Neurology Question Bank

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1. A 63-year-old man develops dense left hemiparesis involving face, arm and leg, left hemisensory loss and a left homonymous hemianopia. Language, attention and cognition are normal and there is no neglect. MRI shows an infarct in the posterior limb of the right internal capsule extending to the optic tract region. Occlusion of which artery is most likely?

The anterior choroidal artery arises from the supraclinoid internal carotid artery and supplies the posterior limb of the internal capsule, optic tract, lateral geniculate body, medial temporal structures and part of the thalamus. Occlusion produces the triad of contralateral hemiparesis, hemisensory loss and homonymous hemianopia, typically without cortical signs. Superior division MCA occlusion produces face and arm weakness with cortical features such as neglect in the non-dominant hemisphere. PCA occlusion causes hemianopia and sensory loss but rarely dense hemiparesis. Medial lenticulostriate branches arise from the ACA and supply the anterior basal ganglia and anterior limb. Pearl: the full triad is uncommon; partial syndromes predominate.

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2. A 28-year-old woman at 22 weeks gestation with multiple sclerosis develops a disabling relapse over 4 days with left leg weakness preventing walking and urinary retention. Infection has been excluded. What is the most appropriate treatment?

Disabling relapses in pregnancy are treated with intravenous methylprednisolone, typically 1 g daily for 3 to 5 days. Methylprednisolone is extensively metabolised by placental 11-beta-hydroxysteroid dehydrogenase type 2, so fetal exposure is low; it is preferred over dexamethasone and betamethasone, which cross the placenta readily. Exposure is best avoided in the first trimester where possible. Plasma exchange is reserved for steroid-refractory severe relapses. Intravenous immunoglobulin has weak evidence for acute relapse treatment. Alemtuzumab is an induction disease-modifying therapy that is contraindicated in pregnancy and has no role in acute relapse management.

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3. A 64-year-old man with known prostate carcinoma reports 3 weeks of thoracic back pain that wakes him at night, and 2 days of leg heaviness with hesitancy of micturition. Power is 4/5 in both legs with a sensory level at T8 and extensor plantars. What is the most appropriate immediate investigation?

Suspected metastatic spinal cord compression requires whole-spine MRI within 24 hours (NICE), because up to a third of patients have multiple levels of epidural disease, and a limited study can miss a second compressive lesion that would change the radiotherapy or surgical field. Imaging only the clinically suspected level therefore risks undertreatment. Plain radiographs are insensitive, missing compression in around 20% of cases, and cannot show epidural soft tissue. Bone scintigraphy detects osseous metastases but does not demonstrate the epidural component or the degree of cord compression. Pearl: start dexamethasone while awaiting the scan.

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4. According to Brain Trauma Foundation guidance for severe traumatic brain injury, what is the recommended cerebral perfusion pressure target for survival and favourable outcome?

Brain Trauma Foundation guidelines recommend a cerebral perfusion pressure of 60-70 mmHg, calculated as mean arterial pressure minus intracranial pressure. Values below 50-60 mmHg risk ischaemia, while aggressively driving perfusion pressure above 70 mmHg with fluids and vasopressors increases the risk of acute respiratory distress syndrome without improving neurological outcome. A target of 40-50 mmHg is clearly ischaemic. Targets of 80-90 mmHg or above 100 mmHg reflect the abandoned Rosner hyperaemic approach. Pearl: the arterial line transducer must be zeroed at the tragus, not the right atrium, for accurate cerebral perfusion pressure.

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5. A 34-year-old woman has 2 months of a fine, fast tremor of both hands, with palpitations, heat intolerance and 5 kg weight loss. She drinks two cups of coffee daily and takes no medications. Examination shows a symmetrical low-amplitude postural tremor of about 10 Hz, brisk reflexes and a resting pulse of 108/min, with no other neurological signs. Which investigation is most appropriate next?

Enhanced physiological tremor is a symmetrical, low-amplitude, high-frequency (about 8–12 Hz) postural tremor caused by increased beta-adrenergic drive or other reversible factors. Causes include thyrotoxicosis, anxiety, caffeine, hypoglycaemia, phaeochromocytoma, alcohol or benzodiazepine withdrawal, and drugs such as salbutamol, lithium, valproate, SSRIs and amiodarone. Her weight loss, heat intolerance and tachycardia point strongly to hyperthyroidism, so thyroid function tests are the priority; treating the cause abolishes the tremor. Dopamine transporter SPECT is for suspected degenerative parkinsonism. Brain MRI is not indicated without focal signs. Ceruloplasmin is appropriate for young patients with atypical tremor, dystonia or liver disease. Pearl: thyroid function should be checked in every new tremor.

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6. What is the mechanism of action of efgartigimod in generalised myasthenia gravis?

