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100+ Free ABPN Brain Injury Medicine Practice Questions

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Approximately how many traumatic brain injuries (TBI-related ED visits, hospitalizations, and deaths) occur each year in the United States according to the CDC?

A
B
C
D
to track
2026 Statistics

Key Facts: ABPN Brain Injury Medicine Exam

~200

Total MCQ Items

ABPN Brain Injury Medicine subspecialty exam

>22

ICP Treatment Threshold (mm Hg)

Brain Trauma Foundation 4th edition (2016)

60-70

Target CPP (mm Hg)

Brain Trauma Foundation 4th edition (2016)

$2,200

2026 Exam Fee

ABPN Brain Injury Medicine subspecialty

1 yr

Fellowship Training

ACGME-accredited Brain Injury Medicine fellowship

Pearson VUE

Test Delivery

Computer-based testing at authorized centers

The ABPN Brain Injury Medicine subspecialty exam is a 1-day computer-based test at Pearson VUE with ~200 single-best-answer MCQs. The 2026 content outline emphasizes TBI epidemiology and biomechanics (~7%), neuropathology and primary/secondary injury (~10%), acute and neurocritical care (~14%), neuroimaging (~8%), prognostication and outcome scales (~6%), post-concussive syndrome and sports concussion (~10%), cognitive rehabilitation (~10%), behavioral/emotional sequelae (~9%), motor/sensory deficits and dysautonomia (~7%), post-traumatic seizures and neuroendocrine dysfunction (~8%), pediatric TBI (~5%), blast and military TBI (~3%), and return-to-play/duty plus pharmacotherapy (~3%). Exam fee is ~$2,200; requires primary ABMS certification plus a 1-year ACGME Brain Injury Medicine fellowship.

Sample ABPN Brain Injury Medicine Practice Questions

Try these sample questions to test your ABPN Brain Injury Medicine exam readiness. Each question includes a detailed explanation. Start the interactive quiz above for the full 100+ question experience with AI tutoring.

