Doug Brunk

DALLAS – The way Lilyana Amezcua, MD, sees it, clinicians should view race and ethnicity as health disparities when assessing individuals with multiple sclerosis.

Whites are predominately affected with MS, “but we have seen changing demographics,” said Dr. Amezcua, of the University of Southern California MS Comprehensive Care and Research Group. “Why are African Americans now at higher risk ... and why do African Americans appear to have more severe disease? Is it a biological difference ... or is it because of poor access” to health care?

At the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis, Dr. Amezcua delivered a presentation entitled “Effect of Race and Ethnicity on MS Presentation and Disease Course.” She called on researchers in the field “to not just take race and ethnicity as any small variable. We need to be cognizant and use the correct methodology, depending on what [question] we want to answer. We need to better define how we ascertain race, how we ascertain ethnicity.”

Dr. Amezcua, who is also the MS fellowship program director at the Keck School of Medicine, disclosed that she receives funding from the National MS Society, the National Institutes of Health, the California Community Foundation, and Biogen.

[email protected]

DALLAS – The way Lilyana Amezcua, MD, sees it, clinicians should view race and ethnicity as health disparities when assessing individuals with multiple sclerosis.

Whites are predominately affected with MS, “but we have seen changing demographics,” said Dr. Amezcua, of the University of Southern California MS Comprehensive Care and Research Group. “Why are African Americans now at higher risk ... and why do African Americans appear to have more severe disease? Is it a biological difference ... or is it because of poor access” to health care?

At the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis, Dr. Amezcua delivered a presentation entitled “Effect of Race and Ethnicity on MS Presentation and Disease Course.” She called on researchers in the field “to not just take race and ethnicity as any small variable. We need to be cognizant and use the correct methodology, depending on what [question] we want to answer. We need to better define how we ascertain race, how we ascertain ethnicity.”

Dr. Amezcua, who is also the MS fellowship program director at the Keck School of Medicine, disclosed that she receives funding from the National MS Society, the National Institutes of Health, the California Community Foundation, and Biogen.

[email protected]

DALLAS – The way Lilyana Amezcua, MD, sees it, clinicians should view race and ethnicity as health disparities when assessing individuals with multiple sclerosis.

Whites are predominately affected with MS, “but we have seen changing demographics,” said Dr. Amezcua, of the University of Southern California MS Comprehensive Care and Research Group. “Why are African Americans now at higher risk ... and why do African Americans appear to have more severe disease? Is it a biological difference ... or is it because of poor access” to health care?

At the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis, Dr. Amezcua delivered a presentation entitled “Effect of Race and Ethnicity on MS Presentation and Disease Course.” She called on researchers in the field “to not just take race and ethnicity as any small variable. We need to be cognizant and use the correct methodology, depending on what [question] we want to answer. We need to better define how we ascertain race, how we ascertain ethnicity.”

Dr. Amezcua, who is also the MS fellowship program director at the Keck School of Medicine, disclosed that she receives funding from the National MS Society, the National Institutes of Health, the California Community Foundation, and Biogen.

[email protected]

DALLAS – In 2 years of follow-up, about 43% of U.S. patients diagnosed with multiple sclerosis (MS) had not received disease-modifying drug (DMD) therapy, a rate that is consistent with other published studies.

The finding comes from a retrospective analysis of claims data presented at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. “This rate of DMD treatment merits further exploration given that evidence suggests the importance of early DMD treatment initiation in patients with a confirmed diagnosis of relapsing forms of MS to help optimize the benefits of treatment,” Amy L. Phillips, PharmD, a study author, said in an interview in advance of the meeting.

Little is known about current DMD treatment patterns in U.S. patients with multiple sclerosis following an increase in the number of available DMDs in recent years, according to Dr. Phillips of the department of health economics and outcomes research at EMD Serono.

“Most previous studies have focused on self-injectable DMDs or self-injectable and infusion DMDs,” she said. “Information about the treatment patterns including oral DMDs is scarce, particularly in large population samples. The objective of our study was to describe treatment patterns and sequences of therapy among U.S. patients with MS newly initiating DMD treatment between Jan. 1, 2011 and June 30, 2015.”

Dr. Phillips, lead study author Jacqueline A. Nicholas, MD, MPH, of the OhioHealth Multiple Sclerosis Center, and their colleagues used data from the IQVIA RWD Adjudicated Claims database to identify patients who had at least two medical claims with a MS diagnosis and at least one DMD claim during the study period. Other eligibility criteria included continuous eligibility with commercial insurance 1 year before (baseline period) and 2 years after (follow-up period) initiation of the DMD, no evidence of DMD use during the baseline period, and being aged between 18 and 63 years.

Of 63,946 diagnostically eligible patients, 36,175 (57%) had a claim for a DMD. The researchers reported findings from 8,251 patients who met all of the eligibility criteria. Their mean age was 43 years, 76% were female, and the mean number of DMDs over 2 years among newly treated patients was 1.27.

The most common first-line DMD therapy was glatiramer acetate (GA, 38%), followed by intramuscular interferon beta (IM IFNb-1a, 14%), subcutaneous interferon beta (SC IFNb-1a, 14%), dimethyl fumarate (DMF, 14%), and fingolimod (9%). DMF was the most common second-line therapy (36%), followed by fingolimod (17%), GA (17%), SC IFNb-1a (8%), and IM IFNb-1a (7%).

“Numerous DMD treatment patterns observed in this study highlight the diverse patient and treatment needs,” Dr. Phillips said. “DMD treatment patterns in MS vary due to the heterogeneity of the disease, physician preferences, and patient needs and treatment goals. Patient-centered care and shared decision making has been shown to improve patient satisfaction and to encourage treatment adherence in MS.”

She acknowledged certain limitations of the study, including the fact that the analysis presents only the most common DMD treatment sequences observed in this patient population.

“Future analyses might examine less common DMD treatment sequences,” she said. “Also, more research is needed to understand how DMD treatment patterns and sequences change over time, and the factors that may be associated with DMD switching and treatment discontinuation.”

She also noted that the administrative claims data studied represent mostly patients with commercial health insurance, limiting the generalizability of the findings. Further, ICD-9 and ICD-10 codes do not distinguish between MS types.

Funding for the study was provided by EMD Serono, the biopharmaceutical business of Merck KGaA, Darmstadt, Germany, in the United States and Canada. Dr. Phillips is an employee of the company.

[email protected]

SOURCE: Phillips A et al. ACTRIMS FORUM 2019, Abstract 001.

DALLAS – In 2 years of follow-up, about 43% of U.S. patients diagnosed with multiple sclerosis (MS) had not received disease-modifying drug (DMD) therapy, a rate that is consistent with other published studies.

The finding comes from a retrospective analysis of claims data presented at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. “This rate of DMD treatment merits further exploration given that evidence suggests the importance of early DMD treatment initiation in patients with a confirmed diagnosis of relapsing forms of MS to help optimize the benefits of treatment,” Amy L. Phillips, PharmD, a study author, said in an interview in advance of the meeting.

Little is known about current DMD treatment patterns in U.S. patients with multiple sclerosis following an increase in the number of available DMDs in recent years, according to Dr. Phillips of the department of health economics and outcomes research at EMD Serono.

“Most previous studies have focused on self-injectable DMDs or self-injectable and infusion DMDs,” she said. “Information about the treatment patterns including oral DMDs is scarce, particularly in large population samples. The objective of our study was to describe treatment patterns and sequences of therapy among U.S. patients with MS newly initiating DMD treatment between Jan. 1, 2011 and June 30, 2015.”

Dr. Phillips, lead study author Jacqueline A. Nicholas, MD, MPH, of the OhioHealth Multiple Sclerosis Center, and their colleagues used data from the IQVIA RWD Adjudicated Claims database to identify patients who had at least two medical claims with a MS diagnosis and at least one DMD claim during the study period. Other eligibility criteria included continuous eligibility with commercial insurance 1 year before (baseline period) and 2 years after (follow-up period) initiation of the DMD, no evidence of DMD use during the baseline period, and being aged between 18 and 63 years.

Of 63,946 diagnostically eligible patients, 36,175 (57%) had a claim for a DMD. The researchers reported findings from 8,251 patients who met all of the eligibility criteria. Their mean age was 43 years, 76% were female, and the mean number of DMDs over 2 years among newly treated patients was 1.27.

The most common first-line DMD therapy was glatiramer acetate (GA, 38%), followed by intramuscular interferon beta (IM IFNb-1a, 14%), subcutaneous interferon beta (SC IFNb-1a, 14%), dimethyl fumarate (DMF, 14%), and fingolimod (9%). DMF was the most common second-line therapy (36%), followed by fingolimod (17%), GA (17%), SC IFNb-1a (8%), and IM IFNb-1a (7%).

“Numerous DMD treatment patterns observed in this study highlight the diverse patient and treatment needs,” Dr. Phillips said. “DMD treatment patterns in MS vary due to the heterogeneity of the disease, physician preferences, and patient needs and treatment goals. Patient-centered care and shared decision making has been shown to improve patient satisfaction and to encourage treatment adherence in MS.”

She acknowledged certain limitations of the study, including the fact that the analysis presents only the most common DMD treatment sequences observed in this patient population.

“Future analyses might examine less common DMD treatment sequences,” she said. “Also, more research is needed to understand how DMD treatment patterns and sequences change over time, and the factors that may be associated with DMD switching and treatment discontinuation.”

She also noted that the administrative claims data studied represent mostly patients with commercial health insurance, limiting the generalizability of the findings. Further, ICD-9 and ICD-10 codes do not distinguish between MS types.

Funding for the study was provided by EMD Serono, the biopharmaceutical business of Merck KGaA, Darmstadt, Germany, in the United States and Canada. Dr. Phillips is an employee of the company.

[email protected]

SOURCE: Phillips A et al. ACTRIMS FORUM 2019, Abstract 001.

DALLAS – In 2 years of follow-up, about 43% of U.S. patients diagnosed with multiple sclerosis (MS) had not received disease-modifying drug (DMD) therapy, a rate that is consistent with other published studies.

The finding comes from a retrospective analysis of claims data presented at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. “This rate of DMD treatment merits further exploration given that evidence suggests the importance of early DMD treatment initiation in patients with a confirmed diagnosis of relapsing forms of MS to help optimize the benefits of treatment,” Amy L. Phillips, PharmD, a study author, said in an interview in advance of the meeting.

Little is known about current DMD treatment patterns in U.S. patients with multiple sclerosis following an increase in the number of available DMDs in recent years, according to Dr. Phillips of the department of health economics and outcomes research at EMD Serono.

“Most previous studies have focused on self-injectable DMDs or self-injectable and infusion DMDs,” she said. “Information about the treatment patterns including oral DMDs is scarce, particularly in large population samples. The objective of our study was to describe treatment patterns and sequences of therapy among U.S. patients with MS newly initiating DMD treatment between Jan. 1, 2011 and June 30, 2015.”

Dr. Phillips, lead study author Jacqueline A. Nicholas, MD, MPH, of the OhioHealth Multiple Sclerosis Center, and their colleagues used data from the IQVIA RWD Adjudicated Claims database to identify patients who had at least two medical claims with a MS diagnosis and at least one DMD claim during the study period. Other eligibility criteria included continuous eligibility with commercial insurance 1 year before (baseline period) and 2 years after (follow-up period) initiation of the DMD, no evidence of DMD use during the baseline period, and being aged between 18 and 63 years.

Of 63,946 diagnostically eligible patients, 36,175 (57%) had a claim for a DMD. The researchers reported findings from 8,251 patients who met all of the eligibility criteria. Their mean age was 43 years, 76% were female, and the mean number of DMDs over 2 years among newly treated patients was 1.27.

