A 67-year-old man presents to the Emergency Department with sudden onset weakness of the left arm and leg that began 2 hours ago. He has a history of hypertension and hyperlipidaemia. On examination, his blood pressure is 168/95 mmHg, heart rate 78 bpm regular, and oxygen saturation 96% on room air. Neurological examination reveals left hemiparesis with increased tone and brisk reflexes. A non-contrast CT head shows no haemorrhage or early ischaemic changes. Which of the following is the maximum time window from symptom onset for administering intravenous thrombolysis in eligible patients with acute ischaemic stroke?
Q52
A 54-year-old woman presents to the Emergency Department with sudden onset of the worst headache of her life, which peaked within 1 minute. She vomited twice and has photophobia. She has a history of polycystic kidney disease. On examination, she is alert and oriented, temperature 37.2°C, BP 165/95 mmHg, pulse 88/min. There is mild neck stiffness but no focal neurological deficit. CT head performed 4 hours after onset shows no abnormality. What is the most appropriate next step?
Q53
A 66-year-old man presents with a 9-month history of progressive memory impairment and behavioral changes. His wife reports he has become disinhibited, making inappropriate comments in public, and has developed a sweet tooth with food preferences he never had before. He has lost interest in his hobbies but shows no concern about his symptoms. On examination, he has mild frontal release signs. MMSE score is 22/30 with particular difficulty in verbal fluency. MRI brain shows bilateral frontal and anterior temporal lobe atrophy. What is the most likely diagnosis?
Q54
A 48-year-old woman with a 15-year history of migraine with aura presents with increasingly frequent attacks despite taking propranolol 80 mg twice daily and using sumatriptan for acute attacks. She has 12 migraine days per month with significant disability. She has tried and failed topiramate due to side effects. Her BMI is 28 kg/m². Blood pressure is 118/76 mmHg. What is the most appropriate next step in management?
Q55
What is the mechanism of action of memantine in the treatment of Alzheimer's dementia?
Q56
A 28-year-old man is brought to the Emergency Department following a witnessed tonic-clonic seizure. He is now post-ictal but becoming more alert. He has no past medical history and takes no medications. Examination shows he is afebrile with Glasgow Coma Scale 14/15. Blood glucose is 5.8 mmol/L, sodium 138 mmol/L, calcium 2.4 mmol/L. He last consumed alcohol 36 hours ago after a heavy weekend of drinking. What is the most appropriate immediate management?
Q57
A 39-year-old woman presents with a 6-week history of progressive confusion, behavioral changes, and myoclonic jerks. MRI brain shows bilateral symmetrical signal changes in the basal ganglia and cortical ribboning on diffusion-weighted imaging. EEG shows generalized periodic complexes. CSF shows elevated protein at 0.8 g/L with normal glucose and cell count. CSF 14-3-3 protein is positive. What is the most likely diagnosis?
Q58
A 74-year-old woman is admitted with acute left hemiparesis. CT head shows a right middle cerebral artery territory infarct with no haemorrhage. She has atrial fibrillation and her CHA2DS2-VASc score is 5. She is not anticoagulated. After initial management, when is the most appropriate time to commence anticoagulation?
Q59
A 57-year-old man with type 2 diabetes presents with a 3-month history of frequent episodes of unilateral throbbing headache lasting 2-3 hours, associated with nausea and photophobia. He has 8-10 episodes per month, causing significant work absence. He takes metformin and gliclazide. Paracetamol provides minimal relief. Neurological examination is normal. What is the most appropriate prophylactic treatment to initiate?
Q60
An 81-year-old woman is admitted from a care home with acute confusion. She has been increasingly agitated over the past 2 days with visual hallucinations of small animals. Her medications include donepezil 10 mg, memantine 20 mg, and rivastigmine patch 9.5 mg/24h for dementia with Lewy bodies diagnosed 3 years ago. On examination, temperature 37.8°C, BP 110/70 mmHg, oxygen saturation 94% on air. Chest is clear and urinalysis shows blood ++ and leucocytes ++. What is the most important immediate management step?
