ABPN Brain Injury Medicine cheat sheet

Diffuse axonal injury results from rotational acceleration-deceleration forces causing shear strain at gray-white junctions; classic sites are the corpus callosum, dorsolateral brainstem, and parasagittal white matter.

Primary injury occurs at impact (contusion, axonal shear, hematoma); secondary injury evolves over hours to days via excitotoxicity, mitochondrial failure, calcium influx, oxidative stress, and neuroinflammation.

Glutamate excitotoxicity drives Ca2+ influx through NMDA receptors, activating calpains, caspases, and phospholipases that degrade cytoskeletal and membrane proteins.

Cerebral autoregulation maintains constant CBF across a mean arterial pressure range of roughly 50-150 mmHg; this curve is right-shifted in chronic hypertension and impaired after severe TBI.

Cerebral perfusion pressure equals mean arterial pressure minus intracranial pressure (CPP = MAP - ICP); normal CPP targets are approximately 60-70 mmHg in adults.

Chronic traumatic encephalopathy is defined neuropathologically by perivascular hyperphosphorylated tau tangles at the depths of cortical sulci, distinct from Alzheimer-type plaque-predominant pathology.

The Monro-Kellie doctrine states that intracranial volume is fixed (brain + blood + CSF); an expanding mass is initially offset by CSF and venous blood displacement before ICP rises steeply.

Cerebral edema types include cytotoxic (intracellular swelling from ATP failure), vasogenic (blood-brain barrier breakdown), interstitial (hydrocephalus), and osmotic.

TBI incidence is highest in two peaks: young adults (15-24 years, largely motor vehicle crashes) and older adults (≥65 years, largely falls); falls are the leading cause overall in many registries.

Males have roughly twice the TBI incidence of females; alcohol intoxication is present in a substantial minority of adult TBI presentations and increases recurrence risk.

Helmet use reduces head injury risk in motorcycle and bicycle crashes; seat belts and airbags reduce severe TBI in motor vehicle occupants.

The Glasgow Coma Scale stratifies severity: severe 3-8, moderate 9-12, mild 13-15 (assessed after resuscitation, excluding sedation/paralysis confounders).

Repeat concussion during incomplete recovery carries risk of second-impact syndrome (malignant cerebral edema) and prolonged recovery; graded return-to-play protocols reduce this risk.

Falls in older adults are mitigated by multifactorial interventions: strength/balance exercise, medication review, vision correction, home hazard modification, and vitamin D where deficient.

Penetrating and blast injuries combine focal tissue destruction with pressure-wave shear; blast TBI often coexists with polytrauma and psychiatric comorbidity.

Anoxic-ischemic brain injury from cardiac arrest preferentially damages hippocampus (CA1), neocortex, cerebellum (Purkinje cells), and basal ganglia.

GCS components: eye opening (1-4), verbal response (1-5), motor response (1-6); motor score best predicts outcome and is least confounded by intubation.

The FOUR score adds brainstem reflexes and respiratory pattern to eye and motor responses, useful when the patient is intubated.

Post-traumatic amnesia duration correlates with injury severity; PTA >24 hours indicates at least moderate injury, and PTA >7 days indicates severe injury.

Loss of consciousness >30 minutes and GCS <13 at 24 hours are standard criteria distinguishing moderate-severe from mild TBI.

The Confusion Assessment Method (CAM) is the standard bedside instrument for delirium; it requires acute onset/fluctuation plus inattention plus either disorganized thinking or altered consciousness.

Neuroimaging: CT without contrast is first-line in acute TBI to exclude hemorrhage, mass effect, and herniation; MRI (SWI, DTI) is more sensitive for axonal injury and microhemorrhage.

The Canadian CT Head Rule and New Orleans Criteria guide CT ordering in mild TBI; both rely on history of loss of consciousness, amnesia, vomiting, age, and mechanism.

Formal neuropsychological testing should be delayed until PTA resolves and acute confusional state clears; effort/validity measures are essential in medicolegal contexts.

Avoid hypoxia (SpO2 <90%) and hypotension (systolic <90-100 mmHg); a single episode of hypotension markedly increases mortality in severe TBI.