The most common first-line DMD therapy was glatiramer acetate (GA, 38%), followed by intramuscular interferon beta (IM IFNb-1a, 14%), subcutaneous interferon beta (SC IFNb-1a, 14%), dimethyl fumarate (DMF, 14%), and fingolimod (9%). DMF was the most common second-line therapy (36%), followed by fingolimod (17%), GA (17%), SC IFNb-1a (8%), and IM IFNb-1a (7%).

“Numerous DMD treatment patterns observed in this study highlight the diverse patient and treatment needs,” Dr. Phillips said. “DMD treatment patterns in MS vary due to the heterogeneity of the disease, physician preferences, and patient needs and treatment goals. Patient-centered care and shared decision making has been shown to improve patient satisfaction and to encourage treatment adherence in MS.”

She acknowledged certain limitations of the study, including the fact that the analysis presents only the most common DMD treatment sequences observed in this patient population.

“Future analyses might examine less common DMD treatment sequences,” she said. “Also, more research is needed to understand how DMD treatment patterns and sequences change over time, and the factors that may be associated with DMD switching and treatment discontinuation.”

She also noted that the administrative claims data studied represent mostly patients with commercial health insurance, limiting the generalizability of the findings. Further, ICD-9 and ICD-10 codes do not distinguish between MS types.

Funding for the study was provided by EMD Serono, the biopharmaceutical business of Merck KGaA, Darmstadt, Germany, in the United States and Canada. Dr. Phillips is an employee of the company.

[email protected]

SOURCE: Phillips A et al. ACTRIMS FORUM 2019, Abstract 001.

DALLAS – A number of sociodemographic factors may influence health and disability insurance access by individuals with multiple sclerosis, including employment, age, gender, disease duration, marital status, and ethnicity, results from a large survey suggest.

“The last similar work was conducted over 10 years ago and so much has happened in the meantime, including the Great Recession and the introduction of the Affordable Care Act, that offers protection for health care but not for other important types of insurance (short- and long-term disability, long-term care, and life),” lead study author Sarah Planchon, PhD, said in an interview in advance of the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. “MS is one of the most costly chronic diseases today. That is not only because of the cost of disease-modifying therapies but also because of lost employment and income. We wanted to better understand the insurance landscape so that we could in turn educate patients and professionals about the protection these insurances offer and advise them on how to obtain these policies.”

In an effort to evaluate factors that affect insurance access in MS, Dr. Planchon, a project scientist at the Mellen Center for Multiple Sclerosis at the Cleveland Clinic in Ohio, and her colleagues used the North American Research Committee on MS (NARCOMS), iConquerMS, and the National Multiple Sclerosis Society to survey 2,507 individuals with the disease regarding insurance, demographic, health, disability, and employment status. They used covariate-adjusted nominal logistic regression to estimate odds ratios for the likelihood of having or not having a type of insurance. The majority of respondents (83%) were female, their mean age was 54 years, 91% were white, 65% were currently married, and their mean disease duration at the time of the survey was 16 years. In addition, 43% were employed full/part-time, and 29% were not employed or retired because of disability. Nearly all respondents (96%) reported having health insurance, while 59% had life insurance, 29% had private long-term disability insurance, 18% had short-term disability insurance, and 10% had long-term care insurance.

The researchers found that employment status had the greatest impact on insurance coverage. Of those with health insurance, 33% were employed full-time, compared with 89% of those with short-term disability insurance, 42% of those with private long-term disability insurance, 44% of those with long-term care insurance, and 41% of those with life insurance. Logistic regression analyses indicated that respondents employed part time were significantly more likely to have short-term disability insurance if they were currently married (odds ratio, 4.4). Short-term disability insurance was significantly more likely among fully employed patients with disease duration of 5-10 years vs. more than 20 years (OR, 2.0). Private long-term disability insurance was significantly associated with female gender (OR, 1.6), age 50-59 years vs. younger than 40 (OR, 1.6), full-time vs. part-time employment (OR, 2.3), and shorter disease duration (ORs, 1.4-1.6 for 6-10, 11-15, and 16-20 years’ duration). Long-term care insurance was associated with older age (ORs, 2.5 and 4.3 for those aged 50-59 and 60-65 vs. younger than 40), and having excellent or good general health status vs. fair or poor (OR, 1.8). Life insurance was associated with non-Hispanic ethnicity (OR, 1.6), full-time vs. part-time employment (OR, 2.4), older age (ORs, 1.6-1.7 for ages 40-49 and 50-59 vs. younger than 40), and marital status (currently/previously married, ORs, 1.6-2.6). Considering the high rate of survey respondents with health insurance, covariate-adjusted modeling was not applicable.

“The number of people with MS who do not have long-term care insurance was surprisingly high,” Dr. Planchon said. “Although the improved treatment climate recently may decrease the long-term disability levels, we do not yet know this with certainty. A large number of people with MS are likely to need long-term care in the future, which often is a significant financial burden to families.” The findings suggest that clinical care teams “need to initiate early discussions of possible long-term needs with their patients,” she continued. “Incorporation of social work teams, who are familiar with the needs of people with MS and insurance options available to them, within MS specialty practices will bolster the comprehensive care of patients and their families.”

She acknowledged certain limitations of the study, including the low proportion of respondents who were Hispanic/Latino and African American (about 4% each). “The insurance landscape may differ in these groups compared to the majority Caucasian population who responded to this survey,” Dr. Planchon said.

The National Multiple Sclerosis Society funded the study. Dr. Planchon reported having no relevant financial disclosures.

[email protected]

SOURCE: Planchon S et al. ACTRIMS Forum 2019, Abstract P295.

DALLAS – A number of sociodemographic factors may influence health and disability insurance access by individuals with multiple sclerosis, including employment, age, gender, disease duration, marital status, and ethnicity, results from a large survey suggest.

“The last similar work was conducted over 10 years ago and so much has happened in the meantime, including the Great Recession and the introduction of the Affordable Care Act, that offers protection for health care but not for other important types of insurance (short- and long-term disability, long-term care, and life),” lead study author Sarah Planchon, PhD, said in an interview in advance of the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. “MS is one of the most costly chronic diseases today. That is not only because of the cost of disease-modifying therapies but also because of lost employment and income. We wanted to better understand the insurance landscape so that we could in turn educate patients and professionals about the protection these insurances offer and advise them on how to obtain these policies.”

In an effort to evaluate factors that affect insurance access in MS, Dr. Planchon, a project scientist at the Mellen Center for Multiple Sclerosis at the Cleveland Clinic in Ohio, and her colleagues used the North American Research Committee on MS (NARCOMS), iConquerMS, and the National Multiple Sclerosis Society to survey 2,507 individuals with the disease regarding insurance, demographic, health, disability, and employment status. They used covariate-adjusted nominal logistic regression to estimate odds ratios for the likelihood of having or not having a type of insurance. The majority of respondents (83%) were female, their mean age was 54 years, 91% were white, 65% were currently married, and their mean disease duration at the time of the survey was 16 years. In addition, 43% were employed full/part-time, and 29% were not employed or retired because of disability. Nearly all respondents (96%) reported having health insurance, while 59% had life insurance, 29% had private long-term disability insurance, 18% had short-term disability insurance, and 10% had long-term care insurance.

The researchers found that employment status had the greatest impact on insurance coverage. Of those with health insurance, 33% were employed full-time, compared with 89% of those with short-term disability insurance, 42% of those with private long-term disability insurance, 44% of those with long-term care insurance, and 41% of those with life insurance. Logistic regression analyses indicated that respondents employed part time were significantly more likely to have short-term disability insurance if they were currently married (odds ratio, 4.4). Short-term disability insurance was significantly more likely among fully employed patients with disease duration of 5-10 years vs. more than 20 years (OR, 2.0). Private long-term disability insurance was significantly associated with female gender (OR, 1.6), age 50-59 years vs. younger than 40 (OR, 1.6), full-time vs. part-time employment (OR, 2.3), and shorter disease duration (ORs, 1.4-1.6 for 6-10, 11-15, and 16-20 years’ duration). Long-term care insurance was associated with older age (ORs, 2.5 and 4.3 for those aged 50-59 and 60-65 vs. younger than 40), and having excellent or good general health status vs. fair or poor (OR, 1.8). Life insurance was associated with non-Hispanic ethnicity (OR, 1.6), full-time vs. part-time employment (OR, 2.4), older age (ORs, 1.6-1.7 for ages 40-49 and 50-59 vs. younger than 40), and marital status (currently/previously married, ORs, 1.6-2.6). Considering the high rate of survey respondents with health insurance, covariate-adjusted modeling was not applicable.

“The number of people with MS who do not have long-term care insurance was surprisingly high,” Dr. Planchon said. “Although the improved treatment climate recently may decrease the long-term disability levels, we do not yet know this with certainty. A large number of people with MS are likely to need long-term care in the future, which often is a significant financial burden to families.” The findings suggest that clinical care teams “need to initiate early discussions of possible long-term needs with their patients,” she continued. “Incorporation of social work teams, who are familiar with the needs of people with MS and insurance options available to them, within MS specialty practices will bolster the comprehensive care of patients and their families.”

She acknowledged certain limitations of the study, including the low proportion of respondents who were Hispanic/Latino and African American (about 4% each). “The insurance landscape may differ in these groups compared to the majority Caucasian population who responded to this survey,” Dr. Planchon said.

The National Multiple Sclerosis Society funded the study. Dr. Planchon reported having no relevant financial disclosures.

[email protected]

SOURCE: Planchon S et al. ACTRIMS Forum 2019, Abstract P295.

DALLAS – A number of sociodemographic factors may influence health and disability insurance access by individuals with multiple sclerosis, including employment, age, gender, disease duration, marital status, and ethnicity, results from a large survey suggest.

“The last similar work was conducted over 10 years ago and so much has happened in the meantime, including the Great Recession and the introduction of the Affordable Care Act, that offers protection for health care but not for other important types of insurance (short- and long-term disability, long-term care, and life),” lead study author Sarah Planchon, PhD, said in an interview in advance of the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. “MS is one of the most costly chronic diseases today. That is not only because of the cost of disease-modifying therapies but also because of lost employment and income. We wanted to better understand the insurance landscape so that we could in turn educate patients and professionals about the protection these insurances offer and advise them on how to obtain these policies.”

In an effort to evaluate factors that affect insurance access in MS, Dr. Planchon, a project scientist at the Mellen Center for Multiple Sclerosis at the Cleveland Clinic in Ohio, and her colleagues used the North American Research Committee on MS (NARCOMS), iConquerMS, and the National Multiple Sclerosis Society to survey 2,507 individuals with the disease regarding insurance, demographic, health, disability, and employment status. They used covariate-adjusted nominal logistic regression to estimate odds ratios for the likelihood of having or not having a type of insurance. The majority of respondents (83%) were female, their mean age was 54 years, 91% were white, 65% were currently married, and their mean disease duration at the time of the survey was 16 years. In addition, 43% were employed full/part-time, and 29% were not employed or retired because of disability. Nearly all respondents (96%) reported having health insurance, while 59% had life insurance, 29% had private long-term disability insurance, 18% had short-term disability insurance, and 10% had long-term care insurance.

The researchers found that employment status had the greatest impact on insurance coverage. Of those with health insurance, 33% were employed full-time, compared with 89% of those with short-term disability insurance, 42% of those with private long-term disability insurance, 44% of those with long-term care insurance, and 41% of those with life insurance. Logistic regression analyses indicated that respondents employed part time were significantly more likely to have short-term disability insurance if they were currently married (odds ratio, 4.4). Short-term disability insurance was significantly more likely among fully employed patients with disease duration of 5-10 years vs. more than 20 years (OR, 2.0). Private long-term disability insurance was significantly associated with female gender (OR, 1.6), age 50-59 years vs. younger than 40 (OR, 1.6), full-time vs. part-time employment (OR, 2.3), and shorter disease duration (ORs, 1.4-1.6 for 6-10, 11-15, and 16-20 years’ duration). Long-term care insurance was associated with older age (ORs, 2.5 and 4.3 for those aged 50-59 and 60-65 vs. younger than 40), and having excellent or good general health status vs. fair or poor (OR, 1.8). Life insurance was associated with non-Hispanic ethnicity (OR, 1.6), full-time vs. part-time employment (OR, 2.4), older age (ORs, 1.6-1.7 for ages 40-49 and 50-59 vs. younger than 40), and marital status (currently/previously married, ORs, 1.6-2.6). Considering the high rate of survey respondents with health insurance, covariate-adjusted modeling was not applicable.

