ABPN Neurology study materials
ABPN Neurology study resources

ABPN Neurology cheat sheet

ABPN Neurology · Keep the key ideas within reach.

Quick reference

Basic Neuroscience and Neuroanatomy

  • Lateral corticospinal tract fibers decussate at the medullary pyramids; a lesion above the decussation causes contralateral spastic weakness, while anterior corticospinal fibers decussate segmentally.

  • Dorsal column fibers carry vibration and proprioception, synapse in nucleus gracilis and cuneatus, and cross as internal arcuate fibers to form the medial lemniscus.

  • Spinothalamic fibers cross one to two segments above entry in the anterior white commissure; a central cord lesion produces suspended cape-like loss of pain and temperature.

  • Posterior communicating artery aneurysm compresses CN III and causes a painful pupil-involving third nerve palsy; microvascular ischemia typically spares the pupil.

  • Lateral medullary (Wallenberg) syndrome: ipsilateral facial pain and temperature loss, Horner syndrome, ataxia, dysphagia, and contralateral body pain and temperature loss.

  • Broca aphasia: nonfluent speech with preserved comprehension from dominant inferior frontal gyrus damage; Wernicke aphasia: fluent speech with poor comprehension from dominant superior temporal damage.

  • Direct basal ganglia pathway (D1) inhibits GPi/SNr and facilitates movement; indirect pathway (D2) increases GPi/SNr inhibition and suppresses movement.

  • Motor homunculus: leg on medial cortex supplied by ACA, face and hand laterally supplied by MCA; occipital cortex is PCA territory.

  • Cerebellar hemispheric lesions cause ipsilateral limb ataxia; vermian lesions cause truncal and gait ataxia.

Quick reference

Behavioral Neurology and Dementia

  • Alzheimer disease: early episodic memory loss, medial temporal and parietal atrophy, amyloid plaques, and tau neurofibrillary tangles; acetylcholinesterase inhibitors or memantine are symptomatic.

  • Behavioral variant frontotemporal dementia: disinhibition, apathy, loss of empathy, hyperorality, and executive deficits with frontal and anterior temporal atrophy; memory is relatively spared early.

  • Dementia with Lewy bodies: fluctuating cognition, visual hallucinations, parkinsonism, REM sleep behavior disorder, and neuroleptic sensitivity; occipital hypometabolism on FDG-PET.

  • Vascular dementia: stepwise decline with executive dysfunction, gait disturbance, urinary symptoms, and focal signs; subcortical white matter hyperintensities are common.

  • Primary progressive aphasia variants: semantic variant with temporal pole atrophy and anomia; logopenic variant with impaired repetition and phonological loop deficits.

  • Delirium: acute fluctuating attention and disorientation, often from drugs, infection, or metabolic derangement; dementia has insidious progressive decline with preserved attention until late.

  • Creutzfeldt-Jakob disease: rapidly progressive dementia, myoclonus, startle, and periodic sharp wave complexes; RT-QuIC and 14-3-3 support diagnosis.

  • Normal pressure hydrocephalus: gait apraxia, urinary incontinence, and dementia, with ventriculomegaly and a positive large-volume lumbar puncture tap test.

  • Gerstmann syndrome: acalculia, agraphia, finger agnosia, and right-left disorientation from dominant inferior parietal lobe damage.

Quick reference

Cerebrovascular Disease

  • Intravenous alteplase is indicated within 4.5 hours of ischemic stroke onset when blood pressure is below 185/110 mm Hg and there is no hemorrhage on CT.

  • Mechanical thrombectomy is standard for large vessel occlusion up to 6 hours and selected patients up to 24 hours using DAWN or DEFUSE-3 imaging criteria.

  • TOAST stroke subtypes: large artery atherosclerosis, cardioembolism, small vessel occlusion, other determined cause, and undetermined cause.

  • Lacunar syndromes: pure motor (posterior limb internal capsule), pure sensory (thalamus), sensorimotor, ataxic hemiparesis, and dysarthria-clumsy hand.

  • ACA infarction: contralateral leg greater than arm weakness, abulia, and incontinence; MCA infarction: face and arm greater than leg weakness, aphasia or neglect.

  • Cerebellar hemorrhage larger than 3 cm or causing brainstem compression warrants surgical evacuation; malignant MCA infarction may require decompressive hemicraniectomy within 48 hours.

