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App Identifies Stress and Missed Sleep as Seizure Triggers
BOSTON—Research using an Apple Watch app to track seizures in people with epilepsy finds that common triggers include stress and missed sleep, according to a preliminary study presented at the 69th Annual Meeting of the American Academy of Neurology. 
Gregory Krauss, MD, Professor of Neurology at Johns Hopkins University in Baltimore, and colleagues conducted the study to identify common seizure triggers and estimate their relative frequency in a US population of people with epilepsy. For the 10-month study, 598 people signed up to track their seizures with an app called EpiWatch that had been created using ResearchKit, a software framework designed by Apple to make it easy for researchers to gather data more frequently and more accurately from participants using an iPhone or Apple Watch.
When a participant felt a seizure aura starting, he or she opened the app. Using the Apple Watch's biosensors, EpiWatch recorded the participant's heart rate and movements for 10 minutes. The app asked him or her to perform tasks to test responsiveness. After the seizure ended, the participant was given a brief survey about seizure type, aura, loss of awareness, and possible seizure triggers.
"The data collected will help researchers better understand epilepsy, while helping people with epilepsy keep a more complete history of their seizures," said Dr. Krauss. "The app also provides helpful tracking of seizures, prescription medication use, and drug side effects--activities that are important in helping people manage their condition."
In all, 40% of the group tracked a total of 1,485 seizures, and 177 participants reported what triggered their seizures. Stress was the most common trigger and was linked to 37% of seizures. Participants also identified lack of sleep as a trigger for 18% of the seizures, menstruation for 12%, and overexertion for 11%. Other reported triggers included diet (9%), missed medications (7%), and fever or infection (6%). Demographics and seizure types were generally similar between participants who reported seizure triggers and those who did not. Seizure triggers did not vary by the type of seizure people had.
The investigators found that stress was more commonly reported as a trigger for participants who worked full-time (35%), compared with those who worked part-time (21%), were unemployed (27%), or were disabled (29%). Nonadherence to medication was reported slightly more frequently among younger participants (ie, ages 16 to 25), among whom 40% reported a missed medication as a trigger, compared with older participants (ie, ages 26 to 66), among whom 34% reported a missed medication.
"Seizures are very unpredictable," said Dr. Krauss. "Our eventual goal is to be able to use wearable technology to predict an oncoming seizure. This could potentially save lives, as well as give people with epilepsy more freedom. The data collected in this study help us take a step in that direction."
BOSTON—Research using an Apple Watch app to track seizures in people with epilepsy finds that common triggers include stress and missed sleep, according to a preliminary study presented at the 69th Annual Meeting of the American Academy of Neurology.
Gregory Krauss, MD, Professor of Neurology at Johns Hopkins University in Baltimore, and colleagues conducted the study to identify common seizure triggers and estimate their relative frequency in a US population of people with epilepsy. For the 10-month study, 598 people signed up to track their seizures with an app called EpiWatch that had been created using ResearchKit, a software framework designed by Apple to make it easy for researchers to gather data more frequently and more accurately from participants using an iPhone or Apple Watch.
When a participant felt a seizure aura starting, he or she opened the app. Using the Apple Watch's biosensors, EpiWatch recorded the participant's heart rate and movements for 10 minutes. The app asked him or her to perform tasks to test responsiveness. After the seizure ended, the participant was given a brief survey about seizure type, aura, loss of awareness, and possible seizure triggers.
"The data collected will help researchers better understand epilepsy, while helping people with epilepsy keep a more complete history of their seizures," said Dr. Krauss. "The app also provides helpful tracking of seizures, prescription medication use, and drug side effects--activities that are important in helping people manage their condition."
In all, 40% of the group tracked a total of 1,485 seizures, and 177 participants reported what triggered their seizures. Stress was the most common trigger and was linked to 37% of seizures. Participants also identified lack of sleep as a trigger for 18% of the seizures, menstruation for 12%, and overexertion for 11%. Other reported triggers included diet (9%), missed medications (7%), and fever or infection (6%). Demographics and seizure types were generally similar between participants who reported seizure triggers and those who did not. Seizure triggers did not vary by the type of seizure people had.
The investigators found that stress was more commonly reported as a trigger for participants who worked full-time (35%), compared with those who worked part-time (21%), were unemployed (27%), or were disabled (29%). Nonadherence to medication was reported slightly more frequently among younger participants (ie, ages 16 to 25), among whom 40% reported a missed medication as a trigger, compared with older participants (ie, ages 26 to 66), among whom 34% reported a missed medication.
"Seizures are very unpredictable," said Dr. Krauss. "Our eventual goal is to be able to use wearable technology to predict an oncoming seizure. This could potentially save lives, as well as give people with epilepsy more freedom. The data collected in this study help us take a step in that direction."
BOSTON—Research using an Apple Watch app to track seizures in people with epilepsy finds that common triggers include stress and missed sleep, according to a preliminary study presented at the 69th Annual Meeting of the American Academy of Neurology.
Gregory Krauss, MD, Professor of Neurology at Johns Hopkins University in Baltimore, and colleagues conducted the study to identify common seizure triggers and estimate their relative frequency in a US population of people with epilepsy. For the 10-month study, 598 people signed up to track their seizures with an app called EpiWatch that had been created using ResearchKit, a software framework designed by Apple to make it easy for researchers to gather data more frequently and more accurately from participants using an iPhone or Apple Watch.
When a participant felt a seizure aura starting, he or she opened the app. Using the Apple Watch's biosensors, EpiWatch recorded the participant's heart rate and movements for 10 minutes. The app asked him or her to perform tasks to test responsiveness. After the seizure ended, the participant was given a brief survey about seizure type, aura, loss of awareness, and possible seizure triggers.
"The data collected will help researchers better understand epilepsy, while helping people with epilepsy keep a more complete history of their seizures," said Dr. Krauss. "The app also provides helpful tracking of seizures, prescription medication use, and drug side effects--activities that are important in helping people manage their condition."
In all, 40% of the group tracked a total of 1,485 seizures, and 177 participants reported what triggered their seizures. Stress was the most common trigger and was linked to 37% of seizures. Participants also identified lack of sleep as a trigger for 18% of the seizures, menstruation for 12%, and overexertion for 11%. Other reported triggers included diet (9%), missed medications (7%), and fever or infection (6%). Demographics and seizure types were generally similar between participants who reported seizure triggers and those who did not. Seizure triggers did not vary by the type of seizure people had.
The investigators found that stress was more commonly reported as a trigger for participants who worked full-time (35%), compared with those who worked part-time (21%), were unemployed (27%), or were disabled (29%). Nonadherence to medication was reported slightly more frequently among younger participants (ie, ages 16 to 25), among whom 40% reported a missed medication as a trigger, compared with older participants (ie, ages 26 to 66), among whom 34% reported a missed medication.
"Seizures are very unpredictable," said Dr. Krauss. "Our eventual goal is to be able to use wearable technology to predict an oncoming seizure. This could potentially save lives, as well as give people with epilepsy more freedom. The data collected in this study help us take a step in that direction."
Extrapolation of AED Efficacy Data From Adults to Pediatric Patients
BOSTON—Across a likely spectrum of syndromes with generalized seizures, the effect of adjunctive antiepileptic drug (AED) treatment on primary generalized tonic-clonic seizures appears similar between adults and children, according to a report presented at the 69th Annual Meeting of the American Academy of Neurology. 
The availability of new AEDs for pediatric patients has been delayed due to the challenges of conducting clinical trials in children. In response to this challenge, the feasibility of extrapolation of adjunctive efficacy results for partial-onset seizures has been previously shown by Pellock et al from adult to pediatric populations when the disease course and pharmacokinetics of drug effects are comparable between populations. In response to a request from the Pediatric Committee of the European Medicines Agency, Douglas Nordli Jr, MD, and colleagues explored the feasibility of extrapolating AED efficacy data from adults to pediatric patients with primary generalized tonic-clonic seizures. Dr. Nordli is the Chief of the Division of Pediatric Neurology and Codirector of the Neurosciences Institute at Children's Hospital Los Angeles.
Dr. Nordli and colleagues conducted literature searches in EMBASE, Medline, and the Cochrane Central Register of Controlled Trials for randomized, placebo-controlled clinical trials of adjunctive AED treatment for primary generalized tonic-clonic seizures in adults and children published from 1970 to 2015. Outcome data, expressed as median percent reduction in seizure frequency and greater than or equal to 50% responder rate, were extracted from eligible trials for adult and pediatric patients receiving adjunctive AEDs or placebo and used to determine the relative strength of baseline-subtracted efficacy measures.
Seven published trials of AED adjunctive therapy for primary generalized tonic-clonic seizures were eligible for quantitative analysis. Dr. Nordli and colleagues found that changes in efficacy measures were similar in adults and children with primary generalized tonic-clonic seizures and were not age-dependent. The 95% confidence intervals for the standardized mean difference in median percent reduction of seizure frequency and estimated risk ratios in greater than or equal to 50% responder rate were consistently in favor of the AED treatment and comparable between adult and pediatric groups.
Dr. Nordli's study was supported by Eisai.
Suggested Reading
Pellock JM, Carman WJ, Thyagarajan V, et al. Efficacy of antiepileptic drugs in adults predicts efficacy in children: a systematic review. Neurology. 2012;79(14):1482-1489.
BOSTON—Across a likely spectrum of syndromes with generalized seizures, the effect of adjunctive antiepileptic drug (AED) treatment on primary generalized tonic-clonic seizures appears similar between adults and children, according to a report presented at the 69th Annual Meeting of the American Academy of Neurology.
The availability of new AEDs for pediatric patients has been delayed due to the challenges of conducting clinical trials in children. In response to this challenge, the feasibility of extrapolation of adjunctive efficacy results for partial-onset seizures has been previously shown by Pellock et al from adult to pediatric populations when the disease course and pharmacokinetics of drug effects are comparable between populations. In response to a request from the Pediatric Committee of the European Medicines Agency, Douglas Nordli Jr, MD, and colleagues explored the feasibility of extrapolating AED efficacy data from adults to pediatric patients with primary generalized tonic-clonic seizures. Dr. Nordli is the Chief of the Division of Pediatric Neurology and Codirector of the Neurosciences Institute at Children's Hospital Los Angeles.
