Clinical Psychiatry News

A novel, once-nightly formulation of sodium oxybate is safe and effective for treating both subjective and objective symptoms of narcolepsy, new research suggests. Top-line results from the phase 3 REST-ON trial released earlier this year showed that the agent known as FT218 (Avadel Pharmaceuticals) met all three of its coprimary efficacy endpoints at all three doses assessed (6 g, 7.5 g, and 9 g). Patients receiving the drug showed significantly greater improvements on the Maintenance of Wakefulness Test (MWT), the Clinical Global Impression of Improvement (CGI-I), and mean weekly attacks of cataplexy, compared with those who received placebo.

The new analyses, which focused on key secondary outcomes, showed that all three doses of the novel agent were associated with significant improvements in sleep quality, refreshing nature of sleep, sleep paralysis, disturbed nocturnal sleep, and scores on the Epworth Sleepiness Scale (ESS).

Principal investigator Michael J. Thorpy, MD, director of the Sleep-Wake Disorders Center at the Montefiore Medical Center, New York, said in a news release that the results represent “the promise of a potential new treatment strategy for physicians and patients.”

“I am particularly impressed by the consistency of results as early as 3 weeks with only a 6-g dose,” he added.

Dr. Thorpy, who is also a professor of neurology at the Albert Einstein College of Medicine, noted that the new formulation will be more convenient for patients. “The advantage of this medication is its once-nightly formulation, so patients don’t need to awaken during the night and can actually have a better night’s sleep,” he said.

Dr. Thorpy presented the study findings at the 2021 annual meeting of the American Academy of Neurology.

FT218 is currently under review by the U.S. Food and Drug Administration, which has set Oct. 15 as the Prescription Drug User Fee Act target date.

Forced awakening

Sodium oxybate was first approved by the FDA in 2002 to treat cataplexy in adults with narcolepsy and was expanded in 2005 to also treat excessive daytime sleepiness (EDS). That formulation is indicated for twice-nightly administration, with the second dose taken 2.5-4 hours after the first.

“The need for forced awakening to take the second dose ... may result in noncompliance, which may lead to reduced efficacy and/or mistimed doses,” the investigators noted.

FT218 is a modified-release version of sodium oxybate. A single 6-g dose of the investigational agent “has shown bioequivalent exposure to twice-nightly immediate-release [sodium oxybate] given as two 3-g doses,” wrote the researchers.

It also currently has Orphan Drug Designation from the FDA for the treatment of narcolepsy.

The randomized, double-blind, placebo-controlled, multicenter REST-ON study was conducted from November 2016 to March 2020 and included patients 16 years or older who had narcolepsy type 1 or type 2.

Patients received the active treatment (n = 107; mean age, 30.9 years; 64.5% women) or placebo (n = 105; mean age, 31.6 years; 71.4% women) according to a four-period forced uptitration dosing schedule of 4.5 g for 1 week, 6 g for 2 weeks, 7.5 g for 5 weeks, and 9 g for 5 weeks.

Secondary outcome measures included the ESS, sleep quality/refreshing nature of sleep on a visual analog scale, sleep paralysis and hypnagogic hallucinations on a sleep symptoms diary, disturbed nocturnal sleep on polysomnographic measures, and number of arousals as defined per the American Academy of Sleep Medicine Score Manual.

Reports of adverse events (AEs) were collected from time of informed consent until 7 days after the last dose received.

Improvement across doses

Results showed that, compared with placebo, improvement in disturbed nocturnal sleep from baseline was significantly greater for the active treatment at 6 g at week 3 (mean between-group difference, –11; P < .001), at 7.5 g at week 8 (mean difference, –17.7; P < .001), and at 9 g at week 13 (mean difference, –22.6; P < .001).

The mean difference between the three doses and placebo for reduction in number of arousals was –11.3 (P < .05), –19.4 (P < .001), and –23.7 (P < .001), respectively. And the 6 g at week 3, 7.5 g at week 8, and 9 g at week 13 doses showed significant (P < .001) improvements versus placebo on the ESS (mean difference, –2.1, –3.2, and –3.9, respectively).

All three doses also showed significant improvement in sleep quality and refreshing nature of sleep (P < .001 for all comparisons), as well as improvement of sleep paralysis (P = .04, P = .02, and P = .04, respectively).

There were no significant differences between FT218 and placebo for improvement in hypnagogic hallucinations. Dr. Thorpy noted that the number of patients with baseline hallucinations “was relatively small,” which may have led to this finding. “Had there been a much larger population with hallucinations, I suspect that we would have seen a statistically significant improvement there as well,” he said.

Generally well tolerated

The investigators noted that FT218 was “generally well tolerated, and the most common adverse reactions were well-known and established sodium oxybate adverse reactions.”

Treatment-related AEs that occurred in more than 2% of the patients receiving FT218 included nausea, dizziness, enuresis, headache, decreased appetite, and vomiting.

Seven serious AEs were reported, including five in those assigned to the active treatment. This included one case each of diabetes inadequate control, paresthesia, perirectal abscess, hypertension, and suicidal ideation. Only the case of suicidal ideation was considered to be a treatment-related AE.

The investigators noted that, although they have not yet delved into subgroup analysis to look for differences among sex, age, or race, they plan to do so in the future.

Overall, the results indicate that “FT218 is an effective agent not only for the major symptoms of sleepiness and cataplexy, but also the quality of sleep at night,” said Dr. Thorpy.

Asked whether he thinks the FDA will approve the drug, he said that it should be “straightforward” because it’s just a different formulation of an already-approved agent. “I very much expect there will not be any problems in this medication being approved,” Dr. Thorpy said.

Benefits ‘sleep architecture’

Commenting on the findings, Logan Schneider, MD, codirector of the Stanford/VA Alzheimer’s Center and clinical assistant professor at the Stanford Sleep Center, Redwood City, Calif., said that the investigators’ focus on these secondary outcomes “was really worthwhile.”

Dr. Schneider, who was not involved in the research, noted that, because the study only included patients with narcolepsy, the results can’t be extrapolated to groups who have other sleep disorders.

Still, “it is worthwhile now to expand beyond the two primary symptoms that are, in my consideration, life threatening: daytime sleepiness and cataplexy. We should also address more of the quality of life and other aspects of narcolepsy, including disturbed nocturnal sleep and sleep quality issues related to that,” he said.

“Being able to address those aspects and say, ‘I have a therapy that clearly helps the multidimensionality of our patients’ is very vindicating,” Dr. Schneider noted.

He was also impressed with the various measures the researchers used, rather than relying just on patient reports, “which are subject to recollection difficulties. This was a nice way to quantify possibly as a diagnostic marker the underlying disruption of sleep, as well as a possible treatment marker to show how well a therapy works.”

“It actually shows a beneficial effect on sleep architecture,” Dr. Schneider said.

The study was funded by Avadel Pharmaceuticals. Dr. Thorpy is a consultant/advisory board member for Avadel, Axsome, Balance Therapeutics, Eisai, Harmony Biosciences, Jazz Pharmaceuticals, NLS Pharmaceuticals, Suven Life Sciences, and Takeda Pharmaceutical. Dr. Schneider reports being an adviser and/or on the speakers’ bureau for similar drugs by Jazz Pharmaceuticals and Harmony Biosciences.

A version of this article first appeared on Medscape.com.

A novel, once-nightly formulation of sodium oxybate is safe and effective for treating both subjective and objective symptoms of narcolepsy, new research suggests. Top-line results from the phase 3 REST-ON trial released earlier this year showed that the agent known as FT218 (Avadel Pharmaceuticals) met all three of its coprimary efficacy endpoints at all three doses assessed (6 g, 7.5 g, and 9 g). Patients receiving the drug showed significantly greater improvements on the Maintenance of Wakefulness Test (MWT), the Clinical Global Impression of Improvement (CGI-I), and mean weekly attacks of cataplexy, compared with those who received placebo.

The new analyses, which focused on key secondary outcomes, showed that all three doses of the novel agent were associated with significant improvements in sleep quality, refreshing nature of sleep, sleep paralysis, disturbed nocturnal sleep, and scores on the Epworth Sleepiness Scale (ESS).

Principal investigator Michael J. Thorpy, MD, director of the Sleep-Wake Disorders Center at the Montefiore Medical Center, New York, said in a news release that the results represent “the promise of a potential new treatment strategy for physicians and patients.”

“I am particularly impressed by the consistency of results as early as 3 weeks with only a 6-g dose,” he added.

Dr. Thorpy, who is also a professor of neurology at the Albert Einstein College of Medicine, noted that the new formulation will be more convenient for patients. “The advantage of this medication is its once-nightly formulation, so patients don’t need to awaken during the night and can actually have a better night’s sleep,” he said.

Dr. Thorpy presented the study findings at the 2021 annual meeting of the American Academy of Neurology.

FT218 is currently under review by the U.S. Food and Drug Administration, which has set Oct. 15 as the Prescription Drug User Fee Act target date.

Forced awakening

Sodium oxybate was first approved by the FDA in 2002 to treat cataplexy in adults with narcolepsy and was expanded in 2005 to also treat excessive daytime sleepiness (EDS). That formulation is indicated for twice-nightly administration, with the second dose taken 2.5-4 hours after the first.

“The need for forced awakening to take the second dose ... may result in noncompliance, which may lead to reduced efficacy and/or mistimed doses,” the investigators noted.

FT218 is a modified-release version of sodium oxybate. A single 6-g dose of the investigational agent “has shown bioequivalent exposure to twice-nightly immediate-release [sodium oxybate] given as two 3-g doses,” wrote the researchers.

It also currently has Orphan Drug Designation from the FDA for the treatment of narcolepsy.

The randomized, double-blind, placebo-controlled, multicenter REST-ON study was conducted from November 2016 to March 2020 and included patients 16 years or older who had narcolepsy type 1 or type 2.

Patients received the active treatment (n = 107; mean age, 30.9 years; 64.5% women) or placebo (n = 105; mean age, 31.6 years; 71.4% women) according to a four-period forced uptitration dosing schedule of 4.5 g for 1 week, 6 g for 2 weeks, 7.5 g for 5 weeks, and 9 g for 5 weeks.

Secondary outcome measures included the ESS, sleep quality/refreshing nature of sleep on a visual analog scale, sleep paralysis and hypnagogic hallucinations on a sleep symptoms diary, disturbed nocturnal sleep on polysomnographic measures, and number of arousals as defined per the American Academy of Sleep Medicine Score Manual.

Reports of adverse events (AEs) were collected from time of informed consent until 7 days after the last dose received.

Improvement across doses

Results showed that, compared with placebo, improvement in disturbed nocturnal sleep from baseline was significantly greater for the active treatment at 6 g at week 3 (mean between-group difference, –11; P < .001), at 7.5 g at week 8 (mean difference, –17.7; P < .001), and at 9 g at week 13 (mean difference, –22.6; P < .001).

The mean difference between the three doses and placebo for reduction in number of arousals was –11.3 (P < .05), –19.4 (P < .001), and –23.7 (P < .001), respectively. And the 6 g at week 3, 7.5 g at week 8, and 9 g at week 13 doses showed significant (P < .001) improvements versus placebo on the ESS (mean difference, –2.1, –3.2, and –3.9, respectively).

All three doses also showed significant improvement in sleep quality and refreshing nature of sleep (P < .001 for all comparisons), as well as improvement of sleep paralysis (P = .04, P = .02, and P = .04, respectively).

There were no significant differences between FT218 and placebo for improvement in hypnagogic hallucinations. Dr. Thorpy noted that the number of patients with baseline hallucinations “was relatively small,” which may have led to this finding. “Had there been a much larger population with hallucinations, I suspect that we would have seen a statistically significant improvement there as well,” he said.

Generally well tolerated

The investigators noted that FT218 was “generally well tolerated, and the most common adverse reactions were well-known and established sodium oxybate adverse reactions.”

Treatment-related AEs that occurred in more than 2% of the patients receiving FT218 included nausea, dizziness, enuresis, headache, decreased appetite, and vomiting.

Seven serious AEs were reported, including five in those assigned to the active treatment. This included one case each of diabetes inadequate control, paresthesia, perirectal abscess, hypertension, and suicidal ideation. Only the case of suicidal ideation was considered to be a treatment-related AE.

The investigators noted that, although they have not yet delved into subgroup analysis to look for differences among sex, age, or race, they plan to do so in the future.

Overall, the results indicate that “FT218 is an effective agent not only for the major symptoms of sleepiness and cataplexy, but also the quality of sleep at night,” said Dr. Thorpy.

Asked whether he thinks the FDA will approve the drug, he said that it should be “straightforward” because it’s just a different formulation of an already-approved agent. “I very much expect there will not be any problems in this medication being approved,” Dr. Thorpy said.

Benefits ‘sleep architecture’

Commenting on the findings, Logan Schneider, MD, codirector of the Stanford/VA Alzheimer’s Center and clinical assistant professor at the Stanford Sleep Center, Redwood City, Calif., said that the investigators’ focus on these secondary outcomes “was really worthwhile.”

Dr. Schneider, who was not involved in the research, noted that, because the study only included patients with narcolepsy, the results can’t be extrapolated to groups who have other sleep disorders.

Still, “it is worthwhile now to expand beyond the two primary symptoms that are, in my consideration, life threatening: daytime sleepiness and cataplexy. We should also address more of the quality of life and other aspects of narcolepsy, including disturbed nocturnal sleep and sleep quality issues related to that,” he said.

“Being able to address those aspects and say, ‘I have a therapy that clearly helps the multidimensionality of our patients’ is very vindicating,” Dr. Schneider noted.

He was also impressed with the various measures the researchers used, rather than relying just on patient reports, “which are subject to recollection difficulties. This was a nice way to quantify possibly as a diagnostic marker the underlying disruption of sleep, as well as a possible treatment marker to show how well a therapy works.”

“It actually shows a beneficial effect on sleep architecture,” Dr. Schneider said.

The study was funded by Avadel Pharmaceuticals. Dr. Thorpy is a consultant/advisory board member for Avadel, Axsome, Balance Therapeutics, Eisai, Harmony Biosciences, Jazz Pharmaceuticals, NLS Pharmaceuticals, Suven Life Sciences, and Takeda Pharmaceutical. Dr. Schneider reports being an adviser and/or on the speakers’ bureau for similar drugs by Jazz Pharmaceuticals and Harmony Biosciences.

A version of this article first appeared on Medscape.com.

A novel, once-nightly formulation of sodium oxybate is safe and effective for treating both subjective and objective symptoms of narcolepsy, new research suggests. Top-line results from the phase 3 REST-ON trial released earlier this year showed that the agent known as FT218 (Avadel Pharmaceuticals) met all three of its coprimary efficacy endpoints at all three doses assessed (6 g, 7.5 g, and 9 g). Patients receiving the drug showed significantly greater improvements on the Maintenance of Wakefulness Test (MWT), the Clinical Global Impression of Improvement (CGI-I), and mean weekly attacks of cataplexy, compared with those who received placebo.

The new analyses, which focused on key secondary outcomes, showed that all three doses of the novel agent were associated with significant improvements in sleep quality, refreshing nature of sleep, sleep paralysis, disturbed nocturnal sleep, and scores on the Epworth Sleepiness Scale (ESS).

Principal investigator Michael J. Thorpy, MD, director of the Sleep-Wake Disorders Center at the Montefiore Medical Center, New York, said in a news release that the results represent “the promise of a potential new treatment strategy for physicians and patients.”

“I am particularly impressed by the consistency of results as early as 3 weeks with only a 6-g dose,” he added.

Dr. Thorpy, who is also a professor of neurology at the Albert Einstein College of Medicine, noted that the new formulation will be more convenient for patients. “The advantage of this medication is its once-nightly formulation, so patients don’t need to awaken during the night and can actually have a better night’s sleep,” he said.

Dr. Thorpy presented the study findings at the 2021 annual meeting of the American Academy of Neurology.

FT218 is currently under review by the U.S. Food and Drug Administration, which has set Oct. 15 as the Prescription Drug User Fee Act target date.

Forced awakening

Sodium oxybate was first approved by the FDA in 2002 to treat cataplexy in adults with narcolepsy and was expanded in 2005 to also treat excessive daytime sleepiness (EDS). That formulation is indicated for twice-nightly administration, with the second dose taken 2.5-4 hours after the first.

“The need for forced awakening to take the second dose ... may result in noncompliance, which may lead to reduced efficacy and/or mistimed doses,” the investigators noted.

FT218 is a modified-release version of sodium oxybate. A single 6-g dose of the investigational agent “has shown bioequivalent exposure to twice-nightly immediate-release [sodium oxybate] given as two 3-g doses,” wrote the researchers.

It also currently has Orphan Drug Designation from the FDA for the treatment of narcolepsy.

The randomized, double-blind, placebo-controlled, multicenter REST-ON study was conducted from November 2016 to March 2020 and included patients 16 years or older who had narcolepsy type 1 or type 2.

Patients received the active treatment (n = 107; mean age, 30.9 years; 64.5% women) or placebo (n = 105; mean age, 31.6 years; 71.4% women) according to a four-period forced uptitration dosing schedule of 4.5 g for 1 week, 6 g for 2 weeks, 7.5 g for 5 weeks, and 9 g for 5 weeks.

Secondary outcome measures included the ESS, sleep quality/refreshing nature of sleep on a visual analog scale, sleep paralysis and hypnagogic hallucinations on a sleep symptoms diary, disturbed nocturnal sleep on polysomnographic measures, and number of arousals as defined per the American Academy of Sleep Medicine Score Manual.

Reports of adverse events (AEs) were collected from time of informed consent until 7 days after the last dose received.

Improvement across doses

Results showed that, compared with placebo, improvement in disturbed nocturnal sleep from baseline was significantly greater for the active treatment at 6 g at week 3 (mean between-group difference, –11; P < .001), at 7.5 g at week 8 (mean difference, –17.7; P < .001), and at 9 g at week 13 (mean difference, –22.6; P < .001).

The mean difference between the three doses and placebo for reduction in number of arousals was –11.3 (P < .05), –19.4 (P < .001), and –23.7 (P < .001), respectively. And the 6 g at week 3, 7.5 g at week 8, and 9 g at week 13 doses showed significant (P < .001) improvements versus placebo on the ESS (mean difference, –2.1, –3.2, and –3.9, respectively).

All three doses also showed significant improvement in sleep quality and refreshing nature of sleep (P < .001 for all comparisons), as well as improvement of sleep paralysis (P = .04, P = .02, and P = .04, respectively).

There were no significant differences between FT218 and placebo for improvement in hypnagogic hallucinations. Dr. Thorpy noted that the number of patients with baseline hallucinations “was relatively small,” which may have led to this finding. “Had there been a much larger population with hallucinations, I suspect that we would have seen a statistically significant improvement there as well,” he said.

Generally well tolerated

The investigators noted that FT218 was “generally well tolerated, and the most common adverse reactions were well-known and established sodium oxybate adverse reactions.”

Treatment-related AEs that occurred in more than 2% of the patients receiving FT218 included nausea, dizziness, enuresis, headache, decreased appetite, and vomiting.

