NEET SS Neurology (DM) Syllabus

Neurology (DM) syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Neurology (DM) in NEET SS, not a summary of it.

1. 1

   Cerebrovascular Disorders

   4 topics

   • Acute Ischemic Stroke
     • Thrombolysis and mechanical thrombectomy windows
     • Stroke etiology (TOAST classification)
     • Secondary prevention strategies
   • Intracerebral and Subarachnoid Hemorrhage
     • Aneurysmal SAH management
     • Vasospasm and delayed ischemia
   • Cerebral Venous Sinus Thrombosis
     • Risk factors and anticoagulation
   • Vascular Malformations and Vasculitis
     • AVM, cavernoma
     • CNS vasculitis
2. 2

   Epilepsy and Disorders of Consciousness

   4 topics

   • Seizure Classification and Epilepsy Syndromes
     • ILAE classification
     • Focal vs generalized epilepsies
   • Antiseizure Medications
     • Mechanisms and drug selection
     • Drug-resistant epilepsy and surgery
   • Status Epilepticus
     • Staged pharmacologic management
   • Coma and Brain Death
     • Localization and prognostication
3. 3

   Movement Disorders and Neurodegeneration

   3 topics

   • Parkinson's Disease and Parkinsonism
     • Dopaminergic therapy and motor complications
     • Atypical parkinsonian syndromes
   • Hyperkinetic Movement Disorders
     • Dystonia, chorea, tremor
     • Wilson's disease and Huntington's disease
   • Dementias
     • Alzheimer's disease and biomarkers
     • Frontotemporal and Lewy body dementia
4. 4

   Neuromuscular Disorders

   4 topics

   • Peripheral Neuropathies
     • Guillain-Barre syndrome and CIDP
     • Hereditary and metabolic neuropathies
   • Disorders of Neuromuscular Junction
     • Myasthenia gravis and Lambert-Eaton
   • Myopathies and Motor Neuron Disease
     • Muscular dystrophies and inflammatory myopathies
     • Amyotrophic lateral sclerosis
   • Electrophysiology (NCS/EMG)
     • Localization of nerve and muscle lesions
5. 5

   Neuroinfections, Demyelination and Headache

   3 topics

   • CNS Infections
     • Bacterial, tubercular and viral meningoencephalitis
     • Autoimmune encephalitis
   • Multiple Sclerosis and Demyelinating Disorders
     • McDonald criteria and disease-modifying therapy
     • NMOSD and MOG-associated disease
   • Headache Disorders
     • Migraine and trigeminal autonomic cephalalgias
     • Idiopathic intracranial hypertension

Neurology (DM) flashcards for NEET SS

21 of 53 cards from the Neurology (DM) deck — real questions with worked answers.

1. What is the maximum time window for IV thrombolysis with alteplase in acute ischemic stroke, and the extended window with tenecteplase/criteria?

   IV alteplase is approved up to 4.5 hours from symptom onset. Mechanical thrombectomy can be extended to 6 hours routinely, and 6-24 hours in selected patients with large-vessel occlusion using perfusion imaging mismatch (DAWN/DEFUSE-3 criteria).

2. List the major absolute contraindications to IV thrombolysis in acute ischemic stroke.

   Intracranial hemorrhage on CT, BP >185/110 uncontrolled, platelets <100,000, INR >1.7, recent major surgery/GI bleed, ischemic stroke within 3 months, active internal bleeding, and blood glucose <50 mg/dL (correct and reassess).

3. What ASPECTS score threshold generally favors mechanical thrombectomy in anterior circulation stroke?

   ASPECTS >=6 (out of 10) indicates limited early ischemic change and favorable outcome with thrombectomy; lower scores suggest a large established infarct core.

4. Describe the classic clinical features distinguishing a lacunar (small-vessel) stroke.

   Lacunar syndromes (pure motor, pure sensory, sensorimotor, ataxic hemiparesis, dysarthria-clumsy hand) lack cortical signs (no aphasia, neglect, or visual field defects) and result from small penetrating artery occlusion, classically lipohyalinosis from hypertension.

5. What is the target blood pressure before and after IV thrombolysis in acute ischemic stroke?

   Before tPA: <185/110 mmHg. After tPA: maintain <180/105 mmHg for 24 hours. In non-thrombolysed patients, permissive hypertension is allowed up to 220/120.

6. What is the most common cause and the classic CT appearance of spontaneous (non-traumatic) intracerebral hemorrhage?

   Hypertension is the most common cause, typically in basal ganglia (putamen), thalamus, pons, and cerebellum. CT shows a hyperdense parenchymal lesion; lobar hemorrhages in the elderly suggest cerebral amyloid angiopathy.

7. What is the ICH score and what variables comprise it?

   The ICH score predicts 30-day mortality using: GCS (3-4=2, 5-12=1, 13-15=0), ICH volume >=30 mL (1), intraventricular hemorrhage (1), infratentorial origin (1), and age >=80 (1). Total 0-6.

