Concussion

Populations and Risk Factors

• Contact sport athletes (hockey, football, rugby, soccer, martial arts) — highest incidence population; repeat concussions are cumulative
• Children and adolescents (ages 5–18) — developing brain is more vulnerable; longer recovery trajectory; catastrophic risk from second impact syndrome
• Older adults (65+) — falls are the leading mechanism; anticoagulant use increases intracranial hemorrhage risk even from mild impacts
• Males have higher overall incidence (sport and occupational exposure), but females report more severe and prolonged symptoms when concussed at comparable force levels
• Military personnel — blast-related mTBI is an increasingly recognized mechanism
• Previous concussion history — each concussion lowers the threshold and extends recovery for subsequent injuries; 3+ concussions significantly increase risk of persistent post-concussion symptoms
• Comorbid migraine, anxiety, depression, ADHD, or learning disability — associated with longer recovery
• Cervical spine instability or pre-existing cervical dysfunction — increases vulnerability to concurrent cervical injury from the same mechanism

Causes and Pathophysiology

Mechanism of Injury

Concussion results from sudden acceleration-deceleration, rotational, or direct impact forces transmitted to the brain. The brain moves within the cranial vault, producing shear strain on axons and cell membranes. Critically, the cervical spine is subjected to the same forces — the head-neck complex functions as a coupled mechanical unit during impact. This means:

• Whiplash-type cervical injury is almost universally co-present in concussion, because the same acceleration-deceleration that injures the brain also injures the cervical spine structures
• Many "persistent concussion symptoms" — particularly headache, dizziness, and neck pain — may originate from cervical injury rather than brain injury, making cervicogenic contribution a central consideration in assessment and treatment

Neurometabolic Cascade

The injury triggers a well-characterized neurometabolic cascade (Giza & Hovda, 2014) that unfolds over hours to weeks:

1. Mechanoporation: The biomechanical forces stretch and shear neuronal cell membranes, creating transient pores (mechanopores). This is not structural tearing (which occurs in severe TBI) but a functional disruption of membrane integrity that alters ion channel behavior.

1. Ionic flux: Mechanoporation causes unregulated release of intracellular potassium (K+) into the extracellular space and influx of calcium (Ca2+) and sodium (Na+) into neurons. This depolarizes neurons indiscriminately, producing the acute symptoms (confusion, disorientation, amnesia, loss of consciousness).

1. Glutamate excitotoxicity: The indiscriminate depolarization causes massive release of glutamate (the brain's primary excitatory neurotransmitter). Glutamate binds NMDA receptors, further driving calcium influx and perpetuating the ionic disturbance in a feed-forward loop. Excessive calcium activates destructive enzymatic cascades (calpains, caspases) that damage the cytoskeleton.

1. Energy crisis: To restore ionic balance, membrane Na+/K+ ATPase pumps work overtime, consuming enormous amounts of ATP. Simultaneously, calcium-overloaded mitochondria become dysfunctional, reducing ATP production. The brain enters an energy crisis — high metabolic demand with impaired energy supply. This mismatch explains why cognitive exertion, physical activity, and sensory stimulation worsen symptoms: the injured brain cannot meet increased metabolic demands.

1. Axonal dysfunction: Calcium-mediated cytoskeletal damage and energy failure impair axonal transport. In mTBI, axons are functionally disrupted but not severed (unlike diffuse axonal injury in severe TBI). This produces the cognitive symptoms — slowed processing, poor concentration, memory difficulty — without focal neurological deficits.

1. Inflammatory response: Neuroinflammatory mediators (cytokines, reactive oxygen species) are released, contributing to secondary injury over hours to days. This inflammatory phase is the rationale for symptom monitoring in the 24–48 hours post-injury.

1. Resolution: The cascade typically resolves over 7–10 days in adults and 2–4 weeks in children as ionic balance is restored, mitochondrial function recovers, and inflammatory markers normalize. Persistent symptoms beyond 4 weeks suggest either ongoing neurometabolic dysfunction or — commonly — that cervicogenic or vestibular components are maintaining the symptom picture.

