User login
ADHD and dyslexia may affect evaluation of concussion
, a new study shows.
“Our results suggest kids with certain learning disorders may respond differently to concussion tests, and this needs to be taken into account when advising on recovery times and when they can return to sport,” said lead author Mathew Stokes, MD. Dr. Stokes is assistant professor of pediatrics and neurology/neurotherapeutics at the University of Texas–Southwestern Medical Center, Dallas.
The study was presented at the American Academy of Neurology Sports Concussion Virtual Conference, held online July 31 to Aug. 1.
Learning disorders affected scores
The researchers analyzed data from participants aged 10-18 years who were enrolled in the North Texas Concussion Registry (ConTex). Participants had been diagnosed with a concussion that was sustained within 30 days of enrollment. The researchers investigated whether there were differences between patients who had no history of learning disorders and those with a history of dyslexia and/or ADD/ADHD with regard to results of clinical testing following concussion.
Of the 1,298 individuals in the study, 58 had been diagnosed with dyslexia, 158 had been diagnosed with ADD/ADHD, and 35 had been diagnosed with both conditions. There was no difference in age, time since injury, or history of concussion between those with learning disorders and those without, but there were more male patients in the ADD/ADHD group.
Results showed that in the dyslexia group, mean time was slower (P = .011), and there was an increase in error scores on the King-Devick (KD) test (P = .028). That test assesses eye movements and involves the rapid naming of numbers that are spaced differently. In addition, those with ADD/ADHD had significantly higher impulse control scores (P = .007) on the ImPACT series of tests, which are commonly used in the evaluation of concussion. Participants with both dyslexia and ADHD demonstrated slower KD times (P = .009) and had higher depression scores and anxiety scores.
Dr. Stokes noted that a limiting factor of the study was that baseline scores were not available. “It is possible that kids with ADD have less impulse control even at baseline, and this would need to be taken into account,” he said. “You may perhaps also expect someone with dyslexia to have a worse score on the KD tests, so we need more data on how these scores are affected from baseline in these individuals. But our results show that when evaluating kids pre- or post concussion, it is important to know about learning disorders, as this will affect how we interpret the data.”
At 3-month follow-up, there were no longer significant differences in anxiety and depression scores for those with and those without learning disorders. “This suggests anxiety and depression may well be worse temporarily after concussion for those with ADD/ADHD but gets better with time,” Dr. Stokes said.
Follow-up data were not available for the other cognitive tests.
Are recovery times longer?
Asked whether young people with these learning disorders needed a longer time to recover after concussion, Dr. Stokes said: “That is a million-dollar question. Studies so far on this have shown conflicting results. Our results add to a growing body of literature on this.” He stressed that it is important to include anxiety and depression scores on both baseline and postconcussion tests. “People don’t tend to think of these symptoms as being associated with concussion, but they are actually very prominent in this situation,” he noted. “Our results suggest that individuals with ADHD may be more prone to anxiety and depression, and a blow to the head may tip them more into these symptoms.”
Discussing the study at a virtual press conference as part of the AAN Sports Concussion meeting, the codirector of the meeting, David Dodick, MD, Mayo Clinic, Scottsdale, Ariz., said: “This is a very interesting and important study which suggests there are differences between adolescents with a history of dyslexia/ADHD and those without these conditions in performance in concussion tests. Understanding the differences in these groups will help health care providers in evaluating these athletes and assisting in counseling them and their families with regard to their risk of injury.
“It is important to recognize that athletes with ADHD, whether or not they are on medication, may take longer to recover from a concussion,” Dr. Dodick added. They also exhibit greater reductions in cognitive skills and visual motor speed regarding hand-eye coordination, he said. There is an increase in the severity of symptoms. “Symptoms that exist in both groups tend to more severe in those individuals with ADHD,” he noted.
“Ascertaining the presence or absence of ADHD or dyslexia in those who are participating in sport is important, especially when trying to interpret the results of baseline testing, the results of postinjury testing, decisions on when to return to play, and assessing for individuals and their families the risk of long-term repeat concussions and adverse outcomes,” he concluded.
The other codirector of the AAN meeting, Brian Hainline, MD, chief medical officer of the National Collegiate Athletic Association, added: “It appears that athletes with ADHD may suffer more with concussion and have a longer recovery time. This can inform our decision making and help these individuals to understand that they are at higher risk.”
Dr. Hainline said this raises another important point: “Concussion is not a homogeneous entity. It is a brain injury that can manifest in multiple parts of the brain, and the way the brain is from a premorbid or comorbid point of view can influence the manifestation of concussion as well,” he said. “All these things need to be taken into account.”
Attentional deficit may itself make an individual more susceptible to sustaining an injury in the first place, he said. “All of this is an evolving body of research which is helping clinicians to make better-informed decisions for athletes who may manifest differently.”
A version of this article originally appeared on Medscape.com.
, a new study shows.
“Our results suggest kids with certain learning disorders may respond differently to concussion tests, and this needs to be taken into account when advising on recovery times and when they can return to sport,” said lead author Mathew Stokes, MD. Dr. Stokes is assistant professor of pediatrics and neurology/neurotherapeutics at the University of Texas–Southwestern Medical Center, Dallas.
The study was presented at the American Academy of Neurology Sports Concussion Virtual Conference, held online July 31 to Aug. 1.
Learning disorders affected scores
The researchers analyzed data from participants aged 10-18 years who were enrolled in the North Texas Concussion Registry (ConTex). Participants had been diagnosed with a concussion that was sustained within 30 days of enrollment. The researchers investigated whether there were differences between patients who had no history of learning disorders and those with a history of dyslexia and/or ADD/ADHD with regard to results of clinical testing following concussion.
Of the 1,298 individuals in the study, 58 had been diagnosed with dyslexia, 158 had been diagnosed with ADD/ADHD, and 35 had been diagnosed with both conditions. There was no difference in age, time since injury, or history of concussion between those with learning disorders and those without, but there were more male patients in the ADD/ADHD group.
Results showed that in the dyslexia group, mean time was slower (P = .011), and there was an increase in error scores on the King-Devick (KD) test (P = .028). That test assesses eye movements and involves the rapid naming of numbers that are spaced differently. In addition, those with ADD/ADHD had significantly higher impulse control scores (P = .007) on the ImPACT series of tests, which are commonly used in the evaluation of concussion. Participants with both dyslexia and ADHD demonstrated slower KD times (P = .009) and had higher depression scores and anxiety scores.
Dr. Stokes noted that a limiting factor of the study was that baseline scores were not available. “It is possible that kids with ADD have less impulse control even at baseline, and this would need to be taken into account,” he said. “You may perhaps also expect someone with dyslexia to have a worse score on the KD tests, so we need more data on how these scores are affected from baseline in these individuals. But our results show that when evaluating kids pre- or post concussion, it is important to know about learning disorders, as this will affect how we interpret the data.”
At 3-month follow-up, there were no longer significant differences in anxiety and depression scores for those with and those without learning disorders. “This suggests anxiety and depression may well be worse temporarily after concussion for those with ADD/ADHD but gets better with time,” Dr. Stokes said.
Follow-up data were not available for the other cognitive tests.
Are recovery times longer?
Asked whether young people with these learning disorders needed a longer time to recover after concussion, Dr. Stokes said: “That is a million-dollar question. Studies so far on this have shown conflicting results. Our results add to a growing body of literature on this.” He stressed that it is important to include anxiety and depression scores on both baseline and postconcussion tests. “People don’t tend to think of these symptoms as being associated with concussion, but they are actually very prominent in this situation,” he noted. “Our results suggest that individuals with ADHD may be more prone to anxiety and depression, and a blow to the head may tip them more into these symptoms.”
Discussing the study at a virtual press conference as part of the AAN Sports Concussion meeting, the codirector of the meeting, David Dodick, MD, Mayo Clinic, Scottsdale, Ariz., said: “This is a very interesting and important study which suggests there are differences between adolescents with a history of dyslexia/ADHD and those without these conditions in performance in concussion tests. Understanding the differences in these groups will help health care providers in evaluating these athletes and assisting in counseling them and their families with regard to their risk of injury.
“It is important to recognize that athletes with ADHD, whether or not they are on medication, may take longer to recover from a concussion,” Dr. Dodick added. They also exhibit greater reductions in cognitive skills and visual motor speed regarding hand-eye coordination, he said. There is an increase in the severity of symptoms. “Symptoms that exist in both groups tend to more severe in those individuals with ADHD,” he noted.
“Ascertaining the presence or absence of ADHD or dyslexia in those who are participating in sport is important, especially when trying to interpret the results of baseline testing, the results of postinjury testing, decisions on when to return to play, and assessing for individuals and their families the risk of long-term repeat concussions and adverse outcomes,” he concluded.
The other codirector of the AAN meeting, Brian Hainline, MD, chief medical officer of the National Collegiate Athletic Association, added: “It appears that athletes with ADHD may suffer more with concussion and have a longer recovery time. This can inform our decision making and help these individuals to understand that they are at higher risk.”
Dr. Hainline said this raises another important point: “Concussion is not a homogeneous entity. It is a brain injury that can manifest in multiple parts of the brain, and the way the brain is from a premorbid or comorbid point of view can influence the manifestation of concussion as well,” he said. “All these things need to be taken into account.”
Attentional deficit may itself make an individual more susceptible to sustaining an injury in the first place, he said. “All of this is an evolving body of research which is helping clinicians to make better-informed decisions for athletes who may manifest differently.”
A version of this article originally appeared on Medscape.com.
, a new study shows.
“Our results suggest kids with certain learning disorders may respond differently to concussion tests, and this needs to be taken into account when advising on recovery times and when they can return to sport,” said lead author Mathew Stokes, MD. Dr. Stokes is assistant professor of pediatrics and neurology/neurotherapeutics at the University of Texas–Southwestern Medical Center, Dallas.
The study was presented at the American Academy of Neurology Sports Concussion Virtual Conference, held online July 31 to Aug. 1.
Learning disorders affected scores
The researchers analyzed data from participants aged 10-18 years who were enrolled in the North Texas Concussion Registry (ConTex). Participants had been diagnosed with a concussion that was sustained within 30 days of enrollment. The researchers investigated whether there were differences between patients who had no history of learning disorders and those with a history of dyslexia and/or ADD/ADHD with regard to results of clinical testing following concussion.
Of the 1,298 individuals in the study, 58 had been diagnosed with dyslexia, 158 had been diagnosed with ADD/ADHD, and 35 had been diagnosed with both conditions. There was no difference in age, time since injury, or history of concussion between those with learning disorders and those without, but there were more male patients in the ADD/ADHD group.
Results showed that in the dyslexia group, mean time was slower (P = .011), and there was an increase in error scores on the King-Devick (KD) test (P = .028). That test assesses eye movements and involves the rapid naming of numbers that are spaced differently. In addition, those with ADD/ADHD had significantly higher impulse control scores (P = .007) on the ImPACT series of tests, which are commonly used in the evaluation of concussion. Participants with both dyslexia and ADHD demonstrated slower KD times (P = .009) and had higher depression scores and anxiety scores.
Dr. Stokes noted that a limiting factor of the study was that baseline scores were not available. “It is possible that kids with ADD have less impulse control even at baseline, and this would need to be taken into account,” he said. “You may perhaps also expect someone with dyslexia to have a worse score on the KD tests, so we need more data on how these scores are affected from baseline in these individuals. But our results show that when evaluating kids pre- or post concussion, it is important to know about learning disorders, as this will affect how we interpret the data.”
At 3-month follow-up, there were no longer significant differences in anxiety and depression scores for those with and those without learning disorders. “This suggests anxiety and depression may well be worse temporarily after concussion for those with ADD/ADHD but gets better with time,” Dr. Stokes said.
Follow-up data were not available for the other cognitive tests.
Are recovery times longer?
Asked whether young people with these learning disorders needed a longer time to recover after concussion, Dr. Stokes said: “That is a million-dollar question. Studies so far on this have shown conflicting results. Our results add to a growing body of literature on this.” He stressed that it is important to include anxiety and depression scores on both baseline and postconcussion tests. “People don’t tend to think of these symptoms as being associated with concussion, but they are actually very prominent in this situation,” he noted. “Our results suggest that individuals with ADHD may be more prone to anxiety and depression, and a blow to the head may tip them more into these symptoms.”
Discussing the study at a virtual press conference as part of the AAN Sports Concussion meeting, the codirector of the meeting, David Dodick, MD, Mayo Clinic, Scottsdale, Ariz., said: “This is a very interesting and important study which suggests there are differences between adolescents with a history of dyslexia/ADHD and those without these conditions in performance in concussion tests. Understanding the differences in these groups will help health care providers in evaluating these athletes and assisting in counseling them and their families with regard to their risk of injury.
“It is important to recognize that athletes with ADHD, whether or not they are on medication, may take longer to recover from a concussion,” Dr. Dodick added. They also exhibit greater reductions in cognitive skills and visual motor speed regarding hand-eye coordination, he said. There is an increase in the severity of symptoms. “Symptoms that exist in both groups tend to more severe in those individuals with ADHD,” he noted.
“Ascertaining the presence or absence of ADHD or dyslexia in those who are participating in sport is important, especially when trying to interpret the results of baseline testing, the results of postinjury testing, decisions on when to return to play, and assessing for individuals and their families the risk of long-term repeat concussions and adverse outcomes,” he concluded.
The other codirector of the AAN meeting, Brian Hainline, MD, chief medical officer of the National Collegiate Athletic Association, added: “It appears that athletes with ADHD may suffer more with concussion and have a longer recovery time. This can inform our decision making and help these individuals to understand that they are at higher risk.”
Dr. Hainline said this raises another important point: “Concussion is not a homogeneous entity. It is a brain injury that can manifest in multiple parts of the brain, and the way the brain is from a premorbid or comorbid point of view can influence the manifestation of concussion as well,” he said. “All these things need to be taken into account.”
Attentional deficit may itself make an individual more susceptible to sustaining an injury in the first place, he said. “All of this is an evolving body of research which is helping clinicians to make better-informed decisions for athletes who may manifest differently.”
A version of this article originally appeared on Medscape.com.
From AAN Sports Concussion Conference
Concussion linked to risk for dementia, Parkinson’s disease, and ADHD
new research suggests. Results from a retrospective, population-based cohort study showed that controlling for socioeconomic status and overall health did not significantly affect this association.
The link between concussion and risk for ADHD and for mood and anxiety disorder was stronger in the women than in the men. In addition, having a history of multiple concussions strengthened the association between concussion and subsequent mood and anxiety disorder, dementia, and Parkinson’s disease compared with experiencing just one concussion.
The findings are similar to those of previous studies, noted lead author Marc P. Morissette, PhD, research assistant at the Pan Am Clinic Foundation in Winnipeg, Manitoba, Canada. “The main methodological differences separating our study from previous studies in this area is a focus on concussion-specific injuries identified from medical records and the potential for study participants to have up to 25 years of follow-up data,” said Dr. Morissette.
The findings were published online July 27 in Family Medicine and Community Health, a BMJ journal.
Almost 190,000 participants
Several studies have shown associations between head injury and increased risk for ADHD, depression, anxiety, Alzheimer’s disease, and Parkinson’s disease. However, many of these studies relied on self-reported medical history, included all forms of traumatic brain injury, and failed to adjust for preexisting health conditions.
An improved understanding of concussion and the risks associated with it could help physicians manage their patients’ long-term needs, the investigators noted.
In the current study, the researchers examined anonymized administrative health data collected between the periods of 1990–1991 and 2014–2015 in the Manitoba Population Research Data Repository at the Manitoba Center for Health Policy.
Eligible patients had been diagnosed with concussion in accordance with standard criteria. Participants were excluded if they had been diagnosed with dementia or Parkinson’s disease before the incident concussion during the study period. The investigators matched three control participants to each included patient on the basis of age, sex, and location.
Study outcome was time from index date (date of first concussion) to diagnosis of ADHD, mood and anxiety disorder, dementia, or Parkinson’s disease. The researchers controlled for socioeconomic status using the Socioeconomic Factor Index, version 2 (SEFI2), and for preexisting medical conditions using the Charlson Comorbidity Index (CCI).
The study included 28,021 men (mean age, 25 years) and 19,462 women (mean age, 30 years) in the concussion group and 81,871 men (mean age, 25 years) and 57,159 women (mean age, 30 years) in the control group. Mean SEFI2 score was approximately −0.05, and mean CCI score was approximately 0.2.
Dose effect?
Results showed that concussion was associated with an increased risk for ADHD (hazard ratio [HR], 1.39), mood and anxiety disorder (HR, 1.72), dementia (HR, 1.72), and Parkinson’s disease (HR, 1.57).
After a concussion, the risk of developing ADHD was 28% higher and the risk of developing mood and anxiety disorder was 7% higher among women than among men. Gender was not associated with risk for dementia or Parkinson’s disease after concussion.
Sustaining a second concussion increased the strength of the association with risk for dementia compared with sustaining a single concussion (HR, 1.62). Similarly, sustaining more than three concussions increased the strength of the association with the risk for mood and anxiety disorders (HR for more than three vs one concussion, 1.22) and Parkinson›s disease (HR, 3.27).
