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Traumatic Brain Injury in the Aging Population: Litigating Medical Issues


By the year 2030 twenty-percent of the population will be 65 years of age or older. Individuals 85 years and older represent the fastest growing segment of the United States population. As a result, litigators must pay attention to this growing segment of client. There are special concerns and unique medical considerations present in litigating a TBI in the elderly that are not present in other cases. Some of those considerations are outlined below.


Many animal and human studies have provided substantial evidence that advanced age is associated with increased mortality and poorer outcome after TBI.

  • It is believed that neuroplasticity, or the ability of the brain to heal itself and reroute brain function around injured portions of the brain, decreases with age.
  • Atrophy of the brain increases with age and this in turn increases the distance between the brain and the skull, making dural vessels more vulnerable with shearing damage (as we saw in the case of Natasha Richardson). (Cummings and Benson, 1992).
  • In a comparison of patients older than and younger than 55 years old, matched for injury severity and gender, it was observed that the older patient group had a significantly longer mean linking the rehabilitation stay, higher total rehab charges and slower rate of improvement on functional measures. (Cifu et al, 1996).
  • In a comparison of psycho-social outcomes at one year post injury of patients with various ages a study found that patients 60 years old and older were significantly more disabled and required more supervision than those younger than 50 years of age. (Rothweiler et al. 1998)
  • In ages 66 to 79 years old, a Glascow Coma scale of less than 11 at the time of the injury was related to an increased risk of nursing home placement in that segment of TBI patients. (Ritchie et al 2000).
  • Plaintiff's counsel should stress the more adverse outcome in an aged client. Jurors are sensitive to the terrors of growing old in an impaired and possibly lonely state. Stress the high divorce rate among TBI victims (Rodger Ll et al. 1997). Stress that these clients face worse outcomes and lives. Stress that the "tipping point" in the life of such a client was the TBI: a once independent person can no longer live alone.


As we have seen earlier, the aging brain is less resilient and has a lower rate of recovery from an equal trauma to that of a younger brain. To further complicate matters, brain scans of clients 50 years of age and older can present challenges not found in representing younger braininjured individuals. In trying to distinguish between traumatically caused abnormalities on a brain scan and those caused by the normal or abnormal processes of aging, there are complex medical issues to be resolved to successfully litigate such a claim.

White matter hyperintensities (WMH), also known as white matter lesions (WML), small vessel disease or cerebral micro-hemorrhages all describe bright foci seen on T-2 weighted MRI images in the human brain. These small abnormalities are generally seen with increasing frequency in the brains of humans fifty years old and older. They are typically seen the deep periventricular region. Only 2% of those 75 years old would have a brain free of WMH.

WMH can be seen with aging and can be caused by trauma. The defense will blame the WMH on age. What are the risk factors of developing WMH? Hypertension and diabetes are the leading risk factors for the development of WMH. They are also seen in patients with a long history of migraine headaches (Porter A et al. 2005), and in increased numbers in people suffering from bipolar disorders.

The presence of WMH on your client's brain MRI must be explained or put into context in order to fully maximize a brain injury claim. While the existence of WMH can cause cognitive, balance and gait problems with an increasing load, there are millions of elderly persons with WMH who have no apparent cognitive defects. Acknowledging the presence of WMH is important not only to assess the past and future cognitive progress of the plaintiff, but the WMH need to be distinguished from MRI abnormalities of the brain caused by trauma to the patient.

Diffuse axonal injury (DAI) is a type of injury to the brain matter which commonly occurs from high speed velocity change accidents and serious falls. More recently, DAI has been shown to exist in a continuum from mild to moderate to severe brain injury cases (Topal NB et al. 2008; Schrader H et al. 2009). Historically it was felt that DAI was only present in severe or coma-inducing types of injuries, which is now not the case. Therefore if WMH or small sites of injury are seen on the brain MRI of a patient who has undergone such forces that would twist or stretch the brain, DAI abnormalities must be distinguished between age-related WMH if the patient is 40 years or older. The person under 40 (especially a person in their teens or twenties) would not be expected to have any WMH. The distinguishing factors in DAI lesions would be that most of the lesions are small (1-5mm), multiple and bilateral. They are predominantly located in discrete brain areas, especially at the gray/white matter junction at the frontal and temporal lobes and in the corpus callosum(Scheid, R et al 2003). The velocity change induced abnormalities on MRI are due to the slight difference in density of brain white matter and gray matter. When these tissues are subjected to extreme forces they blur together or tear. Brain injured patients as opposed to normals have a greater brain volume loss in comparison.

