Iran Specialty Board Neurology cheat sheet

Ischemic stroke thrombolysis window: IV alteplase (0.9 mg/kg, max 90 mg; 10% bolus, rest over 60 min) is approved within 4.5 h of last known well; benefit declines with time, and wake-up stroke may be treated if DWI-FLAIR mismatch on MRI.

Mechanical thrombectomy: indicated for anterior circulation large-vessel occlusion (ICA, M1) within 6 h of onset (and up to 24 h in selected patients with favorable perfusion/clinical mismatch by DAWN/DEFUSE-3 criteria); door-to-groin target < 60-90 min.

NIHSS thresholds: 0-4 minor, 5-15 moderate, 16-20 moderate-severe, >20 severe; a score >= 6 with cortical signs suggests large-vessel occlusion and warrants vascular imaging.

Blood pressure in acute ischemic stroke: permissive hypertension unless thrombolysis (target < 185/110 before, < 180/105 after) or thrombectomy; in hemorrhagic stroke, lower SBP to 130-140 mmHg if presenting SBP 150-220 mmHg.

TOAST classification of ischemic stroke: large-artery atherosclerosis, cardioembolism, small-vessel occlusion (lacunar), other determined etiology, and undetermined etiology.

Intracerebral hemorrhage: spot sign on CT angiography predicts expansion; reversal of anticoagulation (vitamin K plus PCC for warfarin; idarucizumab for dabigatran; andexanet alfa or PCC for factor Xa inhibitors) is time-critical.

Subarachnoid hemorrhage: thunderclap headache, CT sensitivity ~100% within 6 h but falls after 24 h; if CT negative and suspicion persists, lumbar puncture shows xanthochromia after ~12 h.

Cerebral venous sinus thrombosis: hypercoagulable states, pregnancy/puerperium, and oral contraceptives are common triggers; anticoagulation with heparin is first-line even in hemorrhagic infarction.

Stroke mimics (seizure, migraine, hypoglycemia, conversion) account for a substantial share of code-stroke activations; check glucose immediately and consider EEG when postictal deficits are suspected.

Seizure classification (ILAE 2017): focal (aware/impaired awareness; motor/nonmotor) vs generalized (tonic-clonic, absence, myoclonic, atonic, tonic); focal-to-bilateral tonic-clonic is a separate descriptor.

Status epilepticus: define at 5 min of continuous seizure or recurrent seizures without recovery; first-line benzodiazepines (lorazepam 0.1 mg/kg IV, max 4 mg), second-line fosphenytoin/valproate/levetiracetam, then anesthetic infusion.

EEG frequencies: delta < 4 Hz, theta 4-7 Hz, alpha 8-13 Hz, beta 14-30 Hz; alpha rhythm attenuates with eye opening (reactivity) and is posterior-dominant in wakefulness.

Normal sleep EEG: vertex sharp waves in N1, sleep spindles (12-14 Hz) and K-complexes in N2, slow-wave delta in N3, and REM with sawtooth waves and low-voltage mixed frequency.

Interictal epileptiform discharges: spikes < 70 ms, sharp waves 70-200 ms; benign variants include rolandic spikes, 14-and-6 positive bursts, wicket spikes, and breach rhythm (do not over-read as epileptiform).

Juvenile myoclonic epilepsy: myoclonic jerks on awakening, generalized 3-4 Hz polyspike-wave, often photosensitive; first-line valproate (avoid in women of childbearing age) or levetiracetam.

Absence epilepsy: brief impaired awareness with 3 Hz generalized spike-wave, hyperventilation provokes; ethosuximide is first-line for pure absence, valproate if also tonic-clonic.

Drug choice: focal seizures-levetiracetam, lamotrigine, carbamazepine, oxcarbazepine; generalized-valproate, lamotrigine, levetiracetam; avoid carbamazepine/oxcarbazepine in generalized syndromes (may worsen absence/myoclonus).

