Patient Workbook · TBI & Concussion Recovery

The TBI Recovery Audit
Your Environment · Your Inputs · Your Recovery Plan

"You can't consent to what you've never been told."

Every item in this audit is a documented mechanism — not a theory. The same inputs that lower seizure threshold slow or block TBI recovery. This is not about doing everything at once. It is about knowing what is in your environment so you can make informed decisions about what to address first.

My Recovery Audit

Check every item that applies to your current daily life and injury history. The brain after TBI is operating at a lower threshold — the same inputs that trigger seizures in a sensitized brain also block recovery in an injured one.

This is my first documented TBI or concussion

I have had 2 or more concussions (cumulative injury changes recovery trajectory)

My most recent injury was less than 3 months ago (acute phase)

I am still symptomatic more than 3 months after my injury (post-concussion syndrome)

I have a history of whiplash, neck injury, or forceful impact to the upper spine

My injury involved loss of consciousness, even briefly

I was not given specific recovery instructions beyond "rest for a few days"

I returned to screen use, work, or school within 48–72 hours of injury

I have had a difficult birth (forceps, vacuum, prolonged labor) — relevant to cranial structure and baseline resilience

These are the documented effects of unresolved excitotoxicity, mitochondrial dysfunction, and neuroinflammation — the mechanisms that sustain post-concussion syndrome. They are also the symptoms most directly affected by the inputs in this audit.

Persistent headache or head pressure

Light sensitivity (photophobia)

Sound sensitivity (phonophobia)

Cognitive fatigue / brain fog

Difficulty concentrating or word-finding

Memory problems (short-term)

Sleep disturbance — difficulty falling or staying asleep

Mood dysregulation — irritability, anxiety, depression

Balance or vestibular issues

Visual disturbance — blurring, tracking difficulty, eye fatigue

Neck pain or occipital tightness

Barometric pressure sensitivity — symptoms worsen before rain or storms

Symptom crash after screen use or cognitive effort ("PEM-like" pattern)

Fatigue disproportionate to activity level

In seizure disorders, the core mechanism is insufficient GABA (inhibitory) relative to glutamate (excitatory). In TBI, the acute crisis is glutamate excess — the secondary injury cascade. But the sustained post-concussion problem is identical: GABAergic interneurons are preferentially destroyed by excitotoxic damage, leaving the brain with reduced inhibitory infrastructure. The same inputs that deplete GABA in a seizure disorder are blocking recovery here.

Post-concussion symptoms are largely GABAergic in origin. Anxiety, light sensitivity, sound sensitivity, sleep disruption, mood dysregulation, and cognitive fatigue — all documented in MRS (magnetic resonance spectroscopy) studies showing reduced GABA in visual cortex, prefrontal cortex, and hippocampus after concussion. These are not vague complaints. They are the measurable signatures of a brain operating without adequate inhibitory tone.

Post-traumatic epilepsy risk. TBI is one of the most significant risk factors for developing seizures. The excitotoxic damage from the injury — and from every repeat injury — lowers seizure threshold. Hemosiderin deposits (iron released from lysed red blood cells after any brain bleed, including microbleeds from concussion) generate free radicals indefinitely through Fenton chemistry, creating ongoing cortical irritation. Every head injury that caused bleeding deposits iron into cortical tissue. This is the documented mechanism behind delayed-onset post-traumatic epilepsy. The inputs in this audit are relevant on two levels: recovery from TBI and protection against post-traumatic seizures.

