Czech Neurology Board Examination cheat sheet

The corticospinal tract decussates at the medullary pyramids (85–90% in the lateral corticospinal tract); the remainder forms the anterior corticospinal tract and decussates segmentally.

The lateral spinothalamic tract carries pain and temperature; fibers ascend 1–2 segments in Lissauer's tract before synapsing in the dorsal horn, then decussate within 1–2 segments.

The dorsal column–medial lemniscus pathway carries vibration and proprioception; fibers ascend ipsilaterally in the fasciculus gracilis (lower limbs) and cuneatus (upper limbs) and decussate in the medulla.

Broca's area (inferior frontal gyrus, pars opercularis/triangularis, dominant hemisphere) mediates motor speech; Wernicke's area (posterior superior temporal gyrus) mediates comprehension.

The circle of Willis connects anterior and posterior circulations via the anterior communicating artery and posterior communicating arteries; absence of one posterior communicating artery is a common normal variant.

Resting membrane potential approximates the potassium equilibrium potential (about −70 mV); the Na+/K+-ATPase exchanges 3 Na+ out for 2 K+ in.

The monosynaptic stretch reflex arc: Ia afferent from muscle spindle → alpha motor neuron → extrafusal muscle contraction; gamma motor neurons adjust spindle sensitivity.

Cerebrospinal fluid is produced mainly by choroid plexus (~500 mL/day), total volume ~150 mL, and is absorbed by arachnoid granulations into the superior sagittal sinus.

Upper motor neuron signs: spasticity, hyperreflexia, Babinski sign, clonus, loss of superficial abdominal reflexes; lower motor neuron signs: fasciculations, atrophy, hypotonia, areflexia.

Pupil light reflex pathway: retina → optic nerve → optic chiasm → optic tract → pretectal nucleus → bilateral Edinger-Westphal nucleus → CN III → ciliary ganglion → pupil constriction.

A relative afferent pupillary defect (Marcus Gunn pupil) indicates optic nerve or severe retinal disease, not a simple efferent (CN III) lesion.

Horner syndrome: ptosis, miosis, anhidrosis (and facial flushing); localizes to the ipsilateral hypothalamus, brainstem, cervical spinal cord (C8–T2), sympathetic chain, or internal carotid artery.

Aphasia vs dysarthria: aphasia is a language disorder (impaired comprehension, naming, repetition, or fluency); dysarthria is a motor speech disorder with preserved language.

Topographic diagnosis of hemiparesis: face and arm > leg suggests a lateral cortical lesion; leg > arm suggests a medial frontal lesion (anterior cerebral artery territory); pure motor suggests a lacunar lesion in the internal capsule, pons, or corona radiata.

Cerebellar signs: ipsilateral limb ataxia, intention tremor, dysdiadochokinesia, dysmetria, and nystagmus; vermis lesions cause truncal/gait ataxia.

Glasgow Coma Scale: eye opening (1–4), verbal response (1–5), motor response (1–6); total 3–15; score ≤8 is generally an indication to consider airway protection.

Intravenous thrombolysis with alteplase or tenecteplase is indicated within 4.5 hours of ischemic stroke onset after excluding hemorrhage on CT and contraindications (e.g., recent surgery, uncontrolled hypertension >185/110 mmHg).

Mechanical thrombectomy is indicated for large vessel occlusion (ICA, M1, or basilar) within 6 hours of onset; selected patients with salvageable penumbra may benefit up to 24 hours.

The NIHSS quantifies stroke severity (0–42); a score ≥6 often prompts consideration of large vessel occlusion and thrombectomy.

Hemorrhagic transformation risk increases with large infarct volume, severe hypertension, and delayed reperfusion; follow-up imaging is obtained after thrombolysis or thrombectomy.

Subarachnoid hemorrhage: sudden thunderclap headache; CT is highly sensitive within 6 hours; if CT is negative and suspicion persists, lumbar puncture for xanthochromia after 12 hours is performed.

Aneurysmal SAH management includes nimodipine for vasospasm prophylaxis, early aneurysm securing (coiling or clipping), and monitoring for hydrocephalus and hyponatremia.

Malignant middle cerebral artery infarction with mass effect may require decompressive hemicraniectomy, typically within 48 hours in patients ≤60 years.

Brain death criteria require coma, absent brainstem reflexes, and apnea in the absence of confounding factors (hypothermia, drugs, metabolic derangement); ancillary tests may be used when the clinical exam is unreliable.

