The term "cognitive reserve" has been around for approximately twenty years. Only more recently, however, has it become a concept that can be useful to the TBI litigator. Not only will a loss of cognitive reserve through TBI make your client more susceptible to a future of Alzheimer's disease or dementia, but it will cause this neuropathology to onset at a much earlier age. Defense attorneys and IME physicians are not generally prepared to defend a case over loss of cognitive reserve, and they often do not realize the immense future medical costs it can generate until it is too late. For these reasons, the concept should be utilized in every case of objective brain injury and should be part of every TBI case valuation.
What is Cognitive Reserve?
Cognitive reserve is really a fancy term for a common sense notion - that the more brain you have going into an accident or old age, the better your outcome will be. The concept of cognitive reserve ( CR) posits that once the brain reserve capacity of an individual is depleted past a certain threshold, clinical and functional deficits and symptoms will emerge. Thus, every client that you see with a brain injury went into the accident with a certain amount of protection against the ravages of dementia, old age, future brain injury or any other insult to the brain. As a result of an injury, the barrier against these rather horrendous futures is lowered and the individual has less CR. Since dementia robs us of our memories and thus CR can also be talked about as a barrier against loss of "selfhood." There are generally thought to be two models of CR - passive and active.
Passive Cognitive Reserve
This is also known as brain reserve and simply is an assessment of the amount of neuronal and other brain tissue a person has when they go into an accident or injury. Large head circumference (i.e., larger brain size) is associated with greater resilience against cognitive impairment (Perneczky R. et al. 2010; Kesler SR. et al. 2003). In a recent study involving Alzheimer's patients, head circumference was associated with reduced clinical symptomatology for equal rates of brain atrophy. (Perneczky R. et al. 2010).
Active Cognitive Reserve
Every one is born with and develops a certain amount of brain tissue, but the life an individual leads both prior to and after an injury can positively or negatively affect a person's cognitive reserve against that injury, as well as the recovery and level of cognition throughout his or her life after such an injury. For example, persons with higher IQ, higher educational levels, higher occupational attainment, higher physical activity levels and higher degrees of social connections experience less severe clinical and cognitive changes in the presence of Alzheimer, dementia or brain injury. (Tucker AM and Stern Y. 2011; Fairjones SE. et al. 2011; see generally Cognitive Reserve: Theory and Applications edited by Yaakov Stern). It is important to remember that, not only does active CR help protect against an injury, it also mediates and affects the long term outcome and life of the injured person thereafter. Unfortunately, as we shall see, TBI negatively affects almost all of the factors that affect active CR. CR is always lowered in the face of a permanent brain injury.
CR is one of the explanations for why we see such a broad variety of responses to objective brain injury. One client may have a single small lesion and may be unable to function at a previous job while another may have a dozen abnormalities on MR and report little by way of symptoms. The association between brain lesions and cognitive symptoms is not always linear, and CR helps explain why.
Cognitive Reserve and TBI
Unfortunately for victims of TBI, both active and passive cognitive reserve are negatively affected by a brain injury. Not only are millions of neurons lost in the brain because of injury (passive CR), the abilities and possibilities of building up or maintaining a high level of cognitive functioning or occupation (active CR) are lost or diminished. It is known that CR is a moderator of post-concussive symptoms in children and that children with lower cognitive ability and a complicated mild TBI were especially prone to longer term cognitive symptoms. (Fay. TB. et al. 2010).
Of special note is a study done by Ropacki and Elias (Ropacki MT. 2003) in which persons appearing for treatment for brain injury were classified into two groups - a negative premorbid history of closed head injury and positive premorbid history for closed head injury. The authors found that the patients with a positive history of closed head injury had diminished cognitive reserve secondary to the effects of the premorbid insult which resulted in greater cognitive decline following an additional closed head injury, in excess of what might otherwise be expected from that head injury alone.
This study and others can be used to argue not only for a reduction of CR from injury, but the CR literature can explain well documented phenomena of second and third head injuries being cumulative and can turn preexisting head injuries into positive features of your case.
How TBI Negatively Affects Active Cognitive Reserve
There has been a great deal of fascinating recent research involving the brain which describes how a person's environment and social ties are fundamentally important to brain growth and repair. When we talk about active CR, we are talking, in part, about the concept of "neuroplasticity" - the ability of the brain to rewire itself around damaged areas to preserve function. Most neurons in the brain, as it has been well known for sometime, do not repair or replace themselves after injury. Neuroplasticity is the brain's way of getting around the loss of neurons, either by rerouting function or utilizing a different part of the brain to take over for another. This is called "positive neuroplasticity". There is also a concept known as negative neuroplasticity - actions or environments which, rather than promote brain repair and enhancement, have a negative effect on brain repair and function,and can lead to cognitive and structural decline.
The research on these processes shows:
That animals in a zoo, rather than a wild environment, with less "complicated" lives show decreased "dendritic arborization." It is now known that in "enriched environments" the brain actually sends out and builds a higher number of branches in the dendrite of the neuron than it does in impoverished environments. Multiply this times the untold number of neurons in our brain and one can see the important effect that environment plays on the actual structure of the brain. This applies to humans as well;
Stimulating environments and exercise promote neurogenesis (the actual regrowth of brain tissue) in the dentate gyrus (Brown, et al. 2003; van Praag, et al. 2005). Exercise and cognitive stimulation regulate factors that increase neuronal plasticity and resistance to cell death. Environmental enrichment can actually prevent or slow the accumulation of Alzheimer's pathology (Lazarov O, et al. 2005);
In a study with Alzheimer's patients aerobic exercise improved executive function processes in women with mild cognitive impairment (Baker LD. et al. 2010; Nithianantharajah J. et al. 2011);
It has been shown that neuroplasticity, the fundamental mechanism of neuronal adaptation, is disrupted by mood disorders and chronic stress. Hippocampal atrophy has been repeatedly documented from major depression. (Pittenger C. et al. 2008);
Higher educational attainment, higher occupational attainment and higher social standing have all been shown to increase cognitive reserve;
Social ties and the richness of a person's environment provide cognitive reserve that protects against impaired cognition after a stroke (Glymour MM, et al. 2008). Many animal models of environmental enrichment (EE) have been used to show the influence of social stimulation on mitigating cognitive decline. (Redolat R. 2011)
Obviously, a TBI takes away brain cells and structure from the brain, but as can be seen, it negatively affects almost all of the other factors involved in positive neuroplasticity and recovery through active cognitive reserve, as well.