ICP >20-22 mmHg sustained warrants treatment; tiered options include head elevation 30°, CSF drainage, sedation, osmotic therapy (mannitol or hypertonic saline), and decompressive craniectomy.

Hyperventilation to PaCO2 30-35 mmHg is a temporizing bridge for impending herniation only; prophylactic hyperventilation is avoided because it causes ischemia.

Hypertonic saline and mannitol both lower ICP by creating an osmotic gradient; hypertonic saline may be preferred in hypotension, while mannitol risks hypovolemia and renal injury.

Seizure prophylaxis with phenytoin or levetiracetam is indicated for the first 7 days after severe TBI; prophylaxis beyond 7 days does not prevent late post-traumatic epilepsy.

Venous thromboembolism prophylaxis with mechanical devices starts on admission; pharmacologic prophylaxis is typically delayed 24-72 hours pending hemorrhage stability.

Target normothermia and treat fever aggressively; therapeutic hypothermia has not shown outcome benefit in severe adult TBI in randomized trials.

Steroids are contraindicated in severe TBI (CRASH trial showed increased mortality); avoid hypotension and maintain normoglycemia and normal sodium.

Higher-intensity, task-specific, repetitive practice drives activity-dependent neuroplasticity; dosing (repetitions and intensity) predicts motor recovery better than approach alone.

Constraint-induced movement therapy improves upper limb function in selected hemiparetic patients by forcing use of the affected limb and limiting the less affected one.

Recovery follows a decelerating curve steepest in the first 3-6 months; plateau is not fixed, and late gains occur with targeted training.

Disorders of consciousness include coma, vegetative state/unresponsive wakefulness syndrome, and minimally conscious state; the Coma Recovery Scale-Revised is the standard assessment.

Spasticity management is graded: positioning and stretching, then botulinum toxin for focal tone, then intrathecal baclofen or systemic agents for diffuse tone.

Disorders of consciousness and severe TBI require structured caregiver training and environmental enrichment; early mobilization reduces complications including DVT and pneumonia.

Aerobic exercise after concussion should follow a sub-symptom threshold progression; prolonged strict rest beyond 24-48 hours may delay recovery.

Frontal lobe injury commonly produces dysexecutive syndrome: impaired planning, disinhibition, apathy, and poor insight, often with preserved IQ scores.

Temporal lobe injury, especially hippocampal, produces anterograde declarative memory deficits; implicit and procedural learning may be relatively spared.

Post-traumatic depression is common and treatable; SSRIs are first-line, but agents with anticholinergic burden should be avoided given cognitive effects.

Emotional lability and irritability after TBI respond to behavioral strategies, caregiver education, and agents such as beta-blockers or SSRIs; benzodiazepines may worsen cognition.

Psychosis after TBI is more common with temporal or frontal injury and family history; treatment uses atypical antipsychotics at the lowest effective dose.

Apathy is common and often under-recognized; it differs from depression in lacking dysphoria and may respond to dopaminergic agents such as amantadine.

Amantadine accelerates functional recovery in disorders of consciousness during the first 4 weeks of treatment; benefit may wane after discontinuation.

Sleep-wake disturbance after TBI includes insomnia, circadian disruption, and hypersomnia; cognitive behavioral therapy for insomnia is first-line for chronic insomnia.

Heterotopic ossification presents with warmth, swelling, and reduced range of motion near joints; alkaline phosphatase rises early, and bone scan is sensitive before plain films.

Post-traumatic hypopituitarism can occur after moderate-severe TBI; screen for cortisol, thyroid, and gonadal axes when symptoms suggest deficiency.

Paroxysmal sympathetic hyperactivity features episodic tachycardia, hypertension, tachypnea, fever, diaphoresis, and dystonia; treat with beta-blockers, gabapentin, or clonidine.

Venous thromboembolism risk is high after TBI; prophylaxis decision balances hemorrhage progression against clot risk, with IVC filters reserved for contraindications to anticoagulation.

Dysphagia after severe TBI increases aspiration pneumonia risk; bedside swallow screening followed by instrumental assessment (VFSS/FEES) guides diet advancement.

Neuroendocrine and metabolic complications include syndrome of inappropriate antidiuretic hormone and cerebral salt wasting; both cause hyponatremia but differ in volume status.