Dr. Nordli and colleagues conducted literature searches in EMBASE, Medline, and the Cochrane Central Register of Controlled Trials for randomized, placebo-controlled clinical trials of adjunctive AED treatment for primary generalized tonic-clonic seizures in adults and children published from 1970 to 2015. Outcome data, expressed as median percent reduction in seizure frequency and greater than or equal to 50% responder rate, were extracted from eligible trials for adult and pediatric patients receiving adjunctive AEDs or placebo and used to determine the relative strength of baseline-subtracted efficacy measures.
Seven published trials of AED adjunctive therapy for primary generalized tonic-clonic seizures were eligible for quantitative analysis. Dr. Nordli and colleagues found that changes in efficacy measures were similar in adults and children with primary generalized tonic-clonic seizures and were not age-dependent. The 95% confidence intervals for the standardized mean difference in median percent reduction of seizure frequency and estimated risk ratios in greater than or equal to 50% responder rate were consistently in favor of the AED treatment and comparable between adult and pediatric groups.
Dr. Nordli's study was supported by Eisai.
Suggested Reading
Pellock JM, Carman WJ, Thyagarajan V, et al. Efficacy of antiepileptic drugs in adults predicts efficacy in children: a systematic review. Neurology. 2012;79(14):1482-1489.
BOSTON—Across a likely spectrum of syndromes with generalized seizures, the effect of adjunctive antiepileptic drug (AED) treatment on primary generalized tonic-clonic seizures appears similar between adults and children, according to a report presented at the 69th Annual Meeting of the American Academy of Neurology.
The availability of new AEDs for pediatric patients has been delayed due to the challenges of conducting clinical trials in children. In response to this challenge, the feasibility of extrapolation of adjunctive efficacy results for partial-onset seizures has been previously shown by Pellock et al from adult to pediatric populations when the disease course and pharmacokinetics of drug effects are comparable between populations. In response to a request from the Pediatric Committee of the European Medicines Agency, Douglas Nordli Jr, MD, and colleagues explored the feasibility of extrapolating AED efficacy data from adults to pediatric patients with primary generalized tonic-clonic seizures. Dr. Nordli is the Chief of the Division of Pediatric Neurology and Codirector of the Neurosciences Institute at Children's Hospital Los Angeles.
Dr. Nordli and colleagues conducted literature searches in EMBASE, Medline, and the Cochrane Central Register of Controlled Trials for randomized, placebo-controlled clinical trials of adjunctive AED treatment for primary generalized tonic-clonic seizures in adults and children published from 1970 to 2015. Outcome data, expressed as median percent reduction in seizure frequency and greater than or equal to 50% responder rate, were extracted from eligible trials for adult and pediatric patients receiving adjunctive AEDs or placebo and used to determine the relative strength of baseline-subtracted efficacy measures.
Seven published trials of AED adjunctive therapy for primary generalized tonic-clonic seizures were eligible for quantitative analysis. Dr. Nordli and colleagues found that changes in efficacy measures were similar in adults and children with primary generalized tonic-clonic seizures and were not age-dependent. The 95% confidence intervals for the standardized mean difference in median percent reduction of seizure frequency and estimated risk ratios in greater than or equal to 50% responder rate were consistently in favor of the AED treatment and comparable between adult and pediatric groups.
Dr. Nordli's study was supported by Eisai.
Suggested Reading
Pellock JM, Carman WJ, Thyagarajan V, et al. Efficacy of antiepileptic drugs in adults predicts efficacy in children: a systematic review. Neurology. 2012;79(14):1482-1489.
Oral GnRH antagonist offers endometriosis pain relief in trials
VANCOUVER – An oral agent reduced dysmenorrhea and nonmenstrual pelvic pain in endometriosis patients, with more fine control over estrogen levels than historically seen with injectable gonadotropin-releasing hormone (GnRH) agonists, according to findings from two randomized controlled trials.
Elagolix is an oral, nonpeptide, gonadotropin-releasing hormone (GnRH) antagonist being developed by Neurocrine Biosciences and AbbVie. Its dose can be adjusted in an attempt to achieve estrogen levels in the optimal “therapeutic window” that controls endometriosis pain while reducing menopausal symptoms, according to Hugh S. Taylor, MD, professor of obstetrics, gynecology and reproductive services at Yale University, New Haven, Conn., and chief of obstetrics and gynecology at Yale–New Haven Hospital, who presented the research at the World Congress on Endometriosis.
Results from two phase III clinical trials, simultaneously published in the New England Journal of Medicine, show that two different doses of elagolix – 150 mg once daily or 200 mg twice daily – improved moderate or severe endometriosis-associated pain. However, patients taking the drug experienced heightened frequencies of hot flushes and increased serum lipid levels, and decreases from baseline in bone mineral density (N Engl J Med. 2017 May 19. doi: 10.1056/NEJMoa1700089).
Still, the two doses give physicians options in tailoring the drug for their patients, Dr. Taylor said. The key is to keep the levels within the therapeutic window. “That’s always been the goal, and now we have a drug that does that. You can customize it for your patient, using the stronger dose for those who need it,” he said.
He described the results from two parallel clinical trials, one conducted in the United States and Canada (Elaris Endometriosis I, n = 872) and one conducted at 187 sites on five continents (Elaris Endometriosis II, n = 817).
Patients were allowed to use NSAIDs (500 mg of naproxen) or an opioid, or both, as needed. Dr. Taylor reported the results after 6 months of treatment.
Both doses of the drug outperformed placebo in reducing dysmenorrhea at 3 months. In Elaris EM-I, 75.8% in the high-dose group and 46.4% in the low-dose group had a clinically significant reduction in dysmenorrhea and decreased or stable use of analgesics at 3 months, compared with 19.6% in the placebo group. In Elaris EM-II, 72.4% in the high-dose group and 43.4% in the low-dose group achieved a clinically significant reduction, compared with 22.7% in the placebo group (P less than .001 for all comparisons).
For nonmenstrual pelvic pain, the two doses of elagolix again bested placebo. In Elaris EM-I, 54.5% in the high-dose group and 50.4% in the low-dose group achieved a clinically significant reduction and a decreased or stable use of analgesics, compared with 36.5% on placebo (P less than .001 for all). In Elaris EM-II, 57.8% in the high-dose group and 49.8% in the low-dose group achieved a clinically significant response, compared with 36.5% in the placebo group (P less than .001 and P = .003, respectively).
The responses were sustained at 6 months for both outcomes.
In Elaris EM-I, hot flushes were reported by 7.0% of the placebo group, 23.7% of the low-dose group, and 42.3% of the high-dose group (P less than .001). In Elaris EM-II, they were reported in 10.3% of the placebo group, 22.6% of the low-dose group, and 47.6% of the high-dose group (P less than .001).
Patients in the elagolix groups experienced increases in total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides, though the researchers noted that less than 20% of participants in each group had LDL levels higher than 160 mg/dL or triglycerides levels higher than 200 mg/dL at any point during treatment.
There were also decreases in bone mineral density in the elagolix groups, but after 6 months of treatment, a z score of –1.5 or less at the lumbar spine occurred in fewer than 5% of women in the elagolix groups.
The drug should provide a more palatable option to GnRH agonists, according to Dr. Taylor. “This is a big step forward, very effective and much more tolerable. I think having an oral, rapidly acting, reversible drug, with a couple of doses available, will make this much more widely accepted and just as effective.”
The study was sponsored by AbbVie. Dr. Taylor and other researchers on the study reported financial ties to AbbVie and other pharmaceutical companies.
VANCOUVER – An oral agent reduced dysmenorrhea and nonmenstrual pelvic pain in endometriosis patients, with more fine control over estrogen levels than historically seen with injectable gonadotropin-releasing hormone (GnRH) agonists, according to findings from two randomized controlled trials.
Elagolix is an oral, nonpeptide, gonadotropin-releasing hormone (GnRH) antagonist being developed by Neurocrine Biosciences and AbbVie. Its dose can be adjusted in an attempt to achieve estrogen levels in the optimal “therapeutic window” that controls endometriosis pain while reducing menopausal symptoms, according to Hugh S. Taylor, MD, professor of obstetrics, gynecology and reproductive services at Yale University, New Haven, Conn., and chief of obstetrics and gynecology at Yale–New Haven Hospital, who presented the research at the World Congress on Endometriosis.
Results from two phase III clinical trials, simultaneously published in the New England Journal of Medicine, show that two different doses of elagolix – 150 mg once daily or 200 mg twice daily – improved moderate or severe endometriosis-associated pain. However, patients taking the drug experienced heightened frequencies of hot flushes and increased serum lipid levels, and decreases from baseline in bone mineral density (N Engl J Med. 2017 May 19. doi: 10.1056/NEJMoa1700089).
Still, the two doses give physicians options in tailoring the drug for their patients, Dr. Taylor said. The key is to keep the levels within the therapeutic window. “That’s always been the goal, and now we have a drug that does that. You can customize it for your patient, using the stronger dose for those who need it,” he said.
He described the results from two parallel clinical trials, one conducted in the United States and Canada (Elaris Endometriosis I, n = 872) and one conducted at 187 sites on five continents (Elaris Endometriosis II, n = 817).
Patients were allowed to use NSAIDs (500 mg of naproxen) or an opioid, or both, as needed. Dr. Taylor reported the results after 6 months of treatment.
Both doses of the drug outperformed placebo in reducing dysmenorrhea at 3 months. In Elaris EM-I, 75.8% in the high-dose group and 46.4% in the low-dose group had a clinically significant reduction in dysmenorrhea and decreased or stable use of analgesics at 3 months, compared with 19.6% in the placebo group. In Elaris EM-II, 72.4% in the high-dose group and 43.4% in the low-dose group achieved a clinically significant reduction, compared with 22.7% in the placebo group (P less than .001 for all comparisons).
For nonmenstrual pelvic pain, the two doses of elagolix again bested placebo. In Elaris EM-I, 54.5% in the high-dose group and 50.4% in the low-dose group achieved a clinically significant reduction and a decreased or stable use of analgesics, compared with 36.5% on placebo (P less than .001 for all). In Elaris EM-II, 57.8% in the high-dose group and 49.8% in the low-dose group achieved a clinically significant response, compared with 36.5% in the placebo group (P less than .001 and P = .003, respectively).