Focal seizures originate in one hemisphere; generalized seizures involve bilateral networks at onset; classification includes motor vs non-motor onset and awareness (focal aware, focal impaired awareness).

Status epilepticus: continuous seizure ≥5 minutes or recurrent seizures without recovery; first-line benzodiazepines, second-line IV antiseizure medication (e.g., levetiracetam, valproate, fosphenytoin), then anesthetic agents for refractory cases.

Juvenile myoclonic epilepsy: onset in adolescence, myoclonic jerks on awakening, generalized tonic-clonic seizures, and sometimes absence; EEG shows 3–4 Hz generalized spike-wave; often lifelong treatment with valproate or levetiracetam.

Typical absence seizures: brief (seconds) impairment of awareness, 3 Hz generalized spike-wave on EEG, hyperventilation provocation; first-line ethosuximide or valproate.

Sudden unexpected death in epilepsy (SUDEP) risk factors include frequent generalized tonic-clonic seizures, nocturnal seizures, poor medication adherence, and young adult age.

Obstructive sleep apnea diagnosis: apnea-hypopnea index ≥5 with symptoms, or ≥15 without symptoms; first-line treatment is CPAP; avoid sedatives and alcohol.

Narcolepsy type 1: excessive daytime sleepiness, cataplexy, low CSF hypocretin-1; multiple sleep latency test shows mean sleep latency ≤8 minutes and ≥2 sleep-onset REM periods.

REM sleep behavior disorder: dream-enacting behaviors with loss of REM atonia; strongly associated with synucleinopathies (Parkinson's disease, dementia with Lewy bodies, multiple system atrophy).

Guillain-Barré syndrome: acute ascending areflexic weakness, albuminocytologic dissociation in CSF (elevated protein with normal cell count), and demyelinating features on EMG/NCS; treat with IVIG or plasma exchange.

Myasthenia gravis: fatigable weakness, ptosis, diplopia, bulbar symptoms; anti-AChR antibodies in ~85% of generalized cases; repetitive nerve stimulation shows decrement; treat with acetylcholinesterase inhibitors, immunosuppression, and thymectomy in selected patients.

Lambert-Eaton myasthenic syndrome: proximal weakness, hyporeflexia that improves with exercise, autonomic symptoms; anti-VGCC antibodies; associated with small cell lung cancer; repetitive nerve stimulation shows increment.

Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP): progressive or relapsing weakness over ≥8 weeks, demyelinating NCS, elevated CSF protein; treat with IVIG, corticosteroids, or plasma exchange.

Amyotrophic lateral sclerosis: combined upper and lower motor neuron signs, progressive, with bulbar involvement; riluzole and edaravone modestly slow progression; noninvasive ventilation for respiratory insufficiency.

Duchenne muscular dystrophy: X-linked dystrophin deficiency, calf pseudohypertrophy, Gowers sign, elevated CK; corticosteroids slow progression; monitor cardiac and respiratory function.

Myotonic dystrophy type 1: CTG repeat expansion in DMPK; distal weakness, myotonia, cataracts, cardiac conduction defects, and endocrine abnormalities; autosomal dominant.

Peripheral neuropathy evaluation: determine fiber type (large vs small), distribution (mononeuropathy, mononeuropathy multiplex, polyneuropathy), temporal course, and associated systemic disease; NCS/EMG distinguishes axonal from demyelinating.

Multiple sclerosis diagnosis (McDonald criteria): dissemination in space and time demonstrated clinically or by MRI; CSF oligoclonal bands can substitute for dissemination in time.

MS relapse treatment: high-dose corticosteroids (e.g., IV methylprednisolone 1 g daily for 3–5 days) shorten relapse duration but do not alter long-term disability.

Disease-modifying therapies for MS include injectables (interferon beta, glatiramer acetate), oral agents (fingolimod, dimethyl fumarate, teriflunomide, cladribine), and infusions (natalizumab, alemtuzumab, ocrelizumab).

Neuromyelitis optica spectrum disorder (NMOSD): anti-aquaporin-4 antibodies, longitudinally extensive transverse myelitis (≥3 segments), optic neuritis, area postrema syndrome; treat acute attacks with steroids and plasma exchange; prevent with rituximab, eculizumab, or inebilizumab.

MOG antibody-associated disease (MOGAD): optic neuritis, ADEM-like presentations, transverse myelitis; MOG antibodies detected by cell-based assay; often steroid-responsive.

Acute disseminated encephalomyelitis (ADEM): post-infectious, multifocal white matter lesions, encephalopathy; more common in children; treat with high-dose corticosteroids.