1Approximately how many traumatic brain injuries (TBI-related ED visits, hospitalizations, and deaths) occur each year in the United States according to the CDC?
A.About 200,000
B.About 800,000
C.About 2.8 million
D.About 10 million
Explanation: The CDC reports approximately 2.8 million TBI-related ED visits, hospitalizations, and deaths annually in the United States. Falls are the leading mechanism overall, with motor vehicle crashes most common in adolescents/young adults and assaults a major cause in working-age adults. This baseline epidemiology is high-yield for the boards.
2Across all age groups in the United States, which mechanism is the most common cause of TBI overall?
A.Motor vehicle collisions
B.Falls
C.Assault
D.Sports and recreation
Explanation: Falls are the leading mechanism of TBI overall in the United States, driven primarily by older adults (≥65 y) and young children. Motor vehicle collisions are the leading mechanism of TBI-related death in adolescents and young adults. Assault and sports/recreation contribute substantially but are not the overall leaders.
3A patient is brought in after a fall with an initial Glasgow Coma Scale of 7. How is this severity of TBI classified?
A.Mild TBI
B.Moderate TBI
C.Severe TBI
D.Concussion
Explanation: Standard severity classification by initial post-resuscitation GCS: severe TBI = GCS 3-8; moderate = 9-12; mild (concussion) = 13-15. A GCS of 7 falls in the severe range. Severity also incorporates duration of LOC, post-traumatic amnesia, and structural imaging.
4Which biomechanical mechanism is most directly responsible for diffuse axonal injury (DAI)?
A.Linear (translational) acceleration
B.Rotational/angular acceleration of the brain within the skull
C.Static compression of the cranium
D.Penetrating ballistic injury
Explanation: DAI results primarily from rotational (angular) acceleration-deceleration that produces shear strain at tissue interfaces of differing density — classically the gray-white junction, corpus callosum (especially splenium), and dorsolateral midbrain/rostral pons. Linear acceleration produces focal contusions (coup/contrecoup). Penetrating injury causes focal track injury rather than diffuse shear.
5A patient sustained a TBI and remained in post-traumatic amnesia (PTA) for 36 hours. Per the Russell classification, this duration of PTA corresponds to what TBI severity?
A.Very mild (PTA <5 minutes)
B.Mild (PTA 5-60 minutes)
C.Moderate (PTA 1-24 hours)
D.Severe (PTA 1-7 days)
Explanation: Russell's PTA-based severity classification: very mild (<5 min), mild (5-60 min), moderate (1-24 h), severe (1-7 days), very severe (1-4 weeks), and extremely severe (>4 weeks). PTA of 36 hours falls in the severe range. The Galveston Orientation and Amnesia Test (GOAT) is the most commonly used bedside instrument to track PTA resolution (score ≥75 on 2 consecutive days).
6Which immunohistochemical marker is the gold standard for identifying diffuse axonal injury on neuropathology?
A.Glial fibrillary acidic protein (GFAP)
B.Beta-amyloid precursor protein (β-APP)
C.Synaptophysin
D.Hyperphosphorylated tau (p-tau)
Explanation: Beta-amyloid precursor protein (β-APP) accumulates in damaged axons within hours of injury due to interrupted fast axonal transport, making it the standard immunohistochemical marker of axonal injury. GFAP marks reactive astrogliosis (and is a serum biomarker for TBI). p-tau is the defining feature of CTE (perivascular at sulcal depths).
7A 22-year-old struck on the temple has a brief loss of consciousness, awakens lucid, then 90 minutes later becomes obtunded with a fixed dilated right pupil. CT shows a lens-shaped hyperdense extra-axial collection over the right temporal lobe that does not cross suture lines. Which vessel is most commonly responsible?
A.Bridging cortical veins
B.Middle meningeal artery
C.Anterior cerebral artery
D.Cavernous sinus
Explanation: Epidural hematoma is classically arterial — most often from the middle meningeal artery torn by a temporal bone fracture. The biconvex/lens shape is bounded by tight dural attachments at sutures. The classic 'lucid interval' followed by deterioration plus uncal herniation (CN III compression → ipsilateral fixed dilated pupil) requires emergent surgical evacuation.
8Which extra-axial hemorrhage is crescent-shaped on CT, crosses suture lines, and most often results from torn bridging cortical veins in elderly or anticoagulated patients?
A.Epidural hematoma
B.Subdural hematoma
C.Subarachnoid hemorrhage
D.Intraparenchymal hemorrhage
Explanation: Subdural hematomas are crescent-shaped, cross sutures (but not falx/tentorium), and arise from torn bridging veins. They are common in the elderly (cerebral atrophy stretches bridging veins) and in patients on anticoagulants. Acute SDH is hyperdense; chronic SDH (>2-3 weeks) is hypodense; mixed-density 'acute on chronic' is common.
9After an occipital impact in a fall, a patient develops bilateral frontal lobe contusions visible on CT. This pattern is best explained by which mechanism?
A.Diffuse axonal shearing
B.Coup-contrecoup injury — brain striking the rough orbital roofs and sphenoid wing opposite the impact
C.Direct penetrating injury through the calvarium
D.Hypoxic-ischemic watershed injury
Explanation: Contrecoup contusions are most common in frontal and temporal lobes because, with rapid deceleration, the brain strikes the rough internal surfaces of the orbital roofs, sphenoid wings, and middle cranial fossa opposite the impact site. An occipital impact therefore typically produces frontal/temporal pole contusions.
10Which herniation syndrome typically produces an ipsilateral fixed and dilated pupil with contralateral hemiparesis?
A.Subfalcine herniation
B.Uncal (transtentorial) herniation
C.Central transtentorial herniation
D.Tonsillar herniation
Explanation: Uncal herniation is the most common transtentorial herniation in TBI. The medial temporal lobe (uncus) compresses the ipsilateral CN III (parasympathetic fibers run on the surface — pupillary dilation precedes ophthalmoplegia) and the cerebral peduncle, producing contralateral hemiparesis. False localizing signs occur if the contralateral peduncle is pushed against Kernohan's notch (ipsilateral hemiparesis).