The responses were sustained at 6 months for both outcomes.
In Elaris EM-I, hot flushes were reported by 7.0% of the placebo group, 23.7% of the low-dose group, and 42.3% of the high-dose group (P less than .001). In Elaris EM-II, they were reported in 10.3% of the placebo group, 22.6% of the low-dose group, and 47.6% of the high-dose group (P less than .001).
Patients in the elagolix groups experienced increases in total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides, though the researchers noted that less than 20% of participants in each group had LDL levels higher than 160 mg/dL or triglycerides levels higher than 200 mg/dL at any point during treatment.
There were also decreases in bone mineral density in the elagolix groups, but after 6 months of treatment, a z score of –1.5 or less at the lumbar spine occurred in fewer than 5% of women in the elagolix groups.
The drug should provide a more palatable option to GnRH agonists, according to Dr. Taylor. “This is a big step forward, very effective and much more tolerable. I think having an oral, rapidly acting, reversible drug, with a couple of doses available, will make this much more widely accepted and just as effective.”
The study was sponsored by AbbVie. Dr. Taylor and other researchers on the study reported financial ties to AbbVie and other pharmaceutical companies.
VANCOUVER – An oral agent reduced dysmenorrhea and nonmenstrual pelvic pain in endometriosis patients, with more fine control over estrogen levels than historically seen with injectable gonadotropin-releasing hormone (GnRH) agonists, according to findings from two randomized controlled trials.
Elagolix is an oral, nonpeptide, gonadotropin-releasing hormone (GnRH) antagonist being developed by Neurocrine Biosciences and AbbVie. Its dose can be adjusted in an attempt to achieve estrogen levels in the optimal “therapeutic window” that controls endometriosis pain while reducing menopausal symptoms, according to Hugh S. Taylor, MD, professor of obstetrics, gynecology and reproductive services at Yale University, New Haven, Conn., and chief of obstetrics and gynecology at Yale–New Haven Hospital, who presented the research at the World Congress on Endometriosis.
Results from two phase III clinical trials, simultaneously published in the New England Journal of Medicine, show that two different doses of elagolix – 150 mg once daily or 200 mg twice daily – improved moderate or severe endometriosis-associated pain. However, patients taking the drug experienced heightened frequencies of hot flushes and increased serum lipid levels, and decreases from baseline in bone mineral density (N Engl J Med. 2017 May 19. doi: 10.1056/NEJMoa1700089).
Still, the two doses give physicians options in tailoring the drug for their patients, Dr. Taylor said. The key is to keep the levels within the therapeutic window. “That’s always been the goal, and now we have a drug that does that. You can customize it for your patient, using the stronger dose for those who need it,” he said.
He described the results from two parallel clinical trials, one conducted in the United States and Canada (Elaris Endometriosis I, n = 872) and one conducted at 187 sites on five continents (Elaris Endometriosis II, n = 817).
Patients were allowed to use NSAIDs (500 mg of naproxen) or an opioid, or both, as needed. Dr. Taylor reported the results after 6 months of treatment.
Both doses of the drug outperformed placebo in reducing dysmenorrhea at 3 months. In Elaris EM-I, 75.8% in the high-dose group and 46.4% in the low-dose group had a clinically significant reduction in dysmenorrhea and decreased or stable use of analgesics at 3 months, compared with 19.6% in the placebo group. In Elaris EM-II, 72.4% in the high-dose group and 43.4% in the low-dose group achieved a clinically significant reduction, compared with 22.7% in the placebo group (P less than .001 for all comparisons).
For nonmenstrual pelvic pain, the two doses of elagolix again bested placebo. In Elaris EM-I, 54.5% in the high-dose group and 50.4% in the low-dose group achieved a clinically significant reduction and a decreased or stable use of analgesics, compared with 36.5% on placebo (P less than .001 for all). In Elaris EM-II, 57.8% in the high-dose group and 49.8% in the low-dose group achieved a clinically significant response, compared with 36.5% in the placebo group (P less than .001 and P = .003, respectively).
The responses were sustained at 6 months for both outcomes.
In Elaris EM-I, hot flushes were reported by 7.0% of the placebo group, 23.7% of the low-dose group, and 42.3% of the high-dose group (P less than .001). In Elaris EM-II, they were reported in 10.3% of the placebo group, 22.6% of the low-dose group, and 47.6% of the high-dose group (P less than .001).
Patients in the elagolix groups experienced increases in total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides, though the researchers noted that less than 20% of participants in each group had LDL levels higher than 160 mg/dL or triglycerides levels higher than 200 mg/dL at any point during treatment.
There were also decreases in bone mineral density in the elagolix groups, but after 6 months of treatment, a z score of –1.5 or less at the lumbar spine occurred in fewer than 5% of women in the elagolix groups.
The drug should provide a more palatable option to GnRH agonists, according to Dr. Taylor. “This is a big step forward, very effective and much more tolerable. I think having an oral, rapidly acting, reversible drug, with a couple of doses available, will make this much more widely accepted and just as effective.”
The study was sponsored by AbbVie. Dr. Taylor and other researchers on the study reported financial ties to AbbVie and other pharmaceutical companies.
Key clinical point:
Major finding: At 3 and 6 months, the drug achieved a clinically significant reduction in dysmenorrhea for between 43% and 77% of women, compared with placebo (P less than .001).
Data source: Two phase III controlled trials randomizing nearly 1,700 with surgically confirmed endometriosis.
Disclosures: The study was sponsored by AbbVie. Dr. Taylor and other researchers on the study reported financial ties to AbbVie and other pharmaceutical companies.
Infections up the risk for pregnancy-associated stroke in preeclampsia
A host of factors, some of them preventable or treatable, increase the risk of pregnancy-related stroke among women hospitalized for preeclampsia, according to findings from a case-control study of nearly 800 preeclamptic women in New York.
Women who experienced a stroke were roughly seven times more likely to have severe preeclampsia or eclampsia, and about three to four times more likely to have an infection, a prothrombotic state, a coagulopathy, or chronic hypertension, according to the findings (Stroke. 2017 May 25. doi: 10.1161/STROKEAHA.117.017374).
“Prospective studies are needed to confirm these findings and develop interventions aimed at preventing strokes in this uniquely vulnerable group,” they added.
For the study, the investigators used billing data from the 2003-2012 New York State Department of Health inpatient database to identify women aged 12-55 years admitted with preeclampsia.
They matched each woman who experienced pregnancy-associated stroke with three randomly selected controls of the same age, race/ethnicity, and insurance status. They then compared the groups on a set of predefined risk factors.
Results showed that of 88,857 women admitted for preeclampsia during the study period, 0.2% experienced pregnancy-associated stroke, translating to a cumulative incidence of 222 per 100,000 preeclamptic women, a value more than six times that seen in the general pregnant population, the investigators noted.
The majority of strokes occurred post partum (66.5%), but more than a quarter occurred before delivery (27.9%). The single most common type of stroke was hemorrhagic (46.7%).
The 197 women with preeclampsia who experienced pregnancy-associated stroke had a sharply higher rate of in-hospital mortality (13.2%), compared with the 591 controls (0.2%).
In multivariate analysis, women with preeclampsia experiencing stroke were more likely to have severe preeclampsia or eclampsia (odds ratio, 7.2; 95% confidence interval, 4.6-11.3), or infections at the time of admission (OR, 3.0; 95% CI, 1.6-5.8), predominantly genitourinary infections.
Other risk factors for pregnancy-associated stroke included prothrombotic states (OR, 3.5; 95% CI, 1.3-9.2), coagulopathies (OR, 3.1; 95% CI, 1.3-7.1), or chronic hypertension (OR, 3.2; 95% CI, 1.8-5.5).
The findings were similar when women were matched by the severity of preeclampsia, when women with eclampsia were excluded, or when women with only postpartum stroke were included.
Heart disease, multiple gestation, and previous pregnancies were not significantly independently associated with the risk of pregnancy-associated stroke.
“The ethnic and regional diversity of New York State increases the generalizability of our findings,” the investigators wrote. “Matching of cases and controls allowed for nuanced analysis of other risk factors.”
But the study may have missed some cases of preeclampsia not formally diagnosed, and the timing of infections relative to stroke was unknown, they acknowledged. Additionally, they noted that causality cannot be inferred from the observational study, and therefore the results should be interpreted cautiously.
The investigators reported research support from the National Institutes of Health. They had no other financial disclosures.
A host of factors, some of them preventable or treatable, increase the risk of pregnancy-related stroke among women hospitalized for preeclampsia, according to findings from a case-control study of nearly 800 preeclamptic women in New York.
Women who experienced a stroke were roughly seven times more likely to have severe preeclampsia or eclampsia, and about three to four times more likely to have an infection, a prothrombotic state, a coagulopathy, or chronic hypertension, according to the findings (Stroke. 2017 May 25. doi: 10.1161/STROKEAHA.117.017374).
“Prospective studies are needed to confirm these findings and develop interventions aimed at preventing strokes in this uniquely vulnerable group,” they added.
For the study, the investigators used billing data from the 2003-2012 New York State Department of Health inpatient database to identify women aged 12-55 years admitted with preeclampsia.
They matched each woman who experienced pregnancy-associated stroke with three randomly selected controls of the same age, race/ethnicity, and insurance status. They then compared the groups on a set of predefined risk factors.
Results showed that of 88,857 women admitted for preeclampsia during the study period, 0.2% experienced pregnancy-associated stroke, translating to a cumulative incidence of 222 per 100,000 preeclamptic women, a value more than six times that seen in the general pregnant population, the investigators noted.
The majority of strokes occurred post partum (66.5%), but more than a quarter occurred before delivery (27.9%). The single most common type of stroke was hemorrhagic (46.7%).
The 197 women with preeclampsia who experienced pregnancy-associated stroke had a sharply higher rate of in-hospital mortality (13.2%), compared with the 591 controls (0.2%).
In multivariate analysis, women with preeclampsia experiencing stroke were more likely to have severe preeclampsia or eclampsia (odds ratio, 7.2; 95% confidence interval, 4.6-11.3), or infections at the time of admission (OR, 3.0; 95% CI, 1.6-5.8), predominantly genitourinary infections.
