Neurology — MCQs

Neurology UK Medical PG Practice Questions and MCQs

Question 21: A 45-year-old man presents with progressive weakness in his hands, difficulty with fine motor tasks, and muscle twitching. On examination, he has muscle wasting in his hands with fasciculations and hyperreflexia. What is the most likely diagnosis?

A. Carpal tunnel syndrome
B. Cervical myelopathy
C. Motor neuron disease (Correct Answer)
D. Peripheral neuropathy
E. Myasthenia gravis

Explanation: ***Motor neuron disease*** - The combination of **progressive weakness**, **muscle wasting** and **fasciculations** (Lower Motor Neuron signs) with **hyperreflexia** (Upper Motor Neuron signs) is the hallmark presentation of **Motor Neuron Disease (MND)**, most commonly **Amyotrophic Lateral Sclerosis (ALS)**. - This condition involves the degeneration of both upper and lower motor neurons, accounting for the mixed neurological findings observed in the patient. *Carpal tunnel syndrome* - **Carpal tunnel syndrome** is a focal compression neuropathy of the **median nerve**, typically causing **numbness**, tingling, and weakness primarily in the thumb, index, and middle fingers. - It is characterized by isolated **thenar atrophy** and does not present with widespread **fasciculations** or **hyperreflexia**, which indicate a more extensive neurological process. *Cervical myelopathy* - **Cervical myelopathy** results from **spinal cord compression**, typically leading to **Upper Motor Neuron (UMN)** signs (like **hyperreflexia** and spasticity) below the lesion, often accompanied by sensory changes and gait disturbance. - While it can present with some mixed features, the prominent and diffuse **fasciculations** indicative of widespread Lower Motor Neuron involvement are less characteristic than in MND. *Peripheral neuropathy* - **Peripheral neuropathies** primarily affect peripheral nerves, leading to **Lower Motor Neuron (LMN)** signs such as weakness and wasting, but they characteristically cause **hyporeflexia** or **areflexia**. - The presence of **hyperreflexia** in this patient is a crucial finding that effectively rules out a pure peripheral nerve disorder. *Myasthenia gravis* - **Myasthenia gravis** is an autoimmune disorder of the **neuromuscular junction** causing fluctuating muscle weakness that **worsens with activity** and improves with rest, often affecting ocular and bulbar muscles. - It does not cause muscle **wasting** or **fasciculations**, and reflexes typically remain normal, making it inconsistent with the patient's presentation.

Question 22: A 55-year-old man presents with sudden onset diplopia and ptosis affecting his left eye. On examination, his left pupil is dilated and non-reactive to light. Eye movements show limitation in all directions. What is the most likely diagnosis?

A. Myasthenia gravis
B. Third cranial nerve palsy (Correct Answer)
C. Horner's syndrome
D. Fourth cranial nerve palsy
E. Sixth cranial nerve palsy

Explanation: ***Third cranial nerve palsy***- The constellation of **ptosis**, a **dilated and non-reactive pupil**, and **limitation in eye movements** in multiple directions affecting one eye is the hallmark of an **oculomotor nerve (CN III) palsy**.- The involvement of the pupil suggests a **compressive lesion**, such as an **aneurysm** (e.g., posterior communicating artery), which compromises the superficial parasympathetic fibers of CN III.*Myasthenia gravis*- While **ptosis** and **diplopia** are common in myasthenia gravis, the ophthalmoplegia typically **fluctuates** throughout the day and **spares the pupils**.- The **dilated and non-reactive pupil** in this case is a critical differentiating feature that rules out myasthenia gravis.*Horner's syndrome*- Horner's syndrome results from sympathetic pathway disruption, characterized by a triad of mild **ptosis**, **miosis** (constricted pupil), and facial **anhydrosis**.- The patient's **dilated pupil** directly contradicts the **miosis** seen in Horner's syndrome.*Fourth cranial nerve palsy*- A **fourth cranial nerve (trochlear nerve) palsy** affects the **superior oblique muscle**, leading to **vertical diplopia** and difficulty looking down and in.- It does not cause **ptosis**, widespread **extraocular muscle limitation**, or **pupillary abnormalities**, which are prominent in this patient's presentation.*Sixth cranial nerve palsy*- A **sixth cranial nerve (abducens nerve) palsy** affects the **lateral rectus muscle**, causing **horizontal diplopia** due to impaired abduction (outward gaze) of the affected eye.- This condition does not typically cause **ptosis**, a **dilated pupil**, or generalized limitation of eye movements as described.

