TBI & Concussion Recovery: The Functional Approach
A concussion is not a bruise on the brain. There is no bleeding, no structural damage visible on CT or standard MRI.
TBI & Concussion Recovery: The Functional Approach
The Invisible Injury
A concussion is not a bruise on the brain. There is no bleeding, no structural damage visible on CT or standard MRI. This is precisely why it has been dismissed, minimized, and undertreated for decades. The patient looks fine. The scan looks fine. Therefore the patient must be fine.
They are not fine.
A concussion is a neurometabolic injury — a cascade of biochemical disruption that impairs how neurons produce energy, communicate with each other, and regulate inflammation. The damage is functional, not structural. And understanding this cascade is the key to treating it.
The Neurometabolic Cascade
In 2001, Christopher Giza and David Hovda at UCLA published the landmark description of the neurometabolic cascade of concussion — updated in 2014 — that transformed our understanding of what happens inside a concussed brain.
Phase 1: Ionic flux (seconds to minutes). The mechanical force of impact stretches neuronal cell membranes, opening ion channels indiscriminately. Potassium floods out of cells. Sodium and calcium flood in. The neuron depolarizes wildly. To restore ionic balance, the sodium-potassium ATPase pump goes into overdrive — consuming massive amounts of ATP (energy) at exactly the moment the cell is least capable of producing it.
Phase 2: Glutamate excitotoxicity (minutes to hours). The mechanical disruption and ionic chaos trigger massive release of glutamate — the brain’s primary excitatory neurotransmitter. In normal amounts, glutamate is essential. In excess, it is toxic. Glutamate binds NMDA receptors, opening calcium channels further. Intracellular calcium accumulates to dangerous levels, activating destructive enzymes (calpains, caspases) that damage the cell’s internal structures.
Phase 3: Energy crisis (hours to days). The cell is simultaneously burning through ATP to restore ionic balance and unable to produce ATP efficiently because calcium overload has impaired mitochondria. This energy crisis — high demand, low supply — is the metabolic hallmark of concussion. The brain becomes hyperglycolytic initially (burning through glucose reserves), then shifts to a prolonged period of metabolic depression where neurons cannot produce adequate energy. This phase can last 7-10 days in adults and potentially longer in children and adolescents.
Phase 4: Neuroinflammation (days to weeks to months). Microglial activation begins within hours and can persist for weeks, months, or in some cases years. The inflammatory cytokines (IL-1beta, TNF-alpha, IL-6) released by activated microglia impair synaptic function, reduce BDNF, and create oxidative stress. Axonal injury — stretching and shearing of the long white matter tracts — triggers Wallerian degeneration that unfolds over weeks.
Phase 5: Vulnerability window. During recovery, the brain is metabolically fragile. A second impact during this window — before the neurometabolic cascade has resolved — can produce catastrophic, disproportionate injury. This is the basis for return-to-play protocols and why premature clearance is dangerous.
Why Rest Alone Is Not Enough
For years, the standard concussion prescription was “rest in a dark room until symptoms resolve.” This approach — cocooning — felt intuitively right. The brain is injured, so protect it from all stimulation.
Michael Collins and colleagues at the University of Pittsburgh Medical Center began challenging this paradigm around 2014-2016, publishing data showing that prolonged strict rest actually delayed recovery. Patients who rested for more than 1-2 days had worse outcomes than those who began gentle, sub-symptom-threshold activity earlier.
The paradigm has shifted to active recovery. After an initial 24-48 hours of relative rest, gradual reintroduction of physical and cognitive activity — staying below the symptom exacerbation threshold — promotes recovery. The brain needs appropriately dosed activity to heal. Complete deprivation of input can actually delay neuroplastic recovery.
The key phrase is sub-symptom threshold. Activity should not worsen symptoms. If walking for 10 minutes triggers a headache, the dose is 8 minutes. Gradual, calibrated challenge — not avoidance, not pushing through.
Assessment: Finding the Broken Pathways
A concussion is not one injury. It is a collection of pathway-specific injuries that vary from patient to patient. Effective treatment requires identifying which pathways are impaired.
