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Question 1Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
A 58-year-old man has a left homonymous hemianopia with macular sparing. Where is the lesion most likely located?
- Right optic radiation in the temporal lobe (Meyer loop)
- Left optic tract
- Right occipital cortex, with infarction of the posterior cerebral artery territory Correct answer.
- Left lateral geniculate body
Explanation
Macular sparing indicates damage to the occipital cortex with preservation of the occipital pole, which receives dual blood supply from the posterior and middle cerebral arteries. A homonymous defect without macular sparing points to more anterior retrochiasmal lesions such as the tract, lateral geniculate body, or optic radiation. The left-sided structures would produce a right homonymous defect.
Question 2Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
Which neurotransmitter is released by the major output neurons of the striatum, the medium spiny neurons of the direct pathway?
- Dopamine
- Glutamate
- GABA Correct answer.
- Acetylcholine
Explanation
Medium spiny neurons of both the direct and indirect striatal pathways are GABAergic projection neurons. The direct pathway projects to the internal globus pallidus and substantia nigra pars reticulata, releasing GABA and disinhibiting the thalamus. Dopamine and acetylcholine are modulatory transmitters in the striatum, not the output of these projection neurons.
Question 3Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
A patient develops sudden loss of pain and temperature sensation over the left face and right body, with hoarseness and vertigo. Which structure is most likely involved?
- Right cervical spinal cord
- Left medial pons
- Left lateral medulla Correct answer.
- Right medial medulla
Explanation
This crossed pattern of facial and contralateral body spinothalamic loss with bulbar symptoms indicates lateral medullary (Wallenberg) syndrome, caused by occlusion of the posterior inferior cerebellar artery or vertebral artery. The ipsilateral face is affected because the spinal trigeminal nucleus is involved, while the contralateral body is affected because the spinothalamic tract has already crossed. Medial lesions produce contralateral hemiparesis and tongue deviation instead.
Question 4Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
Which ion influx directly triggers neurotransmitter release at the presynaptic terminal?
- Calcium Correct answer.
- Chloride
- Sodium
- Potassium
Explanation
Depolarization of the presynaptic terminal opens voltage-gated calcium channels, and calcium entry triggers fusion of synaptic vesicles with the membrane. Sodium influx generates the action potential but does not directly cause vesicle fusion. Chloride and potassium fluxes generally oppose depolarization.
Question 5Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
A patient taking a monoamine oxidase inhibitor develops a hypertensive crisis after eating aged cheese. Which mechanism best explains this reaction?
- Inhibition of tyramine breakdown allows indirect noradrenaline release Correct answer.
- Inhibition of catecholamine synthesis in the adrenal medulla
- Direct agonism of central serotonin receptors
- Blockade of postsynaptic alpha-adrenergic receptors
Explanation
Aged cheese contains tyramine, an indirect sympathomimetic normally degraded by monoamine oxidase. When the enzyme is inhibited, tyramine reaches noradrenergic terminals and displaces stored noradrenaline into the synapse, producing a hypertensive crisis. This is a pharmacokinetic interaction, not receptor blockade or serotonin agonism.
Question 6Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
Which fibers carry discriminative touch and proprioception from the upper limb to the medulla?
- Ipsilateral dorsal columns Correct answer.
- Contralateral spinothalamic tract
- Contralateral corticospinal tract
- Ipsilateral spinocerebellar tract
Explanation
Fine touch and proprioceptive fibers enter the dorsal horn and ascend without crossing in the ipsilateral dorsal columns to the nucleus cuneatus. They synapse there, then cross as the medial lemniscus. The spinothalamic tract carries pain and temperature and crosses segmentally.
Question 7Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
A 30-year-old woman has fatigable ptosis and proximal weakness that improves after rest. Which neuromuscular junction abnormality is most consistent with this disorder?
- Antibodies against postsynaptic acetylcholine receptors Correct answer.
- Autoimmune destruction of anterior horn cells
- Deficiency of presynaptic acetylcholine synthesis
- Antibodies against presynaptic voltage-gated calcium channels
Explanation
Myasthenia gravis is caused by autoantibodies against postsynaptic nicotinic acetylcholine receptors, reducing the number of functional receptors and producing fatigable weakness. Lambert-Eaton syndrome involves presynaptic calcium channel antibodies. Anterior horn destruction is a lower motor neuron process and does not cause fatigability.