A sensitivity analysis found similar associations between concussion and risk for mood and anxiety disorder among all age groups. Younger participants were at greater risk for ADHD, however, and older participants were at greater risk for dementia and Parkinson’s disease.
Increased awareness of concussion and the outcomes of interest, along with improved diagnostic tools, may have influenced the study’s findings, Dr. Morissette noted. “The sex-based differences may be due to either pathophysiological differences in response to concussive injuries or potentially a difference in willingness to seek medical care or share symptoms, concussion-related or otherwise, with a medical professional,” he said.
“We are hopeful that our findings will encourage practitioners to be cognizant of various conditions that may present in individuals who have previously experienced a concussion,” Dr. Morissette added. “If physicians are aware of the various associations identified following a concussion, it may lead to more thorough clinical examination at initial presentation, along with more dedicated care throughout the patient’s life.”
Association versus causation
Commenting on the research, Steven Erickson, MD, sports medicine specialist at Banner–University Medicine Neuroscience Institute, Phoenix, Ariz., noted that although the study showed an association between concussion and subsequent diagnosis of ADHD, anxiety, and Parkinson’s disease, “this association should not be misconstrued as causation.” He added that the study’s conclusions “are just as likely to be due to labeling theory” or a self-fulfilling prophecy.
“Patients diagnosed with ADHD, anxiety, or Parkinson’s disease may recall concussion and associate the two diagnoses; but patients who have not previously been diagnosed with a concussion cannot draw that conclusion,” said Dr. Erickson, who was not involved with the research.
Citing the apparent gender difference in the strength of the association between concussion and the outcomes of interest, Dr. Erickson noted that women are more likely to report symptoms in general “and therefore are more likely to be diagnosed with ADHD and anxiety disorders” because of differences in reporting rather than incidence of disease.
“Further research needs to be done to definitively determine a causal relationship between concussion and any psychiatric or neurologic diagnosis,” Dr. Erickson concluded.
The study was funded by the Pan Am Clinic Foundation. Dr. Morissette and Dr. Erickson have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
new research suggests. Results from a retrospective, population-based cohort study showed that controlling for socioeconomic status and overall health did not significantly affect this association.
The link between concussion and risk for ADHD and for mood and anxiety disorder was stronger in the women than in the men. In addition, having a history of multiple concussions strengthened the association between concussion and subsequent mood and anxiety disorder, dementia, and Parkinson’s disease compared with experiencing just one concussion.
The findings are similar to those of previous studies, noted lead author Marc P. Morissette, PhD, research assistant at the Pan Am Clinic Foundation in Winnipeg, Manitoba, Canada. “The main methodological differences separating our study from previous studies in this area is a focus on concussion-specific injuries identified from medical records and the potential for study participants to have up to 25 years of follow-up data,” said Dr. Morissette.
The findings were published online July 27 in Family Medicine and Community Health, a BMJ journal.
Almost 190,000 participants
Several studies have shown associations between head injury and increased risk for ADHD, depression, anxiety, Alzheimer’s disease, and Parkinson’s disease. However, many of these studies relied on self-reported medical history, included all forms of traumatic brain injury, and failed to adjust for preexisting health conditions.
An improved understanding of concussion and the risks associated with it could help physicians manage their patients’ long-term needs, the investigators noted.
In the current study, the researchers examined anonymized administrative health data collected between the periods of 1990–1991 and 2014–2015 in the Manitoba Population Research Data Repository at the Manitoba Center for Health Policy.
Eligible patients had been diagnosed with concussion in accordance with standard criteria. Participants were excluded if they had been diagnosed with dementia or Parkinson’s disease before the incident concussion during the study period. The investigators matched three control participants to each included patient on the basis of age, sex, and location.
Study outcome was time from index date (date of first concussion) to diagnosis of ADHD, mood and anxiety disorder, dementia, or Parkinson’s disease. The researchers controlled for socioeconomic status using the Socioeconomic Factor Index, version 2 (SEFI2), and for preexisting medical conditions using the Charlson Comorbidity Index (CCI).
The study included 28,021 men (mean age, 25 years) and 19,462 women (mean age, 30 years) in the concussion group and 81,871 men (mean age, 25 years) and 57,159 women (mean age, 30 years) in the control group. Mean SEFI2 score was approximately −0.05, and mean CCI score was approximately 0.2.
Dose effect?
Results showed that concussion was associated with an increased risk for ADHD (hazard ratio [HR], 1.39), mood and anxiety disorder (HR, 1.72), dementia (HR, 1.72), and Parkinson’s disease (HR, 1.57).
After a concussion, the risk of developing ADHD was 28% higher and the risk of developing mood and anxiety disorder was 7% higher among women than among men. Gender was not associated with risk for dementia or Parkinson’s disease after concussion.
Sustaining a second concussion increased the strength of the association with risk for dementia compared with sustaining a single concussion (HR, 1.62). Similarly, sustaining more than three concussions increased the strength of the association with the risk for mood and anxiety disorders (HR for more than three vs one concussion, 1.22) and Parkinson›s disease (HR, 3.27).
A sensitivity analysis found similar associations between concussion and risk for mood and anxiety disorder among all age groups. Younger participants were at greater risk for ADHD, however, and older participants were at greater risk for dementia and Parkinson’s disease.
Increased awareness of concussion and the outcomes of interest, along with improved diagnostic tools, may have influenced the study’s findings, Dr. Morissette noted. “The sex-based differences may be due to either pathophysiological differences in response to concussive injuries or potentially a difference in willingness to seek medical care or share symptoms, concussion-related or otherwise, with a medical professional,” he said.
“We are hopeful that our findings will encourage practitioners to be cognizant of various conditions that may present in individuals who have previously experienced a concussion,” Dr. Morissette added. “If physicians are aware of the various associations identified following a concussion, it may lead to more thorough clinical examination at initial presentation, along with more dedicated care throughout the patient’s life.”
Association versus causation
Commenting on the research, Steven Erickson, MD, sports medicine specialist at Banner–University Medicine Neuroscience Institute, Phoenix, Ariz., noted that although the study showed an association between concussion and subsequent diagnosis of ADHD, anxiety, and Parkinson’s disease, “this association should not be misconstrued as causation.” He added that the study’s conclusions “are just as likely to be due to labeling theory” or a self-fulfilling prophecy.
“Patients diagnosed with ADHD, anxiety, or Parkinson’s disease may recall concussion and associate the two diagnoses; but patients who have not previously been diagnosed with a concussion cannot draw that conclusion,” said Dr. Erickson, who was not involved with the research.
Citing the apparent gender difference in the strength of the association between concussion and the outcomes of interest, Dr. Erickson noted that women are more likely to report symptoms in general “and therefore are more likely to be diagnosed with ADHD and anxiety disorders” because of differences in reporting rather than incidence of disease.
“Further research needs to be done to definitively determine a causal relationship between concussion and any psychiatric or neurologic diagnosis,” Dr. Erickson concluded.
The study was funded by the Pan Am Clinic Foundation. Dr. Morissette and Dr. Erickson have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
new research suggests. Results from a retrospective, population-based cohort study showed that controlling for socioeconomic status and overall health did not significantly affect this association.
The link between concussion and risk for ADHD and for mood and anxiety disorder was stronger in the women than in the men. In addition, having a history of multiple concussions strengthened the association between concussion and subsequent mood and anxiety disorder, dementia, and Parkinson’s disease compared with experiencing just one concussion.
The findings are similar to those of previous studies, noted lead author Marc P. Morissette, PhD, research assistant at the Pan Am Clinic Foundation in Winnipeg, Manitoba, Canada. “The main methodological differences separating our study from previous studies in this area is a focus on concussion-specific injuries identified from medical records and the potential for study participants to have up to 25 years of follow-up data,” said Dr. Morissette.
The findings were published online July 27 in Family Medicine and Community Health, a BMJ journal.
Almost 190,000 participants
Several studies have shown associations between head injury and increased risk for ADHD, depression, anxiety, Alzheimer’s disease, and Parkinson’s disease. However, many of these studies relied on self-reported medical history, included all forms of traumatic brain injury, and failed to adjust for preexisting health conditions.
An improved understanding of concussion and the risks associated with it could help physicians manage their patients’ long-term needs, the investigators noted.
In the current study, the researchers examined anonymized administrative health data collected between the periods of 1990–1991 and 2014–2015 in the Manitoba Population Research Data Repository at the Manitoba Center for Health Policy.
Eligible patients had been diagnosed with concussion in accordance with standard criteria. Participants were excluded if they had been diagnosed with dementia or Parkinson’s disease before the incident concussion during the study period. The investigators matched three control participants to each included patient on the basis of age, sex, and location.
Study outcome was time from index date (date of first concussion) to diagnosis of ADHD, mood and anxiety disorder, dementia, or Parkinson’s disease. The researchers controlled for socioeconomic status using the Socioeconomic Factor Index, version 2 (SEFI2), and for preexisting medical conditions using the Charlson Comorbidity Index (CCI).
The study included 28,021 men (mean age, 25 years) and 19,462 women (mean age, 30 years) in the concussion group and 81,871 men (mean age, 25 years) and 57,159 women (mean age, 30 years) in the control group. Mean SEFI2 score was approximately −0.05, and mean CCI score was approximately 0.2.
Dose effect?
Results showed that concussion was associated with an increased risk for ADHD (hazard ratio [HR], 1.39), mood and anxiety disorder (HR, 1.72), dementia (HR, 1.72), and Parkinson’s disease (HR, 1.57).
After a concussion, the risk of developing ADHD was 28% higher and the risk of developing mood and anxiety disorder was 7% higher among women than among men. Gender was not associated with risk for dementia or Parkinson’s disease after concussion.
Sustaining a second concussion increased the strength of the association with risk for dementia compared with sustaining a single concussion (HR, 1.62). Similarly, sustaining more than three concussions increased the strength of the association with the risk for mood and anxiety disorders (HR for more than three vs one concussion, 1.22) and Parkinson›s disease (HR, 3.27).
A sensitivity analysis found similar associations between concussion and risk for mood and anxiety disorder among all age groups. Younger participants were at greater risk for ADHD, however, and older participants were at greater risk for dementia and Parkinson’s disease.
Increased awareness of concussion and the outcomes of interest, along with improved diagnostic tools, may have influenced the study’s findings, Dr. Morissette noted. “The sex-based differences may be due to either pathophysiological differences in response to concussive injuries or potentially a difference in willingness to seek medical care or share symptoms, concussion-related or otherwise, with a medical professional,” he said.
“We are hopeful that our findings will encourage practitioners to be cognizant of various conditions that may present in individuals who have previously experienced a concussion,” Dr. Morissette added. “If physicians are aware of the various associations identified following a concussion, it may lead to more thorough clinical examination at initial presentation, along with more dedicated care throughout the patient’s life.”
Association versus causation
Commenting on the research, Steven Erickson, MD, sports medicine specialist at Banner–University Medicine Neuroscience Institute, Phoenix, Ariz., noted that although the study showed an association between concussion and subsequent diagnosis of ADHD, anxiety, and Parkinson’s disease, “this association should not be misconstrued as causation.” He added that the study’s conclusions “are just as likely to be due to labeling theory” or a self-fulfilling prophecy.
“Patients diagnosed with ADHD, anxiety, or Parkinson’s disease may recall concussion and associate the two diagnoses; but patients who have not previously been diagnosed with a concussion cannot draw that conclusion,” said Dr. Erickson, who was not involved with the research.
Citing the apparent gender difference in the strength of the association between concussion and the outcomes of interest, Dr. Erickson noted that women are more likely to report symptoms in general “and therefore are more likely to be diagnosed with ADHD and anxiety disorders” because of differences in reporting rather than incidence of disease.
“Further research needs to be done to definitively determine a causal relationship between concussion and any psychiatric or neurologic diagnosis,” Dr. Erickson concluded.
The study was funded by the Pan Am Clinic Foundation. Dr. Morissette and Dr. Erickson have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
From Family Medicine and Community Health
Consensus document reviews determination of brain death
The document, a result of the World Brain Death Project, surveys the clinical aspects of this determination, such as clinical testing, apnea testing, and the number of examinations required, as well as its social and legal aspects, including documentation, qualifications for making the determination, and religious attitudes toward BD/DNC.
The recommendations are the minimum criteria for BD/DNC, and countries and professional societies may choose to adopt stricter criteria, the authors noted. Seventeen supplements to the consensus statement contain detailed reports on topics the statement examines, including focuses on both adults and children.
“Perhaps the most important points of this project are, first, to show the worldwide acceptance of the concept of BD/DNC and what the minimum requirements are for BD/DNC,” said corresponding author Gene Sung, MD, MPH, director of the neurocritical care and stroke division at the University of Southern California, Los Angeles. Second, “this standard is centered around a clinical determination without the need for other testing.”
The consensus document and supplements were published online Aug. 3 in JAMA.
Comprehensive review
A lack of rigor has led to many differences in the determination of BD/DNC, said Dr. Sung. “Some of the variance that is common are the numbers of exams and examiners that are required and whether ancillary tests are required for determination of BD/DNC. In addition, a lot of guidelines and protocols that are in use are not thorough in detailing how to do the examinations and what to do in different circumstances.”
Professional societies such as the World Federation of Intensive and Critical Care recruited experts in BD/DNC to develop recommendations, which were based on relevant articles that they identified during a literature search. “We wanted to develop a fairly comprehensive document that, along with the 17 supplements, builds a foundation to show how to determine BD/DNC – what the minimum clinical criteria needed are and what to do in special circumstances,” Dr. Sung said.
Major sections of the statement include recommendations for the minimum clinical standards for the determination of BD/DNC in adults and children.
Determination must begin by establishing that the patient has sustained an irreversible brain injury that resulted in the loss of all brain function, according to the authors. Confounders such as pharmacologic paralysis and the effect of CNS depressant medications should be ruled out.
In addition, clinical evaluation must include an assessment for coma and an evaluation for brain stem areflexia. Among other criteria, the pupils should be fixed and nonresponsive to light, the face should not move in response to noxious cranial stimulation, and the gag and cough reflexes should be absent. Apnea testing is recommended to evaluate the responsiveness of respiratory centers in the medulla.
Although the definition of BD/DNC is the same in children as in adults, less evidence is available for the determination of BD/DNC in the very young. The authors thus advised a cautious approach to the evaluation of infants and younger children.
Recommendations vary by age and often require serial examinations, including apnea testing, they noted.
Ancillary testing
The consensus statement also reviews ancillary testing, which the authors recommend be required when the minimum clinical examination, including the apnea test, cannot be completed and when it is in the presence of confounding conditions that cannot be resolved.
The authors recommended digital subtraction angiography, radionuclide studies, and transcranial Doppler ultrasonography as ancillary tests based on blood flow in the brain. However, CT angiography and magnetic resonance angiography not be used.
A lack of guidance makes performing an apnea test in patients receiving extracorporeal membrane oxygenation (ECMO) challenging, according to the authors. Nevertheless, they recommended that the same principles of BD/DNC be applied to adults and children receiving ECMO.
They further recommended a period of preoxygenation before the apnea test, and the document describes in detail the method for administering this test to people receiving ECMO.
Another potentially challenging situation pointed out in the consensus document is the determination of BD/DNC in patients who have been treated with targeted temperature management. Therapeutic hypothermia, particularly if it is preceded or accompanied by sedation, can temporarily impair brain stem reflexes, thus mimicking BD/DNC.
The new document includes a flowchart and step-by-step recommendations as well as suggestions for determining BD/DNC under these circumstances.
Among document limitations acknowledged by the authors is the lack of high-quality data from randomized, controlled trials on which to base their recommendations.
In addition, economic, technological, or personnel limitations may reduce the available options for ancillary testing, they added. Also, the recommendations do not incorporate contributions from patients or social or religious groups, although the authors were mindful of their concerns.
To promote the national and international harmonization of BD/DNC criteria, “medical societies and countries can evaluate their own policies in relation to this document and fix any deficiencies,” Dr. Sung said.
“Many countries do not have any BD/DNC policies and can use the documents from this project to create their own. There may need to be discussions with legal, governmental, religious, and societal leaders to help understand and accept BD/DNC and to help enact policies in different communities,” he added.
Divergent definitions
The determination of death is not simply a scientific question, but also a philosophical, religious, and cultural question, wrote Robert D. Truog, MD, director of the Harvard Center for Bioethics, Boston, and colleagues in an accompanying editorial. Future research should consider cultural differences over these questions.
“Most important is that there be a clear and logical consistency between the definition of death and the tests that are used to diagnose it,” Dr. Truog said.
The concept of whole brain death was advanced as an equivalent to biological death, “such that, when the brain dies, the body literally disintegrates, just as it does after cardiac arrest,” but evidence indicates that this claim is untrue, Dr. Truog said. Current tests also do not diagnose the death of the whole brain.
Another hypothesis is that brain stem death represents the irreversible loss of consciousness and the capacity for spontaneous respiration.