SUDEP risk factors: uncontrolled generalized tonic-clonic seizures, nocturnal seizures, poor adherence, young adult male; counseling on supervision and nocturnal monitoring is evidence-based.

Nerve conduction study: demyelination suggested by conduction velocity < 70-80% of normal, distal latency > 130% of upper limit, F-wave prolongation, conduction block (>50% amplitude drop), and temporal dispersion.

EMG findings: fibrillation potentials and positive sharp waves indicate active denervation (weeks after injury); large-amplitude polyphasic motor units indicate chronic reinnervation; myopathy shows short-duration small-amplitude units with early recruitment.

Guillain-Barré syndrome: progressive ascending weakness with areflexia, albuminocytologic dissociation (high CSF protein with normal cells) after the first week; treat with IVIG or plasma exchange, avoid corticosteroids.

CIDP: progressive or relapsing weakness over >= 8 weeks with demyelinating NCS features and elevated CSF protein; responds to IVIG, steroids, or plasma exchange.

Myasthenia gravis: fatigable weakness, ptosis/diplopia, decrement > 10% on repetitive nerve stimulation, anti-AChR or anti-MuSK antibodies; treat with pyridostigmine, steroids, and steroid-sparing agents; thymectomy for thymoma.

Lambert-Eaton myasthenic syndrome: proximal weakness, hyporeflexia, autonomic symptoms, incremental response > 100-200% on high-frequency repetitive stimulation, anti-VGCC antibodies; screen for small-cell lung cancer.

ALS: upper and lower motor neuron signs in multiple regions without sensory loss; split-hand index and fasciculations; riluzole and edaravone modestly slow progression; noninvasive ventilation improves survival.

Charcot-Marie-Tooth type 1A: demyelinating, uniform slowing of conduction velocities, duplication of PMP22 on chromosome 17p11.2; CMT2 is axonal with normal velocities.

Diabetic neuropathy: distal symmetric polyneuropathy is most common; small-fiber involvement shows reduced intraepidermal nerve fiber density with normal NCS; autonomic testing for gastroparesis and orthostasis.

Mononeuritis multiplex: asymmetric painful weakness suggesting vasculitis, diabetes, or leprosy; nerve biopsy may show necrotizing arteritis; urgent immunosuppression prevents further deficit.

MS diagnosis (2017 McDonald criteria): dissemination in space (>= 1 of 4 typical regions: periventricular, cortical/juxtacortical, infratentorial, spinal cord) and in time (simultaneous enhancing and non-enhancing lesions or new lesion on follow-up); CSF oligoclonal bands can substitute for dissemination in time.

MS phenotypes: clinically isolated syndrome, relapsing-remitting, secondary progressive, and primary progressive; progression independent of relapse activity (PIRA) is a key outcome measure.

MS MRI: ovoid periventricular lesions (Dawson fingers), juxtacortical/cortical lesions, infratentorial lesions, and short-segment cord lesions; enhancing lesions indicate active inflammation.

NMOSD: anti-aquaporin-4 antibodies (cell-based assay), longitudinally extensive transverse myelitis (>= 3 segments), optic neuritis with severe visual loss, area postrema syndrome; treat attacks with IV methylprednisolone and plasma exchange; avoid interferon-beta and fingolimod (may worsen).

MOGAD: anti-MOG antibodies, often bilateral optic neuritis with disc edema, ADEM-like or cortical encephalitis, and conus medullaris involvement; many patients have monophasic course and steroid responsiveness.

Autoimmune encephalitis: anti-NMDAR (psychiatric onset, dyskinesias, ovarian teratoma), anti-LGI1 (faciobrachial dystonic seizures, hyponatremia), anti-GABA-B (small-cell lung cancer); check CSF and serum antibodies, start immunotherapy early.

Optic neuritis: painful monocular visual loss with color desaturation, relative afferent pupillary defect, and pain on eye movement; MRI brain and orbits with contrast; treat with IV methylprednisolone for faster recovery (does not change final outcome).