Question 23: A 65-year-old woman presents with gradual onset hearing loss and tinnitus in her left ear over 6 months. Weber test lateralizes to the right ear. Rinne test is positive bilaterally. What type of hearing loss is this?

A. Conductive hearing loss
B. Sensorineural hearing loss (Correct Answer)
C. Mixed hearing loss
D. Functional hearing loss
E. Normal hearing

Explanation: ***Sensorineural hearing loss*** - The **Weber test** lateralizes to the **unaffected ear** (right ear), which is characteristic of unilateral sensorineural hearing loss because the better cochlea perceives the sound more clearly. - The **Rinne test is positive** (Air Conduction > Bone Conduction) bilaterally, indicating that sound transmission through the outer and middle ear is intact, consistent with a problem in the inner ear or auditory nerve. *Conductive hearing loss* - If this were **conductive hearing loss** in the left ear, the **Weber test** would lateralize to the **affected ear** (left ear) due to the occlusion effect. - Conductive hearing loss in the affected ear would result in a **negative Rinne test** (Bone Conduction > Air Conduction) in that ear, which contradicts the bilateral positive Rinne results. *Mixed hearing loss* - **Mixed hearing loss** involves both conductive and sensorineural components. While a positive Rinne test can occur, the clear lateralization of Weber to the *unaffected* ear strongly points to pure sensorineural loss. - In mixed hearing loss, the conductive component would typically alter the Weber test's lateralization pattern to some extent, or at least suggest a more complex picture than purely SNHL. *Functional hearing loss* - **Functional hearing loss** is a non-organic hearing impairment. The tuning fork test results (Weber lateralizing away from the symptomatic ear and positive Rinne bilaterally) are consistent and indicative of an **organic pathology**. - There are no indications in the clinical scenario (such as inconsistent test results or disproportionate speech understanding) to suggest a non-organic cause. *Normal hearing* - This option is incorrect because the patient presents with **gradual onset hearing loss and tinnitus** in the left ear, which are symptoms of hearing impairment. - While a positive Rinne test is consistent with normal hearing, the **Weber test would not lateralize** to either side if hearing were normal and symmetrical.

Question 24: A 42-year-old man presents with progressive weakness in his arms and legs over 18 months. He has muscle fasciculations, hyperreflexia, and bulbar symptoms including dysarthria. EMG shows widespread denervation. What is the most likely diagnosis?

A. Multiple sclerosis
B. Myasthenia gravis
C. Motor neuron disease (Correct Answer)
D. Guillain-Barré syndrome
E. Cervical myelopathy

Explanation: ***Motor neuron disease*** - This diagnosis is strongly indicated by the presence of both **Upper Motor Neuron (UMN)** signs (hyperreflexia) and **Lower Motor Neuron (LMN)** signs (fasciculations, widespread denervation on EMG). - The 18-month progressive weakness involving the limbs and the presence of **bulbar symptoms** like dysarthria are hallmark features of **Amyotrophic Lateral Sclerosis (ALS)**, the most common form of MND. *Multiple sclerosis* - MS is characterized by **demyelinating lesions** in the central nervous system, causing symptoms that are disseminated in time and space, and typically involves sensory, visual, or cerebellar deficits, not purely motor system degeneration. - It does not typically present with **fasciculations** or widespread **LMN signs** of denervation on EMG, and while UMN signs can be present, the combination seen here is atypical. *Myasthenia gravis* - This condition causes **fluctuating muscle weakness** that worsens with activity and improves with rest, often affecting ocular, bulbar, and limb muscles, but it does not cause **hyperreflexia** (UMN signs) or **fasciculations** (LMN signs). - The pathophysiology involves impaired **neuromuscular transmission**, not a primary motor neuron pathology leading to widespread denervation as evidenced by the EMG. *Guillain-Barré syndrome* - GBS is characterized by an **acute, rapidly progressive ascending paralysis** that evolves over days to a few weeks, which is inconsistent with the 18-month chronic progression described. - It is exclusively a **lower motor neuron disease**, presenting with **areflexia** and flaccid weakness, and specifically lacks any **hyperreflexia** (UMN signs). *Cervical myelopathy* - While cervical myelopathy can cause a combination of UMN signs (below the lesion) and LMN signs (at the level of compression), it typically leads to more localized weakness and sensory changes. - It does not usually result in generalized **widespread denervation** throughout the body and significant **bulbar involvement** (dysarthria) as a primary feature, which strongly points towards a diffuse motor neuron disorder.