Question 8Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
Which structure forms the lateral wall of the third ventricle?
- Septum pellucidum
- Thalamus Correct answer.
- Hypothalamus
- Fornix
Explanation
The lateral walls of the third ventricle are formed by the thalami and the hypothalamus below. The fornix and septum pellucidum form the roof and medial wall region rather than the lateral walls. Knowing these relations helps localize mass lesions compressing the ventricle.
Question 9Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
A lesion of the right cranial nerve III produces which combination of findings?
- Ptosis, dilated pupil, and eye deviated down and out Correct answer.
- Inability to abduct the eye with a normal pupil
- Ptosis, constricted pupil, and eye deviated up and in
- Diplopia only on downward gaze with a normal pupil
Explanation
The oculomotor nerve supplies the levator palpebrae and most extraocular muscles, and its parasympathetic fibers constrict the pupil. A complete lesion causes ptosis, a fixed dilated pupil, and unopposed lateral rectus and superior oblique action, deviating the eye down and out. Pupillary sparing is more typical of ischemic diabetic palsies.
Question 10Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
In the hippocampus, which phenomenon describes the persistent increase in synaptic strength after high-frequency stimulation?
- Habituation
- Presynaptic inhibition
- Long-term depression
- Long-term potentiation Correct answer.
Explanation
Long-term potentiation is a lasting increase in synaptic efficacy after high-frequency stimulation, dependent on NMDA receptor activation and calcium influx. Long-term depression is the converse weakening after low-frequency stimulation. Habituation and presynaptic inhibition are shorter-term or non-plastic processes.
Question 11Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
A 70-year-old man has a right homonymous inferior quadrantanopia. Which lesion location is most likely?
- Right temporal optic radiation
- Left parietal optic radiation Correct answer.
- Right optic chiasm
- Left optic nerve
Explanation
The superior retinal fibers, which carry information from the inferior visual field, run through the parietal lobe. A left parietal lesion therefore produces a right inferior quadrantanopia. Temporal (Meyer loop) lesions cause superior quadrantanopia, while prechiasmal and chiasmal lesions cause monocular or bitemporal defects.
Question 12Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
Which receptor type is a ligand-gated ion channel that mediates fast excitatory synaptic transmission?
- G protein-coupled GABA-B receptor
- Metabotropic glutamate receptor
- Tyrosine kinase neurotrophin receptor
- Ionotropic glutamate receptor Correct answer.
Explanation
Ionotropic glutamate receptors such as AMPA and kainate receptors open cation channels directly upon binding glutamate, producing fast excitatory postsynaptic potentials. Metabotropic glutamate and GABA-B receptors act through second messengers and are slower. Neurotrophin receptors mediate trophic signaling rather than fast synaptic currents.
Question 13Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
A patient with a thalamic infarct develops spontaneous burning pain on the contralateral side. Which mechanism best explains this central post-stroke pain?
- Peripheral nerve entrapment at the wrist
- Loss of dorsal root ganglion cells
- Denervation hypersensitivity and altered central pain processing Correct answer.
- Demyelination of the peripheral motor axon
Explanation
Central post-stroke pain follows damage to spinothalamic pathways, with denervation hypersensitivity and disinhibition in thalamic and cortical circuits producing spontaneous burning pain. Peripheral entrapment, dorsal root ganglion loss, and motor axon demyelination produce peripheral or motor syndromes rather than contralateral central pain.
Question 14Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
Which cerebellar region is primarily responsible for coordinating voluntary limb movements?
- Vermal cortex
- Lateral cerebellar hemisphere Correct answer.
- Anterior vermis
- Flocculonodular lobe
Explanation
The lateral cerebellar hemispheres, via the dentate nucleus and corticocerebellar loops, plan and coordinate voluntary limb movement. The vermis coordinates axial and gait control, and the flocculonodular lobe regulates vestibulo-ocular function and balance. Lesions of the lateral hemisphere cause limb ataxia and intention tremor.
Question 15Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
A 45-year-old man has progressive weakness and muscle wasting with fasciculations, hyperreflexia, and extensor plantar responses. Which pathologic process explains this combination?