Currently, the literature attempting to verify the rate and extent of progression of WMH over time in elderly patients and what that means to their cognition is somewhat unclear. Several studies done in Austria (Schmidt, R et al 2002, 2003, 2005) did not find an association between the evolution of WMH and a decrease in cognitive functioning. However, the same researchers in 2005 (Danderflier, WM et al 2005), found the load of WMH was independently associated with general cognitive functioning in a sample of independently living Danes. Other studies have generally confirmed the relationship between the increased load of WMH and cognitive decline, atrophy, balance problems, and less ability to live independently (See Subcortical Hyperintensities Are Associated with Cognitive Decline in Patients with Mild Cognitive Impairment, Debette et al, 2007). Geriatric depression has been found to be associated with an increase load with WMH (Taylor, WD et al 2003).

In a 2009 study (Cristensen H. et al.) it was found that there was no direct evidence to support the argument that increased education and brain size was protective (the brain reserve hypothesis) of age-related vessel deterioration. They found that WMH and atrophy were not associated with cognitive changes in these elderly patients. However, in an earlier study (Dufouil C. et al. 2003) they found that education modulated the consequences of WMH on cognition and that participants with a higher level of education were protected against cognitive deterioration related to vascular insults to the brain.

Another way to fight defense assertions that WMH are causing all of your clients problems is to compare initial studies of the brain to later studies of the brain at the end of litigation. Comparing two different T-2 weighted images of the brain 2 to 3 years apart will show whether or not there is progression of WMH or whether it is static. If there is no interval change then the argument is in the favor of the plaintiff and will deter assertions that old age silent strokes are causing the current disabilities with the TBI patients.


Atrophy of the brain in the normal population occurs at a slow rate which increases with age. A young person with a TBI can and will suffer atrophy due to the widespread death of brain cells due to trauma. Erin Bigler has done work to suggest that the estimated average brain volume loss with severe TBI is 50cm3. When explaining this to the jury emphasize that billions of synapsis reside in one cubic mm of grey matter (2001b; Mackenzie et al 2002).

In an elderly TBI patient CT and MRI scans will show some atrophy of the brain regardless of the level of the injury. The trick is to determine which brain atrophy is due to the trauma and which is due to the effects of aging. CT scans taken at the time of the emergency room will not show atrophy related to the TBI. Atrophy will only show up months later, thus sequential CTs or MRIs can be compared with the initial CT at the ER to determine if trauma related atrophy has occurred. The natural aging atrophy rate will be much smaller than atrophy seen in the six month period following moderate or severe TBI, and thus they can be distinguished by your medical expert. An abnormal/TBI atrophy can be shown utilizing volumetric CT comparison.


  • Rule out hypertension, Diabetes, migraines and other causes of increased WMH or atrophy.
  • Have your expert radiologist show that the abnormalities seen in your client are located at the gray/white junction rather than being more highly distributed, thus indicating the presence of diffused axonal injury trauma induced abnormalities.
  • Obtain a favorable time-line of your client's condition to fight against the assertion of creeping cognitive decline because of small vessel deterioration. Before and after witnesses can be used to provide ammunition against assertions of pre-accident decline. A patient's general physician can be a highly effective witness on this and other issues.
  • Remember-if there is evidence of pre-existing WMH damage, you assert that the TBI has had a greater adverse effect because the client's brain had already lost cells to vascular disease.
  • If WMH are not shown on the emergency room CT (no MRI likely done until a few weeks or more after the trauma) and show up on MRI a few weeks later, compare this initial MRI to the following MRIs to show a static (i.e. traumatic) condition. This also proves that WMH are not age-related.
  • If both the above are happening (i.e. growing number of WMH after accident in serial MRI's) and there is some proof of objective injury (bruise or other focal bleed), an aggravation argument will work well.


Another difficult situation arises when a client has neuroradiological studies which show abnormalities consistent with Alzheimer's or early dementia (other than the presence of WMH which, was discussed above). Erin Bigler (Bigler ED et al. 2002) did an interesting study regarding the age-related changes in the temporal lobe vs. changes from TBI. They found that age-related changes cause minimal temporal lobe gyral, hypocampal, temporal horn and whitematter atrophy. They found that trauma produced disproportionate white-matter loss associated with increased temporal horn and CSF volumes, and substantial hypocampal atrophy. The hypocampus is relatively susceptible to injury (and thus atrophy) to due trauma. The hypocampus is now known to be an important center of activity regarding human memory. It is now possible to measure hypocampal volume and atrophy with MRI. The list of factors that can cause reduction of hypocampal volume which have been reported in human literature include:

  • Epilepsy, Alzheimer's, dementia, mild cognitive impairment, aging, traumatic brain injury, cardiac arrest, Parkinson's Disease, Huntington's Disease, herpes, Downs Syndrome, survivor of low birth weight, Cushions Disease, depressions, Post-Traumatic Stress Disorder, chronic alcoholism, schizophrenia, borderline personality disorder, Obsessive Compulsive Disorder, anti-social personality disorder. Larger hypocampal volumes have been correlated with autism and fragile x-syndrome. (Geuz E et al. 2005).