“The number of people with MS who do not have long-term care insurance was surprisingly high,” Dr. Planchon said. “Although the improved treatment climate recently may decrease the long-term disability levels, we do not yet know this with certainty. A large number of people with MS are likely to need long-term care in the future, which often is a significant financial burden to families.” The findings suggest that clinical care teams “need to initiate early discussions of possible long-term needs with their patients,” she continued. “Incorporation of social work teams, who are familiar with the needs of people with MS and insurance options available to them, within MS specialty practices will bolster the comprehensive care of patients and their families.”

She acknowledged certain limitations of the study, including the low proportion of respondents who were Hispanic/Latino and African American (about 4% each). “The insurance landscape may differ in these groups compared to the majority Caucasian population who responded to this survey,” Dr. Planchon said.

The National Multiple Sclerosis Society funded the study. Dr. Planchon reported having no relevant financial disclosures.

[email protected]

SOURCE: Planchon S et al. ACTRIMS Forum 2019, Abstract P295.

DALLAS – A battery of smartphone-based tests has been developed to help detect visual pathway disturbances in MS patients and to follow them over time.

“One of the ideas is, can you design something that’s so easy to use and quick that it’s not a burden on the patient?” Randy H. Kardon, MD, PhD, said in an interview at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. “The other was to test a couple of different modalities. By that I mean we test visual acuity, contrast sensitivity, and critical flicker fusion, which is a way of measuring the speed of conduction of nerves in the visual system.”

Dr. Kardon, professor of neuro-ophthalmology at the University of Iowa, Iowa City, worked with colleagues from Aalborg University, Denmark, to study these tests and a novel measure known as the vanishing optotype on 117 patients with MS and 103 age-matched controls. They found that the tests “very nicely discriminated between normal eyes from patients that had MS,” said Dr. Kardon, director of the Iowa City VA Center for Prevention and Treatment of Visual Loss. “Furthermore, we could determine which eyes from the MS patients had previous optic neuritis and which eyes hadn’t. We’re now looking for partners to go forward with larger studies to validate it further and refine these tests even more.”

Dr. Kardon disclosed that he has received funding from the National Eye Institute, the Department of Defense, and from VA Rehabilitation Research and Development. He was also a member of the Novartis steering committee for the OCTiMS study and is a cofounder of MedFace and FaceX.

[email protected]

DALLAS – A battery of smartphone-based tests has been developed to help detect visual pathway disturbances in MS patients and to follow them over time.

“One of the ideas is, can you design something that’s so easy to use and quick that it’s not a burden on the patient?” Randy H. Kardon, MD, PhD, said in an interview at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. “The other was to test a couple of different modalities. By that I mean we test visual acuity, contrast sensitivity, and critical flicker fusion, which is a way of measuring the speed of conduction of nerves in the visual system.”

Dr. Kardon, professor of neuro-ophthalmology at the University of Iowa, Iowa City, worked with colleagues from Aalborg University, Denmark, to study these tests and a novel measure known as the vanishing optotype on 117 patients with MS and 103 age-matched controls. They found that the tests “very nicely discriminated between normal eyes from patients that had MS,” said Dr. Kardon, director of the Iowa City VA Center for Prevention and Treatment of Visual Loss. “Furthermore, we could determine which eyes from the MS patients had previous optic neuritis and which eyes hadn’t. We’re now looking for partners to go forward with larger studies to validate it further and refine these tests even more.”

Dr. Kardon disclosed that he has received funding from the National Eye Institute, the Department of Defense, and from VA Rehabilitation Research and Development. He was also a member of the Novartis steering committee for the OCTiMS study and is a cofounder of MedFace and FaceX.

[email protected]

DALLAS – A battery of smartphone-based tests has been developed to help detect visual pathway disturbances in MS patients and to follow them over time.

“One of the ideas is, can you design something that’s so easy to use and quick that it’s not a burden on the patient?” Randy H. Kardon, MD, PhD, said in an interview at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. “The other was to test a couple of different modalities. By that I mean we test visual acuity, contrast sensitivity, and critical flicker fusion, which is a way of measuring the speed of conduction of nerves in the visual system.”

Dr. Kardon, professor of neuro-ophthalmology at the University of Iowa, Iowa City, worked with colleagues from Aalborg University, Denmark, to study these tests and a novel measure known as the vanishing optotype on 117 patients with MS and 103 age-matched controls. They found that the tests “very nicely discriminated between normal eyes from patients that had MS,” said Dr. Kardon, director of the Iowa City VA Center for Prevention and Treatment of Visual Loss. “Furthermore, we could determine which eyes from the MS patients had previous optic neuritis and which eyes hadn’t. We’re now looking for partners to go forward with larger studies to validate it further and refine these tests even more.”

Dr. Kardon disclosed that he has received funding from the National Eye Institute, the Department of Defense, and from VA Rehabilitation Research and Development. He was also a member of the Novartis steering committee for the OCTiMS study and is a cofounder of MedFace and FaceX.

[email protected]

DALLAS – The rate of spinal cord atrophy at the C1 level is promising as a prognostic biomarker for the future conversion to secondary progressive disease in patients with relapsing remitting multiple sclerosis (RRMS), results from a novel, single-center study suggest.

“Among all magnetic resonance imaging measures, spinal cord area shows the strongest correlations with MS disability and has been shown to discriminate progressive from relapsing remitting disease subtypes,” lead study author Antje Bischof, MD, said in an interview in advance of the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. “In our work, we used a novel method to accurately measure upper cervical cord area at C1 vertebral level from brain MRI. This enabled us to show for the first time that spinal cord atrophy rates are faster in relapsing remitting MS patients who later converted to secondary progressive disease, compared to a matched group of patients who remained relapsing remitting MS over 2 decades.”


Dr. Bischof, a postdoctoral research fellow in the department of neurology at the University of California, San Francisco, and her colleagues matched 54 RRMS patients who converted to secondary progressive MS (SPMS) during the 12-year observation period with 54 RRMS patients who remained RRMS during the observation period, based on demographic and clinical criteria. Additionally, they evaluated 54 age- and sex-matched healthy controls at baseline. From routine T1-weighted brain MRI, they analyzed brain measures and spinal cord area at C1 level over 12 years to evaluate their potential to discriminate between the two matched groups during the preconversion period.

Subjects who developed SPMS showed higher rates of spinal cord atrophy (–2.2% per year; standard error, 0.2) before conversion to a secondary progressive course, compared with their RRMS matches who did not convert to SPMS (–0.7% per year; SE, 0.2; P less than .0001). Their data suggest that this difference exists at least 4 years before conversion to SPMS. “None of the commonly used measures of the brain including global brain volumes like white matter and gray matter, regional brain volumes like thalamus, and MS lesion volumes, discriminated between the patients with relapsing remitting MS who later converted to secondary progressive disease and the patients who remained RRMS,” Dr. Bischof said.

She acknowledged certain limitations of the study, including the small sample size and the fact that the results require confirmation in a second MS cohort in order to be generalizable. “These results suggest cervical cord atrophy rate at C1 level as a prognostic biomarker for the conversion to secondary progressive MS and could be useful for treatment decisions early in the disease course, and for the study of genetic, epidemiologic, and immune variables in MS,” Dr. Bischof concluded.

She reported having no financial disclosures.

[email protected]

SOURCE: Bischof A et al. ACTRIMS Forum 2019, Abstract P157.

DALLAS – The rate of spinal cord atrophy at the C1 level is promising as a prognostic biomarker for the future conversion to secondary progressive disease in patients with relapsing remitting multiple sclerosis (RRMS), results from a novel, single-center study suggest.

“Among all magnetic resonance imaging measures, spinal cord area shows the strongest correlations with MS disability and has been shown to discriminate progressive from relapsing remitting disease subtypes,” lead study author Antje Bischof, MD, said in an interview in advance of the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. “In our work, we used a novel method to accurately measure upper cervical cord area at C1 vertebral level from brain MRI. This enabled us to show for the first time that spinal cord atrophy rates are faster in relapsing remitting MS patients who later converted to secondary progressive disease, compared to a matched group of patients who remained relapsing remitting MS over 2 decades.”


Dr. Bischof, a postdoctoral research fellow in the department of neurology at the University of California, San Francisco, and her colleagues matched 54 RRMS patients who converted to secondary progressive MS (SPMS) during the 12-year observation period with 54 RRMS patients who remained RRMS during the observation period, based on demographic and clinical criteria. Additionally, they evaluated 54 age- and sex-matched healthy controls at baseline. From routine T1-weighted brain MRI, they analyzed brain measures and spinal cord area at C1 level over 12 years to evaluate their potential to discriminate between the two matched groups during the preconversion period.

Subjects who developed SPMS showed higher rates of spinal cord atrophy (–2.2% per year; standard error, 0.2) before conversion to a secondary progressive course, compared with their RRMS matches who did not convert to SPMS (–0.7% per year; SE, 0.2; P less than .0001). Their data suggest that this difference exists at least 4 years before conversion to SPMS. “None of the commonly used measures of the brain including global brain volumes like white matter and gray matter, regional brain volumes like thalamus, and MS lesion volumes, discriminated between the patients with relapsing remitting MS who later converted to secondary progressive disease and the patients who remained RRMS,” Dr. Bischof said.

She acknowledged certain limitations of the study, including the small sample size and the fact that the results require confirmation in a second MS cohort in order to be generalizable. “These results suggest cervical cord atrophy rate at C1 level as a prognostic biomarker for the conversion to secondary progressive MS and could be useful for treatment decisions early in the disease course, and for the study of genetic, epidemiologic, and immune variables in MS,” Dr. Bischof concluded.

She reported having no financial disclosures.

[email protected]

SOURCE: Bischof A et al. ACTRIMS Forum 2019, Abstract P157.

DALLAS – The rate of spinal cord atrophy at the C1 level is promising as a prognostic biomarker for the future conversion to secondary progressive disease in patients with relapsing remitting multiple sclerosis (RRMS), results from a novel, single-center study suggest.

“Among all magnetic resonance imaging measures, spinal cord area shows the strongest correlations with MS disability and has been shown to discriminate progressive from relapsing remitting disease subtypes,” lead study author Antje Bischof, MD, said in an interview in advance of the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. “In our work, we used a novel method to accurately measure upper cervical cord area at C1 vertebral level from brain MRI. This enabled us to show for the first time that spinal cord atrophy rates are faster in relapsing remitting MS patients who later converted to secondary progressive disease, compared to a matched group of patients who remained relapsing remitting MS over 2 decades.”


Dr. Bischof, a postdoctoral research fellow in the department of neurology at the University of California, San Francisco, and her colleagues matched 54 RRMS patients who converted to secondary progressive MS (SPMS) during the 12-year observation period with 54 RRMS patients who remained RRMS during the observation period, based on demographic and clinical criteria. Additionally, they evaluated 54 age- and sex-matched healthy controls at baseline. From routine T1-weighted brain MRI, they analyzed brain measures and spinal cord area at C1 level over 12 years to evaluate their potential to discriminate between the two matched groups during the preconversion period.

