Neurology — MCQs
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A 71-year-old man presents with confusion, falls, and urinary incontinence developing over 4 months. MRI shows ventricular dilatation with periventricular white matter changes. What is the most likely diagnosis?
A 56-year-old man presents with progressive weakness in his hands and forearms over 8 months. He has muscle wasting and fasciculations but no sensory symptoms. Upper motor neuron signs are absent. What is the most likely diagnosis?
A 72-year-old woman presents with sudden onset weakness of her right arm and face, and inability to speak. CT head shows acute infarct in the left middle cerebral artery territory. She presents 6 hours after symptom onset. What is the most appropriate treatment?
A 44-year-old woman presents with sudden onset severe headache, diplopia, and ptosis. CT shows subarachnoid hemorrhage. CT angiogram reveals a posterior communicating artery aneurysm. What cranial nerve is most likely affected?
A 52-year-old man presents with progressive weakness in his hands over 6 months. He has difficulty with fine motor tasks and notices muscle wasting. EMG shows chronic denervation in a C8-T1 distribution. What is the most likely diagnosis?
A 56-year-old man with a history of alcohol excess presents with confusion, ataxia, and nystagmus. He is given IV thiamine and shows rapid improvement. What was the most likely initial diagnosis?
A 38-year-old woman presents with sudden onset severe occipital headache during sexual intercourse. CT head is normal. What is the most appropriate next investigation?
A 72-year-old man presents with progressive memory loss and gait disturbance over 6 months. MRI shows ventricular dilatation with normal cortical sulci. Opening pressure on lumbar puncture is 8 cmH₂O. What is the most likely diagnosis?
A 27-year-old man is brought to the Emergency Department by his girlfriend who witnessed a seizure. She describes that he suddenly stopped talking mid-sentence, turned his head and eyes forcefully to the right, then his right arm started jerking rhythmically for approximately 45 seconds. He did not lose consciousness and was able to describe his symptoms afterwards. He recalls feeling a tingling sensation spreading up his left arm just before the episode. He has no past medical history. Neurological examination is now normal. What is the most likely site of the seizure focus?
A 69-year-old man presents to the Emergency Department with acute onset confusion, right homonymous hemianopia, and inability to recognize familiar faces, including his wife. He cannot describe the features of his own home when asked. There is no limb weakness, sensory loss, or language impairment. CT head performed 3 hours after symptom onset shows a subtle hypodensity in the left occipito-temporal region with no haemorrhage. Which anatomical territory is most likely affected by this stroke?
Neurology UK Medical PG Practice Questions and MCQs
Question 31: A 71-year-old man presents with confusion, falls, and urinary incontinence developing over 4 months. MRI shows ventricular dilatation with periventricular white matter changes. What is the most likely diagnosis?
- A. Alzheimer's disease
- B. Normal pressure hydrocephalus (Correct Answer)
- C. Vascular dementia
- D. Lewy body dementia
- E. Frontotemporal dementia
Explanation: ***Normal pressure hydrocephalus*** - The classic triad of **Normal Pressure Hydrocephalus (NPH)** includes **gait disturbance** (falls), **dementia** (confusion), and **urinary incontinence**, all present in this patient. - The MRI findings of **ventricular dilatation** with **periventricular white matter changes** are characteristic of NPH, indicating CSF accumulation without increased intracranial pressure. *Alzheimer's disease* - Typically presents with **insidious memory loss** as the primary symptom, with gait disturbance and incontinence occurring much later in the disease course. - MRI would classically show **cortical atrophy**, especially of the **hippocampus** and medial temporal lobes, rather than just ventricular dilatation. *Vascular dementia* - Often presents with a **stepwise decline** in cognitive function, reflecting a history of multiple cerebrovascular events, and may include focal neurological deficits. - While periventricular white matter changes can be seen, the specific NPH clinical triad with primarily enlarged ventricles is less characteristic as a primary diagnosis. *Lewy body dementia* - Core features include **fluctuating cognition**, recurrent detailed **visual hallucinations**, and spontaneous **Parkinsonism**. These are not described as prominent features in this case. - Although urinary incontinence can occur, it's typically alongside the other defining features, which are absent here. *Frontotemporal dementia* - Characterized by early and prominent changes in **behavior** (e.g., disinhibition, apathy) or **language function** (aphasia), rather than memory or a triad involving gait and incontinence. - MRI typically shows selective **frontal and temporal lobe atrophy**, not isolated ventricular dilatation with periventricular white matter changes.