Therefore, again, differential diagnoses need to be ruled out if reduction of hypocampal volume is found in a client with supposed TBI damage. There is a study suggesting that the age related decline in MRI volumes of the temporal lobe occur, but that no age-related decrease in hypocampal volume occurs, at least not up to the age of 70 (Sullivan ED et al. 2009). Rates of hypocampal atrophy correlate with changes in clinical status and aging over time in elderly persons who lie along the cognitive continuum from normal to mild impairment to Alzheimer's disease. (Jack CR et al. 2000). Therefore, if other causes are ruled out and hypocampal atrophy is found in a client under the age of 70 then it would be relatable to trauma to the brain.

Ventricular atrophy is also commonly seen in the elderly. An MRI will show increased fluid spaces within the brain. It has been shown that ventricular expansion occurs faster in those developing mild cognitive impairment years prior to clinical symptoms, eventually more rapid expansion occurs 24 months prior to the emergence of clinical symptoms (Carlson NE et al. 2008). What makes this difficult, for litigation purposes, is that ventricular enlargement has been noted as a common sequelae as TBI. Ventriculonegaly was found in 39% of patients with severe head injury and 27% of those with moderate head injury. Increased ventricular size was evident four weeks after injury in 57% of the patients and two months after injury in 69% of the patients. Post traumatic ventriculonegaly was significantly correlated with outcome. (Poca MA et al. 2005).

Therefore, again, the defense will try to show MRI evidence of ventricular atrophy as being a result of pre-existing and age related cognitive decline or even Alzheimer's or dementia, rather than it being a result of TBI. In the case of ventricular atrophy from trauma, the cognitive decline occurs in the patient immediately following the trauma. This could be followed by ventricular enlargement within a few months. There will be no enlargement at the Emergency Room CT scan. This would be contrary to the study cited above when the ventricular enlargement precedes the emergence of dementia by a couple of years.(i.e. ventricular enlargement without cognitive problems). Therefore if pre-existing enlargement is shown (on Emergency Room CT) only an argument of traumatic aggravation of emerging dementia could be made.

Finally, ventricular enlargement can occur as a result of hydrocephalus. Hydrocephalus will often occur as a result of trauma to the head and brain. Most commonly, following a brain bleed the dead blood cells circulating within the cerebral spinal fluid can clog up the fluid drains in the brain, leading to increase intracranial pressure. This increased pressure leads to expansion of the ventricles and atrophy. If your client, following trauma, slowly develops a gait disturbance, that is the most common and first sign of physical symptoms from the emergence of hydrocephalus. Cognitive problems and death can follow. The lifetime insertion of a shunt (the cure) is a serious and costly medical expense.


Much research has been done in the past ten years on whether or not TBI is a risk factor for the developments of Alzheimer's Disease (AD). At present, the majority of studies indicate that TBI is a risk factor for AD, but there are some contradictory studies. When litigating the cases involving the elderly client, the threat raised by TBI of an increased risk for AD or dementia must be brought to the attention of the insurance company and/or the jurors.

Studies have shown that TBI is three times more common in patients with AD (Graves et al. 1990; Henderson et al. 1992; Mayeux et al. 1993; Mortimer et al. 1985). Nemetz et al (1999) involved a study of over 1,000 patients forty years old and older. There it was found that the history of remote TBI was associated with not an increased risk of development of AD, but it showed that TBI patients who developed AD in the median time between TBI and the onset of AD was 10 years vs. an age-adjusted median of 18 years in those without TBI. This suggests that TBI may reduce the time of onset of AD in vulnerable individuals. Although there is significant discrepancy in the literature, there still appears to be an increasing trend to support the hypothesis that TBI is a potential risk factor for AD. Accumulating evidence implicates traumatic brain injury as a possible predisposing factor in AD development (Van Den Heuvel C et al. 2007). Researchers have determined that the destructive cellular pathways that occur following traumatic brain injury are the same as those activated in AD. Persons who have died of AD, upon examination of the brain, often show a build-up of a toxic peptide called Beta Amyloid. This is similar to what happens in the brain after traumatic injury, when neurons die, there is a build-up of beta amyloid in the brain.