Subjects who developed SPMS showed higher rates of spinal cord atrophy (–2.2% per year; standard error, 0.2) before conversion to a secondary progressive course, compared with their RRMS matches who did not convert to SPMS (–0.7% per year; SE, 0.2; P less than .0001). Their data suggest that this difference exists at least 4 years before conversion to SPMS. “None of the commonly used measures of the brain including global brain volumes like white matter and gray matter, regional brain volumes like thalamus, and MS lesion volumes, discriminated between the patients with relapsing remitting MS who later converted to secondary progressive disease and the patients who remained RRMS,” Dr. Bischof said.

She acknowledged certain limitations of the study, including the small sample size and the fact that the results require confirmation in a second MS cohort in order to be generalizable. “These results suggest cervical cord atrophy rate at C1 level as a prognostic biomarker for the conversion to secondary progressive MS and could be useful for treatment decisions early in the disease course, and for the study of genetic, epidemiologic, and immune variables in MS,” Dr. Bischof concluded.

She reported having no financial disclosures.

[email protected]

SOURCE: Bischof A et al. ACTRIMS Forum 2019, Abstract P157.

LAS VEGAS – Despite recent advances in the diagnosis and treatment of posttraumatic stress disorder, researchers have yet to fully understand its pathophysiology.

“We don’t know whether there is just one type of pathophysiology or if there are different mechanisms and different etiologies that contribute to the symptomatic heterogeneity that we see,” Murray B. Stein, MD, MPH, said at an annual psychopharmacology update held by the Nevada Psychiatric Association.

“Many theories currently being studied are inflammatory theories, looking at autonomic dysregulation, glucocorticoid sensitivity, hippocampal volume/dysfunction, and cortical-amygdala circuit dysregulation.”

Dr. Stein expects clinicians to gain an improved understanding of PTSD and a myriad of other conditions in the coming years as the Million Veteran Program (MVP) gets underway. MVP researchers are building one of the world’s largest medical databases by asking 1 million veteran volunteers to provide a blood sample and complete surveys about their health, military experience, lifestyle, and other topics that might contribute to health and disease. They will study how genes influence diseases such as diabetes and cancer, and military-related illnesses, such as PTSD. “It’s an amazing study, where over the next decade, you’re going to hear research findings not just on PTSD but in other areas of mental health and physical health,” said Dr. Stein, distinguished professor of psychiatry and family medicine and public health at the University of California, San Diego. So far, he said, 700,000 veterans are enrolled.


Dr. Stein shared preliminary findings from one component of the MVP study, in which participants complete the PTSD Checklist (PCL-17), a widely used 17-item self-report measure of PTSD symptoms in the past month. Using Manhattan plot analysis, Dr. Stein and his colleagues conducted a PTSD genomewide association study based on PCL-17 total scores. They found several genes significantly associated with PTSD, including LRRIQ3, TRAIP, KCNIP4, PCDHA1, MAD1L1, TSNARE1, EXD3, MGC57346-CRHR1, and TCF4. “This is the first study in the world to find this many genes [associated with PTSD],” said Dr. Stein, a staff psychiatrist with the VA San Diego Healthcare System. “The MAD1L1 gene is also one that’s come up in schizophrenia and in major depression. In fact, if we look at genetic correlations of how PTSD is genetically associated to other disorders that have been studied in this way, like major depression and schizophrenia, we find that there is shared variation. However, there are also unique features, so we are learning what we think is true about mental disorders overall, that in some ways comorbidity is explained by genetic risk, but there are also individual specific risk factors that go with specific disorders.

“We’re exploring each of those genes.”

[email protected]

LAS VEGAS – Despite recent advances in the diagnosis and treatment of posttraumatic stress disorder, researchers have yet to fully understand its pathophysiology.

“We don’t know whether there is just one type of pathophysiology or if there are different mechanisms and different etiologies that contribute to the symptomatic heterogeneity that we see,” Murray B. Stein, MD, MPH, said at an annual psychopharmacology update held by the Nevada Psychiatric Association.

“Many theories currently being studied are inflammatory theories, looking at autonomic dysregulation, glucocorticoid sensitivity, hippocampal volume/dysfunction, and cortical-amygdala circuit dysregulation.”

Dr. Stein expects clinicians to gain an improved understanding of PTSD and a myriad of other conditions in the coming years as the Million Veteran Program (MVP) gets underway. MVP researchers are building one of the world’s largest medical databases by asking 1 million veteran volunteers to provide a blood sample and complete surveys about their health, military experience, lifestyle, and other topics that might contribute to health and disease. They will study how genes influence diseases such as diabetes and cancer, and military-related illnesses, such as PTSD. “It’s an amazing study, where over the next decade, you’re going to hear research findings not just on PTSD but in other areas of mental health and physical health,” said Dr. Stein, distinguished professor of psychiatry and family medicine and public health at the University of California, San Diego. So far, he said, 700,000 veterans are enrolled.


Dr. Stein shared preliminary findings from one component of the MVP study, in which participants complete the PTSD Checklist (PCL-17), a widely used 17-item self-report measure of PTSD symptoms in the past month. Using Manhattan plot analysis, Dr. Stein and his colleagues conducted a PTSD genomewide association study based on PCL-17 total scores. They found several genes significantly associated with PTSD, including LRRIQ3, TRAIP, KCNIP4, PCDHA1, MAD1L1, TSNARE1, EXD3, MGC57346-CRHR1, and TCF4. “This is the first study in the world to find this many genes [associated with PTSD],” said Dr. Stein, a staff psychiatrist with the VA San Diego Healthcare System. “The MAD1L1 gene is also one that’s come up in schizophrenia and in major depression. In fact, if we look at genetic correlations of how PTSD is genetically associated to other disorders that have been studied in this way, like major depression and schizophrenia, we find that there is shared variation. However, there are also unique features, so we are learning what we think is true about mental disorders overall, that in some ways comorbidity is explained by genetic risk, but there are also individual specific risk factors that go with specific disorders.

“We’re exploring each of those genes.”

[email protected]

LAS VEGAS – Despite recent advances in the diagnosis and treatment of posttraumatic stress disorder, researchers have yet to fully understand its pathophysiology.

“We don’t know whether there is just one type of pathophysiology or if there are different mechanisms and different etiologies that contribute to the symptomatic heterogeneity that we see,” Murray B. Stein, MD, MPH, said at an annual psychopharmacology update held by the Nevada Psychiatric Association.

“Many theories currently being studied are inflammatory theories, looking at autonomic dysregulation, glucocorticoid sensitivity, hippocampal volume/dysfunction, and cortical-amygdala circuit dysregulation.”

Dr. Stein expects clinicians to gain an improved understanding of PTSD and a myriad of other conditions in the coming years as the Million Veteran Program (MVP) gets underway. MVP researchers are building one of the world’s largest medical databases by asking 1 million veteran volunteers to provide a blood sample and complete surveys about their health, military experience, lifestyle, and other topics that might contribute to health and disease. They will study how genes influence diseases such as diabetes and cancer, and military-related illnesses, such as PTSD. “It’s an amazing study, where over the next decade, you’re going to hear research findings not just on PTSD but in other areas of mental health and physical health,” said Dr. Stein, distinguished professor of psychiatry and family medicine and public health at the University of California, San Diego. So far, he said, 700,000 veterans are enrolled.


Dr. Stein shared preliminary findings from one component of the MVP study, in which participants complete the PTSD Checklist (PCL-17), a widely used 17-item self-report measure of PTSD symptoms in the past month. Using Manhattan plot analysis, Dr. Stein and his colleagues conducted a PTSD genomewide association study based on PCL-17 total scores. They found several genes significantly associated with PTSD, including LRRIQ3, TRAIP, KCNIP4, PCDHA1, MAD1L1, TSNARE1, EXD3, MGC57346-CRHR1, and TCF4. “This is the first study in the world to find this many genes [associated with PTSD],” said Dr. Stein, a staff psychiatrist with the VA San Diego Healthcare System. “The MAD1L1 gene is also one that’s come up in schizophrenia and in major depression. In fact, if we look at genetic correlations of how PTSD is genetically associated to other disorders that have been studied in this way, like major depression and schizophrenia, we find that there is shared variation. However, there are also unique features, so we are learning what we think is true about mental disorders overall, that in some ways comorbidity is explained by genetic risk, but there are also individual specific risk factors that go with specific disorders.

“We’re exploring each of those genes.”

[email protected]

LAS VEGAS – The way Robert Hudak, MD, sees it, the terms excessive anxiety and anxiety disorders are not interchangeable – and do not mean the same thing.

“People with anxiety disorders have excessive anxiety, but not everyone with excessive anxiety has a psychiatric disorder,” he said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “Any anxiety above baseline can be normal. It’s not necessarily pathological. I think that’s an important point that’s easy to overlook when we’re in clinical practice, and it affects how we approach our patients.”

Anxiety can present in a variety of ways in different individuals. Panic attacks are often the primary chief complaint, and it’s common to hear complaints from family that the person is routinely seeking reassurance. In addition, tics and twitches are not unusual in people with anxiety disorder. “Some of that is brought out by anxiety itself,” said Dr. Hudak, who is a psychiatrist at the University of Pittsburgh. Sleep disturbances or other somatic complaints also are common. “They complain of racing thoughts, increased energy, and depression,” he added. “When someone complains about depression, don’t assume they have a mood disorder. The reason people with anxiety disorders complain about depression is that it really feels awful. Anxiety is incredibly dysphoric.” Physical complaints include shortness of breath, GI distress, dizziness, vague somatic complaints, and skin or gum lesions.

He went on to note that individuals with excessive anxiety virtually never lose consciousness. “The exception is blood/injection/injury phobia,” he said. “That’s the only case in which anxiety will cause loss of consciousness. It happens in virtually no other setting. Ondine’s curse while falling asleep is another symptom that only occurs with anxiety. It’s a sensation that you have to remember to breathe, and breathing is no longer automatic. There are medical conditions that cause Ondine’s curse. However, the patient who complains of Ondine’s curse as they’re falling asleep is pathognomonic for anxiety.”

Dr. Hudak said panic attacks, a discrete period of fear or discomfort, rarely last more than 30 minutes.

“I view panic attacks in three flavors,” he said. “Some people have the cardiovascular flavor with shortness of breath and heart palpitations. Some have what I call the neurological flavor, where the predominant symptoms seem to be dizziness and tingling. Other people have GI flavor, with gut pain, nausea, and diarrhea. Panic attacks are not a psychiatric disorder. It’s a qualifier for any psychiatric disorder.”

Social anxiety disorder, meanwhile, presents as two completely distinct and separate illnesses that have nothing in common with each other.

“The performance subtype of social anxiety really presents like a simple phobia,” Dr. Hudak said. “The treatment for that is really behavioral therapy and cognitive-behavioral therapy, and rarely the use of medications. The generalized type presents with intrusive, [obsessive-compulsive disorder]–like thoughts. Affected individuals describe themselves as ‘paranoid’ or feeling that they are being scrutinized. The categorical versus dimensional diagnosis is being debated.” Individuals with generalized anxiety disorder, on the other hand, have excessive and pervasive worry and anxiety present more days than not for a 6-month period. “The individual finds it difficult to control the worry,” he said. Somatic symptoms include restlessness, fatigue, difficulty concentrating, irritability, muscle tension, and insomnia. Different studies show the prevalence rate between 3% and 8%, affecting more women than men.

The medical work-up for excessive anxiety should consist of history and physical exam, complete blood count, the Chem-7 metabolic test, thyroid-stimulating hormone, and EKG if indicated. Both medications and behavioral therapy are used in the treatment of anxiety disorders. Many patients require both in order to achieve maximum treatment response. “Often, people with less severe illnesses can be managed with therapy alone,” Dr. Hudak said.