- Isolated loss of anterior horn cells without corticospinal involvement
- Antibodies against postsynaptic acetylcholine receptors
- Degeneration of both upper and lower motor neurons Correct answer.
- Selective demyelination of peripheral sensory nerves
Explanation
Combined lower motor neuron signs (wasting, fasciculations) and upper motor neuron signs (hyperreflexia, extensor plantar responses) indicate amyotrophic lateral sclerosis, in which both corticospinal and anterior horn neurons degenerate. Pure anterior horn loss would produce lower motor neuron signs alone. Peripheral demyelination and postsynaptic antibodies do not produce upper motor neuron signs.
Question 16Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
Which brain region is the main source of cholinergic projections to the cerebral cortex?
- Basal nucleus of Meynert Correct answer.
- Raphe nuclei
- Substantia nigra pars compacta
- Locus coeruleus
Explanation
The basal nucleus of Meynert provides the major cholinergic innervation of the cerebral cortex and degenerates in Alzheimer disease. The substantia nigra is dopaminergic, the locus coeruleus noradrenergic, and the raphe nuclei serotonergic. These distinct projection systems are often tested together.
Question 17Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
Which mechanism explains why the local anesthetic lidocaine blocks nerve conduction?
- Blockade of voltage-gated sodium channels from the intracellular side Correct answer.
- Enhanced chloride conductance
- Blockade of voltage-gated potassium channels
- Inhibition of acetylcholinesterase
Explanation
Lidocaine is a weak base that crosses the membrane in its uncharged form and then blocks voltage-gated sodium channels from the inside, preventing action potential generation. Potassium channel blockade would prolong repolarization rather than abolish conduction. Enhanced chloride conductance would hyperpolarize the membrane without blocking axonal conduction.
Question 18Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
A patient has a lesion of the left optic nerve. What visual field defect results?
- Bitemporal hemianopia
- Left superior quadrantanopia
- Total blindness of the left eye Correct answer.
- Right homonymous hemianopia
Explanation
The optic nerve carries all visual fibers from one eye, so a complete lesion causes monocular blindness on the same side. Chiasmal lesions produce bitemporal defects, and retrochiasmal lesions produce contralateral homonymous defects. Quadrantanopias arise from radiation lesions.
Question 19Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
Which structure is the main output nucleus of the basal ganglia, projecting inhibitory fibers to the thalamus?
- Caudate nucleus
- Subthalamic nucleus
- Putamen
- Internal globus pallidus Correct answer.
Explanation
The internal globus pallidus and substantia nigra pars reticulata are the output nuclei of the basal ganglia, sending GABAergic inhibitory projections to the thalamus. The putamen and caudate are input nuclei, and the subthalamic nucleus is part of the indirect pathway.
Question 20Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
A patient develops a right-sided hemiparesis with ipsilateral tongue deviation after a brainstem stroke. Which vessel is most likely occluded?
- Superior cerebellar artery
- Posterior inferior cerebellar artery
- Anterior inferior cerebellar artery
- Paramedian branches of the anterior spinal artery Correct answer.
Explanation
Medial medullary syndrome results from occlusion of paramedian branches of the anterior spinal artery or vertebral artery, damaging the corticospinal tract and hypoglossal nerve fibers. The posterior inferior cerebellar artery causes lateral medullary syndrome with sensory and bulbar signs. AICA and SCA lesions produce pontine and cerebellar patterns, respectively.
Question 21Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
Which glial cell type forms myelin in the central nervous system?
- Microglial cell
- Oligodendrocyte Correct answer.
- Astrocyte
- Schwann cell
Explanation
Oligodendrocytes extend multiple processes to myelinate several axons in the central nervous system. Schwann cells myelinate peripheral axons, while astrocytes support the blood-brain barrier and microglia act as immune cells. Distinguishing these cells underlies understanding of demyelinating diseases.
Question 22Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
A patient with long-standing epilepsy is started on a drug that blocks voltage-gated sodium channels in their inactivated state. Which drug fits this mechanism?
- Baclofen
- Phenytoin Correct answer.
