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About the Author
Randall W. Evans, PhD, ABPP – Clinical Neuro- psychologist, Board Certified in Rehabilitation Psychology, Fellow of the National Academy of Neuropsychology. Formerly a Research Fellow with the National Institutes of Health where his research focused on neuro-pharmacology and neuro-psychological test development. He published extensively in these areas with works appearing in the New England Journal of Medicine, Archives of Physical Medicine and Rehabilitation, Developmental Neurology, and a host of other peer review journals.
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Treating the Aging Traumatic Brain Injured Patient
At least 5.3 million persons in the U.S., or 2% of the population, are currently living with a Traumatic Brain Injury (TBI)-related disability.1 TBI is defined as a “blow or jolt to the head or a penetrating injury that disrupts the function of the brain” with a continuum of severity from mild to moderate to severe.1 Mild TBI (M-TBI) the most commonly diagnosed TBI accounts for approximately 75% of all TBI cases, or roughly 1.1 million new cases in the U.S. per year. 2-3
Definition of M-TBI 4
The presence of any of the following:
- Any period of loss of consciousness
- Any loss of memory for events immediately before or after the accident/trauma
- Any alteration in mental state at the time of the accident/trauma, e.g. felling dazed, disoriented, confused (“seeing stars”)
- Focal neurological deficit(s) that may or may not be transient but where the severity of injury does not exceed any of the following:
- Loss of consciousness of approximately 30 minutes or less
- After 30 minutes, and after Glasgow Coma Scale (GCS) of 13-15 Post-traumatic amnesia (PTA) not greater than 24 hours.
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TBI severity must be carefully assessed and appreciated as it has certain implications for short- and long-term clinical outcomes. The most commonly used scale used during the initial phases (e.g., scene of the trauma, in the ER or ICU) is the Glasgow Coma Scale (GCS) which measures speaking, eye opening and motor abilities on a 15-point scale.5 The higher the score on the GCS, the less severe the injury; with scores categorized into 3 basic levels of functioning.
The Rancho Los Amigos Scale (RLAS, aka “Rancho” 3) has some overlap with the GCS, but emphasizes progress throughout the recovery processand takes on a more chronic injury perspective. In addition to measuring progress, the RLAS is also used to communicate clinical status between healthcare professionals.
Why Focus on TBI and Aging?
The number of persons with TBI-related disabilities in the U.S. is steadily growing. Consider that 28% of TBIs result from falls among those ages 65 or older.1 As this age demographic increases, likely so will the incidence of new TBI cases. Further, as neuro-trauma care in the U.S. advances, the ‘net’ increase of persons living with TBI-related disabilities will rise annually.
The “normal” aging process itself can be viewed as a slow, steady decline of various neurological and physical functions regardless of trauma or disease. When a TBI is super-imposed upon the “normal” aging process, what occurs in many circumstances is a situation where 1 (normal aging) + 1 (TBI) = 3. TBI, especially severe TBI, leaves the injured person with increased “risk factors” for an accelerated aging process.6-8 There is no absolute age that puts TBI patients into a higher risk pool for accelerated aging, rather ranges of ages (e.g., 70 and above) that seem to be associated with a poorer prognosis with respect to TBI recovery.9-11 Moreover, TBI can hasten or exacerbate age-related symptoms/illnesses such as insomnia, cardiovascular disease, cognitive decline, certain cancers, Type 2 diabetes, and depression.12-14
One of the disease states that is getting particular attention within the brain injury research is Dementia of the Alzheimer’s Type (DAT).8 By definition, DAT is a progressive neurological disorder that currently has no known cure. To date, the relationship between TBI and DAT is ambiguous. While some persons with severe TBI share similar levels of functioning when compared to persons suspected of having DAT (e.g. impaired attention and memory, decreased ability to perform activities of daily living, preservative and confabulatory tendencies) the underlying neuron-anatomical and neuron-physiological mechanisms are different in many ways.15 The evidence to date suggests that there may be a causal link (e.g., genetic marker, presence of plaques, neuronal “tangles”) between TBI and DAT with severity of TBI and age at onset as possible mediators.6; 14-16 However, there is conflicting evidence regarding the potential link between TBI and vascular dementia, thus, further research is warranted.6-7
In addition, TBI has been shown to provoke a seizure and for some, epilepsy with injury severity increasing the chance of developing a seizure disorder, including: prolonged coma, skull fractures, “open” (i.e., penetrating) TBI, infection of the meninges, and pre-injury history of seizures.17-18 While seizure disorders appear to be more common among the TBI population than in the non-injured population, even in severe TBI, epilepsy is relatively rare (2-10%).17; 19 However, a recent longitudinal study of 312 persons with moderate to severe TBI found that at a minimum of 10 years post-injury approximately 56% of persons were prescribed anti-convulsant medications.20 The presumed rationale for such a high use of anti-convulsants include: actual seizure disorder, prophylactic usage, and/or behavioral control.
