NEET SS Neurosurgery (MCh) Flashcards

24 sample cards from the Neurosurgery (MCh) deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. What is the Hunt and Hess grading scale used for, and what does Grade I describe?

   It grades clinical severity of aneurysmal subarachnoid hemorrhage to predict prognosis. Grade I = asymptomatic or mild headache and slight nuchal rigidity. Higher grades (IV-V) involve stupor/coma and have worse outcomes.

2. What does the modified Fisher scale predict, and what is the gold-standard investigation for diagnosing SAH when CT is negative?

   The modified Fisher scale grades SAH blood thickness and intraventricular hemorrhage on CT to predict vasospasm risk. If non-contrast CT is negative but clinical suspicion is high, lumbar puncture looking for xanthochromia is the next step; CTA/DSA confirms the aneurysm.

3. What is cerebral vasospasm after SAH, when does it peak, and what is the mainstay of prophylaxis and treatment?

   Delayed arterial narrowing causing ischemia, peaking days 4-14 (max ~day 7) after aneurysmal SAH. Oral nimodipine improves outcomes (neuroprotective). Treatment of symptomatic vasospasm: induced hypertension/euvolemia and endovascular therapy (balloon angioplasty, intra-arterial vasodilators).

4. Compare surgical clipping versus endovascular coiling for ruptured aneurysms (ISAT trial findings).

   ISAT showed coiling had better 1-year outcomes (lower death/dependency) for suitable ruptured aneurysms, but with higher rebleeding and recurrence/retreatment rates than clipping. Clipping offers more durable occlusion. Choice depends on aneurysm morphology, location, and patient factors.

5. What is the Spetzler-Martin grading system for arteriovenous malformations and its three components?

   It grades surgical risk of brain AVMs by summing: size (<3 cm=1, 3-6 cm=2, >6 cm=3), eloquence of adjacent brain (eloquent=1, non=0), and venous drainage (deep=1, superficial=0). Total 1-5; higher grades have higher operative morbidity.

6. Contrast an arteriovenous malformation (AVM) with a cavernous malformation (cavernoma) in terms of angiography and bleeding.

   AVM: high-flow, with a nidus and arteriovenous shunting, visible on angiography (DSA). Cavernoma: low-flow, angiographically occult, 'popcorn' appearance with hemosiderin rim on MRI (T2/GRE/SWI); presents with seizures and lower-pressure hemorrhage.

7. What is a dural arteriovenous fistula, and what classification predicts its hemorrhage risk?

   An abnormal direct shunt between dural arteries and a dural venous sinus or cortical vein. The Borden and Cognard classifications stratify risk by presence of cortical venous reflux/drainage—cortical venous drainage markedly increases hemorrhage and aggressive course risk.

8. What is the most common location of hypertensive intracerebral hemorrhage, and which vessels are responsible?

   The basal ganglia, particularly the putamen, is the most common site. Hemorrhage arises from rupture of lenticulostriate arteries (Charcot-Bouchard microaneurysms). Other sites: thalamus, pons, cerebellum.

9. What are the surgical indications for cerebellar hemorrhage evacuation?

   Cerebellar hematoma >3 cm in diameter, or with neurological deterioration, brainstem compression, or hydrocephalus from fourth ventricle obstruction, warrants urgent surgical evacuation. EVD alone is insufficient and may precipitate upward herniation.

10. What underlying vascular pathology causes lobar hemorrhage in the elderly, and what is its hallmark?

    Cerebral amyloid angiopathy (CAA), from beta-amyloid deposition in cortical/leptomeningeal vessel walls. Hallmark: recurrent lobar (peripheral/cortical) hemorrhages and microbleeds on GRE/SWI in normotensive elderly patients.

11. What did the STICH trials conclude about surgery for supratentorial spontaneous intracerebral hemorrhage?

    STICH I showed no overall benefit of early surgery over initial conservative management for most supratentorial ICH. STICH II suggested a possible small benefit for superficial lobar hematomas without intraventricular hemorrhage, but no clear survival advantage. Deep ICH is generally managed medically.

12. What is cervical spondylotic myelopathy, and what is its definitive treatment?

    Chronic spinal cord compression from degenerative cervical changes (disc, osteophytes, ligamentum flavum hypertrophy) causing gait disturbance, hand clumsiness, hyperreflexia, and Hoffmann/Babinski signs. Definitive treatment is surgical decompression (anterior ACDF or posterior laminectomy/laminoplasty).