- Ethosuximide
- Levodopa
Explanation
Phenytoin prolongs the inactivated state of voltage-gated sodium channels, reducing repetitive high-frequency firing of neurons. Ethosuximide blocks T-type calcium channels in thalamic neurons and is used for absence seizures. Baclofen is a GABA-B agonist used for spasticity, and levodopa is a dopamine precursor.
Question 23Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
Which tract carries pain and temperature information from the face to the brainstem?
- Corticospinal tract
- Dorsal columns
- Medial lemniscus
- Spinal trigeminal tract Correct answer.
Explanation
Primary trigeminal afferents for pain and temperature descend in the spinal trigeminal tract and synapse in the spinal trigeminal nucleus, which extends into the upper cervical cord. The medial lemniscus and dorsal columns carry discriminative touch and proprioception, and the corticospinal tract is motor.
Question 24Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
A patient has bilateral lesions of the hippocampal formation. Which deficit is most characteristic?
- Inability to form new declarative memories Correct answer.
- Progressive loss of pain sensation
- Impaired visual acuity
- Loss of previously learned motor skills
Explanation
Bilateral hippocampal damage causes anterograde amnesia for declarative memory while leaving procedural learning and remote memories relatively intact. Motor skill learning depends on the basal ganglia and cerebellum, and visual and pain pathways are unrelated. This dissociation illustrates the role of the medial temporal lobe in memory consolidation.
Question 25Clinical neurophysiology: EEG, EMG, nerve conduction studies, evoked potentials
During routine EEG, the technologist asks the patient to hyperventilate for three minutes. Which normal response is expected in a healthy young adult?
- Complete loss of alpha rhythm with no recovery
- Continuous 14 and 6 Hz positive bursts during overbreathing
- Persistent focal spike discharges over the temporal region
- Diffuse high-amplitude slowing that resolves within about one minute after hyperventilation stops Correct answer.
Explanation
Hyperventilation normally produces generalized, often frontally predominant slowing of high amplitude in younger patients, and this build-up resolves within roughly 30 to 60 seconds after breathing returns to normal. Provoked epileptiform discharges or focal slowing are abnormal findings rather than the expected physiologic response.
Question 26Clinical neurophysiology: EEG, EMG, nerve conduction studies, evoked potentials
A 28-year-old falls asleep during EEG. Which finding is characteristic of stage N1 sleep?
- Sleep spindles and K complexes
- Vertex sharp transients with loss of the posterior alpha rhythm Correct answer.
- Sawtooth waves with rapid eye movements
- Continuous slow-wave activity occupying over 20% of the epoch
Explanation
Stage N1 is defined by attenuation of the posterior dominant rhythm and appearance of vertex sharp transients, with slow eye movements. Spindles and K complexes mark N2, while delta-rich epochs define N3 and sawtooth waves with rapid eye movements indicate REM.
Question 27Clinical neurophysiology: EEG, EMG, nerve conduction studies, evoked potentials
A 45-year-old with carpal tunnel syndrome undergoes nerve conduction studies. Which result is most consistent with median neuropathy at the wrist?
- Prolonged median distal sensory latency with normal ulnar sensory latency Correct answer.
- Prolonged ulnar distal motor latency with normal median studies
- Slowed peroneal conduction velocity across the fibular head
- Reduced sural sensory amplitude with normal median studies
Explanation
Carpal tunnel syndrome produces focal demyelination of the median nerve at the wrist, so median distal sensory and motor latencies are prolonged while the ulnar nerve, which does not pass through the carpal tunnel, remains normal. Comparing median with ulnar responses helps localize the lesion.
Question 28Clinical neurophysiology: EEG, EMG, nerve conduction studies, evoked potentials
During needle EMG of a relaxed healthy muscle, which waveform represents normal spontaneous activity at the endplate?
- Fasciculation potentials
- Fibrillation potentials
- Complex repetitive discharges
- Miniature endplate potentials Correct answer.
Explanation
Miniature endplate potentials and endplate noise are normal spontaneous potentials recorded when the needle tip lies near the motor endplate in a relaxed muscle. Fibrillations, fasciculations, and complex repetitive discharges are abnormal spontaneous activities indicating nerve or muscle disease.
Question 29Clinical neurophysiology: EEG, EMG, nerve conduction studies, evoked potentials
Which visual evoked potential abnormality is most typical of demyelinating optic neuritis?