  • Subarachnoid hemorrhage: thunderclap headache, CT sensitivity highest within 6 hours, xanthochromia on lumbar puncture; nimodipine reduces delayed cerebral ischemia.

  • Cerebral venous thrombosis presents with headache, seizures, and hemorrhagic infarction; anticoagulation is given even in the presence of hemorrhagic transformation.

  • Basilar artery occlusion causes fluctuating consciousness, quadriparesis, and cranial nerve palsies; early revascularization improves outcome.

Quick reference

Epilepsy and Clinical Neurophysiology

  • Focal temporal lobe seizures: epigastric rising sensation, déjà vu, automatisms, and impaired awareness; EEG may show temporal spikes.

  • Childhood absence epilepsy: 3 Hz generalized spike-and-wave, brief staring without postictal confusion, provoked by hyperventilation; ethosuximide is first line.

  • Juvenile myoclonic epilepsy: morning myoclonic jerks, generalized tonic-clonic seizures, 4-6 Hz polyspike-wave; valproate is effective but teratogenic.

  • Status epilepticus: benzodiazepine first, then fosphenytoin, valproate, or levetiracetam; refractory cases require anesthetic infusion and continuous EEG.

  • Carbamazepine and oxcarbazepine can worsen absence and myoclonic seizures; valproate, levetiracetam, and lamotrigine are broader-spectrum options.

  • West syndrome: infantile spasms, hypsarrhythmia, and developmental regression; treat with ACTH or vigabatrin.

  • Lennox-Gastaut syndrome: multiple seizure types, slow spike-and-wave, drop attacks, and intellectual disability; broad-spectrum therapy is often required.

  • SUDEP risk is increased by uncontrolled generalized tonic-clonic seizures, nocturnal seizures, and young adult age; nocturnal supervision may reduce risk.

Quick reference

Headache and Pain

  • Migraine without aura: 4-72 hours, unilateral pulsating pain, nausea, photophobia, and phonophobia; aura typically lasts 5-60 minutes.

  • Cluster headache: 15-180 minutes of severe periorbital pain with ipsilateral autonomic signs and restlessness; high-flow oxygen and sumatriptan are acute treatments.

  • Trigeminal neuralgia: lancinating V2 or V3 pain triggered by touch; carbamazepine is first line, and MRI evaluates for vascular compression or multiple sclerosis.

  • Medication overuse headache: headache on 15 or more days per month with frequent acute medication use; withdrawal of the offending agent is required.

  • Headache red flags: thunderclap onset, fever with neck stiffness, papilledema, new onset after age 50, positional worsening, and focal neurologic deficit.

  • Idiopathic intracranial hypertension: obese young woman, papilledema, pulsatile tinnitus, and elevated opening pressure; acetazolamide and weight loss are treatments.

  • Giant cell arteritis: age over 50, jaw claudication, scalp tenderness, elevated ESR/CRP, and visual loss; give corticosteroids immediately and confirm with temporal artery biopsy.

  • Postherpetic neuralgia: gabapentin, pregabalin, tricyclic antidepressants, or lidocaine patch; opioids are not first line.

  • Pain transmission: A-delta fibers carry fast sharp pain, C fibers carry slow dull pain, and gate control theory predicts that nonpainful input can modulate pain.

Quick reference

Neuromuscular Disorders

  • Myasthenia gravis: fatigable ptosis and diplopia, bulbar weakness, acetylcholine receptor antibodies, decrement on repetitive nerve stimulation, and jitter on single-fiber EMG.

  • Lambert-Eaton myasthenic syndrome: proximal weakness, autonomic symptoms, reflexes that increase after exercise, voltage-gated calcium channel antibodies, and small cell lung cancer association.

  • Guillain-Barré syndrome: ascending areflexic weakness, albuminocytologic dissociation, nadir within 2-4 weeks, and treatment with IVIG or plasma exchange.

  • Chronic inflammatory demyelinating polyneuropathy: progressive or relapsing weakness over more than 8 weeks, sensory involvement, demyelinating EMG, and response to IVIG, steroids, or plasma exchange.

  • Amyotrophic lateral sclerosis: upper and lower motor neuron signs without sensory loss; riluzole and edaravone modestly slow progression.

  • Myotonic dystrophy type 1: CTG repeat expansion, distal weakness, myotonia, cataracts, and cardiac conduction disease; autosomal dominant with anticipation.