What depletes GABA — same in both TBI and seizures

· Fluoride → inhibits GAD (glutamate→GABA enzyme)

· B6 depletion (OCs, antibiotics, processed food) → GAD cofactor

· Gut dysbiosis → destroys GABA-producing bacteria

· PFAS thyroid disruption → reduces GABA receptor density

· Benzodiazepine tolerance → GABA receptor downregulation

· Aspartame → excitatory load; blocks inhibitory rebound

What GABA deficiency looks like post-TBI

· Anxiety and nervous system hyperreactivity

· Light and sound sensitivity (lowered sensory threshold)

· Sleep onset difficulty and fragmented sleep

· Mood dysregulation / irritability

· Cognitive fatigue disproportionate to effort

· Symptom crash after sensory or cognitive load

I drink fluoridated municipal tap water

I drink filtered water but don't know if the filter removes fluoride

I drink distilled or reverse osmosis water (mineral-stripped — leaches minerals from the body)

I drink from aluminum cans regularly (soda, sparkling water, energy drinks)

I rarely drink plain water throughout the day — dehydration is a significant TBI recovery barrier

Goal: natural spring water (findaspring.com) or non-ozonated bottled spring water · glass or stainless steel containers

After TBI, the brain releases massive amounts of glutamate from injured neurons — the secondary injury cascade. Adding dietary free glutamate to an already-flooded system extends and amplifies this damage. This is the part that doesn't make the discharge paperwork.

I use protein powders (whey, plant-based, collagen with additives) — high free glutamate; feeds secondary injury in recovering brain

I eat processed food daily — packaged, fast food, restaurant more than 3x/week

I use artificial sweeteners — aspartame (diet drinks, Equal), sucralose (Splenda), acesulfame-K

I eat foods with MSG, hydrolyzed protein, yeast extract, or "natural flavors" regularly

I eat conventional (non-organic) produce from the Dirty Dozen list — pyrethroids affect sodium channels

I eat conventional meat, dairy, or farmed fish (subtherapeutic antibiotics destroy GABA-producing gut bacteria)

I skip meals or go more than 4–5 hours without eating — glucose instability impairs neuronal repair

I eat artificial food dyes daily (brightly colored snacks, cereals, drinks)

My child (or I) eat commercially produced candy regularly — gummies, sour candy, hard candy, chocolate

Florida DOH and Lead Safe Mama testing identified lead, arsenic, and cadmium in popular commercial candy brands (Sour Patch Kids, Ring Pops, Nerds, Jolly Ranchers, Airheads, Trolli, Haribo, and others). Lead accumulates in the brain and has no safe threshold for neurological effect. For a brain already recovering from injury, heavy metal burden from daily candy consumption is a documented and unaddressed input.

I drink coffee, tea, or caffeinated beverages daily — adenosine (sleep drive) is critical for brain repair; caffeine blocks it

I use energy drinks (Monster, Red Bull, Celsius, Reign)

I use pre-workout supplements

I take OTC medications containing caffeine (Excedrin, Midol, Anacin, NoDoz)

I take a daily multivitamin

Retinyl palmitate (synthetic vitamin A) raises intracranial pressure — directly contraindicated in the context of TBI. Synthetic D3 raises serum calcium, activating voltage-gated calcium channels. Folic acid (not food-form folate) blocks the folate receptor in MTHFR variants and masks B12 deficiency. TiO₂ coating on the tablet — titanium dioxide, flagged for neurological effects. None of these are what the label implies.

I supplement with Vitamin D (D3 capsules or drops) — soft tissue calcification risk; use morning sunlight and food sources (cod liver oil, fatty fish, pastured egg yolk)

I use fluoride toothpaste (most commercial brands)

Fluoride toothpaste is 1,000–1,500 ppm. Fluoride varnish applied at dental cleanings is 22,600 ppm — directly on oral mucosa. Fluoride inhibits glutamate decarboxylase (GAD), the enzyme that converts glutamate to GABA. For a recovering brain, every daily fluoride exposure is suppressing GABA synthesis at the enzymatic level.

I take OTC antihistamines, pain relievers, or cold medicine regularly

I have taken a fluoroquinolone antibiotic (Cipro, Levaquin, Avelox) in the past 2 years

I cook with nonstick (Teflon/PTFE) pans — especially on high heat

My nonstick pans have scratches or chips in the coating

I drink from aluminum cans regularly

I store or heat food in plastic containers

Non-native EMF activates voltage-gated calcium channels and generates reactive oxygen species — the same pathway that drives neuroinflammation in TBI. Sleep is the primary window for glymphatic clearance and synaptic repair. The bedroom environment determines the quality of that window.

