Neurology — MCQs
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A 19-year-old woman presents to the Emergency Department having had three generalised tonic-clonic seizures in the past hour without regaining consciousness between episodes. She has no history of epilepsy. What is the third-line treatment if initial benzodiazepines and second-line therapy fail to terminate the seizures?
A 71-year-old man with type 2 diabetes presents with sudden onset right homonymous hemianopia but no motor weakness. CT head shows a left occipital infarct. Which vascular territory is most likely affected?
A 34-year-old woman with generalised epilepsy controlled on sodium valproate 1000mg twice daily is planning pregnancy. She had her last seizure 4 years ago. What is the most appropriate adjustment to her antiepileptic medication?
A 68-year-old woman with atrial fibrillation presents to the Emergency Department 3 hours after sudden onset left-sided weakness and dysphasia. CT head shows no haemorrhage. Her NIHSS score is 14. She takes warfarin and her INR is 3.2. Blood pressure is 165/95 mmHg. What is the most appropriate immediate management to enable thrombolysis?
A 52-year-old man with a history of chronic migraine presents to the neurology clinic having tried multiple preventive treatments without success. He experiences 12-15 headache days per month, of which 10 are migrainous. He has tried and failed adequate trials of propranolol, topiramate, and amitriptyline. He is considerably disabled by his headaches and has had to reduce his working hours. He does not overuse acute medications. Which treatment option would be most appropriate to consider next according to NICE guidance?
A 23-year-old woman presents to the Emergency Department following a witnessed seizure at work. Her colleague describes that she suddenly stopped talking mid-conversation, stared blankly ahead for about 30 seconds while smacking her lips, then seemed confused for a few minutes afterwards. She has no memory of the event. She has never had a seizure before and has no significant medical history. Neurological examination is now normal. What type of seizure has she most likely experienced?
Which clinical feature is part of the diagnostic criteria for dementia with Lewy bodies but NOT typically seen in early Alzheimer's disease?
What is the mechanism of action of alteplase in acute ischaemic stroke?
A 67-year-old woman diagnosed with vascular dementia 2 years ago presents with her daughter who is concerned about capacity to manage finances. The patient has been making unusual purchases and has forgotten to pay bills. MMSE score is 20/30. She understands that she has memory problems but insists she can manage her money independently. She can describe what bills need to be paid but has repeatedly forgotten to pay them. What is the most appropriate approach to capacity assessment for financial decisions?
A 42-year-old woman presents with right-sided weakness that developed over 20 minutes and has now completely resolved after 45 minutes. She has no past medical history and takes no regular medications. Examination is entirely normal. Blood pressure is 128/78 mmHg, heart rate is 72 bpm and regular. ECG shows sinus rhythm. Blood glucose is 5.4 mmol/L. She is a non-smoker with BMI of 24. According to current guidelines, what is the most appropriate acute management?
Neurology UK Medical PG Practice Questions and MCQs
Question 91: A 19-year-old woman presents to the Emergency Department having had three generalised tonic-clonic seizures in the past hour without regaining consciousness between episodes. She has no history of epilepsy. What is the third-line treatment if initial benzodiazepines and second-line therapy fail to terminate the seizures?
- A. General anaesthesia with propofol or thiopental (Correct Answer)
- B. Intravenous phenobarbital
- C. Intravenous magnesium sulphate
- D. Oral carbamazepine via nasogastric tube
- E. Intravenous methylprednisolone
Explanation: ***General anaesthesia with propofol or thiopental*** - If **status epilepticus** persists despite initial benzodiazepines (first-line) and a second-line antiepileptic drug (e.g., phenytoin, fosphenytoin, levetiracetam), the condition becomes **refractory status epilepticus**. - Third-line treatment involves inducing **general anaesthesia** with agents like **propofol** or **thiopental** in an **Intensive Care Unit (ICU)** setting, often guided by **EEG monitoring** to achieve burst suppression. *Intravenous phenobarbital* - While **phenobarbital** is an antiepileptic, it is typically considered a **second-line agent** or an alternative if other second-line drugs are contraindicated or ineffective, rather than the designated third-line treatment for refractory status epilepticus after *failure* of second-line therapy. - The critical step after failure of second-line AEDs is escalation to inducing **general anaesthesia** to stop persistent seizure activity. *Intravenous magnesium sulphate* - **Magnesium sulphate** is the specific first-line treatment for seizures occurring in the context of **eclampsia** or pre-eclampsia, which is not indicated in this non-pregnant patient. - It has no role in the standard emergency management protocol for **generalized tonic-clonic status epilepticus** in patients without eclampsia. *Oral carbamazepine via nasogastric tube* - **Oral medications** are inappropriate for terminating acute **status epilepticus** due to their inherently **slow absorption** and delayed onset of action, making them ineffective in an acute life-threatening situation. - **Carbamazepine** is used for the long-term management of epilepsy, not for emergency seizure termination, as it would not achieve therapeutic levels rapidly enough. *Intravenous methylprednisolone* - **Methylprednisolone** is a corticosteroid primarily used for its anti-inflammatory and immunosuppressive effects, and it has **no direct anticonvulsant properties**. - It is not indicated for the immediate termination of **acute seizure activity** or **status epilepticus**, though it might be used to treat underlying inflammatory causes of epilepsy (e.g., autoimmune encephalitis) over a longer course.
Question 92: A 71-year-old man with type 2 diabetes presents with sudden onset right homonymous hemianopia but no motor weakness. CT head shows a left occipital infarct. Which vascular territory is most likely affected?