Question 32: A 56-year-old man presents with progressive weakness in his hands and forearms over 8 months. He has muscle wasting and fasciculations but no sensory symptoms. Upper motor neuron signs are absent. What is the most likely diagnosis?
- A. Motor neuron disease (Correct Answer)
- B. Cervical myelopathy
- C. Peripheral neuropathy
- D. Myasthenia gravis
- E. Polymyositis
Explanation: ***Motor neuron disease***- The presentation of progressive, pure motor weakness, **muscle wasting**, and **fasciculations** without sensory involvement or **upper motor neuron (UMN) signs** (such as spasticity or hyperreflexia) strongly suggests a Motor Neuron Disease (MND), particularly the Progressive Muscular Atrophy subtype which is purely **lower motor neuron (LMN)**.- MND is characterized by the degeneration of motor neurons in the spinal cord and brainstem, leading to these **LMN signs** and ultimately muscle denervation, atrophy, and weakness.*Cervical myelopathy*- This condition involves spinal cord compression, typically causing a mix of **UMN signs** (e.g., hyperreflexia, spasticity) and **sensory deficits** (numbness, tingling) below the level of compression, which are absent in this case.- While it can cause hand weakness and wasting due to LMN damage at the compression site, the absence of **sensory changes** or widespread UMN signs makes MND a more fitting diagnosis.*Peripheral neuropathy*- Peripheral neuropathies affect peripheral nerves, commonly resulting in a combination of **sensory symptoms** (numbness, paresthesias) and motor weakness, often in a **stocking-glove distribution**.- The pure motor presentation and diffuse **fasciculations** are highly characteristic of an anterior horn cell disorder (MND) rather than a peripheral nerve disorder, which typically involves both motor and sensory fibers.*Myasthenia gravis*- This is a neuromuscular junction disorder characterized by **fluctuating, fatigable weakness** that improves with rest, often affecting ocular, bulbar, or proximal limb muscles first.- Myasthenia gravis does not typically cause **muscle wasting** or **fasciculations**, which are prominent and progressive features in the patient's presentation.*Polymyositis*- This is an inflammatory myopathy that primarily causes **symmetrical proximal muscle weakness** (shoulders and hips), making activities like standing or lifting arms difficult.- Polymyositis affects the muscle fibers themselves, not the anterior horn cells, therefore **fasciculations** are absent, and it does not present with the widespread muscle wasting seen in MND.
Question 33: A 72-year-old woman presents with sudden onset weakness of her right arm and face, and inability to speak. CT head shows acute infarct in the left middle cerebral artery territory. She presents 6 hours after symptom onset. What is the most appropriate treatment?
- A. Aspirin
- B. Alteplase
- C. Mechanical thrombectomy (Correct Answer)
- D. Clopidogrel
- E. Heparin
Explanation: ***Mechanical thrombectomy*** - This procedure is indicated for patients with acute stroke due to **large vessel occlusion (LVO)**, such as the MCA territory infarct seen here. - Current guidelines recommend mechanical thrombectomy up to 6 hours after symptom onset, and even up to **24 hours** in carefully selected patients who meet criteria based on advanced imaging (e.g., demonstrating a small core infarct/large **penumbra**). *Aspirin* - Aspirin is an antiplatelet agent used for acute stroke management when reperfusion therapies (thrombolysis/thrombectomy) are contraindicated, or after successful reperfusion to prevent recurrence. - It is not the definitive acute reperfusion treatment required for a symptomatic **large vessel occlusion** at this presentation time. *Alteplase* - The acceptable time window for intravenous thrombolysis with **Alteplase (rtPA)** is generally restricted to 0 to **4.5 hours** after symptom onset. - Since the patient presented at 6 hours, the standard window for IV thrombolysis has expired, making mechanical thrombectomy the preferred reperfusion option if an LVO is confirmed. *Clopidogrel* - Clopidogrel is an antiplatelet medication primarily utilized for the **secondary prevention** of stroke, often in combination with aspirin (dual antiplatelet therapy) for short periods. - It is not an acute reperfusion therapy and would not address the acute **vessel occlusion** causing the symptoms, unlike thrombectomy. *Heparin* - Systemic anticoagulation (like Heparin) is generally not recommended for the routine management of acute ischemic stroke due to the increased risk of **hemorrhagic transformation**. - Anticoagulants are reserved for specific circumstances, such as treating cerebral venous thrombosis or documented arterial dissection, not acute anterior circulation strokes like this MCA infarct.