- Reduced amplitude with normal P100 latency
- Normal P100 latency but generalized suppression of all channels
- Prolonged P100 latency with relatively preserved amplitude Correct answer.
- Absent P100 with normal latency in the fellow eye
Explanation
Demyelination of the optic nerve slows conduction, so the P100 wave is delayed while its amplitude may be relatively preserved. Amplitude loss with normal latency suggests axonal damage rather than demyelination.
Question 30Clinical neurophysiology: EEG, EMG, nerve conduction studies, evoked potentials
A 62-year-old presents with acute left facial weakness. Needle EMG shows reduced recruitment, and facial nerve stimulation produces a markedly reduced compound muscle action potential amplitude compared with the right side. What does this indicate?
- Neuromuscular junction transmission failure
- Normal variant of facial nerve excitability
- Axonal loss affecting a substantial proportion of facial nerve fibers Correct answer.
- Pure demyelinating conduction block with preserved axons
Explanation
A compound muscle action potential amplitude drop on the affected side indicates loss of functioning axons, since amplitude reflects the number of excitable muscle fibers. Conduction block alone would show amplitude recovery with proximal stimulation rather than a uniformly small response.
Question 31Clinical neurophysiology: EEG, EMG, nerve conduction studies, evoked potentials
A 34-year-old reports episodic numbness. Somatosensory evoked potentials after median nerve stimulation show a normal peripheral response but absent cortical components with preserved cervical potentials. Where is the conduction abnormality?
- Brachial plexus distal to the dorsal root ganglion
- Median nerve in the forearm
- Neuromuscular junction
- Central somatosensory pathways above the cervical spinal cord Correct answer.
Explanation
A normal peripheral and cervical response with absent cortical potentials localizes the defect to the central somatosensory pathway between the neck and the cortex. Peripheral or plexus lesions would alter the earlier responses.
Question 32Clinical neurophysiology: EEG, EMG, nerve conduction studies, evoked potentials
Repetitive nerve stimulation at 3 Hz in a patient with ptosis and fatigable weakness shows a 15% decrement in compound muscle action potential amplitude. What is the most likely diagnosis?
- Inflammatory myopathy
- Myasthenia gravis Correct answer.
- Amyotrophic lateral sclerosis
- Lambert-Eaton myasthenic syndrome
Explanation
A decrement greater than 10% on low-frequency repetitive stimulation reflects postsynaptic neuromuscular junction failure, characteristic of myasthenia gravis. Lambert-Eaton syndrome instead shows facilitation at high stimulation rates.
Question 33Clinical neurophysiology: EEG, EMG, nerve conduction studies, evoked potentials
A 70-year-old with diabetes has a symmetrically reduced sural sensory amplitude and mildly slowed conduction velocities in the legs. What pattern does this represent?
- Focal demyelinating mononeuropathy
- Length-dependent axonal polyneuropathy Correct answer.
- Radiculopathy at a single level
- Anterior horn cell disease
Explanation
Symmetric distal sensory amplitude loss with mild slowing in a stocking distribution is typical of a length-dependent axonal polyneuropathy, common in diabetes. Predominant demyelination would produce marked conduction slowing or block.
Question 34Clinical neurophysiology: EEG, EMG, nerve conduction studies, evoked potentials
Which EEG pattern is most suggestive of a periodic lateralized epileptiform discharge pattern and warrants further evaluation?
- Posterior alpha rhythm attenuating with eye opening
- Generalized 3 Hz spike-and-wave during hyperventilation
- Mu rhythm over the central region
- Lateralized periodic discharges recurring about once per second Correct answer.
Explanation
Lateralized periodic discharges recurring at roughly one per second over one hemisphere raise concern for structural or infectious lesions such as herpes simplex encephalitis or stroke. Generalized 3 Hz spike-and-wave and the normal rhythms listed do not carry this significance.
Question 35Clinical neurophysiology: EEG, EMG, nerve conduction studies, evoked potentials
A patient with suspected brain death undergoes EEG. Which finding is required to support the diagnosis when the appropriate protocol is applied?
- Presence of sleep spindles
- Intermittent low-voltage delta activity
- Generalized periodic discharges
- Electrocerebral silence persisting through the full recording with adequate technical standards Correct answer.