“Instead of focusing on biology, [this definition] focuses on values and is based on the claim that when a person is in a state of irreversible apneic unconsciousness, we may consider them to be dead,” said Dr. Truog. He and his coeditorialists argued that the concept of whole brain death should be replaced with that of brain stem death.
“This report should be a call for our profession, as well as for federal and state lawmakers, to reform our laws so that they are consistent with our diagnostic criteria,” Dr. Truog said.
“The most straightforward way of doing this would be to change U.S. law and adopt the British standard of brain stem death, and then refine our testing to make the diagnosis of irreversible apneic unconsciousness as reliable and safe as possible,” he concluded.
The drafting of the consensus statement was not supported by outside funding. Dr. Sung reported no relevant financial relationships. Dr. Truog reported receiving compensation from Sanofi and Covance for participating in data and safety monitoring boards unrelated to the consensus document.
A version of this article originally appeared on Medscape.com.
The document, a result of the World Brain Death Project, surveys the clinical aspects of this determination, such as clinical testing, apnea testing, and the number of examinations required, as well as its social and legal aspects, including documentation, qualifications for making the determination, and religious attitudes toward BD/DNC.
The recommendations are the minimum criteria for BD/DNC, and countries and professional societies may choose to adopt stricter criteria, the authors noted. Seventeen supplements to the consensus statement contain detailed reports on topics the statement examines, including focuses on both adults and children.
“Perhaps the most important points of this project are, first, to show the worldwide acceptance of the concept of BD/DNC and what the minimum requirements are for BD/DNC,” said corresponding author Gene Sung, MD, MPH, director of the neurocritical care and stroke division at the University of Southern California, Los Angeles. Second, “this standard is centered around a clinical determination without the need for other testing.”
The consensus document and supplements were published online Aug. 3 in JAMA.
Comprehensive review
A lack of rigor has led to many differences in the determination of BD/DNC, said Dr. Sung. “Some of the variance that is common are the numbers of exams and examiners that are required and whether ancillary tests are required for determination of BD/DNC. In addition, a lot of guidelines and protocols that are in use are not thorough in detailing how to do the examinations and what to do in different circumstances.”
Professional societies such as the World Federation of Intensive and Critical Care recruited experts in BD/DNC to develop recommendations, which were based on relevant articles that they identified during a literature search. “We wanted to develop a fairly comprehensive document that, along with the 17 supplements, builds a foundation to show how to determine BD/DNC – what the minimum clinical criteria needed are and what to do in special circumstances,” Dr. Sung said.
Major sections of the statement include recommendations for the minimum clinical standards for the determination of BD/DNC in adults and children.
Determination must begin by establishing that the patient has sustained an irreversible brain injury that resulted in the loss of all brain function, according to the authors. Confounders such as pharmacologic paralysis and the effect of CNS depressant medications should be ruled out.
In addition, clinical evaluation must include an assessment for coma and an evaluation for brain stem areflexia. Among other criteria, the pupils should be fixed and nonresponsive to light, the face should not move in response to noxious cranial stimulation, and the gag and cough reflexes should be absent. Apnea testing is recommended to evaluate the responsiveness of respiratory centers in the medulla.
Although the definition of BD/DNC is the same in children as in adults, less evidence is available for the determination of BD/DNC in the very young. The authors thus advised a cautious approach to the evaluation of infants and younger children.
Recommendations vary by age and often require serial examinations, including apnea testing, they noted.
Ancillary testing
The consensus statement also reviews ancillary testing, which the authors recommend be required when the minimum clinical examination, including the apnea test, cannot be completed and when it is in the presence of confounding conditions that cannot be resolved.
The authors recommended digital subtraction angiography, radionuclide studies, and transcranial Doppler ultrasonography as ancillary tests based on blood flow in the brain. However, CT angiography and magnetic resonance angiography not be used.
A lack of guidance makes performing an apnea test in patients receiving extracorporeal membrane oxygenation (ECMO) challenging, according to the authors. Nevertheless, they recommended that the same principles of BD/DNC be applied to adults and children receiving ECMO.
They further recommended a period of preoxygenation before the apnea test, and the document describes in detail the method for administering this test to people receiving ECMO.
Another potentially challenging situation pointed out in the consensus document is the determination of BD/DNC in patients who have been treated with targeted temperature management. Therapeutic hypothermia, particularly if it is preceded or accompanied by sedation, can temporarily impair brain stem reflexes, thus mimicking BD/DNC.
The new document includes a flowchart and step-by-step recommendations as well as suggestions for determining BD/DNC under these circumstances.
Among document limitations acknowledged by the authors is the lack of high-quality data from randomized, controlled trials on which to base their recommendations.
In addition, economic, technological, or personnel limitations may reduce the available options for ancillary testing, they added. Also, the recommendations do not incorporate contributions from patients or social or religious groups, although the authors were mindful of their concerns.
To promote the national and international harmonization of BD/DNC criteria, “medical societies and countries can evaluate their own policies in relation to this document and fix any deficiencies,” Dr. Sung said.
“Many countries do not have any BD/DNC policies and can use the documents from this project to create their own. There may need to be discussions with legal, governmental, religious, and societal leaders to help understand and accept BD/DNC and to help enact policies in different communities,” he added.
Divergent definitions
The determination of death is not simply a scientific question, but also a philosophical, religious, and cultural question, wrote Robert D. Truog, MD, director of the Harvard Center for Bioethics, Boston, and colleagues in an accompanying editorial. Future research should consider cultural differences over these questions.
“Most important is that there be a clear and logical consistency between the definition of death and the tests that are used to diagnose it,” Dr. Truog said.
The concept of whole brain death was advanced as an equivalent to biological death, “such that, when the brain dies, the body literally disintegrates, just as it does after cardiac arrest,” but evidence indicates that this claim is untrue, Dr. Truog said. Current tests also do not diagnose the death of the whole brain.
Another hypothesis is that brain stem death represents the irreversible loss of consciousness and the capacity for spontaneous respiration.
“Instead of focusing on biology, [this definition] focuses on values and is based on the claim that when a person is in a state of irreversible apneic unconsciousness, we may consider them to be dead,” said Dr. Truog. He and his coeditorialists argued that the concept of whole brain death should be replaced with that of brain stem death.
“This report should be a call for our profession, as well as for federal and state lawmakers, to reform our laws so that they are consistent with our diagnostic criteria,” Dr. Truog said.
“The most straightforward way of doing this would be to change U.S. law and adopt the British standard of brain stem death, and then refine our testing to make the diagnosis of irreversible apneic unconsciousness as reliable and safe as possible,” he concluded.
The drafting of the consensus statement was not supported by outside funding. Dr. Sung reported no relevant financial relationships. Dr. Truog reported receiving compensation from Sanofi and Covance for participating in data and safety monitoring boards unrelated to the consensus document.
A version of this article originally appeared on Medscape.com.
The document, a result of the World Brain Death Project, surveys the clinical aspects of this determination, such as clinical testing, apnea testing, and the number of examinations required, as well as its social and legal aspects, including documentation, qualifications for making the determination, and religious attitudes toward BD/DNC.
The recommendations are the minimum criteria for BD/DNC, and countries and professional societies may choose to adopt stricter criteria, the authors noted. Seventeen supplements to the consensus statement contain detailed reports on topics the statement examines, including focuses on both adults and children.
“Perhaps the most important points of this project are, first, to show the worldwide acceptance of the concept of BD/DNC and what the minimum requirements are for BD/DNC,” said corresponding author Gene Sung, MD, MPH, director of the neurocritical care and stroke division at the University of Southern California, Los Angeles. Second, “this standard is centered around a clinical determination without the need for other testing.”
The consensus document and supplements were published online Aug. 3 in JAMA.
Comprehensive review
A lack of rigor has led to many differences in the determination of BD/DNC, said Dr. Sung. “Some of the variance that is common are the numbers of exams and examiners that are required and whether ancillary tests are required for determination of BD/DNC. In addition, a lot of guidelines and protocols that are in use are not thorough in detailing how to do the examinations and what to do in different circumstances.”
Professional societies such as the World Federation of Intensive and Critical Care recruited experts in BD/DNC to develop recommendations, which were based on relevant articles that they identified during a literature search. “We wanted to develop a fairly comprehensive document that, along with the 17 supplements, builds a foundation to show how to determine BD/DNC – what the minimum clinical criteria needed are and what to do in special circumstances,” Dr. Sung said.
Major sections of the statement include recommendations for the minimum clinical standards for the determination of BD/DNC in adults and children.
Determination must begin by establishing that the patient has sustained an irreversible brain injury that resulted in the loss of all brain function, according to the authors. Confounders such as pharmacologic paralysis and the effect of CNS depressant medications should be ruled out.
In addition, clinical evaluation must include an assessment for coma and an evaluation for brain stem areflexia. Among other criteria, the pupils should be fixed and nonresponsive to light, the face should not move in response to noxious cranial stimulation, and the gag and cough reflexes should be absent. Apnea testing is recommended to evaluate the responsiveness of respiratory centers in the medulla.
Although the definition of BD/DNC is the same in children as in adults, less evidence is available for the determination of BD/DNC in the very young. The authors thus advised a cautious approach to the evaluation of infants and younger children.
Recommendations vary by age and often require serial examinations, including apnea testing, they noted.
Ancillary testing
The consensus statement also reviews ancillary testing, which the authors recommend be required when the minimum clinical examination, including the apnea test, cannot be completed and when it is in the presence of confounding conditions that cannot be resolved.
The authors recommended digital subtraction angiography, radionuclide studies, and transcranial Doppler ultrasonography as ancillary tests based on blood flow in the brain. However, CT angiography and magnetic resonance angiography not be used.
A lack of guidance makes performing an apnea test in patients receiving extracorporeal membrane oxygenation (ECMO) challenging, according to the authors. Nevertheless, they recommended that the same principles of BD/DNC be applied to adults and children receiving ECMO.
They further recommended a period of preoxygenation before the apnea test, and the document describes in detail the method for administering this test to people receiving ECMO.
Another potentially challenging situation pointed out in the consensus document is the determination of BD/DNC in patients who have been treated with targeted temperature management. Therapeutic hypothermia, particularly if it is preceded or accompanied by sedation, can temporarily impair brain stem reflexes, thus mimicking BD/DNC.
The new document includes a flowchart and step-by-step recommendations as well as suggestions for determining BD/DNC under these circumstances.
Among document limitations acknowledged by the authors is the lack of high-quality data from randomized, controlled trials on which to base their recommendations.
In addition, economic, technological, or personnel limitations may reduce the available options for ancillary testing, they added. Also, the recommendations do not incorporate contributions from patients or social or religious groups, although the authors were mindful of their concerns.
To promote the national and international harmonization of BD/DNC criteria, “medical societies and countries can evaluate their own policies in relation to this document and fix any deficiencies,” Dr. Sung said.
“Many countries do not have any BD/DNC policies and can use the documents from this project to create their own. There may need to be discussions with legal, governmental, religious, and societal leaders to help understand and accept BD/DNC and to help enact policies in different communities,” he added.
Divergent definitions
The determination of death is not simply a scientific question, but also a philosophical, religious, and cultural question, wrote Robert D. Truog, MD, director of the Harvard Center for Bioethics, Boston, and colleagues in an accompanying editorial. Future research should consider cultural differences over these questions.
“Most important is that there be a clear and logical consistency between the definition of death and the tests that are used to diagnose it,” Dr. Truog said.
The concept of whole brain death was advanced as an equivalent to biological death, “such that, when the brain dies, the body literally disintegrates, just as it does after cardiac arrest,” but evidence indicates that this claim is untrue, Dr. Truog said. Current tests also do not diagnose the death of the whole brain.
Another hypothesis is that brain stem death represents the irreversible loss of consciousness and the capacity for spontaneous respiration.
“Instead of focusing on biology, [this definition] focuses on values and is based on the claim that when a person is in a state of irreversible apneic unconsciousness, we may consider them to be dead,” said Dr. Truog. He and his coeditorialists argued that the concept of whole brain death should be replaced with that of brain stem death.
“This report should be a call for our profession, as well as for federal and state lawmakers, to reform our laws so that they are consistent with our diagnostic criteria,” Dr. Truog said.
“The most straightforward way of doing this would be to change U.S. law and adopt the British standard of brain stem death, and then refine our testing to make the diagnosis of irreversible apneic unconsciousness as reliable and safe as possible,” he concluded.
The drafting of the consensus statement was not supported by outside funding. Dr. Sung reported no relevant financial relationships. Dr. Truog reported receiving compensation from Sanofi and Covance for participating in data and safety monitoring boards unrelated to the consensus document.
A version of this article originally appeared on Medscape.com.
Repetitive hits to the head tied to depression, poor cognition in later life
A history of repetitive hits to the head (RHI), even without noticeable symptoms, is linked to a significantly increased risk of depression and poorer cognition later in life, new research shows.
“We found that a history of exposure to [repetitive hits to the head] from contact sports, military service, or physical abuse, as well as a history of TBI (traumatic brain injury), corresponded to more symptoms of later life depression and worse cognitive function,” lead author Michael Alosco, PhD, associate professor of neurology and codirector of the Boston University Alzheimer’s Disease Center Clinical Core, told Medscape Medical News.
He added that the findings underscore the importance of assessing repetitive head impacts (RHI).
The study was published online June 26 in Neurology.
Largest study to date
It is well known that sustaining a TBI is associated with worse later life cognition or mood problems, said Alosco. However, in the current research the investigators hypothesized that RHI may be a key driver of some of these outcomes, Alosco said.
Previous studies have been small or have only examined male former football players.
“What’s unique about our study is that we focused on a history of RHIs, and it is the largest study of its kind, incorporating over 30,000 males and females with different types of exposure to these RHIs.”
The researchers used data from the Brain Health Registry, an internet-based registry that longitudinally monitors cognition and functioning of participants (age 40 years and older).
Participants completed the Ohio State University TBI Identification Method (OSU TBI-ID) and answered a yes/no question: “Have you ever had a period of time in which you experienced multiple, repeated impacts to your head (eg, history of abuse, contact sports, military duty)?”
Participants also completed the Geriatric Depression Scale (GDS-15), the CogState Battery (CBB), and the Lumos Labs NeuroCognitive Performance Tests (NCPT). Demographic information included age, sex, race/ethnicity, and level of education.
Negative synergistic effect
Of the total sample (N = 13,323, mean age 62 years, 72.5% female, 88.6% White) 725 participants (5%) reported exposure to RHI, with contact sports as the most common cause, followed by physical abuse and then military duty; about 55% (7277 participants) reported TBI.
The researchers noted that 44.4% of those exposed to RHI and 70.3% of those who reported TBI were female. However, those with a history of contact sports were predominantly male and those reporting a history of abuse were predominantly women.
Among study participants who completed the GDS-15, 16.4% reported symptoms of depression, similar to rates reported among community-dwelling older adults.
Compared to the unexposed group, participants who reported TBI with loss of consciousness (LOC) and participants who reported TBI without LOC both had higher scores on the GDS-15 (beta = 0.75 [95% CI, 0.59-0.91] and beta = 0.43 [95% CI, 0.31-0.54], respectively).
A history of RHI was associated with an even higher depression score (beta = 1.24 [95% CI, 0.36-2.12).
Depression increased in tandem with increased exposure, with the lowest GDS-15 scores found in the unexposed group and subsequent increases in scores as exposure to RHI was introduced and TBI severity increased. The GDS scores were highest in those who had RHI plus TBI with LOC.
Participants with a history of RHI and/or TBI also had worse scores on tests of memory, learning, processing speed, and reaction time, compared with unexposed participants.
In particular, TBI with LOC had the most neuropsychological associations.
TBI without LOC had a negative effect on CogState tests measuring Identification and processing speed (beta = 0.004 [95% CI, 0-0.01] and beta = 0.004 [95% CI, 0.0002-0.01], respectively), whereas RHI predicted a worse processing speed score (beta = .02 [95% CI, 0.01-0.05]).
The presence of both RHI and TBI (with or without LOC) had a “synergistic negative effect” on neuropsychological performance, with a “consistent statistically significant finding” for worse neuropsychological test performance for those who had RHI and TBI with LOC, compared with those who had not sustained RHI.
Alosco said the findings highlight the need for clinicians to educate and inform parents/guardians of kids playing (or considering playing) contact sports about the research and potential risks associated with these activities.
If we want to prevent long-term problems, one way is not to expose [people] to these hits. Everyone takes risks in life with everything, but the more we can understand and mitigate the risks, the better,” Alosco said.
“A significant contribution”
Commenting on the findings for Medscape Medical News, Temitayo Oyegbile-Chidi, MD, PhD, a pediatric neurologist with Health Peak Inc, McLean, Virginia, and a member of the American Academy of Neurology, said the study “makes a significant contribution to the literature, as neurologists who specialized in TBI have long yearned to understand the long-term effects of repeated head impact on the brain and cognition.”
Clinicians should “inquire about a history of prior head impacts on all our patients, regardless of age, especially if they are experiencing or showing signs of unexpected cognitive dysfunction or mental health concerns,” said Oyegbile-Chidi, who was not involved with the study.