Interestingly, seizures, if they do occur, are more likely to occur in the acute phase after TBI than in the chronic phase.5 As such, prophylactic use of anti-convulsant medications is deemed as a “best practice” in the days and weeks following injury, but in the event that no seizures occur, and the risk factors are low, then strong consideration should be given to gradually discontinuing anti-convulsant medication usage as it is well known that many anti-convulsant medications carry serious negative side effects including blunting of cognition and potential liver and kidney dysfunction. Because young children and elder adults are the two largest groups at risk for TBI, the issue of aging with TBI and the potential risk for late onset seizure (several years post-injury) remains for as long as 20 years, but then declines significantly as the person ages.19
Unfortunately, late onset (also often referred to as “breakthrough”) seizures are usually more difficult to manage than acute onset seizures. Fortunately, there is considerable research in process that involves diagnostic and treatment approaches to all forms of epilepsy. A valuable resource to review this ongoing research is www.ninds.nih.gov/disorders/epilepsy/epilepsy.htm.
In addition to exploring the relationship between TBI and DAT and TBI and seizure disorders, several studies have explored the influence of TBI on other health conditions such as, arthritis, sleep disorder, higher risk for another TBI, hypertension and obesity, major depression, neuro-muscular disorders, and anxiety disorders.2; 21-24 Taken together, results suggest a higher incidence of each of these conditions among TBI patients as compared to their non-injured counterparts.
Moreover, it is the general consensus that TBI usually aggravates most pre-injury problems, whether they be physical or behavioral in nature.23 Persons with TBI may have blatant, or subtle, problems with self awareness, self monitoring, and insight.22 These deficiencies can impede adherence to treatment recommendations. Further, this lack of psychological savvy can contribute to the social isolation that a significant number of persons with TBI confront, particularly those with severe TBI.25 Since the largest segment of the TBI population is in their late teens and early twenties, many non-injured peers “move on” with their lives and development, leaving the injured person, who may be undergoing months or even years of rehabilitation, behind. |
Featured Course
Traumatic Brain Injury (TBI): The Effects of Aging
(3 CEs) by Randall Evans, Ph.D., ABPP

Taken together, these data suggest that TBI is a major healthcare concern. Moreover, the statistics put the need to understand the impact of the “graying” of this population, and special issues facing the injured person, their families and significant others in perspective. While new neuro-imaging techniques and new medications are being developed to refine diagnosis and treatment of TBI, there are emerging concerns and research data to suggest that TBI, particularly severe TBI, may have a significant impact on the “normal” aging process across the lifespan.
Like their patients, healthcare professionals working with TBI patients face unique challenges. Further, providers of TBI rehabilitation face considerable obstacles as they amend their treatment protocols to assist patients that may be several decades post-injury. The featured course reviews the medical, psychological, and social consequences that can occur following TBI and discusses developing therapies to improve quality-of-life in this population. As the “graying” of America continues, including those with TBI related problems, strict attention must be made to how services and supports are in place for those with TBI and how an injured person decades post-injury will access such services.
References
- Langlois, J.A., et al. Traumatic brain injury in the United States: emergency department visits, hospitalizations, and deaths. Centers for Disease Control and Prevention, National Center for Injury Prevention and Control, 2006.