“In more severe cases, medications can help reduce symptoms to the point where therapy is easier to perform. The bottom line here is that at no time should you treat someone with an anxiety disorder with medications alone. Behavioral therapy is at least as effective as medications, and perhaps more so.”

Many trials of anxiety medications are of short duration and therefore lack evidence of long-term improvement, he said. Commonly used scales often include nonspecific items such as arousal score that can be reduced by sedating medications without improving the actual disorder. If someone has excessive anxiety that is not part of a primary anxiety disorder, Dr. Hudak typically prescribes benzodiazepines. “If someone is anxious because a loved one died, or if they’re nervous about their wedding day, or about taking a board exam, benzos can be used,” he said. “For someone who has an anxiety disorder, I virtually never use benzodiazepines. I generally use medications in the antidepressant category. I probably initiate fewer than five benzodiazepine prescriptions per year for anxiety disorder. There is also data to suggest that using benzodiazepines in patients with anxiety disorder may make cognitive-behavioral therapy more difficult.”

According to Dr. Hudak, selective serotonin reuptake inhibitors seem to have the largest evidence base in panic disorder and are first-line pharmacotherapy for both panic disorder and generalized anxiety disorder, while tricyclic antidepressants (TCAs) usually are considered a second-line therapy. “There is good data behind MAO inhibitors, and there is increasingly good data behind [selective norepinephrine reuptake inhibitors],” he said. “If someone has failed a trial of SSRIs, you may consider trying an SNRI before a TCA. However, I would try multiple SSRIs before ruling out that class of medications. I have had people fail five SSRIs and respond dramatically to the sixth SSRI.”

Dr. Hudak disclosed that he receives royalties from the Cambridge University Press.

[email protected]

LAS VEGAS – The way Robert Hudak, MD, sees it, the terms excessive anxiety and anxiety disorders are not interchangeable – and do not mean the same thing.

“People with anxiety disorders have excessive anxiety, but not everyone with excessive anxiety has a psychiatric disorder,” he said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “Any anxiety above baseline can be normal. It’s not necessarily pathological. I think that’s an important point that’s easy to overlook when we’re in clinical practice, and it affects how we approach our patients.”

Anxiety can present in a variety of ways in different individuals. Panic attacks are often the primary chief complaint, and it’s common to hear complaints from family that the person is routinely seeking reassurance. In addition, tics and twitches are not unusual in people with anxiety disorder. “Some of that is brought out by anxiety itself,” said Dr. Hudak, who is a psychiatrist at the University of Pittsburgh. Sleep disturbances or other somatic complaints also are common. “They complain of racing thoughts, increased energy, and depression,” he added. “When someone complains about depression, don’t assume they have a mood disorder. The reason people with anxiety disorders complain about depression is that it really feels awful. Anxiety is incredibly dysphoric.” Physical complaints include shortness of breath, GI distress, dizziness, vague somatic complaints, and skin or gum lesions.

He went on to note that individuals with excessive anxiety virtually never lose consciousness. “The exception is blood/injection/injury phobia,” he said. “That’s the only case in which anxiety will cause loss of consciousness. It happens in virtually no other setting. Ondine’s curse while falling asleep is another symptom that only occurs with anxiety. It’s a sensation that you have to remember to breathe, and breathing is no longer automatic. There are medical conditions that cause Ondine’s curse. However, the patient who complains of Ondine’s curse as they’re falling asleep is pathognomonic for anxiety.”

Dr. Hudak said panic attacks, a discrete period of fear or discomfort, rarely last more than 30 minutes.

“I view panic attacks in three flavors,” he said. “Some people have the cardiovascular flavor with shortness of breath and heart palpitations. Some have what I call the neurological flavor, where the predominant symptoms seem to be dizziness and tingling. Other people have GI flavor, with gut pain, nausea, and diarrhea. Panic attacks are not a psychiatric disorder. It’s a qualifier for any psychiatric disorder.”

Social anxiety disorder, meanwhile, presents as two completely distinct and separate illnesses that have nothing in common with each other.

“The performance subtype of social anxiety really presents like a simple phobia,” Dr. Hudak said. “The treatment for that is really behavioral therapy and cognitive-behavioral therapy, and rarely the use of medications. The generalized type presents with intrusive, [obsessive-compulsive disorder]–like thoughts. Affected individuals describe themselves as ‘paranoid’ or feeling that they are being scrutinized. The categorical versus dimensional diagnosis is being debated.” Individuals with generalized anxiety disorder, on the other hand, have excessive and pervasive worry and anxiety present more days than not for a 6-month period. “The individual finds it difficult to control the worry,” he said. Somatic symptoms include restlessness, fatigue, difficulty concentrating, irritability, muscle tension, and insomnia. Different studies show the prevalence rate between 3% and 8%, affecting more women than men.

The medical work-up for excessive anxiety should consist of history and physical exam, complete blood count, the Chem-7 metabolic test, thyroid-stimulating hormone, and EKG if indicated. Both medications and behavioral therapy are used in the treatment of anxiety disorders. Many patients require both in order to achieve maximum treatment response. “Often, people with less severe illnesses can be managed with therapy alone,” Dr. Hudak said.

“In more severe cases, medications can help reduce symptoms to the point where therapy is easier to perform. The bottom line here is that at no time should you treat someone with an anxiety disorder with medications alone. Behavioral therapy is at least as effective as medications, and perhaps more so.”

Many trials of anxiety medications are of short duration and therefore lack evidence of long-term improvement, he said. Commonly used scales often include nonspecific items such as arousal score that can be reduced by sedating medications without improving the actual disorder. If someone has excessive anxiety that is not part of a primary anxiety disorder, Dr. Hudak typically prescribes benzodiazepines. “If someone is anxious because a loved one died, or if they’re nervous about their wedding day, or about taking a board exam, benzos can be used,” he said. “For someone who has an anxiety disorder, I virtually never use benzodiazepines. I generally use medications in the antidepressant category. I probably initiate fewer than five benzodiazepine prescriptions per year for anxiety disorder. There is also data to suggest that using benzodiazepines in patients with anxiety disorder may make cognitive-behavioral therapy more difficult.”

According to Dr. Hudak, selective serotonin reuptake inhibitors seem to have the largest evidence base in panic disorder and are first-line pharmacotherapy for both panic disorder and generalized anxiety disorder, while tricyclic antidepressants (TCAs) usually are considered a second-line therapy. “There is good data behind MAO inhibitors, and there is increasingly good data behind [selective norepinephrine reuptake inhibitors],” he said. “If someone has failed a trial of SSRIs, you may consider trying an SNRI before a TCA. However, I would try multiple SSRIs before ruling out that class of medications. I have had people fail five SSRIs and respond dramatically to the sixth SSRI.”

Dr. Hudak disclosed that he receives royalties from the Cambridge University Press.

[email protected]

LAS VEGAS – The way Robert Hudak, MD, sees it, the terms excessive anxiety and anxiety disorders are not interchangeable – and do not mean the same thing.

“People with anxiety disorders have excessive anxiety, but not everyone with excessive anxiety has a psychiatric disorder,” he said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “Any anxiety above baseline can be normal. It’s not necessarily pathological. I think that’s an important point that’s easy to overlook when we’re in clinical practice, and it affects how we approach our patients.”

Anxiety can present in a variety of ways in different individuals. Panic attacks are often the primary chief complaint, and it’s common to hear complaints from family that the person is routinely seeking reassurance. In addition, tics and twitches are not unusual in people with anxiety disorder. “Some of that is brought out by anxiety itself,” said Dr. Hudak, who is a psychiatrist at the University of Pittsburgh. Sleep disturbances or other somatic complaints also are common. “They complain of racing thoughts, increased energy, and depression,” he added. “When someone complains about depression, don’t assume they have a mood disorder. The reason people with anxiety disorders complain about depression is that it really feels awful. Anxiety is incredibly dysphoric.” Physical complaints include shortness of breath, GI distress, dizziness, vague somatic complaints, and skin or gum lesions.

He went on to note that individuals with excessive anxiety virtually never lose consciousness. “The exception is blood/injection/injury phobia,” he said. “That’s the only case in which anxiety will cause loss of consciousness. It happens in virtually no other setting. Ondine’s curse while falling asleep is another symptom that only occurs with anxiety. It’s a sensation that you have to remember to breathe, and breathing is no longer automatic. There are medical conditions that cause Ondine’s curse. However, the patient who complains of Ondine’s curse as they’re falling asleep is pathognomonic for anxiety.”

Dr. Hudak said panic attacks, a discrete period of fear or discomfort, rarely last more than 30 minutes.

“I view panic attacks in three flavors,” he said. “Some people have the cardiovascular flavor with shortness of breath and heart palpitations. Some have what I call the neurological flavor, where the predominant symptoms seem to be dizziness and tingling. Other people have GI flavor, with gut pain, nausea, and diarrhea. Panic attacks are not a psychiatric disorder. It’s a qualifier for any psychiatric disorder.”

Social anxiety disorder, meanwhile, presents as two completely distinct and separate illnesses that have nothing in common with each other.

“The performance subtype of social anxiety really presents like a simple phobia,” Dr. Hudak said. “The treatment for that is really behavioral therapy and cognitive-behavioral therapy, and rarely the use of medications. The generalized type presents with intrusive, [obsessive-compulsive disorder]–like thoughts. Affected individuals describe themselves as ‘paranoid’ or feeling that they are being scrutinized. The categorical versus dimensional diagnosis is being debated.” Individuals with generalized anxiety disorder, on the other hand, have excessive and pervasive worry and anxiety present more days than not for a 6-month period. “The individual finds it difficult to control the worry,” he said. Somatic symptoms include restlessness, fatigue, difficulty concentrating, irritability, muscle tension, and insomnia. Different studies show the prevalence rate between 3% and 8%, affecting more women than men.

The medical work-up for excessive anxiety should consist of history and physical exam, complete blood count, the Chem-7 metabolic test, thyroid-stimulating hormone, and EKG if indicated. Both medications and behavioral therapy are used in the treatment of anxiety disorders. Many patients require both in order to achieve maximum treatment response. “Often, people with less severe illnesses can be managed with therapy alone,” Dr. Hudak said.

“In more severe cases, medications can help reduce symptoms to the point where therapy is easier to perform. The bottom line here is that at no time should you treat someone with an anxiety disorder with medications alone. Behavioral therapy is at least as effective as medications, and perhaps more so.”

Many trials of anxiety medications are of short duration and therefore lack evidence of long-term improvement, he said. Commonly used scales often include nonspecific items such as arousal score that can be reduced by sedating medications without improving the actual disorder. If someone has excessive anxiety that is not part of a primary anxiety disorder, Dr. Hudak typically prescribes benzodiazepines. “If someone is anxious because a loved one died, or if they’re nervous about their wedding day, or about taking a board exam, benzos can be used,” he said. “For someone who has an anxiety disorder, I virtually never use benzodiazepines. I generally use medications in the antidepressant category. I probably initiate fewer than five benzodiazepine prescriptions per year for anxiety disorder. There is also data to suggest that using benzodiazepines in patients with anxiety disorder may make cognitive-behavioral therapy more difficult.”

According to Dr. Hudak, selective serotonin reuptake inhibitors seem to have the largest evidence base in panic disorder and are first-line pharmacotherapy for both panic disorder and generalized anxiety disorder, while tricyclic antidepressants (TCAs) usually are considered a second-line therapy. “There is good data behind MAO inhibitors, and there is increasingly good data behind [selective norepinephrine reuptake inhibitors],” he said. “If someone has failed a trial of SSRIs, you may consider trying an SNRI before a TCA. However, I would try multiple SSRIs before ruling out that class of medications. I have had people fail five SSRIs and respond dramatically to the sixth SSRI.”

Dr. Hudak disclosed that he receives royalties from the Cambridge University Press.