Education and Achievement: Generally, a person who has suffered a TBI will have a reduction in their cognitive abilities. Someone who was aiming for graduate school may settle for a two year degree or may not finish high school or college at all. Because of the educational and cognitive difficulties, the vocational achievement level is obviously lowered because of TBI. (See Himanen L. et al. 2011, 30-year follow up with all levels of TBI in Finland showed that working to normal retirement age occurred with only 11% of the subjects who worked and fulfilled a working career after TBI). Unfortunately, with TBI, there is a global "lowering" of the overall status of the patient because of injury. That is because all areas of life are affected at the same time - lesser or no job, inability to continue high level hobbies, drastically reduced richness and extent of social ties because of personality changes and withdrawal. Because of reduced impulse control or inhibition there is an increased risk of addiction, inappropriate behavior, criminal activity, or divorce. There is also the specter of increased risk of mental illness. Falling from your place in the world (and it does not matter if you started high or in the middle or low, you still feel the fall) is a very powerful stressor on the individual and this magnifies the problems described herein as well.
Physical Exercise: If there are additional orthopaedic injuries associated with the brain injury which do not allow for physical exercise, CR will be adversely affected. Likewise if the TBI is serious enough to cause balance problems or other impediments to exercise that should be taken into account as well.
Enriched Environment: Enriched enrivroment is very important, especially in patients who have suffered a frontal lobe injury. We know that the larger the social network, the more protective the CR. Very commonly those suffering from frontal lobe injuries are described as "becoming a loner." Social isolation, withdrawal, and disinhibition all play a part. Persons with TBI or frontal lobe injury are literally "on a different wavelength" than those around them, hampering the important social networks needed for full recovery and cognitive function. Likewise, we know that increased stress and/or mental disorders such as depression impede CR. Persons with TBI are vastly more likely to have a lifetime of anxiety, depression, or mental illness, than those without such an injury. EE is thus severely impaired for those with TBI. Finally, the richness and diversity of environment which has been noted to improve CR will likely be absent in the context of a TBI survivor.
Prior Closed Head Injury or Other Problems: A history of ADHD, learning disabilities, prior TBI are all well known impediments to full recovery, all other things being equal. In the context of CR, these preexisting conditions have already reduced the CR of the TBI victim before the accident even happened. Thus, the outcome, precisely because of these prior problems, is diminished.
All aspects of the human life that are wired for the brain to increase its CR are adversely affected by TBI. TBI survivors who have lost brain matter and cognitive function are thus doubly hampered - the brain injury affects the active CR processes adversely and healing and normalization are forever impaired and curtailed. It is a snowball effect.
Negative Effectives on Adult Neurogenesis
Despite almost universal belief to the contrary, it is now known that the adult brain is capable of producing new neurons through the human life span with or without injury to the brain. The brain, in some, but not all areas, engages in what is known as "compensatory neurogenesis" following brain damage, which is an aspect of neuroplasticity. Adult neurogenesis has been reported in the dentate gyrus (Altman & Das, 1965; Kaplan & Hinds, 1977; Eriksson et al., 1998), the olfactory bulb (Kaplan & Hinds, 1977; Altman, 1969, Luskin, 1993; Doetsch & Alvarez-Buylla, 1996), the amygdala (Bernier, Bedard, Vinet, Levesque, & Parent, 2002), several regions of the basal ganglia (Zhao et al., 2003; Chmielnicki, Benraiss, Economides, & Goldman, 2004; 2005). There is also research showing neurogenesis in the neocortex, but more research is needed as to where and how the frontal lobe is undergoing neurogenesis.
The brain can attempt to recover from damage by increasing neurogenesis in an area of the brain that can do so, known as local compensatory neurogenesis. Distal compensatory neurogenesis is when the brain builds up in areas other than the area injured to compensate for the loss. Finally, the brain can actually increase neurogenesis in an area that normally does not exhibit neruogenesis after an injury, a process known as induction of compensatory neurogenesis.
How is this relevant to a brain injury case? First, it is not well known by the defense that there is any neurogenesis at all. There is not much evidence of neurogenesis in the frontal lobes, but that day is coming. If an argument by the defense is made regarding neurogenesis or neuroplasticity as leading to full recovery, you need to respond that the factors negatively affecting active cognitive reserve are the same factors that affect adult neurogenesis. In other words, someone after a brain injury is going to have long term factors (Stress, anxiety, depression, lower status, education) and will face the same reduction in natural ongoing adult neurogenesis over what they could have expected without the accident in the long run.
This can been seen in the case of the hippocampus. Very often we see atrophy in the hippocampus associated with TBI cases involving memory loss. If you have a case involving hippocampus atrophy after an accident, you can argue that somehow the normal neurogenesis in the hippocampus has been adversely affected, otherwise there would not be atrophy (assuming non-related depression is ruled out). Are adult generated neurons produced after an accident fully capable of replacing developmentally created neurons? One of the possible causes of seizures post brain injury, could come from the fact that adult generated cells produce action potentials in the brain. (Nakatomi et al., 2002; van Praag et al., 2002).