8. What is the most common cause of spontaneous subarachnoid hemorrhage and the investigation of choice?

   Ruptured saccular (berry) aneurysm, most often at the anterior communicating artery. Non-contrast CT is the initial test (highest sensitivity within 6 hours); if negative with high suspicion, do lumbar puncture looking for xanthochromia. CT angiography/DSA localizes the aneurysm.

9. How is the severity of subarachnoid hemorrhage graded clinically and radiologically?

   Hunt and Hess (clinical, grades 1-5) and WFNS (uses GCS) for clinical grading; the modified Fisher scale grades the amount of subarachnoid/intraventricular blood on CT, predicting vasospasm risk.

10. What is the timing and prevention of cerebral vasospasm after aneurysmal SAH?

    Vasospasm peaks between days 4-14 (most common days 7-10). Oral nimodipine (a calcium channel blocker) for 21 days improves outcomes by reducing delayed cerebral ischemia (though it does not abolish angiographic spasm).

11. What is the classic clinical triad and imaging finding of cerebral venous sinus thrombosis (CVST)?

    Headache (most common, often with raised ICP), seizures, and focal deficits; papilledema may occur. The 'empty delta sign' on contrast CT/CTV and absence of flow on MR venography confirm thrombosis. Hemorrhagic venous infarcts not respecting arterial territories are characteristic.

12. What is the first-line treatment of cerebral venous sinus thrombosis, even in the presence of hemorrhagic infarction?

    Anticoagulation (LMWH or unfractionated heparin acutely, then warfarin/oral anticoagulants) is first-line even when hemorrhagic venous infarction is present, as the benefit outweighs bleeding risk.

13. What are common predisposing/prothrombotic risk factors for CVST?

    Pregnancy/puerperium, oral contraceptives, dehydration, infections (otitis/mastoiditis/sinusitis), thrombophilias (factor V Leiden, protein C/S deficiency, antiphospholipid syndrome), malignancy, and nephrotic syndrome.

14. Differentiate AVM, cavernoma, and developmental venous anomaly in terms of bleeding risk and imaging.

    Arteriovenous malformation (AVM): high-flow nidus with arteriovenous shunting, ~2-4%/year bleed risk. Cavernoma (cavernous malformation): angiographically occult, 'popcorn' lesion with hemosiderin rim on T2*/SWI, lower annual bleed risk. Developmental venous anomaly (DVA): 'caput medusae' appearance, usually benign and should not be resected.

15. What is the most common primary CNS vasculitis and how is it diagnosed?

    Primary angiitis of the CNS (PACNS) presents with headache, encephalopathy, and multifocal strokes. Diagnosis relies on angiography (beading/alternating stenosis-dilatation), CSF showing mild pleocytosis/elevated protein, and ideally brain/leptomeningeal biopsy for confirmation.

16. State the 2017 ILAE basic classification of seizure onset types.

    Seizures are classified by onset as: focal onset (aware or impaired awareness; motor or non-motor), generalized onset (motor: tonic-clonic, etc., or non-motor: absence), and unknown onset, with possible focal-to-bilateral tonic-clonic progression.

17. Describe the EEG and clinical features of childhood absence epilepsy.

    Brief (5-10 sec) episodes of staring/behavioral arrest with impaired awareness, multiple times daily, provoked by hyperventilation; EEG shows generalized 3 Hz spike-and-wave discharges. First-line: ethosuximide (or valproate).

18. What are the defining features of Juvenile Myoclonic Epilepsy (JME)?

    Onset in adolescence with early-morning myoclonic jerks, generalized tonic-clonic seizures, and sometimes absences; EEG shows 4-6 Hz polyspike-and-wave; photosensitivity common. Valproate is most effective; lifelong therapy usually required as relapse is high.

19. What triad defines Lennox-Gastaut syndrome?

    (1) Multiple seizure types (tonic, atonic, atypical absence), (2) characteristic EEG with slow (<2.5 Hz) spike-and-wave and paroxysmal fast activity in sleep, and (3) intellectual impairment. Often drug-resistant.

20. Match these antiseizure drugs to their primary mechanisms: phenytoin, valproate, levetiracetam, lamotrigine, ethosuximide.

    Phenytoin: blocks voltage-gated Na+ channels. Valproate: broad (Na+ channel, increases GABA, T-type Ca2+). Levetiracetam: binds SV2A synaptic vesicle protein. Lamotrigine: blocks Na+ channels (inhibits glutamate release). Ethosuximide: blocks T-type Ca2+ channels (thalamic).

21. Which antiseizure drugs are best avoided in absence and myoclonic seizures because they may worsen them?

    Sodium channel blockers/GABAergics such as carbamazepine, oxcarbazepine, phenytoin, gabapentin, pregabalin, and vigabatrin can worsen absence and myoclonic seizures. Use broad-spectrum agents (valproate, lamotrigine, levetiracetam) instead.

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