Neurology UK Medical PG Practice Questions and MCQs
Question 51: A 67-year-old man presents to the Emergency Department with sudden onset weakness of the left arm and leg that began 2 hours ago. He has a history of hypertension and hyperlipidaemia. On examination, his blood pressure is 168/95 mmHg, heart rate 78 bpm regular, and oxygen saturation 96% on room air. Neurological examination reveals left hemiparesis with increased tone and brisk reflexes. A non-contrast CT head shows no haemorrhage or early ischaemic changes. Which of the following is the maximum time window from symptom onset for administering intravenous thrombolysis in eligible patients with acute ischaemic stroke?
A. 3 hours
B. 4.5 hours (Correct Answer)
C. 6 hours
D. 9 hours
E. 12 hours
Explanation: ***4.5 hours***
- Current clinical guidelines, based on the **ECASS III trial**, state that **intravenous alteplase (rtPA)** can be administered up to **4.5 hours** from the onset of stroke symptoms.
- While treatment is most effective within the first 3 hours, extending the window to **4.5 hours** provides significant benefit for recovery, provided there are no **contraindications** such as intracranial hemorrhage.
*3 hours*
- This was the original **FDA-approved** time window based on the **NINDS trial**; however, it has since been expanded to include eligible patients up to 4.5 hours.
- Restricting treatment to only 3 hours would unnecessarily exclude patients who still derive benefit from **thrombolytic therapy**.
*6 hours*
- The **6-hour window** is more commonly associated with the timeframe for **mechanical thrombectomy** in patients with a **Large Vessel Occlusion (LVO)**.
- For intravenous thrombolysis, the risk of **hemorrhagic transformation** increases significantly beyond the 4.5-hour mark, making it unsuitable as a routine maximum window.
*9 hours*
- While some advanced imaging-guided protocols (using **CT perfusion**) are investigating extended windows for rtPA, it is not the standard maximum window for general practice.
- Administration at this stage without specific **penumbral imaging** criteria is associated with a high risk of **intracranial bleeding**.
*12 hours*
- This time frame far exceeds the safety profile for **intravenous thrombolysis** and is not supported by standard clinical evidence for rtPA.
- In selected patients with large vessel strokes, **mechanical thrombectomy** may be considered up to **24 hours**, but clinical outcomes for IV thrombolysis at this stage are poor.
Question 52: A 54-year-old woman presents to the Emergency Department with sudden onset of the worst headache of her life, which peaked within 1 minute. She vomited twice and has photophobia. She has a history of polycystic kidney disease. On examination, she is alert and oriented, temperature 37.2°C, BP 165/95 mmHg, pulse 88/min. There is mild neck stiffness but no focal neurological deficit. CT head performed 4 hours after onset shows no abnormality. What is the most appropriate next step?
A. Discharge with analgesia and neurology follow-up
B. Perform lumbar puncture to analyze CSF for xanthochromia and red cells (Correct Answer)
C. Arrange CT angiography of cerebral vessels
D. Repeat CT head in 6 hours
E. Start prophylactic nimodipine 60 mg four times daily
Explanation: ***Perform lumbar puncture to analyze CSF for xanthochromia and red cells***
- A **thunderclap headache** in a patient with **polycystic kidney disease** (associated with berry aneurysms) is highly suspicious for **subarachnoid hemorrhage (SAH)**, even if the initial CT is negative.
- When a non-contrast CT head is negative or inconclusive, especially if performed early, a **lumbar puncture** performed at least **12 hours after symptom onset** is the gold standard to look for **xanthochromia** and **red blood cells**.
*Discharge with analgesia and neurology follow-up*
- Discharging the patient is unsafe because a **normal CT scan** does not 100% exclude SAH, particularly if performed within 6 hours of symptom onset, or if there's a small bleed.
- Missing a diagnosis of SAH carries a high risk of subsequent catastrophic **rebleeding** and potentially fatal outcomes.
*Arrange CT angiography of cerebral vessels*
- **CT angiography (CTA)** is used to identify the source of bleeding (e.g., an **aneurysm**) *after* the diagnosis of SAH has been confirmed by CT or CSF analysis.