For those who have sustained single or repeated head impacts with or without associated LOC in the past, “it is important … to keep in mind that depression and cognitive dysfunction may persist or present even many years after the impact was sustained,” she added.
The study was supported by a grant from the National Institutes of Health. Alosco has disclosed no relevant financial relationships. The other authors’ disclosures are listed on the original paper. Oyegbile-Chidi has disclosed no relevant financial relationships.
A history of repetitive hits to the head (RHI), even without noticeable symptoms, is linked to a significantly increased risk of depression and poorer cognition later in life, new research shows.
“We found that a history of exposure to [repetitive hits to the head] from contact sports, military service, or physical abuse, as well as a history of TBI (traumatic brain injury), corresponded to more symptoms of later life depression and worse cognitive function,” lead author Michael Alosco, PhD, associate professor of neurology and codirector of the Boston University Alzheimer’s Disease Center Clinical Core, told Medscape Medical News.
He added that the findings underscore the importance of assessing repetitive head impacts (RHI).
The study was published online June 26 in Neurology.
Largest study to date
It is well known that sustaining a TBI is associated with worse later life cognition or mood problems, said Alosco. However, in the current research the investigators hypothesized that RHI may be a key driver of some of these outcomes, Alosco said.
Previous studies have been small or have only examined male former football players.
“What’s unique about our study is that we focused on a history of RHIs, and it is the largest study of its kind, incorporating over 30,000 males and females with different types of exposure to these RHIs.”
The researchers used data from the Brain Health Registry, an internet-based registry that longitudinally monitors cognition and functioning of participants (age 40 years and older).
Participants completed the Ohio State University TBI Identification Method (OSU TBI-ID) and answered a yes/no question: “Have you ever had a period of time in which you experienced multiple, repeated impacts to your head (eg, history of abuse, contact sports, military duty)?”
Participants also completed the Geriatric Depression Scale (GDS-15), the CogState Battery (CBB), and the Lumos Labs NeuroCognitive Performance Tests (NCPT). Demographic information included age, sex, race/ethnicity, and level of education.
Negative synergistic effect
Of the total sample (N = 13,323, mean age 62 years, 72.5% female, 88.6% White) 725 participants (5%) reported exposure to RHI, with contact sports as the most common cause, followed by physical abuse and then military duty; about 55% (7277 participants) reported TBI.
The researchers noted that 44.4% of those exposed to RHI and 70.3% of those who reported TBI were female. However, those with a history of contact sports were predominantly male and those reporting a history of abuse were predominantly women.
Among study participants who completed the GDS-15, 16.4% reported symptoms of depression, similar to rates reported among community-dwelling older adults.
Compared to the unexposed group, participants who reported TBI with loss of consciousness (LOC) and participants who reported TBI without LOC both had higher scores on the GDS-15 (beta = 0.75 [95% CI, 0.59-0.91] and beta = 0.43 [95% CI, 0.31-0.54], respectively).
A history of RHI was associated with an even higher depression score (beta = 1.24 [95% CI, 0.36-2.12).
Depression increased in tandem with increased exposure, with the lowest GDS-15 scores found in the unexposed group and subsequent increases in scores as exposure to RHI was introduced and TBI severity increased. The GDS scores were highest in those who had RHI plus TBI with LOC.
Participants with a history of RHI and/or TBI also had worse scores on tests of memory, learning, processing speed, and reaction time, compared with unexposed participants.
In particular, TBI with LOC had the most neuropsychological associations.
TBI without LOC had a negative effect on CogState tests measuring Identification and processing speed (beta = 0.004 [95% CI, 0-0.01] and beta = 0.004 [95% CI, 0.0002-0.01], respectively), whereas RHI predicted a worse processing speed score (beta = .02 [95% CI, 0.01-0.05]).
The presence of both RHI and TBI (with or without LOC) had a “synergistic negative effect” on neuropsychological performance, with a “consistent statistically significant finding” for worse neuropsychological test performance for those who had RHI and TBI with LOC, compared with those who had not sustained RHI.
Alosco said the findings highlight the need for clinicians to educate and inform parents/guardians of kids playing (or considering playing) contact sports about the research and potential risks associated with these activities.
If we want to prevent long-term problems, one way is not to expose [people] to these hits. Everyone takes risks in life with everything, but the more we can understand and mitigate the risks, the better,” Alosco said.
“A significant contribution”
Commenting on the findings for Medscape Medical News, Temitayo Oyegbile-Chidi, MD, PhD, a pediatric neurologist with Health Peak Inc, McLean, Virginia, and a member of the American Academy of Neurology, said the study “makes a significant contribution to the literature, as neurologists who specialized in TBI have long yearned to understand the long-term effects of repeated head impact on the brain and cognition.”
Clinicians should “inquire about a history of prior head impacts on all our patients, regardless of age, especially if they are experiencing or showing signs of unexpected cognitive dysfunction or mental health concerns,” said Oyegbile-Chidi, who was not involved with the study.
For those who have sustained single or repeated head impacts with or without associated LOC in the past, “it is important … to keep in mind that depression and cognitive dysfunction may persist or present even many years after the impact was sustained,” she added.
The study was supported by a grant from the National Institutes of Health. Alosco has disclosed no relevant financial relationships. The other authors’ disclosures are listed on the original paper. Oyegbile-Chidi has disclosed no relevant financial relationships.
A history of repetitive hits to the head (RHI), even without noticeable symptoms, is linked to a significantly increased risk of depression and poorer cognition later in life, new research shows.
“We found that a history of exposure to [repetitive hits to the head] from contact sports, military service, or physical abuse, as well as a history of TBI (traumatic brain injury), corresponded to more symptoms of later life depression and worse cognitive function,” lead author Michael Alosco, PhD, associate professor of neurology and codirector of the Boston University Alzheimer’s Disease Center Clinical Core, told Medscape Medical News.
He added that the findings underscore the importance of assessing repetitive head impacts (RHI).
The study was published online June 26 in Neurology.
Largest study to date
It is well known that sustaining a TBI is associated with worse later life cognition or mood problems, said Alosco. However, in the current research the investigators hypothesized that RHI may be a key driver of some of these outcomes, Alosco said.
Previous studies have been small or have only examined male former football players.
“What’s unique about our study is that we focused on a history of RHIs, and it is the largest study of its kind, incorporating over 30,000 males and females with different types of exposure to these RHIs.”
The researchers used data from the Brain Health Registry, an internet-based registry that longitudinally monitors cognition and functioning of participants (age 40 years and older).
Participants completed the Ohio State University TBI Identification Method (OSU TBI-ID) and answered a yes/no question: “Have you ever had a period of time in which you experienced multiple, repeated impacts to your head (eg, history of abuse, contact sports, military duty)?”
Participants also completed the Geriatric Depression Scale (GDS-15), the CogState Battery (CBB), and the Lumos Labs NeuroCognitive Performance Tests (NCPT). Demographic information included age, sex, race/ethnicity, and level of education.
Negative synergistic effect
Of the total sample (N = 13,323, mean age 62 years, 72.5% female, 88.6% White) 725 participants (5%) reported exposure to RHI, with contact sports as the most common cause, followed by physical abuse and then military duty; about 55% (7277 participants) reported TBI.
The researchers noted that 44.4% of those exposed to RHI and 70.3% of those who reported TBI were female. However, those with a history of contact sports were predominantly male and those reporting a history of abuse were predominantly women.
Among study participants who completed the GDS-15, 16.4% reported symptoms of depression, similar to rates reported among community-dwelling older adults.
Compared to the unexposed group, participants who reported TBI with loss of consciousness (LOC) and participants who reported TBI without LOC both had higher scores on the GDS-15 (beta = 0.75 [95% CI, 0.59-0.91] and beta = 0.43 [95% CI, 0.31-0.54], respectively).
A history of RHI was associated with an even higher depression score (beta = 1.24 [95% CI, 0.36-2.12).
Depression increased in tandem with increased exposure, with the lowest GDS-15 scores found in the unexposed group and subsequent increases in scores as exposure to RHI was introduced and TBI severity increased. The GDS scores were highest in those who had RHI plus TBI with LOC.
Participants with a history of RHI and/or TBI also had worse scores on tests of memory, learning, processing speed, and reaction time, compared with unexposed participants.
In particular, TBI with LOC had the most neuropsychological associations.
TBI without LOC had a negative effect on CogState tests measuring Identification and processing speed (beta = 0.004 [95% CI, 0-0.01] and beta = 0.004 [95% CI, 0.0002-0.01], respectively), whereas RHI predicted a worse processing speed score (beta = .02 [95% CI, 0.01-0.05]).
The presence of both RHI and TBI (with or without LOC) had a “synergistic negative effect” on neuropsychological performance, with a “consistent statistically significant finding” for worse neuropsychological test performance for those who had RHI and TBI with LOC, compared with those who had not sustained RHI.
Alosco said the findings highlight the need for clinicians to educate and inform parents/guardians of kids playing (or considering playing) contact sports about the research and potential risks associated with these activities.
If we want to prevent long-term problems, one way is not to expose [people] to these hits. Everyone takes risks in life with everything, but the more we can understand and mitigate the risks, the better,” Alosco said.
“A significant contribution”
Commenting on the findings for Medscape Medical News, Temitayo Oyegbile-Chidi, MD, PhD, a pediatric neurologist with Health Peak Inc, McLean, Virginia, and a member of the American Academy of Neurology, said the study “makes a significant contribution to the literature, as neurologists who specialized in TBI have long yearned to understand the long-term effects of repeated head impact on the brain and cognition.”
Clinicians should “inquire about a history of prior head impacts on all our patients, regardless of age, especially if they are experiencing or showing signs of unexpected cognitive dysfunction or mental health concerns,” said Oyegbile-Chidi, who was not involved with the study.
For those who have sustained single or repeated head impacts with or without associated LOC in the past, “it is important … to keep in mind that depression and cognitive dysfunction may persist or present even many years after the impact was sustained,” she added.
The study was supported by a grant from the National Institutes of Health. Alosco has disclosed no relevant financial relationships. The other authors’ disclosures are listed on the original paper. Oyegbile-Chidi has disclosed no relevant financial relationships.
Blood biomarker detects concussion, shows severity, predicts recovery
(TBI), new research indicates.
“Blood NfL may be used to aid in the diagnosis of patients with concussion or mild TBI [and] to identify individuals at increased risk of developing persistent postconcussive symptoms following TBI,” said lead author Pashtun Shahim, MD, PhD, National Institutes of Health Clinical Center, Bethesda, Md.
“This study is the first to do a detailed assessment of serum NfL chain and advanced brain imaging in multiple cohorts, brain injury severities, and time points after injury. The cohorts included professional athletes and nonathletes, and over time up to 5 years after TBI,” Dr. Shahim added.
The study was published online July 8 in Neurology.
Rapid indicator of neuronal damage
The researchers studied two cohorts of patients with head injuries. In the first, they determined serum and CSF NfL chain levels in professional Swedish ice hockey players (median age, 27 years), including 45 with acute concussion, 31 with repetitive concussions and persistent post-concussive symptoms (PCS), 28 who contributed samples during preseason with no recent concussion, and 14 healthy nonathletes.
CSF and serum NfL concentrations were closely correlated (r = 0.71; P < .0001). Serum NfL distinguished players with persistent PCS due to repetitive concussions from preseason concussion-free players, with an area under the receiver operating characteristic curve of 0.97. Higher CSF and serum NfL levels were associated with a higher number of concussions and severity of PCS after 1 year.
The second cohort involved 230 clinic-based adults (mean age, 43 years), including 162 with TBI and 68 healthy controls. In this cohort, patients with TBI had increased serum NfL concentrations compared with controls for up to 5 years, and these concentrations were able to distinguish between mild, moderate, and severe TBI. Serum NfL also correlated with measures of functional outcome, MRI brain atrophy, and diffusion tensor imaging estimates of traumatic axonal injury.
“Our findings suggest that NfL concentrations in serum offer rapid and accessible means of assessing and predicting neuronal damage in patients with TBI,” the investigators wrote.
What’s needed going forward, said Dr. Shahim, is “validation in larger cohorts for determining what levels of NfL in blood may be associated with a specific type of TBI, and what the levels are in healthy individuals of different ages.”
Not ready for prime time
In an accompanying editorial, Christopher Filley, MD, University of Colorado at Denver, Aurora, noted that NfL “may prove useful in identifying TBI patients at risk for prolonged symptoms and in enabling more focused treatment for these individuals.”
“These reports are richly laden with acute and longitudinal data that not only support the use of NfL as a convenient diagnostic test for TBI, but plausibly correlate with the neuropathology of TBI that is thought to play a major role in immediate and lasting cognitive disability,” he wrote.
Although the origin of TBI-induced cognitive decline is not entirely explained by traumatic axonal injury, “NfL appears to have much promise as a blood test that relates directly to the ubiquitous white matter damage of TBI, revealing a great deal about not only whether a TBI occurred, but also the extent of injury sustained, and how this injury may affect patient outcome for years thereafter,” Dr. Filley wrote.
However, he cautioned more research is needed before the blood test can be routinely applied to TBI diagnosis in clinical practice. “Among the hurdles still ahead are the standardization of measurement techniques across analytical platforms, and the determination of precise cutoffs between normal and abnormal values in different ages groups and at varying levels of TBI severity,” Dr. Filley noted.
The research was supported by the National Institutes of Health, the Department of Defense, the Center for Neuroscience and Regenerative Medicine at the Uniformed Services University, and the Swedish Research Council. Dr. Shahim and Dr. Filley have reported no relevant financial relationships.
This article first appeared on Medscape.com.
(TBI), new research indicates.
“Blood NfL may be used to aid in the diagnosis of patients with concussion or mild TBI [and] to identify individuals at increased risk of developing persistent postconcussive symptoms following TBI,” said lead author Pashtun Shahim, MD, PhD, National Institutes of Health Clinical Center, Bethesda, Md.
“This study is the first to do a detailed assessment of serum NfL chain and advanced brain imaging in multiple cohorts, brain injury severities, and time points after injury. The cohorts included professional athletes and nonathletes, and over time up to 5 years after TBI,” Dr. Shahim added.
The study was published online July 8 in Neurology.
Rapid indicator of neuronal damage
The researchers studied two cohorts of patients with head injuries. In the first, they determined serum and CSF NfL chain levels in professional Swedish ice hockey players (median age, 27 years), including 45 with acute concussion, 31 with repetitive concussions and persistent post-concussive symptoms (PCS), 28 who contributed samples during preseason with no recent concussion, and 14 healthy nonathletes.
CSF and serum NfL concentrations were closely correlated (r = 0.71; P < .0001). Serum NfL distinguished players with persistent PCS due to repetitive concussions from preseason concussion-free players, with an area under the receiver operating characteristic curve of 0.97. Higher CSF and serum NfL levels were associated with a higher number of concussions and severity of PCS after 1 year.
The second cohort involved 230 clinic-based adults (mean age, 43 years), including 162 with TBI and 68 healthy controls. In this cohort, patients with TBI had increased serum NfL concentrations compared with controls for up to 5 years, and these concentrations were able to distinguish between mild, moderate, and severe TBI. Serum NfL also correlated with measures of functional outcome, MRI brain atrophy, and diffusion tensor imaging estimates of traumatic axonal injury.
“Our findings suggest that NfL concentrations in serum offer rapid and accessible means of assessing and predicting neuronal damage in patients with TBI,” the investigators wrote.
What’s needed going forward, said Dr. Shahim, is “validation in larger cohorts for determining what levels of NfL in blood may be associated with a specific type of TBI, and what the levels are in healthy individuals of different ages.”
Not ready for prime time
In an accompanying editorial, Christopher Filley, MD, University of Colorado at Denver, Aurora, noted that NfL “may prove useful in identifying TBI patients at risk for prolonged symptoms and in enabling more focused treatment for these individuals.”
“These reports are richly laden with acute and longitudinal data that not only support the use of NfL as a convenient diagnostic test for TBI, but plausibly correlate with the neuropathology of TBI that is thought to play a major role in immediate and lasting cognitive disability,” he wrote.
Although the origin of TBI-induced cognitive decline is not entirely explained by traumatic axonal injury, “NfL appears to have much promise as a blood test that relates directly to the ubiquitous white matter damage of TBI, revealing a great deal about not only whether a TBI occurred, but also the extent of injury sustained, and how this injury may affect patient outcome for years thereafter,” Dr. Filley wrote.
However, he cautioned more research is needed before the blood test can be routinely applied to TBI diagnosis in clinical practice. “Among the hurdles still ahead are the standardization of measurement techniques across analytical platforms, and the determination of precise cutoffs between normal and abnormal values in different ages groups and at varying levels of TBI severity,” Dr. Filley noted.
The research was supported by the National Institutes of Health, the Department of Defense, the Center for Neuroscience and Regenerative Medicine at the Uniformed Services University, and the Swedish Research Council. Dr. Shahim and Dr. Filley have reported no relevant financial relationships.
This article first appeared on Medscape.com.
(TBI), new research indicates.