Question 34: A 44-year-old woman presents with sudden onset severe headache, diplopia, and ptosis. CT shows subarachnoid hemorrhage. CT angiogram reveals a posterior communicating artery aneurysm. What cranial nerve is most likely affected?
- A. Second (optic)
- B. Third (oculomotor) (Correct Answer)
- C. Fourth (trochlear)
- D. Fifth (trigeminal)
- E. Sixth (abducens)
Explanation: ***Third (oculomotor)*** - The **Oculomotor nerve (CN III)** travels in close proximity to the junction of the internal carotid artery and the **Posterior Communicating Artery (PCoA)**. - An expanding PCoA aneurysm specifically compresses CN III, leading to **ptosis** (paralysis of levator palpebrae superioris), **diplopia** (paralysis of most extraocular muscles), and often a dilated pupil (parasympathetic fiber compression). *Second (optic)* - Lesions of the **Optic nerve (CN II)** primarily result in **visual field defects**, reduced visual acuity, or blindness, but they do not cause diplopia or ptosis. - The nerve's anatomical location is superior and more anterior, making it less susceptible to direct compression by a PCoA aneurysm. *Fourth (trochlear)* - Compression of the **Trochlear nerve (CN IV)** impairs the superior oblique muscle, resulting in vertical and torsional **diplopia**, especially when looking down and in. - Damage to CN IV does not cause ptosis, and it is usually spared in isolated PCoA compression because its course is superior to CN III. *Fifth (trigeminal)* - The **Trigeminal nerve (CN V)** is responsible for sensation of the face and motor function for mastication. - Involvement of CN V causes facial numbness or pain, not deficits in eye movement or eyelid position like ptosis or diplopia. *Sixth (abducens)* - Damage to the **Abducens nerve (CN VI)** paralyzes the lateral rectus muscle, causing isolated horizontal **diplopia** and an inability to abduct the affected eye. - While CN VI can be affected by increased intracranial pressure associated with SAH, it does not cause ptosis, which is a key clinical finding indicating CN III involvement.
Question 35: A 52-year-old man presents with progressive weakness in his hands over 6 months. He has difficulty with fine motor tasks and notices muscle wasting. EMG shows chronic denervation in a C8-T1 distribution. What is the most likely diagnosis?