- It is not the primary diagnostic tool for confirming the presence of **subarachnoid blood** itself if the non-contrast CT is negative and SAH is still suspected.
*Repeat CT head in 6 hours*
- Repeating a non-contrast CT head is not the next most appropriate step, as the sensitivity for detecting blood **decreases over time**; if the initial CT was negative, a subsequent CT is unlikely to reveal blood unless there's a new bleed.
- If clinical suspicion for SAH remains high despite a negative initial CT, **lumbar puncture** is the definitive next diagnostic step.
*Start prophylactic nimodipine 60 mg four times daily*
- **Nimodipine** is a calcium channel blocker used to prevent **delayed cerebral ischemia** caused by vasospasm, which is a common complication *after* a confirmed SAH.
- This is a management step for established SAH and should only be initiated once the **diagnosis of SAH** is definitively established by imaging or CSF analysis.
Question 53: A 66-year-old man presents with a 9-month history of progressive memory impairment and behavioral changes. His wife reports he has become disinhibited, making inappropriate comments in public, and has developed a sweet tooth with food preferences he never had before. He has lost interest in his hobbies but shows no concern about his symptoms. On examination, he has mild frontal release signs. MMSE score is 22/30 with particular difficulty in verbal fluency. MRI brain shows bilateral frontal and anterior temporal lobe atrophy. What is the most likely diagnosis?
A. Alzheimer's dementia
B. Behavioral variant frontotemporal dementia (Correct Answer)
C. Vascular dementia
D. Dementia with Lewy bodies
E. Normal pressure hydrocephalus
Explanation: ***Behavioral variant frontotemporal dementia***
- This diagnosis is characterized by early **behavioral changes** such as **disinhibition**, **apathy**, and **hyperorality** (e.g., developing a sweet tooth and new food preferences), along with **frontal and anterior temporal lobe atrophy** on MRI.
- Key features include **loss of insight** regarding symptoms, executive dysfunction (difficulty in verbal fluency), and frontal release signs, which are all present in the patient.
*Alzheimer's dementia*
- Primarily presents with early and prominent **episodic memory loss** and visuospatial deficits, rather than initial behavioral changes or disinhibition.
- Neuroimaging typically shows **hippocampal atrophy** and temporoparietal involvement, rather than the specific frontal and anterior temporal atrophy seen here.
*Vascular dementia*
- Characterized by a **stepwise decline** in cognitive function, often associated with focal neurological deficits and clear **vascular risk factors** or a history of stroke.
- **MRI** would typically reveal multiple infarcts or significant **white matter disease**, which is not the primary finding in this case.
*Dementia with Lewy bodies*
- Presents with a classic triad of **fluctuating cognition**, recurrent **visual hallucinations**, and features of **parkinsonism**.
- While behavioral symptoms can occur, the prominent early disinhibition and hyperorality without other defining features make this less likely.
*Normal pressure hydrocephalus*
- Clinically defined by the triad of **gait disturbance** (often described as magnetic), **urinary incontinence**, and cognitive decline (typically attention and executive function).
- Imaging characteristically shows **ventriculomegaly** out of proportion to sulcal atrophy, which is distinct from the focal cortical atrophy observed in this patient.
Question 54: A 48-year-old woman with a 15-year history of migraine with aura presents with increasingly frequent attacks despite taking propranolol 80 mg twice daily and using sumatriptan for acute attacks. She has 12 migraine days per month with significant disability. She has tried and failed topiramate due to side effects. Her BMI is 28 kg/m². Blood pressure is 118/76 mmHg. What is the most appropriate next step in management?
A. Switch propranolol to amitriptyline 75 mg at night
B. Add greater occipital nerve block injections
C. Refer for consideration of CGRP monoclonal antibody therapy (Correct Answer)
D. Commence sodium valproate 600 mg twice daily
E. Increase propranolol to 120 mg twice daily
Explanation: ***Refer for consideration of CGRP monoclonal antibody therapy***
- This patient has **chronic migraine** (12 migraine days per month) and has failed two adequate trials of preventive medications (**propranolol** and **topiramate**).
- This failure to respond to conventional oral preventatives is a key criterion for initiating **CGRP monoclonal antibody** therapy, which targets specific pathways involved in migraine.