Bladder and bowel dysfunction are common; anticholinergic agents treat detrusor overactivity but may worsen cognition in older patients.

Pressure injuries and contractures are prevented by repositioning, splinting, and early mobilization; spasticity contributes to contracture formation.

Decision-making capacity requires four elements: understanding, appreciation, reasoning, and expressing a choice; capacity is task-specific, not global.

Surrogate decision-makers apply substituted judgment (what the patient would have wanted) when prior wishes are known, and best-interests standard when they are not.

Informed consent requires disclosure of diagnosis, proposed treatment, alternatives, and material risks, plus voluntariness and capacity.

Disorders of consciousness raise ethical questions about withdrawal of life-sustaining treatment; prognostic uncertainty and family values guide shared decisions.

Mandated reporting laws require clinicians to report suspected abuse, neglect, or exploitation of vulnerable adults, including those with acquired brain injury.

Return-to-work and driving decisions use functional assessment (e.g., on-road driving evaluation, neuropsychological testing) rather than diagnosis alone.

TBI care follows a trauma system model: prehospital triage to designated trauma centers, designated neurocritical care units, and inpatient rehabilitation referral for severe injury.

Medicolegal documentation should record objective findings, functional status, and prognostic reasoning; malingering and effort testing are relevant to validity of cognitive complaints.

Rehabilitation intensity and timing: early initiation of multidisciplinary rehabilitation after stabilization improves functional outcomes in moderate-severe TBI.

Family and caregiver involvement in rehabilitation improves adherence and reduces caregiver burden; caregiver education is a core component of discharge planning.

Functional outcome measures include the Functional Independence Measure (FIM) and Glasgow Outcome Scale-Extended (GOS-E); GOS-E categories range from death to upper good recovery.

Cognitive rehabilitation targets attention, memory, and executive function with compensatory strategies and metacognitive training; evidence supports strategy-based approaches.

Vocational rehabilitation uses job coaching, work hardening, and reasonable accommodations; supported employment improves competitive employment rates.

Assistive technology and environmental modifications (ramps, communication devices, memory aids) reduce disability and support community participation.

Community integration is measured by participation in home, social, and productive activities; barriers include transportation, insurance, and stigma.

Depression and substance use screening should occur throughout rehabilitation; untreated comorbidity predicts poorer functional and vocational outcomes.

Serial neurologic examinations are essential in acute TBI; a decline in GCS or new focal deficit warrants urgent repeat imaging.

Pupillary examination is a key herniation sign: a blown pupil indicates ipsilateral uncal herniation and requires immediate intervention.

The Glasgow Coma Scale should be scored before sedation and after resuscitation; intubated patients receive a verbal score of 1T.

Neuroimaging modalities: CT for acute hemorrhage and fracture; MRI for diffuse axonal injury, contusion evolution, and brainstem injury.

Electroencephalography is indicated for unexplained altered consciousness, suspected nonconvulsive seizures, and post-traumatic seizure evaluation.

Neuropsychological assessment should include premorbid estimate, effort/validity measures, and domain-specific testing (attention, memory, executive, processing speed).

Screening tools for depression after TBI include the PHQ-9; cognitive symptoms can overlap with depression and require careful attribution.

Prognostic factors in severe TBI include age, GCS motor score, pupillary reactivity, CT findings (Marshall classification), and hypotension/hypoxia.

Falls are the leading cause of TBI-related emergency department visits in older adults; prevention includes home safety and medication review.

Motor vehicle crashes are a leading cause of severe TBI in young adults; prevention includes seat belts, airbags, and graduated licensing.

Sports-related concussion prevention includes rule changes, protective equipment, and education; helmets reduce skull fracture and severe injury but do not eliminate concussion.

Alcohol and substance use increase injury risk and complicate acute assessment; screening and brief intervention reduce recurrence.

Firearm-related TBI has high mortality and is a leading cause of TBI death in the United States; prevention includes safe storage counseling.

Blast injury mechanisms include primary (pressure wave), secondary (penetrating fragments), tertiary (body displacement), and quaternary (burns, inhalation).

Anoxic-ischemic injury from cardiac arrest causes selective neuronal vulnerability in hippocampus, neocortex, cerebellum, and basal ganglia; hypothermia after arrest improves outcomes.