ImPACT testing — a computerized neurocognitive assessment measuring verbal memory, visual memory, processing speed, and reaction time. Widely used for baseline and post-injury comparison in athletes. Useful but limited — it captures cognitive function but misses vestibular, oculomotor, and autonomic dysfunction.
VOMS (Vestibular/Ocular Motor Screening) — developed at the University of Pittsburgh. A structured assessment of smooth pursuits, horizontal and vertical saccades, convergence, VOR, and visual motion sensitivity. Each component is scored for symptom provocation. VOMS identifies the specific vestibulo-oculomotor pathways that are disrupted — and these are often the primary drivers of persistent symptoms (headache, dizziness, difficulty reading, motion sensitivity).
Balance assessment — Balance Error Scoring System (BESS), Sensory Organization Test, dynamic posturography. Evaluates the vestibulospinal system and sensory integration.
Neurocognitive testing — formal neuropsychological evaluation for persistent cases. Working memory, processing speed, executive function, attention, verbal and visual memory.
Autonomic testing — heart rate variability, orthostatic vital signs, tilt table if POTS is suspected. Autonomic dysfunction is one of the most underrecognized consequences of concussion.
Metabolic Support: Feeding the Recovering Brain
The neurometabolic cascade creates specific nutritional demands. The brain needs substrates for energy production, membrane repair, neurotransmitter synthesis, and anti-inflammatory defense.
Omega-3 Fatty Acids (DHA)
DHA is not supplementary — it is structural. It comprises 40% of the polyunsaturated fatty acids in neuronal cell membranes. After concussion, membranes are damaged and need rebuilding.
Julian Bailes’ 2011 rat study showed that DHA supplementation before and after TBI significantly reduced axonal injury markers. Julian Mills’ 2011 work demonstrated that omega-3 supplementation reduced brain injury severity in animal models. Michael Lewis has championed high-dose omega-3 for TBI recovery in humans, advocating 2-4 grams of combined EPA/DHA daily, with emphasis on DHA.
The protocol: 2-3 grams of DHA daily for acute recovery. Use triglyceride-form fish oil. Begin as soon as possible after injury.
Creatine
Creatine is not just for athletes. It is a phosphate donor that regenerates ATP — exactly what the energy-depleted post-concussion brain needs. Sakellaris et al. (2008) studied creatine supplementation in pediatric TBI patients (ages 1-18) and found significant improvements in cognitive and behavioral outcomes, reduced ICU stay, and reduced disability.
Dose: 5-10 grams daily for acute recovery, 3-5 grams daily for maintenance. Creatine monohydrate is the most studied form.
Magnesium
Intracellular magnesium drops precipitously after TBI — Vink and colleagues documented this extensively. Magnesium blocks the NMDA receptor (reducing excitotoxicity), supports mitochondrial ATP production, and has anti-inflammatory properties. Magnesium L-threonate is the preferred form for CNS penetration. Dose: 1-2 grams daily (providing 96-144 mg elemental magnesium per gram of threonate salt).
B Vitamins
The methylation cycle — which is essential for neurotransmitter synthesis, DNA repair, and myelin maintenance — is disrupted after TBI. Methylfolate (800-1000 mcg), methylcobalamin (1000-5000 mcg), and P5P (active B6, 50 mg) support recovery.
CoQ10 and PQQ
Mitochondria are directly damaged in concussion. CoQ10 (ubiquinol form, 200-400 mg daily) supports electron transport chain function. PQQ (20 mg daily) stimulates mitochondrial biogenesis — the creation of new mitochondria to replace damaged ones.
Anti-Neuroinflammation Strategies
Curcumin
The BBB-crossing formulations are essential — standard curcumin does not get into the brain in meaningful amounts. Longvida (developed at UCLA — poetic, given that Giza and Hovda’s cascade work was also UCLA) has demonstrated BBB penetration in human studies. Dose: 400-1000 mg daily. Curcumin inhibits NF-kB, reduces microglial activation, and scavenges reactive oxygen species.
Resveratrol and SPMs
Resveratrol (200-500 mg trans-resveratrol daily) activates SIRT1 and Nrf2 pathways, supporting antioxidant defense. Specialized pro-resolving mediators (SPMs — resolvins, protectins, maresins, derived from omega-3s) actively turn off the inflammatory cascade rather than merely suppressing it. SPM Active (Metagenics) provides concentrated SPMs.