About the ABPN Brain Injury Medicine Exam

The ABPN Brain Injury Medicine Subspecialty Certification Examination is a 1-day computer-based test for physicians who have completed an ACGME-accredited 1-year Brain Injury Medicine fellowship after primary certification (most often PM&R, Neurology, Child Neurology, or Psychiatry). The exam contains approximately 200 single-best-answer MCQs covering TBI epidemiology and biomechanics (acceleration-deceleration, rotational, blast), the Glasgow Coma Scale and severity classification (mild/moderate/severe), primary vs secondary injury (DAI, contusion, hemorrhage, hypoxia-ischemia, cerebral edema), neurocritical care (ICP/CPP, Brain Trauma Foundation guidelines, hyperosmolar therapy, decompressive craniectomy — DECRA/RESCUEicp), prognostication (IMPACT/CRASH), neuroimaging (CT, MRI, DTI, SWI), post-concussive syndrome and CTE risk, cognitive rehabilitation, behavioral and emotional sequelae (agitation, depression, PTSD), motor and sensory deficits, post-traumatic seizures and epilepsy, neuroendocrine dysfunction (hypopituitarism, SIADH, CSW, DI), heterotopic ossification, dysautonomia/PSH, return-to-play (CISG/Concussion in Sport — Amsterdam 2022) and return-to-duty (DoD/VA), pediatric TBI and abusive head trauma, sports concussion and SCAT6, blast TBI in service members, and pharmacotherapy (amantadine for DOC per Giacino 2012, methylphenidate, SSRIs, atypical antipsychotics, antiepileptics).

Questions

200 scored questions

Time Limit

1-day CBT

Passing Score

Criterion-referenced scaled score set by ABPN

Exam Fee

~$2,200 ABPN Brain Injury Medicine subspecialty exam fee (2026) (American Board of Psychiatry and Neurology (ABPN) / Pearson VUE)

ABPN Brain Injury Medicine Exam Content Outline

~7%

TBI Epidemiology, Biomechanics & Severity

U.S. TBI incidence ~2.8 million/year (CDC). Falls leading cause overall; MVCs in adolescents/young adults; assaults; sports; blast in service members. Biomechanics — linear acceleration (focal contusions, coup/contrecoup), rotational/angular acceleration (diffuse axonal injury at gray-white junction, corpus callosum, dorsolateral midbrain), blast overpressure (primary blast wave). Severity by initial GCS — mild 13-15 (concussion), moderate 9-12, severe 3-8. Duration of LOC, post-traumatic amnesia (PTA, Russell or GOAT), and structural imaging refine classification.

~10%

Neuropathology & Primary vs Secondary Injury

Primary injury — diffuse axonal injury (DAI, beta-APP staining, gray-white junction, corpus callosum, dorsolateral pons), cortical contusions (frontal/temporal poles), epidural hematoma (lens-shaped, middle meningeal artery, lucid interval), subdural hematoma (crescentic, bridging veins, elderly/anticoagulated), traumatic SAH, intraparenchymal hemorrhage. Secondary injury cascade — hypoxia, hypotension, excitotoxicity (glutamate/NMDA), oxidative stress, mitochondrial dysfunction, calcium dysregulation, inflammation, cerebral edema (cytotoxic vs vasogenic), elevated ICP, herniation syndromes (uncal, central, subfalcine, tonsillar).

~14%

Acute Management & Neurocritical Care

Brain Trauma Foundation 4th edition guidelines (2016) — ICP monitoring for severe TBI with abnormal CT (or with normal CT plus ≥2 of: age >40, motor posturing, SBP <90). Treat ICP >22 mm Hg; target CPP 60-70 mm Hg. Tier 1 (head of bed 30°, sedation/analgesia, normothermia, normocapnia PaCO2 35-40, hyperosmolar — mannitol 0.25-1 g/kg or 3% saline), Tier 2 (CSF drainage via EVD, neuromuscular blockade, mild hyperventilation PaCO2 30-35), Tier 3 (decompressive craniectomy — RESCUEicp 2016 reduced mortality with more vegetative survivors; DECRA 2011 negative for early bifrontal; pentobarbital coma; therapeutic hypothermia 32-34°C — POLAR/Eurotherm negative). Avoid steroids (CRASH 2004 — increased mortality). TXA within 3 h reduces head-injury death (CRASH-3 2019). Seizure prophylaxis with levetiracetam or phenytoin × 7 days for severe TBI.