- Iverson, G.L., et al. Cumulative effects of concussion in amateur athletes. Brain Injury, 2004. 18, p. 433-443.
- Thurman, D., et al. Traumatic brain injury in the United States: A public health perspective. Journal of Head Trauma Rehabilitation, 1999. 14(6): p. 602-615.
- American Congress of Rehabilitation Medicine Head Injury Interdisciplinary Special Interest Group. Definition of mild traumatic brain injury. Journal of Head Trauma Rehabilitation, 1993. 8: p. 86-87.
- Rosenthal, M. Rehabilitation of the adult and child with traumatic brain injury(2cd edition), 1990. Philadelphia, Davis Press.
- Plassman, B., and Evans,R. Aging with traumatic brain injury: the veteran’s story. Presentation to the 2cd Federal Traumatic Brain Injury Interagency Conference, 2006.
- Mehta, K.M., et al. Head trauma and the risk of dementia and Alzheimer’s disease: The Rotterdam Study. Neurology, 1999. 53: p. 1959-1962.
- Salib, E., et al. Head injury and the risk of Alzheimer’s disease: a case control study. International Journal of Geriatric Psychiatry, 1997. 12: p. 363-368.
- Colantino, A., et al. Aging with traumatic brain injury: long term health conditions. International Journal of Rehabilitation Research, 2004. 27(3): p. 209-214.
- Kreutzer, J et al. Traumatic Brain Injury: Family Response and Outcome. Archives of Physical Medicine and Rehabilitation, 1992. 73: p.777-778.
- Pike, J. Medical complications in severe head injury. New Horizons, 1995. 3: p. 534-538.
- Kerr, M.E., et al. Genetics and the central nervous system: apolipoprotein-E and brain injury. American Academy of Clinical Neuroscience Clinical Issues, 1998. IX: 524-p. 530.
- Mayeux, R., et al. Synergistic effects of traumatic head injury and apolipoprotein e-4 in patients with Alzheimer’s disease. Neurology, 1995. XLV: p. 555-557.
- Levin, H., & Kraus, M.E. The frontal lobes and traumatic brain injury. Journal of Neuropsychiatry and Clinical Neuroscience, 1994. 6(4): p. 443-454.
- Nemetz, P.N., et al. Traumatic brain injury and time to onset of Alzheimer’s disease: a population-based study. American Journal of Epidemiology, 1999. 149(1): p. 32-40.
- Jordan, B.D., et al. Apolipoprotein E-4 associated with chronic traumatic brain injury in boxing. Journal of the American Medical Association, 1997. 278(8): p. 136-140.
- Guidice, M. et al. Post-traumatic epilepsy following head injury. Brain Injury, 1987. 1: p.61.
- Russell-Jones, D.L., et al. The frequency and consequences of head injury in epileptic seizures. Journal of Neurology, Neurosurgery, and Psychiatry, 1989. 52: p. 659-662.
- Annergers, J.F., et al. Seizures after head injury: a population study. Neurology, 1980. 30: p. 683.
- Evans, R. Aging Issues and TBI. Presentation at the Lifetime Planning for Individuals with Brain Injuries and Other Cognitive Disorders, 2006. Austin, Texas.
- Bontke, C .F., et al. Medical complications and associated injuries of persons treated in the traumatic brain injury model systems programs. Journal of Head Trauma Rehabilitation, 1993. 8: p. 34-46.
- van Reekum, R., et al. Can traumatic brain injury cause psychiatric disorders? Journal of Neuropsychiatry and Clinical Neuroscience, 2000. 12: p. 316-327.
- Ripley, D. & Weed, R.O. Life care planning for acquired brain injury, in Life care planning and case management handbook, R.O. Weed, Editor. 2004, CRC Press: Boca Rotan p. 313-350.
- Jorge, R.E., et al. Depression and anxiety following traumatic brain injury. Journal of Neuropsychiatry and Clinical Neuroscience, 1993. 5: p. 369-374.
- Wood, R.L., et al. The impact of head injury neurobehavioral sequelae on personal relationships: preliminary findings. Brain Injury, 2005. 19(10): p. 845-851.
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