Falls in older adults often involve polypharmacy (sedatives, antihypertensives); deprescribing reduces fall risk.

Airway management: intubate for GCS ≤8, inability to protect airway, or respiratory failure; preoxygenate and maintain cervical spine precautions.

Cervical spine injury must be assumed in severe TBI until cleared by imaging and clinical criteria (e.g., NEXUS or Canadian C-spine rules).

ICP monitoring is indicated for severe TBI with abnormal CT or for GCS ≤8 with normal CT plus risk factors (age >40, hypotension, motor posturing).

Sedation and analgesia (propofol, fentanyl) reduce ICP and metabolic demand; avoid hypotension and monitor for propofol infusion syndrome.

Decompressive craniectomy for refractory ICP elevation reduces mortality but may increase rates of vegetative state and severe disability (DECRA, RESCUEicp).

Seizure prophylaxis for 7 days after severe TBI reduces early post-traumatic seizures; it does not prevent late epilepsy.

Nutrition: early enteral feeding within 24-48 hours is preferred; avoid parenteral nutrition unless enteral is contraindicated.

Sodium and glucose management: avoid hyperglycemia and hyponatremia; maintain normonatremia and treat SIADH or cerebral salt wasting appropriately.

Post-traumatic stress disorder can occur after TBI and may overlap with post-concussive symptoms; trauma-focused psychotherapy is first-line.

Substance use disorders are common after TBI and worsen outcomes; integrated treatment addressing both conditions is recommended.

Impulse control and aggression after TBI may respond to behavioral plans, caregiver training, and medications such as beta-blockers or mood stabilizers.

Cognitive fatigue is common and disabling; pacing, energy conservation, and treating sleep and mood disorders improve function.

Post-traumatic headache is common after mild TBI; management includes abortive and preventive agents, and medication overuse should be avoided.

Dizziness and vestibular dysfunction after concussion are treated with vestibular rehabilitation; benign paroxysmal positional vertigo responds to canalith repositioning.

Return-to-learn after concussion uses graded academic accommodations, rest breaks, and reduced screen time initially, with progressive return to full workload.

Suicide risk is elevated after TBI; screening for depression and suicidal ideation is essential, especially in the first year after injury.

Post-traumatic epilepsy risk is highest with penetrating injury, cortical contusion, subdural hematoma, and early seizures; prophylaxis beyond 7 days is not recommended.

Hydrocephalus after TBI or subarachnoid hemorrhage may present with declining cognition, gait disturbance, and incontinence; shunt placement can improve symptoms.

Cranial nerve injuries (especially olfactory and optic) occur with skull base fractures; anosmia is common after frontal injury.

Carotid-cavernous fistula and traumatic aneurysm are rare vascular complications; suspect with pulsatile exophthalmos, chemosis, or delayed hemorrhage.

Autonomic dysfunction and paroxysmal sympathetic hyperactivity require exclusion of pain, infection, and bowel/bladder distension before escalating treatment.

Bone health: immobilization and anticonvulsants increase fracture risk; weight-bearing exercise and vitamin D/calcium are considered.

Dysautonomia and temperature dysregulation occur in severe TBI; management includes environmental control and treating triggers.

Medication review: avoid anticholinergics, benzodiazepines, and sedatives that impair cognition; use the Beers criteria in older adults.

Advance directives and healthcare proxies should be documented early; surrogates should follow prior expressed wishes when known.

Capacity assessment is task-specific: a patient may have capacity for treatment consent but not for financial decisions.

Informed consent for research in disorders of consciousness requires special protections; surrogate consent and assent where possible are used.

Mandatory reporting includes suspected elder and dependent adult abuse; clinicians must report to designated agencies.

Disability rights and the Americans with Disabilities Act require reasonable accommodations in employment and education for individuals with TBI.

Driving after TBI requires assessment of vision, cognition, and motor function; on-road testing and state reporting laws guide recommendations.

Return-to-work planning should involve vocational rehabilitation, employer accommodations, and gradual return with modified duties.

Systems of care: trauma center designation, neurocritical care units, inpatient rehabilitation facilities, and community-based programs improve outcomes.

Cerebral blood flow is approximately 50 mL/100 g/min; flow below 20 mL/100 g/min causes EEG slowing, and below 10 mL/100 g/min causes irreversible infarction.