“Blood NfL may be used to aid in the diagnosis of patients with concussion or mild TBI [and] to identify individuals at increased risk of developing persistent postconcussive symptoms following TBI,” said lead author Pashtun Shahim, MD, PhD, National Institutes of Health Clinical Center, Bethesda, Md.
“This study is the first to do a detailed assessment of serum NfL chain and advanced brain imaging in multiple cohorts, brain injury severities, and time points after injury. The cohorts included professional athletes and nonathletes, and over time up to 5 years after TBI,” Dr. Shahim added.
The study was published online July 8 in Neurology.
Rapid indicator of neuronal damage
The researchers studied two cohorts of patients with head injuries. In the first, they determined serum and CSF NfL chain levels in professional Swedish ice hockey players (median age, 27 years), including 45 with acute concussion, 31 with repetitive concussions and persistent post-concussive symptoms (PCS), 28 who contributed samples during preseason with no recent concussion, and 14 healthy nonathletes.
CSF and serum NfL concentrations were closely correlated (r = 0.71; P < .0001). Serum NfL distinguished players with persistent PCS due to repetitive concussions from preseason concussion-free players, with an area under the receiver operating characteristic curve of 0.97. Higher CSF and serum NfL levels were associated with a higher number of concussions and severity of PCS after 1 year.
The second cohort involved 230 clinic-based adults (mean age, 43 years), including 162 with TBI and 68 healthy controls. In this cohort, patients with TBI had increased serum NfL concentrations compared with controls for up to 5 years, and these concentrations were able to distinguish between mild, moderate, and severe TBI. Serum NfL also correlated with measures of functional outcome, MRI brain atrophy, and diffusion tensor imaging estimates of traumatic axonal injury.
“Our findings suggest that NfL concentrations in serum offer rapid and accessible means of assessing and predicting neuronal damage in patients with TBI,” the investigators wrote.
What’s needed going forward, said Dr. Shahim, is “validation in larger cohorts for determining what levels of NfL in blood may be associated with a specific type of TBI, and what the levels are in healthy individuals of different ages.”
Not ready for prime time
In an accompanying editorial, Christopher Filley, MD, University of Colorado at Denver, Aurora, noted that NfL “may prove useful in identifying TBI patients at risk for prolonged symptoms and in enabling more focused treatment for these individuals.”
“These reports are richly laden with acute and longitudinal data that not only support the use of NfL as a convenient diagnostic test for TBI, but plausibly correlate with the neuropathology of TBI that is thought to play a major role in immediate and lasting cognitive disability,” he wrote.
Although the origin of TBI-induced cognitive decline is not entirely explained by traumatic axonal injury, “NfL appears to have much promise as a blood test that relates directly to the ubiquitous white matter damage of TBI, revealing a great deal about not only whether a TBI occurred, but also the extent of injury sustained, and how this injury may affect patient outcome for years thereafter,” Dr. Filley wrote.
However, he cautioned more research is needed before the blood test can be routinely applied to TBI diagnosis in clinical practice. “Among the hurdles still ahead are the standardization of measurement techniques across analytical platforms, and the determination of precise cutoffs between normal and abnormal values in different ages groups and at varying levels of TBI severity,” Dr. Filley noted.
The research was supported by the National Institutes of Health, the Department of Defense, the Center for Neuroscience and Regenerative Medicine at the Uniformed Services University, and the Swedish Research Council. Dr. Shahim and Dr. Filley have reported no relevant financial relationships.
This article first appeared on Medscape.com.
Epilepsy after TBI linked to worse 12-month outcomes
findings from an analysis of a large, prospective database suggest. “We found that patients essentially have a 10-times greater risk of developing posttraumatic epilepsy and seizures at 12 months [post injury] if the presenting Glasgow Coma Scale GCS) is less than 8,” said lead author John F. Burke, MD, PhD, University of California, San Francisco, in presenting the findings as part of the virtual annual meeting of the American Association of Neurological Surgeons.
Assessing risk factors
While posttraumatic epilepsy represents an estimated 20% of all cases of symptomatic epilepsy, many questions remain on those most at risk and on the long-term effects of posttraumatic epilepsy on TBI outcomes. To probe those issues, Dr. Burke and colleagues turned to the multicenter TRACK-TBI database, which has prospective, longitudinal data on more than 2,700 patients with traumatic brain injuries and is considered the largest source of prospective data on posttraumatic epilepsy.
Using the criteria of no previous epilepsy and having 12 months of follow-up, the team identified 1,493 patients with TBI. In addition, investigators identified 182 orthopedic controls (included and prospectively followed because they have injuries but not specifically head trauma) and 210 controls who are friends of the patients and who do not have injuries but allow researchers to control for socioeconomic and environmental factors.
Of the 1,493 patients with TBI, 41 (2.7%) were determined to have posttraumatic epilepsy, assessed according to a National Institute of Neurological Disorders and Stroke epilepsy screening questionnaire, which is designed to identify patients with posttraumatic epilepsy symptoms. There were no reports of epilepsy symptoms using the screening tool among the controls. Dr. Burke noted that the 2.7% was in agreement with historical reports.
In comparing patients with TBI who did and did not have posttraumatic epilepsy, no differences were observed in the groups in terms of gender, although there was a trend toward younger age among those with PTE (mean age, 35.4 years with posttraumatic injury vs. 41.5 without; P = .05).
A major risk factor for the development of posttraumatic epilepsy was presenting GCS scores. Among those with scores of less than 8, indicative of severe injury, the rate of posttraumatic epilepsy was 6% at 6 months and 12.5% at 12 months. In contrast, those with TBI presenting with GCS scores between 13 and 15, indicative of minor injury, had an incidence of posttraumatic epilepsy of 0.9% at 6 months and 1.4% at 12 months.
Imaging findings in the two groups showed that hemorrhage detected on CT imaging was associated with a significantly higher risk for posttraumatic epilepsy (P < .001).
“The main takeaway is that any hemorrhage in the brain is a major risk factor for developing seizures,” Dr. Burke said. “Whether it is subdural, epidural blood, subarachnoid or contusion, any blood confers a very [high] risk for developing seizures.”
Posttraumatic epilepsy was linked to poorer longer-term outcomes even for patients with lesser injury: Among those with TBI and GCS of 13-15, the mean Glasgow Outcome Scale Extended (GOSE) score at 12 months among those without posttraumatic epilepsy was 7, indicative of a good recovery with minor defects, whereas the mean GOSE score for those with PTE was 4.6, indicative of moderate to severe disability (P < .001).
“It was surprising to us that PTE-positive patients had a very significant decrease in GOSE, compared to PTE-negative patients,” Dr. Burke said. “There was a nearly 2-point drop in the GOSE and that was extremely significant.”
A multivariate analysis showed there was still a significant independent risk for a poor GOSE score with posttraumatic epilepsy after controlling for GCS score, head CT findings, and age (P < .001).
The authors also looked at mood outcomes using the Brief Symptom Inventory–18, which showed significant worse effect in those with posttraumatic epilepsy after multivariate adjustment (P = .01). Additionally, a highly significant worse effect in cognitive outcomes on the Rivermead cognitive metric was observed with posttraumatic epilepsy (P = .001).
“On all metrics tested, posttraumatic epilepsy worsened outcomes,” Dr. Burke said.
He noted that the study has some key limitations, including the 12-month follow-up. A previous study showed a linear increase in posttraumatic follow-up up to 30 years. “The fact that we found 41 patients at 12 months indicates there are probably more that are out there who are going to develop seizures, but because we don’t have the follow-up we can’t look at that.”
Although the screening questionnaires are effective, “the issue is these people are not being seen by an epileptologist or having scalp EEG done, and we need a more accurate way to do this,” he said. A new study, TRACK-TBI EPI, will address those limitations and a host of other issues with a 5-year follow-up.
Capturing the nuances of brain injury
Commenting on the study as a discussant, neurosurgeon Uzma Samadani, MD, PhD, of the Minneapolis Veterans Affairs Medical Center and CentraCare in Minneapolis, suggested that the future work should focus on issues including the wide-ranging mechanisms that could explain the seizure activity.
“For example, it’s known that posttraumatic epilepsy or seizures can be triggered by abnormal conductivity due to multiple different mechanisms associated with brain injury, such as endocrine dysfunction, cortical-spreading depression, and many others,” said Dr. Samadani, who has been a researcher on the TRACK-TBI study.
Factors ranging from genetic differences to comorbid conditions such as alcoholism can play a role in brain injury susceptibility, Dr. Samadani added. Furthermore, outcome measures currently available simply may not capture the unknown nuances of brain injury.
“We have to ask, are these an all-or-none phenomena, or is aberrant electrical activity after brain injury a continuum of dysfunction?” Dr. Samadani speculated.
“I would caution that we are likely underestimating the non–easily measurable consequences of brain injury,” she said. “And the better we can quantitate susceptibility, classify the nature of injury and target acute management, the less posttraumatic epilepsy/aberrant electrical activity our patients will have.”
Dr. Burke and Dr. Samadani disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
findings from an analysis of a large, prospective database suggest. “We found that patients essentially have a 10-times greater risk of developing posttraumatic epilepsy and seizures at 12 months [post injury] if the presenting Glasgow Coma Scale GCS) is less than 8,” said lead author John F. Burke, MD, PhD, University of California, San Francisco, in presenting the findings as part of the virtual annual meeting of the American Association of Neurological Surgeons.
Assessing risk factors
While posttraumatic epilepsy represents an estimated 20% of all cases of symptomatic epilepsy, many questions remain on those most at risk and on the long-term effects of posttraumatic epilepsy on TBI outcomes. To probe those issues, Dr. Burke and colleagues turned to the multicenter TRACK-TBI database, which has prospective, longitudinal data on more than 2,700 patients with traumatic brain injuries and is considered the largest source of prospective data on posttraumatic epilepsy.
Using the criteria of no previous epilepsy and having 12 months of follow-up, the team identified 1,493 patients with TBI. In addition, investigators identified 182 orthopedic controls (included and prospectively followed because they have injuries but not specifically head trauma) and 210 controls who are friends of the patients and who do not have injuries but allow researchers to control for socioeconomic and environmental factors.
Of the 1,493 patients with TBI, 41 (2.7%) were determined to have posttraumatic epilepsy, assessed according to a National Institute of Neurological Disorders and Stroke epilepsy screening questionnaire, which is designed to identify patients with posttraumatic epilepsy symptoms. There were no reports of epilepsy symptoms using the screening tool among the controls. Dr. Burke noted that the 2.7% was in agreement with historical reports.
In comparing patients with TBI who did and did not have posttraumatic epilepsy, no differences were observed in the groups in terms of gender, although there was a trend toward younger age among those with PTE (mean age, 35.4 years with posttraumatic injury vs. 41.5 without; P = .05).
A major risk factor for the development of posttraumatic epilepsy was presenting GCS scores. Among those with scores of less than 8, indicative of severe injury, the rate of posttraumatic epilepsy was 6% at 6 months and 12.5% at 12 months. In contrast, those with TBI presenting with GCS scores between 13 and 15, indicative of minor injury, had an incidence of posttraumatic epilepsy of 0.9% at 6 months and 1.4% at 12 months.
Imaging findings in the two groups showed that hemorrhage detected on CT imaging was associated with a significantly higher risk for posttraumatic epilepsy (P < .001).
“The main takeaway is that any hemorrhage in the brain is a major risk factor for developing seizures,” Dr. Burke said. “Whether it is subdural, epidural blood, subarachnoid or contusion, any blood confers a very [high] risk for developing seizures.”
Posttraumatic epilepsy was linked to poorer longer-term outcomes even for patients with lesser injury: Among those with TBI and GCS of 13-15, the mean Glasgow Outcome Scale Extended (GOSE) score at 12 months among those without posttraumatic epilepsy was 7, indicative of a good recovery with minor defects, whereas the mean GOSE score for those with PTE was 4.6, indicative of moderate to severe disability (P < .001).
“It was surprising to us that PTE-positive patients had a very significant decrease in GOSE, compared to PTE-negative patients,” Dr. Burke said. “There was a nearly 2-point drop in the GOSE and that was extremely significant.”
A multivariate analysis showed there was still a significant independent risk for a poor GOSE score with posttraumatic epilepsy after controlling for GCS score, head CT findings, and age (P < .001).
The authors also looked at mood outcomes using the Brief Symptom Inventory–18, which showed significant worse effect in those with posttraumatic epilepsy after multivariate adjustment (P = .01). Additionally, a highly significant worse effect in cognitive outcomes on the Rivermead cognitive metric was observed with posttraumatic epilepsy (P = .001).
“On all metrics tested, posttraumatic epilepsy worsened outcomes,” Dr. Burke said.
He noted that the study has some key limitations, including the 12-month follow-up. A previous study showed a linear increase in posttraumatic follow-up up to 30 years. “The fact that we found 41 patients at 12 months indicates there are probably more that are out there who are going to develop seizures, but because we don’t have the follow-up we can’t look at that.”
Although the screening questionnaires are effective, “the issue is these people are not being seen by an epileptologist or having scalp EEG done, and we need a more accurate way to do this,” he said. A new study, TRACK-TBI EPI, will address those limitations and a host of other issues with a 5-year follow-up.
Capturing the nuances of brain injury
Commenting on the study as a discussant, neurosurgeon Uzma Samadani, MD, PhD, of the Minneapolis Veterans Affairs Medical Center and CentraCare in Minneapolis, suggested that the future work should focus on issues including the wide-ranging mechanisms that could explain the seizure activity.
“For example, it’s known that posttraumatic epilepsy or seizures can be triggered by abnormal conductivity due to multiple different mechanisms associated with brain injury, such as endocrine dysfunction, cortical-spreading depression, and many others,” said Dr. Samadani, who has been a researcher on the TRACK-TBI study.
Factors ranging from genetic differences to comorbid conditions such as alcoholism can play a role in brain injury susceptibility, Dr. Samadani added. Furthermore, outcome measures currently available simply may not capture the unknown nuances of brain injury.
“We have to ask, are these an all-or-none phenomena, or is aberrant electrical activity after brain injury a continuum of dysfunction?” Dr. Samadani speculated.
“I would caution that we are likely underestimating the non–easily measurable consequences of brain injury,” she said. “And the better we can quantitate susceptibility, classify the nature of injury and target acute management, the less posttraumatic epilepsy/aberrant electrical activity our patients will have.”
Dr. Burke and Dr. Samadani disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
findings from an analysis of a large, prospective database suggest. “We found that patients essentially have a 10-times greater risk of developing posttraumatic epilepsy and seizures at 12 months [post injury] if the presenting Glasgow Coma Scale GCS) is less than 8,” said lead author John F. Burke, MD, PhD, University of California, San Francisco, in presenting the findings as part of the virtual annual meeting of the American Association of Neurological Surgeons.
Assessing risk factors
While posttraumatic epilepsy represents an estimated 20% of all cases of symptomatic epilepsy, many questions remain on those most at risk and on the long-term effects of posttraumatic epilepsy on TBI outcomes. To probe those issues, Dr. Burke and colleagues turned to the multicenter TRACK-TBI database, which has prospective, longitudinal data on more than 2,700 patients with traumatic brain injuries and is considered the largest source of prospective data on posttraumatic epilepsy.
Using the criteria of no previous epilepsy and having 12 months of follow-up, the team identified 1,493 patients with TBI. In addition, investigators identified 182 orthopedic controls (included and prospectively followed because they have injuries but not specifically head trauma) and 210 controls who are friends of the patients and who do not have injuries but allow researchers to control for socioeconomic and environmental factors.
Of the 1,493 patients with TBI, 41 (2.7%) were determined to have posttraumatic epilepsy, assessed according to a National Institute of Neurological Disorders and Stroke epilepsy screening questionnaire, which is designed to identify patients with posttraumatic epilepsy symptoms. There were no reports of epilepsy symptoms using the screening tool among the controls. Dr. Burke noted that the 2.7% was in agreement with historical reports.
In comparing patients with TBI who did and did not have posttraumatic epilepsy, no differences were observed in the groups in terms of gender, although there was a trend toward younger age among those with PTE (mean age, 35.4 years with posttraumatic injury vs. 41.5 without; P = .05).
A major risk factor for the development of posttraumatic epilepsy was presenting GCS scores. Among those with scores of less than 8, indicative of severe injury, the rate of posttraumatic epilepsy was 6% at 6 months and 12.5% at 12 months. In contrast, those with TBI presenting with GCS scores between 13 and 15, indicative of minor injury, had an incidence of posttraumatic epilepsy of 0.9% at 6 months and 1.4% at 12 months.
Imaging findings in the two groups showed that hemorrhage detected on CT imaging was associated with a significantly higher risk for posttraumatic epilepsy (P < .001).
“The main takeaway is that any hemorrhage in the brain is a major risk factor for developing seizures,” Dr. Burke said. “Whether it is subdural, epidural blood, subarachnoid or contusion, any blood confers a very [high] risk for developing seizures.”
Posttraumatic epilepsy was linked to poorer longer-term outcomes even for patients with lesser injury: Among those with TBI and GCS of 13-15, the mean Glasgow Outcome Scale Extended (GOSE) score at 12 months among those without posttraumatic epilepsy was 7, indicative of a good recovery with minor defects, whereas the mean GOSE score for those with PTE was 4.6, indicative of moderate to severe disability (P < .001).