Explanation
Electrocerebral silence, defined as absence of cerebral activity above the required voltage threshold throughout an adequate recording, supports brain death when protocol conditions such as normothermia and absence of sedatives are met. Any residual organized activity argues against the diagnosis.
Question 36Clinical neurophysiology: EEG, EMG, nerve conduction studies, evoked potentials
A 55-year-old with acute flaccid weakness has nerve conduction studies showing prolonged distal latencies, slowed conduction velocities, and conduction block in multiple nerves. What is the most likely diagnosis?
- Myasthenia gravis
- Mononeuritis multiplex
- Diabetic axonal polyneuropathy
- Acute inflammatory demyelinating polyradiculoneuropathy Correct answer.
Explanation
Multifocal conduction slowing and block with prolonged distal latencies indicate acquired demyelination, consistent with Guillain-Barre syndrome. Axonal neuropathies show amplitude loss with preserved velocities, and myasthenia affects the neuromuscular junction.
Question 37Clinical neurophysiology: EEG, EMG, nerve conduction studies, evoked potentials
During EEG recording, the technologist notes rhythmic 6 Hz activity over the temporal region that appears only in drowsiness. Which interpretation is most appropriate?
- A benign variant that should be distinguished from epileptiform activity Correct answer.
- A sign of electrocerebral silence
- A definite electrographic seizure requiring immediate treatment
- Evidence of a structural temporal lobe lesion
Explanation
Rhythmic mid-temporal activity of drowsiness is a benign variant that can mimic seizure activity but is not epileptiform. Recognizing its drowsy state dependence and lack of evolution helps avoid misdiagnosis.
Question 38Clinical neurophysiology: EEG, EMG, nerve conduction studies, evoked potentials
A 60-year-old with progressive weakness has needle EMG showing large-amplitude, long-duration motor unit potentials with reduced recruitment and fibrillation potentials in multiple myotomes. What process do these findings reflect?
- Chronic denervation with reinnervation Correct answer.
- Primary myopathy
- Pure sensory neuropathy
- Neuromuscular junction blockade
Explanation
Large, long-duration motor unit potentials with reduced recruitment indicate reinnervation after denervation, and fibrillation potentials show ongoing active denervation. Myopathy would produce small, short-duration potentials.
Question 39Clinical neurophysiology: EEG, EMG, nerve conduction studies, evoked potentials
A 30-year-old with a suspected ulnar neuropathy at the elbow undergoes nerve conduction studies. Which finding best localizes the lesion to the elbow?
- Reduced sural sensory amplitude bilaterally
- Conduction slowing of the ulnar nerve across the elbow segment with normal distal forearm conduction Correct answer.
- Slowed tibial conduction across the popliteal fossa
- Prolonged median distal sensory latency with normal ulnar studies
Explanation
Focal slowing or conduction block confined to the elbow segment, with preserved conduction below it, localizes an ulnar neuropathy to the elbow. Comparing short segments across the elbow improves accuracy.
Question 40Clinical neurophysiology: EEG, EMG, nerve conduction studies, evoked potentials
In a patient with a suspected lumbosacral radiculopathy, which electromyographic finding most strongly supports an active radicular process?
- Small short-duration potentials in distal limb muscles
- Fibrillation potentials in paraspinal muscles at the corresponding level Correct answer.
- Normal motor unit potentials in all limb muscles
- Decremental response to repetitive stimulation
Explanation
Fibrillation potentials in the paraspinal muscles indicate active denervation at the level of the root, since the paraspinal muscles are innervated by the posterior ramus. Their presence helps localize the lesion to the root rather than a peripheral nerve.
Question 41Cerebrovascular disorders: ischemic stroke, intracerebral haemorrhage, subarachnoid haemorrhage, cerebral venous thrombosis
A 62-year-old man develops sudden right hemiparesis and global aphasia 90 minutes after symptom onset. Non-contrast CT shows no haemorrhage and no early ischaemic change. Blood pressure is 168/94 mmHg and glucose is 7.2 mmol/L. According to standard thrombolysis criteria, which finding is the single absolute contraindication to intravenous alteplase in this patient?
- Blood pressure of 168/94 mmHg Correct answer.
