Neurodegenerative Processes and Brain Injury

Brain injury can predispose the brain to neurodegenerative processes and may be implicated in a host of diseases such as chronic traumatic encephalopathy (CTE), Parkinson’s disease multiple scelerosis, amyotrophic lateral scelerosis, stroke, epilepsy, Alzheimer’s disease and others. The simplified explanations in this post allow us to consider whether we are monitoring and treating neuroinflammatory influences chronically and properly after brain injury.


  1. We do not know when neurodegenerative processes fully abate after an injury, or whether they actually do at all. Because we have no true clinical biomarkers that alert us to the cessation or the continuation of pathophysiologic processes within the brain, we instead equate observed improvements in outward function as hallmarks of improved neurophysiologic function.
  1. We do not know if neurodegenerative processes vary with different genomic factors.
  1. We do know that metabolism within the brain changes after injury, at least temporarily. We also know that metabolism of oxygen, glucose, and lipids produce undesirable waste products that are ideally removed from the brain.
  1. We recognize there seems to be a necessary interplay between proinflammatory and anti-inflammatory processes in the brain and that the endocrine and immune systems interact inextricably to produce a metabolic homeostasis. We have evidence that alterations in the blood-brain barrier (BBB), designed to control what passes into and out of the brain, may persist over long periods of time and change with aging.
  1. Microglia are cells in the brain responsible for dealing with pathogens and/or damaged, dying or dead cells within the brain. After brain injury we know that microglial activation and deactivation changes to an abnormal process whereby microglia do not necessarily deactivate. After brain injury, the metabolic waste products may not be removed from the brain via the BBB efficiently, and may serve to excite inflammatory processes within the brain.
  1. Infections outside the brain that are normally prevented from entering the brain may actually do so with greater ease, and as a result, microglia sensitivity may be primed, resulting in their overactivation.

Associated Considerations

  1. What behavioral influences ought to be considered for chronic management after brain injury? They may include sleep, diet, and exercise. Each of these is known to influence inflammation and immune system function around the body.
  1. Endocrine interventions may provide for neuroprotection and facilitation of improved metabolic function and reduction of metabolic stress within the brain. This results in healthier cells, less programmed cell death, and perhaps longer functioning of previously uninjured cells, thus preserving neurologic reserve and probably function. So hormone replacement therapy may be beneficial in providing neuroprotection and restitution of metabolic function.
  1. Additionally, endocrine therapies that seek to accelerate recovery by pursuit of high normal ranges in replacement therapies or supraphysiologic levels for a treatment period, should perhaps be explored.
  1. Interventions may be useful that actively address neuroinflammation pharmacologically. Given the complexity of neuroinflammatory processes and their consequences, it seems probable that a multifaceted approach will be necessary to fully facilitate an interruption of what can be self-perpetuating inflammatory processes within the brain or prevent recurrent reactivation of primed inflammatory processes.

So, we must consider whether an approach that addresses behaviorally accessible avenues such as diet, sleep, and exercise combined synergistically with endocrine, immune dietary and exercise interventions to quiet inflammatory processes in a previously injured brain has utility in accelerating recovery, furthering recovery, providing neuroprotection for residual, as of yet, uninjured cells, and/or preventing neurodegenerative processes to be accelerated over those of normal aging.


Value-based treatment and outcomes is a largely discussed topic in national healthcare today. Unfortunately though, there is not a unanimous definition of “value” within traumatic brain injury (TBI) rehabilitation.

The value-based treatment and outcomes model promotes the most effective and results driven practices to be implemented in the most cost-effective ways available. Value is the perceived benefit to a patient’s health, as determined by the difference created from the inverse relationship between better treatments and lower costs.

The greater the difference, the greater the value. By this logic, a person would determine the value of a new clothing item not only by the article’s look, fit, durability, etc., but also by accumulating those benefits and weighing them in comparison to the cost of the item.

I argue that the term “value” in value-based treatment and outcomes ought to refer to the value received by the patient, and less so, perhaps, by the payer.

In this example, the purchaser is also the person ascribing perceived value to the purchase, whereas the party paying for a healthcare service is rarely the party receiving the service. It is in this divide between the paying party and the receiving party where the perception of value often varies.

In healthcare, value to the paying party may be defined as a need to meet the contractual obligation of coverage in the most cost-effective manner possible. Reiterating value-based treatment and outcomes, the two components necessary are the most effective care and the most cost-effective means.