“It was surprising to us that PTE-positive patients had a very significant decrease in GOSE, compared to PTE-negative patients,” Dr. Burke said. “There was a nearly 2-point drop in the GOSE and that was extremely significant.”
A multivariate analysis showed there was still a significant independent risk for a poor GOSE score with posttraumatic epilepsy after controlling for GCS score, head CT findings, and age (P < .001).
The authors also looked at mood outcomes using the Brief Symptom Inventory–18, which showed significant worse effect in those with posttraumatic epilepsy after multivariate adjustment (P = .01). Additionally, a highly significant worse effect in cognitive outcomes on the Rivermead cognitive metric was observed with posttraumatic epilepsy (P = .001).
“On all metrics tested, posttraumatic epilepsy worsened outcomes,” Dr. Burke said.
He noted that the study has some key limitations, including the 12-month follow-up. A previous study showed a linear increase in posttraumatic follow-up up to 30 years. “The fact that we found 41 patients at 12 months indicates there are probably more that are out there who are going to develop seizures, but because we don’t have the follow-up we can’t look at that.”
Although the screening questionnaires are effective, “the issue is these people are not being seen by an epileptologist or having scalp EEG done, and we need a more accurate way to do this,” he said. A new study, TRACK-TBI EPI, will address those limitations and a host of other issues with a 5-year follow-up.
Capturing the nuances of brain injury
Commenting on the study as a discussant, neurosurgeon Uzma Samadani, MD, PhD, of the Minneapolis Veterans Affairs Medical Center and CentraCare in Minneapolis, suggested that the future work should focus on issues including the wide-ranging mechanisms that could explain the seizure activity.
“For example, it’s known that posttraumatic epilepsy or seizures can be triggered by abnormal conductivity due to multiple different mechanisms associated with brain injury, such as endocrine dysfunction, cortical-spreading depression, and many others,” said Dr. Samadani, who has been a researcher on the TRACK-TBI study.
Factors ranging from genetic differences to comorbid conditions such as alcoholism can play a role in brain injury susceptibility, Dr. Samadani added. Furthermore, outcome measures currently available simply may not capture the unknown nuances of brain injury.
“We have to ask, are these an all-or-none phenomena, or is aberrant electrical activity after brain injury a continuum of dysfunction?” Dr. Samadani speculated.
“I would caution that we are likely underestimating the non–easily measurable consequences of brain injury,” she said. “And the better we can quantitate susceptibility, classify the nature of injury and target acute management, the less posttraumatic epilepsy/aberrant electrical activity our patients will have.”
Dr. Burke and Dr. Samadani disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
FROM AANS 2020
Persistent posttraumatic headache risk factors confirmed
It also revealed a surprisingly high frequency of misdiagnosis. The original sample included 500 patients drawn from the Stanford Research Repository Cohort Discovery Tool, but a review found 200 records that were misdiagnosed and had to be excluded.
“It’s very easy to label someone who suffered a head injury and say this is the reason why they have this (headache),” said lead author Tommy Chan, MBBS, a headache fellow in the department of neurology at Stanford (Calif.) University, in an interview. Such patients are often seen by ED or primary care physicians who do not have a lot of experience with posttraumatic headache, and that can lead to negative consequences if a low-pressure headache is mistaken as stemming from a skull fracture. “It’s a very different treatment plan for one versus the other,” said Dr. Chan in an interview.
He noted that it can help to take a patient history that includes the preaccident headache frequency and determine if there was a change in frequency post injury.
Dr. Chan presented the results at the virtual annual meeting of the American Headache Society.
“The results are what one might expect, although we haven’t studied it enough to really know. We haven’t systematically characterized these risk factors for chronic posttraumatic headache very well, [so] it’s useful to have this information,” said Andrew Charles, MD, professor neurology at the University of California, Los Angeles, and director of the UCLA Goldberg Migraine Program, who was not involved in the study. However, Dr. Charles emphasized the need to confirm the results prospectively.
Defining risk factors
The analysis found that a history of migraines, medication overuse, psychological disorders, and new posttraumatic headache–associated comorbidities were all associated with a greater risk for persistent posttraumatic headache. None of those came as a surprise, “but we live in a world where medicine is practiced based on evidence, and providers want to see data to support that. I think that this will help with resource allocation. It’s important to address [a patient’s] overuse of medications, or if they’re having psychological symptoms,” said Dr. Chan.
A total of 150 patients in the analysis had acute posttraumatic headache (mean duration, 0.7 months) while 150 had persistent posttraumatic headache (mean duration, 24 months; P < .00001). Clinical factors associated with risk of persistent headache included a history migraine (relative risk, 2.4; P < .0001), a previous head injury (odds ratio, 5.8; P < .0001), medication overuse (RR, 2.6; P < .0001), preexisting psychological history (OR, 5; P < .0001), and new posttraumatic headache–associated comorbidities, such as vertigo or posttraumatic stress disorder (RR, 9.8; P < .0001).
Identifying patient subgroups
The researchers also identified four subcategories of patients with persistent posttraumatic headache, each with differing risk factors and clinical characteristics. It’s too soon to use these identifiers to make clinical recommendations, but Dr. Chan hopes that further study of these groups will be informative. “It might point us toward (the idea) that each patient population is actually different, even within the chronic persistent posttraumatic headache population, we can’t group them all under the same umbrella term. If we can tease out that a patient has truly had a head injury, but no history of migraine, no overuse of medication, no psychological history, and no other associated symptoms, this would be a very interesting population to study because they would help us understand the pathophysiology [of persistent posttraumatic headache].”
Although the study was conducted by defining persistent posttraumatic headache as lasting at least 3 months, Dr. Chan took issue with that commonly held definition. That choice is arbitrary, with no pathophysiological basis or data to support it, and is based more on clinical trials testing preventative treatments. But when it is used in clinical practice, it can muddy communication with patients. “When this timeline is told to a patient, and when it’s not achieved, they might become disappointed. We should not put too much emphasis on time. Everybody is different,” he said.
The study did not receive any funding. Dr. Chan had no relevant financial disclosures. Dr. Charles consults for consults for Amgen, BioHaven, Eli Lilly, Novartis, and Lundbeck.
It also revealed a surprisingly high frequency of misdiagnosis. The original sample included 500 patients drawn from the Stanford Research Repository Cohort Discovery Tool, but a review found 200 records that were misdiagnosed and had to be excluded.
“It’s very easy to label someone who suffered a head injury and say this is the reason why they have this (headache),” said lead author Tommy Chan, MBBS, a headache fellow in the department of neurology at Stanford (Calif.) University, in an interview. Such patients are often seen by ED or primary care physicians who do not have a lot of experience with posttraumatic headache, and that can lead to negative consequences if a low-pressure headache is mistaken as stemming from a skull fracture. “It’s a very different treatment plan for one versus the other,” said Dr. Chan in an interview.
He noted that it can help to take a patient history that includes the preaccident headache frequency and determine if there was a change in frequency post injury.
Dr. Chan presented the results at the virtual annual meeting of the American Headache Society.
“The results are what one might expect, although we haven’t studied it enough to really know. We haven’t systematically characterized these risk factors for chronic posttraumatic headache very well, [so] it’s useful to have this information,” said Andrew Charles, MD, professor neurology at the University of California, Los Angeles, and director of the UCLA Goldberg Migraine Program, who was not involved in the study. However, Dr. Charles emphasized the need to confirm the results prospectively.
Defining risk factors
The analysis found that a history of migraines, medication overuse, psychological disorders, and new posttraumatic headache–associated comorbidities were all associated with a greater risk for persistent posttraumatic headache. None of those came as a surprise, “but we live in a world where medicine is practiced based on evidence, and providers want to see data to support that. I think that this will help with resource allocation. It’s important to address [a patient’s] overuse of medications, or if they’re having psychological symptoms,” said Dr. Chan.
A total of 150 patients in the analysis had acute posttraumatic headache (mean duration, 0.7 months) while 150 had persistent posttraumatic headache (mean duration, 24 months; P < .00001). Clinical factors associated with risk of persistent headache included a history migraine (relative risk, 2.4; P < .0001), a previous head injury (odds ratio, 5.8; P < .0001), medication overuse (RR, 2.6; P < .0001), preexisting psychological history (OR, 5; P < .0001), and new posttraumatic headache–associated comorbidities, such as vertigo or posttraumatic stress disorder (RR, 9.8; P < .0001).
Identifying patient subgroups
The researchers also identified four subcategories of patients with persistent posttraumatic headache, each with differing risk factors and clinical characteristics. It’s too soon to use these identifiers to make clinical recommendations, but Dr. Chan hopes that further study of these groups will be informative. “It might point us toward (the idea) that each patient population is actually different, even within the chronic persistent posttraumatic headache population, we can’t group them all under the same umbrella term. If we can tease out that a patient has truly had a head injury, but no history of migraine, no overuse of medication, no psychological history, and no other associated symptoms, this would be a very interesting population to study because they would help us understand the pathophysiology [of persistent posttraumatic headache].”
Although the study was conducted by defining persistent posttraumatic headache as lasting at least 3 months, Dr. Chan took issue with that commonly held definition. That choice is arbitrary, with no pathophysiological basis or data to support it, and is based more on clinical trials testing preventative treatments. But when it is used in clinical practice, it can muddy communication with patients. “When this timeline is told to a patient, and when it’s not achieved, they might become disappointed. We should not put too much emphasis on time. Everybody is different,” he said.
The study did not receive any funding. Dr. Chan had no relevant financial disclosures. Dr. Charles consults for consults for Amgen, BioHaven, Eli Lilly, Novartis, and Lundbeck.
It also revealed a surprisingly high frequency of misdiagnosis. The original sample included 500 patients drawn from the Stanford Research Repository Cohort Discovery Tool, but a review found 200 records that were misdiagnosed and had to be excluded.
“It’s very easy to label someone who suffered a head injury and say this is the reason why they have this (headache),” said lead author Tommy Chan, MBBS, a headache fellow in the department of neurology at Stanford (Calif.) University, in an interview. Such patients are often seen by ED or primary care physicians who do not have a lot of experience with posttraumatic headache, and that can lead to negative consequences if a low-pressure headache is mistaken as stemming from a skull fracture. “It’s a very different treatment plan for one versus the other,” said Dr. Chan in an interview.
He noted that it can help to take a patient history that includes the preaccident headache frequency and determine if there was a change in frequency post injury.
Dr. Chan presented the results at the virtual annual meeting of the American Headache Society.
“The results are what one might expect, although we haven’t studied it enough to really know. We haven’t systematically characterized these risk factors for chronic posttraumatic headache very well, [so] it’s useful to have this information,” said Andrew Charles, MD, professor neurology at the University of California, Los Angeles, and director of the UCLA Goldberg Migraine Program, who was not involved in the study. However, Dr. Charles emphasized the need to confirm the results prospectively.
Defining risk factors
The analysis found that a history of migraines, medication overuse, psychological disorders, and new posttraumatic headache–associated comorbidities were all associated with a greater risk for persistent posttraumatic headache. None of those came as a surprise, “but we live in a world where medicine is practiced based on evidence, and providers want to see data to support that. I think that this will help with resource allocation. It’s important to address [a patient’s] overuse of medications, or if they’re having psychological symptoms,” said Dr. Chan.
A total of 150 patients in the analysis had acute posttraumatic headache (mean duration, 0.7 months) while 150 had persistent posttraumatic headache (mean duration, 24 months; P < .00001). Clinical factors associated with risk of persistent headache included a history migraine (relative risk, 2.4; P < .0001), a previous head injury (odds ratio, 5.8; P < .0001), medication overuse (RR, 2.6; P < .0001), preexisting psychological history (OR, 5; P < .0001), and new posttraumatic headache–associated comorbidities, such as vertigo or posttraumatic stress disorder (RR, 9.8; P < .0001).
Identifying patient subgroups
The researchers also identified four subcategories of patients with persistent posttraumatic headache, each with differing risk factors and clinical characteristics. It’s too soon to use these identifiers to make clinical recommendations, but Dr. Chan hopes that further study of these groups will be informative. “It might point us toward (the idea) that each patient population is actually different, even within the chronic persistent posttraumatic headache population, we can’t group them all under the same umbrella term. If we can tease out that a patient has truly had a head injury, but no history of migraine, no overuse of medication, no psychological history, and no other associated symptoms, this would be a very interesting population to study because they would help us understand the pathophysiology [of persistent posttraumatic headache].”
Although the study was conducted by defining persistent posttraumatic headache as lasting at least 3 months, Dr. Chan took issue with that commonly held definition. That choice is arbitrary, with no pathophysiological basis or data to support it, and is based more on clinical trials testing preventative treatments. But when it is used in clinical practice, it can muddy communication with patients. “When this timeline is told to a patient, and when it’s not achieved, they might become disappointed. We should not put too much emphasis on time. Everybody is different,” he said.
The study did not receive any funding. Dr. Chan had no relevant financial disclosures. Dr. Charles consults for consults for Amgen, BioHaven, Eli Lilly, Novartis, and Lundbeck.
FROM AHS 2020
Prior head injury is associated with severe Parkinson’s disease phenotype
according to research presented online as part of the 2020 American Academy of Neurology Science Highlights.
Neurologists have identified various phenotypes among patients with Parkinson’s disease; however, the factors that determine these phenotypes, which may include genetic and environmental variables, are poorly understood. Ethan G. Brown, MD, assistant professor of neurology at the University of California, San Francisco, and colleagues hypothesized that head injury, which is a risk factor for Parkinson’s disease, would be associated with a more severe phenotype.
“Head injury is a risk factor for other conditions that involve cognitive impairment,” said Dr. Brown. “The mechanisms of how head injury contributes to neurodegenerative disease are not clear, but may be related to the initiation of an inflammatory cascade that can have a long-term, chronic effect. We hypothesized that these long-term sequelae may contribute to symptoms in Parkinson’s disease.”
An analysis of data from two cohorts
The researchers examined the relationship between head injury and clinical features by analyzing data for two cohorts of patients with Parkinson’s disease. Through an online survey, the investigators elicited information about head injury and other exposures from participants in the Parkinson’s Progression Markers Initiative (PPMI) and the Fox Insight (FI) study. Dr. Brown and colleagues determined disease phenotypes for participants in PPMI using baseline Movement Disorder Society-Unified Parkinson’s Disease Rating Scale (MDS-UPDRS) score and 5-year change in Montreal Cognitive Assessment score. For participants in FI, the researchers determined phenotypes using baseline self-reported MDS-UPDRS-II score and self-reported cognitive impairment. They used parametric and nonparametric tests as appropriate and adjusted the results for age, sex, and smoking history.
In all, 267 participants with Parkinson’s disease in PPMI and 25,308 in FI submitted information about head injury. In the PPMI cohort, head injury before Parkinson’s disease diagnosis was associated with greater nonmotor symptom burden at enrollment. The mean MDS-UPDRS-I score was 7.73 among participants with any injury, compared with 6.19 among participants with no injury. Similarly, the mean MDS-UPDRS-I score was 8.29 among participants with severe head injury, compared with 6.19 among participants with no injury. Motor symptoms were worse among participants with severe injury (MDS-UPDRS-II score, 8.35). Among 110 participants who were followed for 5 years, patients who reported severe head injury before diagnosis had a decline in cognitive function. The mean change in Montreal Cognitive Assessment score was –0.60 for patients with severe head injury and 0.76 in those with no head injury.
“The improvement from baseline in the participants with Parkinson’s disease but without head injury was small and not statistically significant,” said Dr. Brown. The increase could have resulted from practice effect, although it is not certain, he added. “We are continuing to evaluate other, more sensitive tests of cognitive impairment to try to understand these results more completely in this population.”
In the FI cohort, participants who reported a prior head injury had more motor symptoms (MDS-UPDRS-II, 14.4), compared with those without head injury (MDS-UPDRS-II, 12.1). Also, the risk of self-reported cognitive impairment was elevated in participants who reported head injury (odds ratio, 1.58).
“The results most affected by the self-reported nature of [the] FI [data] are the cognitive impairment results,” said Dr. Brown. “Subjective cognitive impairment ... is very different from objective cognitive impairment, which could be measured through in-person testing in the PPMI cohort. Many factors may contribute to noticing cognitive decline, some of which can be measured and controlled for, but some cannot. There may be a correlation between subjective cognitive decline and true cognitive impairment, but this has not been fully studied in Parkinson’s disease.”
The search for the underlying mechanism
Clarifying whether the relationship between head injury and Parkinson’s disease phenotype is causal or whether falling is an early indication of worse symptoms will require more longitudinal data. “We would like to further characterize the differences between people with Parkinson’s disease with and without a history of head injury,” said Dr. Brown. “More detailed understanding of these phenotypic differences could point to an underlying mechanism, or whether or not other comorbid conditions are involved. We would also like to understand whether genetics plays a role.”