Distinguishing Mild TBI from Severe TBI

Second Impact Syndrome

Second impact syndrome occurs when a second concussion is sustained before the neurometabolic cascade from the first has fully resolved. The still-dysregulated brain loses cerebrovascular autoregulation, resulting in rapid, catastrophic cerebral edema, raised intracranial pressure, and potential brainstem herniation. It is rare but carries near-100% morbidity and up to 50% mortality. It is almost exclusively reported in children and adolescents, which is the basis for the more conservative return-to-play protocols in pediatric populations and the legislative framework of Rowan's Law in Ontario.

Cervicogenic Contribution to Persistent Symptoms

The acceleration-deceleration mechanism that causes concussion simultaneously injures cervical structures:

• Upper cervical facet joints (C0–C3) — irritation produces cervicogenic headache that mimics and overlaps with post-concussion headache
• Suboccipital muscles — acute protective guarding transitions to chronic hypertonicity; sustained suboccipital tension contributes to headache via cervicotrigeminal convergence (the same mechanism as in migraine)
• Vestibular input from upper cervical proprioceptors — cervical injury disrupts vestibular-cervical integration, producing dizziness and balance dysfunction that is clinically indistinguishable from central vestibular concussion symptoms
• SCM and upper trapezius — whiplash-component injury produces neck pain, restricted cervical AROM, and referred headache patterns

Research increasingly supports that a significant proportion of persistent post-concussion symptoms (especially headache, dizziness, and cognitive fatigue beyond 4 weeks) are maintained by cervicogenic dysfunction rather than ongoing brain pathology (Patricios et al., 2023). This is directly relevant to MT scope — the cervicogenic component is treatable.

Signs and Symptoms

Acute Presentation (0–72 hours)

Symptoms are organized by domain:

• Physical: headache (most common symptom, ~90%), dizziness, nausea/vomiting, balance disturbance, visual disturbance (blurred or double vision), sensitivity to light (photophobia) and noise (phonophobia), tinnitus, fatigue
• Cognitive: confusion, disorientation, feeling "in a fog," slowed processing speed, difficulty concentrating, short-term memory impairment, amnesia (retrograde and/or anterograde around the event)
• Emotional: irritability, emotional lability, anxiety, sadness; emotional symptoms may not present immediately
• Sleep: drowsiness, difficulty falling asleep, sleeping more or less than usual; sleep disturbance is both a symptom and a recovery impediment

Loss of consciousness occurs in only 10–20% of concussions. Its absence does not exclude the diagnosis.

Persistent Post-Concussion Symptoms (>4 weeks)

When symptoms persist beyond 4 weeks in adults (or beyond 4 weeks in children, per Amsterdam 2022), the condition is described as persistent post-concussion symptoms (the term "post-concussion syndrome" is being phased out as a formal diagnosis due to its non-specific criteria). Key features:

• Headache, dizziness, and cognitive fatigue are the most common persistent symptoms
• Cervicogenic headache is a major contributor — often the primary treatable component
• Vestibular dysfunction (dizziness provoked by head movement, visual motion sensitivity) may require specialized vestibular rehabilitation
• Psychological factors (anxiety about recovery, activity avoidance, depression) contribute to symptom persistence and must be addressed concurrently
• Recovery beyond 3 months is still expected in most cases, but the timeline is less predictable

Recovery Timeline

Assessment Profile

Subjective Presentation

• Chief complaint: headache following a head impact or acceleration-deceleration injury; "foggy" thinking, difficulty concentrating; dizziness; sensitivity to light and noise; may report neck pain and stiffness (whiplash component); symptoms may worsen with cognitive or physical exertion
• Pain quality: headache is typically diffuse, pressure-like or dull aching; may have throbbing component; cervicogenic headache is characteristically unilateral occipital-to-frontal; neck pain is dull, aching, positional
• Onset: acute onset from identifiable impact or acceleration-deceleration event; establish exact mechanism of injury (direction of force, whether head struck a surface, sport vs. MVA vs. fall); establish timeline — how many days/weeks since injury; prior concussion history is critical (number, proximity, recovery time for each)
• Aggravating factors: cognitive exertion (reading, screens, schoolwork), physical exertion, bright or flickering lights, loud or busy environments, head movement (especially rotation), sustained visual focus, multi-sensory environments (grocery stores, malls)
• Easing factors: rest in a dark quiet room (during acute phase); symptom-limited activity (after initial 24–48 hours); neck support; sleep (though sleep itself may be disrupted)
• Red flags: worsening headache despite rest; seizure activity; repeated vomiting (beyond initial event); slurred speech or worsening confusion; one pupil larger than the other (nonreactive or unequal pupils); weakness or numbness in extremities; inability to recognize people or places; increasing drowsiness or inability to be awakened; clear fluid from nose or ears (CSF leak); any focal neurological deficit → emergency referral; do not treat — these suggest intracranial hemorrhage, cerebral edema, or skull fracture

