MTBI and Anoxia Lecture Review

Concussion Defined and Diagnostic Criteria

• Mild Traumatic Brain Injury (MTBI) is clinically defined by specific thresholds using the Glasgow Coma Scale (GCS) and other clinical presentations:

  • GCS Score: Typically ranges from $13-15$.

  • Loss of Consciousness (LOC): Must not exceed $30$ minutes. It is critical to note that a patient does NOT have to lose consciousness to be diagnosed with a concussion.

  • Post-Traumatic Amnesia (PTA) and Altered Mental State: Must last for less than $24$ hours.

  • Symptom Manifestation: Symptoms may not appear immediately; they can be delayed by several hours following the initial injury.

• Symptom Burden Checklists: Standardized tools are used for assessment, most notably the SCAT5 (Sport Concussion Assessment Tool - 5th Edition).

Pathophysiology and Metabolic Cascade

• Nature of Injury: Concussion is a functional rather than structural injury to the brain. There is typically a metabolic dysfunction characterized by a "cascade effect."

• Recovery Timeline: Most individuals fully recover within $3$ months. However, $10-20\%$ of cases develop post-concussive syndrome, which involves residual deficits that can last from months to years.

• The Metabolic Cascade:

  • Involves the release of excitatory neurotransmitters.

  • Abnormal ion fluxes occur across cell membranes.

  • Glucose Metabolism: There is an initial increase in glucose metabolism.

  • Lactic Acid Accumulation: This leads to inflammation.

  • Duration: This physiological state can persist for roughly $30$ days.

• Macrophysiological Insult: The injury affects the Autonomic Nervous System (ANS) and the control of Cerebral Blood Flow (CBF) and cardiac rhythm.

Neurophysiological Insights and EEG

• Imaging Limitations: Because there is no structural damage, a concussion cannot be seen on standard medical imaging (e.g., MRI or CT scan).

• Functional Assessment: Clinicians look at neuropsychology, symptom checklists, balance, and postural control. Traditionally, there has been no clear physiological picture of brain function post-concussion.

• Role of EEG:

  • EEG studies have noted a reduction in activity in concussed persons.

  • This reduction persists even when there are no significant clinical differences in ImPACT scores or balance skills.

  • Concussed individuals may use more brain resources to mask an inability to produce normal "power" compared to a healthy person. This compensation for a physiological problem could itself lead to further issues.

  • Functional resolution (clinical symptoms disappearing) may happen faster than physiological resolution (the brain returning to a normal state).

  • This suggests that current clinical assessment tools may not be sensitive enough for many mTBI cases.

Multiple Concussions and Second Impact Syndrome (SIS)

• Risks of Multiple Injuries: Repeated concussions can lead to an increased susceptibility to future concussions, specific neuropsychiatric needs, and cognitive problems later in life.

• Second Impact Syndrome (SIS):

  • This occurs when a second injury happens after a concussion while the brain is still recovering. It occurs without a hematoma but features significant brain swelling.

  • A second injury anywhere on the body after a mild concussion can trigger this, as the first concussion disrupts autoregulation.

  • The second injury causes a catecholamine surge, leading the brain to swell significantly.

  • This condition is life-threatening.

• Pathophysiology of SIS:

  • Cerebral Autoregulation: This refers to the "tone" of arteries maintained to ensure steady perfusion. Dysregulation occurs post-injury.

  • Blood Pressure (BP) Impacts: If autoregulation is affected or absent, systemic BP changes can severely alter Cerebral Blood Flow (CBF).

  • Roughly $20-30\%$ of mTBI patients have autoregulation problems.

  • Catecholamine Surge: This is a sympathetic response to injury that increases BP and Heart Rate (HR) within seconds. Combined with poor autoregulation, it results in rapid and profound brain engorgement.

PT Assessment of MTBI

• Core Components of Assessment:

  • Patient Education.

  • Activity intolerance and tolerance levels.

  • Vestibular function.

  • High-level balance dysfunction.

  • Post-traumatic headache management.

  • TMJ Disorder: Screening for jaw-related issues.

  • Attention and dual-task performance.

  • Participation in activities and the ability to return to those activities.

• Cognitive and Clinical Tools:

  • Arousal / Attention: Use of ImPACT (Immediate Post-concussion Assessment and Cognitive Testing) to track recovery of attention span, working memory, reaction time, and non-verbal problem solving.