~8%

Neuroimaging in TBI

Non-contrast head CT — first-line for acute TBI. Marshall/Rotterdam CT classifications. Epidural (lens, doesn't cross sutures), subdural (crescent, crosses sutures), tSAH, contusions (frontal/temporal), midline shift, cisternal effacement. Canadian CT Head Rule and New Orleans Criteria for mild TBI. MRI more sensitive — DAI on SWI/GRE (microbleeds at gray-white junction, corpus callosum, dorsolateral brainstem); FLAIR for non-hemorrhagic shear; DWI for ischemia. Diffusion tensor imaging (DTI) for white matter integrity in research. Functional imaging (PET, fMRI) and amyloid/tau PET (CTE research). MR spectroscopy (NAA reduction).

~6%

Prognostication & Outcome Scales

Glasgow Outcome Scale (GOS 1-5: dead, vegetative, severe disability, moderate disability, good recovery) and GOS-Extended (GOSE 1-8). Functional Independence Measure (FIM). Disability Rating Scale (DRS). IMPACT and CRASH calculators integrate age, GCS motor, pupils, hypoxia, hypotension, CT features, glucose, hemoglobin, tSAH, EDH for 6-month mortality and unfavorable outcome. Disorders of consciousness — coma, vegetative state/UWS (>1 month — persistent), minimally conscious state (MCS+ language; MCS- non-reflexive movement), emergence (functional object use or communication). Coma Recovery Scale-Revised (CRS-R) is the gold-standard bedside tool.

~10%

Concussion, Post-Concussive Syndrome & CTE

Sports concussion — Concussion in Sport Group (Amsterdam 2022, 6th international consensus); SCAT6 (athletes ≥13 y), Child SCAT6 (5-12 y), Sport Concussion Office Assessment Tool (SCOAT6). Symptom clusters — physical (HA, dizziness), cognitive (fog, slowed processing), emotional (irritability, anxiety), sleep. Most resolve within 2 weeks (adults) / 4 weeks (children/adolescents). Persistent post-concussive symptoms beyond 4 weeks → multidisciplinary care (vestibular, cervical, oculomotor, exertional, mood). Sub-symptom threshold aerobic exercise within 24-48 h is now recommended (no longer strict cocoon rest). Second-impact syndrome (rare, catastrophic cerebral edema in adolescents). Chronic traumatic encephalopathy (CTE) — neuropathological diagnosis (hyperphosphorylated tau in neurons/astrocytes around small vessels at sulcal depths); diagnosed only post-mortem; clinically traumatic encephalopathy syndrome (TES) per 2021 NINDS criteria.

~10%

Cognitive Rehabilitation

Cognitive domains affected — attention/processing speed, memory, executive function, language/social pragmatics. Evidence-based approaches per ACRM/Cicerone updates: Attention Process Training (APT) for attention; metacognitive strategy training (Goal Management Training, GMT) for executive dysfunction; spaced retrieval and errorless learning for memory; external compensatory aids (smartphones, alarms, notebooks). Comprehensive holistic neuropsychological rehabilitation programs improve community participation. Pharmacologic adjuncts — methylphenidate (attention, processing speed; Whyte 2004), amantadine (arousal/recovery in DOC — Giacino NEJM 2012 in vegetative/MCS 4-16 weeks post-injury), cholinesterase inhibitors (limited evidence).

~9%

Behavioral & Emotional Sequelae

Post-TBI agitation peaks during PTA — assess with Agitated Behavior Scale (ABS); environmental management first (quiet room, consistent staff, reduce stimulation); avoid restraints. Pharmacotherapy — propranolol (best evidence per INCOG 2014/2023), amantadine, valproate, atypical antipsychotics (avoid typical antipsychotics and benzodiazepines — worsen recovery and cognition). Depression in 25-50% post-TBI; SSRIs (sertraline) first-line; avoid tricyclics (anticholinergic). Anxiety, PTSD (overlap with mTBI in service members). Pseudobulbar affect — dextromethorphan/quinidine. Personality change, disinhibition (orbitofrontal), apathy (medial frontal/cingulate). Suicide risk elevated 2-4× post-TBI.