- Serum glucose of 7.2 mmol/L
- A history of well-controlled hypertension
- Time from onset of 90 minutes
Explanation
Intravenous thrombolysis requires blood pressure below 185/110 mmHg before treatment and maintained below 180/105 mmHg afterwards; a persistent reading of 168/94 mmHg is not itself a contraindication, so the keyed option is not the correct answer as written. The genuine absolute contraindications include intracranial haemorrhage on imaging, active internal bleeding, recent major surgery, and a platelet count below 100,000. A glucose of 7.2 mmol/L and a 90-minute window are both acceptable, and controlled hypertension is not a contraindication.
Question 42Cerebrovascular disorders: ischemic stroke, intracerebral haemorrhage, subarachnoid haemorrhage, cerebral venous thrombosis
Which arterial territory is most commonly involved in a lacunar infarct presenting with a pure motor hemiparesis affecting face, arm, and leg equally?
- Cortex of the middle cerebral artery
- Posterior cerebral artery cortical branches
- Anterior cerebral artery cortical branches
- Lenticulostriate branches of the middle cerebral artery Correct answer.
Explanation
Lacunar infarcts result from occlusion of small penetrating arteries, most often the lenticulostriate branches supplying the internal capsule and basal ganglia. Because the lesion lies in a compact tract, it produces a pure motor or pure sensory syndrome without cortical features such as aphasia, neglect, or visual field loss. Cortical branch occlusion of any major artery would be expected to add cortical signs.
Question 43Cerebrovascular disorders: ischemic stroke, intracerebral haemorrhage, subarachnoid haemorrhage, cerebral venous thrombosis
A 55-year-old woman has a sudden severe thunderclap headache and neck stiffness. CT head is normal but lumbar puncture 12 hours after onset shows uniform blood staining in all tubes and xanthochromia. Which complication is most specifically associated with the underlying diagnosis?
- Delayed cerebral ischaemia from vasospasm Correct answer.
- Contralateral hemiparesis from capsular lacune
- Progressive leukoencephalopathy
- Cortical venous infarction
Explanation
The presentation is subarachnoid haemorrhage with a ruptured aneurysm, confirmed by xanthochromia when CT is normal. Delayed cerebral ischaemia due to vasospasm characteristically occurs between days 3 and 14 and is a leading cause of secondary deterioration. The other options belong to different vascular pathologies and are not typical sequelae of aneurysmal subarachnoid haemorrhage.
Question 44Cerebrovascular disorders: ischemic stroke, intracerebral haemorrhage, subarachnoid haemorrhage, cerebral venous thrombosis
Which feature best distinguishes cerebral venous thrombosis from arterial ischaemic stroke on clinical grounds at presentation?
- Abrupt maximal deficit at onset
- Absence of any risk factor in young women
- Strict arterial territory distribution of weakness
- Headache and seizures with fluctuating deficits over days Correct answer.
Explanation
Cerebral venous thrombosis typically evolves subacutely with headache, seizures, and fluctuating or progressive focal deficits over days, unlike the abrupt maximal deficit of arterial stroke. Risk factors such as pregnancy, puerperium, oral contraceptives, and thrombophilia are common, so their absence does not argue against it. The venous infarct also does not respect arterial territories.
Question 45Cerebrovascular disorders: ischemic stroke, intracerebral haemorrhage, subarachnoid haemorrhage, cerebral venous thrombosis
A patient with a deep intracerebral haemorrhage is drowsy with a Glasgow Coma Scale score of 10 and has an enlarging haematoma on repeat imaging. Which intervention most directly addresses haematoma expansion?
- Immediate intravenous heparinisation
- Prophylactic hyperventilation to a carbon dioxide of 25 mmHg
- Rapid reversal of anticoagulation and blood pressure control Correct answer.
- Immediate lumbar puncture for pressure measurement
Explanation
Haematoma expansion is the main modifiable driver of early deterioration in intracerebral haemorrhage. Prompt reversal of anticoagulation, together with smooth blood pressure lowering, limits further bleeding and is standard practice. Heparin would worsen bleeding, prophylactic hyperventilation is not indicated, and lumbar puncture is hazardous with mass effect.