Other risk factors for pregnancy-associated stroke included prothrombotic states (OR, 3.5; 95% CI, 1.3-9.2), coagulopathies (OR, 3.1; 95% CI, 1.3-7.1), or chronic hypertension (OR, 3.2; 95% CI, 1.8-5.5).
The findings were similar when women were matched by the severity of preeclampsia, when women with eclampsia were excluded, or when women with only postpartum stroke were included.
Heart disease, multiple gestation, and previous pregnancies were not significantly independently associated with the risk of pregnancy-associated stroke.
“The ethnic and regional diversity of New York State increases the generalizability of our findings,” the investigators wrote. “Matching of cases and controls allowed for nuanced analysis of other risk factors.”
But the study may have missed some cases of preeclampsia not formally diagnosed, and the timing of infections relative to stroke was unknown, they acknowledged. Additionally, they noted that causality cannot be inferred from the observational study, and therefore the results should be interpreted cautiously.
The investigators reported research support from the National Institutes of Health. They had no other financial disclosures.
A host of factors, some of them preventable or treatable, increase the risk of pregnancy-related stroke among women hospitalized for preeclampsia, according to findings from a case-control study of nearly 800 preeclamptic women in New York.
Women who experienced a stroke were roughly seven times more likely to have severe preeclampsia or eclampsia, and about three to four times more likely to have an infection, a prothrombotic state, a coagulopathy, or chronic hypertension, according to the findings (Stroke. 2017 May 25. doi: 10.1161/STROKEAHA.117.017374).
“Prospective studies are needed to confirm these findings and develop interventions aimed at preventing strokes in this uniquely vulnerable group,” they added.
For the study, the investigators used billing data from the 2003-2012 New York State Department of Health inpatient database to identify women aged 12-55 years admitted with preeclampsia.
They matched each woman who experienced pregnancy-associated stroke with three randomly selected controls of the same age, race/ethnicity, and insurance status. They then compared the groups on a set of predefined risk factors.
Results showed that of 88,857 women admitted for preeclampsia during the study period, 0.2% experienced pregnancy-associated stroke, translating to a cumulative incidence of 222 per 100,000 preeclamptic women, a value more than six times that seen in the general pregnant population, the investigators noted.
The majority of strokes occurred post partum (66.5%), but more than a quarter occurred before delivery (27.9%). The single most common type of stroke was hemorrhagic (46.7%).
The 197 women with preeclampsia who experienced pregnancy-associated stroke had a sharply higher rate of in-hospital mortality (13.2%), compared with the 591 controls (0.2%).
In multivariate analysis, women with preeclampsia experiencing stroke were more likely to have severe preeclampsia or eclampsia (odds ratio, 7.2; 95% confidence interval, 4.6-11.3), or infections at the time of admission (OR, 3.0; 95% CI, 1.6-5.8), predominantly genitourinary infections.
Other risk factors for pregnancy-associated stroke included prothrombotic states (OR, 3.5; 95% CI, 1.3-9.2), coagulopathies (OR, 3.1; 95% CI, 1.3-7.1), or chronic hypertension (OR, 3.2; 95% CI, 1.8-5.5).
The findings were similar when women were matched by the severity of preeclampsia, when women with eclampsia were excluded, or when women with only postpartum stroke were included.
Heart disease, multiple gestation, and previous pregnancies were not significantly independently associated with the risk of pregnancy-associated stroke.
“The ethnic and regional diversity of New York State increases the generalizability of our findings,” the investigators wrote. “Matching of cases and controls allowed for nuanced analysis of other risk factors.”
But the study may have missed some cases of preeclampsia not formally diagnosed, and the timing of infections relative to stroke was unknown, they acknowledged. Additionally, they noted that causality cannot be inferred from the observational study, and therefore the results should be interpreted cautiously.
The investigators reported research support from the National Institutes of Health. They had no other financial disclosures.
FROM STROKE
Key clinical point:
Major finding: Independent risk factors for pregnancy-associated stroke were severe preeclampsia or eclampsia (OR, 7.2), infections (OR, 3.0), prothrombotic states (OR, 3.5), coagulopathies (OR, 3.1), or chronic hypertension (OR, 3.2).
Data source: A matched, case-control study of 788 women from a New York inpatient database who were hospitalized for preeclampsia.
Disclosures: The investigators reported research support from the National Institutes of Health. They had no other financial disclosures.
MS May Have a Measurable Prodrome
A Large Case–Control Analysis
Previous studies have provided evidence for an MS prodrome that occurs years before a demyelinating event or the onset of clinical symptoms. Many of these studies, however, have been limited by a retrospective design or by the absence of a control group.
To analyze the question further, Dr. Tremlett and colleagues examined data from linked health administrative and clinical databases in the Canadian provinces of British Columbia, Saskatchewan, Manitoba, and Nova Scotia, which were chosen for their geographic diversity and comprehensive data. The researchers created a health administrative cohort, which was based on administrative data, and an MS clinic-derived cohort, which used administrative and clinical data. The study’s primary outcome was all-cause use of health care during each of the five years before the health administrative index date (ie, the first demyelinating disease-related claim) or clinical index date (ie, the date of MS symptom onset).
Health Care Use Increased in Prodromal MS
The health administrative cohort included 14,428 people with MS and 72,059 matched controls. In all, 10,525 (73%) of the patients with MS were women, and their mean age at the health administrative index date was 43. Compared with controls, annual health care use increased steadily between five years and one year before the first demyelinating disease claim in these patients.
The mean number of hospital admissions was 26% higher in people with MS than in controls in the fifth year before the index date, and 78% higher in the year before the index date. The mean number of physician claims was 24% higher in people with MS than in controls in the fifth year before the index date, and 88% higher in people with MS than in controls in the year before the index date. Also, the mean number of prescribed drug classes was 23% higher in people with MS than in matched controls in the fifth year before the index date, and 49% higher in people with MS than in controls in the year before the index date.
The MS clinic cohort included 3,202 people with MS and 16,006 matched controls. In all, 2,368 (74%) of people with MS were women, and the mean age at the clinical index date was approximately 37. Compared with the health administrative cohort, this cohort had similar patterns for physician claims and prescriptions, although the differences in use in each of the five years mostly did not reach statistical significance.
“To gain a better insight into the MS prodrome, the complex reasons for increased health care use will need to be established, for example, through access of additional administrative data such as the specific diagnostic codes related to a hospital admission or physician visit, or the therapeutic drug class for a prescription,” Dr. Tremlett concluded.
—Erik Greb
Suggested Reading
Wijnands JMA, Kingwell E, Zhu F, et al. Health-care use before a first demyelinating event suggestive of a multiple sclerosis prodrome: a matched cohort study. Lancet Neurol. 2017 Apr 20 [Epub ahead of print].
A Large Case–Control Analysis
Previous studies have provided evidence for an MS prodrome that occurs years before a demyelinating event or the onset of clinical symptoms. Many of these studies, however, have been limited by a retrospective design or by the absence of a control group.
To analyze the question further, Dr. Tremlett and colleagues examined data from linked health administrative and clinical databases in the Canadian provinces of British Columbia, Saskatchewan, Manitoba, and Nova Scotia, which were chosen for their geographic diversity and comprehensive data. The researchers created a health administrative cohort, which was based on administrative data, and an MS clinic-derived cohort, which used administrative and clinical data. The study’s primary outcome was all-cause use of health care during each of the five years before the health administrative index date (ie, the first demyelinating disease-related claim) or clinical index date (ie, the date of MS symptom onset).
Health Care Use Increased in Prodromal MS
The health administrative cohort included 14,428 people with MS and 72,059 matched controls. In all, 10,525 (73%) of the patients with MS were women, and their mean age at the health administrative index date was 43. Compared with controls, annual health care use increased steadily between five years and one year before the first demyelinating disease claim in these patients.
The mean number of hospital admissions was 26% higher in people with MS than in controls in the fifth year before the index date, and 78% higher in the year before the index date. The mean number of physician claims was 24% higher in people with MS than in controls in the fifth year before the index date, and 88% higher in people with MS than in controls in the year before the index date. Also, the mean number of prescribed drug classes was 23% higher in people with MS than in matched controls in the fifth year before the index date, and 49% higher in people with MS than in controls in the year before the index date.
The MS clinic cohort included 3,202 people with MS and 16,006 matched controls. In all, 2,368 (74%) of people with MS were women, and the mean age at the clinical index date was approximately 37. Compared with the health administrative cohort, this cohort had similar patterns for physician claims and prescriptions, although the differences in use in each of the five years mostly did not reach statistical significance.
“To gain a better insight into the MS prodrome, the complex reasons for increased health care use will need to be established, for example, through access of additional administrative data such as the specific diagnostic codes related to a hospital admission or physician visit, or the therapeutic drug class for a prescription,” Dr. Tremlett concluded.
—Erik Greb
Suggested Reading
Wijnands JMA, Kingwell E, Zhu F, et al. Health-care use before a first demyelinating event suggestive of a multiple sclerosis prodrome: a matched cohort study. Lancet Neurol. 2017 Apr 20 [Epub ahead of print].
A Large Case–Control Analysis
Previous studies have provided evidence for an MS prodrome that occurs years before a demyelinating event or the onset of clinical symptoms. Many of these studies, however, have been limited by a retrospective design or by the absence of a control group.
To analyze the question further, Dr. Tremlett and colleagues examined data from linked health administrative and clinical databases in the Canadian provinces of British Columbia, Saskatchewan, Manitoba, and Nova Scotia, which were chosen for their geographic diversity and comprehensive data. The researchers created a health administrative cohort, which was based on administrative data, and an MS clinic-derived cohort, which used administrative and clinical data. The study’s primary outcome was all-cause use of health care during each of the five years before the health administrative index date (ie, the first demyelinating disease-related claim) or clinical index date (ie, the date of MS symptom onset).
Health Care Use Increased in Prodromal MS
The health administrative cohort included 14,428 people with MS and 72,059 matched controls. In all, 10,525 (73%) of the patients with MS were women, and their mean age at the health administrative index date was 43. Compared with controls, annual health care use increased steadily between five years and one year before the first demyelinating disease claim in these patients.
The mean number of hospital admissions was 26% higher in people with MS than in controls in the fifth year before the index date, and 78% higher in the year before the index date. The mean number of physician claims was 24% higher in people with MS than in controls in the fifth year before the index date, and 88% higher in people with MS than in controls in the year before the index date. Also, the mean number of prescribed drug classes was 23% higher in people with MS than in matched controls in the fifth year before the index date, and 49% higher in people with MS than in controls in the year before the index date.