*Switch propranolol to amitriptyline 75 mg at night*
- While **amitriptyline** is a valid preventive, the patient has already failed two first-line preventatives, making advanced therapies like CGRP inhibitors more appropriate at this stage.
- **75 mg** is a high starting dose, often associated with significant **sedation** and **anticholinergic side effects**, which could worsen patient compliance and quality of life.
*Add greater occipital nerve block injections*
- **Greater occipital nerve blocks** are typically used for acute migraine attacks, **cluster headaches**, or as a bridge therapy, rather than a long-term preventive for chronic migraine.
- They offer temporary relief and do not address the systemic **pathophysiology** of frequent, disabling migraine attacks effectively.
*Commence sodium valproate 600 mg twice daily*
- **Sodium valproate** carries a significant **teratogenic risk** and is generally contraindicated in women of **childbearing potential** unless strict pregnancy prevention measures are in place.
- It also has other side effects like **weight gain** and hair loss, making it less favorable than CGRP inhibitors for a patient who has failed other preventatives.
*Increase propranolol to 120 mg twice daily*
- The patient is already on **160 mg daily** of propranolol (80 mg BID) and is still experiencing 12 migraine days per month, indicating suboptimal efficacy.
- Increasing the dose further is unlikely to provide significant additional benefit and would heighten the risk of **dose-dependent side effects** such as **bradycardia** and **fatigue**.
Question 55: What is the mechanism of action of memantine in the treatment of Alzheimer's dementia?
A. Reversible inhibition of acetylcholinesterase
B. Irreversible inhibition of acetylcholinesterase
C. NMDA receptor antagonist reducing glutamate excitotoxicity (Correct Answer)
D. Selective serotonin reuptake inhibitor
E. Dopamine receptor agonist
Explanation: ***NMDA receptor antagonist reducing glutamate excitotoxicity***- Memantine is a **non-competitive, low-affinity NMDA receptor antagonist** that modulates glutamatergic neurotransmission.- This action helps to prevent excessive neuronal stimulation and **excitotoxicity** caused by overactive glutamate signaling, a significant factor in the progression of Alzheimer's disease.*Reversible inhibition of acetylcholinesterase*- This mechanism describes the action of drugs like **donepezil**, **rivastigmine**, and **galantamine**, which are also used in Alzheimer's treatment.- These drugs increase the availability of **acetylcholine** in the synaptic cleft, targeting the cholinergic deficit in the disease.*Irreversible inhibition of acetylcholinesterase*- This mechanism is associated with toxic agents such as **organophosphates** and is not a therapeutic approach for Alzheimer's dementia.- Irreversible inhibition would lead to a severe and sustained **cholinergic crisis**, which is life-threatening.*Selective serotonin reuptake inhibitor*- **SSRIs** are primarily used to treat mood disorders like **depression and anxiety** by increasing serotonin levels in the brain.- While these conditions can co-occur with Alzheimer's, SSRIs do not address the core **neurodegenerative pathology** of the disease.*Dopamine receptor agonist*- **Dopamine receptor agonists** are typically used in the management of **Parkinson's disease** and restless leg syndrome.- Their mechanism involves enhancing dopaminergic activity and is not directly relevant to the **cholinergic or glutamatergic imbalances** characteristic of Alzheimer's.
Question 56: A 28-year-old man is brought to the Emergency Department following a witnessed tonic-clonic seizure. He is now post-ictal but becoming more alert. He has no past medical history and takes no medications. Examination shows he is afebrile with Glasgow Coma Scale 14/15. Blood glucose is 5.8 mmol/L, sodium 138 mmol/L, calcium 2.4 mmol/L. He last consumed alcohol 36 hours ago after a heavy weekend of drinking. What is the most appropriate immediate management?
A. Discharge with neurology follow-up and advise not to drive
B. Administer intravenous lorazepam 4 mg
C. Start oral levetiracetam 500 mg twice daily
D. Admit for chlordiazepoxide regimen and thiamine supplementation (Correct Answer)
E. Arrange urgent CT head and EEG before discharge
Explanation: ***Admit for chlordiazepoxide regimen and thiamine supplementation***
- This patient is experiencing an **alcohol withdrawal seizure**, which typically occurs **12-48 hours** after the last drink following a period of heavy consumption.
