Iraqi Board Neurology cheat sheet

Corticospinal tract decussates at the medullary pyramids (~85%); lateral corticospinal tract carries limb motor fibers, anterior tract carries axial muscles.

Internal capsule: anterior limb (thalamocortical), genu (corticobulbar), posterior limb (corticospinal) - a small posterior limb lesion causes dense contralateral hemiparesis.

MCA territory: lateral frontal, parietal, superior temporal cortex plus basal ganglia via lenticulostriates; ACA: medial frontal/parietal, leg > arm weakness.

Brainstem rule of 4: mid-pons lesions affect CN 6/7 plus contralateral hemiparesis; medulla lesions affect CN 9-12 with contralateral spinothalamic loss.

Cerebellar signs: vermis → truncal ataxia; hemisphere → ipsilateral limb dysmetria and intention tremor; flocculonodular → nystagmus and vertigo.

Resting membrane potential ≈ −70 mV set by K+ conductance; threshold ≈ −55 mV; action potential depolarization from voltage-gated Na+ influx, repolarization from K+ efflux.

EEG frequencies: delta <4 Hz, theta 4-7 Hz, alpha 8-13 Hz (posterior, eyes closed), beta 14-30 Hz; sleep spindles 11-16 Hz in N2.

UMN lesion: spasticity, hyperreflexia, Babinski sign, no fasciculations; LMN lesion: flaccidity, atrophy, fasciculations, areflexia.

Ischemic neuron 24-48 h: red neurons (eosinophilic cytoplasm, pyknotic nucleus); 1-2 weeks: macrophages; months-years: glial scar.

Astrocytes express GFAP; reactive gliosis is the CNS scar. Microglia derive from yolk-sac myeloid progenitors and are the resident phagocytes.

Oligodendrocytes myelinate CNS (one cell, many axons); Schwann cells myelinate PNS (one cell, one internode).

Prion disease: spongiform change, neuronal loss, PrP amyloid plaques (kuru plaques in variant CJD); no inflammation.

Lewy bodies: alpha-synuclein, eosinophilic intracytoplasmic inclusions with halo; nigral loss causes parkinsonism.

Neurofibrillary tangles: hyperphosphorylated tau; Braak staging correlates with cognitive decline better than plaque counts.

Amyloid angiopathy: Aβ deposition in leptomeningeal and cortical vessels, causing lobar hemorrhage in the elderly.

CT hyperdensity: acute blood, calcification, bone, iodine contrast; MRI DWI hyperintensity detects cytotoxic edema within minutes of infarction.

MRI T1: fat bright, CSF dark; T2: water bright; FLAIR suppresses CSF to show periventricular and cortical lesions.

Gadolinium enhancement implies blood-brain barrier breakdown: tumor, abscess, active demyelination, subacute infarct.

NCS: demyelination → prolonged distal latency, slowed conduction velocity (<70% of normal), conduction block, F-wave prolongation; axonal loss → reduced amplitude.

EMG: fibrillation potentials and positive sharp waves indicate active denervation; large polyphasic units indicate reinnervation.

EEG in encephalopathy: generalized slowing; triphasic waves in hepatic/metabolic encephalopathy; burst suppression indicates severe cortical depression.

Periodic lateralized epileptiform discharges (PLEDs) suggest acute structural lesion (stroke, HSV encephalitis) and carry seizure risk.

Repetitive nerve stimulation: >10% decrement in myasthenia gravis; incremental response in Lambert-Eaton syndrome.

NIHSS thresholds: <5 minor, 5-15 moderate, >15 severe; tPA window 0-4.5 h with BP <185/110 mmHg and no hemorrhage on CT.

Large vessel occlusion with mismatch on perfusion imaging may undergo thrombectomy up to 24 h; time is brain for anterior circulation.

TOAST subtypes: large artery atherosclerosis, cardioembolism, small vessel (lacunar), other determined, undetermined.

Lacunar syndromes: pure motor, pure sensory, sensorimotor, ataxic hemiparesis, dysarthria-clumsy hand - due to single deep perforator infarct.

