Eric R. Braverman, M.D. | PATH Medical
Centers for Disease Control and Prevention (CDC) estimated that approximately 3.8 million Americans receive concussions annually, but several reasons indicate that this number may be too conservative. Because of the difficulty of diagnosing concussions, millions of Americans are undiagnosed. 1,608 subjects were recruited and enrolled in a study at a multispecialty private practice group in Manhattan. 292 patients reported concussions, indicating a prevalence rate of 22%. This figure is staggering compared to the severely underestimated 1% put forth by the CDC, which raises questions regarding the efficacy of concussion diagnosis as well as other common diagnoses at the primary care level. Similar to the concussion epidemic, my BMI study with New York State Governor Cuomo’s former Commissioner of Health, Nirav Shah, found a 59% obesity rate by age 70 when utilizing proper measurements like the DEXA scan and leptin blood test compared to the NHANES obesity rate of 34% using BMI alone (Shah and Braverman, 2012).
Clinically, concussion patients present with additional neuropsychiatric conditions including: depression, anxiety, insomnia, obesity, violence, and mood instability. Individuals suffering from neuropsychiatric conditions often self-medicate using substances like marijuana for insomnia and anxiety treatment, cocaine for fatigue and depression, and alcohol for relaxation and mood enhancement. Obese individuals suffer from food addiction, leptin resistance and dopamine deficiency. Demented persons typically have further rates of head trauma and cognitive or thinking misperceptions, which results in long-term legal and illegal narcotic abuse. Traumatic injuries such as PTSD and other related conditions add to problems of brain health. Crime and violence occurs as the sequelae of brain health neglect: creating a society that fails those with brain disorders. Board-certified psychiatrists often treat these patients without asking for a concussion medical history. These physicians need to be re-trained to look at a medical history that includes concussion history. Therefore, it is no surprise that with no analysis of the first concussion, sports stars like Chris Benoit and Jovan Belcher have suffered fatal consequences of chronic traumatic encephalopathy (CTE) while athletes such as Muhammad Ali and Tony Dorsett have likely cases of dementia and CTE. The answer to combatting brain disease is through preventative treatments that ultimately reshape the way health care focuses its efforts on the brain – which should be the most tested organ.
Mass underdiagnosis of concussions can lead to a lack of precaution in recently concussed individuals, resulting in further injuries to the brain. Current studies have elucidated a link between early adulthood concussions and patterns of decline in late adulthood associated with abnormal aging. Existing methods of detecting concussions include neuropsychological testing, which is often ineffective as individuals purposely fail a baseline test in order to conceal signs of cognitive impairment when a concussion is sustained. While no test is perfect and indeed many athletes can fake tests (i.e. failed on purpose), it is therefore important to start neurocognitive testing earlier in life during or prior to high school when individuals have no incentive to manipulate results. In contrast, electrophysiological assessment of P300 latency and amplitude has proved to be accurate and has been termed ‘the lie detector test’ of concussion diagnosis. Patients with a history of concussion typically have slower processing speeds and decreased voltage on the P300 and may develop chronic traumatic encephalopathy, which is a degenerative brain disease often seen in athletes who suffer repeated blows to the head. P300 measurements taken in the period of middle to late adulthood and after years of sports performance, may be able to detect the lingering effects of concussions even after symptoms identified by neuropsychological evaluations have subsided.
Every person with a history of concussion should undergo examination with a P300. The P300 is inexpensive, widely available to researchers, and can be easily implemented in the clinic (Braverman et al., 2015; Braverman et al., 2013). Extracting specific ERPs from the P300 serve as “brain vital signs,” critical for subsequent evaluation of dysfunction in concussion cases (Hajra et al., 2016). Examination with the P300 is imperative as concussions are risk factors for early-onset Alzheimer’s disease (EOAD) and may lead to disinhibition (Mendez et al, 2015) as well as cause depressive symptoms, anxiety, substance misuse, behavior and/or cognitive changes, and sleep disorders (Finkbeiner et al., 2016; Tkachenko et al., 2016). Concussions can also affect the brain’s structure by increasing dendritic branching and reducing synaptic density, which are associated with impulsivity (Hehar et al, 2015).
In regards to P300 results, we often see slowed processing speeds and decreased voltage. The negative correlations between response time and P300 amplitude suggest that the time necessary to accurately respond to targets increases as the efficiency of allocating processing resources decreases during highly demanding working memory tasks (Ozen et al. 2013). Concussion victims typically show a decrease in P300 amplitude and latency, an effect presumed to reflect alterations in attentional-cognitive processes, with the degree of impairment strongly related to the severity of post-concussion symptoms (Moore et al., 2014; Theriault et al., 2009; Dupuis et al., 2000; Pratap-Chand et al., 1988). These results suggest that a history of concussions may lead to persisting neurophysiological abnormalities that may even be present long after neuropsychological testing ceases to identify concussion symptoms. These results also disagree with those of other studies that suggest that there are either no long-term P300 abnormalities in individuals with histories of concussions, or that those abnormalities persist for up to six months after the last concussion was sustained. Further research should be conducted to investigate possible correlations between these shortened P300 latencies and the prevalence of neuropsychiatric disorders seen as a result of concussions.