  • SAC (Standardized Assessment of Concussion): A short sideline test performed minutes post-injury. It should not be used in isolation to determine severity or return-to-play readiness.

  • Vestibular and Balance: Assessments often check for BPPV. Tools include computerized posturography (Neurocom SOT and BESS), as well as HiMAT, DGI, FGA, and mini BESTest.

  • Self-Reports: DHI (Dizziness Handicap Inventory) and ABC (Activity-specific Balance Confidence scale).

• Symptom Screening:

  • Post-Concussion Scale: A $21$-item self-report questionnaire.

  • SCAT: Includes an $18$-item screen and a $7$-item follow-up for symptoms.

  • Screening for headache, TMJ pain, and cervical/shoulder issues.

Clinical Trajectories of Concussion

Evidence suggests total rest is not required for everyone. Patients often fall into one of six trajectories to determine treatment goals:

1. Cognitive / Fatigue

• Clinical Picture: Poor concentration, poor multitasking, reduced skill acquisition, increased distractibility, and low energy.

• Client Reports: Non-specific headache and difficulty concentrating.

• Assessment Findings: SCAT5 shows elevated cognitive symptoms; decreased processing speed; normal vestibular, oculomotor, balance, and postural stability exams.

2. Post-Traumatic Migraine

• Clinical Picture: Migraine symptoms, nausea, and photophobia. Stress and anxiety exacerbate symptoms.

• Client Reports: Elevated SCAT5 numbers for headaches, nausea, and sound sensitivity.

• Assessment Findings: Normal vestibular/oculomotor screen (except for increased headache during testing); normal balance and postural exams.

3. Cervical

• Clinical Picture: Cervical tightness, muscle spasms, and occipital headaches.

• Client Reports: Neck pain and stiffness.

• Assessment Findings: Increased SCAT5 score for neck pain; decreased cervical Range of Motion (ROM); "lazy" or poor effort during oculomotor/vestibular exams; normal balance and postural stability.

4. Anxiety / Mood

• Clinical Picture: Feeling anxious, depressed, or overwhelmed; disturbed sleep patterns.

• Client Reports: Increased SCAT5 scores for emotional components.

• Assessment Findings: Normal neurocognitive skills; normal balance and postural stability; potential headaches or "fog" during vestibular/oculomotor testing.

5. Vestibular

• Clinical Picture: Problems with balance and vision during head movements; brain fog; dizziness; nausea; loss of balance or falls. Overstimulation in busy environments.

• Client Reports: Elevated SCAT5 scores for headache, dizziness, and fog.

• Assessment Findings: Decreased balance and postural stability (increased sway); reduced neurocognition; positive vestibular/oculomotor exam.

6. Ocular

• Clinical Picture: Vision and tracking problems; frontal headaches; difficulty with screens or tracking objects.

• Client Reports: Elevated SCAT5 scores for blurry vision.

• Assessment Findings: Positive oculomotor exam; presence of nystagmus.

PT Intervention and Management Strategies

• Predictors of Recovery:

  • Reporting > 4 symptoms suggests a recovery period of > 1 week.

  • Prior concussions, amnesia at the time of injury, dizziness, nausea, and LOC also suggest recovery will take more than $7$ days.

  • Common Symptoms in Adults: Headache/pressure, low energy, feeling "off," and concentration difficulties.

  • Higher initial PCS (Post-Concussion Scale) scores correlate to prolonged symptoms; even a $1$-point change is clinically significant.

• The "Old Model" of Return to Activity: Focused on total rest (cognitive and physical) followed by a graded return. In this model, the patient must be symptom-free for $24$ hours at each stage to progress. This usually involves a minimum of $1$ week ($7$ steps).

• Controlled Exercise and Modern Management:

  • Total rest reduces Cerebral Blood Flow (CBF), which can actually prevent the brain from mediating the metabolic cascade, thereby prolonging symptoms.

  • Sub-symptom Threshold Aerobic Activity: Safe and enhances recovery by releasing BDNF (Brain-Derived Neurotrophic Factor), which is neuroprotective.

• Trajectory-Specific Management:

  • Cognitive/Fatigue: Reduce physical/cognitive demands, regulate sleep, light walking, and cognitive retraining when asymptomatic.