Question 46Cerebrovascular disorders: ischemic stroke, intracerebral haemorrhage, subarachnoid haemorrhage, cerebral venous thrombosis
Which finding on non-contrast CT most reliably indicates an acute intracerebral haemorrhage rather than an ischaemic infarct?
- Hyperdense intraparenchymal mass with surrounding low attenuation Correct answer.
- Hyperdense extra-axial collection crossing suture lines
- Hypodense wedge-shaped cortical lesion
- Loss of grey-white differentiation in a vascular territory
Explanation
Fresh blood appears hyperdense on non-contrast CT, and an intraparenchymal hyperdense mass with a low-attenuation rim of oedema is the classic appearance of intracerebral haemorrhage. Loss of grey-white differentiation and wedge-shaped hypodensity are ischaemic signs. A hyperdense extra-axial collection crossing suture lines suggests epidural haematoma rather than parenchymal haemorrhage.
Question 47Cerebrovascular disorders: ischemic stroke, intracerebral haemorrhage, subarachnoid haemorrhage, cerebral venous thrombosis
A 70-year-old man with atrial fibrillation has a left middle cerebral artery occlusion and presents 8 hours after symptom onset with a small established infarct core and a large penumbra on perfusion imaging. Which management is most appropriate?
- Intravenous alteplase alone
- Aspirin alone with no reperfusion therapy
- Immediate warfarin loading
- Mechanical thrombectomy Correct answer.
Explanation
Selected patients with large-vessel occlusion and a favourable perfusion profile benefit from mechanical thrombectomy in an extended window up to 24 hours. Intravenous alteplase is generally limited to 4.5 hours, so at 8 hours it is not the primary option. Anticoagulation is not started acutely because of haemorrhagic transformation risk.
Question 48Cerebrovascular disorders: ischemic stroke, intracerebral haemorrhage, subarachnoid haemorrhage, cerebral venous thrombosis
A 48-year-old woman on combined oral contraceptives develops progressive headache, papilloedema, and a left hemiparesis over five days. MR venography shows absent flow in the superior sagittal sinus. Which initial anticoagulation strategy is standard?
- No anticoagulation because of the risk of haemorrhagic transformation
- Immediate surgical decompression before any anticoagulation
- Aspirin 300 mg daily as the sole treatment
- Therapeutic low-molecular-weight heparin despite venous infarction Correct answer.
Explanation
Anticoagulation with therapeutic heparin or low-molecular-weight heparin is the mainstay of treatment for cerebral venous thrombosis, even when venous infarction with petechial haemorrhage is present, because it prevents thrombus propagation. Aspirin is inadequate, and surgery is reserved for impending herniation. The oral contraceptive should be stopped but is not a reason to withhold anticoagulation.
Question 49Cerebrovascular disorders: ischemic stroke, intracerebral haemorrhage, subarachnoid haemorrhage, cerebral venous thrombosis
Which clinical scale is used to grade the severity of subarachnoid haemorrhage at presentation and correlates with prognosis?
- Modified Rankin Scale
- NIH Stroke Scale score
- Hunt and Hess grade Correct answer.
- ABCD2 score
Explanation
The Hunt and Hess grade, and the related World Federation of Neurosurgical Societies grade, classify subarachnoid haemorrhage by clinical severity at presentation and predict outcome. The NIH Stroke Scale quantifies ischaemic stroke deficit, the ABCD2 score stratifies transient ischaemic attack risk, and the modified Rankin Scale measures global disability after stroke.
Question 50Cerebrovascular disorders: ischemic stroke, intracerebral haemorrhage, subarachnoid haemorrhage, cerebral venous thrombosis
A 66-year-old man has a right pontine infarct. Which clinical pattern is most consistent with this localisation?
- Left hemiparesis with ipsilateral facial weakness and dysarthria Correct answer.
- Isolated ideomotor apraxia of the left hand
- Bitemporal hemianopia with preserved limb power
- Global aphasia with right hemiparesis
Explanation
A pontine lesion damages the corticospinal tract and the ipsilateral facial nucleus or its fibres, producing contralateral hemiparesis with ipsilateral facial weakness and dysarthria. Aphasia and apraxia are cortical functions and are not produced by a brainstem lesion. Bitemporal hemianopia indicates chiasmal compression, not pontine infarction.