Question 25: A 62-year-old man presents with progressive memory loss, confusion, and behavioral changes over 6 months. MRI shows generalized atrophy. CSF shows elevated tau protein and decreased amyloid-β42. What is the most likely diagnosis?

A. Vascular dementia
B. Alzheimer's disease (Correct Answer)
C. Frontotemporal dementia
D. Lewy body dementia
E. Normal pressure hydrocephalus

Explanation: ***Alzheimer's disease*** - The clinical presentation of progressive **memory loss**, confusion, and behavioral changes over 6 months, combined with generalized atrophy on MRI, is highly suggestive of **Alzheimer's disease (AD)**. - The characteristic cerebrospinal fluid (CSF) findings—**elevated tau protein** (reflecting neuronal degeneration) and **decreased amyloid-β42** (reflecting amyloid plaque deposition)—are key biomarkers for AD. *Vascular dementia* - This diagnosis typically presents with a **stepwise cognitive decline** and often focal neurological deficits following cerebrovascular events, rather than a gradual progression focused on memory loss. - Neuroimaging usually reveals specific **infarcts** or extensive white matter lesions, not just generalized atrophy, and CSF biomarkers are not typically elevated tau and decreased amyloid-β42. *Frontotemporal dementia* - Often characterized by prominent early **behavioral disturbances** (e.g., disinhibition, apathy) or **language difficulties** (aphasia), with memory often relatively preserved initially. - CSF biomarkers for tau and amyloid-β42 are generally **normal** or less specific in frontotemporal dementia compared to AD. *Lewy body dementia* - Key distinguishing features include recurrent, well-formed **visual hallucinations**, spontaneous **Parkinsonism**, and significant fluctuations in attention and cognition. - While amyloid-β42 can be reduced, the presence of **elevated tau protein** in CSF, combined with the absence of the core clinical features, makes AD more likely. *Normal pressure hydrocephalus* - Characterized by the classic triad of **gait disturbance** (often magnetic gait), **urinary incontinence**, and **dementia**, with gait disturbance usually being a prominent early feature. - MRI typically shows **ventriculomegaly** disproportionate to sulcal atrophy, and CSF analysis does not show the characteristic biomarker pattern of elevated tau and decreased amyloid-β42.

Question 26: A 29-year-old woman presents with sudden onset severe headache during sexual intercourse. She has no focal neurological signs but is photophobic. CT head shows subarachnoid hemorrhage. What is the most appropriate immediate management?

A. Surgical clipping
B. Endovascular coiling
C. Conservative management
D. Lumbar puncture
E. Nimodipine and aneurysm securement (Correct Answer)

Explanation: ***Nimodipine and aneurysm securement***- This option includes the two critical immediate interventions for confirmed SAH: securing the source (clipping or coiling) to prevent re-bleeding, and starting **Nimodipine** to prevent vasospasm.- **Nimodipine**, a calcium channel blocker, is initiated immediately (up to 96 hours) upon diagnosis to prevent delayed cerebral ischemia due to **vasospasm**, which is the leading cause of morbidity after SAH.*Surgical clipping*- Clipping is one method for definitive securement of the aneurysm but does not include mention of the vital need for concurrent and immediate **vasospasm** prophylaxis using **Nimodipine**.- **Surgical clipping** is typically chosen for aneurysms with wide necks or specific anatomic locations less suitable for coiling.*Endovascular coiling*- **Coiling** is often the less invasive, preferred method chosen for definitive aneurysm securement but fails to encompass the essential role of concurrent Nimodipine in the comprehensive immediate management plan.- Immediate securement is necessary to mitigate the high risk of **re-bleeding** (especially within the first 24 hours), which is associated with high mortality.*Conservative management*- This is inappropriate management for SAH confirmed on CT, as the high risk of **re-bleeding** and **vasospasm** necessitates urgent intervention.- Immediate aggressive care, including securing the source and medical management like blood pressure control and **Nimodipine**, is mandated.*Lumbar puncture*- **Lumbar puncture (LP)** is a diagnostic tool used only when SAH is suspected clinically (thunderclap headache) but the initial non-contrast CT scan is negative or indeterminate.- Since the CT scan *confirmed* SAH in this patient, LP is unnecessary and may delay the initiation of crucial life-saving interventions and aneurysm securement.