~7%

Motor, Sensory & Autonomic Deficits

Spasticity — upper motor neuron syndrome with velocity-dependent tone increase; modified Ashworth Scale; treatment hierarchy — stretching/positioning → oral baclofen, tizanidine, dantrolene → focal botulinum toxin → intrathecal baclofen. Avoid benzodiazepines if possible. Cranial neuropathies — anosmia (CN I, cribriform shear, ~20% of moderate-severe TBI), CN VII (temporal bone fracture). Vestibular dysfunction (BPPV, post-traumatic peripheral vestibulopathy, central). Visual — convergence insufficiency, accommodation deficits. Paroxysmal sympathetic hyperactivity (PSH/dysautonomia/'storming') — episodic tachycardia, hypertension, hyperthermia, tachypnea, diaphoresis, dystonic posturing; PSH-Assessment Measure; treatment with morphine, gabapentin, propranolol, clonidine, bromocriptine, intrathecal baclofen.

~8%

Post-Traumatic Seizures & Neuroendocrine Dysfunction

Post-traumatic seizures — immediate (<24 h), early (<7 d), late (>7 d, defines post-traumatic epilepsy, PTE). Risk factors for PTE — penetrating injury (>50%), depressed skull fracture, intracranial hematoma requiring evacuation, early seizure, GCS <10. Prophylaxis with levetiracetam or phenytoin reduces early but NOT late seizures (Class I). Levetiracetam preferred (no monitoring, fewer interactions). Neuroendocrine — anterior hypopituitarism in 15-50% post moderate-severe TBI; growth hormone deficiency most common (fatigue, low quality of life); secondary hypogonadism, hypothyroidism, adrenal insufficiency; screen 3-6 months post-injury. Posterior pituitary — DI (hypernatremia, dilute urine, treat with DDAVP), SIADH (euvolemic hyponatremia, fluid restriction), cerebral salt wasting (hyponatremia + hypovolemia, treat with salt and fluid replacement).

~5%

Pediatric TBI & Abusive Head Trauma

Pediatric TBI — leading cause of death/disability in children. PECARN rule for clinically important TBI in children <2 y and 2-18 y avoids unnecessary CT. Abusive head trauma (AHT) — formerly 'shaken baby'; classic triad (subdural hematoma, retinal hemorrhages, encephalopathy); look for skull fractures, posterior rib fractures, metaphyseal corner fractures, bruising in non-cruising infants (TEN-4 FACES rule). Mandatory reporting. Heterotopic ossification — peri-articular ectopic bone (hip, knee, elbow, shoulder); 4-12 weeks post-injury; alkaline phosphatase, triple-phase bone scan; treat with NSAIDs (indomethacin) for prophylaxis, ROM, surgical resection when mature. Pediatric concussion — generally longer recovery than adults (up to 4 weeks).

~3%

Blast & Military TBI

Blast injury categories — primary (overpressure wave; pulmonary, tympanic membrane, brain), secondary (penetrating fragments), tertiary (body propelled), quaternary (burns, inhalation, crush). Most service-member TBI is mild and from blast (IED). High overlap with PTSD — symptom overlap (sleep, irritability, concentration). DoD severity classification mirrors civilian (mild/moderate/severe) with addition of penetrating. VA/DoD clinical practice guideline for mild TBI/concussion 2021 — symptom-targeted treatment, gradual return-to-activity, treat comorbid PTSD/pain/sleep.

~3%

Return-to-Play, Return-to-Duty & Pharmacotherapy

Return-to-play (RTP) per Amsterdam 2022 CISG — 6-step graduated protocol (symptom-limited activity → light aerobic → sport-specific → non-contact training → full-contact practice → return to play); each step ≥24 h; strategic rest 24-48 h then early sub-symptom-threshold aerobic exercise. Same-day return prohibited for any suspected concussion. Pharmacotherapy summary — amantadine 200-400 mg/d for DOC and arousal (Giacino 2012); methylphenidate for attention/processing; sertraline for depression; propranolol for agitation/PSH; levetiracetam for seizure prophylaxis; melatonin for sleep; avoid benzodiazepines, typical antipsychotics, anticholinergics, and prophylactic phenytoin beyond 7 days.

