What is Traumatic Brain Injury?
The brain has about 10 billion capillaries in a highly specialized endothelial lining flush with tight junctions, basement membranes, pericytes & astrocyte projections. This blood-brain barrier (BBB) admits molecules sized at 400 daltons and less (as a comparison, alcohol is 200 daltons per molecule which is how it can land in our stomach and impact our brain to get us drunk so quickly) & uses transportors for everything bigger for influx & efflux (waste). This is the brain’s first protection against external chemical and metabolic assaults.
With an injury like a concussion, the initial injury can include shearing & compression of brain tissue, possible hypoxia, ischemia, edema & perhaps elevations in intercranial pressures which can be dangerous for tissue. There may also be disruption of the blood vessels, axons & cell membranes resulting in possible further decreased oxygen delivery to neurons and an increased need for glucose in the brain to address all these traumas. The greater need for influx of nutrients and oxygen and greater efflux of wastes results in a more permeable BBB, aka ‘leaky brain’.
Secondary damage can result from a significant increase in free radicals & oxidative stress leading to further damage of nerve cells, an increase in neuronal inflammatory mediators acutely the first month & subacutely the first 6 weeks but can become chronic. Other possible damage includes an increase in brain glutamate & increased intracellular calcium & neuronal death, neurotransmitter dysfunction (may need dopamine/serotonin /acetylcholine support), excitotoxicity (leading to increased free radical formation, inflammation, and brain edema), disrupted brain cell metabolism, mitochondrial damage & poor cellular function.
Inflammation and excitotoxicity are the initial neuroprotective mechanism. Brain tissue damage releases the endogenous danger signals (extracellular ATP & HMGB) which bind to TLR4 on neurons & glia to activate an immune response. Activated microglia can shift from anti-inflammatory to pro-inflammatory & migrate to injured tissue which is how we heal- we need to be alerted to a problem in order to address it. This process, however, also results in an increase of proinflammatory cytokines & reactive oxygen species.
A chronically excitotoxic state, perhaps mediated by TNFa, IL1b, IL6 and other mediators, is where the inflammation exceeds its initial usefulness and can begin to beget its own problems. Overstimulation of NMDA & AMPA with excessive intracellular calcium can lead to enzyme activation, which can damage the neuronal cytoskeleton, membranes & DNA. Ongoing mitochondrial damage can result in loss of mitochondrial ATP production. Chronic microglial activation may mediate CTE (chronic traumatic encephalopathy). Disruption of the physical structure of axons and dendrites can interrupt communication and may persist symptomatically for years.
The leaky BBB may also allow food antigens, abnormal peptides, viruses or other noxious chemical or metabolic toxins into brain circulation. As the body/brain try to clean up these further insults with the typical pathway of communication via inflammation, auto-reactive antibodies, T lymphocytes, damaged astrocytes, free radicals, proinflammatory cytokines and glutamate may damage brain proteins and structure further, resulting in poor removal of wastes from the brain, poor clearance of excitotoxins & poor healing of TBI. This all serves to lower brain reserve and resilience.
Regarding concussion or other head trauma:
Even if hitting your head doesn’t cause a skull fracture or other obvious wound or injury, your squishy brain may still bump up against the inside of your very hard skull. There are mechanisms in place to cushion this blow, but if you find yourself with symptoms of forgetfulness, agitation, headache or others, you may have a concussion. It’s important to address this aggressively to care for your brain.
The issue is that when the brain gets hurt, the blood-brain barrier that protects the brain from the rest of the body gets more permeable. This happens so the body can get more healing factors to the brain and take away waste products from injuries, but it also means that non-desirable elements like toxins and organisms can more easily pass into these same elements. This is even worse if you’ve had previous head injuries/concussions (they are cumulative, meaning damage accumulates and worsens with each injury), if you’re over 55 years old, and if you have more inflammation already in your system (poor diet, poor sleep, lots of stress, old trauma, sedentary life, etc). This program below addresses all of these issues.
What is treatment like at Center for Healing Neurology?
Our primary goal is to restore our patients to their daily routine and active life. As a neurology team, we have access to pharmaceuticals that are appropriate for each individual patient. We also use our integrative medicine training for nutraceuticals, nutritional guidance and biocranial therapy.
Our program is personalized based on the mechanism of action, the symptoms, and the impact on quality of life. It includes a complete history and physical examination and further diagnostics which may include imaging, autonomic nervous system testing, neuroendocrine evaluation, electrophysiology, and more. Treatment focuses on returning functionality to your life in the best way we can and may include appropriate use of pharmaceuticals, nutraceuticals, nutritional guidance, biocranial therapy, compression training, regenerative medicine, and more.
The critical work is to limit excitotoxicity after brain injury and offer the brain luscious calm in which to address damage and completely resolve all inflammation. This is why typical neurorehabilitation has ‘brain rest’ as its foundation followed by slow retraining.
Traumatic Brain Injury Program
We help you:
A) Decrease neuroinflammation
B) Enhance perfusion of oxygen and nutrients
C) Encourage and guide best healing with diet, lifestyle, and nutraceutical support
D) Regenerate neuronal cellular components and work to restore optimal performance
E) Prevent further progression as well as modify risks for cognitive decline