My Wi-Fi router is on overnight (not on a timer)

I charge my phone on or near my nightstand

I have a smart TV, streaming stick, or other device in my bedroom

My smart meter is on a bedroom wall or within 15 feet of where I sleep

I can see a cell tower, power lines, or electrical infrastructure from my home

I have solar panels on or near the house (inverter creates dirty electricity)

I use LED lighting in my bedroom or main living areas in the evening

My bedroom is not fully dark at night

I use Bluetooth headphones or earbuds regularly (including while sleeping)

Screen use after TBI imposes metabolic demand on a brain that is already in energy deficit. Light sensitivity and post-exertion symptom crashes are signs that the recovery threshold is being exceeded.

I use screens within 1 hour of bedtime

I returned to full screen use (work, phone, TV) within 1 week of injury

My symptoms worsen after screen use — I use screens anyway

I game in a dark room or with high-contrast backlighting

I use wireless headphones during screen sessions

I have not been told the specific screen exposure thresholds relevant to TBI recovery

Sleep is not passive rest after TBI — it is when glymphatic clearance of excess glutamate and metabolic waste occurs, when synaptic consolidation and repair happens, and when cortisol resets. Disrupting it extends every symptom.

I do not get outdoor morning sunlight within the first hour after waking

My first light exposure is a screen (phone, computer, TV)

I sleep fewer than 7–8 hours most nights

I wake with a dry mouth or have been told I snore or stop breathing

I sleep on my back — lateral sleep supports glymphatic flow

My sleep schedule is irregular — different bedtimes each night

I take sleep medication or antihistamines to sleep

List your current medications. Check any flag items that apply.

Current medications

Supplements / OTC used regularly

Flag items — check any that apply:

I take acetaminophen (Tylenol) regularly for TBI headaches — depletes glutathione, the brain's primary antioxidant defense; the #1 cause of acute liver failure in the US

I take NSAIDs (ibuprofen, naproxen) regularly — GI and renal burden; magnesium interaction

I take a proton pump inhibitor (Prilosec, Nexium, Prevacid) — depletes magnesium, the brain's natural NMDA channel blocker

I take a benzodiazepine (Xanax, Valium, Ativan, Klonopin) — GABA receptor downregulation during tolerance; rebound excitability

I take oral contraceptives — deplete B6 and folate; B6 is required for GABA synthesis

I take corticosteroids (prednisone, methylprednisolone) — blood sugar dysregulation affects neuronal stability and repair

I take a daily antihistamine (Benadryl) — anticholinergic burden impairs cognitive recovery

I take iron supplements

Free iron generates hydroxyl radicals via Fenton chemistry — the same mechanism responsible for hemosiderin-related post-traumatic cortical irritation. Iron supplementation without confirmed deficiency adds to an oxidative environment in a brain already managing iron from microbleeds. Serum ferritin testing before supplementing is worth discussing with a provider.

I am currently taking or recently completed a course of antibiotics

I take medication for post-traumatic seizures (AED) — same nutrient depletion profile as seizure disorder; see Seizure Threshold Audit for full AED flag list

Not all antibiotics carry the same neurological risk. Check any class you have taken — recently or repeatedly in the past. Use this list to start a conversation with your prescriber.

Fluoroquinolone — Cipro, Levaquin, Avelox, Floxin, Factive, Noroxin, Baxdela

Published side effects: seizures (FDA Black Box Warning), confusion, hallucinations, dizziness, insomnia, tendon rupture, and peripheral neuropathy (which may be permanent). Also disrupts gut bacteria that produce GABA and neurotransmitter precursors. Discuss with your provider: Is there a lower-risk alternative given my TBI history?