  • Duchenne muscular dystrophy: X-linked dystrophin deficiency, Gowers sign, calf pseudohypertrophy, elevated creatine kinase, and cardiomyopathy; corticosteroids slow decline.

  • Charcot-Marie-Tooth type 1A: demyelinating neuropathy from PMP22 duplication, pes cavus, hammer toes, and slow nerve conduction velocities.

  • Botulism: descending flaccid paralysis, autonomic dysfunction, and pupillary dilation from presynaptic acetylcholine release blockade.

Quick reference

Movement Disorders

  • Parkinson disease: asymmetric resting tremor, bradykinesia, rigidity, and postural instability; levodopa is the most effective symptomatic therapy.

  • Progressive supranuclear palsy: vertical supranuclear gaze palsy, early falls, axial rigidity, and midbrain atrophy with the hummingbird sign.

  • Multiple system atrophy: autonomic failure, cerebellar ataxia, and parkinsonism; MRI may show the hot cross bun sign in the pons.

  • Corticobasal syndrome: asymmetric apraxia, alien limb phenomenon, cortical sensory loss, and dystonia.

  • Huntington disease: CAG repeat expansion, chorea, psychiatric symptoms, dementia, and caudate atrophy; autosomal dominant with anticipation.

  • Essential tremor: bilateral action and postural tremor, alcohol responsiveness, and treatment with propranolol or primidone.

  • Tardive dyskinesia: involuntary oro-bucco-lingual movements after dopamine antagonist exposure; treat with VMAT2 inhibitors such as valbenazine or deutetrabenazine.

  • Wilson disease: low ceruloplasmin, elevated urinary copper, Kayser-Fleischer rings, liver disease, and psychiatric symptoms; chelation therapy is essential.

  • Restless legs syndrome: urge to move legs at rest, worse in evening, relieved by movement; iron deficiency should be evaluated.

Quick reference

Demyelinating, Infectious, and Autoimmune Disorders of the Nervous System

  • Multiple sclerosis 2017 McDonald criteria require dissemination in space and time; typical MRI regions are periventricular, juxtacortical, infratentorial, and spinal cord.

  • Neuromyelitis optica spectrum disorder: AQP4-IgG, severe optic neuritis, longitudinally extensive transverse myelitis, and area postrema syndrome; complement inhibitors prevent relapse.

  • MOG antibody disease: optic neuritis, ADEM-like presentations, and transverse myelitis; MOG-IgG testing confirms.

  • ADEM: post-infectious encephalopathy with multifocal white matter lesions, often in children; corticosteroids are first-line treatment.

  • Herpes simplex encephalitis: fever, seizures, confusion, and temporal lobe involvement; CSF PCR and early intravenous acyclovir are standard.

  • Neurosyphilis: CSF VDRL, pleocytosis, and elevated protein; intravenous penicillin G is treatment.

  • Lyme neuroborreliosis: facial nerve palsy, radiculitis, and CSF pleocytosis; doxycycline or ceftriaxone is effective.

  • Progressive multifocal leukoencephalopathy: JC virus, progressive asymmetric white matter lesions without mass effect or enhancement; natalizumab and immunosuppression increase risk.

  • Anti-NMDA receptor encephalitis: young women, ovarian teratoma, psychiatric symptoms, seizures, dyskinesias, and hypoventilation; immunotherapy and tumor removal are indicated.

Quick reference

Neuro-oncology, Neuro-ophthalmology, and Neuro-otology

  • Glioblastoma: IDH-wildtype, ring-enhancing intra-axial mass with central necrosis and edema, often crossing the corpus callosum; temozolomide and radiation follow resection.

  • Meningioma: extra-axial, homogeneously enhancing mass with a dural tail; most are benign and observation or resection is based on symptoms and growth.

  • Pituitary adenoma: bitemporal hemianopia from optic chiasm compression; prolactinomas are treated with dopamine agonists.

  • Spinal cord compression: back pain, weakness, sensory level, and bowel or bladder dysfunction; urgent MRI and dexamethasone are indicated.

  • Papilledema: bilateral optic disc swelling from raised intracranial pressure, often with absent spontaneous venous pulsations and enlarged blind spots.

  • Optic neuritis: painful monocular vision loss, reduced color vision, relative afferent pupillary defect, and Uhthoff phenomenon; brain MRI predicts multiple sclerosis risk.