Cerebral ischemia triggers the ischemic cascade: ATP depletion, Na+/K+ pump failure, depolarization, glutamate release, calcium influx, and cell death.

Blood-brain barrier disruption after TBI permits vasogenic edema; tight junction proteins (claudins, occludin) are degraded by matrix metalloproteinases.

Neuroinflammation involves microglial activation, cytokine release (IL-1β, TNF-α), and leukocyte infiltration, contributing to secondary injury.

Axonal injury evolves over hours to days; APP immunohistochemistry and silver staining detect axonal pathology, and DTI shows white matter integrity loss.

The hippocampus and prefrontal cortex are vulnerable to excitotoxicity and hypoxia, explaining memory and executive deficits after TBI.

Cerebral autoregulation impairment after TBI makes blood pressure support critical; both hypotension and hypertension can worsen injury.

Neurogenesis and plasticity occur in the subventricular zone and dentate gyrus; rehabilitation and enriched environments may enhance plasticity.

TBI is a leading cause of death and disability worldwide; low- and middle-income countries have higher incidence and mortality.

Older adults have higher TBI mortality and worse functional outcomes than younger adults with similar injury severity.

Alcohol intoxication at time of injury is associated with increased mortality and complications in TBI.

Prevention strategies: primary (prevent injury), secondary (reduce injury severity), and tertiary (reduce disability and recurrence).

Helmet laws and seat belt laws reduce severe TBI incidence at the population level.

Concussion in sports: removal from play and graded return-to-sport reduce risk of prolonged recovery and second-impact syndrome.

Falls prevention in older adults includes exercise, vision correction, medication review, and home modification.

Firearm injury is a leading cause of TBI death in the US; safe storage and counseling are prevention strategies.

GCS motor score is the strongest predictor of outcome among GCS components.

Pupillary reactivity and the pupillary light reflex are key prognostic indicators in severe TBI.

CT findings associated with poor outcome include midline shift, subdural hematoma, contusion, and traumatic subarachnoid hemorrhage.

The Marshall CT classification stratifies TBI severity based on imaging findings.

Post-traumatic amnesia duration is a core measure of injury severity and predicts functional outcome.

Neuropsychological assessment should include validity/effort testing, especially in medicolegal contexts.

Screening for depression and anxiety after TBI is recommended; the PHQ-9 is commonly used.

EEG is indicated for unexplained altered consciousness and suspected nonconvulsive seizures.

Avoid hypotension (systolic <90 mmHg) and hypoxia (SpO2 <90%) to prevent secondary injury.

ICP monitoring is indicated for severe TBI with abnormal CT or risk factors.

CPP target is approximately 60-70 mmHg in adults; individualize based on autoregulation status.

Hyperosmolar therapy with mannitol or hypertonic saline treats elevated ICP; monitor osmolarity and renal function.

Hyperventilation is a temporizing measure for impending herniation only; avoid prophylactic hyperventilation.

Seizure prophylaxis for 7 days after severe TBI; no benefit beyond 7 days.

VTE prophylaxis with mechanical devices initially; pharmacologic prophylaxis when hemorrhage is stable.

Avoid steroids in severe TBI; CRASH trial showed increased mortality.

Task-specific, repetitive practice drives neuroplasticity and functional recovery.

Constraint-induced movement therapy improves upper limb function in selected patients.

Recovery is fastest in the first 3-6 months but can continue for years with targeted training.

Disorders of consciousness assessment uses the Coma Recovery Scale-Revised.

Spasticity management is graded: positioning, botulinum toxin, intrathecal baclofen.

Early mobilization reduces complications such as DVT and pneumonia.

Aerobic exercise after concussion follows a sub-symptom threshold progression.

Caregiver training and environmental enrichment support recovery in severe TBI.

Frontal lobe injury causes dysexecutive syndrome with impaired planning, disinhibition, and poor insight.

Temporal lobe injury causes anterograde declarative memory deficits; procedural learning may be spared.

SSRIs are first-line for post-traumatic depression; avoid anticholinergic burden.

Emotional lability and irritability respond to behavioral strategies and agents such as beta-blockers or SSRIs.