In a study of rats, Itoh, T et al. (2009) report increases in amyloid precursor protein (APP) in the region surrounding injury in the cerebral cortex. Results suggested that the overexpression of APP is related to the induction of Alzheimer's type dementia and that trauma to the brain is an important risk factor for the disease. Likewise, the chemical composition of those undergoing post-injury brain monitoring was looked at for levels of amyloid protein by microdialysis. Results suggested that high levels of these substances were found post injury, again showing a biological link between TBI and Alzheimer's (Marklund N et al. 2009).

However, the presence of amyloid deposition in a client's brain, especially if it were shown to pre-exist any traumatic brain injury, can not always be pointed to, to suggest cognitive impairment by the defense. Aizenstein HJ et al (2008) found that 21% of an unimpaired group of elderly persons showed evidence of early deposition of amyloid protein in the brain, which can be used to argue against the inevitability of cognitive decline when amyloid shows up as a preexisting condition in an elderly client's brain.


Diffused Tensor Imaging (DTI) MR is a new and very useful software package that can be run on a normal MRI machine. DTI looks at white matter tracts in the brain and whether or not water molecules can travel through them(meaning they have been broken) or around them(meaning they are intact). DTI can predict the approximate time of an acute injury by looking at the damaged tissue (MacDonald CL et al. 2007). DTI can show white matter abnormalities without hemorrhagic lesions being present. It can show damaged neural fibers related to cognitively dysfunctional TBI, and thus appears to be more sensitive to TBI than normal MRI.

DTI has been shown to be useful in distinguishing traumatic brain injury from dementia caused by Alzheimer's disease and in diagnosing Alzheimer's disease itself. It appears that DTI can show abnormalities in the splenium of the corpus collosum, as a marker for the development of Alzheimer's. (Duan JT et al. 2006). Using DTI the white matter in the splenium can be analyzed and can help distinguish between individuals on the continuum from normal to mild cognitive impairment (MCI) to full blown AD. (Ukmar M et al. 2008).


  • Have a neruoradiologist look at the initial CT scans if there is any question of preexisting Alzheimer's.
  • Get before and after witnesses to establish a temporal cognitive decline following the accident but not before the accident.
  • Remember that a TBI can hasten the onset of AD, so if there is a legitimate argument that it was pre-existing in some way then go for aggravation.
  • Stress that TBI and Alzheimer's have similar biological mechanisms.


Parkinson's disease and MS are commonly found in the elderly population with or without traumatic brain injury.

Medical studies on Parkinson's disease and traumatic brain injuries do not lead to the conclusion that trauma and brain injury can cause Parkinson's Disease. (Factor SA et al. 1988; Williams DB et al. 1991) A small study (Goetz CG, Stebbins GT 1991) found that patients with pre-existing Parkinson's disease compared to a controlled group of Parkinson's patients who suffered a head trauma in a car accident, the Parkinson's symptoms of the injured group were worse for several months, but came back to baseline. There is some research that suggests that some head trauma can shorten the time that Parkinson's disease can manifest itself in an individual, but the value of that research is unclear.

There is no current evidence that brain trauma can give rise to MS. However, the emotional stress of undergoing a serious accident, injuries, inconveniences, and changes in lifestyle associated with a serious accident, can aggravate the symptoms in a MS patient (Buljevac D et al, 2003; Mohr et al, 2000; Esposito et al, 2002). One of the cases I handled happened to involve a young lady who was wholly unaware that she had MS as she had been completely asymptomatic until shortly after a motorcycle accident. She had a spinal MRI a few months before the accident, which upon rereading showed an MS lesion to be in existence. In that case it was easy to show that the MS became manifest and symptomatic in this individual based upon the trauma. The trauma had sped up the process.


  • Make sure the pre and post treating physician records indicate an aggravation of symptoms or need for more medication within a couple of weeks of the trauma. It doesn't have to happen immediately, but the aggravation needs to be quick and it needs to be borne out by the medical records, not just the testimony of the patient and family.
  • If the client has low grade MS and is fully functioning, the accident can reduce their ability to work and engage in the activities of daily life.
  • A change in MS medication can be thousands of dollars per month, so developing an aggravation case involving such a change or increase in medical costs can be significant.
  • Current research will survive a Daubert or Frye challenge as to stress aggravating MS, but will not survive a challenge that trauma caused MS.


A little known adverse consequence of TBI in middle-age or in the elderly is that almost all private insurance plans providing long term nursing home care will automatically disqualify an applicant who has suffered an objective traumatic brain injury. How much of a problem is this? How does this play into TBI litigation?