The MS clinic cohort included 3,202 people with MS and 16,006 matched controls. In all, 2,368 (74%) of people with MS were women, and the mean age at the clinical index date was approximately 37. Compared with the health administrative cohort, this cohort had similar patterns for physician claims and prescriptions, although the differences in use in each of the five years mostly did not reach statistical significance.
“To gain a better insight into the MS prodrome, the complex reasons for increased health care use will need to be established, for example, through access of additional administrative data such as the specific diagnostic codes related to a hospital admission or physician visit, or the therapeutic drug class for a prescription,” Dr. Tremlett concluded.
—Erik Greb
Suggested Reading
Wijnands JMA, Kingwell E, Zhu F, et al. Health-care use before a first demyelinating event suggestive of a multiple sclerosis prodrome: a matched cohort study. Lancet Neurol. 2017 Apr 20 [Epub ahead of print].
How Can Neurologists Diagnose Traumatic Encephalopathy Syndrome?
BOSTON—Proposed diagnostic criteria for probable or possible chronic traumatic encephalopathy (CTE), a progressive neurodegenerative disease associated with repetitive brain trauma, include a history of head impacts and various core clinical and supportive features. 
The preliminary criteria, which were presented by Andrew Budson, MD, Professor of Neurology at Boston University School of Medicine, at the 69th Annual Meeting of the American Academy of Neurology, primarily were designed for research purposes, but can serve as a guide for neurologists for the diagnosis of traumatic encephalopathy syndrome. CTE is a neuropathologic diagnosis, whereas traumatic encephalopathy syndrome is a clinical diagnosis. In addition to presenting the general criteria, Dr. Budson shared diagnostic subtypes, potential biomarkers, and treatment options.
General Criteria
There are five general criteria that patients must meet to receive a diagnosis of traumatic encephalopathy syndrome, said Dr. Budson. First, there must be a history of impacts to the head based on types of injuries (eg, mild or severe traumatic brain injury, concussions, or subconcussive trauma) and sources of exposure, such as military service or involvement in contact sports for a minimum of six years, including at least two years at the college level or higher.
Second, patients must not have another neurologic disorder that likely accounts for the clinical features. Third, clinical features must be present for at least 12 months. The fourth requirement is that at least one core clinical feature (ie, cognitive, behavioral, or mood features) must be present and considered a change from baseline. Finally, at least two of nine supportive features must be present.
Core Clinical and Supportive Features
Of the core clinical features, difficulties in cognition must be reported by the patient, an informant, or a clinician and substantiated by standardized tests. Core behavioral clinical features include emotionally explosive behavior or physical and verbal abuse. Core mood clinical features include feeling overly sad, depressed, or hopeless.
In addition to core clinical features, two of the following supportive features must be present: impulsivity, anxiety, apathy, paranoia, suicidality, headache, motor signs (eg, dysarthria, dysgraphia, or other features of parkinsonism), documented decline for at least a year, or delayed onset of clinical features after a significant head impact exposure (usually at least two years).
Syndrome Subtypes
Patients may have one of four possible traumatic encephalopathy syndrome diagnostic subtypes. A behavioral/mood variant is more common among younger patients, whereas a cognitive variant is more common in older populations, said Dr. Budson. Patients also may have a mixed variant or dementia. Patients with the dementia subtype must have a progressive course of cognitive core clinical features, with or without behavior or mood features. In addition, patients with dementia must have cognitive impairment that interferes with their ability to function independently during normal daily activities.
Biomarkers and Treatment
Cavum septum pellucidum, cavum vergae, or fenestrations on neuroimaging are potential CTE biomarkers, said Dr. Budson. Normal beta amyloid CSF levels, elevated CSF p-tau/tau ratio, negative amyloid imaging, as well as cortical atrophy beyond that expected for age could also be signs of CTE. Potential experimental biomarkers include positive tau imaging and cortical thinning based on MRI.
Once physicians have made a diagnosis of probable or possible CTE, there are several treatments that may benefit patients, although no medications are approved for the treatment of CTE. Cholinesterase inhibitors may help to treat memory impairment, said Dr. Budson. For patients with depression and anxiety, selective serotonin reuptake inhibitors may be helpful. For patients with violent or explosive behavior, atypical neuroleptics may be efficacious. Memantine may benefit patients with moderate or severe dementia. Finally, to manage agitation, a combination of dextromethorphan and quinidine may be a treatment option.
—Erica Tricarico
Suggested Reading
Montenigro PH, Baugh CM, Daneshvar DH, et al. Clinical subtypes of chronic traumatic encephalopathy: literature review and proposed research diagnostic criteria for traumatic encephalopathy syndrome. Alzheimers Res Ther. 2014;6(5):68.
BOSTON—Proposed diagnostic criteria for probable or possible chronic traumatic encephalopathy (CTE), a progressive neurodegenerative disease associated with repetitive brain trauma, include a history of head impacts and various core clinical and supportive features.
The preliminary criteria, which were presented by Andrew Budson, MD, Professor of Neurology at Boston University School of Medicine, at the 69th Annual Meeting of the American Academy of Neurology, primarily were designed for research purposes, but can serve as a guide for neurologists for the diagnosis of traumatic encephalopathy syndrome. CTE is a neuropathologic diagnosis, whereas traumatic encephalopathy syndrome is a clinical diagnosis. In addition to presenting the general criteria, Dr. Budson shared diagnostic subtypes, potential biomarkers, and treatment options.
General Criteria
There are five general criteria that patients must meet to receive a diagnosis of traumatic encephalopathy syndrome, said Dr. Budson. First, there must be a history of impacts to the head based on types of injuries (eg, mild or severe traumatic brain injury, concussions, or subconcussive trauma) and sources of exposure, such as military service or involvement in contact sports for a minimum of six years, including at least two years at the college level or higher.
Second, patients must not have another neurologic disorder that likely accounts for the clinical features. Third, clinical features must be present for at least 12 months. The fourth requirement is that at least one core clinical feature (ie, cognitive, behavioral, or mood features) must be present and considered a change from baseline. Finally, at least two of nine supportive features must be present.
Core Clinical and Supportive Features
Of the core clinical features, difficulties in cognition must be reported by the patient, an informant, or a clinician and substantiated by standardized tests. Core behavioral clinical features include emotionally explosive behavior or physical and verbal abuse. Core mood clinical features include feeling overly sad, depressed, or hopeless.
In addition to core clinical features, two of the following supportive features must be present: impulsivity, anxiety, apathy, paranoia, suicidality, headache, motor signs (eg, dysarthria, dysgraphia, or other features of parkinsonism), documented decline for at least a year, or delayed onset of clinical features after a significant head impact exposure (usually at least two years).
Syndrome Subtypes
Patients may have one of four possible traumatic encephalopathy syndrome diagnostic subtypes. A behavioral/mood variant is more common among younger patients, whereas a cognitive variant is more common in older populations, said Dr. Budson. Patients also may have a mixed variant or dementia. Patients with the dementia subtype must have a progressive course of cognitive core clinical features, with or without behavior or mood features. In addition, patients with dementia must have cognitive impairment that interferes with their ability to function independently during normal daily activities.
Biomarkers and Treatment
Cavum septum pellucidum, cavum vergae, or fenestrations on neuroimaging are potential CTE biomarkers, said Dr. Budson. Normal beta amyloid CSF levels, elevated CSF p-tau/tau ratio, negative amyloid imaging, as well as cortical atrophy beyond that expected for age could also be signs of CTE. Potential experimental biomarkers include positive tau imaging and cortical thinning based on MRI.
Once physicians have made a diagnosis of probable or possible CTE, there are several treatments that may benefit patients, although no medications are approved for the treatment of CTE. Cholinesterase inhibitors may help to treat memory impairment, said Dr. Budson. For patients with depression and anxiety, selective serotonin reuptake inhibitors may be helpful. For patients with violent or explosive behavior, atypical neuroleptics may be efficacious. Memantine may benefit patients with moderate or severe dementia. Finally, to manage agitation, a combination of dextromethorphan and quinidine may be a treatment option.
—Erica Tricarico
Suggested Reading
Montenigro PH, Baugh CM, Daneshvar DH, et al. Clinical subtypes of chronic traumatic encephalopathy: literature review and proposed research diagnostic criteria for traumatic encephalopathy syndrome. Alzheimers Res Ther. 2014;6(5):68.
BOSTON—Proposed diagnostic criteria for probable or possible chronic traumatic encephalopathy (CTE), a progressive neurodegenerative disease associated with repetitive brain trauma, include a history of head impacts and various core clinical and supportive features.
The preliminary criteria, which were presented by Andrew Budson, MD, Professor of Neurology at Boston University School of Medicine, at the 69th Annual Meeting of the American Academy of Neurology, primarily were designed for research purposes, but can serve as a guide for neurologists for the diagnosis of traumatic encephalopathy syndrome. CTE is a neuropathologic diagnosis, whereas traumatic encephalopathy syndrome is a clinical diagnosis. In addition to presenting the general criteria, Dr. Budson shared diagnostic subtypes, potential biomarkers, and treatment options.
General Criteria
There are five general criteria that patients must meet to receive a diagnosis of traumatic encephalopathy syndrome, said Dr. Budson. First, there must be a history of impacts to the head based on types of injuries (eg, mild or severe traumatic brain injury, concussions, or subconcussive trauma) and sources of exposure, such as military service or involvement in contact sports for a minimum of six years, including at least two years at the college level or higher.
Second, patients must not have another neurologic disorder that likely accounts for the clinical features. Third, clinical features must be present for at least 12 months. The fourth requirement is that at least one core clinical feature (ie, cognitive, behavioral, or mood features) must be present and considered a change from baseline. Finally, at least two of nine supportive features must be present.
Core Clinical and Supportive Features
Of the core clinical features, difficulties in cognition must be reported by the patient, an informant, or a clinician and substantiated by standardized tests. Core behavioral clinical features include emotionally explosive behavior or physical and verbal abuse. Core mood clinical features include feeling overly sad, depressed, or hopeless.