Simply meeting the contractual obligation of coverage, however, is not always sufficient to the provision of most effective care, and many times this approach unfortunately reduces the discussion of treatment to that of costs involved, thus limiting the duration of TBI residential programs and rehabilitation treatments.

The transition of health insurance from nonprofit to for-profit and the need to continually satisfy shareholders’ financial expectations can stand in tension to the need to provide the most effective care, especially if that care seems more costly. Furthermore, the tremendous complexity of acquired brain injury is unrivaled by any other medical diagnosis. This complexity is rarely understood by health plan professionals whose job is to review benefits and coverage and approve an individual’s treatment, resulting in cost-based decision making over efficacy-based decision-making. 

On the other hand, the value of the same services to the person receiving them may place a greater level of importance on most effective care. For example, while being able to ambulate with a normal gait and endurance may be of great value to the patient, the payer may want to forego costs necessary for such an end result and instead settle for the patient’s ability to ambulate with less efficiency and for very simple purposes, i.e., short distances or with supervision. 

I argue that the term “value” in value-based treatment and outcomes ought to refer to the value received by the patient, and less so, perhaps, by the payer. Do individuals with TBI ascribe the highest value to a “functional” outcome, or to an outcome that represents the maximization of their post-injury ability? Is “functional” the highest value outcome, and if, so, for whom? 

That the payer may find relatively little motivation and, therefore, value in paying for the most effective service available is, unfortunately, disconnected from the values of the person needing or receiving the services. And, that the patient may not be aware of all that they should be about treatment choices, treatment efficacy, and prognosis, leaves patients remarkably vulnerable to treaters, payers and others.

This disconnect serves as a disquieting confound to the value-based treatment and outcomes model in healthcare. The value intended to result from a difference between most-effective care and the most cost-effective means is diminished to a value found only through the latter half of the equation, cost-effectiveness.

Given the strikingly different definitions of value between a payer and a patient, the issue can be ethically challenging and quite pointed. Ultimately, the obligation for all parties should be to the value-based treatment and outcomes model, and this model should not be jeopardized.

Social Isolation after Brain Injury

Effects of brain injury can permeate beyond reckonable and documented impairments. Social isolation is one such often unmeasured and unnoticed effect. Stark contrasts in lifestyle before and after brain injury, such as social isolation, impact the injured person, family members, and friends.

Additionally, social isolation shares a causal relationship with depression. Social isolation’s potential to cause such widespread and negative changes after brain injury necessitates serious consideration and investigation.

Brain injuries can rob individuals of physical, communicative, cognitive, emotional and behavioral skills. When these skills are impaired, individuals are challenged with the difficulty of reintegrating into their pre-injury lifestyle. No longer providing the same level of support for their family and friends, their role shifts and relationships are altered. Self-worth is largely derived from social interaction with others. A life redefined by injury is a monumental shift, and in that transition, social isolation often awaits.

Though a downward spiral toward social isolation is caused by disconnect from family and friends, they are not necessarily to blame. The injured person’s difficulties in returning to work may bring about financial struggle. They may depend heavily on friends and family for daily care. Behavioral changes can be enough to cause significant discomfort for loved ones.

Stress, responsibility, and worry come with the support of a brain injured person. Many of those involved in supporting roles will drift away or lessen their involvement substantially. Those who do stay may still feel disconnected from their injured loved one. As such, through no fault of any one party, social isolation sets in as a considerable problem. The social isolation associated with brain injury perpetuates the stark contrasts in lifestyle listed above, and consequentially negatively impacts the brain injured person and those in their sphere of support.

Additionally, social isolation’s causal relationship with depression is a dismal outlook for people with brain injury. The incidence of depression five to seven years after brain injury ranges between 40 to 60% according to research literature. Though social isolation is not definitively the cause of each case of depression, there is enough room to believe it’s a significant contributor.

Through the instances explained above, social isolation is a serious problem for both the individual with brain injury and their family members. Detection of social isolation is difficult in its complexities, and solutions are few and far between. There is a significant need for investigation and development of solutions to address social isolation.

Depression is best treated by a combination of counseling, medication, and exercise. Counseling can focus on individuals’ reactions to their circumstance, and efforts to change their circumstance. Counseling can provide coping mechanisms for the injured person and family. Medications, when appropriately applied, can be used to effect the neurotransmitter systems involved in depression as well as help with sleep and anxiety. Exercise can bring about improved feelings of well-being and help to regulate the body’s production of endorphins.

Above all, depression mandates the involvement of professionals who can undertake careful investigation of the cause of depression, and numerous treatment modalities for depression.