Seven serious AEs were reported, including five in those assigned to the active treatment. This included one case each of diabetes inadequate control, paresthesia, perirectal abscess, hypertension, and suicidal ideation. Only the case of suicidal ideation was considered to be a treatment-related AE.

The investigators noted that, although they have not yet delved into subgroup analysis to look for differences among sex, age, or race, they plan to do so in the future.

Overall, the results indicate that “FT218 is an effective agent not only for the major symptoms of sleepiness and cataplexy, but also the quality of sleep at night,” said Dr. Thorpy.

Asked whether he thinks the FDA will approve the drug, he said that it should be “straightforward” because it’s just a different formulation of an already-approved agent. “I very much expect there will not be any problems in this medication being approved,” Dr. Thorpy said.

Benefits ‘sleep architecture’

Commenting on the findings, Logan Schneider, MD, codirector of the Stanford/VA Alzheimer’s Center and clinical assistant professor at the Stanford Sleep Center, Redwood City, Calif., said that the investigators’ focus on these secondary outcomes “was really worthwhile.”

Dr. Schneider, who was not involved in the research, noted that, because the study only included patients with narcolepsy, the results can’t be extrapolated to groups who have other sleep disorders.

Still, “it is worthwhile now to expand beyond the two primary symptoms that are, in my consideration, life threatening: daytime sleepiness and cataplexy. We should also address more of the quality of life and other aspects of narcolepsy, including disturbed nocturnal sleep and sleep quality issues related to that,” he said.

“Being able to address those aspects and say, ‘I have a therapy that clearly helps the multidimensionality of our patients’ is very vindicating,” Dr. Schneider noted.

He was also impressed with the various measures the researchers used, rather than relying just on patient reports, “which are subject to recollection difficulties. This was a nice way to quantify possibly as a diagnostic marker the underlying disruption of sleep, as well as a possible treatment marker to show how well a therapy works.”

“It actually shows a beneficial effect on sleep architecture,” Dr. Schneider said.

The study was funded by Avadel Pharmaceuticals. Dr. Thorpy is a consultant/advisory board member for Avadel, Axsome, Balance Therapeutics, Eisai, Harmony Biosciences, Jazz Pharmaceuticals, NLS Pharmaceuticals, Suven Life Sciences, and Takeda Pharmaceutical. Dr. Schneider reports being an adviser and/or on the speakers’ bureau for similar drugs by Jazz Pharmaceuticals and Harmony Biosciences.

A version of this article first appeared on Medscape.com.

Motor problems in children may be a harbinger of serious mental illness, new research suggests.

Investigators found that motor abnormalities were twice as common among those who develop psychosis or depression, compared with their counterparts in the general population, suggesting that these abnormalities may help predict vulnerability and provide an opportunity for early intervention.

“We have learned there are motor signs that are measurable in adolescence [that are] more prevalent in these disorders,” said lead investigator Katherine S. F. Damme, PhD, adolescent development and preventive treatment program (ADAPT), Northwestern University, Chicago. 

A core symptom

There has been a lot of interest in the pathophysiology of psychosis and in detecting it early, said Dr. Damme. “It has devastating effects, and early intervention is of great importance,” she added.

However, previous research has typically focused on affect or cognition, rather than on motor signs, despite the fact that motor signs are a “core symptom of both psychosis and depression.”

The prevalence and presentation of motor signs in adolescence, which is a “critical time for identifying these risk markers” because of their proximity to the onset of psychosis, has been understudied, Dr. Damme said.

For their study, the investigators gathered motor function data from the Adolescent Brain Cognitive Development Study (ABCD), which included 10,835 children aged 9-11 years with broad demographic diversity from 21 sites across the United States.

Overall, 27.6% of the children were reported to have least one motor sign; approximately 3% were reported to have two or more motor signs.

The most common of these was dyscoordination, which was endorsed by 19.3% of participants. In addition, 8.8% were reported to have had experienced developmental motor delays, 1.5% had psychomotor agitation, and 0.3% had psychomotor retardation.

The investigators determined that 4.6% of participants met criteria for depression, 2.6% for a psychosis, and 1.8% for comorbid psychosis and depression.

Motor signs were much more common among children with depression, psychosis, or both than among those who did not have these conditions; 45.8% reported having at least one motor sign.

Developmental motor delays and dyscoordination occurred at about the same rate in both patients with depression and those with psychosis. Rates were higher among patients with both of these conditions than among those with either condition alone.

In contrast, psychomotor agitation was more common among patients with depression alone and among those with comorbid depression and psychosis than among patients with psychosis alone. The rate of psychomotor retardation was increased among patients with psychosis alone but was less common among patients with comorbidity than in the healthy control group.

Familial vulnerability

The investigators also assessed participants who had not been diagnosed with a mental illness but who had a family history of depression only (28.9%), a relative with psychosis-like experiences (0.6%), or a family history of both depression and psychosis experiences (1.8%).

Although the effect size was smaller, there was a higher rate of motor signs among participants with a family history of these conditions, Dr. Damme said. “Again, we see that it’s elevated across developmental motor delays and at a similar rate in people who have depression and psychosis.”

In addition, psychomotor agitation was linked to depression with psychosis and depression without it.

Sensorimotor connectivity network data for the cohort indicated there was no main effect of diagnosis on corticostriatal connectivity.

However, more depressive symptoms were related to less connectivity (P = .024). There was a similar finding for psychotic-like experiences. The total number of such experiences related to lower connectivity (P < .001).

During the postpresentation discussion, Ian Kelleher, MD, PhD, honorary clinical lecturer in psychiatry at the Royal College of Surgeons in Ireland, Dublin, said he was “surprised” by the finding that the rate of psychomotor retardation was lower among participants with psychosis and depression.

Dr. Damme noted that some of the motor sign item ratings came by way of a child interview and that some of these item ratings came from the adults in the children’s lives.

She added that she was not entirely sure whether asking an 8- to 11-year-old in a clinical interview whether they are experiencing motor signs “might be the best way to get at motor slowing.”

Subtle features

Commenting on the findings in an interview, Peter F. Liddle, MD, PhD, professor of psychiatry, at the University of Nottingham (England), noted that the “features we’re talking about are pretty subtle.

“What I’ve been wondering about for some time is whether we should be getting video recordings and using machine learning approaches to teach a computer to recognize normal movements vs abnormal movements, and particularly facial expression,” said Dr. Liddle, who was not involved with the research.

He called the current study “interesting” but noted several factors that affect the potential utility of the findings in predicting outcomes.

First, they “may not be very good for distinguishing schizophrenia from mood disorders; but if the question is simply determining which young person might go on to develop a significant mental disorder, then it may be useful,” Dr. Liddle said.

He endorsed the investigators’ conclusion that motor abnormalities may be a transdiagnostic marker. Beyond that, they may be “more useful as a predictor of the likely long-term severity, but that’s my own hypothesis based on my work,” he added.

Another question concerns the sensitivity of motor abnormalities as a predictive marker. With the rate of the abnormalities identified in those who developed psychosis and depression about double the rate in the overall population, “it sounds like those assessors were fairly sensitive. … but not all that specific,” said Dr. Liddle.

A third issue relates to treatment. “By the time people get sent to a psychiatrist for assessment for possible impending psychotic illness, they’ve often already had medication,” typically an antidepressant or antipsychotic.

“It’s very well established that dopamine-blocking antipsychotics produce hypokinesia and also dyskinesia,” which could then become a confounding factor, Dr. Liddle said.

The study was funded by grants from the National Institute of Mental Health. The study authors and Dr. Liddle have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Motor problems in children may be a harbinger of serious mental illness, new research suggests.

Investigators found that motor abnormalities were twice as common among those who develop psychosis or depression, compared with their counterparts in the general population, suggesting that these abnormalities may help predict vulnerability and provide an opportunity for early intervention.

“We have learned there are motor signs that are measurable in adolescence [that are] more prevalent in these disorders,” said lead investigator Katherine S. F. Damme, PhD, adolescent development and preventive treatment program (ADAPT), Northwestern University, Chicago. 

A core symptom

There has been a lot of interest in the pathophysiology of psychosis and in detecting it early, said Dr. Damme. “It has devastating effects, and early intervention is of great importance,” she added.

However, previous research has typically focused on affect or cognition, rather than on motor signs, despite the fact that motor signs are a “core symptom of both psychosis and depression.”

The prevalence and presentation of motor signs in adolescence, which is a “critical time for identifying these risk markers” because of their proximity to the onset of psychosis, has been understudied, Dr. Damme said.

For their study, the investigators gathered motor function data from the Adolescent Brain Cognitive Development Study (ABCD), which included 10,835 children aged 9-11 years with broad demographic diversity from 21 sites across the United States.

Overall, 27.6% of the children were reported to have least one motor sign; approximately 3% were reported to have two or more motor signs.

The most common of these was dyscoordination, which was endorsed by 19.3% of participants. In addition, 8.8% were reported to have had experienced developmental motor delays, 1.5% had psychomotor agitation, and 0.3% had psychomotor retardation.

The investigators determined that 4.6% of participants met criteria for depression, 2.6% for a psychosis, and 1.8% for comorbid psychosis and depression.

Motor signs were much more common among children with depression, psychosis, or both than among those who did not have these conditions; 45.8% reported having at least one motor sign.

Developmental motor delays and dyscoordination occurred at about the same rate in both patients with depression and those with psychosis. Rates were higher among patients with both of these conditions than among those with either condition alone.

In contrast, psychomotor agitation was more common among patients with depression alone and among those with comorbid depression and psychosis than among patients with psychosis alone. The rate of psychomotor retardation was increased among patients with psychosis alone but was less common among patients with comorbidity than in the healthy control group.

Familial vulnerability

The investigators also assessed participants who had not been diagnosed with a mental illness but who had a family history of depression only (28.9%), a relative with psychosis-like experiences (0.6%), or a family history of both depression and psychosis experiences (1.8%).

Although the effect size was smaller, there was a higher rate of motor signs among participants with a family history of these conditions, Dr. Damme said. “Again, we see that it’s elevated across developmental motor delays and at a similar rate in people who have depression and psychosis.”

In addition, psychomotor agitation was linked to depression with psychosis and depression without it.

Sensorimotor connectivity network data for the cohort indicated there was no main effect of diagnosis on corticostriatal connectivity.

However, more depressive symptoms were related to less connectivity (P = .024). There was a similar finding for psychotic-like experiences. The total number of such experiences related to lower connectivity (P < .001).

During the postpresentation discussion, Ian Kelleher, MD, PhD, honorary clinical lecturer in psychiatry at the Royal College of Surgeons in Ireland, Dublin, said he was “surprised” by the finding that the rate of psychomotor retardation was lower among participants with psychosis and depression.

Dr. Damme noted that some of the motor sign item ratings came by way of a child interview and that some of these item ratings came from the adults in the children’s lives.

She added that she was not entirely sure whether asking an 8- to 11-year-old in a clinical interview whether they are experiencing motor signs “might be the best way to get at motor slowing.”

Subtle features

Commenting on the findings in an interview, Peter F. Liddle, MD, PhD, professor of psychiatry, at the University of Nottingham (England), noted that the “features we’re talking about are pretty subtle.

“What I’ve been wondering about for some time is whether we should be getting video recordings and using machine learning approaches to teach a computer to recognize normal movements vs abnormal movements, and particularly facial expression,” said Dr. Liddle, who was not involved with the research.

He called the current study “interesting” but noted several factors that affect the potential utility of the findings in predicting outcomes.

First, they “may not be very good for distinguishing schizophrenia from mood disorders; but if the question is simply determining which young person might go on to develop a significant mental disorder, then it may be useful,” Dr. Liddle said.

He endorsed the investigators’ conclusion that motor abnormalities may be a transdiagnostic marker. Beyond that, they may be “more useful as a predictor of the likely long-term severity, but that’s my own hypothesis based on my work,” he added.

Another question concerns the sensitivity of motor abnormalities as a predictive marker. With the rate of the abnormalities identified in those who developed psychosis and depression about double the rate in the overall population, “it sounds like those assessors were fairly sensitive. … but not all that specific,” said Dr. Liddle.

A third issue relates to treatment. “By the time people get sent to a psychiatrist for assessment for possible impending psychotic illness, they’ve often already had medication,” typically an antidepressant or antipsychotic.

“It’s very well established that dopamine-blocking antipsychotics produce hypokinesia and also dyskinesia,” which could then become a confounding factor, Dr. Liddle said.

The study was funded by grants from the National Institute of Mental Health. The study authors and Dr. Liddle have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Motor problems in children may be a harbinger of serious mental illness, new research suggests.

Investigators found that motor abnormalities were twice as common among those who develop psychosis or depression, compared with their counterparts in the general population, suggesting that these abnormalities may help predict vulnerability and provide an opportunity for early intervention.

“We have learned there are motor signs that are measurable in adolescence [that are] more prevalent in these disorders,” said lead investigator Katherine S. F. Damme, PhD, adolescent development and preventive treatment program (ADAPT), Northwestern University, Chicago. 

A core symptom

There has been a lot of interest in the pathophysiology of psychosis and in detecting it early, said Dr. Damme. “It has devastating effects, and early intervention is of great importance,” she added.

However, previous research has typically focused on affect or cognition, rather than on motor signs, despite the fact that motor signs are a “core symptom of both psychosis and depression.”

The prevalence and presentation of motor signs in adolescence, which is a “critical time for identifying these risk markers” because of their proximity to the onset of psychosis, has been understudied, Dr. Damme said.

For their study, the investigators gathered motor function data from the Adolescent Brain Cognitive Development Study (ABCD), which included 10,835 children aged 9-11 years with broad demographic diversity from 21 sites across the United States.

Overall, 27.6% of the children were reported to have least one motor sign; approximately 3% were reported to have two or more motor signs.

The most common of these was dyscoordination, which was endorsed by 19.3% of participants. In addition, 8.8% were reported to have had experienced developmental motor delays, 1.5% had psychomotor agitation, and 0.3% had psychomotor retardation.

The investigators determined that 4.6% of participants met criteria for depression, 2.6% for a psychosis, and 1.8% for comorbid psychosis and depression.

Motor signs were much more common among children with depression, psychosis, or both than among those who did not have these conditions; 45.8% reported having at least one motor sign.

Developmental motor delays and dyscoordination occurred at about the same rate in both patients with depression and those with psychosis. Rates were higher among patients with both of these conditions than among those with either condition alone.

In contrast, psychomotor agitation was more common among patients with depression alone and among those with comorbid depression and psychosis than among patients with psychosis alone. The rate of psychomotor retardation was increased among patients with psychosis alone but was less common among patients with comorbidity than in the healthy control group.

Familial vulnerability

The investigators also assessed participants who had not been diagnosed with a mental illness but who had a family history of depression only (28.9%), a relative with psychosis-like experiences (0.6%), or a family history of both depression and psychosis experiences (1.8%).

Although the effect size was smaller, there was a higher rate of motor signs among participants with a family history of these conditions, Dr. Damme said. “Again, we see that it’s elevated across developmental motor delays and at a similar rate in people who have depression and psychosis.”

In addition, psychomotor agitation was linked to depression with psychosis and depression without it.

Sensorimotor connectivity network data for the cohort indicated there was no main effect of diagnosis on corticostriatal connectivity.

However, more depressive symptoms were related to less connectivity (P = .024). There was a similar finding for psychotic-like experiences. The total number of such experiences related to lower connectivity (P < .001).

During the postpresentation discussion, Ian Kelleher, MD, PhD, honorary clinical lecturer in psychiatry at the Royal College of Surgeons in Ireland, Dublin, said he was “surprised” by the finding that the rate of psychomotor retardation was lower among participants with psychosis and depression.

Dr. Damme noted that some of the motor sign item ratings came by way of a child interview and that some of these item ratings came from the adults in the children’s lives.

She added that she was not entirely sure whether asking an 8- to 11-year-old in a clinical interview whether they are experiencing motor signs “might be the best way to get at motor slowing.”

Subtle features

Commenting on the findings in an interview, Peter F. Liddle, MD, PhD, professor of psychiatry, at the University of Nottingham (England), noted that the “features we’re talking about are pretty subtle.

“What I’ve been wondering about for some time is whether we should be getting video recordings and using machine learning approaches to teach a computer to recognize normal movements vs abnormal movements, and particularly facial expression,” said Dr. Liddle, who was not involved with the research.

He called the current study “interesting” but noted several factors that affect the potential utility of the findings in predicting outcomes.

First, they “may not be very good for distinguishing schizophrenia from mood disorders; but if the question is simply determining which young person might go on to develop a significant mental disorder, then it may be useful,” Dr. Liddle said.

He endorsed the investigators’ conclusion that motor abnormalities may be a transdiagnostic marker. Beyond that, they may be “more useful as a predictor of the likely long-term severity, but that’s my own hypothesis based on my work,” he added.

Another question concerns the sensitivity of motor abnormalities as a predictive marker. With the rate of the abnormalities identified in those who developed psychosis and depression about double the rate in the overall population, “it sounds like those assessors were fairly sensitive. … but not all that specific,” said Dr. Liddle.

A third issue relates to treatment. “By the time people get sent to a psychiatrist for assessment for possible impending psychotic illness, they’ve often already had medication,” typically an antidepressant or antipsychotic.

“It’s very well established that dopamine-blocking antipsychotics produce hypokinesia and also dyskinesia,” which could then become a confounding factor, Dr. Liddle said.

The study was funded by grants from the National Institute of Mental Health. The study authors and Dr. Liddle have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Social and economic disparities are linked to an increased risk for psychosis in Black and Latino communities, new research shows.

Results of a literature review of social and economic disparities in mental illness suggest that “structural racism” contributes to social and environmental conditions that affect psychosis risk.

“Black and Latino people suffer disproportionately from psychosis risk factors, at the neighborhood level and at the individual level, in large part as a result of structural racism,” study investigator Deidre M. Anglin, PhD, associate professor, department of psychology, City College of New York (N.Y.), told reporters attending a press briefing.

The social environment, which, for minorities, involves disadvantage and discrimination, may account for this increased psychosis risk, perhaps even more so than genetics, she said. Structural racism “is a critical public health threat,” Dr. Anglin added.

The findings were presented at the virtual American Psychiatric Association annual meeting and were simultaneously published online May 3 in The American Journal of Psychiatry.
 

Perpetual disadvantage

Dr. Anglin and colleagues examined U.S.-based evidence connecting characteristics of social environments with outcomes across the psychosis continuum – from psychotic experiences to schizophrenia.

Citing numerous studies, the researchers highlighted three key areas that reflect social and environmental conditions that may affect psychosis risk, and that disproportionately affect minorities. These were neighborhood factors, trauma in a U.S. context, and racial disparities during the prenatal and perinatal periods.

The data that were related to neighborhoods revealed “just how much racism has historically structured U.S. neighborhoods in ways that generationally perpetuate disadvantage for racially minoritized communities,” said Dr. Anglin.

“This happens through inequitable access to resources, such as health care, clean air, education, [and] employment, but also in terms of disproportionate exposure to environmental toxins and stressors,” she said.

These neighborhood factors are associated with cumulative stress that may be linked to heightened risk for psychosis, the investigators noted.