Observation

• Local inspection: no visible injury in most concussions (the brain injury is internal); may observe facial/scalp bruising, lacerations, or swelling if direct impact occurred; periorbital ecchymosis ("raccoon eyes") or mastoid ecchymosis (Battle's sign) are red flags for basilar skull fracture
• Posture: forward head posture and guarded cervical posture from whiplash component; protective shoulder elevation; general postural instability — patient may sway or need to widen base of support; observe for listing or lean during quiet standing
• Gait: may show balance impairment — tandem gait (heel-to-toe) difficulty is a clinical sign; observe for unsteadiness, widened base, or veering; gait disturbance in the acute phase reflects vestibular and proprioceptive disruption, not motor pathway damage (which would indicate severe TBI)

Palpation

• Tone: suboccipital hypertonicity (rectus capitis posterior major/minor, obliquus capitis superior/inferior) — consistently present due to acute protective guarding from the acceleration-deceleration mechanism; upper trapezius and SCM bilateral hypertonicity — whiplash component; cervical paraspinals (semispinalis, splenius capitis) — guarding pattern; muscle tone reflects protective guarding (LMN pattern), not spasticity (UMN); if velocity-dependent spasticity is present, this is not a concussion — refer for neuroimaging
• Tenderness: upper cervical segmental tenderness at C1–C3 articular pillars — indicates facet joint irritation from the same mechanism that caused the concussion; suboccipital attachments at the inferior nuchal line and occiput (C0–C1 junction) — characteristically tender and the primary MT treatment target; SCM and upper trapezius attachment sites (mastoid process, clavicular/sternal attachments) — whiplash-related tenderness; scalp tenderness may be present over the impact site; palpation of cervical structures should reproduce or partially reproduce the patient's headache pattern if cervicogenic contribution is present — this is a positive clinical finding confirming MT treatment relevance
• Temperature: usually normal; localized warmth over cervical paraspinals in the acute phase (first 48–72 hours) may reflect acute inflammatory response in whiplash-injured tissues
• Tissue quality: suboccipital muscles exhibit ropy, fibrotic texture in the subacute-to-chronic phase (>1 week); palpable TrPs in suboccipital muscles, upper trapezius, and SCM — clinically significant and a primary treatment target; reduced C0–C2 intersegmental joint play on PA glide and rotational assessment; upper trapezius and SCM may show taut bands with characteristic referral patterns (upper trapezius: temporal referral; SCM: periorbital and frontal referral)

Motion Assessment

• AROM: cervical AROM is typically restricted from the co-present cervical injury — expect limitation in rotation, lateral flexion, and extension; the pattern of restriction is non-capsular (injury-specific rather than proportional); restricted cervical AROM that reproduces headache confirms cervicogenic contribution and is a key assessment finding; compare bilateral rotation carefully for asymmetry
• PROM / end-feel: guarded/protective end-feel through restricted ranges in the acute phase; may transition to firm or leathery end-feel in the subacute phase as soft tissue fibrosis develops; PROM slightly exceeds AROM (protective guarding reduces active range)
• Resisted testing: cervical and upper extremity strength should be normal — any focal weakness is a red flag for structural brain injury or cervical nerve root injury and requires referral; isometric cervical testing may provoke headache through increased ICP effect — note but do not force through

Special Test Cluster

The SOT cluster for concussion is oriented toward red flag exclusion and cervicogenic differentiation rather than direct confirmation. Concussion is a clinical diagnosis based on mechanism and symptom constellation, not a single confirmatory test.

Note: The SCOAT6 (Sport Concussion Office Assessment Tool 6) is the office-based companion to the SCAT6, designed for clinical follow-up rather than sideline assessment. For MT purposes, familiarity with SCAT6 structure is essential; the SCOAT6 is used by physicians for return-to-play clearance.

Differential Assessment