Metronidazole / Tinidazole — Flagyl · Tindamax (same class, same risks)

Published side effects: seizures (listed in prescribing information), confusion, dizziness, headache, coordination problems, slurred speech, peripheral neuropathy, nausea, and metallic taste. Discuss with your provider: Is there an alternative for this infection that does not carry the same CNS risk?

Cephalosporin — 1st gen: Keflex (cephalexin), Duricef (cefadroxil), Ancef (IV) · 2nd gen: Ceftin, Cefzil, Ceclor · 3rd gen: Omnicef, Suprax, Vantin, Rocephin (injection) · 4th gen: Maxipime (IV)

Published side effects: seizures (listed in prescribing information), myoclonus (muscle jerking), encephalopathy, confusion, and dizziness. Risk increases if kidney function is impaired — cephalexin is primarily cleared by the kidneys and accumulates when clearance is reduced. Particularly relevant for a brain with lowered threshold post-TBI. Discuss with your provider: Has my kidney function been checked recently? Is there an alternative?

TMP-SMX — Bactrim, Septra

Published side effects: anemia, rash, nausea, and kidney effects. Can raise blood levels of certain medications — relevant if taking any neurological or psychiatric drugs. Discuss with your provider: Do I need medication level monitoring during this course?

Amoxicillin (Amoxil), doxycycline (Vibramycin, Doryx), azithromycin (Zithromax / Z-pack), clindamycin (Cleocin), nitrofurantoin (Macrobid, Macrodantin)

Lower neurological risk compared to the classes above. All antibiotics disrupt gut bacteria that produce GABA and neurotransmitter precursors. Discuss with your provider: What probiotic support is appropriate during and after this course?

I have taken 3 or more antibiotic courses in the past 12 months

I have never taken a probiotic after an antibiotic course

A routine dental appointment involves several agents that directly affect brain threshold. For someone recovering from TBI, the mechanisms are the same as for seizure disorders — the fluoride and epinephrine burden is relevant to any neurologically compromised brain.

I received topical fluoride varnish (22,600 ppm — 15x toothpaste concentration) at my last dental cleaning

My local anesthetic contained epinephrine — published side effects include rapid heartbeat, elevated blood pressure, anxiety, headache; can elevate intracranial pressure and lower seizure threshold

I received nitrous oxide sedation — published side effects include nausea, headache, and with repeated use: B12 depletion leading to nerve damage and neurological decline

I have amalgam fillings that have not been safely removed

I have dental work planned and have not discussed my TBI history with my dentist

Before your next dental appointment

Print the TBI dental information sheet and bring it to your appointment. It covers epinephrine/ICP, fluoride varnish, nitrous/B12, cervical positioning, sensory sensitivity, amalgam, and the emergency protocol. Download: Dental Care & Anesthesia — TBI Patient Information Sheet

My audit summary — what stands out most:

My Action Plan

Organized by what to remove, what to add, and what to test. Start with the removes — reducing the daily neurological burden is the first step in any recovery.

Remove — Reduce Ongoing Burden

Remove protein powders (whey, soy, pea, collagen with additives) — free glutamate feeds secondary injury

Remove aspartame, sucralose, acesulfame-K from all food and drink

Remove MSG, hydrolyzed protein, yeast extract, "natural flavors" in processed food

Remove energy drinks, pre-workout, and high-caffeine beverages

Remove artificial food dyes (Red 40, Yellow 5, Yellow 6, Blue 1)

Why this matters for TBI: The excitotoxic cascade following brain injury — the secondary injury process — is directly amplified by dietary free glutamate. This is the mechanism. Protein powders given to TBI patients in hospital and rehab settings are a documented example of feeding the very process that is extending injury.