U.S. studies show that rates of adverse childhood experiences, such as abuse and emotional and physical neglect, are higher among racial and ethnic minorities.

Police victimization and gun violence disproportionately affect racial minorities and create what the investigators call “a unique type of collective trauma” in the United States. They note that Black men have a 1 in 1,000 chance of being victims of lethal force by police over their lifetimes. By comparison, White men have a 39 in 100,000 chance.

One study of a diverse sample from four large U.S. urban centers showed that those who self-reported different types of police victimization were more likely to report psychotic experiences. Another study showed that greater exposure to gun violence fatalities, regardless of police involvement, was positively associated with psychotic experiences.
 

Obstetric complications

A variety of obstetric complications, including infection, maternal inflammation, and stress, have been associated with increased risk for psychotic disorders in U.S. samples.

“What we saw emerge from the literature is that Black women in the U.S. are at substantially increased risk for many of these obstetrical complications compared to White women, and this is not necessarily explained by socioeconomic status,” said Dr. Anglin.

Neighborhood- and individual-level factors appear to affect the disparity in these outcomes. A recent study revealed that exposure to environmental contaminants such as air pollution is associated with higher rates of preterm birth and low birth weight differentially in Black mothers compared with other mothers, “possibly as a result of an interaction between prenatal stress and contaminants,” the investigators noted.

Research also indicates that Black women are more likely to have lower levels of cortisol during the second trimester of pregnancy compared with women of other racial and ethnic groups. Cortisol is essential for fetal growth. Evidence links lower cortisol levels in later stages of pregnancy with decreased fetal growth in individuals who develop schizophrenia.

Black women have higher levels of certain stress biomarkers, including inflammatory C-reactive protein and adrenocorticotropic hormone, in mid- to late pregnancy, compared with White women of the same socioeconomic status.

Such findings “highlight a complex picture” involving maternal cortisol levels and other stress biomarkers, “potentially leading to poor birth outcomes and subsequent risk for psychotic disorders in adulthood,” the investigators noted.

The researchers call for the dismantling of structural racism and the social policies and norms it shapes. They also recommend changes in health care policy and in the approach to early intervention for psychosis among Black and other racially-minoritized groups.

“Altogether, the current evidence suggests the need to identify, address, and tackle the social determinants deeply ingrained in U.S. society, in tandem with empowering the most marginalized communities,” the researchers wrote.

“We recommend that the field of psychiatry devote considerably more effort to addressing structural racism and social determinants of psychosis in funding priorities, training, and intervention development,” they added.

Dr. Anglin suggests that mental health providers use what she called a “cultural formulation interview” that takes a person’s environmental and social context into consideration. Studies show that incorporating this into clinical practice helps reduce misdiagnosis of mental illness in Black populations, she said.
 

Call to action

Commenting on the findings in an interview, Ned H. Kalin, MD, editor of The American Journal of Psychiatry and professor and chair of the department of psychiatry, University of Wisconsin, Madison, said the study was well done and serves as a “call to action” to address the impact of structural racism on mental health issues and psychiatric diseases.

The article highlights the need for “collecting better data” on structural racism, said Dr. Kalin. “We know it’s a big issue, but we can’t even quantitate it, so we need some fundamental measures to use as a benchmark as we move forward, as we try to make change.”

He noted that racism “is so embedded in one’s experience and in our society that we sort of don’t even think about it as a trauma.”

In psychiatry, for example, trauma is often thought of as a loss or a traumatic event. “We don’t typically think of trauma as an experience that pervades one’s entire life,” but that needs to change, he said. “At the individual level and in the doctor’s office, being sensitive to and aware of these issues is absolutely critical.”

Dr. Anglin and Dr. Kalin have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Social and economic disparities are linked to an increased risk for psychosis in Black and Latino communities, new research shows.

Results of a literature review of social and economic disparities in mental illness suggest that “structural racism” contributes to social and environmental conditions that affect psychosis risk.

“Black and Latino people suffer disproportionately from psychosis risk factors, at the neighborhood level and at the individual level, in large part as a result of structural racism,” study investigator Deidre M. Anglin, PhD, associate professor, department of psychology, City College of New York (N.Y.), told reporters attending a press briefing.

The social environment, which, for minorities, involves disadvantage and discrimination, may account for this increased psychosis risk, perhaps even more so than genetics, she said. Structural racism “is a critical public health threat,” Dr. Anglin added.

The findings were presented at the virtual American Psychiatric Association annual meeting and were simultaneously published online May 3 in The American Journal of Psychiatry.
 

Perpetual disadvantage

Dr. Anglin and colleagues examined U.S.-based evidence connecting characteristics of social environments with outcomes across the psychosis continuum – from psychotic experiences to schizophrenia.

Citing numerous studies, the researchers highlighted three key areas that reflect social and environmental conditions that may affect psychosis risk, and that disproportionately affect minorities. These were neighborhood factors, trauma in a U.S. context, and racial disparities during the prenatal and perinatal periods.

The data that were related to neighborhoods revealed “just how much racism has historically structured U.S. neighborhoods in ways that generationally perpetuate disadvantage for racially minoritized communities,” said Dr. Anglin.

“This happens through inequitable access to resources, such as health care, clean air, education, [and] employment, but also in terms of disproportionate exposure to environmental toxins and stressors,” she said.

These neighborhood factors are associated with cumulative stress that may be linked to heightened risk for psychosis, the investigators noted.

U.S. studies show that rates of adverse childhood experiences, such as abuse and emotional and physical neglect, are higher among racial and ethnic minorities.

Police victimization and gun violence disproportionately affect racial minorities and create what the investigators call “a unique type of collective trauma” in the United States. They note that Black men have a 1 in 1,000 chance of being victims of lethal force by police over their lifetimes. By comparison, White men have a 39 in 100,000 chance.

One study of a diverse sample from four large U.S. urban centers showed that those who self-reported different types of police victimization were more likely to report psychotic experiences. Another study showed that greater exposure to gun violence fatalities, regardless of police involvement, was positively associated with psychotic experiences.
 

Obstetric complications

A variety of obstetric complications, including infection, maternal inflammation, and stress, have been associated with increased risk for psychotic disorders in U.S. samples.

“What we saw emerge from the literature is that Black women in the U.S. are at substantially increased risk for many of these obstetrical complications compared to White women, and this is not necessarily explained by socioeconomic status,” said Dr. Anglin.

Neighborhood- and individual-level factors appear to affect the disparity in these outcomes. A recent study revealed that exposure to environmental contaminants such as air pollution is associated with higher rates of preterm birth and low birth weight differentially in Black mothers compared with other mothers, “possibly as a result of an interaction between prenatal stress and contaminants,” the investigators noted.

Research also indicates that Black women are more likely to have lower levels of cortisol during the second trimester of pregnancy compared with women of other racial and ethnic groups. Cortisol is essential for fetal growth. Evidence links lower cortisol levels in later stages of pregnancy with decreased fetal growth in individuals who develop schizophrenia.

Black women have higher levels of certain stress biomarkers, including inflammatory C-reactive protein and adrenocorticotropic hormone, in mid- to late pregnancy, compared with White women of the same socioeconomic status.

Such findings “highlight a complex picture” involving maternal cortisol levels and other stress biomarkers, “potentially leading to poor birth outcomes and subsequent risk for psychotic disorders in adulthood,” the investigators noted.

The researchers call for the dismantling of structural racism and the social policies and norms it shapes. They also recommend changes in health care policy and in the approach to early intervention for psychosis among Black and other racially-minoritized groups.

“Altogether, the current evidence suggests the need to identify, address, and tackle the social determinants deeply ingrained in U.S. society, in tandem with empowering the most marginalized communities,” the researchers wrote.

“We recommend that the field of psychiatry devote considerably more effort to addressing structural racism and social determinants of psychosis in funding priorities, training, and intervention development,” they added.

Dr. Anglin suggests that mental health providers use what she called a “cultural formulation interview” that takes a person’s environmental and social context into consideration. Studies show that incorporating this into clinical practice helps reduce misdiagnosis of mental illness in Black populations, she said.
 

Call to action

Commenting on the findings in an interview, Ned H. Kalin, MD, editor of The American Journal of Psychiatry and professor and chair of the department of psychiatry, University of Wisconsin, Madison, said the study was well done and serves as a “call to action” to address the impact of structural racism on mental health issues and psychiatric diseases.

The article highlights the need for “collecting better data” on structural racism, said Dr. Kalin. “We know it’s a big issue, but we can’t even quantitate it, so we need some fundamental measures to use as a benchmark as we move forward, as we try to make change.”

He noted that racism “is so embedded in one’s experience and in our society that we sort of don’t even think about it as a trauma.”

In psychiatry, for example, trauma is often thought of as a loss or a traumatic event. “We don’t typically think of trauma as an experience that pervades one’s entire life,” but that needs to change, he said. “At the individual level and in the doctor’s office, being sensitive to and aware of these issues is absolutely critical.”

Dr. Anglin and Dr. Kalin have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Social and economic disparities are linked to an increased risk for psychosis in Black and Latino communities, new research shows.

Results of a literature review of social and economic disparities in mental illness suggest that “structural racism” contributes to social and environmental conditions that affect psychosis risk.

“Black and Latino people suffer disproportionately from psychosis risk factors, at the neighborhood level and at the individual level, in large part as a result of structural racism,” study investigator Deidre M. Anglin, PhD, associate professor, department of psychology, City College of New York (N.Y.), told reporters attending a press briefing.

The social environment, which, for minorities, involves disadvantage and discrimination, may account for this increased psychosis risk, perhaps even more so than genetics, she said. Structural racism “is a critical public health threat,” Dr. Anglin added.

The findings were presented at the virtual American Psychiatric Association annual meeting and were simultaneously published online May 3 in The American Journal of Psychiatry.
 

Perpetual disadvantage

Dr. Anglin and colleagues examined U.S.-based evidence connecting characteristics of social environments with outcomes across the psychosis continuum – from psychotic experiences to schizophrenia.

Citing numerous studies, the researchers highlighted three key areas that reflect social and environmental conditions that may affect psychosis risk, and that disproportionately affect minorities. These were neighborhood factors, trauma in a U.S. context, and racial disparities during the prenatal and perinatal periods.

The data that were related to neighborhoods revealed “just how much racism has historically structured U.S. neighborhoods in ways that generationally perpetuate disadvantage for racially minoritized communities,” said Dr. Anglin.

“This happens through inequitable access to resources, such as health care, clean air, education, [and] employment, but also in terms of disproportionate exposure to environmental toxins and stressors,” she said.

These neighborhood factors are associated with cumulative stress that may be linked to heightened risk for psychosis, the investigators noted.

U.S. studies show that rates of adverse childhood experiences, such as abuse and emotional and physical neglect, are higher among racial and ethnic minorities.

Police victimization and gun violence disproportionately affect racial minorities and create what the investigators call “a unique type of collective trauma” in the United States. They note that Black men have a 1 in 1,000 chance of being victims of lethal force by police over their lifetimes. By comparison, White men have a 39 in 100,000 chance.

One study of a diverse sample from four large U.S. urban centers showed that those who self-reported different types of police victimization were more likely to report psychotic experiences. Another study showed that greater exposure to gun violence fatalities, regardless of police involvement, was positively associated with psychotic experiences.
 

Obstetric complications

A variety of obstetric complications, including infection, maternal inflammation, and stress, have been associated with increased risk for psychotic disorders in U.S. samples.

“What we saw emerge from the literature is that Black women in the U.S. are at substantially increased risk for many of these obstetrical complications compared to White women, and this is not necessarily explained by socioeconomic status,” said Dr. Anglin.

Neighborhood- and individual-level factors appear to affect the disparity in these outcomes. A recent study revealed that exposure to environmental contaminants such as air pollution is associated with higher rates of preterm birth and low birth weight differentially in Black mothers compared with other mothers, “possibly as a result of an interaction between prenatal stress and contaminants,” the investigators noted.

Research also indicates that Black women are more likely to have lower levels of cortisol during the second trimester of pregnancy compared with women of other racial and ethnic groups. Cortisol is essential for fetal growth. Evidence links lower cortisol levels in later stages of pregnancy with decreased fetal growth in individuals who develop schizophrenia.

Black women have higher levels of certain stress biomarkers, including inflammatory C-reactive protein and adrenocorticotropic hormone, in mid- to late pregnancy, compared with White women of the same socioeconomic status.

Such findings “highlight a complex picture” involving maternal cortisol levels and other stress biomarkers, “potentially leading to poor birth outcomes and subsequent risk for psychotic disorders in adulthood,” the investigators noted.

The researchers call for the dismantling of structural racism and the social policies and norms it shapes. They also recommend changes in health care policy and in the approach to early intervention for psychosis among Black and other racially-minoritized groups.

“Altogether, the current evidence suggests the need to identify, address, and tackle the social determinants deeply ingrained in U.S. society, in tandem with empowering the most marginalized communities,” the researchers wrote.

“We recommend that the field of psychiatry devote considerably more effort to addressing structural racism and social determinants of psychosis in funding priorities, training, and intervention development,” they added.

Dr. Anglin suggests that mental health providers use what she called a “cultural formulation interview” that takes a person’s environmental and social context into consideration. Studies show that incorporating this into clinical practice helps reduce misdiagnosis of mental illness in Black populations, she said.
 

Call to action

Commenting on the findings in an interview, Ned H. Kalin, MD, editor of The American Journal of Psychiatry and professor and chair of the department of psychiatry, University of Wisconsin, Madison, said the study was well done and serves as a “call to action” to address the impact of structural racism on mental health issues and psychiatric diseases.

The article highlights the need for “collecting better data” on structural racism, said Dr. Kalin. “We know it’s a big issue, but we can’t even quantitate it, so we need some fundamental measures to use as a benchmark as we move forward, as we try to make change.”

He noted that racism “is so embedded in one’s experience and in our society that we sort of don’t even think about it as a trauma.”

In psychiatry, for example, trauma is often thought of as a loss or a traumatic event. “We don’t typically think of trauma as an experience that pervades one’s entire life,” but that needs to change, he said. “At the individual level and in the doctor’s office, being sensitive to and aware of these issues is absolutely critical.”

Dr. Anglin and Dr. Kalin have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Editor in Chief of this news organization Eric Topol, MD, founder and director of the Scripps Research Translational Institute in La Jolla, Calif., and professor of molecular medicine, has been closely following COVID-19 data since the pandemic began. He spoke with writer Miriam E. Tucker about the latest on SARS-CoV-2 variants and their impact on vaccine efficacy. The conversation serves as a follow-up to his April 13, 2021, New York Times opinion piece, in which he advised readers that “all variants are innocent until proven guilty.”

You have expressed overall confidence in the efficacy of the vaccines thus far despite the emergence of variants, with some caveats. How do you see the current situation?

The Centers for Disease Control and Prevention has designated five “variants of concern,” but only three of them are real concerns – B.1.1.7, first detected in the United Kingdom; P.1, in Brazil and Japan; and B.1.351, in South Africa. Yet, all three are susceptible to our current vaccines.

The U.K. B.1.1.7 is the worst variant of all because it’s hypertransmissible, so I call it a “superspreader strain.” It also causes more severe illness independent of the spread, so it’s a double whammy. It’s clear that it also causes more deaths. The only arguable point is whether it’s 30% or 50% more deaths, but regardless, it’s more lethal and more transmissible.

The B.1.1.7 is going to be the dominant strain worldwide. It could develop new mutations within it that could come back to haunt us. We must keep watch.

But for now, it’s fully responsive to all the vaccines, which is great because if we didn’t have them, we wouldn’t have gotten through this U.S. pandemic like we have, and neither would Israel and the United Kingdom and other countries that have been able to get out of the crisis. We met the enemy and put it in check.

As for the South Africa variant of concern, B.1.351, we just got some encouraging news showing that it›s very responsive to the Pfizer/BioNTech mRNA vaccine in large numbers of people. The study was conducted in Qatar following that country’s mass immunization campaign in which a total of 385,853 people had received at least one vaccine dose and 265,410 had completed the two doses as of March 31, 2021.

At 2 weeks past the second dose, the vaccine was 75% effective at preventing any documented infection with the B.1.351 variant and 89.5% effective against B.1.1.7. The vaccine’s effectiveness against severe, critical, or fatal COVID-19 was greater than 97.4% for all circulating strains in Qatar, where B.1.1.7 and B.1.351 are most prominent.

We also know that B.1.351 is very responsive to the Johnson & Johnson vaccine and the Novavax [vaccine in development] to a lesser degree. It is the most immune-evading variant we’ve seen thus far, with the highest likelihood of providing some vaccine resistance, yet not enough to interfere with vaccination campaigns. So that’s great news.

The caveats here are that you definitely need two doses of the mRNA vaccines to combat the B.1.351 variant. Also, the AstraZeneca vaccine failed to prevent it in South Africa. However, that study was hard to judge because it was underpowered for number of people with mild infections. So, it didn’t look as if it had any efficacy, but maybe it would if tested in a real trial.

The P.1 (Brazil) variant is the second-highest concern after B.1.1.7 because it’s the only one in the United States that’s still headed up. It seems to be competing a bit with B.1.1.7 here. We know it was associated with the crisis in Brazil, in Chile, and some other South American countries. It has some immune escape, but not as bad as B.1.351. It also appears to have somewhat greater transmissibility but not as much as B.1.1.7.

With P.1, we just don’t know enough yet. It was difficult to assess in Brazil because they were in the midst of a catastrophe – like India is now – and you don’t know how much of it is dragged by the catastrophe vs driving it.

We have to respond to P.1 carefully. There are some good data that it does respond to the Chinese vaccine Sinovac and the AstraZeneca vaccine, and it appears to respond to the others as well, based on serum studies. So it doesn’t look like vaccines will be the worry with this variant. Rather, it could be competing with B.1.1.7 and could lead to breakthrough infections in vaccinated people or reinfections in unvaccinated people who had COVID-19. We need several more weeks to sort it out.

Although the B.1.427 and B.1.429 variants initially seen in California remain on the CDC’s concern list, I’m not worried about them.
 

You mentioned the current COVID-19 crisis in India, where a new variant has been described as a “double mutant,” but on Twitter you called it a “scariant.” Why?

First of all, the B.1.617 variant isn’t a double mutant. It has 15 mutations. It’s a stupid term, focusing on two mutations which largely have been put aside as to concern. One of them is the L452R, which is the same as one of the California variants, and that hasn’t proved to be particularly serious or concerning. The other is the 484Q, and it’s not clear whether that has any function.

The B.1.617 is not the driver of the catastrophe in India. It may be contributing a small amount, but it has been overhyped as the double mutant that’s causing it all. Adding to that are what I call “scariant” headlines here in the United States when a few cases of that variant have been seen.

I coined the term scariant in early February because it was a pretty clear trend. People don’t know what variants are. They know a little bit about mutations but not variants, and they’re scared. A few variants are concerning, but we keep learning more and more things to decrease the concern. That’s why I wrote the New York Times op-ed, to try to provide some reassurance, since there’s such paranoia.
 

Do you think booster vaccinations will be necessary? If so, will those be of the original vaccines or new ones that incorporate the variants?