- A. Carpal tunnel syndrome
- B. Cervical radiculopathy
- C. Motor neuron disease (Correct Answer)
- D. Thoracic outlet syndrome
- E. Ulnar neuropathy
Explanation: ***Motor neuron disease*** - The progressive **hand weakness** over 6 months, difficulty with **fine motor tasks**, and significant **muscle wasting** in the hands are classic features of **Motor Neuron Disease (MND)**, particularly **Amyotrophic Lateral Sclerosis (ALS)**. - EMG showing **chronic denervation** in the C8-T1 distribution strongly indicates degeneration of **anterior horn cells** (lower motor neurons), which are the primary pathology in MND, affecting the muscles supplied by these segments. *Carpal tunnel syndrome* - This condition is caused by **median nerve compression** at the wrist, leading predominantly to **numbness** and **tingling** in the first three and a half digits, with possible **thenar muscle atrophy** in later stages. - The extensive **chronic denervation** across the entire C8-T1 distribution, as shown by EMG, is much broader than the isolated median nerve involvement characteristic of carpal tunnel syndrome. *Cervical radiculopathy* - **Cervical radiculopathy** results from compression of a **cervical nerve root**, typically causing **neck pain** radiating into the arm, **sensory deficits**, and weakness in a specific myotome. - While C8 radiculopathy can affect hand muscles, the purely motor, relentlessly progressive course with prominent widespread **muscle wasting** without significant pain or sensory symptoms is more suggestive of a primary motor neuron disorder. *Thoracic outlet syndrome* - **Neurogenic Thoracic Outlet Syndrome (TOS)** involves compression of the **brachial plexus** (often the lower trunk, C8-T1) leading to hand **muscle wasting** (Gilliatt-Sumner hand) and sensory symptoms. - However, the severe and diffuse **chronic denervation** and the relentless progressive nature of the weakness, without the positional exacerbations or specific sensory patterns often seen in TOS, point away from this diagnosis. *Ulnar neuropathy* - **Ulnar neuropathy** specifically affects muscles supplied by the ulnar nerve, such as the **hypothenar muscles** and **interossei**, leading to characteristic **'claw hand'** deformity and sensory loss in the little finger and half of the ring finger. - The clinical presentation of weakness and the EMG findings indicating denervation in the entire **C8-T1 distribution** are more widespread than would be expected from an isolated ulnar nerve lesion.
Question 36: A 56-year-old man with a history of alcohol excess presents with confusion, ataxia, and nystagmus. He is given IV thiamine and shows rapid improvement. What was the most likely initial diagnosis?
- A. Alcohol withdrawal
- B. Wernicke's encephalopathy (Correct Answer)
- C. Korsakoff's psychosis
- D. Hepatic encephalopathy
- E. Cerebellar stroke
Explanation: ***Wernicke's encephalopathy*** - This diagnosis is strongly supported by the classic triad of symptoms: **confusion** (encephalopathy), **ataxia**, and **nystagmus** (or other ophthalmoplegia) in a patient with chronic **alcohol excess**.- The rapid improvement following the administration of IV **thiamine** is characteristic, as Wernicke's encephalopathy is caused by acute deficiency of thiamine (Vitamin B1).*Alcohol withdrawal*- Primary symptoms include autonomic hyperactivity such as **tachycardia**, **tremors**, hypertension, and potential hallucinations or seizures (delirium tremens).- While confusion may occur in severe alcohol withdrawal, the specific triad of nystagmus and ataxia strongly points toward Wernicke's, and **benzodiazepines**, not thiamine, are the primary agents for acute withdrawal.*Korsakoff's psychosis*- This condition is the chronic form following Wernicke's encephalopathy, characterized mainly by **severe anterograde and retrograde amnesia** and **confabulation**.- It typically does not involve the acute ocular symptoms or global confusion seen in the initial presentation.*Hepatic encephalopathy*- This condition results from advanced liver failure (common in alcoholics) and leads to altered mental status, often accompanied by **asterixis** (flapping tremor).- Although confusion is present, the specific combination of ataxia and nystagmus is less characteristic of hepatic encephalopathy, and treatment involves lowering **ammonia** levels, not IV thiamine.*Cerebellar stroke*- A stroke would present with the **sudden onset** of neurological deficits, including ataxia and potentially nystagmus, often accompanied by severe headache or vertigo.- Crucially, stroke symptoms are structural and irreversible in the short term, meaning they would not resolve rapidly with a nutritional supplement like **IV thiamine**.
Question 37: A 38-year-old woman presents with sudden onset severe occipital headache during sexual intercourse. CT head is normal. What is the most appropriate next investigation?