In addition to core clinical features, two of the following supportive features must be present: impulsivity, anxiety, apathy, paranoia, suicidality, headache, motor signs (eg, dysarthria, dysgraphia, or other features of parkinsonism), documented decline for at least a year, or delayed onset of clinical features after a significant head impact exposure (usually at least two years).
Syndrome Subtypes
Patients may have one of four possible traumatic encephalopathy syndrome diagnostic subtypes. A behavioral/mood variant is more common among younger patients, whereas a cognitive variant is more common in older populations, said Dr. Budson. Patients also may have a mixed variant or dementia. Patients with the dementia subtype must have a progressive course of cognitive core clinical features, with or without behavior or mood features. In addition, patients with dementia must have cognitive impairment that interferes with their ability to function independently during normal daily activities.
Biomarkers and Treatment
Cavum septum pellucidum, cavum vergae, or fenestrations on neuroimaging are potential CTE biomarkers, said Dr. Budson. Normal beta amyloid CSF levels, elevated CSF p-tau/tau ratio, negative amyloid imaging, as well as cortical atrophy beyond that expected for age could also be signs of CTE. Potential experimental biomarkers include positive tau imaging and cortical thinning based on MRI.
Once physicians have made a diagnosis of probable or possible CTE, there are several treatments that may benefit patients, although no medications are approved for the treatment of CTE. Cholinesterase inhibitors may help to treat memory impairment, said Dr. Budson. For patients with depression and anxiety, selective serotonin reuptake inhibitors may be helpful. For patients with violent or explosive behavior, atypical neuroleptics may be efficacious. Memantine may benefit patients with moderate or severe dementia. Finally, to manage agitation, a combination of dextromethorphan and quinidine may be a treatment option.
—Erica Tricarico
Suggested Reading
Montenigro PH, Baugh CM, Daneshvar DH, et al. Clinical subtypes of chronic traumatic encephalopathy: literature review and proposed research diagnostic criteria for traumatic encephalopathy syndrome. Alzheimers Res Ther. 2014;6(5):68.
Breast cancer liquid biopsies don’t change outcomes....yet
LAS VEGAS – Although circulating tumor cells are prognostic in breast cancer, they aren’t likely to become a part of routine practice until they’ve been shown to improve outcomes, and that hasn’t happened yet, according to Anthony Lucci, MD, professor of breast surgical oncology at MD Anderson Cancer Center, Houston.
MD Anderson and other institutions have established that in breast cancer, from baseline through treatment follow-up, the presence of circulating tumor cells (CTCs) in the blood predicts worse outcomes in both metastatic and local disease, even among women who have a pathologic complete response to treatment. 
That knowledge has not yet translated into better outcomes. In a pivotal trial, survival was no better in metastatic breast cancer when women were switched to an alternative chemotherapy regimen after their CTC levels did not fall in response to first-line treatment, compared with women who remained on their initial agent despite persistently high CTCs (J Clin Oncol. 2014 Nov 1;32[31]:3483-9).
“When we tried to switch chemotherapy” based on CTCs, “it really didn’t make a difference, so no one is really quite sure yet what to do with this information. We can’t tell a patient that they are likely to have a much worse outcome, but there’s nothing we can do about it,” and “I don’t think payers will pay” for CTC testing in breast cancer until “we establish a predictive benefit, and show what agents will reduce CTCs and improve outcomes,” Dr. Lucci said at the American Society of Breast Surgeons annual meeting.
Even so, the promise of CTCs as a clinical tool is too great to abandon research, and work continues at MD Anderson and elsewhere. It’s thought that tumor cells in the blood aren’t simply a marker of disease, but rather microscopic disease in themselves that contributes to recurrence and progression. It’s possible that cells shed by tumors lie dormant in the bone marrow, then reactivate and reseed the original tumor site or give rise to distant metastases.
CTCs are similar to tumor cells that have been found in the bone marrow of women with apparently quiescent breast cancer, but finding them in the blood means “you don’t have to poke a needle in someone’s bone. You can just take a sample of their blood, and it tells you the same information,” Dr. Lucci said.
CTCs have been shown in breast cancer to rise and fall depending on tumor response. “In the future, I do think we will [use them] as a serial monitoring tool and a guide to therapy.” There might even be a role for breast cancer screening, he said.
Analyzing the blood for evidence of solid tumors – popularly called “liquid biopsy” – has shown benefits in a variety of cancers, particularly for identifying disease, and in some cases mutations, sooner than with conventional methods. Science is catching up to the old-school notion that cancer spreads through the blood.
Another approach is to look for circulating tumor DNA, which has been shown to be useful for early detection in gynecologic cancers. The idea is that a few tumor cells shatter and spill their genetic material into the blood early on. “In the majority of breast cancer patients,” however, “you don’t find actionable mutations” with circulating tumor DNA, especially in earlier-stage, nonmetastatic disease. “There’s not enough DNA released into the blood,” Dr. Lucci said.
But “we need to be monitoring the blood on a routine basis” for breast cancer clues. “That, I think, is the wave of the future. Just looking at x-rays and waiting for something to happen is too late,” he said.
Dr. Lucci had no disclosures related to his talk.
LAS VEGAS – Although circulating tumor cells are prognostic in breast cancer, they aren’t likely to become a part of routine practice until they’ve been shown to improve outcomes, and that hasn’t happened yet, according to Anthony Lucci, MD, professor of breast surgical oncology at MD Anderson Cancer Center, Houston.
MD Anderson and other institutions have established that in breast cancer, from baseline through treatment follow-up, the presence of circulating tumor cells (CTCs) in the blood predicts worse outcomes in both metastatic and local disease, even among women who have a pathologic complete response to treatment.
That knowledge has not yet translated into better outcomes. In a pivotal trial, survival was no better in metastatic breast cancer when women were switched to an alternative chemotherapy regimen after their CTC levels did not fall in response to first-line treatment, compared with women who remained on their initial agent despite persistently high CTCs (J Clin Oncol. 2014 Nov 1;32[31]:3483-9).
“When we tried to switch chemotherapy” based on CTCs, “it really didn’t make a difference, so no one is really quite sure yet what to do with this information. We can’t tell a patient that they are likely to have a much worse outcome, but there’s nothing we can do about it,” and “I don’t think payers will pay” for CTC testing in breast cancer until “we establish a predictive benefit, and show what agents will reduce CTCs and improve outcomes,” Dr. Lucci said at the American Society of Breast Surgeons annual meeting.
Even so, the promise of CTCs as a clinical tool is too great to abandon research, and work continues at MD Anderson and elsewhere. It’s thought that tumor cells in the blood aren’t simply a marker of disease, but rather microscopic disease in themselves that contributes to recurrence and progression. It’s possible that cells shed by tumors lie dormant in the bone marrow, then reactivate and reseed the original tumor site or give rise to distant metastases.
CTCs are similar to tumor cells that have been found in the bone marrow of women with apparently quiescent breast cancer, but finding them in the blood means “you don’t have to poke a needle in someone’s bone. You can just take a sample of their blood, and it tells you the same information,” Dr. Lucci said.
CTCs have been shown in breast cancer to rise and fall depending on tumor response. “In the future, I do think we will [use them] as a serial monitoring tool and a guide to therapy.” There might even be a role for breast cancer screening, he said.
Analyzing the blood for evidence of solid tumors – popularly called “liquid biopsy” – has shown benefits in a variety of cancers, particularly for identifying disease, and in some cases mutations, sooner than with conventional methods. Science is catching up to the old-school notion that cancer spreads through the blood.
Another approach is to look for circulating tumor DNA, which has been shown to be useful for early detection in gynecologic cancers. The idea is that a few tumor cells shatter and spill their genetic material into the blood early on. “In the majority of breast cancer patients,” however, “you don’t find actionable mutations” with circulating tumor DNA, especially in earlier-stage, nonmetastatic disease. “There’s not enough DNA released into the blood,” Dr. Lucci said.
But “we need to be monitoring the blood on a routine basis” for breast cancer clues. “That, I think, is the wave of the future. Just looking at x-rays and waiting for something to happen is too late,” he said.
Dr. Lucci had no disclosures related to his talk.
LAS VEGAS – Although circulating tumor cells are prognostic in breast cancer, they aren’t likely to become a part of routine practice until they’ve been shown to improve outcomes, and that hasn’t happened yet, according to Anthony Lucci, MD, professor of breast surgical oncology at MD Anderson Cancer Center, Houston.
MD Anderson and other institutions have established that in breast cancer, from baseline through treatment follow-up, the presence of circulating tumor cells (CTCs) in the blood predicts worse outcomes in both metastatic and local disease, even among women who have a pathologic complete response to treatment.
That knowledge has not yet translated into better outcomes. In a pivotal trial, survival was no better in metastatic breast cancer when women were switched to an alternative chemotherapy regimen after their CTC levels did not fall in response to first-line treatment, compared with women who remained on their initial agent despite persistently high CTCs (J Clin Oncol. 2014 Nov 1;32[31]:3483-9).
“When we tried to switch chemotherapy” based on CTCs, “it really didn’t make a difference, so no one is really quite sure yet what to do with this information. We can’t tell a patient that they are likely to have a much worse outcome, but there’s nothing we can do about it,” and “I don’t think payers will pay” for CTC testing in breast cancer until “we establish a predictive benefit, and show what agents will reduce CTCs and improve outcomes,” Dr. Lucci said at the American Society of Breast Surgeons annual meeting.
Even so, the promise of CTCs as a clinical tool is too great to abandon research, and work continues at MD Anderson and elsewhere. It’s thought that tumor cells in the blood aren’t simply a marker of disease, but rather microscopic disease in themselves that contributes to recurrence and progression. It’s possible that cells shed by tumors lie dormant in the bone marrow, then reactivate and reseed the original tumor site or give rise to distant metastases.
CTCs are similar to tumor cells that have been found in the bone marrow of women with apparently quiescent breast cancer, but finding them in the blood means “you don’t have to poke a needle in someone’s bone. You can just take a sample of their blood, and it tells you the same information,” Dr. Lucci said.
CTCs have been shown in breast cancer to rise and fall depending on tumor response. “In the future, I do think we will [use them] as a serial monitoring tool and a guide to therapy.” There might even be a role for breast cancer screening, he said.
Analyzing the blood for evidence of solid tumors – popularly called “liquid biopsy” – has shown benefits in a variety of cancers, particularly for identifying disease, and in some cases mutations, sooner than with conventional methods. Science is catching up to the old-school notion that cancer spreads through the blood.