Switch to natural spring water (findaspring.com) or non-ozonated bottled spring water

Switch to glass or stainless steel — no aluminum cans for daily beverages

Replace nonstick pans with cast iron, carbon steel, stainless steel, or glass

Switch toothpaste: no fluoride, no NHA, no SLS, no TiO₂ — tooth powder or verified clean brand

Remove synthetic multivitamins, Vitamin D3 supplements, folic acid

Check all OTC medications for hidden caffeine, artificial dyes, and sweeteners

Request epinephrine-free anesthetic and opt out of fluoride varnish at dental cleanings

Router off at night — use a smart plug timer

Phone charged in another room overnight — not on the nightstand

All screens removed from bedroom

Replace LED bedroom lighting with incandescent or low-flicker bulbs for evening use

Blackout curtains — no external light sources during sleep

Limit screen exposure in the acute recovery phase — stop before symptoms worsen

Add — Rebuild What Was Depleted

Morning sunlight: eyes open, outdoors, within 30–60 minutes of waking — regulates cortisol, melatonin, and circadian rhythm; all three govern repair windows

Lateral sleep position: left or right side — maximizes glymphatic clearance of excess glutamate and metabolic waste from the brain overnight

Consistent sleep/wake time: same time every day — circadian regularity governs the repair cycle

Bare feet on ground outdoors: grass, soil, sand — 10–20 minutes daily alongside morning sunlight

Gentle movement: walking (not intense exercise) — supports cerebral blood flow without metabolic overload

These are food sources, not prescriptions. Skip any food you are allergic or sensitive to — multiple sources are listed for each nutrient so alternatives are available.

DHA: wild salmon, sardines, mackerel, pastured egg yolks, fish roe — structural repair of neuronal membranes

Magnesium: pumpkin seeds, dark leafy greens, dark chocolate (unsweetened), legumes, avocado — NMDA receptor blocker; anti-excitotoxic

Choline: egg yolks (pastured), liver, beef — phospholipid synthesis; critical for myelin and membrane repair

Thiamine (B1): pork, liver, sunflower seeds — mitochondrial energy production in neurons

Zinc: oysters, red meat, pumpkin seeds, liver — antioxidant; synaptic signaling repair

Folate (food form): liver, lentils, dark leafy greens, avocado — not folic acid supplement

Stable glucose: protein + fat with every meal, no long gaps — glucose instability is a primary driver of post-concussion cognitive symptoms

CoQ10 from food: beef heart, organ meats — mitochondrial electron transport; neuronal energy production

Raw sauerkraut (refrigerated, not shelf-stable) — 1–2 tablespoons with meals

Kimchi (fermented, not vinegar-based)

Kefir from pasture dairy (if tolerated)

Bone broth from pasture-raised animals

Test — Know Your Baseline

RBC Magnesium (not serum)

Full thyroid panel: TSH, free T3, free T4, TPO antibodies

Morning cortisol (8am blood draw) + DHEA-S

Serum iron, ferritin, TIBC, transferrin saturation

Serum copper + ceruloplasmin

Serum zinc

Methylmalonic acid (functional B12 — more sensitive than serum B12)

Homocysteine (elevated = B12/folate/B6 deficiency; neurological risk marker)

Fasting insulin + glucose (HbA1c alone insufficient)

hs-CRP (high-sensitivity C-reactive protein — neuroinflammation marker)

MTHFR gene variants (one-time — determines folic acid safety)

Hormonal panel if symptoms include mood, sleep, or cycle disruption

My change timeline — what I started and when:

Week 1 — I removed:

Week 2 — I added:

What I noticed changing:

Labs I requested (date):

Doctor Visit Prep

Bring this page to your appointment. Fill in before you go. The goal is to use your appointment time efficiently — specific symptoms, specific questions, specific requests.

Provider name

Appointment date

Appointment type

Current medications + doses

Date of injury

Mechanism of injury

Headache

Brain fog / concentration

Light sensitivity

Sound sensitivity

Sleep quality

Mood / irritability / anxiety

Balance / vestibular

Fatigue after activity

Changes since last appointment:

1.

2.

3.

4.

5.

Check the ones you want to ask for. Bring this list.