In addition to the P300, primary care physicians require more tools to identify ‘silent’ concussion injuries in their patient population, such as implementation of a concussion history questionnaire (Figure 1) as well as utilization of the 3T MRI coupled with NeuroQuant® software. Since the 3T MRI has an increased resolution 15 times that of 1.5T MRI, areas of anatomical atrophy can be readily screened and detected. Both children and adults can suffer from increased rates of cerebral atrophy, often a result of head trauma like concussions (Tables 1-2). In light of the gross underestimation of concussion incidences annually in the United States and recent findings regarding long-term effects, the measurement of P300 components and cerebral atrophy should be considered standard practice in primary care.
Braverman ER, Blum K, Hussman KL, Han D, Dushaj K, et al. Evoked potentials and memory/cognition tests validate brain atrophy as measured by 3T MRI (NeuroQuant) in cognitively impaired patients. PLoS One. 2015; 10(8): e0133609.
Braverman ER, Blum K, Damle UJ, Kerner M, Dushaj K, et al. Evoked potentials and neuropsychological tests validate positron emission topography (PET) brain metabolism in cognitively impaired patients. PLoS One. 2013; 8(3): e55398.
Dupuis F, Johnston KM, Lavoie M, Lepore F, Lassonde M. Concussions in athletes produce brain dysfunction as revealed by event-related potentials. Neuroreport. 2000 Dec 18; 11(18): 4087-92.
Finkbeiner NW, Max JE, Longman S, Debert C. Knowing What We Don’t Know: Long-Term Psychiatric Outcomes following Adult Concussion in Sports.
Can J Psychiatry. 2016; 61(5): 270-6.
Hajra SG, Liu CC, Song X, Fickling S, Lie LE, et al. Developing Brain Vital Signs: Initial Framework for Monitoring Brain Function Changes Over Time. Front Neurosci. 2016; 10: 211.
Hehar H, Yeates K, Kolb B, Esser MJ, Mychasiuk R. Impulsivity and Concussion in Juvenile Rats: Examining Molecular and Structural Aspects of the Frontostriatal Pathway. PLoS One. 2015; 10(10): e0139842.
Mendez MF, Paholpak P, Lin A, Zhang JY, Teng E. Prevalence of Traumatic Brain Injury in Early Versus Late-Onset Alzheimer’s Disease. J Alzheimers Dis. 2015; 47(4): 985-993.
Moore RD, Hillman CH, Broglio SP. The Persistent Influence of Concussive Injuries on Cognitive Control and Neuroelectric Function. Journal of Athletic Training. 2014; 49(1): 24-35.
Ozen LJ, Itier RJ, Preston FF, Fernandes MA. Long-term working memory deficits after concussion: electrophysiological evidence. Brain Inj. 2013; 27(11): 1244-55.
Pratap-Chand R, Sinniah M, Salem, FA. Cognitive evoked potential (P300): a metric for cerebral concussion. Acta Neurol Scand. 1988 Sep; 78(3): 185-9.
Shah NR, Braverman ER. Measuring adiposity in patients: the utility of body mass index (BMI), percent body fat, and leptin. PLoS One. 2012; 7(4): e33308.
Theriault M, De Beaumont L, Gosselin N, Filipinni M, Lassonde M. Electrophysiological abnormalities in well functioning multiple concussed athletes. Brain Inj. 2009 Oct; 23(11): 899-906.
Tkachenko N, Singh K, Hasanaj L, Serrano L, Kothare SV. Sleep Disorders Associated With Mild Traumatic Brain Injury Using Sport Concussion Assessment Tool 3. Pediatr Neurol. 2016; 57: 46-50.e1.
|Findings||Percent Positive (N=172 subjects)|
|Small Vessel Ischemia||80 (47%)|
|Empty Sella||15 (9%)|
|Hippocampal Atrophy||54 (31%)|
|Temporal Atrophy||69 (40%)|
|Central Atrophy||89 (52%)|
|Bilateral Atrophy||20 (12%)|
|Findings||Average Age||Percent Positive (N=19 subjects)|
|Hippocampal Atrophy||20 years||1/16 (6%)|
|Temporal Atrophy||21.4 years||5/16 (31%)|
|Frontal Atrophy||20.2 years||4/9 (44%)|
|Parietal Atrophy||24.5 years||2/9 (22%)|
|Limbic Atrophy||23.5 years||2/9 (22%)|
|Concussion||18.5 years||2/18 (11%)|
|Demyelination||19 years||1/18 (5.5%)|
|Bilateral Atrophy||25 years||1/18 (5.5%)|
|Reduced Fractional Anisotropy in Frontal Lobes||20 years||2/16 (12.5%)|
|Reduced Fractional Anisotropy in Centrum Semivale||21.1 years||15/16 (94%)|
|Periatrial||17 years||1/16 (6%)|