As we go forward, there’s still potential for new variants that we haven’t seen yet that combine the worst of all features – transmissibility and immune evasion – especially since we have a world where COVID-19 is unchecked. So, we’re not out of it yet, but at least for the moment, we have vaccines that are capable of protecting against all variants.

In most people, the immune response against SARS-CoV-2 is very durable and strong and may well last for years. With the most closely related SARS-CoV-1, people still had immune responses up to 18 years later. However, some people will have less robust vaccine responses, including the elderly and the immunocompromised. If they don’t have great responses to the vaccine to start with, over time they’re likely to become more vulnerable, especially if they’re exposed to the variants with some degree of immune evasion.

I think we need to study these individuals post vaccination. A lot of people fit into those categories, including seniors, people being treated for cancer or autoimmune conditions, or post organ transplant. We could set up a prospective study to see whether they develop symptomatic COVID-19 and if so, from what – the original strain, B.1.1.7, or the newer variants.

That’s where I think booster shots may be needed. They may not be necessary across the board, but perhaps just in these special subgroups.

All of the current vaccines can be tweaked to include new variants, but the need for that is uncertain as of now. Moderna is working on a so-called bivalent vaccine that includes the original SARS-CoV-2 strain plus the B.1.351 variant, but it isn’t clear that that’s going to be necessary.

Currently, at least 200 COVID-19 vaccines are in development. There will be vaccines you can inhale, room temperature mRNA vaccines, and potentially even oral vaccines.

In the near future, Novavax is close, and there will likely be a two-dose Johnson & Johnson version that has the same potency as the mRNA vaccines. There are a lot of moving parts here.

There may be a step down in efficacy from mRNA to the others, though, and that shouldn’t be discounted. All of the available vaccines so far protect very well against severe disease and death, but some are less effective against mild to moderate infections, which may then lead to long COVID. We don’t yet know whether those who get mild infection post vaccination can still get long COVID.
 

What do you think it will take to achieve herd immunity?

I prefer the term “containment.” It’s quantitative. If you get to an infection rate of less than 1 in 100,000 people, as they’ve done in Israel, with 0.8 per 100,000, then you have the virus in check, and there will be very little spread when it’s at that controlled rate, with no outbreaks. The United States is currently at about 15 per 100,000. California is at 4. That still has to get lower.

It will be a challenge to get to President Biden’s goal of having 70% of U.S. adults given at least one dose by July 4. We’re now at about 57%. To get that next 13% of adults is going to take an all-out effort: mobile units, going to homes, making it ultraconvenient, education for people with safety concerns, incentivization, and days off.

We also need to get employers, universities, and health systems to get to the mandatory level. We haven’t done that yet. Some universities have mandated it for students, faculty, and staff. We need it in more health care systems. Right now, we only have a couple. We mandate flu shots, and flu is nothing, compared with COVID-19. And the COVID-19 vaccine is far more efficacious – flu shots are 40% efficacious, while these are 95%. COVID-19 is a tenfold more lethal and serious disease, and much more spreadable.

People are using the lack of full licensure by the Food and Drug Administration – as opposed to emergency use authorization – as an excuse not to get vaccinated. A biologics license application takes time to approve. Meanwhile, we have hundreds of millions of doses that have been well tolerated and incredibly effective.

Another aspect to consider regarding containment is that about 110 million Americans have already had COVID-19, even though only about 30 million cases have been confirmed. Most of these people have immune protection, although it’s not as good as if they have one vaccine dose. But they have enough protection to be part of the story here of the wall against COVID-19 and will help us get through this.

That’s a silver lining of having an unchecked epidemic for the entire year of 2020. The good part is that’s helping to get us to achieve an incredible level of containment when we haven’t even been close. Right now, we’re as good as the country has been in the pandemic, but we still have a long gap to get down to that 1 per 100,000. That’s what we should be working toward, and we can get there.

A version of this article first appeared on Medscape.com.

Editor in Chief of this news organization Eric Topol, MD, founder and director of the Scripps Research Translational Institute in La Jolla, Calif., and professor of molecular medicine, has been closely following COVID-19 data since the pandemic began. He spoke with writer Miriam E. Tucker about the latest on SARS-CoV-2 variants and their impact on vaccine efficacy. The conversation serves as a follow-up to his April 13, 2021, New York Times opinion piece, in which he advised readers that “all variants are innocent until proven guilty.”

You have expressed overall confidence in the efficacy of the vaccines thus far despite the emergence of variants, with some caveats. How do you see the current situation?

The Centers for Disease Control and Prevention has designated five “variants of concern,” but only three of them are real concerns – B.1.1.7, first detected in the United Kingdom; P.1, in Brazil and Japan; and B.1.351, in South Africa. Yet, all three are susceptible to our current vaccines.

The U.K. B.1.1.7 is the worst variant of all because it’s hypertransmissible, so I call it a “superspreader strain.” It also causes more severe illness independent of the spread, so it’s a double whammy. It’s clear that it also causes more deaths. The only arguable point is whether it’s 30% or 50% more deaths, but regardless, it’s more lethal and more transmissible.

The B.1.1.7 is going to be the dominant strain worldwide. It could develop new mutations within it that could come back to haunt us. We must keep watch.

But for now, it’s fully responsive to all the vaccines, which is great because if we didn’t have them, we wouldn’t have gotten through this U.S. pandemic like we have, and neither would Israel and the United Kingdom and other countries that have been able to get out of the crisis. We met the enemy and put it in check.

As for the South Africa variant of concern, B.1.351, we just got some encouraging news showing that it›s very responsive to the Pfizer/BioNTech mRNA vaccine in large numbers of people. The study was conducted in Qatar following that country’s mass immunization campaign in which a total of 385,853 people had received at least one vaccine dose and 265,410 had completed the two doses as of March 31, 2021.

At 2 weeks past the second dose, the vaccine was 75% effective at preventing any documented infection with the B.1.351 variant and 89.5% effective against B.1.1.7. The vaccine’s effectiveness against severe, critical, or fatal COVID-19 was greater than 97.4% for all circulating strains in Qatar, where B.1.1.7 and B.1.351 are most prominent.

We also know that B.1.351 is very responsive to the Johnson & Johnson vaccine and the Novavax [vaccine in development] to a lesser degree. It is the most immune-evading variant we’ve seen thus far, with the highest likelihood of providing some vaccine resistance, yet not enough to interfere with vaccination campaigns. So that’s great news.

The caveats here are that you definitely need two doses of the mRNA vaccines to combat the B.1.351 variant. Also, the AstraZeneca vaccine failed to prevent it in South Africa. However, that study was hard to judge because it was underpowered for number of people with mild infections. So, it didn’t look as if it had any efficacy, but maybe it would if tested in a real trial.

The P.1 (Brazil) variant is the second-highest concern after B.1.1.7 because it’s the only one in the United States that’s still headed up. It seems to be competing a bit with B.1.1.7 here. We know it was associated with the crisis in Brazil, in Chile, and some other South American countries. It has some immune escape, but not as bad as B.1.351. It also appears to have somewhat greater transmissibility but not as much as B.1.1.7.

With P.1, we just don’t know enough yet. It was difficult to assess in Brazil because they were in the midst of a catastrophe – like India is now – and you don’t know how much of it is dragged by the catastrophe vs driving it.

We have to respond to P.1 carefully. There are some good data that it does respond to the Chinese vaccine Sinovac and the AstraZeneca vaccine, and it appears to respond to the others as well, based on serum studies. So it doesn’t look like vaccines will be the worry with this variant. Rather, it could be competing with B.1.1.7 and could lead to breakthrough infections in vaccinated people or reinfections in unvaccinated people who had COVID-19. We need several more weeks to sort it out.

Although the B.1.427 and B.1.429 variants initially seen in California remain on the CDC’s concern list, I’m not worried about them.
 

You mentioned the current COVID-19 crisis in India, where a new variant has been described as a “double mutant,” but on Twitter you called it a “scariant.” Why?

First of all, the B.1.617 variant isn’t a double mutant. It has 15 mutations. It’s a stupid term, focusing on two mutations which largely have been put aside as to concern. One of them is the L452R, which is the same as one of the California variants, and that hasn’t proved to be particularly serious or concerning. The other is the 484Q, and it’s not clear whether that has any function.

The B.1.617 is not the driver of the catastrophe in India. It may be contributing a small amount, but it has been overhyped as the double mutant that’s causing it all. Adding to that are what I call “scariant” headlines here in the United States when a few cases of that variant have been seen.

I coined the term scariant in early February because it was a pretty clear trend. People don’t know what variants are. They know a little bit about mutations but not variants, and they’re scared. A few variants are concerning, but we keep learning more and more things to decrease the concern. That’s why I wrote the New York Times op-ed, to try to provide some reassurance, since there’s such paranoia.
 

Do you think booster vaccinations will be necessary? If so, will those be of the original vaccines or new ones that incorporate the variants?

As we go forward, there’s still potential for new variants that we haven’t seen yet that combine the worst of all features – transmissibility and immune evasion – especially since we have a world where COVID-19 is unchecked. So, we’re not out of it yet, but at least for the moment, we have vaccines that are capable of protecting against all variants.

In most people, the immune response against SARS-CoV-2 is very durable and strong and may well last for years. With the most closely related SARS-CoV-1, people still had immune responses up to 18 years later. However, some people will have less robust vaccine responses, including the elderly and the immunocompromised. If they don’t have great responses to the vaccine to start with, over time they’re likely to become more vulnerable, especially if they’re exposed to the variants with some degree of immune evasion.

I think we need to study these individuals post vaccination. A lot of people fit into those categories, including seniors, people being treated for cancer or autoimmune conditions, or post organ transplant. We could set up a prospective study to see whether they develop symptomatic COVID-19 and if so, from what – the original strain, B.1.1.7, or the newer variants.

That’s where I think booster shots may be needed. They may not be necessary across the board, but perhaps just in these special subgroups.

All of the current vaccines can be tweaked to include new variants, but the need for that is uncertain as of now. Moderna is working on a so-called bivalent vaccine that includes the original SARS-CoV-2 strain plus the B.1.351 variant, but it isn’t clear that that’s going to be necessary.

Currently, at least 200 COVID-19 vaccines are in development. There will be vaccines you can inhale, room temperature mRNA vaccines, and potentially even oral vaccines.

In the near future, Novavax is close, and there will likely be a two-dose Johnson & Johnson version that has the same potency as the mRNA vaccines. There are a lot of moving parts here.

There may be a step down in efficacy from mRNA to the others, though, and that shouldn’t be discounted. All of the available vaccines so far protect very well against severe disease and death, but some are less effective against mild to moderate infections, which may then lead to long COVID. We don’t yet know whether those who get mild infection post vaccination can still get long COVID.
 

What do you think it will take to achieve herd immunity?

I prefer the term “containment.” It’s quantitative. If you get to an infection rate of less than 1 in 100,000 people, as they’ve done in Israel, with 0.8 per 100,000, then you have the virus in check, and there will be very little spread when it’s at that controlled rate, with no outbreaks. The United States is currently at about 15 per 100,000. California is at 4. That still has to get lower.

It will be a challenge to get to President Biden’s goal of having 70% of U.S. adults given at least one dose by July 4. We’re now at about 57%. To get that next 13% of adults is going to take an all-out effort: mobile units, going to homes, making it ultraconvenient, education for people with safety concerns, incentivization, and days off.

We also need to get employers, universities, and health systems to get to the mandatory level. We haven’t done that yet. Some universities have mandated it for students, faculty, and staff. We need it in more health care systems. Right now, we only have a couple. We mandate flu shots, and flu is nothing, compared with COVID-19. And the COVID-19 vaccine is far more efficacious – flu shots are 40% efficacious, while these are 95%. COVID-19 is a tenfold more lethal and serious disease, and much more spreadable.

People are using the lack of full licensure by the Food and Drug Administration – as opposed to emergency use authorization – as an excuse not to get vaccinated. A biologics license application takes time to approve. Meanwhile, we have hundreds of millions of doses that have been well tolerated and incredibly effective.

Another aspect to consider regarding containment is that about 110 million Americans have already had COVID-19, even though only about 30 million cases have been confirmed. Most of these people have immune protection, although it’s not as good as if they have one vaccine dose. But they have enough protection to be part of the story here of the wall against COVID-19 and will help us get through this.

That’s a silver lining of having an unchecked epidemic for the entire year of 2020. The good part is that’s helping to get us to achieve an incredible level of containment when we haven’t even been close. Right now, we’re as good as the country has been in the pandemic, but we still have a long gap to get down to that 1 per 100,000. That’s what we should be working toward, and we can get there.

A version of this article first appeared on Medscape.com.

Editor in Chief of this news organization Eric Topol, MD, founder and director of the Scripps Research Translational Institute in La Jolla, Calif., and professor of molecular medicine, has been closely following COVID-19 data since the pandemic began. He spoke with writer Miriam E. Tucker about the latest on SARS-CoV-2 variants and their impact on vaccine efficacy. The conversation serves as a follow-up to his April 13, 2021, New York Times opinion piece, in which he advised readers that “all variants are innocent until proven guilty.”

You have expressed overall confidence in the efficacy of the vaccines thus far despite the emergence of variants, with some caveats. How do you see the current situation?

The Centers for Disease Control and Prevention has designated five “variants of concern,” but only three of them are real concerns – B.1.1.7, first detected in the United Kingdom; P.1, in Brazil and Japan; and B.1.351, in South Africa. Yet, all three are susceptible to our current vaccines.

The U.K. B.1.1.7 is the worst variant of all because it’s hypertransmissible, so I call it a “superspreader strain.” It also causes more severe illness independent of the spread, so it’s a double whammy. It’s clear that it also causes more deaths. The only arguable point is whether it’s 30% or 50% more deaths, but regardless, it’s more lethal and more transmissible.

The B.1.1.7 is going to be the dominant strain worldwide. It could develop new mutations within it that could come back to haunt us. We must keep watch.

But for now, it’s fully responsive to all the vaccines, which is great because if we didn’t have them, we wouldn’t have gotten through this U.S. pandemic like we have, and neither would Israel and the United Kingdom and other countries that have been able to get out of the crisis. We met the enemy and put it in check.

As for the South Africa variant of concern, B.1.351, we just got some encouraging news showing that it›s very responsive to the Pfizer/BioNTech mRNA vaccine in large numbers of people. The study was conducted in Qatar following that country’s mass immunization campaign in which a total of 385,853 people had received at least one vaccine dose and 265,410 had completed the two doses as of March 31, 2021.

At 2 weeks past the second dose, the vaccine was 75% effective at preventing any documented infection with the B.1.351 variant and 89.5% effective against B.1.1.7. The vaccine’s effectiveness against severe, critical, or fatal COVID-19 was greater than 97.4% for all circulating strains in Qatar, where B.1.1.7 and B.1.351 are most prominent.

We also know that B.1.351 is very responsive to the Johnson & Johnson vaccine and the Novavax [vaccine in development] to a lesser degree. It is the most immune-evading variant we’ve seen thus far, with the highest likelihood of providing some vaccine resistance, yet not enough to interfere with vaccination campaigns. So that’s great news.

The caveats here are that you definitely need two doses of the mRNA vaccines to combat the B.1.351 variant. Also, the AstraZeneca vaccine failed to prevent it in South Africa. However, that study was hard to judge because it was underpowered for number of people with mild infections. So, it didn’t look as if it had any efficacy, but maybe it would if tested in a real trial.

The P.1 (Brazil) variant is the second-highest concern after B.1.1.7 because it’s the only one in the United States that’s still headed up. It seems to be competing a bit with B.1.1.7 here. We know it was associated with the crisis in Brazil, in Chile, and some other South American countries. It has some immune escape, but not as bad as B.1.351. It also appears to have somewhat greater transmissibility but not as much as B.1.1.7.

With P.1, we just don’t know enough yet. It was difficult to assess in Brazil because they were in the midst of a catastrophe – like India is now – and you don’t know how much of it is dragged by the catastrophe vs driving it.

We have to respond to P.1 carefully. There are some good data that it does respond to the Chinese vaccine Sinovac and the AstraZeneca vaccine, and it appears to respond to the others as well, based on serum studies. So it doesn’t look like vaccines will be the worry with this variant. Rather, it could be competing with B.1.1.7 and could lead to breakthrough infections in vaccinated people or reinfections in unvaccinated people who had COVID-19. We need several more weeks to sort it out.

Although the B.1.427 and B.1.429 variants initially seen in California remain on the CDC’s concern list, I’m not worried about them.
 

You mentioned the current COVID-19 crisis in India, where a new variant has been described as a “double mutant,” but on Twitter you called it a “scariant.” Why?

First of all, the B.1.617 variant isn’t a double mutant. It has 15 mutations. It’s a stupid term, focusing on two mutations which largely have been put aside as to concern. One of them is the L452R, which is the same as one of the California variants, and that hasn’t proved to be particularly serious or concerning. The other is the 484Q, and it’s not clear whether that has any function.

The B.1.617 is not the driver of the catastrophe in India. It may be contributing a small amount, but it has been overhyped as the double mutant that’s causing it all. Adding to that are what I call “scariant” headlines here in the United States when a few cases of that variant have been seen.

I coined the term scariant in early February because it was a pretty clear trend. People don’t know what variants are. They know a little bit about mutations but not variants, and they’re scared. A few variants are concerning, but we keep learning more and more things to decrease the concern. That’s why I wrote the New York Times op-ed, to try to provide some reassurance, since there’s such paranoia.
 

Do you think booster vaccinations will be necessary? If so, will those be of the original vaccines or new ones that incorporate the variants?

As we go forward, there’s still potential for new variants that we haven’t seen yet that combine the worst of all features – transmissibility and immune evasion – especially since we have a world where COVID-19 is unchecked. So, we’re not out of it yet, but at least for the moment, we have vaccines that are capable of protecting against all variants.

In most people, the immune response against SARS-CoV-2 is very durable and strong and may well last for years. With the most closely related SARS-CoV-1, people still had immune responses up to 18 years later. However, some people will have less robust vaccine responses, including the elderly and the immunocompromised. If they don’t have great responses to the vaccine to start with, over time they’re likely to become more vulnerable, especially if they’re exposed to the variants with some degree of immune evasion.

I think we need to study these individuals post vaccination. A lot of people fit into those categories, including seniors, people being treated for cancer or autoimmune conditions, or post organ transplant. We could set up a prospective study to see whether they develop symptomatic COVID-19 and if so, from what – the original strain, B.1.1.7, or the newer variants.

That’s where I think booster shots may be needed. They may not be necessary across the board, but perhaps just in these special subgroups.

All of the current vaccines can be tweaked to include new variants, but the need for that is uncertain as of now. Moderna is working on a so-called bivalent vaccine that includes the original SARS-CoV-2 strain plus the B.1.351 variant, but it isn’t clear that that’s going to be necessary.

Currently, at least 200 COVID-19 vaccines are in development. There will be vaccines you can inhale, room temperature mRNA vaccines, and potentially even oral vaccines.

In the near future, Novavax is close, and there will likely be a two-dose Johnson & Johnson version that has the same potency as the mRNA vaccines. There are a lot of moving parts here.