Lion’s Mane Mushroom
Hericium erinaceus stimulates nerve growth factor (NGF) synthesis — demonstrated by Kawagishi, expanded by Mori and colleagues. NGF supports neuronal survival, axonal regrowth, and remyelination — all critical after TBI. Dose: 1-3 grams daily of a dual extract (fruiting body + mycelium, capturing both hericenones and erinacines).
Hyperbaric Oxygen Therapy
Hyperbaric oxygen therapy (HBOT) delivers oxygen at greater-than-atmospheric pressure, dramatically increasing dissolved oxygen in plasma and cerebrospinal fluid. The brain after concussion is often hypoperfused — reduced blood flow means reduced oxygen delivery, perpetuating the energy crisis.
Paul Harch has been the most vocal clinical advocate, publishing case series showing improvements in post-concussion symptoms with HBOT at 1.5 ATA. Boussi-Gross et al. (2013) published a randomized controlled trial showing significant improvements in cognitive function and brain metabolism (SPECT imaging) in patients with chronic post-concussion syndrome treated with HBOT (1.5 ATA, 60 sessions). Hadanny et al. (2022) demonstrated improvements in brain MRI microstructure and cognitive function in a randomized controlled trial.
Protocol: 1.3-1.5 ATA, 60-minute sessions, 40-60 sessions total. Some practitioners use mild HBOT (1.3 ATA) which can be done in portable chambers. Higher pressures (2.0+ ATA) are used for acute severe TBI in hospital settings.
The mechanism is not simply “more oxygen.” HBOT upregulates hypoxia-inducible factor (HIF) signaling, stimulates angiogenesis (new blood vessel formation), mobilizes stem cells, and reduces neuroinflammation.
Vestibular Rehabilitation
Vestibular dysfunction is present in 50-80% of concussion patients and is one of the strongest predictors of prolonged recovery. The vestibular system takes a direct hit in most concussions because of its anatomical position — the inner ear structures and brainstem vestibular nuclei are vulnerable to rotational acceleration forces.
Gaze stabilization exercises — VOR x1 and x2 training. The patient fixates on a stationary target while moving the head horizontally and vertically, gradually increasing speed. This retrains the vestibulo-ocular reflex to accurately stabilize vision during head movement.
Habituation exercises — repeated exposure to movements or visual environments that provoke dizziness, at sub-symptom-threshold intensity. The brain gradually recalibrates its response. Brandt-Daroff exercises are a classic habituation protocol.
Balance training — progressive challenge: firm surface with eyes open, firm surface eyes closed, foam surface eyes open, foam surface eyes closed, tandem stance, single leg stance, with head movements, with cognitive dual-tasking. Each progression challenges a different aspect of sensory integration.
Vision Therapy
Convergence insufficiency — the inability to maintain inward eye alignment when focusing on near targets — is one of the most common and most underdiagnosed consequences of concussion. Patients report difficulty reading, blurred vision at near, headache with screen use, words “swimming” on the page. Standard eye exams often miss it because visual acuity (the Snellen chart) is normal.
Convergence training — pencil push-ups, Brock string exercises, vectogram training. Saccadic training — improving the speed and accuracy of rapid eye movements. Prism lenses — yoked prisms or micro-prisms can provide immediate symptom relief while rehabilitation progresses, by shifting the visual midline and reducing the demand on impaired pathways.
Neuro-optometrists (NORA or COVD-certified) are the specialists trained in post-concussion vision rehabilitation.
The Cervical Spine Connection
The upper cervical spine — atlas (C1) and axis (C2) — is intimately connected to the vestibular system, the vertebral arteries, and the brainstem. Whiplash-type forces that cause concussion simultaneously injure the cervical spine in the majority of cases. Suboccipital muscle tension and upper cervical joint dysfunction can perpetuate headache, dizziness, and autonomic symptoms long after the brain itself has healed.
Manual therapy — osteopathic manipulation, chiropractic adjustment of the upper cervical spine, soft tissue work to the suboccipital muscles (rectus capitis posterior major and minor, obliquus capitis superior and inferior) — often produces dramatic improvement in post-concussion symptoms, particularly cervicogenic headache and cervicogenic dizziness.