Anti-NMDA receptor encephalitis: psychiatric symptoms, memory loss, seizures, dyskinesias, autonomic instability, hypoventilation; associated with ovarian teratoma; treat with steroids, IVIG/plasma exchange, and tumor removal.

Optic neuritis: painful vision loss, relative afferent pupillary defect, decreased color vision; MRI brain to assess MS risk; treat with IV corticosteroids for faster recovery.

Parkinson's disease diagnosis requires bradykinesia plus rest tremor or rigidity; levodopa is the most effective symptomatic treatment; motor complications include wearing-off and dyskinesias.

Atypical parkinsonism red flags: early falls, early cognitive impairment, prominent autonomic failure, vertical gaze palsy, alien limb, or poor levodopa response suggest MSA, DLB, PSP, or CBD.

Essential tremor: bilateral postural/kinetic tremor of hands and head, improved by alcohol; first-line treatment propranolol or primidone.

Huntington's disease: autosomal dominant CAG repeat expansion in HTT; chorea, cognitive decline, psychiatric symptoms; onset typically in midlife; treat chorea with tetrabenazine or deutetrabenazine.

Alzheimer's disease: progressive episodic memory impairment; MRI shows medial temporal atrophy; biomarkers include low CSF Aβ42 and elevated tau; cholinesterase inhibitors and memantine provide modest symptomatic benefit.

Dementia with Lewy bodies: fluctuating cognition, visual hallucinations, parkinsonism, REM sleep behavior disorder; neuroleptic sensitivity; treat cognitive symptoms with cholinesterase inhibitors.

Frontotemporal dementia: behavioral variant (disinhibition, apathy, hyperorality) or language variants (primary progressive aphasia); associated with FTLD-tau or FTLD-TDP pathology; no approved disease-modifying therapy.

Wilson's disease: autosomal recessive ATP7B mutation, copper accumulation; Kayser-Fleischer rings, liver disease, tremor, dystonia, psychiatric symptoms; treat with chelating agents (penicillamine, trientine) or zinc.

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

Meningioma: typically extra-axial, dural-based, enhancing mass; WHO grade 1 in most cases; observation for asymptomatic small lesions; surgery for symptomatic or growing tumors.

Brain metastases: most common adult brain tumors; treat with surgery, stereotactic radiosurgery, or whole-brain radiotherapy depending on number and size; corticosteroids for edema.

Primary CNS lymphoma: diffuse large B-cell lymphoma; periventricular enhancing lesions; diagnosis requires biopsy (CSF cytology often negative); treat with high-dose methotrexate-based regimens.

Bacterial meningitis: empiric therapy includes vancomycin plus a third-generation cephalosporin (e.g., ceftriaxone); add ampicillin for Listeria in patients >50 years or immunocompromised; dexamethasone before or with first antibiotic dose in pneumococcal meningitis.

Herpes simplex encephalitis: temporal lobe involvement, fever, headache, seizures, confusion; CSF shows lymphocytic pleocytosis and elevated protein; treat empirically with IV acyclovir until PCR is negative.

Lyme neuroborreliosis: facial nerve palsy (often bilateral), meningitis, radiculoneuritis; CSF shows lymphocytic pleocytosis; treat with ceftriaxone or doxycycline.

Progressive multifocal leukoencephalopathy (PML): JC virus infection of oligodendrocytes; seen with immunosuppression (e.g., natalizumab, HIV); MRI shows non-enhancing white matter lesions; treatment is restoration of immune function.

Migraine with aura: fully reversible visual, sensory, or language symptoms developing over ≥5 minutes and lasting 5–60 minutes, followed by headache; treat acute attacks with triptans or NSAIDs; preventive options include topiramate, propranolol, amitriptyline, and CGRP monoclonal antibodies.

Cluster headache: severe unilateral orbital/supraorbital pain lasting 15–180 minutes with ipsilateral autonomic symptoms (lacrimation, rhinorrhea, ptosis); treat acute attacks with high-flow oxygen or subcutaneous sumatriptan; prevent with verapamil.

Medication-overuse headache: headache on ≥15 days/month with regular overuse of acute medications (e.g., triptans or opioids ≥10 days/month, simple analgesics ≥15 days/month); treat by withdrawing the overused medication.

Giant cell arteritis: age >50, new headache, jaw claudication, visual symptoms, elevated ESR/CRP; treat immediately with high-dose corticosteroids and confirm with temporal artery biopsy.

Trigeminal neuralgia: paroxysmal electric-shock-like facial pain in V2/V3 distribution, triggered by touch or chewing; first-line carbamazepine or oxcarbazepine; consider microvascular decompression if refractory.