There may be a step down in efficacy from mRNA to the others, though, and that shouldn’t be discounted. All of the available vaccines so far protect very well against severe disease and death, but some are less effective against mild to moderate infections, which may then lead to long COVID. We don’t yet know whether those who get mild infection post vaccination can still get long COVID.
 

What do you think it will take to achieve herd immunity?

I prefer the term “containment.” It’s quantitative. If you get to an infection rate of less than 1 in 100,000 people, as they’ve done in Israel, with 0.8 per 100,000, then you have the virus in check, and there will be very little spread when it’s at that controlled rate, with no outbreaks. The United States is currently at about 15 per 100,000. California is at 4. That still has to get lower.

It will be a challenge to get to President Biden’s goal of having 70% of U.S. adults given at least one dose by July 4. We’re now at about 57%. To get that next 13% of adults is going to take an all-out effort: mobile units, going to homes, making it ultraconvenient, education for people with safety concerns, incentivization, and days off.

We also need to get employers, universities, and health systems to get to the mandatory level. We haven’t done that yet. Some universities have mandated it for students, faculty, and staff. We need it in more health care systems. Right now, we only have a couple. We mandate flu shots, and flu is nothing, compared with COVID-19. And the COVID-19 vaccine is far more efficacious – flu shots are 40% efficacious, while these are 95%. COVID-19 is a tenfold more lethal and serious disease, and much more spreadable.

People are using the lack of full licensure by the Food and Drug Administration – as opposed to emergency use authorization – as an excuse not to get vaccinated. A biologics license application takes time to approve. Meanwhile, we have hundreds of millions of doses that have been well tolerated and incredibly effective.

Another aspect to consider regarding containment is that about 110 million Americans have already had COVID-19, even though only about 30 million cases have been confirmed. Most of these people have immune protection, although it’s not as good as if they have one vaccine dose. But they have enough protection to be part of the story here of the wall against COVID-19 and will help us get through this.

That’s a silver lining of having an unchecked epidemic for the entire year of 2020. The good part is that’s helping to get us to achieve an incredible level of containment when we haven’t even been close. Right now, we’re as good as the country has been in the pandemic, but we still have a long gap to get down to that 1 per 100,000. That’s what we should be working toward, and we can get there.

A version of this article first appeared on Medscape.com.

An investigational, orally dissolving film formulation of dexmedetomidine (BXCL501, BioXcel Therapeutics) may offer rapid relief from acute agitation related to schizophrenia or bipolar disorder (BD), results of two phase 3, randomized, placebo-controlled trials show.
 

For both disorders, BXCL501 showed “superiority over placebo” by meeting the primary endpoint of reduction of agitation as measured by the excited component of the Positive and Negative Syndrome Scale (PANSS), study investigator Leslie Citrome, MD, MPH, department of psychiatry and behavioral sciences, New York Medical College, Valhalla, said in an interview.

The findings were presented at the annual meeting of the American Psychiatric Association, which was held as a virtual live event.
 

Noninvasive option

Acute agitation in patients with schizophrenia or BD is often encountered in emergency departments (EDs) and inpatient units. When nondrug tactics fail to calm the patient, drug options include injectable antipsychotics or benzodiazepines. BXCL501 is a thin, orally dissolving film for sublingual or buccal use.

“Dexmedetomidine is a highly-selective alpha-2a receptor agonist and we haven’t really had one of those before in psychiatry for this purpose. And we haven’t had much in the way of orally dissolving thin films that are absorbed in the oral mucosa so this represents an opportunity to provide a potential intervention that does not require an injection and yet could possibly be of use in people who are agitated,” Dr. Citrome said.

The study, known as SERENITY I, included 380 adults (mean age 45.6 years, 63% male) with schizophrenia, schizoaffective disorder, or schizophreniform disorder, and acute agitation in the ED (total score ≥ 14 on the PANSS-Excited Component (PEC) scale at baseline and a score ≥ 4 on at least one of the five PEC items).

Patients were randomly allocated to a single oral dose of BXCL501: 120 mcg, 180 mcg, or placebo. A total of 372 patients (97.9%) completed the study.

Mean PEC total score was 17.6 at baseline. The mean change from baseline in the PEC total score at 2 hours (primary endpoint) was -8.5 and -10.3 with BXCL501 120 mcg and 180 mcg, respectively, versus -4.8 for placebo (P < .0001 vs. placebo).

PEC response rates (≥ 40% reduction from baseline) were 80.6% and 89.6% with BXCL501 120 mcg and 180 mcg versus 47.6% with placebo (P < .0001 vs. placebo).

Compared with placebo, significant improvement in the Clinical Global Impression–Improvement scale (CGI-I) was observed with both BXCL501 doses at 1 and 2 hours after dosing and in the Agitation and Calmness Evaluation Scale (ACES) at 2 hours post dosing.

The incidence of adverse events (AE) was 39.5%, 37.3%, and 15.1% with BXCL501 120 mg, 180 mg, and placebo groups.

All AEs were mild or moderate. The most common AEs with BXCL501 were somnolence, dizziness, dry mouth, hypotension, orthostatic hypotension, hypoesthesia, and paresthesia. No drug-related severe or serious AEs occurred.
 

Nipping it in the bud

SERENITY II had a similar design. This study included 380 adults (mean age 48, 55% female) with bipolar I or II disorder and acute agitation in the ED (total score ≥14 on the PEC scale at baseline and a score ≥4 on at least one PEC item). A total of 362 (95.3%) of patients completed the study.

Mean PEC total score was 18 at baseline. The mean change from baseline in the PEC total score at 2 hours (primary endpoint) was -9.0 and -10.4 with BXCL501 120 mcg and 180 mcg, respectively, versus -4.9 for placebo (P < .0001 vs. placebo).

Bipolar patients also saw significant improvement on the secondary outcomes of CGI-I and ACES, with an adverse event profile similar to that seen in patients with schizophrenia.

BXCL501 demonstrated “rapid, robust and clinically meaningful efficacy” in both patient populations and represents a “novel, noninvasive and well tolerated treatment of agitation,” the investigators concluded in their APA abstracts.

“Patients who are agitated are in psychic pain and they want relief from this psychic pain. We’re also worried that they might get worse and that agitation escalates to aggression potentially requiring restraints. We want to avoid that,” Dr. Citrome said.

“By nipping it in the bud with a pharmacological intervention, we can ease their psychic pain and we can manage a potentially dangerous situation. Offering an oral medicine that would work quickly would be ideal in my mind and patients might potentially be more accepting of that than an injection,” Dr. Citrome said.

Based on the SERENITY I and II data, BioXcel Therapeutics has submitted a new drug application to the Food and Drug Administration.
 

Negotiation first, medication second 

Reached for comment, Samoon Ahmad, MD, professor, department of psychiatry, New York (N.Y.) University, cautioned that, “when we talk about treating an agitated patient, medication is only part of the picture.

“There is a negotiating process with the patient. Number one, you offer them an environment that is conducive to making them feel calm, safe, and secure and that they are being listened to. Providing all of those things sometimes can be very helpful,” said Dr. Ahmad, who serves as unit chief of inpatient psychiatry at Bellevue Hospital Center in New York City.

“If someone starts throwing chairs at you or assaulting you, that is not really the time to negotiate a medicine; you basically have to restrain the patient, and many times give them intramuscular medicine,” Dr. Ahmad said.

He also noted that patients in the SERENITY trials had moderate to severe acute agitation.

“These are people you can potentially negotiate with. But again, when a patient crosses a certain line, you have to immediately do something and that could be intramuscular injection or something oral, which they may spit right in your face, which has happened numerous times,” Dr. Ahmad said.

“I don’t think intramuscular options will ever go away but an oral agent could be a useful tool as well,” said Dr. Ahmad, founder of the Integrative Center for Wellness in New York City.

He cautioned that clinicians are not going to be using this medicine in their offices. “If a patient walks in and is floridly psychotic, you will need to call 911. We’re really talking about its use either in the ED or acute inpatient setting,” Dr. Ahmad said.

A version of this article first appeared on Medscape.com.

An investigational, orally dissolving film formulation of dexmedetomidine (BXCL501, BioXcel Therapeutics) may offer rapid relief from acute agitation related to schizophrenia or bipolar disorder (BD), results of two phase 3, randomized, placebo-controlled trials show.
 

For both disorders, BXCL501 showed “superiority over placebo” by meeting the primary endpoint of reduction of agitation as measured by the excited component of the Positive and Negative Syndrome Scale (PANSS), study investigator Leslie Citrome, MD, MPH, department of psychiatry and behavioral sciences, New York Medical College, Valhalla, said in an interview.

The findings were presented at the annual meeting of the American Psychiatric Association, which was held as a virtual live event.
 

Noninvasive option

Acute agitation in patients with schizophrenia or BD is often encountered in emergency departments (EDs) and inpatient units. When nondrug tactics fail to calm the patient, drug options include injectable antipsychotics or benzodiazepines. BXCL501 is a thin, orally dissolving film for sublingual or buccal use.

“Dexmedetomidine is a highly-selective alpha-2a receptor agonist and we haven’t really had one of those before in psychiatry for this purpose. And we haven’t had much in the way of orally dissolving thin films that are absorbed in the oral mucosa so this represents an opportunity to provide a potential intervention that does not require an injection and yet could possibly be of use in people who are agitated,” Dr. Citrome said.

The study, known as SERENITY I, included 380 adults (mean age 45.6 years, 63% male) with schizophrenia, schizoaffective disorder, or schizophreniform disorder, and acute agitation in the ED (total score ≥ 14 on the PANSS-Excited Component (PEC) scale at baseline and a score ≥ 4 on at least one of the five PEC items).

Patients were randomly allocated to a single oral dose of BXCL501: 120 mcg, 180 mcg, or placebo. A total of 372 patients (97.9%) completed the study.

Mean PEC total score was 17.6 at baseline. The mean change from baseline in the PEC total score at 2 hours (primary endpoint) was -8.5 and -10.3 with BXCL501 120 mcg and 180 mcg, respectively, versus -4.8 for placebo (P < .0001 vs. placebo).

PEC response rates (≥ 40% reduction from baseline) were 80.6% and 89.6% with BXCL501 120 mcg and 180 mcg versus 47.6% with placebo (P < .0001 vs. placebo).

Compared with placebo, significant improvement in the Clinical Global Impression–Improvement scale (CGI-I) was observed with both BXCL501 doses at 1 and 2 hours after dosing and in the Agitation and Calmness Evaluation Scale (ACES) at 2 hours post dosing.

The incidence of adverse events (AE) was 39.5%, 37.3%, and 15.1% with BXCL501 120 mg, 180 mg, and placebo groups.

All AEs were mild or moderate. The most common AEs with BXCL501 were somnolence, dizziness, dry mouth, hypotension, orthostatic hypotension, hypoesthesia, and paresthesia. No drug-related severe or serious AEs occurred.
 

Nipping it in the bud

SERENITY II had a similar design. This study included 380 adults (mean age 48, 55% female) with bipolar I or II disorder and acute agitation in the ED (total score ≥14 on the PEC scale at baseline and a score ≥4 on at least one PEC item). A total of 362 (95.3%) of patients completed the study.

Mean PEC total score was 18 at baseline. The mean change from baseline in the PEC total score at 2 hours (primary endpoint) was -9.0 and -10.4 with BXCL501 120 mcg and 180 mcg, respectively, versus -4.9 for placebo (P < .0001 vs. placebo).

Bipolar patients also saw significant improvement on the secondary outcomes of CGI-I and ACES, with an adverse event profile similar to that seen in patients with schizophrenia.

BXCL501 demonstrated “rapid, robust and clinically meaningful efficacy” in both patient populations and represents a “novel, noninvasive and well tolerated treatment of agitation,” the investigators concluded in their APA abstracts.

“Patients who are agitated are in psychic pain and they want relief from this psychic pain. We’re also worried that they might get worse and that agitation escalates to aggression potentially requiring restraints. We want to avoid that,” Dr. Citrome said.

“By nipping it in the bud with a pharmacological intervention, we can ease their psychic pain and we can manage a potentially dangerous situation. Offering an oral medicine that would work quickly would be ideal in my mind and patients might potentially be more accepting of that than an injection,” Dr. Citrome said.

Based on the SERENITY I and II data, BioXcel Therapeutics has submitted a new drug application to the Food and Drug Administration.
 

Negotiation first, medication second 

Reached for comment, Samoon Ahmad, MD, professor, department of psychiatry, New York (N.Y.) University, cautioned that, “when we talk about treating an agitated patient, medication is only part of the picture.

“There is a negotiating process with the patient. Number one, you offer them an environment that is conducive to making them feel calm, safe, and secure and that they are being listened to. Providing all of those things sometimes can be very helpful,” said Dr. Ahmad, who serves as unit chief of inpatient psychiatry at Bellevue Hospital Center in New York City.

“If someone starts throwing chairs at you or assaulting you, that is not really the time to negotiate a medicine; you basically have to restrain the patient, and many times give them intramuscular medicine,” Dr. Ahmad said.

He also noted that patients in the SERENITY trials had moderate to severe acute agitation.

“These are people you can potentially negotiate with. But again, when a patient crosses a certain line, you have to immediately do something and that could be intramuscular injection or something oral, which they may spit right in your face, which has happened numerous times,” Dr. Ahmad said.

“I don’t think intramuscular options will ever go away but an oral agent could be a useful tool as well,” said Dr. Ahmad, founder of the Integrative Center for Wellness in New York City.

He cautioned that clinicians are not going to be using this medicine in their offices. “If a patient walks in and is floridly psychotic, you will need to call 911. We’re really talking about its use either in the ED or acute inpatient setting,” Dr. Ahmad said.

A version of this article first appeared on Medscape.com.

An investigational, orally dissolving film formulation of dexmedetomidine (BXCL501, BioXcel Therapeutics) may offer rapid relief from acute agitation related to schizophrenia or bipolar disorder (BD), results of two phase 3, randomized, placebo-controlled trials show.
 

For both disorders, BXCL501 showed “superiority over placebo” by meeting the primary endpoint of reduction of agitation as measured by the excited component of the Positive and Negative Syndrome Scale (PANSS), study investigator Leslie Citrome, MD, MPH, department of psychiatry and behavioral sciences, New York Medical College, Valhalla, said in an interview.

The findings were presented at the annual meeting of the American Psychiatric Association, which was held as a virtual live event.
 

Noninvasive option

Acute agitation in patients with schizophrenia or BD is often encountered in emergency departments (EDs) and inpatient units. When nondrug tactics fail to calm the patient, drug options include injectable antipsychotics or benzodiazepines. BXCL501 is a thin, orally dissolving film for sublingual or buccal use.

“Dexmedetomidine is a highly-selective alpha-2a receptor agonist and we haven’t really had one of those before in psychiatry for this purpose. And we haven’t had much in the way of orally dissolving thin films that are absorbed in the oral mucosa so this represents an opportunity to provide a potential intervention that does not require an injection and yet could possibly be of use in people who are agitated,” Dr. Citrome said.

The study, known as SERENITY I, included 380 adults (mean age 45.6 years, 63% male) with schizophrenia, schizoaffective disorder, or schizophreniform disorder, and acute agitation in the ED (total score ≥ 14 on the PANSS-Excited Component (PEC) scale at baseline and a score ≥ 4 on at least one of the five PEC items).

Patients were randomly allocated to a single oral dose of BXCL501: 120 mcg, 180 mcg, or placebo. A total of 372 patients (97.9%) completed the study.

Mean PEC total score was 17.6 at baseline. The mean change from baseline in the PEC total score at 2 hours (primary endpoint) was -8.5 and -10.3 with BXCL501 120 mcg and 180 mcg, respectively, versus -4.8 for placebo (P < .0001 vs. placebo).

PEC response rates (≥ 40% reduction from baseline) were 80.6% and 89.6% with BXCL501 120 mcg and 180 mcg versus 47.6% with placebo (P < .0001 vs. placebo).

Compared with placebo, significant improvement in the Clinical Global Impression–Improvement scale (CGI-I) was observed with both BXCL501 doses at 1 and 2 hours after dosing and in the Agitation and Calmness Evaluation Scale (ACES) at 2 hours post dosing.

The incidence of adverse events (AE) was 39.5%, 37.3%, and 15.1% with BXCL501 120 mg, 180 mg, and placebo groups.

All AEs were mild or moderate. The most common AEs with BXCL501 were somnolence, dizziness, dry mouth, hypotension, orthostatic hypotension, hypoesthesia, and paresthesia. No drug-related severe or serious AEs occurred.
 

Nipping it in the bud

SERENITY II had a similar design. This study included 380 adults (mean age 48, 55% female) with bipolar I or II disorder and acute agitation in the ED (total score ≥14 on the PEC scale at baseline and a score ≥4 on at least one PEC item). A total of 362 (95.3%) of patients completed the study.

Mean PEC total score was 18 at baseline. The mean change from baseline in the PEC total score at 2 hours (primary endpoint) was -9.0 and -10.4 with BXCL501 120 mcg and 180 mcg, respectively, versus -4.9 for placebo (P < .0001 vs. placebo).

Bipolar patients also saw significant improvement on the secondary outcomes of CGI-I and ACES, with an adverse event profile similar to that seen in patients with schizophrenia.

BXCL501 demonstrated “rapid, robust and clinically meaningful efficacy” in both patient populations and represents a “novel, noninvasive and well tolerated treatment of agitation,” the investigators concluded in their APA abstracts.

“Patients who are agitated are in psychic pain and they want relief from this psychic pain. We’re also worried that they might get worse and that agitation escalates to aggression potentially requiring restraints. We want to avoid that,” Dr. Citrome said.

“By nipping it in the bud with a pharmacological intervention, we can ease their psychic pain and we can manage a potentially dangerous situation. Offering an oral medicine that would work quickly would be ideal in my mind and patients might potentially be more accepting of that than an injection,” Dr. Citrome said.

Based on the SERENITY I and II data, BioXcel Therapeutics has submitted a new drug application to the Food and Drug Administration.
 

Negotiation first, medication second 

Reached for comment, Samoon Ahmad, MD, professor, department of psychiatry, New York (N.Y.) University, cautioned that, “when we talk about treating an agitated patient, medication is only part of the picture.

“There is a negotiating process with the patient. Number one, you offer them an environment that is conducive to making them feel calm, safe, and secure and that they are being listened to. Providing all of those things sometimes can be very helpful,” said Dr. Ahmad, who serves as unit chief of inpatient psychiatry at Bellevue Hospital Center in New York City.

“If someone starts throwing chairs at you or assaulting you, that is not really the time to negotiate a medicine; you basically have to restrain the patient, and many times give them intramuscular medicine,” Dr. Ahmad said.

He also noted that patients in the SERENITY trials had moderate to severe acute agitation.

“These are people you can potentially negotiate with. But again, when a patient crosses a certain line, you have to immediately do something and that could be intramuscular injection or something oral, which they may spit right in your face, which has happened numerous times,” Dr. Ahmad said.

“I don’t think intramuscular options will ever go away but an oral agent could be a useful tool as well,” said Dr. Ahmad, founder of the Integrative Center for Wellness in New York City.