[email protected]

LAS VEGAS – Despite the strides that clinicians like Anthony L. Rostain, MD, have made in better understanding and treating patients with ADHD, it remains virtually impossible to predict how a child with the disorder will fare in adulthood.

“We cannot predict the trajectory of the disorder,” Dr. Rostain said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “We’re still learning about the variables that affect clinical course. There are many determinants to the trajectory.”

Dr. Rostain, professor of psychiatry and pediatrics at the University of Pennsylvania, Philadelphia, said ADHD commonly presents with numerous other neurodevelopmental disorders and with comorbid psychiatric conditions like bipolar disorder and anxiety.

“In psychiatry, we tend to see the more complicated patients, the ones with multiple comorbidities,” he said. “The most important change in the way we think about people with ADHD has to do with the growing emphasis on how it affects executive functions, in particular the cognitive, affective, and behavioral consequences of executive dysfunction. In this growingly complex world, with what some describe as ‘distracted minds’ emerging from being immersed in all our technology, it’s sometimes hard to tell: Is this person distracted because they’re always looking at their cell phone, or do they have intrinsic difficulty with managing attention?

“That’s going to become a greater challenge as children grow up in this world filled with shiny screens and devices that make [it] easier to connect with others but also harder to set a goal and follow it to its conclusion.”

ADHD changes over time, Dr. Rostain continued, but there is no single theory or biological explanation to explain its heterogeneity. “There is no cookie-cutter approach; you have to individualize when you are treating the individual in your office,” he said.

It is widely accepted that ADHD arises from biological factors, but social factors likely influence the degree of impairment, risk for comorbid disorders, and access to resources, said Dr. Rostain, who is also codirector of the developmental neuropsychiatry program at The Children’s Hospital of Philadelphia and medical director of the Adult ADHD Treatment and Research Program at Penn Medicine.

“Risk factors like experiencing trauma, being raised in adversity, or having an unstable family structure or lack of community support make the disorder more difficult to treat,” he said. “If there were one thing we could do to prevent ADHD, it might be to prevent pregnant women from drinking or to reduce poverty and violence, but that’s beyond the scope of this talk.”

He also noted that, because of epigenetics, ADHD risk factors express themselves early in some individuals and later in others. “We’re convinced that developmental disorders unfold in a nonlinear fashion,” he said. “Life [with ADHD] is curvy, not a straight line.”

Numerous studies of ADHD neurobiology have demonstrated frontal subcortical and cerebellar dysfunction – smaller striatal structures in particular. “In MRI studies, we also see difficulties with the differential maturation of important neural circuits, along with the persistence of cortical thickening where it should be thinning,” Dr. Rostain said. He went on to note that the normal brain consists of three main networks: the salience network, “which tells us whether to pay attention or to relax,” the attention and control network, and the default mode network, “which is where our mind goes when we’re daydreaming,” he said. “All of us are constantly switching between attention and daydreaming. That’s normal. In ADHD, the balance and synchrony between the default mode and the attention network is disrupted. Individuals with ADHD either remain too long in the default mode, or their attentional system isn’t powered up enough to keep them paying attention and following through during nonrewarding tasks.”

The presentation of ADHD symptoms tends to differ in children, compared with adults. For example, children with the disorder tend to be squirmy, can’t sit still, are restless, and can’t play or work quietly. On the other hand, adults tend to complain about inefficiencies at work, not being able to finish projects, not being able to sit through meetings. They tend to drive too quickly, and they often talk excessively, and make inappropriate comments. “The symptoms of ADHD emerge from disruptions or inefficiencies in basic functions, whether those are executive functions or motivational processes,” he said. “All of this is thought to be the result of genetic unfolding throughout the lifespan.”

The goal of ADHD medical therapy is to alter catecholamine tone in the prefrontal cortex, an area of the brain “designed to help us guide our thinking toward distal goals and navigate the world around us,” Dr. Rostain said. “It allows us also to inhibit actions that are task-irrelevant or are not serving our purposes. It also enable us to regulate emotions.” In his opinion, the medical treatment of ADHD should focus on helping the prefrontal cortex function optimally. “How much we can do – that remains to be seen – but that’s really where the action is,” he said. “From a functional standpoint, that’s what are we trying to achieve. When we have guided attention and when our responses to the world are appropriate, we can say that we’re ‘in the zone.’ That means we can listen, understand, make sense of the world, and deviate or shift direction if something gets in the way of our goals. Our responses should be flexible. We should be able to say, ‘That doesn’t work? Let me try something else.’ This indicates that the norepinephrine and dopamine circuits of the frontal cortex are optimally operating.”

On the other hand, individuals with ADHD find themselves in what Dr. Rostain described as an “unguided attention state” characterized by distraction and poor impulse control. “We also see it in people who are sleep deprived,” he said. “This could be untreated ADHD. If we treat ADHD properly, we move individuals into the optimal zone. But if we overdo it, if our medications are prescribed at doses that are higher than optimal, what you then see is excessive stimulation of the norepinephrine and dopamine systems. This leads to misguided attention, overfocusing, and mental inflexibility. People in this state report extreme amounts of stress and distress.”

Dr. Rostain recommends that medication plans be embedded in a comprehensive treatment approach that starts with psychoeducation. “When treating ADHD, we’re not going to turn a lion into a lamb, and we’re not going to make someone want to study if they don’t like school,” he said. “One of my patients, a college student, told me that, with the medication I prescribed for him, he was able to sit down and read for the first time for 3 hours straight. I said, ‘Great. Did you read your physics book? He said, No. I read Wired magazine.’ So while he was very focused, he didn’t concentrate on what he needed to focus on.”

Dr. Rostain supports the notion of a triad model of care with psychosocial interventions, medical interventions, and educational/workplace interventions “to improve the performance of demanded tasks, and to achieve a sense of being supported by that environment rather than being criticized,” he said. “If you ask most adults with ADHD what school was like, what will they tell you? They usually say it was bad or terrible, like a prison. If you ask them to describe it, they may have trouble remembering a lot of it, because it was so difficult for them.”

Dr. Rostain reported having received scientific advisory board honoraria from Shire, Ironshore, and Arbor. He also has received consultant honoraria from Major League Baseball, the National Football League, and from SUNY/Upstate.

[email protected]

LAS VEGAS – Despite the strides that clinicians like Anthony L. Rostain, MD, have made in better understanding and treating patients with ADHD, it remains virtually impossible to predict how a child with the disorder will fare in adulthood.

“We cannot predict the trajectory of the disorder,” Dr. Rostain said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “We’re still learning about the variables that affect clinical course. There are many determinants to the trajectory.”

Dr. Rostain, professor of psychiatry and pediatrics at the University of Pennsylvania, Philadelphia, said ADHD commonly presents with numerous other neurodevelopmental disorders and with comorbid psychiatric conditions like bipolar disorder and anxiety.

“In psychiatry, we tend to see the more complicated patients, the ones with multiple comorbidities,” he said. “The most important change in the way we think about people with ADHD has to do with the growing emphasis on how it affects executive functions, in particular the cognitive, affective, and behavioral consequences of executive dysfunction. In this growingly complex world, with what some describe as ‘distracted minds’ emerging from being immersed in all our technology, it’s sometimes hard to tell: Is this person distracted because they’re always looking at their cell phone, or do they have intrinsic difficulty with managing attention?

“That’s going to become a greater challenge as children grow up in this world filled with shiny screens and devices that make [it] easier to connect with others but also harder to set a goal and follow it to its conclusion.”

ADHD changes over time, Dr. Rostain continued, but there is no single theory or biological explanation to explain its heterogeneity. “There is no cookie-cutter approach; you have to individualize when you are treating the individual in your office,” he said.

It is widely accepted that ADHD arises from biological factors, but social factors likely influence the degree of impairment, risk for comorbid disorders, and access to resources, said Dr. Rostain, who is also codirector of the developmental neuropsychiatry program at The Children’s Hospital of Philadelphia and medical director of the Adult ADHD Treatment and Research Program at Penn Medicine.

“Risk factors like experiencing trauma, being raised in adversity, or having an unstable family structure or lack of community support make the disorder more difficult to treat,” he said. “If there were one thing we could do to prevent ADHD, it might be to prevent pregnant women from drinking or to reduce poverty and violence, but that’s beyond the scope of this talk.”

He also noted that, because of epigenetics, ADHD risk factors express themselves early in some individuals and later in others. “We’re convinced that developmental disorders unfold in a nonlinear fashion,” he said. “Life [with ADHD] is curvy, not a straight line.”

Numerous studies of ADHD neurobiology have demonstrated frontal subcortical and cerebellar dysfunction – smaller striatal structures in particular. “In MRI studies, we also see difficulties with the differential maturation of important neural circuits, along with the persistence of cortical thickening where it should be thinning,” Dr. Rostain said. He went on to note that the normal brain consists of three main networks: the salience network, “which tells us whether to pay attention or to relax,” the attention and control network, and the default mode network, “which is where our mind goes when we’re daydreaming,” he said. “All of us are constantly switching between attention and daydreaming. That’s normal. In ADHD, the balance and synchrony between the default mode and the attention network is disrupted. Individuals with ADHD either remain too long in the default mode, or their attentional system isn’t powered up enough to keep them paying attention and following through during nonrewarding tasks.”

The presentation of ADHD symptoms tends to differ in children, compared with adults. For example, children with the disorder tend to be squirmy, can’t sit still, are restless, and can’t play or work quietly. On the other hand, adults tend to complain about inefficiencies at work, not being able to finish projects, not being able to sit through meetings. They tend to drive too quickly, and they often talk excessively, and make inappropriate comments. “The symptoms of ADHD emerge from disruptions or inefficiencies in basic functions, whether those are executive functions or motivational processes,” he said. “All of this is thought to be the result of genetic unfolding throughout the lifespan.”

The goal of ADHD medical therapy is to alter catecholamine tone in the prefrontal cortex, an area of the brain “designed to help us guide our thinking toward distal goals and navigate the world around us,” Dr. Rostain said. “It allows us also to inhibit actions that are task-irrelevant or are not serving our purposes. It also enable us to regulate emotions.” In his opinion, the medical treatment of ADHD should focus on helping the prefrontal cortex function optimally. “How much we can do – that remains to be seen – but that’s really where the action is,” he said. “From a functional standpoint, that’s what are we trying to achieve. When we have guided attention and when our responses to the world are appropriate, we can say that we’re ‘in the zone.’ That means we can listen, understand, make sense of the world, and deviate or shift direction if something gets in the way of our goals. Our responses should be flexible. We should be able to say, ‘That doesn’t work? Let me try something else.’ This indicates that the norepinephrine and dopamine circuits of the frontal cortex are optimally operating.”

On the other hand, individuals with ADHD find themselves in what Dr. Rostain described as an “unguided attention state” characterized by distraction and poor impulse control. “We also see it in people who are sleep deprived,” he said. “This could be untreated ADHD. If we treat ADHD properly, we move individuals into the optimal zone. But if we overdo it, if our medications are prescribed at doses that are higher than optimal, what you then see is excessive stimulation of the norepinephrine and dopamine systems. This leads to misguided attention, overfocusing, and mental inflexibility. People in this state report extreme amounts of stress and distress.”

Dr. Rostain recommends that medication plans be embedded in a comprehensive treatment approach that starts with psychoeducation. “When treating ADHD, we’re not going to turn a lion into a lamb, and we’re not going to make someone want to study if they don’t like school,” he said. “One of my patients, a college student, told me that, with the medication I prescribed for him, he was able to sit down and read for the first time for 3 hours straight. I said, ‘Great. Did you read your physics book? He said, No. I read Wired magazine.’ So while he was very focused, he didn’t concentrate on what he needed to focus on.”