Apathy differs from depression in lacking dysphoria and may respond to dopaminergic agents.

Amantadine accelerates recovery in disorders of consciousness during the first 4 weeks.

CBT-I is first-line for chronic insomnia after TBI.

Suicide risk is elevated after TBI; screen for depression and suicidal ideation.

Heterotopic ossification presents with warmth, swelling, and reduced range of motion; alkaline phosphatase rises early.

Post-traumatic hypopituitarism can occur after moderate-severe TBI; screen cortisol, thyroid, and gonadal axes.

Paroxysmal sympathetic hyperactivity features episodic tachycardia, hypertension, tachypnea, fever, and diaphoresis.

VTE risk is high after TBI; balance prophylaxis against hemorrhage progression.

Dysphagia increases aspiration risk; bedside screening followed by instrumental assessment guides diet.

SIADH and cerebral salt wasting both cause hyponatremia but differ in volume status.

Pressure injuries and contractures are prevented by repositioning, splinting, and early mobilization.

Avoid anticholinergics, benzodiazepines, and sedatives that impair cognition, especially in older adults.

Capacity requires understanding, appreciation, reasoning, and expressing a choice; it is task-specific.

Surrogate decision-makers use substituted judgment when prior wishes are known, best interests otherwise.

Informed consent requires disclosure of diagnosis, treatment, alternatives, and material risks.

Disorders of consciousness raise ethical questions about withdrawal of life-sustaining treatment; shared decision-making is essential.

Mandated reporting laws require reporting suspected abuse, neglect, or exploitation of vulnerable adults.

Driving and return-to-work decisions use functional assessment rather than diagnosis alone.

TBI care follows a trauma system model with designated trauma centers and neurocritical care units.

Medicolegal documentation should record objective findings, functional status, and prognostic reasoning.

Diffuse axonal injury results from rotational acceleration-deceleration forces causing shear strain at gray-white junctions.

Primary injury occurs at impact; secondary injury evolves via excitotoxicity, mitochondrial failure, and neuroinflammation.

Glutamate excitotoxicity drives calcium influx through NMDA receptors, activating calpains and caspases.

Cerebral autoregulation maintains constant CBF across MAP 50-150 mmHg; impaired after severe TBI.

CPP = MAP - ICP; normal CPP target is 60-70 mmHg in adults.

CTE is defined by perivascular hyperphosphorylated tau tangles at sulcal depths.

Monro-Kellie doctrine: intracranial volume is fixed; expanding mass is offset by CSF and venous blood displacement.

Cerebral edema types include cytotoxic, vasogenic, interstitial, and osmotic.

TBI incidence peaks in young adults (15-24 years) and older adults (≥65 years).

Falls are the leading cause of TBI in older adults; motor vehicle crashes lead in young adults.

Males have roughly twice the TBI incidence of females.

Alcohol intoxication is present in a substantial minority of adult TBI presentations.

Helmet and seat belt use reduce severe TBI risk.

GCS stratifies severity: severe 3-8, moderate 9-12, mild 13-15.

Repeat concussion during incomplete recovery risks second-impact syndrome.

Anoxic-ischemic injury from cardiac arrest damages hippocampus, neocortex, cerebellum, and basal ganglia.

GCS components: eye 1-4, verbal 1-5, motor 1-6; motor score best predicts outcome.

FOUR score adds brainstem reflexes and respiratory pattern for intubated patients.

PTA >24 hours indicates at least moderate injury; PTA >7 days indicates severe injury.

Loss of consciousness >30 minutes and GCS <13 at 24 hours distinguish moderate-severe from mild TBI.

CAM is the standard bedside instrument for delirium.

CT without contrast is first-line in acute TBI; MRI (SWI, DTI) is more sensitive for axonal injury.

Canadian CT Head Rule and New Orleans Criteria guide CT ordering in mild TBI.

Neuropsychological testing should be delayed until PTA resolves; effort/validity measures are essential.

Avoid hypoxia (SpO2 <90%) and hypotension (systolic <90-100 mmHg) in severe TBI.

ICP >20-22 mmHg sustained warrants treatment: head elevation, CSF drainage, sedation, osmotic therapy, decompressive craniectomy.