- A. MRI brain
- B. Lumbar puncture (Correct Answer)
- C. CT angiogram
- D. Carotid Doppler
- E. EEG
Explanation: ***Lumbar puncture*** - This clinical presentation (sudden, severe headache during exertion—**thunderclap headache**) is characteristic of **subarachnoid hemorrhage (SAH)**, mandating investigation even if the initial non-contrast CT head is normal. - **Lumbar puncture** is necessary to look for **xanthochromia** (pigments from hemoglobin breakdown), which effectively confirms SAH, especially when the CT scan is negative or performed >6 hours after symptom onset. *MRI brain* - While useful for detecting non-hemorrhagic causes of thunderclap headache (e.g., **reversible cerebral vasoconstriction syndrome (RCVS)**), **MRI is inferior to LP** for detecting small amounts of acute SAH. - The primary immediate goal is ruling out the highly lethal diagnosis, **subarachnoid hemorrhage**, for which LP is the necessary confirmatory step following a negative CT. *CT angiogram* - **CT angiogram** is used to identify the underlying vascular lesion, such as a **saccular aneurysm**, *after* the diagnosis of SAH has been confirmed by either CT or LP. - It is not the appropriate *initial* confirmatory test for the presence of blood in the subarachnoid space itself. *Carotid Doppler* - This investigation is primarily used to evaluate for **carotid artery stenosis** or fibromuscular dysplasia, which are not typical causes of isolated thunderclap headache. - It assesses blood flow in the extracranial neck vessels and does not play a role in the urgent ruling out of an acute intracerebral bleed like **SAH**. *EEG* - **EEG** (Electroencephalogram) is utilized primarily for the diagnosis of **seizure disorders**, seizure monitoring, or assessing encephalopathies. - It has no utility in the urgent initial evaluation or diagnosis of a patient presenting with an acute **thunderclap headache**.
Question 38: A 72-year-old man presents with progressive memory loss and gait disturbance over 6 months. MRI shows ventricular dilatation with normal cortical sulci. Opening pressure on lumbar puncture is 8 cmH₂O. What is the most likely diagnosis?
- A. Alzheimer's disease
- B. Normal pressure hydrocephalus (Correct Answer)
- C. Vascular dementia
- D. Parkinson's disease
- E. Progressive supranuclear palsy
Explanation: ***Normal pressure hydrocephalus***- The patient's presentation of progressive **memory loss** (dementia) and **gait disturbance**, combined with MRI showing **ventricular dilatation with normal cortical sulci** and a **normal CSF opening pressure** (8 cmH₂O), is the classic diagnostic triad and findings for **Normal Pressure Hydrocephalus (NPH)**.- NPH is a potentially **reversible cause of dementia**, and the imaging finding of prominent ventricles with preserved cortical sulci, often described as "tight high convexity," is crucial for diagnosis.*Alzheimer's disease*- While Alzheimer's disease causes progressive **memory loss**, MRI typically demonstrates significant **cortical atrophy**, particularly of the medial temporal lobes and hippocampus, which is contrary to the normal cortical sulci observed here.- Gait disturbance usually appears much later in the disease, and the CSF findings are not consistent with the primary pathology of **amyloid plaques** and neurofibrillary tangles.*Vascular dementia*- This diagnosis requires evidence of significant **cerebrovascular disease** such as multiple infarcts or extensive white matter lesions on MRI, which are not described in this case.- The cognitive decline in vascular dementia is often characterized by a **stepwise pattern** of deterioration rather than the gradual progression seen here.*Parkinson's disease*- Parkinson's disease is primarily a **movement disorder** characterized by **bradykinesia**, **resting tremor**, and rigidity, not initially by progressive memory loss and hydrocephalus.- Although dementia can occur, it is typically later in the disease course (Parkinson's Disease Dementia), and the MRI findings of ventricular dilatation with normal sulci are not typical for Parkinson's.*Progressive supranuclear palsy*- This atypical parkinsonism is characterized by prominent **vertical gaze palsy** (supranuclear ophthalmoplegia), axial rigidity, and early falls, symptoms not reported in this patient.- While some atrophy may be seen, the specific imaging pattern of **ventricular enlargement with normal cortical sulci** and normal CSF pressure is not characteristic of PSP.
Question 39: A 27-year-old man is brought to the Emergency Department by his girlfriend who witnessed a seizure. She describes that he suddenly stopped talking mid-sentence, turned his head and eyes forcefully to the right, then his right arm started jerking rhythmically for approximately 45 seconds. He did not lose consciousness and was able to describe his symptoms afterwards. He recalls feeling a tingling sensation spreading up his left arm just before the episode. He has no past medical history. Neurological examination is now normal. What is the most likely site of the seizure focus?