Dr. Rostain supports the notion of a triad model of care with psychosocial interventions, medical interventions, and educational/workplace interventions “to improve the performance of demanded tasks, and to achieve a sense of being supported by that environment rather than being criticized,” he said. “If you ask most adults with ADHD what school was like, what will they tell you? They usually say it was bad or terrible, like a prison. If you ask them to describe it, they may have trouble remembering a lot of it, because it was so difficult for them.”

Dr. Rostain reported having received scientific advisory board honoraria from Shire, Ironshore, and Arbor. He also has received consultant honoraria from Major League Baseball, the National Football League, and from SUNY/Upstate.

[email protected]

LAS VEGAS – Despite the strides that clinicians like Anthony L. Rostain, MD, have made in better understanding and treating patients with ADHD, it remains virtually impossible to predict how a child with the disorder will fare in adulthood.

“We cannot predict the trajectory of the disorder,” Dr. Rostain said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “We’re still learning about the variables that affect clinical course. There are many determinants to the trajectory.”

Dr. Rostain, professor of psychiatry and pediatrics at the University of Pennsylvania, Philadelphia, said ADHD commonly presents with numerous other neurodevelopmental disorders and with comorbid psychiatric conditions like bipolar disorder and anxiety.

“In psychiatry, we tend to see the more complicated patients, the ones with multiple comorbidities,” he said. “The most important change in the way we think about people with ADHD has to do with the growing emphasis on how it affects executive functions, in particular the cognitive, affective, and behavioral consequences of executive dysfunction. In this growingly complex world, with what some describe as ‘distracted minds’ emerging from being immersed in all our technology, it’s sometimes hard to tell: Is this person distracted because they’re always looking at their cell phone, or do they have intrinsic difficulty with managing attention?

“That’s going to become a greater challenge as children grow up in this world filled with shiny screens and devices that make [it] easier to connect with others but also harder to set a goal and follow it to its conclusion.”

ADHD changes over time, Dr. Rostain continued, but there is no single theory or biological explanation to explain its heterogeneity. “There is no cookie-cutter approach; you have to individualize when you are treating the individual in your office,” he said.

It is widely accepted that ADHD arises from biological factors, but social factors likely influence the degree of impairment, risk for comorbid disorders, and access to resources, said Dr. Rostain, who is also codirector of the developmental neuropsychiatry program at The Children’s Hospital of Philadelphia and medical director of the Adult ADHD Treatment and Research Program at Penn Medicine.

“Risk factors like experiencing trauma, being raised in adversity, or having an unstable family structure or lack of community support make the disorder more difficult to treat,” he said. “If there were one thing we could do to prevent ADHD, it might be to prevent pregnant women from drinking or to reduce poverty and violence, but that’s beyond the scope of this talk.”

He also noted that, because of epigenetics, ADHD risk factors express themselves early in some individuals and later in others. “We’re convinced that developmental disorders unfold in a nonlinear fashion,” he said. “Life [with ADHD] is curvy, not a straight line.”

Numerous studies of ADHD neurobiology have demonstrated frontal subcortical and cerebellar dysfunction – smaller striatal structures in particular. “In MRI studies, we also see difficulties with the differential maturation of important neural circuits, along with the persistence of cortical thickening where it should be thinning,” Dr. Rostain said. He went on to note that the normal brain consists of three main networks: the salience network, “which tells us whether to pay attention or to relax,” the attention and control network, and the default mode network, “which is where our mind goes when we’re daydreaming,” he said. “All of us are constantly switching between attention and daydreaming. That’s normal. In ADHD, the balance and synchrony between the default mode and the attention network is disrupted. Individuals with ADHD either remain too long in the default mode, or their attentional system isn’t powered up enough to keep them paying attention and following through during nonrewarding tasks.”

The presentation of ADHD symptoms tends to differ in children, compared with adults. For example, children with the disorder tend to be squirmy, can’t sit still, are restless, and can’t play or work quietly. On the other hand, adults tend to complain about inefficiencies at work, not being able to finish projects, not being able to sit through meetings. They tend to drive too quickly, and they often talk excessively, and make inappropriate comments. “The symptoms of ADHD emerge from disruptions or inefficiencies in basic functions, whether those are executive functions or motivational processes,” he said. “All of this is thought to be the result of genetic unfolding throughout the lifespan.”

The goal of ADHD medical therapy is to alter catecholamine tone in the prefrontal cortex, an area of the brain “designed to help us guide our thinking toward distal goals and navigate the world around us,” Dr. Rostain said. “It allows us also to inhibit actions that are task-irrelevant or are not serving our purposes. It also enable us to regulate emotions.” In his opinion, the medical treatment of ADHD should focus on helping the prefrontal cortex function optimally. “How much we can do – that remains to be seen – but that’s really where the action is,” he said. “From a functional standpoint, that’s what are we trying to achieve. When we have guided attention and when our responses to the world are appropriate, we can say that we’re ‘in the zone.’ That means we can listen, understand, make sense of the world, and deviate or shift direction if something gets in the way of our goals. Our responses should be flexible. We should be able to say, ‘That doesn’t work? Let me try something else.’ This indicates that the norepinephrine and dopamine circuits of the frontal cortex are optimally operating.”

On the other hand, individuals with ADHD find themselves in what Dr. Rostain described as an “unguided attention state” characterized by distraction and poor impulse control. “We also see it in people who are sleep deprived,” he said. “This could be untreated ADHD. If we treat ADHD properly, we move individuals into the optimal zone. But if we overdo it, if our medications are prescribed at doses that are higher than optimal, what you then see is excessive stimulation of the norepinephrine and dopamine systems. This leads to misguided attention, overfocusing, and mental inflexibility. People in this state report extreme amounts of stress and distress.”

Dr. Rostain recommends that medication plans be embedded in a comprehensive treatment approach that starts with psychoeducation. “When treating ADHD, we’re not going to turn a lion into a lamb, and we’re not going to make someone want to study if they don’t like school,” he said. “One of my patients, a college student, told me that, with the medication I prescribed for him, he was able to sit down and read for the first time for 3 hours straight. I said, ‘Great. Did you read your physics book? He said, No. I read Wired magazine.’ So while he was very focused, he didn’t concentrate on what he needed to focus on.”

Dr. Rostain supports the notion of a triad model of care with psychosocial interventions, medical interventions, and educational/workplace interventions “to improve the performance of demanded tasks, and to achieve a sense of being supported by that environment rather than being criticized,” he said. “If you ask most adults with ADHD what school was like, what will they tell you? They usually say it was bad or terrible, like a prison. If you ask them to describe it, they may have trouble remembering a lot of it, because it was so difficult for them.”

Dr. Rostain reported having received scientific advisory board honoraria from Shire, Ironshore, and Arbor. He also has received consultant honoraria from Major League Baseball, the National Football League, and from SUNY/Upstate.

[email protected]

LAS VEGAS – Assessing the risk of major congenital malformations related to antipsychotic exposure requires detailed assessment of other sources of risk, including those related to the diagnosis and associated behaviors, according to Jonathan M. Meyer, MD.

Doug Brunk/MDedge News

However, the largest study to date showed no significant difference in rates of major congenital malformations for those with one or more prescriptions for atypical antipsychotics in the first trimester, compared with pregnancies with no first trimester antipsychotic exposure.

In the U.S. general population, the estimated risk of major birth defects is 2%-4%, Dr. Meyer, a clinical professor of psychiatry at the University of California, San Diego, said at an annual psychopharmacology update held by the Nevada Psychiatric Association.

Medications represent one source of risk for major congenital malformations in patients with psychiatric illness. Other factors include lifestyle factors such substance abuse and smoking, diet and physical activity, adherence with medical/prenatal care regimens, general medical disease burden, and unknown genetic risk because of the illness itself.

Until recently, published studies examining antipsychotic exposure and the risk for congenital malformations have been flawed because of numerous factors, Dr. Meyer said, including the small sample size of live births, absence of systematic collection of risk data prior to and during pregnancy, and failure to examine all possible covariates that might moderate the risk potentially attributable to the medication itself.

For example, researchers led by Frank Habermann, PhD, prospectively evaluated three cohorts who were followed in a psychiatry consultation in Freiburg, Germany: 453 women who received atypical antipsychotics in the first trimester of pregnancy (group A); 238 women who received typical antipsychotics in the first trimester of pregnancy (group B); and 1,104 women who had no records of treatment with medications associated with harmful fetal effects (group C).

Covariates included maternal age, alcohol consumption, smoking habits, number of previous spontaneous abortions, number of previous malformed children, and gestational week at delivery (J Clin Psychopharmacol. 2013;33[4]:453-62).

The researchers found that 5.2% of women in group A gave birth to a child with a major congenital malformation, compared with 5% in group B and 2.5% in group C. Nonsignificant associations were observed between group A vs. B (adjusted odds ratio, 1.26; 95% confidence interval, 0.57-2.82) and group B vs. C (adjusted OR, 1.71; 95% CI, 0.78-3.76). The only significant association noted was between group A and C (adjusted OR, 2.17; 95% CI, 1.20-3.91). However, Dr. Meyer emphasized limitations of the study, including its small sample size and certain missing covariates, including illegal substance use.

[email protected]

LAS VEGAS – Assessing the risk of major congenital malformations related to antipsychotic exposure requires detailed assessment of other sources of risk, including those related to the diagnosis and associated behaviors, according to Jonathan M. Meyer, MD.

Doug Brunk/MDedge News

However, the largest study to date showed no significant difference in rates of major congenital malformations for those with one or more prescriptions for atypical antipsychotics in the first trimester, compared with pregnancies with no first trimester antipsychotic exposure.

In the U.S. general population, the estimated risk of major birth defects is 2%-4%, Dr. Meyer, a clinical professor of psychiatry at the University of California, San Diego, said at an annual psychopharmacology update held by the Nevada Psychiatric Association.

Medications represent one source of risk for major congenital malformations in patients with psychiatric illness. Other factors include lifestyle factors such substance abuse and smoking, diet and physical activity, adherence with medical/prenatal care regimens, general medical disease burden, and unknown genetic risk because of the illness itself.

Until recently, published studies examining antipsychotic exposure and the risk for congenital malformations have been flawed because of numerous factors, Dr. Meyer said, including the small sample size of live births, absence of systematic collection of risk data prior to and during pregnancy, and failure to examine all possible covariates that might moderate the risk potentially attributable to the medication itself.

For example, researchers led by Frank Habermann, PhD, prospectively evaluated three cohorts who were followed in a psychiatry consultation in Freiburg, Germany: 453 women who received atypical antipsychotics in the first trimester of pregnancy (group A); 238 women who received typical antipsychotics in the first trimester of pregnancy (group B); and 1,104 women who had no records of treatment with medications associated with harmful fetal effects (group C).

Covariates included maternal age, alcohol consumption, smoking habits, number of previous spontaneous abortions, number of previous malformed children, and gestational week at delivery (J Clin Psychopharmacol. 2013;33[4]:453-62).

The researchers found that 5.2% of women in group A gave birth to a child with a major congenital malformation, compared with 5% in group B and 2.5% in group C. Nonsignificant associations were observed between group A vs. B (adjusted odds ratio, 1.26; 95% confidence interval, 0.57-2.82) and group B vs. C (adjusted OR, 1.71; 95% CI, 0.78-3.76). The only significant association noted was between group A and C (adjusted OR, 2.17; 95% CI, 1.20-3.91). However, Dr. Meyer emphasized limitations of the study, including its small sample size and certain missing covariates, including illegal substance use.

[email protected]

LAS VEGAS – Assessing the risk of major congenital malformations related to antipsychotic exposure requires detailed assessment of other sources of risk, including those related to the diagnosis and associated behaviors, according to Jonathan M. Meyer, MD.

Doug Brunk/MDedge News

However, the largest study to date showed no significant difference in rates of major congenital malformations for those with one or more prescriptions for atypical antipsychotics in the first trimester, compared with pregnancies with no first trimester antipsychotic exposure.