Another approach is to look for circulating tumor DNA, which has been shown to be useful for early detection in gynecologic cancers. The idea is that a few tumor cells shatter and spill their genetic material into the blood early on. “In the majority of breast cancer patients,” however, “you don’t find actionable mutations” with circulating tumor DNA, especially in earlier-stage, nonmetastatic disease. “There’s not enough DNA released into the blood,” Dr. Lucci said.
But “we need to be monitoring the blood on a routine basis” for breast cancer clues. “That, I think, is the wave of the future. Just looking at x-rays and waiting for something to happen is too late,” he said.
Dr. Lucci had no disclosures related to his talk.
AT ASBS 2017
Desmoplastic trichoepithelioma may co-occur with BCC
SYDNEY, AUSTRALIA – Watchful waiting may not be the safest approach for managing patients with desmoplastic trichoepithelioma, according to a speaker at the annual meeting of the Australasian College of Dermatologists, who described five cases of the benign tumor combined with basal cell carcinoma.
Desmoplastic trichoepithelioma (DTE), a rare benign tumor that typically presents as a small, slow-growing, asymptomatic, skin-colored lesion on the face, with a depressed nonulcerated center and often raised edges, is managed with watchful waiting or local excision. While its key histopathologic features are narrow cords or strands of basaloid cells, numerous small keratin-filled cysts, and a surrounding desmoplastic core, DTE can be confused with morpheaform basal cell carcinoma (BCC), Tristan Blake, MD, dermatology registrar at Royal Brisbane and Womens’ Hospital, Brisbane, Australia, said at the meeting.
“At this stage, there’s no way to confidently say, looking at the slides, if those cases were desmoplastic trichoepithelioma arising in basal cell carcinoma or vice versa, or if they were a single tumor with divergent differentiation, or an occlusion of two separate tumors,” he said.
Dr. Blake added that this was the first time, to his knowledge, that such a combination had been reported, and that the finding had the potential to change the way DTE is managed.
“How can you now confidently elect to leave or watch the desmoplastic trichoepithelioma patients you have, knowing that not an insignificant portion might also harbor BCC or develop BCC in the future?” he said. This dilemma is made more acute by the fact that DTEs are typically found in younger patients and on the face, he added.
Two dermatopathologists involved in the retrospective review of cases reported that histochemistry was not particularly useful in differentiating DTE from other tumors, he noted.
Patients in the study were also interviewed about their tumors and reported no symptoms; when asked how long the lesions had been there prior to diagnosis, those who could recall said the lesions had likely been present for decades.
In an interview, Dr. Blake said that the discovery of coexisting DTE and BCC was a surprise, and cast doubt on the practice of watchful waiting.
No conflicts of interest were declared.
SYDNEY, AUSTRALIA – Watchful waiting may not be the safest approach for managing patients with desmoplastic trichoepithelioma, according to a speaker at the annual meeting of the Australasian College of Dermatologists, who described five cases of the benign tumor combined with basal cell carcinoma.
Desmoplastic trichoepithelioma (DTE), a rare benign tumor that typically presents as a small, slow-growing, asymptomatic, skin-colored lesion on the face, with a depressed nonulcerated center and often raised edges, is managed with watchful waiting or local excision. While its key histopathologic features are narrow cords or strands of basaloid cells, numerous small keratin-filled cysts, and a surrounding desmoplastic core, DTE can be confused with morpheaform basal cell carcinoma (BCC), Tristan Blake, MD, dermatology registrar at Royal Brisbane and Womens’ Hospital, Brisbane, Australia, said at the meeting.
“At this stage, there’s no way to confidently say, looking at the slides, if those cases were desmoplastic trichoepithelioma arising in basal cell carcinoma or vice versa, or if they were a single tumor with divergent differentiation, or an occlusion of two separate tumors,” he said.
Dr. Blake added that this was the first time, to his knowledge, that such a combination had been reported, and that the finding had the potential to change the way DTE is managed.
“How can you now confidently elect to leave or watch the desmoplastic trichoepithelioma patients you have, knowing that not an insignificant portion might also harbor BCC or develop BCC in the future?” he said. This dilemma is made more acute by the fact that DTEs are typically found in younger patients and on the face, he added.
Two dermatopathologists involved in the retrospective review of cases reported that histochemistry was not particularly useful in differentiating DTE from other tumors, he noted.
Patients in the study were also interviewed about their tumors and reported no symptoms; when asked how long the lesions had been there prior to diagnosis, those who could recall said the lesions had likely been present for decades.
In an interview, Dr. Blake said that the discovery of coexisting DTE and BCC was a surprise, and cast doubt on the practice of watchful waiting.
No conflicts of interest were declared.
SYDNEY, AUSTRALIA – Watchful waiting may not be the safest approach for managing patients with desmoplastic trichoepithelioma, according to a speaker at the annual meeting of the Australasian College of Dermatologists, who described five cases of the benign tumor combined with basal cell carcinoma.
Desmoplastic trichoepithelioma (DTE), a rare benign tumor that typically presents as a small, slow-growing, asymptomatic, skin-colored lesion on the face, with a depressed nonulcerated center and often raised edges, is managed with watchful waiting or local excision. While its key histopathologic features are narrow cords or strands of basaloid cells, numerous small keratin-filled cysts, and a surrounding desmoplastic core, DTE can be confused with morpheaform basal cell carcinoma (BCC), Tristan Blake, MD, dermatology registrar at Royal Brisbane and Womens’ Hospital, Brisbane, Australia, said at the meeting.
“At this stage, there’s no way to confidently say, looking at the slides, if those cases were desmoplastic trichoepithelioma arising in basal cell carcinoma or vice versa, or if they were a single tumor with divergent differentiation, or an occlusion of two separate tumors,” he said.
Dr. Blake added that this was the first time, to his knowledge, that such a combination had been reported, and that the finding had the potential to change the way DTE is managed.
“How can you now confidently elect to leave or watch the desmoplastic trichoepithelioma patients you have, knowing that not an insignificant portion might also harbor BCC or develop BCC in the future?” he said. This dilemma is made more acute by the fact that DTEs are typically found in younger patients and on the face, he added.
Two dermatopathologists involved in the retrospective review of cases reported that histochemistry was not particularly useful in differentiating DTE from other tumors, he noted.
Patients in the study were also interviewed about their tumors and reported no symptoms; when asked how long the lesions had been there prior to diagnosis, those who could recall said the lesions had likely been present for decades.
In an interview, Dr. Blake said that the discovery of coexisting DTE and BCC was a surprise, and cast doubt on the practice of watchful waiting.
No conflicts of interest were declared.
AT ACDASM 2017
Key clinical point: Watchful waiting may no longer be the obvious choice for desmoplastic trichoepithelioma, with evidence that the benign tumor may co-occur with basal cell carcinoma.
Major finding: Researchers reported five cases in which both DTE and BCC were identified in the same pathology specimen.
Data source: A retrospective review of 27 patients with DTE, which included reexamination of specimens.
Disclosures: No conflicts of interest were declared.
Alzheimer’s mortality in U.S. grew from 1999 to 2014
The rate of death attributable to Alzheimer’s disease increased by more than 50% from 1999 to 2014 in the United States, according to a report from the Centers for Disease Control and Prevention.
According to data collected from the National Vital Statistics System, the total number of Alzheimer’s deaths was 44,536 in 1999 and 93,541 in 2014. The mortality in 1999 was 16.5 per 100,000 people, and in 2014 it was 25.4 per 100,000 people, a rate increase of 54.5%. Alzheimer’s was the sixth most common cause of death in 2014, accounting for 3.6% of all U.S. deaths.
Mississippi, Louisiana, Arkansas, South Dakota, and Tennessee had mortality increases of more than 100%; Mississippi’s 164.1% increase from 13.3 to 35.2 per 100,000 people was the greatest during the study period. Maine, Montana, and Maryland saw decreases in mortality, with the percentages falling 23.5%, 9.9%, and 6.1%, respectively.
“An increasing number of Alzheimer’s deaths coupled with an increasing number of patients dying at home suggests that there is an increasing number of caregivers of persons with Alzheimer’s. It is likely that these caregivers might benefit from interventions such as education, respite care, and case management that can lessen the potential burden of caregiving,” the CDC investigators concluded.
Find the full study in MMWR (2017;66[20]:521-6).
The rate of death attributable to Alzheimer’s disease increased by more than 50% from 1999 to 2014 in the United States, according to a report from the Centers for Disease Control and Prevention.
According to data collected from the National Vital Statistics System, the total number of Alzheimer’s deaths was 44,536 in 1999 and 93,541 in 2014. The mortality in 1999 was 16.5 per 100,000 people, and in 2014 it was 25.4 per 100,000 people, a rate increase of 54.5%. Alzheimer’s was the sixth most common cause of death in 2014, accounting for 3.6% of all U.S. deaths.
Mississippi, Louisiana, Arkansas, South Dakota, and Tennessee had mortality increases of more than 100%; Mississippi’s 164.1% increase from 13.3 to 35.2 per 100,000 people was the greatest during the study period. Maine, Montana, and Maryland saw decreases in mortality, with the percentages falling 23.5%, 9.9%, and 6.1%, respectively.
“An increasing number of Alzheimer’s deaths coupled with an increasing number of patients dying at home suggests that there is an increasing number of caregivers of persons with Alzheimer’s. It is likely that these caregivers might benefit from interventions such as education, respite care, and case management that can lessen the potential burden of caregiving,” the CDC investigators concluded.
Find the full study in MMWR (2017;66[20]:521-6).
The rate of death attributable to Alzheimer’s disease increased by more than 50% from 1999 to 2014 in the United States, according to a report from the Centers for Disease Control and Prevention.
According to data collected from the National Vital Statistics System, the total number of Alzheimer’s deaths was 44,536 in 1999 and 93,541 in 2014. The mortality in 1999 was 16.5 per 100,000 people, and in 2014 it was 25.4 per 100,000 people, a rate increase of 54.5%. Alzheimer’s was the sixth most common cause of death in 2014, accounting for 3.6% of all U.S. deaths.