He cautioned that clinicians are not going to be using this medicine in their offices. “If a patient walks in and is floridly psychotic, you will need to call 911. We’re really talking about its use either in the ED or acute inpatient setting,” Dr. Ahmad said.

A version of this article first appeared on Medscape.com.

Chronic insomnia is often underrecognized and misunderstood in primary care, sleep expert Christopher Lettieri, MD, told attendees at the annual meeting of the American College of Physicians.

Too often, medications are the treatment of choice, and when used long term they can perpetuate a problematic cycle, said Dr. Lettieri, professor in pulmonary, critical care, and sleep medicine at Johns Hopkins University, Baltimore.

However, medications alone won’t work without other behavior modifications and they come with potential side effects, he said in his talk. Prescription medications typically don’t treat the cause of the insomnia, just the symptoms.

“In the 15 years I’ve been practicing sleep medicine, I can honestly say I only have a handful of patients that I treat with long-term pharmacotherapy,” Dr. Lettieri said.

He said he typically uses pharmacotherapy only when conservative measures have failed or to help jump-start patients to behavior modifications.

Restricted sleep is a good place to start for chronic insomnia, he continued.

Physicians should ask patients the latest time they can wake up to make it to school, work, etc. If that time is 6 a.m., the goal is to move bedtime back to 10 p.m.–11 p.m. If the patient, however, is unable to sleep until 12:30 a.m., move bedtime there, he said.

Though the 5.5-hour window is not ideal, it’s better to get into bed when ready for sleep. From there, try to get the patient to move bedtime back 15 minutes each week as they train themselves to fall asleep earlier, he said.

“I promise you this works in the majority of patients and doesn’t require any medication. You can also accomplish this with one or two office visits, so it is not a huge drain on resources,” he said.
 

Sleep specialists in short supply

Cognitive-behavioral therapy (CBT) is “without question the best way to treat chronic insomnia and it’s recommended as first-line therapy by all published guidelines,” Dr. Lettieri said.

He defined chronic insomnia as happening most nights over at least 3 months. It affects twice as many women as men.

CBT offers a formalized way of changing sleep patterns with the help of an expert in sleep behavior disorders. It combines cognitive therapies with education about sleep and stimulus control and uses techniques such as mindfulness and relaxation.

However, most programs take 4-8 sessions with a sleep medicine provider and are usually not covered by insurance. In addition, the number of insomnia specialists is not nearly adequate to meet demand, he added.

Online and mobile-platform CBT programs are widely effective, Dr. Lettieri said. Many are free and all are convenient for patients to use. He said many of his patients use Sleepio, but many other online programs are effective.

“You can provide sufficient therapy for many of your patients and reserve CBT for patients who can’t be fixed with more conservative measures,” he said.
 

Insomnia among older patients

Interest in helping older patients with insomnia dominated the chat session associated with the talk.

Insomnia increases with age and older patients have often been using prescription or over-the-counter sleep aids for decades.

Additionally, “insomnia is the second-most common reason why people get admitted to long-term care facilities, second only to urinary incontinence,” Dr. Lettieri said.

If physicians use medications with older patients, he said, extra caution is needed. Older people have more neurocognitive impairments than younger adults and may already be taking several other medications. Sleep medications may come with longer elimination half-lives. Polypharmacy may increase risk for falls and have other consequences.

“If you have to go to a medication, try something simple like melatonin,” he said, adding that it should be pharmaceutical grade and extended release.

Also, bright lights during the day, movement throughout the day, and dim lights closer to bedtime are especially important for the elderly, Dr. Lettieri said.

Andrew Corr, MD, a geriatric specialist in primary care with the Riverside (Calif.) Medical Clinic, said in an interview the main message he will take back to his physician group is more CBT and less medication.

He said that, although he has long known CBT is the top first-line treatment, it is difficult to find experts in his area who are trained to do CBT for insomnia, so he was glad to hear online programs and self-directed reading are typically effective.

He also said there’s a common misperception that there’s no harm in prescribing medications such as trazodone (Desyrel), an antidepressant commonly used off label as a sleep aid.

Dr. Lettieri’s talk highlighted his recommendation against using trazodone for sleep. “Despite several recommendations against its use for insomnia, it is still commonly prescribed. You just shouldn’t use it for insomnia,” Dr. Lettieri said.

“It has no measurable effect in a third of patients and at least unacceptable side effects in another third.  Right off the bat, it’s not efficacious in two thirds of patients.”

Additionally, priapism, a prolonged erection, has been associated with trazodone, Dr. Lettieri said, “and I have literally never met a patient on trazodone who was counseled about this.”

Trazodone also has a black box warning from the Food and Drug Administration warning about increased risk for suicidal thoughts.

Dr. Lettieri and Dr. Corr disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Chronic insomnia is often underrecognized and misunderstood in primary care, sleep expert Christopher Lettieri, MD, told attendees at the annual meeting of the American College of Physicians.

Too often, medications are the treatment of choice, and when used long term they can perpetuate a problematic cycle, said Dr. Lettieri, professor in pulmonary, critical care, and sleep medicine at Johns Hopkins University, Baltimore.

However, medications alone won’t work without other behavior modifications and they come with potential side effects, he said in his talk. Prescription medications typically don’t treat the cause of the insomnia, just the symptoms.

“In the 15 years I’ve been practicing sleep medicine, I can honestly say I only have a handful of patients that I treat with long-term pharmacotherapy,” Dr. Lettieri said.

He said he typically uses pharmacotherapy only when conservative measures have failed or to help jump-start patients to behavior modifications.

Restricted sleep is a good place to start for chronic insomnia, he continued.

Physicians should ask patients the latest time they can wake up to make it to school, work, etc. If that time is 6 a.m., the goal is to move bedtime back to 10 p.m.–11 p.m. If the patient, however, is unable to sleep until 12:30 a.m., move bedtime there, he said.

Though the 5.5-hour window is not ideal, it’s better to get into bed when ready for sleep. From there, try to get the patient to move bedtime back 15 minutes each week as they train themselves to fall asleep earlier, he said.

“I promise you this works in the majority of patients and doesn’t require any medication. You can also accomplish this with one or two office visits, so it is not a huge drain on resources,” he said.
 

Sleep specialists in short supply

Cognitive-behavioral therapy (CBT) is “without question the best way to treat chronic insomnia and it’s recommended as first-line therapy by all published guidelines,” Dr. Lettieri said.

He defined chronic insomnia as happening most nights over at least 3 months. It affects twice as many women as men.

CBT offers a formalized way of changing sleep patterns with the help of an expert in sleep behavior disorders. It combines cognitive therapies with education about sleep and stimulus control and uses techniques such as mindfulness and relaxation.

However, most programs take 4-8 sessions with a sleep medicine provider and are usually not covered by insurance. In addition, the number of insomnia specialists is not nearly adequate to meet demand, he added.

Online and mobile-platform CBT programs are widely effective, Dr. Lettieri said. Many are free and all are convenient for patients to use. He said many of his patients use Sleepio, but many other online programs are effective.

“You can provide sufficient therapy for many of your patients and reserve CBT for patients who can’t be fixed with more conservative measures,” he said.
 

Insomnia among older patients

Interest in helping older patients with insomnia dominated the chat session associated with the talk.

Insomnia increases with age and older patients have often been using prescription or over-the-counter sleep aids for decades.

Additionally, “insomnia is the second-most common reason why people get admitted to long-term care facilities, second only to urinary incontinence,” Dr. Lettieri said.

If physicians use medications with older patients, he said, extra caution is needed. Older people have more neurocognitive impairments than younger adults and may already be taking several other medications. Sleep medications may come with longer elimination half-lives. Polypharmacy may increase risk for falls and have other consequences.

“If you have to go to a medication, try something simple like melatonin,” he said, adding that it should be pharmaceutical grade and extended release.

Also, bright lights during the day, movement throughout the day, and dim lights closer to bedtime are especially important for the elderly, Dr. Lettieri said.

Andrew Corr, MD, a geriatric specialist in primary care with the Riverside (Calif.) Medical Clinic, said in an interview the main message he will take back to his physician group is more CBT and less medication.

He said that, although he has long known CBT is the top first-line treatment, it is difficult to find experts in his area who are trained to do CBT for insomnia, so he was glad to hear online programs and self-directed reading are typically effective.

He also said there’s a common misperception that there’s no harm in prescribing medications such as trazodone (Desyrel), an antidepressant commonly used off label as a sleep aid.

Dr. Lettieri’s talk highlighted his recommendation against using trazodone for sleep. “Despite several recommendations against its use for insomnia, it is still commonly prescribed. You just shouldn’t use it for insomnia,” Dr. Lettieri said.

“It has no measurable effect in a third of patients and at least unacceptable side effects in another third.  Right off the bat, it’s not efficacious in two thirds of patients.”

Additionally, priapism, a prolonged erection, has been associated with trazodone, Dr. Lettieri said, “and I have literally never met a patient on trazodone who was counseled about this.”

Trazodone also has a black box warning from the Food and Drug Administration warning about increased risk for suicidal thoughts.

Dr. Lettieri and Dr. Corr disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Chronic insomnia is often underrecognized and misunderstood in primary care, sleep expert Christopher Lettieri, MD, told attendees at the annual meeting of the American College of Physicians.

Too often, medications are the treatment of choice, and when used long term they can perpetuate a problematic cycle, said Dr. Lettieri, professor in pulmonary, critical care, and sleep medicine at Johns Hopkins University, Baltimore.

However, medications alone won’t work without other behavior modifications and they come with potential side effects, he said in his talk. Prescription medications typically don’t treat the cause of the insomnia, just the symptoms.

“In the 15 years I’ve been practicing sleep medicine, I can honestly say I only have a handful of patients that I treat with long-term pharmacotherapy,” Dr. Lettieri said.

He said he typically uses pharmacotherapy only when conservative measures have failed or to help jump-start patients to behavior modifications.

Restricted sleep is a good place to start for chronic insomnia, he continued.

Physicians should ask patients the latest time they can wake up to make it to school, work, etc. If that time is 6 a.m., the goal is to move bedtime back to 10 p.m.–11 p.m. If the patient, however, is unable to sleep until 12:30 a.m., move bedtime there, he said.

Though the 5.5-hour window is not ideal, it’s better to get into bed when ready for sleep. From there, try to get the patient to move bedtime back 15 minutes each week as they train themselves to fall asleep earlier, he said.

“I promise you this works in the majority of patients and doesn’t require any medication. You can also accomplish this with one or two office visits, so it is not a huge drain on resources,” he said.
 

Sleep specialists in short supply

Cognitive-behavioral therapy (CBT) is “without question the best way to treat chronic insomnia and it’s recommended as first-line therapy by all published guidelines,” Dr. Lettieri said.

He defined chronic insomnia as happening most nights over at least 3 months. It affects twice as many women as men.

CBT offers a formalized way of changing sleep patterns with the help of an expert in sleep behavior disorders. It combines cognitive therapies with education about sleep and stimulus control and uses techniques such as mindfulness and relaxation.

However, most programs take 4-8 sessions with a sleep medicine provider and are usually not covered by insurance. In addition, the number of insomnia specialists is not nearly adequate to meet demand, he added.

Online and mobile-platform CBT programs are widely effective, Dr. Lettieri said. Many are free and all are convenient for patients to use. He said many of his patients use Sleepio, but many other online programs are effective.

“You can provide sufficient therapy for many of your patients and reserve CBT for patients who can’t be fixed with more conservative measures,” he said.
 

Insomnia among older patients

Interest in helping older patients with insomnia dominated the chat session associated with the talk.

Insomnia increases with age and older patients have often been using prescription or over-the-counter sleep aids for decades.

Additionally, “insomnia is the second-most common reason why people get admitted to long-term care facilities, second only to urinary incontinence,” Dr. Lettieri said.

If physicians use medications with older patients, he said, extra caution is needed. Older people have more neurocognitive impairments than younger adults and may already be taking several other medications. Sleep medications may come with longer elimination half-lives. Polypharmacy may increase risk for falls and have other consequences.

“If you have to go to a medication, try something simple like melatonin,” he said, adding that it should be pharmaceutical grade and extended release.

Also, bright lights during the day, movement throughout the day, and dim lights closer to bedtime are especially important for the elderly, Dr. Lettieri said.

Andrew Corr, MD, a geriatric specialist in primary care with the Riverside (Calif.) Medical Clinic, said in an interview the main message he will take back to his physician group is more CBT and less medication.

He said that, although he has long known CBT is the top first-line treatment, it is difficult to find experts in his area who are trained to do CBT for insomnia, so he was glad to hear online programs and self-directed reading are typically effective.

He also said there’s a common misperception that there’s no harm in prescribing medications such as trazodone (Desyrel), an antidepressant commonly used off label as a sleep aid.

Dr. Lettieri’s talk highlighted his recommendation against using trazodone for sleep. “Despite several recommendations against its use for insomnia, it is still commonly prescribed. You just shouldn’t use it for insomnia,” Dr. Lettieri said.

“It has no measurable effect in a third of patients and at least unacceptable side effects in another third.  Right off the bat, it’s not efficacious in two thirds of patients.”

Additionally, priapism, a prolonged erection, has been associated with trazodone, Dr. Lettieri said, “and I have literally never met a patient on trazodone who was counseled about this.”

Trazodone also has a black box warning from the Food and Drug Administration warning about increased risk for suicidal thoughts.

Dr. Lettieri and Dr. Corr disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Every spring, I look forward to attending the American Psychiatric Association’s annual meeting. It has become a ritual that starts many months before the actual conference.

Submissions for presentations are due in September, so the planning often starts in the late summer. Hotel and plane reservations are made in January, and the meeting itself begins in May.

The city that hosts the event changes each year but, for me, many things do not. The Clinical Psychiatry News editorial board meeting takes place on Monday morning at 7 a.m., and I scour the program for what sessions to attend. In recent years, I have made a point of writing an article for about one of the sessions while still at the meeting – in 2019 I wrote about the improv-acting workshops I attended – something that just doesn’t translate to a Zoom experience.

I go with the same friend every year, I always attend the Hopkins alumni reception, and I organize dinner at a nice restaurant for friends. I have collected so many funny stories and memories over the years that it would be hard to catalog them all. There was the time in Toronto that I set up a meal at a restaurant named Susur – a meal like no other I’ve ever had – and the check arrived with a jaw-dropping sum that I had not anticipated. In San Diego, we watched a gorgeous sunset over the Pacific Ocean from the veranda of the Hotel Coronado. There was the time I sunbathed on the beach in Waikiki with my book editor, and the notable distress when my colleague’s husband called from the airport to say he was not permitted to board his plane in Baltimore to join us in California! There are funny stories, but there is the sadness that one friend who joined us for so many of these events has died.

I always find the program options to be overwhelming: There is so much going on at once that it can be hard to decide what to go to. I try to attend a mix of sessions, some that are inspiring or entertaining, and others that will be informative for clinical issues.

The speakers have been incredible and over the years I’ve heard then-Vice President Joseph Biden, retired quarterback Terry Bradshaw, Oliver Sacks, Alan Alda, Archbishop Desmond Tutu, and perhaps my favorite – Lorraine Bracco, the actress who played Dr. Melfi on “The Sopranos” – to name just a few. And, of course, the opportunity to get the continuing medical education credits I need for licensing is just one more reason to attend.

Last year in May I was still adjusting to my “new” career from home with a computer screen. I had been scheduled to participate in several panels for the meeting in Philadelphia, but extra computer hours had no appeal. And while the fatigue of doing telemental health has eased, I still avoid extra hours interacting with my computer screen and I did not attend this year’s meeting. Without the lure of friends, fun, and the novelty of being somewhere new, my APA experience would have to wait for real life.

Virtual APA has had a drop in participation. In 2019, the last real-life convention in San Francisco, there were 700 scientific sessions and 11,000 professionals in attendance. This year’s virtual conference hosted 135 sessions with more than 7,000 attendees. Attendance was down, but so were costs associated with live conventions and the APA is considering the addition of a virtual component when the annual meeting returns to the in-person venue.

Tom Abdallah is a medical student at Weill Cornell Medicine–Qatar in Education City. He has never attended an in-person APA annual meeting, but he joined for this year’s virtual sessions. “The scientific sessions were fantastic and diverse. Networking was limited in comparison to in-person conferences. The meeting was very well organized, and it gave me the opportunity to attend without worrying about travel.”

Steven Daviss, MD, a psychiatrist in Maryland, also commented on the ease and financial benefit of attending the meeting from his home office. He calculated that the cost was much less: $350 for virtual APA, compared with approximately $3,500 for the real thing, allowing for transportation, hotels, meals out, and lost income. “But,” said Dr. Daviss, “engagement with colleagues was minimal.”

APA Assembly member Annette Hanson, MD, has continued to go into work throughout the pandemic. Still, she noted that meetings and committee work have made sure she does not miss out on the “Zoom fatigue” that everyone else is feeling. The virtual APA was tiring for her.

“It was brutal. There was the APA Assembly 1 weekend, right after evening Zoom reference committee meetings the week before. Then virtual APA the next weekend. By the end of the week, I had worked every day for 3 weeks straight, including my more-than-full-time job!”

It has been a challenging time, to say the least, and it has certainly helped that videoconferencing has allowed us to be there for our patients and for each other in so many different circumstances. Former APA President Paul Summergrad, MD, talked about how virtual meetings can be very good as educational tools, but he conveyed what I have been feeling in a sentence: “I miss the social aspect of meetings.”

Please get your vaccine, and I hope to see you in New Orleans next May!

Dr. Miller is coauthor of “Committed: The Battle Over Involuntary Psychiatric Care” (Baltimore: Johns Hopkins University Press, 2016). She has a private practice and is assistant professor of psychiatry and behavioral sciences at Johns Hopkins, both in Baltimore.

Every spring, I look forward to attending the American Psychiatric Association’s annual meeting. It has become a ritual that starts many months before the actual conference.

Submissions for presentations are due in September, so the planning often starts in the late summer. Hotel and plane reservations are made in January, and the meeting itself begins in May.

The city that hosts the event changes each year but, for me, many things do not. The Clinical Psychiatry News editorial board meeting takes place on Monday morning at 7 a.m., and I scour the program for what sessions to attend. In recent years, I have made a point of writing an article for about one of the sessions while still at the meeting – in 2019 I wrote about the improv-acting workshops I attended – something that just doesn’t translate to a Zoom experience.

I go with the same friend every year, I always attend the Hopkins alumni reception, and I organize dinner at a nice restaurant for friends. I have collected so many funny stories and memories over the years that it would be hard to catalog them all. There was the time in Toronto that I set up a meal at a restaurant named Susur – a meal like no other I’ve ever had – and the check arrived with a jaw-dropping sum that I had not anticipated. In San Diego, we watched a gorgeous sunset over the Pacific Ocean from the veranda of the Hotel Coronado. There was the time I sunbathed on the beach in Waikiki with my book editor, and the notable distress when my colleague’s husband called from the airport to say he was not permitted to board his plane in Baltimore to join us in California! There are funny stories, but there is the sadness that one friend who joined us for so many of these events has died.