If a family or an individual has the financial means of obtaining long-term care insurance prior to receiving a TBI injury and planned to obtain it, the attorney for that client should investigate the long term financial implications of the injury and how it will play out in the field of long-term care. A review of many of the leading insurers' applications for long term care insurance shows the difficulty that TBI clients will face when trying to make such application. If any of the application questions listed below are answered in the affirmative, all of the applications state on page one that it is unnecessary to fill out the rest of the application as the long-term care insurance will not be offered if any answer is yes. (For example, if you answered "yes" to any question in this insurability profile we recommend you do not submit this application.) Some examples include:

  • Brain disorder
  • Do you have any progressive memory disorder or memory disorder for which you take medication?
  • Have you ever been diagnosed with chronic memory loss, frequent or persistent forgetfulness or organic brain syndrome?
  • Have you ever been medically diagnosed as having frequent or persistent forgetfulness or memory loss? Organic brain syndrome?

If the client is obviously going to fail in their application for long-term insurance due to a litigated TBI injury, steps need to be taken to determine the value of the loss of that future benefit to the individual. A 2007 survey by Genworth (Genworth.com) found that the costs of single room nursing care on an annual basis fluctuated wildly with a high in Alaska of $196,000.00 a year and a low in Louisiana and Missouri of $44,000.00 a year. They found there was a 5% rate of annual medical inflation on nursing home care. The annual costs can be determined on a state by state basis. The average stay in a nursing home is two to three years with five years being the longest average stay. Therefore, the claim would be that the individual and their family would have to private pay for long-term nursing care in the clients lifetime at an average of $75,000.00 a year times 3 to 5 years.

Because the injury sustained by the client is significant enough to block the ability to obtain long-term care, it also would be seen as significant enough to increase the likelihood of dementia or Alzheimer's disease. Thus, the TBI causes a Catch 22, one-two punch against the client - they are more susceptible to the need for long term care because of declining cognitive ability in their future, and at the same time they are blocked from the ability to take out insurance for that particular future concern.


As baby boomers age, the percentage of clients who may have used marijuana has increased. In defense of TBI claims, defense attorneys will latch upon any allegations or proof that the client has smoked or does smoke marijuana. This can come up through direct testimony of the Plaintiff, testimony from friends or relatives, a failed drug test or from medical records.

In most jurisdictions the admissibility of this information would be subject to the balancing test of whether the probative value of such information outweighs the prejudicial effect of such information on the jury. The defense will try to establish that the use of marijuana is relevant because of the following:

  • it had a downward effect on neuropsychological tests battery results;
  • it adversely affects the recovery of the client from TBI;
  • it adversely affects wage and job aspects of the claim.

However, recent medical research can be cited by the Plaintiffs to suggest that the active ingredient in marijuana "cannabinoids" are now thought to play an important role in actually protecting the brain from neuro-trauma following injury. The research cited below can be used to offset the mild amount of research that can be thrown towards the Plaintiff to suggest decreased recovery or test results due to occasional marijuana use. If other Plaintiff or defense physicians can be given the research cited below, they can address the possible protective effects of the marijuana use and thus neutralize or take away the defense's ability to have the whole issue become admissible at trial. The research is as follows:

  • "Endocannabinoids and Traumatic Brain Injury" (Mechoulam, R 2007). This study showed that there are various neuro-protective effects of cannabinoids.
  • "The Therapeutic Potential of the Cannabinoids in Neuroprotection" (Grundy RI, 2002). The study cites the ability of cannabinoids to modulate neurotransmission and to act as anti-inflammatory and antioxidative agents. Both post trauma inflamation and post traumatic oxidation are methods of secondary brain injury following the acute phase.
  • "Therapeutic Potential of Cannabinoids in CNS Disease" (Croxford JL, 2003). This study found that evidence suggest cannabinoids may prove useful in Parkinson's disease in that dexanadinol (HU-211), a synthetic cannabinoid is currently being assessed in clinical trial for traumatic brain injury and stroke.
  • "Cannabinoids as Therapeutic Agents for Ablating Neuroinflammatory Disease" (Cabral GA et al. 2008). When studying the early phases of post traumatic brain inflammation they noted that the cannabinoid's receptor system may prove therapeutically manageable in reducing neuropathogenic disorders, including closed head injuries.

Using some of the above research, a Motions in Limine should be drafted to exclude any reference to marijuana use, arguing that any "adverse" consequence of use is countered by its possible "benefit" and that the whole issue is based upon criminalizing the plaintiff.



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