Warfarin is preferred over DOACs for mechanical valves and moderate-severe mitral stenosis; DOACs are first-line for nonvalvular atrial fibrillation.

Basilar artery occlusion: fluctuating consciousness, quadriparesis, cranial nerve palsies; high mortality and often missed on initial CT.

Cerebral venous thrombosis: headache, seizures, papilledema; treat with heparin even in the presence of hemorrhagic infarct.

ICH: stop antithrombotics, control BP to ~140 mmHg systolic, reverse anticoagulation; cerebellar hematoma >3 cm or brainstem compression warrants surgery.

Focal onset: temporal lobe most common, with automatisms, déjà vu, epigastric rising aura, postictal confusion; often hippocampal sclerosis on MRI.

Absence seizures: 3 Hz generalized spike-and-wave, brief staring with immediate recovery, hyperventilation provokes, ethosuximide first-line.

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

Status epilepticus: benzodiazepine first (lorazepam IV or midazolam IM), then second-line (levetiracetam, fosphenytoin, valproate), then anesthetic infusion.

First-line drugs: focal - carbamazepine, lamotrigine, levetiracetam; generalized tonic-clonic - valproate, lamotrigine; absence - ethosuximide, valproate.

Carbamazepine and phenytoin worsen absence and myoclonic seizures; avoid in generalized epilepsy syndromes.

Sudden unexpected death in epilepsy (SUDEP) risk factors: frequent generalized tonic-clonic seizures, nocturnal seizures, poor adherence, young adult male.

Pregnancy: lamotrigine and levetiracetam have the lowest malformation rates; valproate carries highest risk (neural tube defects, cognitive impairment).

Migraine without aura: ≥5 attacks of 4-72 h, unilateral, pulsating, moderate-severe, aggravated by activity, with nausea or photophobia/phonophobia.

Aura: fully reversible visual, sensory, or speech symptoms developing over ≥5 min, each lasting 5-60 min, followed by headache within 60 min.

Red flags (SNOOP): systemic symptoms, neurologic deficit, onset sudden (thunderclap), older age >50, pattern change, positional, papilledema.

Cluster headache: severe unilateral periorbital pain with ipsilateral autonomic signs, 15-180 min, circadian; high-flow oxygen and sumatriptan are acute treatments.

Trigeminal neuralgia: brief electric shock-like paroxysms in V2/V3, triggered by touch or chewing; carbamazepine first-line; MRI to exclude vascular loop or mass.

Giant cell arteritis: age >50, new headache, jaw claudication, elevated ESR/CRP; start steroids immediately, biopsy within 2 weeks.

Medication-overuse headache: headache ≥15 days/month with regular acute medication use; treat by withdrawal and prophylaxis.

Idiopathic intracranial hypertension: young obese female, papilledema, pulsatile tinnitus, normal CSF; acetazolamide and weight loss.

Parkinson disease: asymmetric resting tremor, bradykinesia, rigidity, postural instability; responds to levodopa; nigrostriatal dopaminergic loss.

Levodopa-induced dyskinesia and wearing-off are motor complications; manage with COMT inhibitors, MAO-B inhibitors, dopamine agonists, or deep brain stimulation.

Progressive supranuclear palsy: vertical supranuclear gaze palsy, early falls, axial rigidity; tauopathy with hummingbird sign on MRI.

Multiple system atrophy: autonomic failure plus parkinsonism (MSA-P) or cerebellar signs (MSA-C); alpha-synuclein glial cytoplasmic inclusions.

Essential tremor: bilateral postural/action tremor of hands and head, improves with alcohol; propranolol and primidone are first-line.

Huntington disease: autosomal dominant CAG repeat expansion in HTT; chorea, psychiatric symptoms, dementia; caudate atrophy on MRI.

ALS: combined UMN and LMN signs in ≥2 regions, no sensory loss, normal sphincter function; riluzole and edaravone modestly slow progression.

Wilson disease: age <40, tremor, dystonia, psychiatric change, Kayser-Fleischer rings, low ceruloplasmin, elevated urinary copper; treat with chelators.

Guillain-Barré syndrome: ascending symmetric weakness, areflexia, albuminocytologic dissociation, nadir by 4 weeks; IVIG or plasma exchange.