Disease-modifying therapy in MS: high-efficacy agents (natalizumab, ocrelizumab, alemtuzumab) for aggressive disease; monitor for PML (natalizumab, JC virus antibody index), infusion reactions, and infections.

Neuromyelitis optica spectrum: pregnancy and postpartum increase relapse risk; continue immunosuppression during pregnancy with agents such as azathioprine or rituximab under specialist guidance.

Parkinson disease: asymmetric resting tremor, bradykinesia, rigidity, and postural instability (late); diagnosis requires bradykinesia plus one other cardinal sign; levodopa is the most effective symptomatic therapy.

Parkinson plus syndromes: MSA (autonomic failure, cerebellar signs), PSP (vertical supranuclear gaze palsy, early falls), CBD (asymmetric cortical signs, alien limb), and DLB (early dementia, visual hallucinations, parkinsonism).

Drug-induced parkinsonism: dopamine-blocking antipsychotics and antiemetics (metoclopramide) are common culprits; it is often symmetric and may persist for months after withdrawal.

Essential tremor: bilateral postural/kinetic tremor of hands, head, or voice, often alcohol-responsive; first-line propranolol or primidone; distinguish from dystonic tremor and PD resting tremor.

Huntington disease: autosomal dominant CAG repeat expansion in HTT (>= 36 pathogenic); chorea, cognitive decline, psychiatric symptoms; treat chorea with tetrabenazine or deutetrabenazine.

Wilson disease: autosomal recessive ATP7B mutation, low ceruloplasmin, elevated urinary copper, Kayser-Fleischer rings; treat with chelators (penicillamine, trientine) or zinc.

Restless legs syndrome: urge to move legs worse at rest and evening, relieved by movement; check ferritin (target > 75-100 ng/mL) and treat with dopamine agonists or alpha-2-delta ligands (gabapentin, pregabalin).

Tardive dyskinesia: involuntary oro-buccal-lingual movements after chronic dopamine antagonist exposure; treat with VMAT2 inhibitors (valbenazine, deutetrabenazine) and avoid anticholinergics, which worsen it.

Corticobasal syndrome: asymmetric rigidity, apraxia, cortical sensory loss, and alien limb phenomenon; often due to CBD or PSP pathology; no disease-modifying therapy exists.

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

Migraine with aura: fully reversible visual, sensory, or speech symptoms spreading over >= 5 min, lasting 5-60 min, followed by headache within 60 min; differentiate from TIA and seizure.

Medication-overuse headache: headache on >= 15 days/month with regular overuse of acute medications (triptans/opioids/combination analgesics >= 10 days/month; simple analgesics >= 15 days/month) for > 3 months.

Cluster headache: severe unilateral orbital/temporal pain with ipsilateral autonomic features (ptosis, miosis, lacrimation, rhinorrhea), attacks lasting 15-180 min; high-flow oxygen and subcutaneous sumatriptan abort; verapamil is first-line prophylaxis.

Trigeminal neuralgia: paroxysmal electric-shock pain in V2/V3, triggered by touch, chewing, or cold; carbamazepine or oxcarbazepine first-line; MRI to exclude vascular compression or mass.

Giant cell arteritis: headache in patients > 50 years with jaw claudication, scalp tenderness, elevated ESR/CRP; start high-dose corticosteroids immediately and obtain temporal artery biopsy within 2 weeks.

Idiopathic intracranial hypertension: headache, transient visual obscurations, pulsatile tinnitus, papilledema; lumbar puncture opening pressure > 25 cm H2O; treat with acetazolamide and weight loss.

Red flags (SNOOP): systemic symptoms, neurologic signs, onset sudden (thunderclap), older age (> 50), pattern change, positional, papilledema, pregnancy, and trauma warrant urgent imaging.