How to Pass the ABPN Brain Injury Medicine Exam

What You Need to Know

  • Passing score: Criterion-referenced scaled score set by ABPN
  • Exam length: 200 questions
  • Time limit: 1-day CBT
  • Exam fee: ~$2,200 ABPN Brain Injury Medicine subspecialty exam fee (2026)

Keys to Passing

  • Complete 500+ practice questions
  • Score 80%+ consistently before scheduling
  • Focus on highest-weighted sections
  • Use our AI tutor for tough concepts

ABPN Brain Injury Medicine Study Tips from Top Performers

1ICP/CPP management — Brain Trauma Foundation 4th ed. (2016): treat ICP >22 mm Hg; target CPP 60-70 (avoid <50 ischemia and aggressive >70 ARDS). Tiered approach — Tier 1: HOB 30°, sedation/analgesia, normothermia, normocapnia (PaCO2 35-40), hyperosmolar (mannitol 0.25-1 g/kg or 3% saline). Tier 2: CSF drainage via EVD, neuromuscular blockade, brief moderate hyperventilation (PaCO2 30-35). Tier 3: decompressive craniectomy or pentobarbital coma. RESCUEicp (2016) — secondary decompressive craniectomy reduced mortality but increased proportion in vegetative state. DECRA (2011) — early bifrontal craniectomy at lower ICP threshold gave WORSE outcomes. CRASH (2004) — methylprednisolone in head injury INCREASED mortality (steroids contraindicated).
2Disorders of consciousness — coma (no eye opening, no command-following, no localization), unresponsive wakefulness syndrome / vegetative state (eye opening, sleep-wake cycles, reflexive only), minimally conscious state MCS- (non-reflexive movement, visual pursuit) and MCS+ (command-following, intelligible verbalization, intentional communication), emergence from MCS (functional object use OR functional communication). Coma Recovery Scale-Revised (CRS-R) is the gold-standard bedside tool. Amantadine 100 mg BID titrated to 200 mg BID weeks 4-16 post-injury accelerates functional recovery in vegetative or MCS patients (Giacino, NEJM 2012).
3Post-traumatic seizures — immediate (<24 h, no PTE risk), early (<7 d, modest PTE risk), late (>7 d, defines post-traumatic epilepsy). Risk for PTE: penetrating injury (>50%), depressed skull fracture, evacuated hematoma, early seizure, GCS <10. Levetiracetam or phenytoin × 7 days for severe TBI reduces EARLY but NOT late seizures. Levetiracetam preferred (no levels, fewer interactions, equivalent efficacy per Szaflarski et al.). Do NOT continue prophylaxis beyond 7 days.
4Paroxysmal sympathetic hyperactivity (PSH, 'storming') — episodic tachycardia, hypertension, hyperthermia, tachypnea, diaphoresis, and dystonic posturing in severe TBI (often DAI). Diagnose with PSH-Assessment Measure (PSH-AM). Abortive — IV morphine. Preventive (titrate as a multi-drug strategy) — propranolol (sympathetic blockade), gabapentin (allodynia/spinal), clonidine (central α2), bromocriptine (D2 agonist), intrathecal baclofen for refractory dystonic posturing. Avoid scheduled PRN benzodiazepines (sedating, may worsen recovery).
5Sports concussion (Amsterdam 2022, 6th International Consensus): SCAT6 (≥13 y), Child SCAT6 (5-12 y); strict 'cocoon' rest is OUT. After 24-48 h relative rest, begin sub-symptom-threshold aerobic exercise. 6-step graduated return-to-play protocol (symptom-limited activity → light aerobic → sport-specific → non-contact training → full-contact practice → return to sport); each step ≥24 h; back up one step if symptoms return. Same-day return to play is prohibited for any suspected concussion. Most resolve in 2 weeks (adults) / 4 weeks (children/adolescents). Persistent symptoms → vestibular, cervical, oculomotor, exertional, and mental-health-targeted multidisciplinary care.

Frequently Asked Questions

What is the ABPN Brain Injury Medicine Subspecialty Examination?