13. Differentiate the typical clinical pattern of lumbar disc herniation (radiculopathy) from lumbar spinal stenosis (neurogenic claudication).

    Disc herniation: dermatomal radicular leg pain, positive straight-leg raise, often worse with sitting/flexion. Lumbar stenosis: neurogenic claudication—bilateral leg pain/heaviness worsened by standing/walking (extension) and relieved by sitting/flexion (shopping-cart sign).

14. What is cauda equina syndrome and why is it a surgical emergency?

    Compression of the lumbosacral nerve roots causing saddle anesthesia, bilateral leg weakness/sciatica, bladder/bowel dysfunction (urinary retention then overflow incontinence), and reduced anal tone. It is a surgical emergency requiring urgent decompression (ideally within 48 hours) to prevent permanent deficits.

15. Which lumbar disc levels are most commonly herniated, and which nerve root is typically compressed by a posterolateral herniation?

    L4-L5 and L5-S1 are most common. A posterolateral (paracentral) herniation typically compresses the traversing root (the lower-numbered level's exiting root): e.g., L4-L5 disc compresses the L5 root; L5-S1 disc compresses the S1 root.

16. What is spondylolisthesis, and how is its severity graded?

    Anterior slippage of one vertebral body over the one below (commonly L5 on S1, isthmic or degenerative type). Graded by the Meyerding classification by percentage slip: Grade I (<25%), II (25-50%), III (50-75%), IV (75-100%), V (spondyloptosis, >100%).

17. What are the types of Chiari malformation, and what defines a Chiari I malformation?

    Chiari I: caudal herniation of cerebellar tonsils =5 mm below the foramen magnum; often associated with syringomyelia. Chiari II: herniation of vermis, brainstem, and fourth ventricle, associated with myelomeningocele. III and IV are rarer/more severe.

18. What is myelomeningocele, and what is the most common associated cranial anomaly?

    An open neural tube defect with herniation of meninges and neural tissue through a vertebral defect (failure of neural tube closure). It is almost always associated with Chiari II malformation and hydrocephalus. Folic acid supplementation reduces risk.

19. In pediatric hydrocephalus, contrast communicating versus non-communicating (obstructive) hydrocephalus with examples.

    Non-communicating (obstructive): blockage within the ventricular system, e.g., aqueductal stenosis, posterior fossa tumor. Communicating: impaired CSF absorption at arachnoid granulations or extraventricular flow obstruction, e.g., post-meningitic, post-hemorrhagic. CSF can still exit ventricles in communicating type.

20. What is the most common malignant brain tumor of childhood, and where does it arise?

    Medulloblastoma, a WHO grade 4 embryonal tumor arising in the cerebellum (vermis/fourth ventricle). It can cause obstructive hydrocephalus and 'drop metastases' via CSF. Molecular subgroups: WNT (best prognosis), SHH, Group 3 (worst), Group 4.

21. What is the surgical target and indication for deep brain stimulation in Parkinson's disease?

    Subthalamic nucleus (STN) and globus pallidus internus (GPi) are the primary targets. Indication: advanced PD with motor fluctuations and dyskinesias that remain levodopa-responsive but poorly controlled medically. STN allows medication reduction; GPi is better for dyskinesia control.

22. What is the gold-standard surgical treatment for medically refractory classic trigeminal neuralgia, and the leading causative mechanism?

    Microvascular decompression (MVD), which relieves neurovascular compression—most commonly by the superior cerebellar artery on the trigeminal nerve root entry zone. It offers the most durable pain relief; percutaneous procedures and stereotactic radiosurgery are alternatives.

23. In epilepsy surgery, what is the most common procedure for mesial temporal lobe epilepsy, and what pathology is typically found?

    Anterior temporal lobectomy with amygdalohippocampectomy (or selective amygdalohippocampectomy). The characteristic pathology is mesial temporal/hippocampal sclerosis. It is highly effective for drug-resistant mesial temporal lobe epilepsy.

24. What is the surgical target for essential tremor, and which functional procedure is used for it?

    The ventral intermediate nucleus (VIM) of the thalamus. Treatment options: deep brain stimulation of VIM, thalamotomy, or MR-guided focused ultrasound thalamotomy. It controls contralateral limb tremor refractory to medication (e.g., propranolol, primidone).

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