Tension-type headache: bilateral, pressing, mild-moderate, not aggravated by activity, without nausea; treat with NSAIDs and limit acute medication to avoid chronification.

Glioblastoma (WHO grade 4): IDH-wildtype, MGMT promoter methylation predicts temozolomide benefit; standard of care is maximal safe resection followed by radiotherapy with concurrent and adjuvant temozolomide.

Meningioma: usually extra-axial, dural-based, enhancing with a dural tail; WHO grade 1 in most; asymptomatic small lesions can be observed, symptomatic or growing lesions are resected or irradiated.

Brain metastases: most common adult brain tumors; lung, breast, melanoma, and renal cell carcinoma are common sources; treat with surgery for single accessible lesion, stereotactic radiosurgery, or whole-brain radiotherapy depending on number and status.

Primary CNS lymphoma: periventricular enhancing lesions, often in immunocompromised patients; stereotactic biopsy is diagnostic; high-dose methotrexate-based chemotherapy is first-line; avoid steroids before biopsy (may obscure histology).

Pituitary adenoma: bitemporal hemianopia from optic chiasm compression, prolactin elevation; prolactinoma treated with dopamine agonists (cabergoline), others with transsphenoidal surgery.

Vestibular schwannoma: unilateral sensorineural hearing loss, tinnitus, imbalance; MRI with contrast shows enhancing cerebellopontine angle mass; management is observation, radiosurgery, or microsurgery.

Paraneoplastic syndromes: anti-Hu (small-cell lung cancer, sensory neuronopathy), anti-Yo (ovarian/breast cancer, cerebellar degeneration), anti-NMDA receptor (ovarian teratoma); treat the underlying tumor.

Increased intracranial pressure from tumor: corticosteroids (dexamethasone) reduce peritumoral edema; mannitol or hypertonic saline for acute herniation; seizure prophylaxis is not routinely indicated unless seizures occur.

Carcinomatous meningitis: multifocal cranial nerve palsies, headache, and hydrocephalus; CSF cytology and MRI with contrast; treat with intrathecal chemotherapy and radiotherapy.

Bacterial meningitis: empiric therapy in adults is vancomycin plus a third-generation cephalosporin (ceftriaxone) with ampicillin added if Listeria risk (age > 50, immunocompromised); dexamethasone before or with first antibiotic dose reduces hearing loss in pneumococcal disease.

CSF profiles: bacterial (high neutrophils, low glucose, high protein), viral (lymphocytic pleocytosis, normal glucose), tuberculous (lymphocytic, very low glucose, high protein, may have xanthochromia), fungal (lymphocytic, low glucose).

HSV encephalitis: fever, headache, altered consciousness, seizures, and temporal lobe involvement on MRI; start IV acyclovir immediately and confirm with CSF PCR; EEG may show periodic lateralized epileptiform discharges (PLEDs).

Neurosyphilis: may present as meningitis, meningovascular disease, general paresis, or tabes dorsalis; CSF VDRL is specific but insensitive; treat with IV penicillin G for 10-14 days.

HIV-associated neurocognitive disorder: spectrum from asymptomatic to HIV-associated dementia; treat with antiretroviral therapy; check CSF viral load and exclude opportunistic infections.

Progressive multifocal leukoencephalopathy: JC virus reactivation, usually in immunocompromised patients; MRI shows asymmetric non-enhancing white matter lesions; treatment is restoring immune function (IRIS may occur).

Toxoplasmosis vs CNS lymphoma: toxoplasmosis shows multiple ring-enhancing lesions with surrounding edema, often in basal ganglia; treat empirically and reassess in 2-3 weeks; lymphoma is usually solitary and periventricular.

Lyme neuroborreliosis: facial nerve palsy (often bilateral), lymphocytic meningitis, radiculoneuritis; serology with ELISA confirmed by Western blot; treat with ceftriaxone or doxycycline.