- A. Right frontal lobe
- B. Left frontal lobe (Correct Answer)
- C. Right temporal lobe
- D. Left parietal lobe
- E. Left occipital lobe
Explanation: ***Left frontal lobe*** - The forced head and eye deviation to the **right** (versive movement) is caused by activation of the **frontal eye fields** in the contralateral (**left**) hemisphere. - Rhythmic jerking of the right arm indicate seizure activity in the **primary motor cortex** located in the **left frontal lobe**, with preserved consciousness defining it as a **focal aware seizure**. *Right frontal lobe* - Seizures in this region would cause **left-sided** motor manifestations and head deviation to the **left**, which contradicts the patient's right-arm jerking. - Motor and versive symptoms in epilepsy typically localize to the **contralateral** side of the brain focus. *Right temporal lobe* - Seizures here usually involve **impaired awareness**, **automatisms** (like lip-smacking), and **epigastric auras**, none of which were described. - Motor features in temporal lobe epilepsy are usually **dystonic posturing** rather than rhythmic clonic jerking or forced eye deviation. *Left parietal lobe* - While the sensory aura (tingling) suggests **somatosensory cortex** involvement, the prominent **versive eye movements** and rhythmic motor jerking are more specific to frontal lobe activation. - Parietal lobe seizures typically present with **paresthesias** or distorted body image rather than primary motor rhythmic jerking and eye deviation. *Left occipital lobe* - Seizures in this focus primarily manifest as **visual phenomena**, such as flashing lights, colors, or temporary **scotomas**. - Although they can spread to the frontal lobe, the lack of visual symptoms at the onset makes a **primary occipital focus** highly unlikely.
Question 40: A 69-year-old man presents to the Emergency Department with acute onset confusion, right homonymous hemianopia, and inability to recognize familiar faces, including his wife. He cannot describe the features of his own home when asked. There is no limb weakness, sensory loss, or language impairment. CT head performed 3 hours after symptom onset shows a subtle hypodensity in the left occipito-temporal region with no haemorrhage. Which anatomical territory is most likely affected by this stroke?
- A. Left anterior cerebral artery
- B. Left middle cerebral artery
- C. Left posterior cerebral artery (Correct Answer)
- D. Basilar artery
- E. Left anterior choroidal artery
Explanation: ***Left posterior cerebral artery*** - The **posterior cerebral artery (PCA)** supplies the **occipital lobe** and **inferior temporal lobe**; damage here explains the **right homonymous hemianopia** and **prosopagnosia** (inability to recognise faces via the fusiform gyrus). - The patient exhibits **topographical disorientation** and preserved motor/language functions, which are classic signs of a **PCA territory** infarct sparing the motor cortex and Broca's/Wernicke's areas. *Left anterior cerebral artery* - Infarction in the **ACA** territory typically presents with contralateral **lower limb weakness** and sensory loss due to involvement of the medial homunculus. - It may also cause personality changes or **urinary incontinence**, none of which are present in this clinical scenario. *Left middle cerebral artery* - **MCA** strokes usually present with contralateral **hemiparesis** (face and arm worse than leg) and **aphasia** if the dominant hemisphere is involved. - This patient has no **limb weakness** or **language impairment**, making an MCA territory infarct highly unlikely. *Basilar artery* - **Basilar artery** occlusion often leads to severe **brainstem dysfunction**, including cranial nerve palsies, quadriplegia, or decreased levels of consciousness (“locked-in syndrome”). - While it can lead to bilateral PCA symptoms, a focal left-sided hypodensity and lack of brainstem signs point away from a mainstem basilar event. *Left anterior choroidal artery* - Occlusion of this artery typically results in a triad of hemiparesis, hemisensory loss, and **homonymous hemianopia** due to its supply to the **internal capsule** and optic tract. - The absence of **motor and sensory deficits** in this patient excludes the involvement of the internal capsule and thalamic structures supplied by this vessel.
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