In the U.S. general population, the estimated risk of major birth defects is 2%-4%, Dr. Meyer, a clinical professor of psychiatry at the University of California, San Diego, said at an annual psychopharmacology update held by the Nevada Psychiatric Association.

Medications represent one source of risk for major congenital malformations in patients with psychiatric illness. Other factors include lifestyle factors such substance abuse and smoking, diet and physical activity, adherence with medical/prenatal care regimens, general medical disease burden, and unknown genetic risk because of the illness itself.

Until recently, published studies examining antipsychotic exposure and the risk for congenital malformations have been flawed because of numerous factors, Dr. Meyer said, including the small sample size of live births, absence of systematic collection of risk data prior to and during pregnancy, and failure to examine all possible covariates that might moderate the risk potentially attributable to the medication itself.

For example, researchers led by Frank Habermann, PhD, prospectively evaluated three cohorts who were followed in a psychiatry consultation in Freiburg, Germany: 453 women who received atypical antipsychotics in the first trimester of pregnancy (group A); 238 women who received typical antipsychotics in the first trimester of pregnancy (group B); and 1,104 women who had no records of treatment with medications associated with harmful fetal effects (group C).

Covariates included maternal age, alcohol consumption, smoking habits, number of previous spontaneous abortions, number of previous malformed children, and gestational week at delivery (J Clin Psychopharmacol. 2013;33[4]:453-62).

The researchers found that 5.2% of women in group A gave birth to a child with a major congenital malformation, compared with 5% in group B and 2.5% in group C. Nonsignificant associations were observed between group A vs. B (adjusted odds ratio, 1.26; 95% confidence interval, 0.57-2.82) and group B vs. C (adjusted OR, 1.71; 95% CI, 0.78-3.76). The only significant association noted was between group A and C (adjusted OR, 2.17; 95% CI, 1.20-3.91). However, Dr. Meyer emphasized limitations of the study, including its small sample size and certain missing covariates, including illegal substance use.

[email protected]

LAS VEGAS – Diagnosing postpartum depression can be tricky because of the wide range of body changes that occur during the postpartum period, but vigilance is warranted with mothers who express a lack of sleep and a lack of social support.

Doug Brunk/MDedge News

One of the best questions to ask is: “Are you able to sleep when the baby sleeps?” Susan Hatters Friedman, MD, said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “This gives you information about depression and insomnia. Make sure to ask about anxiety symptoms. Also ask about any thoughts of suicide or harming the infant, and support from family and friends when she’s under stress and taking care of the baby.”

According to Dr. Friedman, a perinatal and forensic psychiatrist at Case Western Reserve University, Cleveland, social risk factors for postpartum depression (PPD) include being a victim of intimate partner violence and/or abuse, negative life events, decreased social support, relationship issues, and socioeconomic status. Psychological risk factors include anxiety/depression in pregnancy, personal or family history of PPD, and substance misuse. Biological risk factors include medical illness, multiple births, and having an infant with low birth weight/prematurity.

PPD affects 10%-20% of new mothers and peaks at 12 weeks. Postpartum psychosis, meanwhile, occurs in about 1-2 of every 1,000 deliveries. Anxiety comorbidity is common.

In the neonatal intensive care unit (NICU), PPD rates might increase from 28% to 70% depending on the study. Risk factors include personal or family history, disturbed relationships, unfavorable socioeconomic factors, and stressful life events. Obstetrical risk factors might include conception by assisted reproductive technologies and having a stillbirth in the year before conception. NICU-specific risk factors include less-effective coping strategies, greater perception of maternal role disruption, and decreased perception of nursing support. “A lot of mothers [in the NICU] talk to me about being on a roller roaster every day about what’s going to happen with their baby,” Dr. Friedman said.

The most widely used measure to screen for PPD is the 10-item self-rating Edinburgh Postnatal Depression Scale . A total score of 10 or more is considered a flag for the need to follow up for possible depressive symptoms. She advises clinicians to pay particular attention to how patients respond to item No. 10 on the scale, which reads, “The thought of harming myself has occurred to me.” (Optional answers range from “Yes, quite often” to “Never.”) She also recommends administering the screen at both pediatric and obstetrical office visits, “because mothers are more likely to attend a pediatrics appointment than her own [postpartum] follow-up.”

The differential diagnosis of PPD includes the baby blues, postpartum psychosis, postpartum anxiety/PTSD, medical causes, substance use disorder, and PPD in bipolar disorder. Baby blues is not synonymous with PPD. It affects the majority (50%-80%) of new mothers and is characterized by emotional sensitivity, mood lability, and irritability. It usually occurs within 5 days and resolves by the second week post partum.

Postpartum psychosis (PPP) occurs in about 1-2 of every 1,000 deliveries, typically in the first 2 weeks after delivery. The onset occurs rapidly, and PPP is most frequently correlated with bipolar disorder over time. PPP itself is characterized by grandiose bizarre delusions, mood lability, hallucinations, confusion, and disorganized behavior. “This can occur as a new onset of mental illness as well, so getting collateral information about her behaviors is important,” she said.

Dr. Friedman explained that those events occur post partum largely because of sleep deprivation and increasing stress as the woman adjusts to a mothering role. Hormonal shifts also occur, with a drop in estrogen levels. Obstetrical complications also might factor in.

[email protected]

LAS VEGAS – Diagnosing postpartum depression can be tricky because of the wide range of body changes that occur during the postpartum period, but vigilance is warranted with mothers who express a lack of sleep and a lack of social support.

Doug Brunk/MDedge News

One of the best questions to ask is: “Are you able to sleep when the baby sleeps?” Susan Hatters Friedman, MD, said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “This gives you information about depression and insomnia. Make sure to ask about anxiety symptoms. Also ask about any thoughts of suicide or harming the infant, and support from family and friends when she’s under stress and taking care of the baby.”

According to Dr. Friedman, a perinatal and forensic psychiatrist at Case Western Reserve University, Cleveland, social risk factors for postpartum depression (PPD) include being a victim of intimate partner violence and/or abuse, negative life events, decreased social support, relationship issues, and socioeconomic status. Psychological risk factors include anxiety/depression in pregnancy, personal or family history of PPD, and substance misuse. Biological risk factors include medical illness, multiple births, and having an infant with low birth weight/prematurity.

PPD affects 10%-20% of new mothers and peaks at 12 weeks. Postpartum psychosis, meanwhile, occurs in about 1-2 of every 1,000 deliveries. Anxiety comorbidity is common.

In the neonatal intensive care unit (NICU), PPD rates might increase from 28% to 70% depending on the study. Risk factors include personal or family history, disturbed relationships, unfavorable socioeconomic factors, and stressful life events. Obstetrical risk factors might include conception by assisted reproductive technologies and having a stillbirth in the year before conception. NICU-specific risk factors include less-effective coping strategies, greater perception of maternal role disruption, and decreased perception of nursing support. “A lot of mothers [in the NICU] talk to me about being on a roller roaster every day about what’s going to happen with their baby,” Dr. Friedman said.

The most widely used measure to screen for PPD is the 10-item self-rating Edinburgh Postnatal Depression Scale . A total score of 10 or more is considered a flag for the need to follow up for possible depressive symptoms. She advises clinicians to pay particular attention to how patients respond to item No. 10 on the scale, which reads, “The thought of harming myself has occurred to me.” (Optional answers range from “Yes, quite often” to “Never.”) She also recommends administering the screen at both pediatric and obstetrical office visits, “because mothers are more likely to attend a pediatrics appointment than her own [postpartum] follow-up.”

The differential diagnosis of PPD includes the baby blues, postpartum psychosis, postpartum anxiety/PTSD, medical causes, substance use disorder, and PPD in bipolar disorder. Baby blues is not synonymous with PPD. It affects the majority (50%-80%) of new mothers and is characterized by emotional sensitivity, mood lability, and irritability. It usually occurs within 5 days and resolves by the second week post partum.

Postpartum psychosis (PPP) occurs in about 1-2 of every 1,000 deliveries, typically in the first 2 weeks after delivery. The onset occurs rapidly, and PPP is most frequently correlated with bipolar disorder over time. PPP itself is characterized by grandiose bizarre delusions, mood lability, hallucinations, confusion, and disorganized behavior. “This can occur as a new onset of mental illness as well, so getting collateral information about her behaviors is important,” she said.

Dr. Friedman explained that those events occur post partum largely because of sleep deprivation and increasing stress as the woman adjusts to a mothering role. Hormonal shifts also occur, with a drop in estrogen levels. Obstetrical complications also might factor in.

[email protected]

LAS VEGAS – Diagnosing postpartum depression can be tricky because of the wide range of body changes that occur during the postpartum period, but vigilance is warranted with mothers who express a lack of sleep and a lack of social support.

Doug Brunk/MDedge News

One of the best questions to ask is: “Are you able to sleep when the baby sleeps?” Susan Hatters Friedman, MD, said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “This gives you information about depression and insomnia. Make sure to ask about anxiety symptoms. Also ask about any thoughts of suicide or harming the infant, and support from family and friends when she’s under stress and taking care of the baby.”

According to Dr. Friedman, a perinatal and forensic psychiatrist at Case Western Reserve University, Cleveland, social risk factors for postpartum depression (PPD) include being a victim of intimate partner violence and/or abuse, negative life events, decreased social support, relationship issues, and socioeconomic status. Psychological risk factors include anxiety/depression in pregnancy, personal or family history of PPD, and substance misuse. Biological risk factors include medical illness, multiple births, and having an infant with low birth weight/prematurity.

PPD affects 10%-20% of new mothers and peaks at 12 weeks. Postpartum psychosis, meanwhile, occurs in about 1-2 of every 1,000 deliveries. Anxiety comorbidity is common.

In the neonatal intensive care unit (NICU), PPD rates might increase from 28% to 70% depending on the study. Risk factors include personal or family history, disturbed relationships, unfavorable socioeconomic factors, and stressful life events. Obstetrical risk factors might include conception by assisted reproductive technologies and having a stillbirth in the year before conception. NICU-specific risk factors include less-effective coping strategies, greater perception of maternal role disruption, and decreased perception of nursing support. “A lot of mothers [in the NICU] talk to me about being on a roller roaster every day about what’s going to happen with their baby,” Dr. Friedman said.

The most widely used measure to screen for PPD is the 10-item self-rating Edinburgh Postnatal Depression Scale . A total score of 10 or more is considered a flag for the need to follow up for possible depressive symptoms. She advises clinicians to pay particular attention to how patients respond to item No. 10 on the scale, which reads, “The thought of harming myself has occurred to me.” (Optional answers range from “Yes, quite often” to “Never.”) She also recommends administering the screen at both pediatric and obstetrical office visits, “because mothers are more likely to attend a pediatrics appointment than her own [postpartum] follow-up.”

The differential diagnosis of PPD includes the baby blues, postpartum psychosis, postpartum anxiety/PTSD, medical causes, substance use disorder, and PPD in bipolar disorder. Baby blues is not synonymous with PPD. It affects the majority (50%-80%) of new mothers and is characterized by emotional sensitivity, mood lability, and irritability. It usually occurs within 5 days and resolves by the second week post partum.

Postpartum psychosis (PPP) occurs in about 1-2 of every 1,000 deliveries, typically in the first 2 weeks after delivery. The onset occurs rapidly, and PPP is most frequently correlated with bipolar disorder over time. PPP itself is characterized by grandiose bizarre delusions, mood lability, hallucinations, confusion, and disorganized behavior. “This can occur as a new onset of mental illness as well, so getting collateral information about her behaviors is important,” she said.

Dr. Friedman explained that those events occur post partum largely because of sleep deprivation and increasing stress as the woman adjusts to a mothering role. Hormonal shifts also occur, with a drop in estrogen levels. Obstetrical complications also might factor in.

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