RBC Magnesium

Free T3, Free T4, TSH

Morning cortisol (8am)

DHEA-S

Serum iron, ferritin, TIBC

hs-CRP (neuroinflammation)

Serum copper + ceruloplasmin

Methylmalonic acid (B12)

Homocysteine

Fasting insulin + glucose

MTHFR gene variants

Hormonal panel (if applicable)

Questions my provider has not yet asked — that I want to raise:

Has cervical spine involvement been assessed? My injury involved the neck/upper back.

Has anyone assessed my sleep for airway compromise or sleep-disordered breathing?

My symptoms have a hormonal pattern — can we assess hormone levels in relation to my cycle? (women)

What nutrients do my current medications deplete, and how do we monitor for that over time?

Has the role of dietary excitotoxins in secondary injury been discussed in the context of my recovery?

If I need surgery or dental work, which anesthetics are lower-risk given my TBI history?

My fluoride exposure is significant — has this been considered as a factor in my recovery?

What my provider said:

Medication or treatment changes:

Labs ordered:

Follow-up date:

What I still need to follow up on:

Daily Symptom Log

Track symptoms, suspected triggers, sleep, and what you changed. Patterns emerge in 2–4 weeks. Bring this to your next appointment.

Rate headache, fog, and mood 1–10 · S = screen-heavy day · E = exercise · M = menstrual · A = antibiotic · Note any food changes or notable exposures

Day / Date
Headache / Fog (1–10)
Sleep hrs + quality
Mood / Sensitivity
Trigger / Change noted

Clean Alternatives

Practical swaps for the highest-burden inputs. Every category here has a documented mechanism for why it matters in TBI recovery.

Natural spring water — findaspring.com

Non-ozonated bottled spring water (Mountain Valley, Tourmaline, Gerolsteiner)

Not RO, not distilled, not tap. Glass or stainless container.

Tooth powder: baking soda (daily base) + pascalite clay (periodic/acute only — adult use, work with practitioner; contains naturally occurring trace minerals including lead as listed by manufacturer)

Verified clean brands: check EWG Skin Deep, Mamavation, Lead Safe Mama

Avoid: fluoride, NHA (nano-hydroxyapatite), SLS (sodium lauryl sulfate), TiO₂, carrageenan. See: toothpaste.html

Cast iron (well-seasoned)

Carbon steel

Stainless steel (18/10)

Glass or enameled cast iron (Le Creuset, Lodge)

Replace nonstick regardless of whether the surface appears damaged — PFAS off-gas at cooking temperatures.

Pasture-raised eggs, meat, and dairy — no subtherapeutic antibiotics

Wild-caught fish — not farmed

Organic for EWG Dirty Dozen produce minimum

EWG Dirty Dozen: ewg.org/foodnews

EWG Skin Deep — ewg.org/skindeep — personal care and supplement ingredient database

Mamavation — mamavation.com — PFAS and toxin testing database for food and personal care

Lead Safe Mama — tamararubin.com — heavy metal testing in food, supplements, and household products

Open Food Facts — world.openfoodfacts.org — ingredient scanner; searchable by additive

MSG hidden names listmsg-excitotoxins.html → Hidden Names tab — full three-tier list to bring grocery shopping

MSG & Excitotoxins — full mechanism on why dietary free glutamate matters specifically for brain injury and TBI recovery

Non-Native EMF — voltage-gated calcium channels, neuroinflammation, and the bedroom environment

Seizures — all brain threshold mechanisms apply; informed consent tab has the full input-by-input breakdown

Dental Care & Neurological Conditions — printable patient information sheet for your dental appointments

Fluoride — enzyme inhibition, mitochondrial disruption, and why fluoride burden matters in recovery

Drug Library — full entry for any medication — includes nutrient depletions, excipients, and recovery considerations

This workbook was prepared using research from theundoctored.com · Allie Johnson, DNM, DIM, PNM · Educational resource — not medical advice.