  • Migraine: Pharmacological intervention and increased cardiovascular activity (sub-symptom threshold).

  • Anxiety/Mood: Sub-symptom threshold exertional activity for emotional release; psychological counseling; addressing isolation/identity issues.

  • Vestibular: Vestibulo-spinal training (balance/posture), sensory interaction training, and Vestibulo-ocular training (VOR: gaze stability; VMS: gradual exposure to provocative stimuli).

  • Ocular: Exercises for convergence efficiency and dual-tasking vision with balance activities.

  • Cervical: Stretching, ROM, Soft Tissue Mobilization (STM), strengthening when asymptomatic, and pain modalities (thermal/electrical).

Anoxia: Causes and Pathophysiology

• Medical Causes:

  • Status asthmaticus.

  • Cardiac or respiratory arrest.

  • Carbon monoxide poisoning.

  • Near drowning.

  • Obstructive Sleep Apnea (OSA).

  • Acute Respiratory Distress Syndrome (ARDS).

  • General cardio/pulmonary disorders.

• Traumatic Causes:

  • Trauma to the chest or airway.

  • Head injury affecting respiratory drive centers.

  • Increased edema reducing overall oxygenation.

• Basic Neuropathology of Anoxia:

  • Blood vessel damage (reperfusion/oxygenation injury).

  • Excitotoxicity.

  • Inflammatory processes.

  • Apoptosis signaling.

  • Cell death and atrophy.

Localization of Anoxic Damage

• Anatomical Progression: Damage typically moves from distal to proximal.

• Watershed / Border Zones: Regions at the ends of vascular distribution lines are high risk:

  • ACA-MCA zone (Anterior).

  • MCA-PCA zone (Posterior).

  • Intermediate Zone: Between superficial MCA and deep MCA/ACA branches.

  • Central White Matter: Fornix and corpus callosum.

• High Metabolic Demand Regions: Regions most susceptible to anoxia due to their energy needs:

  • Hippocampus: Responsible for memory.

  • Purkinje Fibers: Located in the cerebellum.

  • Thalamus: The brain's relay center.

  • Basal Ganglia: Deep structures for motor modulation.

• Duration Impact: Injury starts focal at distal high-metabolic regions but becomes diffuse and potentially catastrophic as anoxic time increases.

Major Structural Consequences of Anoxia

• Hippocampus (Most Common Gray Matter Structure):

  • Results in Short-Term Memory (STM) deficits and difficulty with new learning.

  • Confusion and Declarative Memory issues (amnesia for facts/events).

  • Damage leads to Wallerian Degeneration in the output pathways: fornix, mammillary bodies, and anterior thalamus.

• Basal Ganglia:

  • Often involves the Globus Pallidus, leading to paralysis or Parkinsonism traits.

  • Proximity to the internal capsule and corticospinal tracts leads to significant motor impairment and extra-pyramidal signs.

• Corpus Callosum:

  • The largest white matter tract; transfers information between hemispheres.

  • While highly vascularized, it is at the distal end of distribution. Damage can result in Alien Hand Syndrome.

• White Matter:

  • Includes the Fornix (output for the hippocampus).

  • Wallerian degeneration leads to atrophy/necrosis of white matter and breakdown of myelin integrity.

  • This causes cognitive impairment, specifically in memory and executive function.

• Diffuse Damage and Atrophy:

  • Cortical sulci and gyri shrink while ventricular volumes increase.

  • Timeline: Global generalized cerebral atrophy can be observed from acute care discharge up to $1-2$ years post-injury, affecting physical, cognitive, and behavioral functions.

Prognosis and Rehab Interventions for Anoxia

• Predictability: Much like TBI, prognosis is difficult to predict. More diffuse and prolonged anoxia correlates with poorer outcomes.

• Limiting Factors: Cognition is often the most limiting factor; permanent damage is more likely in anoxic cases than in TBI.

• Rehabilitation Realities:

  • Anoxia patients are often referred to rehab later than TBI patients.

  • Length of Stay (LOS) is typically the same as TBI, but with worse cognitive and functional outcomes.

  • Progress is generally slower, but success is possible through creative, non-systematic approaches tailored to the specific injury pattern.