I always find the program options to be overwhelming: There is so much going on at once that it can be hard to decide what to go to. I try to attend a mix of sessions, some that are inspiring or entertaining, and others that will be informative for clinical issues.

The speakers have been incredible and over the years I’ve heard then-Vice President Joseph Biden, retired quarterback Terry Bradshaw, Oliver Sacks, Alan Alda, Archbishop Desmond Tutu, and perhaps my favorite – Lorraine Bracco, the actress who played Dr. Melfi on “The Sopranos” – to name just a few. And, of course, the opportunity to get the continuing medical education credits I need for licensing is just one more reason to attend.

Last year in May I was still adjusting to my “new” career from home with a computer screen. I had been scheduled to participate in several panels for the meeting in Philadelphia, but extra computer hours had no appeal. And while the fatigue of doing telemental health has eased, I still avoid extra hours interacting with my computer screen and I did not attend this year’s meeting. Without the lure of friends, fun, and the novelty of being somewhere new, my APA experience would have to wait for real life.

Virtual APA has had a drop in participation. In 2019, the last real-life convention in San Francisco, there were 700 scientific sessions and 11,000 professionals in attendance. This year’s virtual conference hosted 135 sessions with more than 7,000 attendees. Attendance was down, but so were costs associated with live conventions and the APA is considering the addition of a virtual component when the annual meeting returns to the in-person venue.

Tom Abdallah is a medical student at Weill Cornell Medicine–Qatar in Education City. He has never attended an in-person APA annual meeting, but he joined for this year’s virtual sessions. “The scientific sessions were fantastic and diverse. Networking was limited in comparison to in-person conferences. The meeting was very well organized, and it gave me the opportunity to attend without worrying about travel.”

Steven Daviss, MD, a psychiatrist in Maryland, also commented on the ease and financial benefit of attending the meeting from his home office. He calculated that the cost was much less: $350 for virtual APA, compared with approximately $3,500 for the real thing, allowing for transportation, hotels, meals out, and lost income. “But,” said Dr. Daviss, “engagement with colleagues was minimal.”

APA Assembly member Annette Hanson, MD, has continued to go into work throughout the pandemic. Still, she noted that meetings and committee work have made sure she does not miss out on the “Zoom fatigue” that everyone else is feeling. The virtual APA was tiring for her.

“It was brutal. There was the APA Assembly 1 weekend, right after evening Zoom reference committee meetings the week before. Then virtual APA the next weekend. By the end of the week, I had worked every day for 3 weeks straight, including my more-than-full-time job!”

It has been a challenging time, to say the least, and it has certainly helped that videoconferencing has allowed us to be there for our patients and for each other in so many different circumstances. Former APA President Paul Summergrad, MD, talked about how virtual meetings can be very good as educational tools, but he conveyed what I have been feeling in a sentence: “I miss the social aspect of meetings.”

Please get your vaccine, and I hope to see you in New Orleans next May!

Dr. Miller is coauthor of “Committed: The Battle Over Involuntary Psychiatric Care” (Baltimore: Johns Hopkins University Press, 2016). She has a private practice and is assistant professor of psychiatry and behavioral sciences at Johns Hopkins, both in Baltimore.

Every spring, I look forward to attending the American Psychiatric Association’s annual meeting. It has become a ritual that starts many months before the actual conference.

Submissions for presentations are due in September, so the planning often starts in the late summer. Hotel and plane reservations are made in January, and the meeting itself begins in May.

The city that hosts the event changes each year but, for me, many things do not. The Clinical Psychiatry News editorial board meeting takes place on Monday morning at 7 a.m., and I scour the program for what sessions to attend. In recent years, I have made a point of writing an article for about one of the sessions while still at the meeting – in 2019 I wrote about the improv-acting workshops I attended – something that just doesn’t translate to a Zoom experience.

I go with the same friend every year, I always attend the Hopkins alumni reception, and I organize dinner at a nice restaurant for friends. I have collected so many funny stories and memories over the years that it would be hard to catalog them all. There was the time in Toronto that I set up a meal at a restaurant named Susur – a meal like no other I’ve ever had – and the check arrived with a jaw-dropping sum that I had not anticipated. In San Diego, we watched a gorgeous sunset over the Pacific Ocean from the veranda of the Hotel Coronado. There was the time I sunbathed on the beach in Waikiki with my book editor, and the notable distress when my colleague’s husband called from the airport to say he was not permitted to board his plane in Baltimore to join us in California! There are funny stories, but there is the sadness that one friend who joined us for so many of these events has died.

I always find the program options to be overwhelming: There is so much going on at once that it can be hard to decide what to go to. I try to attend a mix of sessions, some that are inspiring or entertaining, and others that will be informative for clinical issues.

The speakers have been incredible and over the years I’ve heard then-Vice President Joseph Biden, retired quarterback Terry Bradshaw, Oliver Sacks, Alan Alda, Archbishop Desmond Tutu, and perhaps my favorite – Lorraine Bracco, the actress who played Dr. Melfi on “The Sopranos” – to name just a few. And, of course, the opportunity to get the continuing medical education credits I need for licensing is just one more reason to attend.

Last year in May I was still adjusting to my “new” career from home with a computer screen. I had been scheduled to participate in several panels for the meeting in Philadelphia, but extra computer hours had no appeal. And while the fatigue of doing telemental health has eased, I still avoid extra hours interacting with my computer screen and I did not attend this year’s meeting. Without the lure of friends, fun, and the novelty of being somewhere new, my APA experience would have to wait for real life.

Virtual APA has had a drop in participation. In 2019, the last real-life convention in San Francisco, there were 700 scientific sessions and 11,000 professionals in attendance. This year’s virtual conference hosted 135 sessions with more than 7,000 attendees. Attendance was down, but so were costs associated with live conventions and the APA is considering the addition of a virtual component when the annual meeting returns to the in-person venue.

Tom Abdallah is a medical student at Weill Cornell Medicine–Qatar in Education City. He has never attended an in-person APA annual meeting, but he joined for this year’s virtual sessions. “The scientific sessions were fantastic and diverse. Networking was limited in comparison to in-person conferences. The meeting was very well organized, and it gave me the opportunity to attend without worrying about travel.”

Steven Daviss, MD, a psychiatrist in Maryland, also commented on the ease and financial benefit of attending the meeting from his home office. He calculated that the cost was much less: $350 for virtual APA, compared with approximately $3,500 for the real thing, allowing for transportation, hotels, meals out, and lost income. “But,” said Dr. Daviss, “engagement with colleagues was minimal.”

APA Assembly member Annette Hanson, MD, has continued to go into work throughout the pandemic. Still, she noted that meetings and committee work have made sure she does not miss out on the “Zoom fatigue” that everyone else is feeling. The virtual APA was tiring for her.

“It was brutal. There was the APA Assembly 1 weekend, right after evening Zoom reference committee meetings the week before. Then virtual APA the next weekend. By the end of the week, I had worked every day for 3 weeks straight, including my more-than-full-time job!”

It has been a challenging time, to say the least, and it has certainly helped that videoconferencing has allowed us to be there for our patients and for each other in so many different circumstances. Former APA President Paul Summergrad, MD, talked about how virtual meetings can be very good as educational tools, but he conveyed what I have been feeling in a sentence: “I miss the social aspect of meetings.”

Please get your vaccine, and I hope to see you in New Orleans next May!

Dr. Miller is coauthor of “Committed: The Battle Over Involuntary Psychiatric Care” (Baltimore: Johns Hopkins University Press, 2016). She has a private practice and is assistant professor of psychiatry and behavioral sciences at Johns Hopkins, both in Baltimore.

Asking a patient who has concerns about memory loss–particular questions can guide referral decisions, according to new research.

Initial questions should zero in on what the patient is forgetting, said Megan Richie, MD, a neurohospitalist at the University of California, San Francisco, who spoke to a virtual audience at the American College of Physicians (ACP) annual Internal Medicine meeting.

Is the patient forgetting to buy things in a store, having trouble recalling events, forgetting important dates? How often do these incidents occur?

These questions “will help get at how pervasive and how likely the memory loss is affecting their lives, versus a subjective complaint that doesn’t have much impact on the day-to-day function,” she said.

It’s also important to ask whether other neurocognitive symptoms accompany the memory loss, Dr. Richie noted.

Does the patient search for words, struggle with attention, or have problems with executive function? Does the patient have psychiatric symptoms, such as hallucinations or delusions, or other neurologic complaints, including weakness, numbness, vision change, or movement disorders?

“When you know how many neurocognitive symptoms they have, think about how [those symptoms] are affecting their safety and functional status. How are they on their activities of daily living?” Dr. Richie suggests.

Also ask whether the patient is taking medications and whether they drive a vehicle. If they do drive, do they get lost?

“These are all going to help you determine the acuity of the workup,” she said.

After a thorough history, cognitive screening is the next consideration.
 

Cognitive screening can be performed in minutes

One of the tests Dr. Richie recommends is the Mini-Cog. It takes 3 minutes to administer and has been formally recommended by the Alzheimer’s Association because it can be completed in the time frame of a Medicare wellness visit, she said.

It entails a three-word recall and clock-drawing test.

Dr. Richie said it’s important to eliminate some key causes first: “Certainly if the patient has signs and symptoms of depression, pseudodementia is a very real and treatable disease you do not want to miss and should consider in these patients,” she pointed out.

Systemic medical conditions can also lead to memory loss.

If there’s an acute component to the complaint, a new infection or medication withdrawal or a side effect could be driving it, so that’s key in questioning.

Dr. Richie explained that the American Academy of Neurology recommends a very limited workup.

“It’s really just to check their thyroid, their vitamin B12 levels, and then a one-time picture of their brain, which can be either MRI or a CT, to look for structural problems or vascular dementia or hydrocephalus, etc.”

“You do not routinely need spinal fluid testing or an EEG,” she emphasized.

Signs that a neurologist should be involved include a rapid decline, signs of potential seizures, or that the patient doesn’t seem safe in their condition.

Neuropsychological testing is helpful, but it takes nearly 3 hours and may not be a good choice for restless or aggressive patients, Dr. Richie said.

Such testing is often not available, and if it is, insurance coverage is often a barrier because many plans don’t cover it.

Patients often ask about drugs and supplements they see advertised to help with memory loss. Medications are not helpful for mild cognitive impairment, although there is evidence that some are beneficial for patients with dementia, Dr. Richie said.

Celine Goetz, MD, assistant professor of internal medicine at Rush University Medical Center, Chicago, Illinois, told this news organization that it’s easy to relate to the fear that patients and families feel when cognitive impairment begins to emerge.

“[Dr.] Richie’s talk was right on point for internists like myself who see many patients with memory complaints, cognitive impairment, and dementia. I think we’re all terrified of losing our memory and the social and functional impairment that comes with that,” she said.

Although cognitive impairment and dementia aren’t curable or reversible, Dr. Goetz noted, internists can help patients optimize management of conditions such as diabetes and heart disease, which can affect cognitive function.

Dr. Richie pointed out that some interventions lack evidence for the treatment of mild cognitive impairment, but Dr. Goetz emphasized that resources are plentiful and can be effective in combination.

“Engaging social workers, pharmacists, nutritionists, physical and occupational therapists, and, on the inpatient side, delirium protocols, chaplains, and music therapists make a huge difference in patient care,” she said.

Dr. Richie and Dr. Goetz report no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Asking a patient who has concerns about memory loss–particular questions can guide referral decisions, according to new research.

Initial questions should zero in on what the patient is forgetting, said Megan Richie, MD, a neurohospitalist at the University of California, San Francisco, who spoke to a virtual audience at the American College of Physicians (ACP) annual Internal Medicine meeting.

Is the patient forgetting to buy things in a store, having trouble recalling events, forgetting important dates? How often do these incidents occur?

These questions “will help get at how pervasive and how likely the memory loss is affecting their lives, versus a subjective complaint that doesn’t have much impact on the day-to-day function,” she said.

It’s also important to ask whether other neurocognitive symptoms accompany the memory loss, Dr. Richie noted.

Does the patient search for words, struggle with attention, or have problems with executive function? Does the patient have psychiatric symptoms, such as hallucinations or delusions, or other neurologic complaints, including weakness, numbness, vision change, or movement disorders?

“When you know how many neurocognitive symptoms they have, think about how [those symptoms] are affecting their safety and functional status. How are they on their activities of daily living?” Dr. Richie suggests.

Also ask whether the patient is taking medications and whether they drive a vehicle. If they do drive, do they get lost?

“These are all going to help you determine the acuity of the workup,” she said.

After a thorough history, cognitive screening is the next consideration.
 

Cognitive screening can be performed in minutes

One of the tests Dr. Richie recommends is the Mini-Cog. It takes 3 minutes to administer and has been formally recommended by the Alzheimer’s Association because it can be completed in the time frame of a Medicare wellness visit, she said.

It entails a three-word recall and clock-drawing test.

Dr. Richie said it’s important to eliminate some key causes first: “Certainly if the patient has signs and symptoms of depression, pseudodementia is a very real and treatable disease you do not want to miss and should consider in these patients,” she pointed out.

Systemic medical conditions can also lead to memory loss.

If there’s an acute component to the complaint, a new infection or medication withdrawal or a side effect could be driving it, so that’s key in questioning.

Dr. Richie explained that the American Academy of Neurology recommends a very limited workup.

“It’s really just to check their thyroid, their vitamin B12 levels, and then a one-time picture of their brain, which can be either MRI or a CT, to look for structural problems or vascular dementia or hydrocephalus, etc.”

“You do not routinely need spinal fluid testing or an EEG,” she emphasized.

Signs that a neurologist should be involved include a rapid decline, signs of potential seizures, or that the patient doesn’t seem safe in their condition.

Neuropsychological testing is helpful, but it takes nearly 3 hours and may not be a good choice for restless or aggressive patients, Dr. Richie said.

Such testing is often not available, and if it is, insurance coverage is often a barrier because many plans don’t cover it.

Patients often ask about drugs and supplements they see advertised to help with memory loss. Medications are not helpful for mild cognitive impairment, although there is evidence that some are beneficial for patients with dementia, Dr. Richie said.

Celine Goetz, MD, assistant professor of internal medicine at Rush University Medical Center, Chicago, Illinois, told this news organization that it’s easy to relate to the fear that patients and families feel when cognitive impairment begins to emerge.

“[Dr.] Richie’s talk was right on point for internists like myself who see many patients with memory complaints, cognitive impairment, and dementia. I think we’re all terrified of losing our memory and the social and functional impairment that comes with that,” she said.

Although cognitive impairment and dementia aren’t curable or reversible, Dr. Goetz noted, internists can help patients optimize management of conditions such as diabetes and heart disease, which can affect cognitive function.

Dr. Richie pointed out that some interventions lack evidence for the treatment of mild cognitive impairment, but Dr. Goetz emphasized that resources are plentiful and can be effective in combination.

“Engaging social workers, pharmacists, nutritionists, physical and occupational therapists, and, on the inpatient side, delirium protocols, chaplains, and music therapists make a huge difference in patient care,” she said.

Dr. Richie and Dr. Goetz report no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Asking a patient who has concerns about memory loss–particular questions can guide referral decisions, according to new research.

Initial questions should zero in on what the patient is forgetting, said Megan Richie, MD, a neurohospitalist at the University of California, San Francisco, who spoke to a virtual audience at the American College of Physicians (ACP) annual Internal Medicine meeting.

Is the patient forgetting to buy things in a store, having trouble recalling events, forgetting important dates? How often do these incidents occur?

These questions “will help get at how pervasive and how likely the memory loss is affecting their lives, versus a subjective complaint that doesn’t have much impact on the day-to-day function,” she said.

It’s also important to ask whether other neurocognitive symptoms accompany the memory loss, Dr. Richie noted.

Does the patient search for words, struggle with attention, or have problems with executive function? Does the patient have psychiatric symptoms, such as hallucinations or delusions, or other neurologic complaints, including weakness, numbness, vision change, or movement disorders?

“When you know how many neurocognitive symptoms they have, think about how [those symptoms] are affecting their safety and functional status. How are they on their activities of daily living?” Dr. Richie suggests.

Also ask whether the patient is taking medications and whether they drive a vehicle. If they do drive, do they get lost?

“These are all going to help you determine the acuity of the workup,” she said.

After a thorough history, cognitive screening is the next consideration.
 

Cognitive screening can be performed in minutes

One of the tests Dr. Richie recommends is the Mini-Cog. It takes 3 minutes to administer and has been formally recommended by the Alzheimer’s Association because it can be completed in the time frame of a Medicare wellness visit, she said.

It entails a three-word recall and clock-drawing test.

Dr. Richie said it’s important to eliminate some key causes first: “Certainly if the patient has signs and symptoms of depression, pseudodementia is a very real and treatable disease you do not want to miss and should consider in these patients,” she pointed out.

Systemic medical conditions can also lead to memory loss.

If there’s an acute component to the complaint, a new infection or medication withdrawal or a side effect could be driving it, so that’s key in questioning.

Dr. Richie explained that the American Academy of Neurology recommends a very limited workup.

“It’s really just to check their thyroid, their vitamin B12 levels, and then a one-time picture of their brain, which can be either MRI or a CT, to look for structural problems or vascular dementia or hydrocephalus, etc.”

“You do not routinely need spinal fluid testing or an EEG,” she emphasized.

Signs that a neurologist should be involved include a rapid decline, signs of potential seizures, or that the patient doesn’t seem safe in their condition.

Neuropsychological testing is helpful, but it takes nearly 3 hours and may not be a good choice for restless or aggressive patients, Dr. Richie said.

Such testing is often not available, and if it is, insurance coverage is often a barrier because many plans don’t cover it.

Patients often ask about drugs and supplements they see advertised to help with memory loss. Medications are not helpful for mild cognitive impairment, although there is evidence that some are beneficial for patients with dementia, Dr. Richie said.

Celine Goetz, MD, assistant professor of internal medicine at Rush University Medical Center, Chicago, Illinois, told this news organization that it’s easy to relate to the fear that patients and families feel when cognitive impairment begins to emerge.

“[Dr.] Richie’s talk was right on point for internists like myself who see many patients with memory complaints, cognitive impairment, and dementia. I think we’re all terrified of losing our memory and the social and functional impairment that comes with that,” she said.

Although cognitive impairment and dementia aren’t curable or reversible, Dr. Goetz noted, internists can help patients optimize management of conditions such as diabetes and heart disease, which can affect cognitive function.

Dr. Richie pointed out that some interventions lack evidence for the treatment of mild cognitive impairment, but Dr. Goetz emphasized that resources are plentiful and can be effective in combination.

“Engaging social workers, pharmacists, nutritionists, physical and occupational therapists, and, on the inpatient side, delirium protocols, chaplains, and music therapists make a huge difference in patient care,” she said.

Dr. Richie and Dr. Goetz report no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Physicians and nonphysicians clearly differ in whether or not a PhD or EdD should be able to call themselves ‘doctor,’ a new Medscape poll Who Should Get to Be Called ‘Doctor’? shows. The topic has clearly struck a nerve, since a record number of respondents – over 12,000 – voted in the poll.

Most physicians think it’s appropriate for people with other doctorate degrees such as a PhD or EdD to call themselves ‘doctor,’ although slightly more than half said it depends on the context.