The neonatal Fc receptor (FcRn) normally rescues IgG from lysosomal degradation and recycles it back into the circulation, giving IgG its long half-life. Efgartigimod is an engineered IgG1 Fc fragment that binds FcRn with high affinity. This diverts IgG, including pathogenic AChR antibodies, to lysosomal breakdown and lowers total IgG by about 60–70% within weeks. Other IgG classes and antibody production are unaffected. In the ADAPT trial it produced rapid, clinically meaningful improvement in AChR-positive generalised MG, given as treatment cycles. Other FcRn antagonists include rozanolixizumab and nipocalimab. C5 inhibition describes eculizumab. CD20 depletion describes rituximab. IL-6 receptor blockade describes tocilizumab and satralizumab.

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7. A 49-year-old man develops acute vertigo, vomiting, hoarseness and dysphagia two days after neck manipulation. There is right ptosis and miosis, loss of pain and temperature sensation over the right face and over the left arm, trunk and leg, right limb ataxia and a reduced right gag reflex. Limb strength and tongue movements are normal. Where is the lesion most likely located?

This is lateral medullary (Wallenberg) syndrome, here probably from right vertebral artery dissection. Structures involved are the spinal trigeminal nucleus and tract (ipsilateral facial pain and temperature loss), lateral spinothalamic tract (contralateral body), nucleus ambiguus (ipsilateral palatal and vocal cord weakness), descending sympathetic fibres (ipsilateral Horner syndrome), inferior cerebellar peduncle (ipsilateral ataxia) and vestibular nuclei (vertigo, nystagmus). The pyramids and hypoglossal nuclei lie medially and are spared, so there is no weakness. Medial medullary lesions cause tongue weakness and contralateral hemiparesis. Lateral pontine (AICA) lesions add facial palsy and deafness. Vertebral artery occlusion is a more frequent cause than isolated PICA occlusion.

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8. A 55-year-old man survived an out-of-hospital cardiac arrest 6 weeks ago after 15 minutes of resuscitation. He is now alert and cognitively intact but has sudden shock-like jerks of his arms and legs whenever he reaches for objects, speaks or tries to walk, causing frequent falls. The jerks are absent at rest, and EEG shows no ongoing seizures. Which drug is most appropriate?

Chronic post-hypoxic myoclonus (Lance-Adams syndrome) develops days to weeks after hypoxic brain injury in patients who regain consciousness. It is a cortical action and intention myoclonus that is stimulus-sensitive and disabling, often with negative myoclonus causing falls. It differs from acute post-anoxic myoclonic status in comatose patients, which carries a poor prognosis. Treatment uses drugs effective in cortical myoclonus, such as levetiracetam, piracetam, valproate and clonazepam, often in combination. Sodium channel blockers such as carbamazepine and phenytoin can worsen myoclonus. Haloperidol has no role. Pearl: the prognosis of Lance-Adams syndrome is relatively favourable, and many patients improve over months with rehabilitation.

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9. A 58-year-old woman is brought in with 2 days of fever, headache, odd behaviour and word-finding difficulty, followed by a focal seizure with impaired awareness. Temperature is 38.7 °C, GCS 13 and there is no papilloedema. CT head is normal; MRI is scheduled for tomorrow. What is the most appropriate immediate management?

Fever, behavioural change, aphasia and seizures suggest HSV-1 encephalitis, which has about 70% mortality untreated and roughly 10–20% with treatment, with worse outcomes when treatment is delayed beyond 48 hours. UK (ABN/BIA) and IDSA guidelines recommend IV aciclovir 10 mg/kg every 8 hours, adjusted for renal function, within 6 hours of suspecting encephalitis, without waiting for MRI or PCR results. Lumbar puncture should be performed as soon as it is safe, and the course is typically 14–21 days. Oral valaciclovir does not reliably achieve adequate CSF concentrations for acute encephalitis. Withholding treatment pending imaging or PCR risks irreversible temporal lobe necrosis.

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10. For drug-susceptible tuberculous meningitis in adults, what total duration of antituberculous therapy is recommended by major guidelines?

Standard therapy for drug-susceptible CNS tuberculosis is an intensive phase of isoniazid, rifampicin, pyrazinamide and ethambutol for 2 months, followed by a continuation phase of isoniazid and rifampicin. ATS/CDC/IDSA (2016) recommend a total of 9–12 months, and WHO recommends 12 months (2HRZE/10HR) for adults, because of uncertain CSF penetration of some drugs (ethambutol and, once meninges heal, rifampicin) and the catastrophic consequences of relapse. The 6-month regimen applies to pulmonary tuberculosis, and 4-month rifapentine–moxifloxacin regimens are not recommended for meningitis. Pyridoxine should accompany isoniazid to prevent neuropathy. A shorter intensified regimen is an option only in children.