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AN62.1-6 | Cranial nerve nuclei & Cerebral hemispheres — Practice Quiz
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The chorda tympani branch of CN VII carries which functional components?
Correct! Chorda tympani = SVA (taste from anterior 2/3 tongue) + GVE (preganglionic parasympathetic to submandibular and sublingual glands via submandibular ganglion).
Bell's palsy = entire CN VII LMN palsy. If lesion is at/above the geniculate ganglion (proximal): all branches affected including chorda tympani → loss of taste (ant 2/3) + dry eye (greater petrosal) + hyperacusis (nerve to stapedius) + facial weakness. If lesion is BELOW geniculate (distal, near stylomastoid) → only facial motor weakness, taste preserved.
Incorrect. Chorda tympani = SVA (taste, ant 2/3) + GVE (salivary glands). It does NOT carry the facial motor component (that is the facial nerve's main trunk exiting via stylomastoid foramen).
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A patient presents with fluent speech, normal articulation, but makes many word substitution errors (paraphasias) and cannot comprehend spoken or written language. The lesion is in:
Correct! Wernicke's aphasia: FLUENT speech but incomprehensible (jargon, paraphasias) + impaired COMPREHENSION. Damage to area 22 in the posterior superior temporal gyrus (left hemisphere). Contrast with Broca's: non-fluent but comprehension intact.
Aphasia types: Broca's (motor) = non-fluent, agrammatic, comprehension intact, frustrated patient. Wernicke's (sensory) = fluent, paraphasias/neologisms, poor comprehension, patient unaware. Conduction = fluent, comprehension intact, repetition impaired (arcuate fasciculus damage). Global = all aspects impaired = large MCA territory.
Incorrect. Fluent + paraphasias + impaired comprehension = Wernicke's aphasia = area 22 (left superior temporal gyrus). Non-fluent + intact comprehension = Broca's (area 44/45).
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A patient with an anterior cerebral artery (ACA) territory infarct develops weakness predominantly affecting the contralateral leg. This is because the motor cortex representation for the leg is located:
Correct! Motor cortex homunculus: LEG is on the MEDIAL surface (paracentral lobule) = ACA territory. ARM and FACE are on the lateral convex surface = MCA territory. ACA infarct → contralateral leg weakness + sensory loss (paracentral lobule).
Somatotopic motor cortex: medial surface (ACA) → leg. Lateral surface (MCA) → arm (lateral) → face (most lateral). ACA infarct signs: contralateral leg paresis + sensory loss + frontal lobe signs (abulia, urinary incontinence from damage to supplementary motor area and cingulate cortex).
Incorrect. ACA territory = medial hemisphere = paracentral lobule = leg representation. MCA = lateral hemisphere = arm + face. This explains why ACA strokes present with leg > arm weakness (opposite to MCA strokes).
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A hypertensive patient develops sudden contralateral hemiplegia with face and arm > leg involvement. CT shows a small lacunar infarct in the internal capsule. The most likely location is the:
Correct! Posterior limb of internal capsule: anterior 2/3 = corticospinal (arm medial → leg lateral); genu = corticobulbar (face). Pure motor stroke (face + arm + leg) or capsular pure motor hemiplegia = posterior limb lenticulostriate infarct.
Lacunar infarcts — small deep infarcts from occlusion of small perforating arteries in Indian hypertensives. Four classical syndromes: (1) Pure motor hemiplegia = posterior limb IC or pons. (2) Pure sensory stroke = VPL thalamus. (3) Ataxic hemiparesis = posterior limb IC or pons. (4) Clumsy hand-dysarthria = genu IC or pons.
Incorrect. Pure motor hemiplegia = posterior limb (corticospinal) ± genu (corticobulbar). Anterior limb = frontopontine. Retrolenticular = optic radiation (hemianopia).
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In Parkinson's disease, the loss of dopamine from the substantia nigra causes bradykinesia primarily through:
Correct! Parkinson's bradykinesia mechanism: SN dopamine loss → D2 receptors (indirect pathway, inhibitory) less activated → indirect pathway MORE ACTIVE → STN more active → GPi more active → thalamus MORE INHIBITED → motor cortex LESS ACTIVATED → bradykinesia, rigidity.
L-DOPA therapy mechanism: replaces depleted dopamine in striatum. Activates D1 (direct pathway facilitatory) + D2 (indirect pathway suppressive) → restores balance → reduces bradykinesia + rigidity. On periods (L-DOPA working) vs off periods (wearing off). Late complication: dyskinesias (too much dopamine → overactive direct pathway → chorea-like movements).
Incorrect. SN dopamine loss → indirect pathway overactive → STN overactive → GPi overactive → thalamus inhibited → reduced motor output. Dopamine normally FACILITATES direct pathway (D1) and INHIBITS indirect pathway (D2). Loss of both → net increase in GPi inhibition of thalamus.