Idiopathic intracranial hypertension: headache, papilledema, elevated opening pressure (>25 cm CSF in adults), normal CSF composition; treat with weight loss, acetazolamide, and sometimes CSF shunting.

Postherpetic neuralgia: persistent pain ≥3 months after herpes zoster; treat with gabapentin, pregabalin, tricyclic antidepressants, or topical lidocaine; prevention with zoster vaccination.

Bell's palsy: acute unilateral lower facial weakness, often with postauricular pain; treat with corticosteroids within 72 hours; add antivirals in severe cases; eye protection for incomplete closure.

CT is first-line for acute stroke to exclude hemorrhage; MRI with diffusion-weighted imaging is more sensitive for acute ischemia and detects lesions within minutes.

MRI contraindications include ferromagnetic implants, pacemakers (unless MRI-conditional), and metallic foreign bodies; gadolinium contrast is avoided in severe renal impairment due to nephrogenic systemic fibrosis risk.

EEG: 3 Hz generalized spike-wave in absence epilepsy; hypsarrhythmia in infantile spasms; periodic lateralized epileptiform discharges (PLEDs) suggest acute structural lesion or infection; burst suppression in severe encephalopathy.

EMG/NCS: demyelinating neuropathy shows slowed conduction velocity, prolonged distal latency, and conduction block; axonal neuropathy shows reduced amplitude with relatively preserved conduction velocity.

Repetitive nerve stimulation: decrement >10% suggests myasthenia gravis; increment >100% suggests Lambert-Eaton myasthenic syndrome.

Lumbar puncture: opening pressure normally 10–20 cm CSF; bacterial meningitis shows neutrophilic pleocytosis, low glucose, high protein; viral meningitis shows lymphocytic pleocytosis with normal glucose.

Evoked potentials: visual evoked potentials detect demyelination of the optic nerve; somatosensory evoked potentials assess dorsal column pathway; brainstem auditory evoked potentials assess CN VIII and brainstem.

Transcranial Doppler: elevated mean flow velocities (>120 cm/s) suggest vasospasm after subarachnoid hemorrhage; also used for sickle cell stroke risk screening.

Post-stroke rehabilitation should begin early (within 24–48 hours once medically stable) with multidisciplinary therapy; constraint-induced movement therapy improves upper limb function in selected patients.

Spasticity management: physical therapy, oral baclofen or tizanidine, focal botulinum toxin injections, and intrathecal baclofen for severe generalized spasticity.

Neuropsychological assessment domains include attention, memory, language, visuospatial function, executive function, and mood; the Mini-Mental State Examination is a screening tool, not a diagnostic test.

Delirium: acute fluctuating attention and awareness disturbance; identify and treat underlying cause; avoid antipsychotics unless necessary for severe agitation; nonpharmacologic measures first.

Palliative care in neurology focuses on symptom control (pain, dyspnea, spasticity, secretions), advance care planning, and psychosocial support for patients and families.

Amyotrophic lateral sclerosis multidisciplinary care includes noninvasive ventilation for respiratory insufficiency, percutaneous endoscopic gastrostomy for dysphagia, and communication aids.

Depression after stroke is common; screen with PHQ-9 or similar; treat with SSRIs and psychotherapy; pseudobulbar affect may respond to dextromethorphan/quinidine.

Brain death and organ donation: confirm death by neurologic criteria per institutional protocol; discuss organ donation with families in coordination with transplant services.

Informed consent requires capacity, disclosure of material risks and alternatives, and voluntariness; document the discussion; emergency treatment may proceed without consent if life-threatening and no surrogate is available.

Capacity assessment: patient can understand relevant information, appreciate consequences, reason, and communicate a choice; capacity is task-specific.

Confidentiality: disclose patient information only with consent or as required by law (e.g., mandatory reporting of certain communicable diseases, court order); GDPR and local health law apply.

Advance directives and durable power of attorney for healthcare should be honored; if absent, surrogate decision-making follows local legal hierarchy.

Medical documentation: record contemporaneous notes, informed consent, and critical conversations; electronic records must comply with data protection regulations.

Duty to report: impaired driving in epilepsy or dementia may require reporting per local law; notify public health authorities of notifiable diseases (e.g., meningococcal meningitis).

Research ethics: institutional review board approval, informed consent, and declaration of conflicts of interest are required before conducting human subject research.

Telemedicine in neurology: ensure patient identity verification, privacy, documentation, and licensure in the jurisdiction where the patient is located.