CIDP: progression >8 weeks, proximal and distal weakness, demyelinating NCS; responds to IVIG, steroids, or plasma exchange.

Myasthenia gravis: fatigable ptosis and diplopia, bulbar weakness, anti-AChR antibodies, decrement on RNS; pyridostigmine and immunosuppression.

Lambert-Eaton syndrome: proximal weakness, autonomic symptoms, anti-VGCC antibodies, incremental response on high-frequency RNS; paraneoplastic with small cell lung cancer.

Diabetic neuropathy: symmetric distal sensory polyneuropathy (stocking-glove), most common; tight glycemic control is the only proven prevention.

Charcot-Marie-Tooth type 1: autosomal dominant, demyelinating, pes cavus, hammer toes, uniform slowing of conduction velocity.

Mononeuritis multiplex: asymmetric painful neuropathy in vasculitis, diabetes, or leprosy; nerve biopsy may show vasculitis.

Bell palsy: unilateral lower facial weakness sparing forehead is UMN; Bell palsy involves entire hemiface; steroids within 72 h improve outcome.

Multiple sclerosis: dissemination in space and time; McDonald criteria use MRI lesions in ≥2 of 4 regions (periventricular, cortical/juxtacortical, infratentorial, spinal cord).

Oligoclonal bands in CSF support MS and reflect intrathecal IgG synthesis; CSF pleocytosis is usually <50 cells.

Neuromyelitis optica spectrum disorder: anti-AQP4 antibodies, longitudinally extensive transverse myelitis (≥3 segments), optic neuritis, area postrema syndrome.

MOG antibody disease: bilateral optic neuritis, ADEM-like presentation, conus myelitis; often steroid-responsive with relapses on withdrawal.

MS relapse: high-dose IV methylprednisolone for 3-5 days; disease-modifying therapy reduces relapse rate and MRI activity but is not for acute relapse.

Acute disseminated encephalomyelitis (ADEM): post-infectious, encephalopathy plus multifocal white matter lesions, common in children; usually monophasic.

Anti-NMDA receptor encephalitis: psychiatric symptoms, dyskinesias, autonomic instability, ovarian teratoma; treat with steroids, IVIG, and tumor removal.

Progressive multifocal leukoencephalopathy: JC virus, non-enhancing white matter lesions, seen with natalizumab and immunosuppression; restore immune function.

Bacterial meningitis: fever, neck stiffness, altered mental status; CSF shows neutrophilic pleocytosis, low glucose, high protein; start empiric antibiotics before LP if unstable.

Empiric adult bacterial meningitis: ceftriaxone plus vancomycin; add ampicillin for Listeria if age >50 or immunocompromised; dexamethasone before first antibiotic dose.

HSV encephalitis: fever, confusion, seizures, temporal lobe involvement on MRI; CSF PCR for HSV; treat with IV acyclovir.

Tuberculous meningitis: subacute course, basilar meningeal enhancement, hydrocephalus, low CSF glucose; treat with 4-drug regimen plus steroids.

Cerebral malaria: Plasmodium falciparum, impaired consciousness, seizures, retinal whitening; treat with IV artesunate.

Cysticercosis: seizures in endemic areas, calcified lesions or cysts with scolex; albendazole plus steroids for parenchymal disease.

Rabies: exposure history, hydrophobia, aerophobia, encephalitis; post-exposure prophylaxis with wound care, vaccine, and immunoglobulin.

HIV neurology: toxoplasmosis (ring-enhancing lesions, treat with pyrimethamine-sulfadiazine), primary CNS lymphoma (periventricular, EBV-positive), cryptococcal meningitis (India ink).

Glioblastoma: IDH-wildtype, MGMT promoter methylation predicts temozolomide response; treatment is maximal resection plus radiotherapy with temozolomide.

Low-grade glioma: IDH-mutant, 1p/19q codeletion defines oligodendroglioma and predicts chemosensitivity.

Meningioma: extra-axial, dural tail, homogeneously enhancing, often calcified; observation for asymptomatic small lesions.