The PPMI and FI studies are funded by the Michael J. Fox Foundation. Dr. Brown has received compensation from HiOscar, NEJM Knowledge Plus, and Rune Labs and has received research support from Gateway Institute for Brain Research.
SOURCE: Brown EG et al. AAN 2020, Abstract S17.002.
according to research presented online as part of the 2020 American Academy of Neurology Science Highlights.
Neurologists have identified various phenotypes among patients with Parkinson’s disease; however, the factors that determine these phenotypes, which may include genetic and environmental variables, are poorly understood. Ethan G. Brown, MD, assistant professor of neurology at the University of California, San Francisco, and colleagues hypothesized that head injury, which is a risk factor for Parkinson’s disease, would be associated with a more severe phenotype.
“Head injury is a risk factor for other conditions that involve cognitive impairment,” said Dr. Brown. “The mechanisms of how head injury contributes to neurodegenerative disease are not clear, but may be related to the initiation of an inflammatory cascade that can have a long-term, chronic effect. We hypothesized that these long-term sequelae may contribute to symptoms in Parkinson’s disease.”
An analysis of data from two cohorts
The researchers examined the relationship between head injury and clinical features by analyzing data for two cohorts of patients with Parkinson’s disease. Through an online survey, the investigators elicited information about head injury and other exposures from participants in the Parkinson’s Progression Markers Initiative (PPMI) and the Fox Insight (FI) study. Dr. Brown and colleagues determined disease phenotypes for participants in PPMI using baseline Movement Disorder Society-Unified Parkinson’s Disease Rating Scale (MDS-UPDRS) score and 5-year change in Montreal Cognitive Assessment score. For participants in FI, the researchers determined phenotypes using baseline self-reported MDS-UPDRS-II score and self-reported cognitive impairment. They used parametric and nonparametric tests as appropriate and adjusted the results for age, sex, and smoking history.
In all, 267 participants with Parkinson’s disease in PPMI and 25,308 in FI submitted information about head injury. In the PPMI cohort, head injury before Parkinson’s disease diagnosis was associated with greater nonmotor symptom burden at enrollment. The mean MDS-UPDRS-I score was 7.73 among participants with any injury, compared with 6.19 among participants with no injury. Similarly, the mean MDS-UPDRS-I score was 8.29 among participants with severe head injury, compared with 6.19 among participants with no injury. Motor symptoms were worse among participants with severe injury (MDS-UPDRS-II score, 8.35). Among 110 participants who were followed for 5 years, patients who reported severe head injury before diagnosis had a decline in cognitive function. The mean change in Montreal Cognitive Assessment score was –0.60 for patients with severe head injury and 0.76 in those with no head injury.
“The improvement from baseline in the participants with Parkinson’s disease but without head injury was small and not statistically significant,” said Dr. Brown. The increase could have resulted from practice effect, although it is not certain, he added. “We are continuing to evaluate other, more sensitive tests of cognitive impairment to try to understand these results more completely in this population.”
In the FI cohort, participants who reported a prior head injury had more motor symptoms (MDS-UPDRS-II, 14.4), compared with those without head injury (MDS-UPDRS-II, 12.1). Also, the risk of self-reported cognitive impairment was elevated in participants who reported head injury (odds ratio, 1.58).
“The results most affected by the self-reported nature of [the] FI [data] are the cognitive impairment results,” said Dr. Brown. “Subjective cognitive impairment ... is very different from objective cognitive impairment, which could be measured through in-person testing in the PPMI cohort. Many factors may contribute to noticing cognitive decline, some of which can be measured and controlled for, but some cannot. There may be a correlation between subjective cognitive decline and true cognitive impairment, but this has not been fully studied in Parkinson’s disease.”
The search for the underlying mechanism
Clarifying whether the relationship between head injury and Parkinson’s disease phenotype is causal or whether falling is an early indication of worse symptoms will require more longitudinal data. “We would like to further characterize the differences between people with Parkinson’s disease with and without a history of head injury,” said Dr. Brown. “More detailed understanding of these phenotypic differences could point to an underlying mechanism, or whether or not other comorbid conditions are involved. We would also like to understand whether genetics plays a role.”
The PPMI and FI studies are funded by the Michael J. Fox Foundation. Dr. Brown has received compensation from HiOscar, NEJM Knowledge Plus, and Rune Labs and has received research support from Gateway Institute for Brain Research.
SOURCE: Brown EG et al. AAN 2020, Abstract S17.002.
according to research presented online as part of the 2020 American Academy of Neurology Science Highlights.
Neurologists have identified various phenotypes among patients with Parkinson’s disease; however, the factors that determine these phenotypes, which may include genetic and environmental variables, are poorly understood. Ethan G. Brown, MD, assistant professor of neurology at the University of California, San Francisco, and colleagues hypothesized that head injury, which is a risk factor for Parkinson’s disease, would be associated with a more severe phenotype.
“Head injury is a risk factor for other conditions that involve cognitive impairment,” said Dr. Brown. “The mechanisms of how head injury contributes to neurodegenerative disease are not clear, but may be related to the initiation of an inflammatory cascade that can have a long-term, chronic effect. We hypothesized that these long-term sequelae may contribute to symptoms in Parkinson’s disease.”
An analysis of data from two cohorts
The researchers examined the relationship between head injury and clinical features by analyzing data for two cohorts of patients with Parkinson’s disease. Through an online survey, the investigators elicited information about head injury and other exposures from participants in the Parkinson’s Progression Markers Initiative (PPMI) and the Fox Insight (FI) study. Dr. Brown and colleagues determined disease phenotypes for participants in PPMI using baseline Movement Disorder Society-Unified Parkinson’s Disease Rating Scale (MDS-UPDRS) score and 5-year change in Montreal Cognitive Assessment score. For participants in FI, the researchers determined phenotypes using baseline self-reported MDS-UPDRS-II score and self-reported cognitive impairment. They used parametric and nonparametric tests as appropriate and adjusted the results for age, sex, and smoking history.
In all, 267 participants with Parkinson’s disease in PPMI and 25,308 in FI submitted information about head injury. In the PPMI cohort, head injury before Parkinson’s disease diagnosis was associated with greater nonmotor symptom burden at enrollment. The mean MDS-UPDRS-I score was 7.73 among participants with any injury, compared with 6.19 among participants with no injury. Similarly, the mean MDS-UPDRS-I score was 8.29 among participants with severe head injury, compared with 6.19 among participants with no injury. Motor symptoms were worse among participants with severe injury (MDS-UPDRS-II score, 8.35). Among 110 participants who were followed for 5 years, patients who reported severe head injury before diagnosis had a decline in cognitive function. The mean change in Montreal Cognitive Assessment score was –0.60 for patients with severe head injury and 0.76 in those with no head injury.
“The improvement from baseline in the participants with Parkinson’s disease but without head injury was small and not statistically significant,” said Dr. Brown. The increase could have resulted from practice effect, although it is not certain, he added. “We are continuing to evaluate other, more sensitive tests of cognitive impairment to try to understand these results more completely in this population.”
In the FI cohort, participants who reported a prior head injury had more motor symptoms (MDS-UPDRS-II, 14.4), compared with those without head injury (MDS-UPDRS-II, 12.1). Also, the risk of self-reported cognitive impairment was elevated in participants who reported head injury (odds ratio, 1.58).
“The results most affected by the self-reported nature of [the] FI [data] are the cognitive impairment results,” said Dr. Brown. “Subjective cognitive impairment ... is very different from objective cognitive impairment, which could be measured through in-person testing in the PPMI cohort. Many factors may contribute to noticing cognitive decline, some of which can be measured and controlled for, but some cannot. There may be a correlation between subjective cognitive decline and true cognitive impairment, but this has not been fully studied in Parkinson’s disease.”
The search for the underlying mechanism
Clarifying whether the relationship between head injury and Parkinson’s disease phenotype is causal or whether falling is an early indication of worse symptoms will require more longitudinal data. “We would like to further characterize the differences between people with Parkinson’s disease with and without a history of head injury,” said Dr. Brown. “More detailed understanding of these phenotypic differences could point to an underlying mechanism, or whether or not other comorbid conditions are involved. We would also like to understand whether genetics plays a role.”
The PPMI and FI studies are funded by the Michael J. Fox Foundation. Dr. Brown has received compensation from HiOscar, NEJM Knowledge Plus, and Rune Labs and has received research support from Gateway Institute for Brain Research.
SOURCE: Brown EG et al. AAN 2020, Abstract S17.002.
FROM AAN 2020
Blue light improves concussion symptoms
a new study has found. Exposure to blue light in the morning through a special device may be a “critical factor” in resetting the circadian rhythm and helping people who have suffered a concussion, author William D. “Scott” Killgore, MD, professor of psychiatry, psychology, and medical imaging, the University of Arizona College of Medicine, Tucson, told Medscape Medical News.
“This is very new, so I wouldn’t say it’s the treatment of choice, but we should start looking at using this system as a nonpharmacologic way to perhaps help patients recover faster from a concussion,” he said.
The findings were released March 2 ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology. The AAN canceled the meeting and released abstracts and access to presenters for press coverage.
About half of patients with a concussion experience sleep problems, including problems falling asleep, staying asleep, and waking up in the middle of the night, said Dr. Killgore.
Poor sleep interrupts the brain’s repair mechanism. “Sleep is important for cleaning out the neurotoxins that build up in your brain during the day. Sleep also helps build oligodendrocyte precursor cells that provide insulation around nerve cells,” he said.
Master clock
Blue light stimulates receptors in the back of the retina that respond only to this wavelength of light, said Dr. Killgore. “It specifically projects to an area in the hypothalamus – essentially the brain’s master clock – that regulates your sleep-wake schedules. So exposure to that bright light essentially resets your circadian rhythm.”
That master clock involves regulating the brain’s production of melatonin. Morning exposure to blue light shifts that production to facilitate sleep at the appropriate time.
The ideal time to be exposed to blue light is from about 8:00 to 11:00 AM. “Timing is critical,” said Dr. Killgore. “If you get light at the wrong time, it will reset your circadian rhythm in the wrong direction.”
Previous research has shown that exposure to blue light leads to improved sleep, which is widely believed to lead to improved mood.
A separate study conducted by Dr. Killgore and colleagues that involved another group of mTBI patients was recently published in Neurobiology of Disease. That study showed that the participants who received blue light experienced a shift in circadian timing of about an hour. “They were going to sleep an hour earlier and waking up an hour earlier,” said Dr. Killgore.
The blue light also appeared to change brain structure and brain function, among other things, he said.
The current study included 35 patients who had suffered an mTBI within the previous 18 months. Most injuries were sports related and occurred while playing football or soccer or riding a bike.
Participants were randomly assigned to use a device fitted with a blue LED light (peak wavelength, 469 nm) or one fitted with an amber-colored LED light. They were instructed to use the device every morning for 30 minutes within 2 hours of waking.
The blue-light group comprised five men and 12 women (mean age, 25.5 years). The amber-light group comprised eight men and 10 women (mean age, 26.3 years).
Researchers told participants only that the study was exploring various aspects of light. “Subjects didn’t know if they were getting a control or active device,” said Dr. Killgore.
Researchers used the Beck Depression Inventory (BDI) to evaluate depression symptoms and the Rivermead Post-Concussion Symptom Questionnaire (RPCSQ). This 16-item questionnaire assesses symptoms in the acute stage as well as those that are more chronic.
After 6 weeks, the blue-light group had lower scores on the BDI compared to the amber-light group (P = .005).
“We found that in the amber-light group, there was essentially no change in terms of depression,” said Dr. Killgore. “But those who got the blue light showed a significant reduction in depressive symptoms, about a 22% decline overall relative to baseline, so a nice drop in overall depression.”
Changes in BDI scores were significantly positively associated with changes in the total chronic symptom score (P = .002) in the blue-light group but not the amber-light group. “Those who got blue light showed a significant reduction in the number of symptoms associated with concussion whereas those who got the amber light stayed the same,” said Dr. Killgore.
There were similar findings for somatic symptoms, such as headache and pain (P = .031), and for cognitive symptoms (P = .014) in the blue-light group.
“These subjects were having fewer problems remembering and paying attention, so their concentration seemed to be improving, at least subjectively,” commented Dr. Killgore.
There was no significant benefit from the blue light for emotional symptoms. “There was a decline, but it wasn’t statistically significant, even though there was a decline in depression,” said Dr. Killgore.
This, he explained, could be due to the small sample size and the greater sensitivity of the BDI for emotional symptoms relative to the RPCSQ. “The BDI has 21 items that are all focused on aspects of depression, whereas the RPCSQ only asks one item for depression and one item for irritability/anger.”
Less daytime sleepiness
The researchers also found a significant improvement in daytime sleepiness. “Subjects were much less sleepy by the end of the study if they got blue light than if they got amber light,” said Dr. Killgore.
Participants wore an actigraphy device that took sleep measurements. Early results indicate that blue-light recipients were getting more sleep by the end of the study.
Researchers are now analyzing additional data to see whether the improvements in depression and post-concussion symptoms are linked to improved sleep. They also gathered data from brain imaging that will be analyzed at a later date.
Dr. Killgore and his colleagues aim to determine what distinguishes people who respond to blue-light therapy from those who don’t. “We want to know what it is that would allow some people to be more responsive than others, so we’re going to be exploring skin color, eye color, genetic factors, and other factors,” he said.
They’re also conducting a study of blue-light therapy in patients with posttraumatic stress disorder, 90% of whom have sleep problems.
“This is quite fascinating,” said Dr. Killgore. “It looks like if you get blue light after your treatment, the treatment sticks better than if you didn’t get the blue light. We think that sleep is probably playing an important role in that.”
Several light devices are available, ranging in price from about $100 to $200.
Commenting on the research, concussion expert Frank Conidi, MD, director of the Florida Center for Headache and Sports Neurology, Port St. Lucie, said the study is interesting from a number of perspectives.
For one thing, it shows that blue-light therapy “provides an inexpensive and minimally invasive way to treat concussion,” he said.
Dr. Conidi said he would recommend blue-light therapy for concussion patients. “I could see neurology practices offering the device to patients as an in-office treatment or to take home for a small fee. I think athletes would be quite receptive to this, as they’re always looking for nonpharmacological ways to treat concussion.”
Dr. Conidi noted that the new results are consistent with other studies that show that decreased depression and improved sleep help with somatic symptoms.
From a research perspective, the study provides a “stepping stone” for larger trials, said Dr. Conidi. He would like to see more studies of acute concussion, such as studies as to whether the therapy shortens the duration of symptoms.
“I would also like to see controlled studies on headache and vestibular symptoms, which are the two most common,” he said.
The study was funded by the US Department of Defense. Killgore and Conidi have disclosed no relevant financial relationships.
This article first appeared on Medscape.com.
a new study has found. Exposure to blue light in the morning through a special device may be a “critical factor” in resetting the circadian rhythm and helping people who have suffered a concussion, author William D. “Scott” Killgore, MD, professor of psychiatry, psychology, and medical imaging, the University of Arizona College of Medicine, Tucson, told Medscape Medical News.
“This is very new, so I wouldn’t say it’s the treatment of choice, but we should start looking at using this system as a nonpharmacologic way to perhaps help patients recover faster from a concussion,” he said.
The findings were released March 2 ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology. The AAN canceled the meeting and released abstracts and access to presenters for press coverage.
About half of patients with a concussion experience sleep problems, including problems falling asleep, staying asleep, and waking up in the middle of the night, said Dr. Killgore.
Poor sleep interrupts the brain’s repair mechanism. “Sleep is important for cleaning out the neurotoxins that build up in your brain during the day. Sleep also helps build oligodendrocyte precursor cells that provide insulation around nerve cells,” he said.
Master clock
Blue light stimulates receptors in the back of the retina that respond only to this wavelength of light, said Dr. Killgore. “It specifically projects to an area in the hypothalamus – essentially the brain’s master clock – that regulates your sleep-wake schedules. So exposure to that bright light essentially resets your circadian rhythm.”
That master clock involves regulating the brain’s production of melatonin. Morning exposure to blue light shifts that production to facilitate sleep at the appropriate time.
The ideal time to be exposed to blue light is from about 8:00 to 11:00 AM. “Timing is critical,” said Dr. Killgore. “If you get light at the wrong time, it will reset your circadian rhythm in the wrong direction.”
Previous research has shown that exposure to blue light leads to improved sleep, which is widely believed to lead to improved mood.
A separate study conducted by Dr. Killgore and colleagues that involved another group of mTBI patients was recently published in Neurobiology of Disease. That study showed that the participants who received blue light experienced a shift in circadian timing of about an hour. “They were going to sleep an hour earlier and waking up an hour earlier,” said Dr. Killgore.
The blue light also appeared to change brain structure and brain function, among other things, he said.
The current study included 35 patients who had suffered an mTBI within the previous 18 months. Most injuries were sports related and occurred while playing football or soccer or riding a bike.
Participants were randomly assigned to use a device fitted with a blue LED light (peak wavelength, 469 nm) or one fitted with an amber-colored LED light. They were instructed to use the device every morning for 30 minutes within 2 hours of waking.
The blue-light group comprised five men and 12 women (mean age, 25.5 years). The amber-light group comprised eight men and 10 women (mean age, 26.3 years).