- Immediate management requires a **benzodiazepine regimen** (e.g., chlordiazepoxide) to prevent further seizures or **delirium tremens**, and **thiamine** to prevent **Wernicke's encephalopathy**.
*Discharge with neurology follow-up and advise not to drive*
- Discharging this patient prematurely is dangerous because he is at high risk for **recurrent seizures** or progression to **delirium tremens** within the withdrawal window.
- While **DVLA advice** regarding driving cessation is necessary eventually, it is not the immediate priority for an unstable patient in withdrawal.
*Administer intravenous lorazepam 4 mg*
- **Intravenous lorazepam** is the first-line treatment for **active seizures** or **status epilepticus**.
- Since the patient is currently **post-ictal** and not actively seizing, prophylactic oral benzodiazepines are more appropriate than emergency IV boluses.
*Start oral levetiracetam 500 mg twice daily*
- Long-term **anti-epileptic drugs (AEDs)** like levetiracetam are not indicated for **provoked seizures** like those caused by alcohol withdrawal.
- The management focus must be on treating the **underlying withdrawal state** rather than a primary seizure disorder like epilepsy.
*Arrange urgent CT head and EEG before discharge*
- An **EEG** is generally not useful in the emergency setting for a clear **provoked seizure** and does not change immediate management.
- A **CT head** is only indicated if there is a history of trauma, **focal neurological deficits**, or if it is a first-ever non-provoked seizure, which is not the case here.
Question 57: A 39-year-old woman presents with a 6-week history of progressive confusion, behavioral changes, and myoclonic jerks. MRI brain shows bilateral symmetrical signal changes in the basal ganglia and cortical ribboning on diffusion-weighted imaging. EEG shows generalized periodic complexes. CSF shows elevated protein at 0.8 g/L with normal glucose and cell count. CSF 14-3-3 protein is positive. What is the most likely diagnosis?
A. Anti-NMDA receptor encephalitis
B. Sporadic Creutzfeldt-Jakob disease (Correct Answer)
C. Progressive multifocal leukoencephalopathy
D. Hashimoto's encephalopathy
E. Variant Creutzfeldt-Jakob disease
Explanation: ***Sporadic Creutzfeldt-Jakob disease***
- This diagnosis is strongly supported by the **rapidly progressive confusion** and **behavioral changes** coupled with **myoclonic jerks** over a 6-week period.
- Key diagnostic features include **bilateral symmetrical signal changes in the basal ganglia** and **cortical ribboning on diffusion-weighted imaging (DWI)** on MRI, **generalized periodic complexes** on EEG, and a **positive CSF 14-3-3 protein** test.
*Anti-NMDA receptor encephalitis*
- This condition typically presents with a more varied clinical picture including **prominent psychiatric symptoms**, seizures, dyskinesias, and autonomic instability, but usually lacks the characteristic MRI findings of **cortical ribboning** and **basal ganglia changes** seen here.
- The definitive diagnosis requires the detection of **anti-NMDA receptor antibodies**, and the EEG findings are usually not generalized periodic complexes.
*Progressive multifocal leukoencephalopathy*
- Caused by the **JC virus**, this disease primarily affects **immunocompromised individuals** and presents with focal neurological deficits related to **demyelination in the white matter**.
- MRI typically shows **asymmetrical white matter lesions** without cortical ribboning or basal ganglia involvement, and it does not feature the specific EEG periodic complexes or positive CSF 14-3-3 protein.
*Hashimoto's encephalopathy*
- While it can cause confusion and myoclonus, it is a **steroid-responsive** encephalopathy often associated with high titers of **anti-thyroid antibodies (e.g., anti-TPO)**, which are not mentioned.
- It lacks the specific MRI findings of **cortical ribboning** and **basal ganglia hyperintensity** on DWI, the characteristic EEG periodic complexes, and the **positive CSF 14-3-3 protein** seen in this patient.