  • Nonarteritic anterior ischemic optic neuropathy: painless altitudinal visual loss with sectoral disc edema in older patients with vascular risk factors.

  • Vestibular schwannoma: unilateral sensorineural hearing loss and tinnitus; gadolinium MRI shows an enhancing internal auditory canal mass.

  • Benign paroxysmal positional vertigo: brief positional vertigo with upbeat torsional nystagmus on Dix-Hallpike; canalith repositioning is curative.

Quick reference

Child Neurology

  • Simple febrile seizure: age 6 months to 5 years, generalized, under 15 minutes, no recurrence within 24 hours; daily antiepileptic therapy is not indicated.

  • Neonatal seizures: often subtle with apnea or autonomic changes; hypoglycemia and hypocalcemia must be checked, and phenobarbital is first line.

  • Cerebral palsy: nonprogressive motor impairment; spastic diplegia is associated with periventricular leukomalacia in preterm infants.

  • Fragile X syndrome: FMR1 CGG repeat expansion, macroorchidism, long face, autism, and intellectual disability.

  • Rett syndrome: MECP2 mutation in girls, developmental regression, hand-wringing stereotypies, and acquired microcephaly.

  • Tuberous sclerosis: TSC1 or TSC2 mutation, ash-leaf spots, facial angiofibromas, cortical tubers, subependymal giant cell astrocytoma, and infantile spasms.

  • Neurofibromatosis type 1: NF1 mutation, café-au-lait spots, axillary freckling, Lisch nodules, optic glioma, and pheochromocytoma.

  • Dravet syndrome: SCN1A mutation, prolonged febrile seizures, developmental regression, and temperature-sensitive seizures.

  • Chiari II malformation: myelomeningocele, hydrocephalus, and tectal plate beaking; associated with folate deficiency prevention.

Quick reference

Neurotrauma

  • Glasgow Coma Scale: eye 4, verbal 5, motor 6; scores 13-15 are mild, 9-12 moderate, and 3-8 severe traumatic brain injury.

  • Epidural hematoma: middle meningeal artery injury, biconvex shape on CT, temporal bone fracture, and a lucid interval.

  • Subdural hematoma: bridging vein tearing, crescent-shaped collection, elderly patients and anticoagulation are risk factors.

  • Diffuse axonal injury: gray-white junction, corpus callosum, and brainstem lesions; MRI susceptibility-weighted imaging is more sensitive than CT.

  • Cushing reflex: hypertension with bradycardia and irregular respiration indicates raised intracranial pressure and impending herniation.

  • Cerebral perfusion pressure equals mean arterial pressure minus intracranial pressure; target is typically 60-70 mm Hg after severe traumatic brain injury.

  • Neurogenic shock: hypotension and bradycardia from loss of sympathetic tone after cervical spinal cord injury; spinal shock is areflexia without hypotension.

  • Central cord syndrome: hyperextension injury with greater arm than leg weakness; surgical decompression is considered for persistent compression.

Quick reference

Toxic, Metabolic, and Nutritional Disorders

  • Wernicke encephalopathy: ophthalmoplegia, ataxia, and confusion from thiamine deficiency; give intravenous thiamine before glucose to prevent Korsakoff syndrome.

  • Vitamin B12 deficiency: subacute combined degeneration with dorsal column and corticospinal signs, paresthesias, and macrocytic anemia.

  • Hepatic encephalopathy: asterixis, confusion, and elevated ammonia; lactulose and rifaximin reduce ammonia production.

  • Carbon monoxide poisoning: bilateral globus pallidus lesions and cherry-red skin; treat with high-flow oxygen or hyperbaric oxygen.

  • Methanol poisoning: severe metabolic acidosis, visual loss, and putaminal necrosis; fomepizole or ethanol blocks metabolism.

  • Ethylene glycol poisoning: metabolic acidosis, oxalate crystals, and hypocalcemia; fomepizole is antidotal.

  • Organophosphate poisoning: SLUDGE and DUMBELS from acetylcholinesterase inhibition; atropine and pralidoxime are treatments.

  • Serotonin syndrome: hyperthermia, clonus, hyperreflexia, and agitation after serotonergic drugs; stop the agent and give cyproheptadine if severe.

  • Osmotic demyelination syndrome: rapid correction of hyponatremia causes pontine and extrapontine demyelination; correct sodium slowly.