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Violent flinging (ballistic) movements of the contralateral arm and leg suddenly develop after a small infarct on MRI. The lesion is in the:
Correct! Hemiballismus = contralateral subthalamic nucleus (STN) damage. STN normally drives GPi inhibition (indirect pathway). Loss of STN → GPi underactive → thalamus DISINHIBITED → motor cortex OVERACTIVATED → violent contralateral proximal limb movements.
Hemiballismus is a neurological emergency (exhaustion, injury risk). Treatment: haloperidol or valproate to reduce movements. STN infarcts are typically lacunar from hypertension or diabetes. Most hemiballismus resolves spontaneously over weeks to months as perilesional oedema resolves and circuits reorganise.
Incorrect. Hemiballismus = CONTRALATERAL STN damage. Remember: basal ganglia pathways are ipsilateral to their deep nucleus but the OUTPUT to the cortex is still contralateral (thalamus → motor cortex → corticospinal crosses). Right STN → left hemiballismus.
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The ventroposterolateral (VPL) nucleus of the thalamus receives sensory information from the body via:
Correct! VPL receives: (1) Medial lemniscus (fine touch, vibration, proprioception from body) + (2) Lateral spinothalamic tract (pain and temperature from body). Output → primary somatosensory cortex (areas 1,2,3) → contralateral body sensation.
Thalamic pain syndrome (Déjerine-Roussy syndrome): VPL thalamic infarct (PCA territory perforator) causes transient contralateral sensory loss, then persistent contralateral spontaneous burning pain (thalamic pain). Common in PCA territory strokes in Indian patients with hypertension.
Incorrect. VPL = body sensory relay (medial lemniscus + spinothalamic). VPM = face (trigeminothalamic). LGN = visual. MGN = auditory. Anterior thalamus = mammillothalamic (limbic/Papez circuit).
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ADH (antidiuretic hormone/vasopressin) and oxytocin are synthesised in the hypothalamus and released from the posterior pituitary. They are produced in:
Correct! ADH and oxytocin are synthesised in the supraoptic nucleus (SON, mainly ADH) and paraventricular nucleus (PVN, mainly oxytocin + ADH). They travel along axons (hypothalamo-hypophyseal tract) to be stored and released from the posterior pituitary (neurohypophysis).
SIADH (syndrome of inappropriate ADH) vs Diabetes Insipidus: SIADH = too much ADH → water retention → dilutional hyponatraemia → confusion, seizures. DI = too little ADH → large volumes of dilute urine → hypernatraemia. Common causes in India: TBM (DI and SIADH both), head injury (DI), lung cancer (SIADH).
Incorrect. ADH + oxytocin = synthesised in SON and PVN → transported down axons → released from posterior pituitary. Damage to SON/PVN or hypothalamo-hypophyseal tract → diabetes insipidus (ADH deficiency = polyuria + polydipsia with dilute urine).
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A 40-year-old woman presents with sudden "thunderclap" headache. CT shows diffuse subarachnoid haemorrhage. Angiography reveals an aneurysm at the anterior communicating artery. Anterior communicating artery aneurysms specifically may cause which additional clinical sign?
Correct! AComm aneurysms sit near the frontal lobes and olfactory tracts. Rupture or mass effect may cause anosmia (CN I compression from the aneurysm or blood tracking into the olfactory groove) + personality change/abulia (frontal lobe ischaemia from vasospasm or direct compression).
Berry aneurysm sites and their specific CN/structure risks: (1) AComm = frontal + olfactory. (2) PComm = CN III (ipsilateral pupil-involved palsy). (3) MCA bifurcation = temporal lobe. (4) Basilar tip = CN III bilateral + midbrain. SAH management: CT to diagnose, LP if CT negative (xanthochromia in CSF), CTA/DSA for aneurysm, neurosurgical clipping or endovascular coiling.
Incorrect. AComm aneurysms: located at junction of both ACAs in the midline, near the olfactory tracts and frontal lobes. CN III palsy = PComm aneurysm. Bitemporal hemianopia = pituitary tumour compressing optic chiasm.
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Occlusion of the left middle cerebral artery (MCA) in the dominant hemisphere typically causes all of the following EXCEPT:
Correct! Left MCA occlusion causes: right hemiplegia (arm + face > leg), aphasia (left = dominant), right homonymous hemianopia (optic radiation). It does NOT cause isolated leg monoplegia — that is an ACA territory sign (medial surface = paracentral lobule = leg representation).
Stroke territory diagnosis from clinical signs: (1) ACA = leg weakness + frontal signs + urinary incontinence. (2) MCA = arm + face + aphasia (left) or neglect (right) + hemianopia. (3) PCA = hemianopia (prominent) + thalamic sensory. (4) Basilar = bilateral signs + CN involvement + vertigo/nausea. (5) Lacunar = pure motor or pure sensory.
Incorrect. Isolated right leg monoplegia = ACA territory (paracentral lobule). MCA territory involves lateral surface = arm + face + aphasia + hemianopia. MCA does NOT supply the leg's primary motor/sensory cortex significantly.
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