The differential diagnosis between vestibular-driven and cervicogenic dizziness is critical: cervicogenic dizziness is provoked by neck movement or sustained postures, relieved by addressing cervical dysfunction, and is not associated with true vertigo (room spinning).
Autonomic Recovery
Post-concussion autonomic dysfunction manifests as exercise intolerance, resting tachycardia, orthostatic symptoms, heat intolerance, and impaired heart rate variability. The autonomic control centers in the brainstem (medulla) are vulnerable to concussive forces.
HRV biofeedback — resonance frequency breathing (typically 5.5-6 breaths per minute) trains the baroreceptor reflex and improves vagal tone. Daily practice for 10-20 minutes, guided by HRV monitoring (devices like HeartMath Inner Balance or Elite HRV).
Vagal toning — cold water face immersion (activates the diving reflex), gargling vigorously, singing or humming (vibrates the vagus through the laryngeal muscles), slow exhalation breathing (4 counts in, 8 counts out).
Buffalo Concussion Treadmill Test (BCTT) — developed by John Leddy at the University of Buffalo. The patient walks on a treadmill with gradually increasing speed and incline while heart rate and symptoms are monitored. The heart rate at which symptoms are provoked is identified as the symptom-exacerbation threshold. The patient then exercises daily at 80% of that threshold heart rate for 20 minutes. Retest every 2-3 weeks — the threshold typically rises progressively until the patient can exercise at maximum intensity without symptoms.
This graded exercise approach has been shown to accelerate recovery from concussion, particularly in adolescents. It directly addresses the autonomic dysfunction and deconditioning that perpetuate post-concussion syndrome.
Photobiomodulation
Transcranial photobiomodulation (tPBM) uses near-infrared light (typically 810nm wavelength) applied to the scalp to penetrate the skull and reach cortical tissue. The photons are absorbed by cytochrome c oxidase in the mitochondrial electron transport chain, directly enhancing ATP production.
Margaret Naeser at Boston University and Michael Hamblin at Harvard/Massachusetts General Hospital have been the leading researchers. Naeser’s pilot studies and case series demonstrated improvements in cognitive function, sleep, and PTSD symptoms in chronic TBI patients treated with transcranial LED therapy. The light reaches 2-3 cm into the brain — sufficient to affect cortical tissue.
Protocol: 810nm wavelength, pulsed at 10 or 40 Hz, applied to forehead (prefrontal cortex) and other regions based on symptoms, 20-30 minutes per session, 3x/week for 6-12 weeks. Devices range from clinical-grade (Vielight Neuro Gamma, Thor Photomedicine) to consumer devices.
The mechanism extends beyond ATP production: tPBM reduces neuroinflammation (shifts microglia from M1 to M2 phenotype), increases cerebral blood flow, upregulates BDNF, and supports mitochondrial biogenesis.
Timeline and Return-to-Activity
Recovery is not linear. Expect fluctuations. The general timeline:
- Acute phase (0-72 hours): Relative rest. Avoid screens, reading, and cognitively demanding tasks. Light walking is acceptable.
- Subacute phase (3-14 days): Gradual return to light cognitive and physical activity below symptom threshold. Begin metabolic support aggressively.
- Recovery phase (2-6 weeks): Most uncomplicated concussions resolve. Begin targeted rehabilitation of identified deficits (vestibular, oculomotor, autonomic).
- Persistent post-concussion syndrome (>3 months): Indicates specific pathway dysfunction that requires targeted intervention. This is where the functional approach is most valuable — identifying the specific generators (vestibular, cervicogenic, oculomotor, autonomic, inflammatory, metabolic) and addressing each one.
Return-to-activity follows a stepwise protocol: symptom-free at rest, then light aerobic exercise, then sport-specific exercise, then non-contact training drills, then full-contact practice, then full competition. Each step requires 24 hours without symptom recurrence before advancing.
The functional medicine layer runs underneath all of this: resolve neuroinflammation, support mitochondrial recovery, optimize sleep, address the cervical spine, feed the brain the raw materials it needs to rebuild.
A concussion is not an event. It is a process. And the process of healing requires as much precision and intention as the injury was random and violent. What would your recovery look like if every pathway received exactly the input it needed to rebuild?