*Variant Creutzfeldt-Jakob disease*
- This form of prion disease typically affects **much younger patients** (often under 30) and presents with early and prominent **psychiatric symptoms** and sensory disturbances, before the onset of frank dementia.
- MRI in vCJD classically shows the **"pulvinar sign"** (hyperintensity in the posterior thalamus) rather than the bilateral basal ganglia changes and cortical ribboning on DWI found in sporadic CJD.
Question 58: A 74-year-old woman is admitted with acute left hemiparesis. CT head shows a right middle cerebral artery territory infarct with no haemorrhage. She has atrial fibrillation and her CHA2DS2-VASc score is 5. She is not anticoagulated. After initial management, when is the most appropriate time to commence anticoagulation?
A. Immediately, as the stroke is cardioembolic
B. After 24 hours if repeat CT shows no haemorrhagic transformation
C. After 48 hours regardless of repeat imaging
D. After 14 days following repeat CT to exclude haemorrhagic transformation (Correct Answer)
E. Anticoagulation is contraindicated following ischaemic stroke
Explanation: ***After 14 days following repeat CT to exclude haemorrhagic transformation***
- In patients with a **large ischaemic stroke** like an MCA territory infarct, anticoagulation is generally delayed for **14 days** to significantly reduce the risk of **haemorrhagic transformation** within the infarcted tissue.
- A **repeat CT head** is essential at the end of this period to confirm the absence of bleeding before initiating long-term anticoagulation for **atrial fibrillation** and secondary stroke prevention.
*Immediately, as the stroke is cardioembolic*
- Initiating anticoagulation **immediately** after a large acute ischaemic stroke carries a high risk of **symptomatic intracranial haemorrhage**, which can dramatically worsen clinical outcomes.
- Current guidelines typically recommend starting **antiplatelet therapy** (e.g., aspirin) in the acute phase, reserving anticoagulation for a later, safer window.
*After 24 hours if repeat CT shows no haemorrhagic transformation*
- A 24-hour delay is insufficient for a **large MCA territory infarct** as the risk of **haemorrhagic transformation** remains elevated throughout the first week post-stroke.
- This shorter timeframe is usually considered for **minor ischaemic strokes** or for initiating antiplatelets, not for full anticoagulation in major events.
*After 48 hours regardless of repeat imaging*
- While 48-72 hours might be considered for **mild to moderate strokes**, it is generally still too early for a **large infarct** like an MCA territory stroke due to the high risk of bleeding.
- Commencing anticoagulation without **follow-up imaging** to exclude haemorrhagic transformation is unsafe, as the infarct area is still highly vulnerable.
*Anticoagulation is contraindicated following ischaemic stroke*
- Anticoagulation is **not contraindicated** but rather **temporarily delayed** following an ischaemic stroke, especially when the cause is **atrial fibrillation**.
- It is crucial for **secondary prevention** of future cardioembolic strokes, as the long-term benefits typically outweigh the risks once the acute bleeding risk has subsided.
Question 59: A 57-year-old man with type 2 diabetes presents with a 3-month history of frequent episodes of unilateral throbbing headache lasting 2-3 hours, associated with nausea and photophobia. He has 8-10 episodes per month, causing significant work absence. He takes metformin and gliclazide. Paracetamol provides minimal relief. Neurological examination is normal. What is the most appropriate prophylactic treatment to initiate?
A. Propranolol 80 mg twice daily
B. Topiramate 25 mg at night, increasing gradually (Correct Answer)
C. Amitriptyline 10 mg at night, increasing to 50-75 mg
D. Sodium valproate 300 mg twice daily
E. Pizotifen 0.5 mg at night
Explanation: ***Topiramate 25 mg at night, increasing gradually***
- **Topiramate** is a first-line agent for migraine prophylaxis and is particularly advantageous in this patient with **Type 2 Diabetes** as it is associated with **weight loss** and can improve glycemic control.
- The dosage must be **titrated slowly** to mitigate common side effects such as **paresthesia**, cognitive slowing, and the risk of renal calculi.
*Propranolol 80 mg twice daily*
- **Propranolol** is a first-line prophylactic, but beta-blockers can **mask the symptoms of hypoglycemia**, posing a risk to patients on insulin secretagogues like **gliclazide**.