Researchers told participants only that the study was exploring various aspects of light. “Subjects didn’t know if they were getting a control or active device,” said Dr. Killgore.
Researchers used the Beck Depression Inventory (BDI) to evaluate depression symptoms and the Rivermead Post-Concussion Symptom Questionnaire (RPCSQ). This 16-item questionnaire assesses symptoms in the acute stage as well as those that are more chronic.
After 6 weeks, the blue-light group had lower scores on the BDI compared to the amber-light group (P = .005).
“We found that in the amber-light group, there was essentially no change in terms of depression,” said Dr. Killgore. “But those who got the blue light showed a significant reduction in depressive symptoms, about a 22% decline overall relative to baseline, so a nice drop in overall depression.”
Changes in BDI scores were significantly positively associated with changes in the total chronic symptom score (P = .002) in the blue-light group but not the amber-light group. “Those who got blue light showed a significant reduction in the number of symptoms associated with concussion whereas those who got the amber light stayed the same,” said Dr. Killgore.
There were similar findings for somatic symptoms, such as headache and pain (P = .031), and for cognitive symptoms (P = .014) in the blue-light group.
“These subjects were having fewer problems remembering and paying attention, so their concentration seemed to be improving, at least subjectively,” commented Dr. Killgore.
There was no significant benefit from the blue light for emotional symptoms. “There was a decline, but it wasn’t statistically significant, even though there was a decline in depression,” said Dr. Killgore.
This, he explained, could be due to the small sample size and the greater sensitivity of the BDI for emotional symptoms relative to the RPCSQ. “The BDI has 21 items that are all focused on aspects of depression, whereas the RPCSQ only asks one item for depression and one item for irritability/anger.”
Less daytime sleepiness
The researchers also found a significant improvement in daytime sleepiness. “Subjects were much less sleepy by the end of the study if they got blue light than if they got amber light,” said Dr. Killgore.
Participants wore an actigraphy device that took sleep measurements. Early results indicate that blue-light recipients were getting more sleep by the end of the study.
Researchers are now analyzing additional data to see whether the improvements in depression and post-concussion symptoms are linked to improved sleep. They also gathered data from brain imaging that will be analyzed at a later date.
Dr. Killgore and his colleagues aim to determine what distinguishes people who respond to blue-light therapy from those who don’t. “We want to know what it is that would allow some people to be more responsive than others, so we’re going to be exploring skin color, eye color, genetic factors, and other factors,” he said.
They’re also conducting a study of blue-light therapy in patients with posttraumatic stress disorder, 90% of whom have sleep problems.
“This is quite fascinating,” said Dr. Killgore. “It looks like if you get blue light after your treatment, the treatment sticks better than if you didn’t get the blue light. We think that sleep is probably playing an important role in that.”
Several light devices are available, ranging in price from about $100 to $200.
Commenting on the research, concussion expert Frank Conidi, MD, director of the Florida Center for Headache and Sports Neurology, Port St. Lucie, said the study is interesting from a number of perspectives.
For one thing, it shows that blue-light therapy “provides an inexpensive and minimally invasive way to treat concussion,” he said.
Dr. Conidi said he would recommend blue-light therapy for concussion patients. “I could see neurology practices offering the device to patients as an in-office treatment or to take home for a small fee. I think athletes would be quite receptive to this, as they’re always looking for nonpharmacological ways to treat concussion.”
Dr. Conidi noted that the new results are consistent with other studies that show that decreased depression and improved sleep help with somatic symptoms.
From a research perspective, the study provides a “stepping stone” for larger trials, said Dr. Conidi. He would like to see more studies of acute concussion, such as studies as to whether the therapy shortens the duration of symptoms.
“I would also like to see controlled studies on headache and vestibular symptoms, which are the two most common,” he said.
The study was funded by the US Department of Defense. Killgore and Conidi have disclosed no relevant financial relationships.
This article first appeared on Medscape.com.
a new study has found. Exposure to blue light in the morning through a special device may be a “critical factor” in resetting the circadian rhythm and helping people who have suffered a concussion, author William D. “Scott” Killgore, MD, professor of psychiatry, psychology, and medical imaging, the University of Arizona College of Medicine, Tucson, told Medscape Medical News.
“This is very new, so I wouldn’t say it’s the treatment of choice, but we should start looking at using this system as a nonpharmacologic way to perhaps help patients recover faster from a concussion,” he said.
The findings were released March 2 ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology. The AAN canceled the meeting and released abstracts and access to presenters for press coverage.
About half of patients with a concussion experience sleep problems, including problems falling asleep, staying asleep, and waking up in the middle of the night, said Dr. Killgore.
Poor sleep interrupts the brain’s repair mechanism. “Sleep is important for cleaning out the neurotoxins that build up in your brain during the day. Sleep also helps build oligodendrocyte precursor cells that provide insulation around nerve cells,” he said.
Master clock
Blue light stimulates receptors in the back of the retina that respond only to this wavelength of light, said Dr. Killgore. “It specifically projects to an area in the hypothalamus – essentially the brain’s master clock – that regulates your sleep-wake schedules. So exposure to that bright light essentially resets your circadian rhythm.”
That master clock involves regulating the brain’s production of melatonin. Morning exposure to blue light shifts that production to facilitate sleep at the appropriate time.
The ideal time to be exposed to blue light is from about 8:00 to 11:00 AM. “Timing is critical,” said Dr. Killgore. “If you get light at the wrong time, it will reset your circadian rhythm in the wrong direction.”
Previous research has shown that exposure to blue light leads to improved sleep, which is widely believed to lead to improved mood.
A separate study conducted by Dr. Killgore and colleagues that involved another group of mTBI patients was recently published in Neurobiology of Disease. That study showed that the participants who received blue light experienced a shift in circadian timing of about an hour. “They were going to sleep an hour earlier and waking up an hour earlier,” said Dr. Killgore.
The blue light also appeared to change brain structure and brain function, among other things, he said.
The current study included 35 patients who had suffered an mTBI within the previous 18 months. Most injuries were sports related and occurred while playing football or soccer or riding a bike.
Participants were randomly assigned to use a device fitted with a blue LED light (peak wavelength, 469 nm) or one fitted with an amber-colored LED light. They were instructed to use the device every morning for 30 minutes within 2 hours of waking.
The blue-light group comprised five men and 12 women (mean age, 25.5 years). The amber-light group comprised eight men and 10 women (mean age, 26.3 years).
Researchers told participants only that the study was exploring various aspects of light. “Subjects didn’t know if they were getting a control or active device,” said Dr. Killgore.
Researchers used the Beck Depression Inventory (BDI) to evaluate depression symptoms and the Rivermead Post-Concussion Symptom Questionnaire (RPCSQ). This 16-item questionnaire assesses symptoms in the acute stage as well as those that are more chronic.
After 6 weeks, the blue-light group had lower scores on the BDI compared to the amber-light group (P = .005).
“We found that in the amber-light group, there was essentially no change in terms of depression,” said Dr. Killgore. “But those who got the blue light showed a significant reduction in depressive symptoms, about a 22% decline overall relative to baseline, so a nice drop in overall depression.”
Changes in BDI scores were significantly positively associated with changes in the total chronic symptom score (P = .002) in the blue-light group but not the amber-light group. “Those who got blue light showed a significant reduction in the number of symptoms associated with concussion whereas those who got the amber light stayed the same,” said Dr. Killgore.
There were similar findings for somatic symptoms, such as headache and pain (P = .031), and for cognitive symptoms (P = .014) in the blue-light group.
“These subjects were having fewer problems remembering and paying attention, so their concentration seemed to be improving, at least subjectively,” commented Dr. Killgore.
There was no significant benefit from the blue light for emotional symptoms. “There was a decline, but it wasn’t statistically significant, even though there was a decline in depression,” said Dr. Killgore.
This, he explained, could be due to the small sample size and the greater sensitivity of the BDI for emotional symptoms relative to the RPCSQ. “The BDI has 21 items that are all focused on aspects of depression, whereas the RPCSQ only asks one item for depression and one item for irritability/anger.”
Less daytime sleepiness
The researchers also found a significant improvement in daytime sleepiness. “Subjects were much less sleepy by the end of the study if they got blue light than if they got amber light,” said Dr. Killgore.
Participants wore an actigraphy device that took sleep measurements. Early results indicate that blue-light recipients were getting more sleep by the end of the study.
Researchers are now analyzing additional data to see whether the improvements in depression and post-concussion symptoms are linked to improved sleep. They also gathered data from brain imaging that will be analyzed at a later date.
Dr. Killgore and his colleagues aim to determine what distinguishes people who respond to blue-light therapy from those who don’t. “We want to know what it is that would allow some people to be more responsive than others, so we’re going to be exploring skin color, eye color, genetic factors, and other factors,” he said.
They’re also conducting a study of blue-light therapy in patients with posttraumatic stress disorder, 90% of whom have sleep problems.
“This is quite fascinating,” said Dr. Killgore. “It looks like if you get blue light after your treatment, the treatment sticks better than if you didn’t get the blue light. We think that sleep is probably playing an important role in that.”
Several light devices are available, ranging in price from about $100 to $200.
Commenting on the research, concussion expert Frank Conidi, MD, director of the Florida Center for Headache and Sports Neurology, Port St. Lucie, said the study is interesting from a number of perspectives.
For one thing, it shows that blue-light therapy “provides an inexpensive and minimally invasive way to treat concussion,” he said.
Dr. Conidi said he would recommend blue-light therapy for concussion patients. “I could see neurology practices offering the device to patients as an in-office treatment or to take home for a small fee. I think athletes would be quite receptive to this, as they’re always looking for nonpharmacological ways to treat concussion.”
Dr. Conidi noted that the new results are consistent with other studies that show that decreased depression and improved sleep help with somatic symptoms.
From a research perspective, the study provides a “stepping stone” for larger trials, said Dr. Conidi. He would like to see more studies of acute concussion, such as studies as to whether the therapy shortens the duration of symptoms.
“I would also like to see controlled studies on headache and vestibular symptoms, which are the two most common,” he said.
The study was funded by the US Department of Defense. Killgore and Conidi have disclosed no relevant financial relationships.
This article first appeared on Medscape.com.
TBI deaths from falls on the rise
A 17% surge in mortality from fall-related traumatic brain injuries from 2008 to 2017 was driven largely by increases among those aged 75 years and older, according to investigators from the Centers for Disease Control and Prevention.
Nationally, the rate of deaths from traumatic brain injuries (TBIs) caused by unintentional falls rose from 3.86 per 100,000 population in 2008 to 4.52 per 100,000 in 2017, as the number of deaths went from 12,311 to 17,408, said Alexis B. Peterson, PhD, and Scott R. Kegler, PhD, of the CDC’s National Center for Injury Prevention and Control in Atlanta.
“This increase might be explained by longer survival following the onset of common diseases such as stroke, cancer, and heart disease or be attributable to the increasing population of older adults in the United States,” they suggested in the Mortality and Morbidity Weekly Report.
The rate of fall-related TBI among Americans aged 75 years and older increased by an average of 2.6% per year from 2008 to 2017, compared with 1.8% in those aged 55-74. Over that same time, death rates dropped for those aged 35-44 (–0.3%), 18-34 (–1.1%), and 0-17 (–4.3%), they said, based on data from the National Vital Statistics System’s multiple cause-of-death database.
The death rate increased fastest in residents of rural areas (2.9% per year), but deaths from fall-related TBI were up at all levels of urbanization. The largest central cities and fringe metro areas were up by 1.4% a year, with larger annual increases seen in medium-size cities (2.1%), small cities (2.2%), and small towns (2.1%), Dr. Peterson and Dr. Kegler said.
Rates of TBI-related mortality in general are higher in rural areas, they noted, and “heterogeneity in the availability and accessibility of resources (e.g., access to high-level trauma centers and rehabilitative services) can result in disparities in postinjury outcomes.”
State-specific rates increased in 45 states, although Alaska was excluded from the analysis because of its small number of cases (less than 20). Increases were significant in 29 states, but none of the changes were significant in the 4 states with lower rates at the end of the study period, the investigators reported.
“In older adults, evidence-based fall prevention strategies can prevent falls and avert costly medical expenditures,” Dr. Peterson and Dr. Kegler said, suggesting that health care providers “consider prescribing exercises that incorporate balance, strength and gait activities, such as tai chi, and reviewing and managing medications linked to falls.”
SOURCE: Peterson AB, Kegler SR. MMWR. 2019 Mar 6;69(9):225-30.
A 17% surge in mortality from fall-related traumatic brain injuries from 2008 to 2017 was driven largely by increases among those aged 75 years and older, according to investigators from the Centers for Disease Control and Prevention.
Nationally, the rate of deaths from traumatic brain injuries (TBIs) caused by unintentional falls rose from 3.86 per 100,000 population in 2008 to 4.52 per 100,000 in 2017, as the number of deaths went from 12,311 to 17,408, said Alexis B. Peterson, PhD, and Scott R. Kegler, PhD, of the CDC’s National Center for Injury Prevention and Control in Atlanta.
“This increase might be explained by longer survival following the onset of common diseases such as stroke, cancer, and heart disease or be attributable to the increasing population of older adults in the United States,” they suggested in the Mortality and Morbidity Weekly Report.
The rate of fall-related TBI among Americans aged 75 years and older increased by an average of 2.6% per year from 2008 to 2017, compared with 1.8% in those aged 55-74. Over that same time, death rates dropped for those aged 35-44 (–0.3%), 18-34 (–1.1%), and 0-17 (–4.3%), they said, based on data from the National Vital Statistics System’s multiple cause-of-death database.
The death rate increased fastest in residents of rural areas (2.9% per year), but deaths from fall-related TBI were up at all levels of urbanization. The largest central cities and fringe metro areas were up by 1.4% a year, with larger annual increases seen in medium-size cities (2.1%), small cities (2.2%), and small towns (2.1%), Dr. Peterson and Dr. Kegler said.
Rates of TBI-related mortality in general are higher in rural areas, they noted, and “heterogeneity in the availability and accessibility of resources (e.g., access to high-level trauma centers and rehabilitative services) can result in disparities in postinjury outcomes.”
State-specific rates increased in 45 states, although Alaska was excluded from the analysis because of its small number of cases (less than 20). Increases were significant in 29 states, but none of the changes were significant in the 4 states with lower rates at the end of the study period, the investigators reported.
“In older adults, evidence-based fall prevention strategies can prevent falls and avert costly medical expenditures,” Dr. Peterson and Dr. Kegler said, suggesting that health care providers “consider prescribing exercises that incorporate balance, strength and gait activities, such as tai chi, and reviewing and managing medications linked to falls.”
SOURCE: Peterson AB, Kegler SR. MMWR. 2019 Mar 6;69(9):225-30.
A 17% surge in mortality from fall-related traumatic brain injuries from 2008 to 2017 was driven largely by increases among those aged 75 years and older, according to investigators from the Centers for Disease Control and Prevention.
Nationally, the rate of deaths from traumatic brain injuries (TBIs) caused by unintentional falls rose from 3.86 per 100,000 population in 2008 to 4.52 per 100,000 in 2017, as the number of deaths went from 12,311 to 17,408, said Alexis B. Peterson, PhD, and Scott R. Kegler, PhD, of the CDC’s National Center for Injury Prevention and Control in Atlanta.
“This increase might be explained by longer survival following the onset of common diseases such as stroke, cancer, and heart disease or be attributable to the increasing population of older adults in the United States,” they suggested in the Mortality and Morbidity Weekly Report.
The rate of fall-related TBI among Americans aged 75 years and older increased by an average of 2.6% per year from 2008 to 2017, compared with 1.8% in those aged 55-74. Over that same time, death rates dropped for those aged 35-44 (–0.3%), 18-34 (–1.1%), and 0-17 (–4.3%), they said, based on data from the National Vital Statistics System’s multiple cause-of-death database.
The death rate increased fastest in residents of rural areas (2.9% per year), but deaths from fall-related TBI were up at all levels of urbanization. The largest central cities and fringe metro areas were up by 1.4% a year, with larger annual increases seen in medium-size cities (2.1%), small cities (2.2%), and small towns (2.1%), Dr. Peterson and Dr. Kegler said.
Rates of TBI-related mortality in general are higher in rural areas, they noted, and “heterogeneity in the availability and accessibility of resources (e.g., access to high-level trauma centers and rehabilitative services) can result in disparities in postinjury outcomes.”
State-specific rates increased in 45 states, although Alaska was excluded from the analysis because of its small number of cases (less than 20). Increases were significant in 29 states, but none of the changes were significant in the 4 states with lower rates at the end of the study period, the investigators reported.
“In older adults, evidence-based fall prevention strategies can prevent falls and avert costly medical expenditures,” Dr. Peterson and Dr. Kegler said, suggesting that health care providers “consider prescribing exercises that incorporate balance, strength and gait activities, such as tai chi, and reviewing and managing medications linked to falls.”
SOURCE: Peterson AB, Kegler SR. MMWR. 2019 Mar 6;69(9):225-30.
FROM MMWR