Autoimmune encephalitis vs infectious encephalitis: early CSF and MRI, and antibody testing; empiric acyclovir plus antibiotics until HSV and bacterial causes excluded; immunotherapy (steroids, IVIG, plasma exchange) if autoimmune suspected.

Alzheimer disease: insidious episodic memory loss, medial temporal atrophy on MRI, temporoparietal hypometabolism on FDG-PET; CSF shows low amyloid-beta42 and high phosphorylated tau; cholinesterase inhibitors for mild-moderate disease and memantine for moderate-severe.

Frontotemporal dementia: behavioral variant (disinhibition, apathy, hyperorality) or primary progressive aphasia (semantic or nonfluent/agrammatic); MRI shows frontal and temporal atrophy; no approved disease-modifying therapy.

Lewy body dementia: fluctuating cognition, visual hallucinations, parkinsonism, REM sleep behavior disorder, and neuroleptic sensitivity; avoid typical antipsychotics; cholinesterase inhibitors may help.

Vascular dementia: stepwise decline with focal signs, white matter hyperintensities, and infarcts; control vascular risk factors; distinguish from mixed Alzheimer-vascular pathology.

Delirium: acute fluctuating inattention with altered consciousness; common triggers include infection, medications (anticholinergics, benzodiazepines), pain, and withdrawal; treat the underlying cause and avoid restraints.

Mild cognitive impairment: objective cognitive impairment with preserved activities of daily living; annual conversion to dementia ~10%; evaluate reversible causes (B12, TSH, depression, sleep apnea).

Primary progressive aphasia: semantic variant (anomia, loss of word meaning, anterior temporal atrophy) vs nonfluent/agrammatic (effortful speech, apraxia, left inferior frontal atrophy); speech therapy is the main intervention.

Normal pressure hydrocephalus: gait disturbance, urinary incontinence, and cognitive decline with ventriculomegaly; large-volume lumbar puncture or external lumbar drain trial predicts shunt response.

Creutzfeldt-Jakob disease: rapidly progressive dementia with myoclonus, startle, periodic sharp wave complexes on EEG, and elevated 14-3-3 or RT-QuIC in CSF; no effective treatment.

Third nerve palsy: pupil-involving palsy with ptosis and down-and-out eye suggests compressive lesion (posterior communicating artery aneurysm); obtain urgent CTA. Pupil-sparing suggests microvascular ischemia (diabetes, hypertension).

Sixth nerve palsy: horizontal diplopia worse in lateral gaze; in adults, consider increased intracranial pressure, microvascular ischemia, and pontine lesions; MRI is indicated if nonisolated or progressive.

Internuclear ophthalmoplegia: impaired adduction of the ipsilateral eye with abducting nystagmus of the contralateral eye; lesion in the medial longitudinal fasciculus; bilateral in MS, unilateral in brainstem stroke.

Horner syndrome: ptosis, miosis, and anhidrosis; postganglionic lesions (carotid dissection) may spare facial sweating; test with apraclonidine and image the carotid and chest as indicated.

Papilledema: bilateral optic disc swelling from raised intracranial pressure, with preserved visual acuity early and enlarged blind spot; perform fundoscopy, then neuroimaging and lumbar puncture.

Anterior ischemic optic neuropathy: sudden painless monocular visual loss with altitudinal field defect and swollen disc; giant cell arteritis must be excluded in older patients with systemic symptoms.

Vestibular neuritis: acute prolonged vertigo with nausea, horizontal-torsional nystagmus, positive head impulse test, and no hearing loss; treat with short course of vestibular suppressants and vestibular rehabilitation.

Benign paroxysmal positional vertigo: brief positional vertigo with torsional nystagmus on Dix-Hallpike; treat with Epley canalith repositioning; no imaging needed in typical cases.

Bell palsy: acute unilateral lower facial weakness with inability to close the eye; corticosteroids within 72 h improve outcome; add antivirals for severe cases; eye protection to prevent exposure keratopathy.