Brain metastases: most common adult brain tumor; gray-white junction, multiple; treat with surgery or stereotactic radiosurgery plus whole-brain radiotherapy.

Pituitary adenoma: bitemporal hemianopia from optic chiasm compression; prolactinoma treated with dopamine agonists first.

Cerebellopontine angle mass: vestibular schwannoma (CN VIII, hearing loss, tinnitus) versus meningioma versus epidermoid.

Increased intracranial pressure: headache worse lying down, vomiting, papilledema, Cushing triad (hypertension, bradycardia, irregular respiration) in herniation.

Primary CNS lymphoma: periventricular enhancing lesions, EBV-associated in immunocompromised; avoid steroids before biopsy because they can cause tumor lysis.

Febrile seizures: age 6 months to 5 years, fever without CNS infection; simple (<15 min, generalized, once in 24 h) has low epilepsy risk.

Neonatal seizures: subtle, tonic, or clonic; common causes are hypoxic-ischemic encephalopathy, hypoglycemia, and infection; EEG monitoring is required.

Cerebral palsy: nonprogressive motor disorder from early brain injury; spastic diplegia is associated with prematurity and periventricular leukomalacia.

Duchenne muscular dystrophy: X-linked dystrophin deficiency, boys, Gowers sign, calf pseudohypertrophy, elevated CK; steroids slow progression.

Spinal muscular atrophy: SMN1 deletion, anterior horn cell loss, hypotonia; treat with nusinersen or gene therapy.

Neural tube defects: folic acid supplementation preconception reduces risk; Chiari II malformation with myelomeningocele.

Kernicterus: bilirubin encephalopathy with basal ganglia injury; prevent by phototherapy and exchange transfusion in severe neonatal jaundice.

Rett syndrome: MECP2 mutation, girls, regression after 6-18 months, hand wringing, microcephaly, seizures.

Trinucleotide repeat disorders: Huntington (CAG), fragile X (CGG), Friedreich ataxia (GAA), myotonic dystrophy (CTG); anticipation occurs with paternal or maternal transmission depending on disease.

Mitochondrial inheritance: maternal transmission, heteroplasmy, MELAS (m.3243A>G), MERRF, Leber hereditary optic neuropathy (m.11778G>A).

Duchenne/Becker: X-linked recessive dystrophin gene; carrier females may have mild symptoms.

Neurofibromatosis type 1: NF1 gene, café-au-lait macules, neurofibromas, optic glioma, Lisch nodules; type 2: NF2 gene, bilateral vestibular schwannomas.

Tuberous sclerosis: TSC1/TSC2, facial angiofibromas, cortical tubers, subependymal giant cell astrocytoma, renal angiomyolipoma.

Spinocerebellar ataxia: autosomal dominant CAG repeats, progressive ataxia with anticipation; genetic testing confirms subtype.

Charcot-Marie-Tooth: CMT1A from PMP22 duplication, demyelinating; CMT2 is axonal; inheritance can be AD, AR, or X-linked.

Fragile X syndrome: FMR1 CGG expansion >200 repeats, intellectual disability, macroorchidism, long face, autism features.

Dominant hemisphere (usually left): language, praxis, calculation; nondominant: visuospatial attention, prosody, hemineglect.

Broca aphasia: nonfluent, effortful speech with preserved comprehension; Wernicke aphasia: fluent but meaningless speech with poor comprehension.

Conduction aphasia: impaired repetition with preserved fluency and comprehension; lesion of arcuate fasciculus.

Global aphasia: large MCA territory lesion with all language functions impaired; transcortical aphasia spares repetition.

Alzheimer disease: episodic memory loss first, medial temporal atrophy, amyloid and tau biomarkers; cholinesterase inhibitors for mild-moderate disease.

Frontotemporal dementia: behavioral variant with disinhibition and apathy, or primary progressive aphasia; pick atrophy of frontal and temporal lobes.

Delirium versus dementia: delirium is acute, fluctuating, with inattention; dementia is chronic and progressive with preserved consciousness.

Gerstmann syndrome: agraphia, acalculia, finger agnosia, left-right confusion; lesion of dominant angular gyrus.