Question 27: A 57-year-old man presents with progressive memory loss and language difficulties over 10 months. MRI shows asymmetric frontotemporal atrophy. CSF shows elevated tau but normal amyloid-β42. What is the most likely diagnosis?

A. Alzheimer's disease
B. Frontotemporal dementia (Correct Answer)
C. Lewy body dementia
D. Vascular dementia
E. Creutzfeldt-Jakob disease

Explanation: ***Frontotemporal dementia*** - The combination of **progressive language difficulties** (suggesting a primary progressive aphasia variant of FTD) and **asymmetric frontotemporal atrophy** on MRI is highly indicative of this diagnosis, aligning with the patient's 10-month progression of symptoms. - The CSF finding of **normal amyloid-β42** is crucial, as it argues against typical Alzheimer's disease, leaving FTD as the most likely diagnosis given the neuroanatomical localization and clinical picture. *Alzheimer's disease* - Typical AD initially presents with prominent **episodic memory loss** and MRI usually demonstrates primary atrophy in the **medial temporal lobes** (hippocampi), not the frontotemporal regions. - The classic CSF profile for AD requires **lowered amyloid-β42** (reflecting deposition into plaques) alongside elevated total tau, which is inconsistent with the normal amyloid-β42 level seen here. *Lewy body dementia* - This condition is characterized by core features including early and persistent **visual hallucinations**, **fluctuating cognition** (attention), and features of parkinsonism, which are not described in the patient. - While cognitive decline is present, the specific pattern of **language difficulties** and focal **frontotemporal atrophy** points away from Lewy body dementia. *Vascular dementia* - Vascular dementia typically presents with a **stepwise decline** in cognitive function, often related to multiple strokes or lacunar infarcts, and usually has a history of cerebrovascular risk factors. - The MRI would show extensive evidence of **cerebrovascular disease** (infarcts or diffuse white matter hyperintensities) rather than primary asymmetric lobar atrophy. *Creutzfeldt-Jakob disease* - CJD is characterized by an extremely **rapidly progressive** course (dementia often develops over weeks or a few months, not 10 months) accompanied by myoclonus, ataxia, or visual disturbance. - MRI is highly sensitive, often showing pathognomonic **diffusion restriction** in the cortex (**cortical ribboning**) or basal ganglia, which is inconsistent with the focal atrophy described.

Question 28: A 50-year-old man presents with progressive weakness in his arms and legs over 18 months. He has muscle fasciculations, hyperreflexia, and bulbar symptoms. EMG shows widespread denervation. What is the prognosis?

A. Complete recovery expected
B. Slow progression over decades
C. Stable course with proper treatment
D. Progressive decline over 2-5 years (Correct Answer)
E. Rapid deterioration within months

Explanation: ***Progressive decline over 2-5 years***- The clinical presentation with **progressive weakness**, combined **upper motor neuron (hyperreflexia)** and **lower motor neuron (fasciculations, widespread denervation)** signs, and **bulbar symptoms** is highly characteristic of **Amyotrophic Lateral Sclerosis (ALS)**.- ALS is a rapidly progressive neurodegenerative disease, with the majority of patients experiencing a fatal outcome, typically due to **respiratory failure**, within **2 to 5 years** from symptom onset.*Complete recovery expected*- ALS is a **universally fatal** neurodegenerative disorder with no known cure, characterized by the irreversible degeneration of motor neurons.- Therefore, expecting complete recovery is incorrect; the disease course is one of continuous and irreversible progression.*Slow progression over decades*- While some rare variants or other motor neuron diseases (e.g., Primary Lateral Sclerosis) may have a slower course, typical sporadic ALS progresses rapidly over a few years, not decades.- The 18-month history of progressive weakness and the classic constellation of UMN/LMN signs are inconsistent with a very prolonged, decades-long progression.*Stable course with proper treatment*- Current treatments for ALS, such as **riluzole** and **edaravone**, offer only modest benefits, typically extending survival by a few months, and do not halt the progression or stabilize the disease.- Although supportive care improves quality of life, the underlying neurodegeneration ensures a continuous and ultimately terminal decline.*Rapid deterioration within months*- While ALS progression rates can vary, a typical course leading to death usually spans **2 to 5 years**, not just a few months.- Deterioration within a few months would suggest an exceptionally aggressive variant or an alternative acute condition, which is less consistent with the described **18-month progressive history**.