The controversy over who gets to be called a doctor was reignited when a Wall Street Journal opinion piece criticized First Lady Jill Biden, EdD, for wanting to be called “Dr Biden.” The piece also challenged the idea that having a PhD is worth the honorific of ‘doctor.’

Medical ethicist Arthur Caplan, PhD, disagreed with that viewpoint, saying the context matters. For example, he prefers to be called “professor” when he’s introduced to the public rather than “doctor” to avoid any confusion about his professional status.

More than 12,000 clinicians including physicians, medical students, nurses, pharmacists, and other health care professionals responded to the poll. The non-MD clinicians were the most likely to say it was always appropriate to be called “doctor” while physicians were the least likely.
 

Context matters

Large percentages of clinicians – 54% of doctors, 62% of medical students, and 41% of nurses – said that the context matters for being called “doctor.’’

“I earned my PhD in 1995 and my MD in 2000. I think it is contextual. In a research or University setting, “Dr.” seems appropriate for a PhD. That same person in public should probably not hold themselves out as “Dr.” So, maybe MDs and DOs can choose, while others maintain the title in their specific setting.” 

Some readers proposed that people with MDs call themselves physicians rather than doctors. Said one: “Anyone with a terminal doctorate degree has the right to use the word doctor.  As a physician when someone asks what I do, I say: ‘I am a physician.’ Problem solved. There can only be one physician but there are many types of doctors.”

Physicians and nurses differed most in their views. Just 24% of physicians said it was always appropriate for people with other doctorate degrees to call themselves doctor whereas about an equal number (22%) thought it was never appropriate.

In contrast, 43% of nurses (including advance practice nurses) said it was always appropriate for people with non-MD doctorates to be called doctor. Only 16% said it’s never appropriate. 

This difference may reflect the growing number of nurses with doctorate degrees, either a DNP or PhD, who want to be called doctor in clinical settings.

Age made a difference too. Only 16% of physicians younger than age 45 said it was always appropriate for people with non-MD doctorate degrees to be called doctor, compared with 27% of physicians aged 45 and up.

Medical students (31%) were also more likely than physicians to say it was always appropriate for non-MD doctorates to use the title “doctor” and 64% said it depends on the context. This was noteworthy because twice as many medical students as physicians (16% vs. 8%) said they work in academia, research, or military government settings.
 

Too many ‘doctors’ confuse the public

Physicians (70%) were also more likely to say it was always or often confusing for the public to hear someone without a medical degree addressed as “doctor.” Only 6% of physicians thought it was never or rarely confusing.

Nurses disagreed. Just 45% said that it was always or often confusing while 16% said it was never or rarely confusing.

Medical students were more aligned with physicians on this issue – 60% said it was always or often confusing to the public and just 10% said it was never or rarely confusing.  

One reader commented, “The problem is the confusion the ‘doctor’ title causes for patients, especially in a hospital setting. Is the ‘doctor’ a physician, a pharmacist, a psychologist, a nurse, etc., etc.? We need to think not of our own egos but if and how  the confusion about this plethora of titles may be hindering good patient care.”

These concerns are not unfounded. The American Medical Association reported in its Truth in Advertising campaign that “patients mistake physicians with nonphysician providers” based on an online survey of 802 adults in 2018. The participants thought these specialists were MDs: dentists (61%), podiatrists (67%), optometrists (47%), psychologists (43%), doctors of nursing (39%), and chiropractors (27%).

The AMA has advocated that states pass the “Health Care Professional Transparency Act,” which New Jersey has enacted. The law requires all health care professionals dealing with patients to wear a name tag that clearly identifies their licensure. Health care professionals must also display their education, training, and licensure in their office.

A version of this article first appeared on Medscape.com.

Physicians and nonphysicians clearly differ in whether or not a PhD or EdD should be able to call themselves ‘doctor,’ a new Medscape poll Who Should Get to Be Called ‘Doctor’? shows. The topic has clearly struck a nerve, since a record number of respondents – over 12,000 – voted in the poll.

Most physicians think it’s appropriate for people with other doctorate degrees such as a PhD or EdD to call themselves ‘doctor,’ although slightly more than half said it depends on the context.

The controversy over who gets to be called a doctor was reignited when a Wall Street Journal opinion piece criticized First Lady Jill Biden, EdD, for wanting to be called “Dr Biden.” The piece also challenged the idea that having a PhD is worth the honorific of ‘doctor.’

Medical ethicist Arthur Caplan, PhD, disagreed with that viewpoint, saying the context matters. For example, he prefers to be called “professor” when he’s introduced to the public rather than “doctor” to avoid any confusion about his professional status.

More than 12,000 clinicians including physicians, medical students, nurses, pharmacists, and other health care professionals responded to the poll. The non-MD clinicians were the most likely to say it was always appropriate to be called “doctor” while physicians were the least likely.
 

Context matters

Large percentages of clinicians – 54% of doctors, 62% of medical students, and 41% of nurses – said that the context matters for being called “doctor.’’

“I earned my PhD in 1995 and my MD in 2000. I think it is contextual. In a research or University setting, “Dr.” seems appropriate for a PhD. That same person in public should probably not hold themselves out as “Dr.” So, maybe MDs and DOs can choose, while others maintain the title in their specific setting.” 

Some readers proposed that people with MDs call themselves physicians rather than doctors. Said one: “Anyone with a terminal doctorate degree has the right to use the word doctor.  As a physician when someone asks what I do, I say: ‘I am a physician.’ Problem solved. There can only be one physician but there are many types of doctors.”

Physicians and nurses differed most in their views. Just 24% of physicians said it was always appropriate for people with other doctorate degrees to call themselves doctor whereas about an equal number (22%) thought it was never appropriate.

In contrast, 43% of nurses (including advance practice nurses) said it was always appropriate for people with non-MD doctorates to be called doctor. Only 16% said it’s never appropriate. 

This difference may reflect the growing number of nurses with doctorate degrees, either a DNP or PhD, who want to be called doctor in clinical settings.

Age made a difference too. Only 16% of physicians younger than age 45 said it was always appropriate for people with non-MD doctorate degrees to be called doctor, compared with 27% of physicians aged 45 and up.

Medical students (31%) were also more likely than physicians to say it was always appropriate for non-MD doctorates to use the title “doctor” and 64% said it depends on the context. This was noteworthy because twice as many medical students as physicians (16% vs. 8%) said they work in academia, research, or military government settings.
 

Too many ‘doctors’ confuse the public

Physicians (70%) were also more likely to say it was always or often confusing for the public to hear someone without a medical degree addressed as “doctor.” Only 6% of physicians thought it was never or rarely confusing.

Nurses disagreed. Just 45% said that it was always or often confusing while 16% said it was never or rarely confusing.

Medical students were more aligned with physicians on this issue – 60% said it was always or often confusing to the public and just 10% said it was never or rarely confusing.  

One reader commented, “The problem is the confusion the ‘doctor’ title causes for patients, especially in a hospital setting. Is the ‘doctor’ a physician, a pharmacist, a psychologist, a nurse, etc., etc.? We need to think not of our own egos but if and how  the confusion about this plethora of titles may be hindering good patient care.”

These concerns are not unfounded. The American Medical Association reported in its Truth in Advertising campaign that “patients mistake physicians with nonphysician providers” based on an online survey of 802 adults in 2018. The participants thought these specialists were MDs: dentists (61%), podiatrists (67%), optometrists (47%), psychologists (43%), doctors of nursing (39%), and chiropractors (27%).

The AMA has advocated that states pass the “Health Care Professional Transparency Act,” which New Jersey has enacted. The law requires all health care professionals dealing with patients to wear a name tag that clearly identifies their licensure. Health care professionals must also display their education, training, and licensure in their office.

A version of this article first appeared on Medscape.com.

Physicians and nonphysicians clearly differ in whether or not a PhD or EdD should be able to call themselves ‘doctor,’ a new Medscape poll Who Should Get to Be Called ‘Doctor’? shows. The topic has clearly struck a nerve, since a record number of respondents – over 12,000 – voted in the poll.

Most physicians think it’s appropriate for people with other doctorate degrees such as a PhD or EdD to call themselves ‘doctor,’ although slightly more than half said it depends on the context.

The controversy over who gets to be called a doctor was reignited when a Wall Street Journal opinion piece criticized First Lady Jill Biden, EdD, for wanting to be called “Dr Biden.” The piece also challenged the idea that having a PhD is worth the honorific of ‘doctor.’

Medical ethicist Arthur Caplan, PhD, disagreed with that viewpoint, saying the context matters. For example, he prefers to be called “professor” when he’s introduced to the public rather than “doctor” to avoid any confusion about his professional status.

More than 12,000 clinicians including physicians, medical students, nurses, pharmacists, and other health care professionals responded to the poll. The non-MD clinicians were the most likely to say it was always appropriate to be called “doctor” while physicians were the least likely.
 

Context matters

Large percentages of clinicians – 54% of doctors, 62% of medical students, and 41% of nurses – said that the context matters for being called “doctor.’’

“I earned my PhD in 1995 and my MD in 2000. I think it is contextual. In a research or University setting, “Dr.” seems appropriate for a PhD. That same person in public should probably not hold themselves out as “Dr.” So, maybe MDs and DOs can choose, while others maintain the title in their specific setting.” 

Some readers proposed that people with MDs call themselves physicians rather than doctors. Said one: “Anyone with a terminal doctorate degree has the right to use the word doctor.  As a physician when someone asks what I do, I say: ‘I am a physician.’ Problem solved. There can only be one physician but there are many types of doctors.”

Physicians and nurses differed most in their views. Just 24% of physicians said it was always appropriate for people with other doctorate degrees to call themselves doctor whereas about an equal number (22%) thought it was never appropriate.

In contrast, 43% of nurses (including advance practice nurses) said it was always appropriate for people with non-MD doctorates to be called doctor. Only 16% said it’s never appropriate. 

This difference may reflect the growing number of nurses with doctorate degrees, either a DNP or PhD, who want to be called doctor in clinical settings.

Age made a difference too. Only 16% of physicians younger than age 45 said it was always appropriate for people with non-MD doctorate degrees to be called doctor, compared with 27% of physicians aged 45 and up.

Medical students (31%) were also more likely than physicians to say it was always appropriate for non-MD doctorates to use the title “doctor” and 64% said it depends on the context. This was noteworthy because twice as many medical students as physicians (16% vs. 8%) said they work in academia, research, or military government settings.
 

Too many ‘doctors’ confuse the public

Physicians (70%) were also more likely to say it was always or often confusing for the public to hear someone without a medical degree addressed as “doctor.” Only 6% of physicians thought it was never or rarely confusing.

Nurses disagreed. Just 45% said that it was always or often confusing while 16% said it was never or rarely confusing.

Medical students were more aligned with physicians on this issue – 60% said it was always or often confusing to the public and just 10% said it was never or rarely confusing.  

One reader commented, “The problem is the confusion the ‘doctor’ title causes for patients, especially in a hospital setting. Is the ‘doctor’ a physician, a pharmacist, a psychologist, a nurse, etc., etc.? We need to think not of our own egos but if and how  the confusion about this plethora of titles may be hindering good patient care.”

These concerns are not unfounded. The American Medical Association reported in its Truth in Advertising campaign that “patients mistake physicians with nonphysician providers” based on an online survey of 802 adults in 2018. The participants thought these specialists were MDs: dentists (61%), podiatrists (67%), optometrists (47%), psychologists (43%), doctors of nursing (39%), and chiropractors (27%).

The AMA has advocated that states pass the “Health Care Professional Transparency Act,” which New Jersey has enacted. The law requires all health care professionals dealing with patients to wear a name tag that clearly identifies their licensure. Health care professionals must also display their education, training, and licensure in their office.

A version of this article first appeared on Medscape.com.

Recently, a patient excitedly told me during her session that she had been coming to see me for about 24 years. This was followed by positive remarks about where she was at the point when she first walked into my office.

Her progress has been slow but steady – and today, she finds herself at a much better place even within the context of having to deal with life’s complications. Her surprise about the longevity of this therapeutic relationship was easily and comfortably balanced by the pleasant feeling of well-being.

This interaction reminded me of a conversation I had with a friend of mine, an ophthalmologist who once asked me a related question: Why is it that people have been coming to see me for decades and I have not been able to “fix” them? Does that make me feel badly?

I clearly remember my response, which started in more of a defensive mode but ended with some self-reflection. I reminded him that, in his specialty, like many other fields of medicine, we don’t get to “fix” a lot. In fact, the majority of the conditions we deal with are chronic and lingering.

However, during the process of reminding him to look in the mirror, I was also able to articulate that many of these patients came into my office in potentially dire situations, including experiencing severe depression and suicidal thoughts, ignoring basic needs such as hygiene, feeling paralyzed with panic attacks, or having complete inability to deal with day-to-day situations.

Decades later, many of these patients, while still struggling with some ongoing issues, appeared to be alive and well – and we have wonderful interactions in our office where I get to talk to them about exciting things they’re looking forward to doing with their families or for themselves. Similar analogies can be applied to almost all medical specialties. An endocrinologist might help a patient with severe diabetes or hypothyroid disease get the illness under control but is not able to fix the problem. Clearly, patients’ quality of life improves tremendously through treatment with medications and with education about lifestyle changes, such as exercise and diet.

Even in the case of surgeons who may successfully remove the problem tissue or tumor, the patient is not in fact “fixed” and still requires ongoing medical care, psychosocial interventions, and pharmacotherapy to maintain or improve upon quality of life.

My patient’s remarks led to a similar, delightful therapeutic session reflecting on her progress and what it meant to both of us. We physicians certainly find it very frustrating that we are unable to fix things and make people feel completely better. However, it is important to reflect on the difference our contribution to the process of healing makes for our patients and the impact it has on their quality of life – which is meaningful to them, however small it may be.

Even in the most severe medical or psychiatric cases, we can provide hope and encouragement, which could lead to minimal or no improvement in the pathological condition but may in fact improve patients’ outlook and willingness to carry on with dignity and satisfaction. It could do us all a lot of good to think of ourselves as healers – not fixers.
 

Dr. Awan, a psychiatrist, is medical director of Pennsylvania Counseling Services in Reading. He disclosed no conflicts of interest.

Recently, a patient excitedly told me during her session that she had been coming to see me for about 24 years. This was followed by positive remarks about where she was at the point when she first walked into my office.

Her progress has been slow but steady – and today, she finds herself at a much better place even within the context of having to deal with life’s complications. Her surprise about the longevity of this therapeutic relationship was easily and comfortably balanced by the pleasant feeling of well-being.

This interaction reminded me of a conversation I had with a friend of mine, an ophthalmologist who once asked me a related question: Why is it that people have been coming to see me for decades and I have not been able to “fix” them? Does that make me feel badly?

I clearly remember my response, which started in more of a defensive mode but ended with some self-reflection. I reminded him that, in his specialty, like many other fields of medicine, we don’t get to “fix” a lot. In fact, the majority of the conditions we deal with are chronic and lingering.

However, during the process of reminding him to look in the mirror, I was also able to articulate that many of these patients came into my office in potentially dire situations, including experiencing severe depression and suicidal thoughts, ignoring basic needs such as hygiene, feeling paralyzed with panic attacks, or having complete inability to deal with day-to-day situations.

Decades later, many of these patients, while still struggling with some ongoing issues, appeared to be alive and well – and we have wonderful interactions in our office where I get to talk to them about exciting things they’re looking forward to doing with their families or for themselves. Similar analogies can be applied to almost all medical specialties. An endocrinologist might help a patient with severe diabetes or hypothyroid disease get the illness under control but is not able to fix the problem. Clearly, patients’ quality of life improves tremendously through treatment with medications and with education about lifestyle changes, such as exercise and diet.

Even in the case of surgeons who may successfully remove the problem tissue or tumor, the patient is not in fact “fixed” and still requires ongoing medical care, psychosocial interventions, and pharmacotherapy to maintain or improve upon quality of life.

My patient’s remarks led to a similar, delightful therapeutic session reflecting on her progress and what it meant to both of us. We physicians certainly find it very frustrating that we are unable to fix things and make people feel completely better. However, it is important to reflect on the difference our contribution to the process of healing makes for our patients and the impact it has on their quality of life – which is meaningful to them, however small it may be.

Even in the most severe medical or psychiatric cases, we can provide hope and encouragement, which could lead to minimal or no improvement in the pathological condition but may in fact improve patients’ outlook and willingness to carry on with dignity and satisfaction. It could do us all a lot of good to think of ourselves as healers – not fixers.
 

Dr. Awan, a psychiatrist, is medical director of Pennsylvania Counseling Services in Reading. He disclosed no conflicts of interest.

Recently, a patient excitedly told me during her session that she had been coming to see me for about 24 years. This was followed by positive remarks about where she was at the point when she first walked into my office.

Her progress has been slow but steady – and today, she finds herself at a much better place even within the context of having to deal with life’s complications. Her surprise about the longevity of this therapeutic relationship was easily and comfortably balanced by the pleasant feeling of well-being.

This interaction reminded me of a conversation I had with a friend of mine, an ophthalmologist who once asked me a related question: Why is it that people have been coming to see me for decades and I have not been able to “fix” them? Does that make me feel badly?

I clearly remember my response, which started in more of a defensive mode but ended with some self-reflection. I reminded him that, in his specialty, like many other fields of medicine, we don’t get to “fix” a lot. In fact, the majority of the conditions we deal with are chronic and lingering.

However, during the process of reminding him to look in the mirror, I was also able to articulate that many of these patients came into my office in potentially dire situations, including experiencing severe depression and suicidal thoughts, ignoring basic needs such as hygiene, feeling paralyzed with panic attacks, or having complete inability to deal with day-to-day situations.

Decades later, many of these patients, while still struggling with some ongoing issues, appeared to be alive and well – and we have wonderful interactions in our office where I get to talk to them about exciting things they’re looking forward to doing with their families or for themselves. Similar analogies can be applied to almost all medical specialties. An endocrinologist might help a patient with severe diabetes or hypothyroid disease get the illness under control but is not able to fix the problem. Clearly, patients’ quality of life improves tremendously through treatment with medications and with education about lifestyle changes, such as exercise and diet.

Even in the case of surgeons who may successfully remove the problem tissue or tumor, the patient is not in fact “fixed” and still requires ongoing medical care, psychosocial interventions, and pharmacotherapy to maintain or improve upon quality of life.

My patient’s remarks led to a similar, delightful therapeutic session reflecting on her progress and what it meant to both of us. We physicians certainly find it very frustrating that we are unable to fix things and make people feel completely better. However, it is important to reflect on the difference our contribution to the process of healing makes for our patients and the impact it has on their quality of life – which is meaningful to them, however small it may be.

Even in the most severe medical or psychiatric cases, we can provide hope and encouragement, which could lead to minimal or no improvement in the pathological condition but may in fact improve patients’ outlook and willingness to carry on with dignity and satisfaction. It could do us all a lot of good to think of ourselves as healers – not fixers.
 

Dr. Awan, a psychiatrist, is medical director of Pennsylvania Counseling Services in Reading. He disclosed no conflicts of interest.