Workers Compensation Guidelines in Treating Brain Injury

In 1977, Ed Breen of the Home Insurance Company identified a problem within the healthcare provisions for workers injured on the job. He approached a group of academics with a win-win solution, if it could be accomplished.

A number of individuals acquired catastrophic brain injuries in the scope of their employment with Mr. Breen’s company. Despite months of treatment in hospitals, these people were often left with tremendous levels of disability. Such disability translated to a very poor quality of life for the injured persons and their families, and a very high cost of continued care over the injured persons’ lifetimes.

Mr. Breen’s solution:

Reduce their levels of disability to an extent greater than that achieved at the hospitals, which leads to:

  1. Improvements in quality of life for the injured persons and their families
  2. Reduction in overall costs of lifetime care

So, advances were made over the last 40 years in treatment of people who have sustained brain injuries through work-related incidents. Worker’s compensation professionals specifically designed an entire continuum of treatment to manage the catastrophic claims of their parent companies in concert with health professionals. Treatment was extended to rehabilitation in post-acute care; results spoke for themselves with many more people returning to higher levels of productivity and overall health, thus reducing long-term health costs.

Worker’s compensation has improved brain-injured persons’ level of care from what it was in 1977. I ask now, is that enough?

In California, the guidelines that are used by carriers and utilization reviews organizations are simple. They are presented from the Medical Treatment Utilization Schedule (MTUS) below in their entirety:

“Patient rehabilitation after traumatic brain injury is divided into two periods: acute and subacute. In the beginning of rehabilitation therapist evaluates patient’s functional status, later he uses methods and means of treatment, and evaluates effectiveness of rehabilitation. Early ambulation is very important for patients with coma. Therapy consists of prevention of complications, improvement of muscle force, and range of motions, balance, movement coordination, endurance and cognitive functions. Early rehabilitation is necessary for traumatic brain injury patients and use of therapy methods can help to regain lost functions and to come back to the society. (Colorado, 2005) (Brown, 2005) (Franckeviciute, 2005) (Driver, 2004) (Shiel, 2001)”

The above definition does not reference the continuum of treatment that has been used consistently over the last four decades. The continuum is shown below:



It is said that if “one has treated one person with a brain injury, they have treated one person with a brain injury.” That is to say, no two people who sustain a brain injury are alike. Brain injury is one of the most, if not the most, complicated medical conditions to be encountered. And, brain injury is often accompanied by other system injury or involvement.

Not only is brain injury tremendously complex, but so must be treatment for brain injury. The above continuum provides for numerous treatment setting options, each with distinct dosing advantages for specific subgroups of patients who are experiencing unique constellations of deficits following brain injury. These deficits can include medical, physical, communicative, cognitive, psychological, and/or behavioral disorders requiring careful selection of the treatment setting most likely to properly dose treatment of the problems presented by any given individual.

So, why does the State of California operate under such simplistic guidelines?  Is this the best we can do?

One solution may be to adopt other guidelines that have far better information to offer pertaining to brain injury. Two of these include the Colorado Medical Treatment Guidelines (2012) and the Official Disability Guidelines.

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.