Question 29: A 68-year-old man presents with progressive memory loss and parkinsonian features. He has visual hallucinations of people and animals. His symptoms fluctuate significantly throughout the day. What is the most likely diagnosis?

A. Alzheimer's disease
B. Parkinson's disease with dementia
C. Lewy body dementia (Correct Answer)
D. Vascular dementia
E. Frontotemporal dementia

Explanation: ***Lewy body dementia***- This diagnosis is strongly suggested by the core diagnostic features: progressive **memory loss**, spontaneous **parkinsonism**, recurrent, detailed **visual hallucinations** (often of people and animals), and significant **fluctuating cognition** throughout the day.- LBD is definitively characterized histologically by the presence of **alpha-synuclein** inclusions (*Lewy bodies*) in the cerebral cortex and brainstem.*Alzheimer's disease*- The primary presentation of AD is typically insidious and progressive decline in **memory** and executive function, often without early or prominent motor symptoms.- While visual hallucinations can occur in later stages of AD, neither significant cognitive fluctuation nor early, prominent **visual hallucinations** are characteristic features.*Parkinson's disease with dementia*- The definitive criterion for PDD is that the onset of **motor symptoms** must precede the development of dementia by at least **one year** (the "one-year rule").- Although PDD involves both motor and cognitive decline, the early co-occurrence of dementia, parkinsonism, and profound **visual hallucinations** points away from PDD and towards LBD.*Vascular dementia*- This condition typically presents with an abrupt or **step-wise decline** in cognitive function, strongly linked to a history of strokes or **cerebrovascular disease**.- Symptoms often reflect focal brain injury, resulting in specific **focal neurological deficits** or significant executive dysfunction, which contrasts with the global symptoms seen here.*Frontotemporal dementia*- FTD classically presents with initial changes in **behavior** (e.g., apathy, disinhibition) or severe language impairment (aphasia), rather than primary memory loss or parkinsonism.- The severe, early, recurrent **visual hallucinations** and fluctuating cognition seen in this patient are not typical features of any FTD subtype.

Question 30: A 42-year-old man presents with progressive weakness in his hands and forearms. He has muscle wasting and fasciculations but preserved reflexes. Sensory examination is normal. EMG shows chronic denervation. What is the most likely diagnosis?

A. Cervical radiculopathy
B. Motor neuron disease (Correct Answer)
C. Peripheral neuropathy
D. Myasthenia gravis
E. Inclusion body myositis

Explanation: ***Motor neuron disease***- This diagnosis is strongly suggested by the progressive **muscle wasting**, **weakness**, and **fasciculations** (signs of lower motor neuron degeneration) restricted to the motor system.- The crucial differentiating features are the **normal sensory examination** and **preserved reflexes**, along with EMG showing **chronic denervation** without primary myopathic changes.*Cervical radiculopathy*- Would typically present with **radicular pain** and often involves **sensory changes** (paresthesias or sensory loss) in a specific dermatome.- EMG abnormalities would be restricted to muscles innervated by the specific affected **nerve root**, not multiple, potentially unrelated, muscle groups in hands and forearms.*Peripheral neuropathy*- Characteristically causes both motor and **sensory symptoms** (numbness, paresthesias), often in a **stocking-glove distribution**, which are absent here.- Deep tendon reflexes are typically **reduced or absent** (hyporeflexia or areflexia), contradicting the preserved reflexes observed in this patient.*Myasthenia gravis*- Characterized by **fluctuating and fatigable weakness** that worsens with sustained activity and improves with rest, but without **muscle atrophy** or **fasciculations**.- EMG shows a **decremental response** on repetitive nerve stimulation, not the chronic denervation changes consistent with motor neuron disease.*Inclusion body myositis*- This is an inflammatory myopathy (muscle disease), so EMG would show **myopathic changes** (short duration, small amplitude motor unit potentials), not the chronic denervation changes described.- While it can cause distal forearm weakness and spares sensory function, it typically affects the **quadriceps** early and reflexes may be impaired, unlike the preserved reflexes here.

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