Spinal cord syndromes: complete transection (loss below level), Brown-Sequard (ipsilateral motor/proprioception loss, contralateral pain/temperature loss), central cord (upper > lower weakness, often cervical spondylosis), anterior cord (motor and pain/temperature loss with preserved proprioception), and posterior cord (loss of proprioception and vibration).

Cauda equina syndrome: saddle anesthesia, urinary retention, bilateral leg weakness, and areflexia; urgent MRI and decompression within 24-48 h prevent permanent deficit.

Cervical radiculopathy: dermatomal pain and weakness, diminished reflex (C5 biceps, C6 brachioradialis, C7 triceps); MRI if progressive deficit or red flags; most improve with conservative care.

Lumbar radiculopathy: L4 (quadriceps, patellar reflex), L5 (dorsiflexion, EHL), S1 (plantarflexion, Achilles reflex); straight-leg raise is sensitive for L5-S1; surgery for progressive weakness or cauda equina.

Spinal cord injury: immobilize and assess with ASIA score; methylprednisolone is not routinely recommended; prevent autonomic dysreflexia (hypertension, bradycardia, headache) by treating the trigger (bladder, bowel, skin).

Neurorehabilitation after stroke: high-intensity, task-specific practice improves motor recovery; constraint-induced movement therapy for upper limb; early mobilization within 24-48 h when medically stable.

Gait rehabilitation: body-weight-supported treadmill training and robotic-assisted gait training may improve walking in incomplete spinal cord injury and stroke; assess with the Functional Ambulation Category.

Spasticity: treat with botulinum toxin for focal spasticity, baclofen (oral or intrathecal) for generalized, and physical therapy; assess with the Modified Ashworth Scale.

Neurogenic bladder: intermittent catheterization is preferred; anticholinergics or beta-3 agonists for detrusor overactivity; urodynamic testing guides management in spinal cord injury.

Neurotransmitters: glutamate (excitatory, NMDA/AMPA receptors), GABA (inhibitory, GABA-A/B), dopamine (nigrostriatal, mesolimbic, mesocortical, tuberoinfundibular pathways), acetylcholine (nicotinic/muscarinic), and serotonin (raphe nuclei).

Cerebral blood flow: normal ~50 mL/100 g/min; electrical failure below ~20 mL/100 g/min, membrane failure and infarction below ~10 mL/100 g/min; autoregulation maintains flow between MAP 60-160 mmHg.

Monro-Kellie doctrine: the skull is a rigid container with brain, blood, and CSF; increases in one compartment must be offset by decreases in others, or intracranial pressure rises.

Neurogenetics: autosomal dominant (Huntington, spinocerebellar ataxias, familial ALS), autosomal recessive (Wilson, Friedreich ataxia), X-linked (Duchenne, Fragile X), mitochondrial (MELAS, MERRF, Leigh); trinucleotide repeat disorders show anticipation.

CT imaging: hyperdense acute hemorrhage, hypodense ischemia after hours, loss of gray-white differentiation and insular ribbon sign in early MCA stroke; CTA for large-vessel occlusion and spot sign.

MRI sequences: DWI detects acute ischemia within minutes (restricted diffusion), FLAIR for edema and demyelination, T2* and SWI for hemorrhage and microbleeds, and gadolinium enhancement for blood-brain barrier breakdown.

Brain death criteria: unresponsive coma, absent brainstem reflexes, and apnea test with PaCO2 rise to >= 60 mmHg (or 20 mmHg above baseline); exclude confounders (hypothermia, drugs, metabolic derangement).

Elevated intracranial pressure: head elevation 30 degrees, hyperventilation to PaCO2 30-35 mmHg as a temporizing measure, hypertonic saline or mannitol, and decompressive craniectomy for refractory cases.

Critical care EEG: nonconvulsive status epilepticus should be suspected in unexplained coma; continuous EEG monitoring is recommended for status epilepticus and after cardiac arrest (burst suppression for refractory cases).