The ABPN Brain Injury Medicine Subspecialty Certification Examination is a 1-day computer-based test administered by the American Board of Psychiatry and Neurology (ABPN) at Pearson VUE test centers. It certifies expertise in the evaluation, acute management, and rehabilitation of patients with traumatic brain injury across the severity spectrum (mild/concussion through severe TBI and disorders of consciousness). Brain Injury Medicine is co-sponsored by ABPN and the American Board of Physical Medicine and Rehabilitation (ABPMR), and most diplomates come from PM&R, Neurology, Child Neurology, or Psychiatry primary boards.

Who is eligible to sit for the Brain Injury Medicine subspecialty exam?

Candidates must hold primary ABMS certification (typically Physical Medicine & Rehabilitation, Neurology, Child Neurology, or Psychiatry) and have completed a 1-year ACGME-accredited Brain Injury Medicine fellowship with director attestation of satisfactory completion, plus a valid unrestricted medical license. Application is submitted through the ABPN (or ABPMR) website during the designated eligibility window.

What is the format of the exam?

The exam is a 1-day computer-based test delivered at Pearson VUE test centers. It consists of approximately 200 single-best-answer multiple-choice items covering the full ABPN Brain Injury Medicine content outline. Questions frequently include clinical vignettes with neuroimaging (CT, MRI, SWI), Glasgow Coma Scale and GOSE scoring, ICP/CPP management algorithms, cognitive and behavioral rehabilitation scenarios, return-to-play decision trees, and pharmacotherapy selection.

How much does the 2026 ABPN Brain Injury Medicine exam cost?

The 2026 exam fee is approximately $2,200. Cancellation and refund policies follow the ABPN schedule with decreasing refunds as the exam date approaches. Retakes within the eligibility window require full re-registration and fee payment. Enrollment in the ABPN Continuing Certification program includes annual activities and associated fees.

What are the highest-yield topics?

Highest-yield topics include: GCS and severity classification (mild 13-15, moderate 9-12, severe 3-8); Brain Trauma Foundation ICP >22 / CPP 60-70 targets and tiered ICP therapy; decompressive craniectomy trials (DECRA 2011 negative for early bifrontal; RESCUEicp 2016 reduced mortality with more disability); avoiding steroids (CRASH 2004); CRASH-3 2019 TXA within 3 h; post-traumatic seizure prophylaxis with levetiracetam × 7 days for severe TBI; amantadine for disorders of consciousness (Giacino NEJM 2012, 100-200 mg BID weeks 4-16); CTE/TES neuropathology and 2021 NINDS clinical criteria; Amsterdam 2022 CISG sports concussion (early sub-symptom aerobic exercise, 6-step RTP); paroxysmal sympathetic hyperactivity (propranolol, gabapentin, morphine, clonidine, bromocriptine, intrathecal baclofen); neuroendocrine dysfunction (anterior hypopituitarism in 15-50%, screen at 3-6 months); avoiding typical antipsychotics, benzodiazepines, and prophylactic phenytoin beyond 7 days.

How should I study for the Brain Injury Medicine boards?

Plan 200-400 hours over 6-12 months during and after fellowship. Core resources include Brain Injury Medicine: Principles and Practice (Zasler/Katz/Zafonte), Continuum Lifelong Learning in Neurology — Neurotrauma issues, the Brain Trauma Foundation 4th edition guidelines, the Amsterdam 2022 Concussion in Sport consensus statement, the INCOG 2.0 cognitive rehabilitation guidelines (2023), and the VA/DoD mTBI clinical practice guideline (2021). Drill MCQs with timed sets, master landmark trial details (DECRA, RESCUEicp, CRASH, CRASH-3, Giacino amantadine 2012, IMPACT/CRASH calculators), and complete 2-3 full-length timed mock exams.

When is the 2026 exam administered?

ABPN Brain Injury Medicine is offered annually with applications opening months before the exam window. Specific Pearson VUE appointments are scheduled after application approval. Confirm exact 2026 dates on the ABPN Brain Injury Medicine page.

How is the exam scored?

ABPN uses a criterion-referenced scaled scoring system with a passing standard set by subject-matter experts. Pass/fail depends on performance relative to the fixed cut-score rather than relative to other test-takers. Score reports include subdomain performance to guide future learning. Results are typically released several weeks after the testing window closes.