Hyperventilation to PaCO2 30-35 mmHg is a temporizing bridge for impending herniation only.

Hypertonic saline and mannitol lower ICP by creating an osmotic gradient.

Seizure prophylaxis with phenytoin or levetiracetam is indicated for the first 7 days after severe TBI.

VTE prophylaxis with mechanical devices starts on admission; pharmacologic prophylaxis delayed 24-72 hours pending hemorrhage stability.

Target normothermia and treat fever aggressively; therapeutic hypothermia has not shown benefit in severe adult TBI.

Steroids are contraindicated in severe TBI (CRASH trial showed increased mortality).

Higher-intensity, task-specific, repetitive practice drives activity-dependent neuroplasticity.

Constraint-induced movement therapy improves upper limb function in selected hemiparetic patients.

Recovery follows a decelerating curve steepest in the first 3-6 months.

Disorders of consciousness include coma, unresponsive wakefulness syndrome, and minimally conscious state; CRS-R is the standard assessment.

Spasticity management is graded: positioning and stretching, botulinum toxin, intrathecal baclofen.

Early mobilization reduces complications including DVT and pneumonia.

Aerobic exercise after concussion follows a sub-symptom threshold progression.

Caregiver training and environmental enrichment support recovery in severe TBI.

Frontal lobe injury commonly produces dysexecutive syndrome with impaired planning, disinhibition, and poor insight.

Temporal lobe injury, especially hippocampal, produces anterograde declarative memory deficits.

Post-traumatic depression is common and treatable; SSRIs are first-line.

Emotional lability and irritability respond to behavioral strategies and agents such as beta-blockers or SSRIs.

Psychosis after TBI is more common with temporal or frontal injury and family history.

Apathy differs from depression in lacking dysphoria and may respond to dopaminergic agents.

Amantadine accelerates functional recovery in disorders of consciousness during the first 4 weeks.

CBT-I is first-line for chronic insomnia after TBI.

Heterotopic ossification presents with warmth, swelling, and reduced range of motion; alkaline phosphatase rises early.

Post-traumatic hypopituitarism can occur after moderate-severe TBI; screen for cortisol, thyroid, and gonadal axes.

Paroxysmal sympathetic hyperactivity features episodic tachycardia, hypertension, tachypnea, fever, diaphoresis, and dystonia.

VTE risk is high after TBI; prophylaxis decision balances hemorrhage progression against clot risk.

Dysphagia after severe TBI increases aspiration pneumonia risk; bedside swallow screening followed by instrumental assessment guides diet.

SIADH and cerebral salt wasting both cause hyponatremia but differ in volume status.

Bladder and bowel dysfunction are common; anticholinergic agents treat detrusor overactivity but may worsen cognition.

Pressure injuries and contractures are prevented by repositioning, splinting, and early mobilization.

Decision-making capacity requires understanding, appreciation, reasoning, and expressing a choice.

Surrogate decision-makers apply substituted judgment when prior wishes are known, best interests otherwise.

Informed consent requires disclosure of diagnosis, treatment, alternatives, and material risks.

Disorders of consciousness raise ethical questions about withdrawal of life-sustaining treatment.

Mandated reporting laws require reporting suspected abuse, neglect, or exploitation of vulnerable adults.

Return-to-work and driving decisions use functional assessment rather than diagnosis alone.

TBI care follows a trauma system model with designated trauma centers and neurocritical care units.

Medicolegal documentation should record objective findings, functional status, and prognostic reasoning.

Diffuse axonal injury results from rotational acceleration-deceleration forces causing shear strain at gray-white junctions.

Primary injury occurs at impact; secondary injury evolves via excitotoxicity, mitochondrial failure, and neuroinflammation.

Glutamate excitotoxicity drives calcium influx through NMDA receptors, activating calpains and caspases.

Cerebral autoregulation maintains constant CBF across MAP 50-150 mmHg; impaired after severe TBI.

CPP = MAP - ICP; normal CPP target is 60-70 mmHg in adults.

CTE is defined by perivascular hyperphosphorylated tau tangles at sulcal depths.

Monro-Kellie doctrine: intracranial volume is fixed; expanding mass is offset by CSF and venous blood displacement.

Cerebral edema types include cytotoxic, vasogenic, interstitial, and osmotic.