- It may also lead to **weight gain** or metabolic changes that are undesirable in the management of diabetes.
*Amitriptyline 10 mg at night, increasing to 50-75 mg*
- **Amitriptyline** is an effective second-line option but is frequently associated with **weight gain** and increased appetite, which can worsen **insulin resistance** in diabetic patients.
- Side effects such as **sedation** and anticholinergic effects (e.g., dry mouth, blurred vision) may be poorly tolerated compared to other prophylactic agents.
*Sodium valproate 300 mg twice daily*
- Although effective for migraines, **sodium valproate** is typically reserved for refractory cases due to its significant metabolic profile, including **weight gain** and potential hepatotoxicity.
- It also carries a high risk of **teratogenicity**, making it a less favorable first-line choice compared to topiramate, even in male patients, in the context of diabetes.
*Pizotifen 0.5 mg at night*
- **Pizotifen** is rarely used in contemporary practice as a first-line agent due to its common side effects of **significant weight gain** and sedation.
- Its efficacy is generally considered lower than that of **topiramate** or **propranolol** for chronic migraine prevention.
Question 60: An 81-year-old woman is admitted from a care home with acute confusion. She has been increasingly agitated over the past 2 days with visual hallucinations of small animals. Her medications include donepezil 10 mg, memantine 20 mg, and rivastigmine patch 9.5 mg/24h for dementia with Lewy bodies diagnosed 3 years ago. On examination, temperature 37.8°C, BP 110/70 mmHg, oxygen saturation 94% on air. Chest is clear and urinalysis shows blood ++ and leucocytes ++. What is the most important immediate management step?
A. Start oral haloperidol 0.5 mg twice daily for agitation
B. Discontinue all antidementia medications
C. Start intravenous antibiotics for urinary tract infection (Correct Answer)
D. Arrange urgent CT head to exclude subdural haematoma
E. Start oral lorazepam 0.5 mg as required for agitation
Explanation: ***Start intravenous antibiotics for urinary tract infection***
- The patient's acute confusion, agitation, and visual hallucinations suggest **delirium**, which is acutely superimposed on her pre-existing **dementia with Lewy bodies**.
- The presence of **fever** (37.8°C) and a **positive urinalysis** (blood ++, leucocytes ++) strongly indicates a **urinary tract infection (UTI)** as the precipitating cause, making prompt intravenous antibiotics the most crucial immediate management step to treat the underlying cause of delirium.
*Start oral haloperidol 0.5 mg twice daily for agitation*
- Patients with **dementia with Lewy bodies (DLB)** are extremely sensitive to **neuroleptics** like haloperidol, which can cause severe adverse effects including worsening parkinsonism, rigidity, and potentially life-threatening complications.
- **Haloperidol** is largely contraindicated in DLB due to this high sensitivity, and its use for agitation would carry significant risks without addressing the underlying infection.
*Discontinue all antidementia medications*
- Abruptly stopping **cholinesterase inhibitors** (donepezil, rivastigmine) and **NMDA receptor antagonists** (memantine) can lead to a rapid and significant worsening of cognitive function and behavioral symptoms.
- While a medication review might be part of long-term care, discontinuing these medications is not the immediate priority for an acute delirious state caused by an infection.
*Arrange urgent CT head to exclude subdural haematoma*
- While neuroimaging can be important in delirium, this patient has clear evidence of an **infectious cause (UTI)** with fever and positive urinalysis, which is a more immediate and treatable explanation for her acute confusion.
- An urgent **CT head** is not the most important immediate step as there is no specific history of trauma or new focal neurological signs to suggest a subdural haematoma as the primary cause.
*Start oral lorazepam 0.5 mg as required for agitation*
- **Benzodiazepines** like **lorazepam** can exacerbate **delirium** in older adults, increasing confusion, sedation, and the risk of falls, rather than resolving the core issue.
- Management of agitation in delirium should primarily focus on treating the underlying cause; benzodiazepines are generally reserved for severe, dangerous agitation as a last resort and used with extreme caution.