Mississippi, Louisiana, Arkansas, South Dakota, and Tennessee had mortality increases of more than 100%; Mississippi’s 164.1% increase from 13.3 to 35.2 per 100,000 people was the greatest during the study period. Maine, Montana, and Maryland saw decreases in mortality, with the percentages falling 23.5%, 9.9%, and 6.1%, respectively.
“An increasing number of Alzheimer’s deaths coupled with an increasing number of patients dying at home suggests that there is an increasing number of caregivers of persons with Alzheimer’s. It is likely that these caregivers might benefit from interventions such as education, respite care, and case management that can lessen the potential burden of caregiving,” the CDC investigators concluded.
Find the full study in MMWR (2017;66[20]:521-6).
FROM MMWR
My face is all red!
My grandson is almost 3. He is, of course, very advanced in many areas, including self-awareness.
At the moment he is suffering from Fifth Disease. (See how advanced he is – he skipped right over Diseases One through Four!) Every now and then his face clouds over as he announces, to anyone and no one, “My face is all red!”
I am not worried about long-term psychic harm. A moment later his face lights up as he looks up at the sky. “It’s a helicopter!” he declares.
By the way, does his behavior remind you of anyone else you’ve met? How about all your patients with rosacea or facial keratosis pilaris who stop by the office to say, “My face is all red!” If they didn’t notice this themselves, others have been happy to help. “You’re all red!” say their family, friends, and coworkers. “Are you all right?”
What about patients like those? Would you call them vain, or cosmetically oriented?
It seems to me that the behavior of little kids – too young to elaborate their psychological musings – sheds light on the way their elders behave, or the way they will themselves when they grow up. Years ago, I was about to laser the face of a woman with an old pulsed-dye unit that left deep-purple bruises. Her job was to train monkeys for the blind. “I need makeup,” she said. “When my monkeys see red spots on my face, they get very upset and start to point at me.”
“Not just monkeys,” I replied.
To take another example, many years ago I saw a little tyke about 18 months old. His parents were concerned about a mole on his palm.
He was not happy to let me examine him, and he let me know. “It’s OK,” I said, in my most condescending, clueless adult voice. “Your Mom and Dad just asked me to check your boo-boo.”
That set him off. “No boo-boo!” he shouted. “No boo-boo!”
Well, silly me, I later realized. The tyke was right: Of course it was not a boo-boo. A boo-boo is an assault on the integrity of the body: a cut, a scrape, a burn, something new, painful, hard to look at. That is why 9.8 out of 10 people whom we freeze, burn, or puncture look the other way while we do it. It’s also why kids dial their screams down to whimpers when we hide what we froze, burned, or punctured by covering it with a Band-Aid. Now the boo-boo is out of sight.
The tyke’s mole, on the other hand, is not an insult to the body but a part of it. It’s him.
Fast forward 15 years and ask a teen with a large (but not giant) hairy congenital nevus if she wants it off. She does not. “That’s me,” she explains.
Or ask an adult with what you would think is a disfiguring facial port-wine stain what growing up with that was like. “It was fine,” they reply. “Strangers sometimes commented, but my friends knew that was just how I looked.”
Or listen to folks who want their liver spots lasered off. They point to a dozen or so, then add, “But don’t take off that one! That’s always been there. That’s just me.”
If you listen for it, you can pick up how early a lot of adult behavior starts. Little ones destined to be lifetime pickers start scraping off anything that’s raised above the skin. Teens finicky about facial moles or minute perturbations in their complexion grow into fussy adults.
We grownups learn to embroider our primal responses with words, thoughts, feeling, explanations. Kids just come out and say what they think – “My face is all red!”
Soon my grandson will have overcome his Fifth Disease without, I hope, graduating to any higher numbers. His other grandfather is a retired engineer who used to design helicopters. By next year I expect that our mutual grandson will be able to identify anything flying overhead by make and model number.
As I said, he’s very advanced.
Also cute as all get-out, (temporary) red face and all.
Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available at amazon.com and barnesandnoble.com. Write to him at [email protected]
My grandson is almost 3. He is, of course, very advanced in many areas, including self-awareness.
At the moment he is suffering from Fifth Disease. (See how advanced he is – he skipped right over Diseases One through Four!) Every now and then his face clouds over as he announces, to anyone and no one, “My face is all red!”
I am not worried about long-term psychic harm. A moment later his face lights up as he looks up at the sky. “It’s a helicopter!” he declares.
By the way, does his behavior remind you of anyone else you’ve met? How about all your patients with rosacea or facial keratosis pilaris who stop by the office to say, “My face is all red!” If they didn’t notice this themselves, others have been happy to help. “You’re all red!” say their family, friends, and coworkers. “Are you all right?”
What about patients like those? Would you call them vain, or cosmetically oriented?
It seems to me that the behavior of little kids – too young to elaborate their psychological musings – sheds light on the way their elders behave, or the way they will themselves when they grow up. Years ago, I was about to laser the face of a woman with an old pulsed-dye unit that left deep-purple bruises. Her job was to train monkeys for the blind. “I need makeup,” she said. “When my monkeys see red spots on my face, they get very upset and start to point at me.”
“Not just monkeys,” I replied.
To take another example, many years ago I saw a little tyke about 18 months old. His parents were concerned about a mole on his palm.
He was not happy to let me examine him, and he let me know. “It’s OK,” I said, in my most condescending, clueless adult voice. “Your Mom and Dad just asked me to check your boo-boo.”
That set him off. “No boo-boo!” he shouted. “No boo-boo!”
Well, silly me, I later realized. The tyke was right: Of course it was not a boo-boo. A boo-boo is an assault on the integrity of the body: a cut, a scrape, a burn, something new, painful, hard to look at. That is why 9.8 out of 10 people whom we freeze, burn, or puncture look the other way while we do it. It’s also why kids dial their screams down to whimpers when we hide what we froze, burned, or punctured by covering it with a Band-Aid. Now the boo-boo is out of sight.
The tyke’s mole, on the other hand, is not an insult to the body but a part of it. It’s him.
Fast forward 15 years and ask a teen with a large (but not giant) hairy congenital nevus if she wants it off. She does not. “That’s me,” she explains.
Or ask an adult with what you would think is a disfiguring facial port-wine stain what growing up with that was like. “It was fine,” they reply. “Strangers sometimes commented, but my friends knew that was just how I looked.”
Or listen to folks who want their liver spots lasered off. They point to a dozen or so, then add, “But don’t take off that one! That’s always been there. That’s just me.”
If you listen for it, you can pick up how early a lot of adult behavior starts. Little ones destined to be lifetime pickers start scraping off anything that’s raised above the skin. Teens finicky about facial moles or minute perturbations in their complexion grow into fussy adults.
We grownups learn to embroider our primal responses with words, thoughts, feeling, explanations. Kids just come out and say what they think – “My face is all red!”
Soon my grandson will have overcome his Fifth Disease without, I hope, graduating to any higher numbers. His other grandfather is a retired engineer who used to design helicopters. By next year I expect that our mutual grandson will be able to identify anything flying overhead by make and model number.
As I said, he’s very advanced.
Also cute as all get-out, (temporary) red face and all.
Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available at amazon.com and barnesandnoble.com. Write to him at [email protected]
My grandson is almost 3. He is, of course, very advanced in many areas, including self-awareness.
At the moment he is suffering from Fifth Disease. (See how advanced he is – he skipped right over Diseases One through Four!) Every now and then his face clouds over as he announces, to anyone and no one, “My face is all red!”
I am not worried about long-term psychic harm. A moment later his face lights up as he looks up at the sky. “It’s a helicopter!” he declares.
By the way, does his behavior remind you of anyone else you’ve met? How about all your patients with rosacea or facial keratosis pilaris who stop by the office to say, “My face is all red!” If they didn’t notice this themselves, others have been happy to help. “You’re all red!” say their family, friends, and coworkers. “Are you all right?”
What about patients like those? Would you call them vain, or cosmetically oriented?
It seems to me that the behavior of little kids – too young to elaborate their psychological musings – sheds light on the way their elders behave, or the way they will themselves when they grow up. Years ago, I was about to laser the face of a woman with an old pulsed-dye unit that left deep-purple bruises. Her job was to train monkeys for the blind. “I need makeup,” she said. “When my monkeys see red spots on my face, they get very upset and start to point at me.”
“Not just monkeys,” I replied.
To take another example, many years ago I saw a little tyke about 18 months old. His parents were concerned about a mole on his palm.
He was not happy to let me examine him, and he let me know. “It’s OK,” I said, in my most condescending, clueless adult voice. “Your Mom and Dad just asked me to check your boo-boo.”
That set him off. “No boo-boo!” he shouted. “No boo-boo!”
Well, silly me, I later realized. The tyke was right: Of course it was not a boo-boo. A boo-boo is an assault on the integrity of the body: a cut, a scrape, a burn, something new, painful, hard to look at. That is why 9.8 out of 10 people whom we freeze, burn, or puncture look the other way while we do it. It’s also why kids dial their screams down to whimpers when we hide what we froze, burned, or punctured by covering it with a Band-Aid. Now the boo-boo is out of sight.
The tyke’s mole, on the other hand, is not an insult to the body but a part of it. It’s him.
Fast forward 15 years and ask a teen with a large (but not giant) hairy congenital nevus if she wants it off. She does not. “That’s me,” she explains.
Or ask an adult with what you would think is a disfiguring facial port-wine stain what growing up with that was like. “It was fine,” they reply. “Strangers sometimes commented, but my friends knew that was just how I looked.”
Or listen to folks who want their liver spots lasered off. They point to a dozen or so, then add, “But don’t take off that one! That’s always been there. That’s just me.”
If you listen for it, you can pick up how early a lot of adult behavior starts. Little ones destined to be lifetime pickers start scraping off anything that’s raised above the skin. Teens finicky about facial moles or minute perturbations in their complexion grow into fussy adults.
We grownups learn to embroider our primal responses with words, thoughts, feeling, explanations. Kids just come out and say what they think – “My face is all red!”
Soon my grandson will have overcome his Fifth Disease without, I hope, graduating to any higher numbers. His other grandfather is a retired engineer who used to design helicopters. By next year I expect that our mutual grandson will be able to identify anything flying overhead by make and model number.
As I said, he’s very advanced.
Also cute as all get-out, (temporary) red face and all.
Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available at amazon.com and barnesandnoble.com. Write to him at [email protected]