- A. Posterior cerebral artery (Correct Answer)
- B. Middle cerebral artery
- C. Anterior cerebral artery
- D. Posterior inferior cerebellar artery
- E. Anterior choroidal artery
Explanation: ***Posterior cerebral artery***- The **posterior cerebral artery (PCA)** supplies the **occipital lobe**, and an infarct here typically results in a **contralateral homonymous hemianopia** often with **macular sparing** if the middle cerebral artery provides collateral supply.- The absence of **motor weakness** is a classic sign of an isolated PCA stroke, as it spares the motor tracts of the internal capsule and frontal lobes.*Middle cerebral artery*- An infarct in the **middle cerebral artery (MCA)** territory usually presents with **contralateral hemiparesis** and **hemisensory loss**, primarily affecting the face and arm.- While it can cause homonymous hemianopia, it is almost always accompanied by **neurological deficits** such as **aphasia** (dominant) or **hemispatial neglect** (non-dominant).*Anterior cerebral artery*- The **anterior cerebral artery (ACA)** supplies the **medial portion** of the frontal and parietal lobes.- Clinical presentation typically involves **contralateral lower limb weakness** and sensory loss, rather than primary visual field defects.*Posterior inferior cerebellar artery*- Infarction of the **posterior inferior cerebellar artery (PICA)** leads to **Lateral Medullary Syndrome** (Wallenberg syndrome).- It is characterized by **ataxia**, **vertigo**, and **ipsilateral facial sensory loss**, but does not cause a homonymous hemianopia.*Anterior choroidal artery*- The **anterior choroidal artery** supplies the **posterior limb of the internal capsule**, which would typically lead to **hemiparesis** and hemisensory loss.- While it can cause visual field defects by affecting the **optic tract** or lateral geniculate nucleus, isolated occipital findings on CT points directly to the PCA.
Question 93: A 34-year-old woman with generalised epilepsy controlled on sodium valproate 1000mg twice daily is planning pregnancy. She had her last seizure 4 years ago. What is the most appropriate adjustment to her antiepileptic medication?
- A. Switch to lamotrigine monotherapy with gradual dose titration (Correct Answer)
- B. Continue sodium valproate but reduce dose to 500mg twice daily
- C. Add folic acid 5mg daily and continue current medication
- D. Switch to levetiracetam immediately and stop sodium valproate
- E. Stop all antiepileptic drugs as she has been seizure-free for 4 years
Explanation: ***Switch to lamotrigine monotherapy with gradual dose titration*** - **Sodium valproate** is highly teratogenic, associated with a 10% risk of **major congenital malformations** and a 30-40% risk of **neurodevelopmental delay**; it must be avoided in women of childbearing potential. - **Lamotrigine** or **levetiracetam** are the preferred alternatives in pregnancy due to their lower teratogenic profile, provided they are introduced with **gradual titration** to maintain seizure control during the transition. *Continue sodium valproate but reduce dose to 500mg twice daily* - Even at lower doses, **valproate** remains significantly more teratogenic than other AEDs, and there is no "safe" dose for the developing fetus. - Current guidelines state that valproate should only be used if there is no other effective treatment, which is not evidenced here as a **switch** has not been attempted. *Add folic acid 5mg daily and continue current medication* - While **high-dose folic acid (5mg)** is mandatory for all women on AEDs to reduce **neural tube defect** risk, it does not mitigate the high neurodevelopmental risks specifically linked to **valproate**. - Continuing valproate when safer options exist violates the **Valproate Pregnancy Prevention Programme** (Prevent) regulations. *Switch to levetiracetam immediately and stop sodium valproate* - An **abrupt switch** or sudden cessation of valproate carries a high risk of **breakthrough seizures** and potentially **status epilepticus**, which poses a risk to both the mother and a future fetus. - Medications should be cross-tapered gradually to ensure **therapeutic levels** are maintained throughout the transition process. *Stop all antiepileptic drugs as she has been seizure-free for 4 years* - While she has been seizure-free, the physiological changes in pregnancy (such as increased **plasma volume** and stress) can lower the **seizure threshold**. - Decisions to stop AEDs should be made well in advance of pregnancy with specialist guidance; stopping now without a safety net risks **seizure recurrence** during a high-risk period.
Question 94: A 68-year-old woman with atrial fibrillation presents to the Emergency Department 3 hours after sudden onset left-sided weakness and dysphasia. CT head shows no haemorrhage. Her NIHSS score is 14. She takes warfarin and her INR is 3.2. Blood pressure is 165/95 mmHg. What is the most appropriate immediate management to enable thrombolysis?
- A. Administer intravenous prothrombin complex concentrate (Correct Answer)
- B. Give oral vitamin K 10mg and wait 6 hours
- C. Give fresh frozen plasma immediately
- D. Wait for INR to fall to <1.7 naturally before considering thrombolysis
- E. Proceed directly with alteplase as she is within the time window
Explanation: ***Administer intravenous prothrombin complex concentrate***- Rapid reversal of **anticoagulation** is essential because an **INR >1.7** is a contraindication for thrombolysis in acute ischemic stroke.- **Prothrombin complex concentrate (PCC)** is the preferred agent as it provides immediate replacement of **clotting factors** (II, VII, IX, X) compared to other methods.*Give oral vitamin K 10mg and wait 6 hours*- **Vitamin K** takes several hours to synthesize new clotting factors, which is far too slow for the **4.5-hour thrombolysis window**.- While vitamin K is often given alongside PCC for sustained reversal, it cannot be used as a **monotherapy** in an emergency setting.*Give fresh frozen plasma immediately*- **Fresh frozen plasma (FFP)** requires large volumes and blood group matching, which causes significant delays in the **hyperacute** setting.- It is less effective and carries a higher risk of **fluid overload** compared to the more concentrated and faster-acting **PCC**.*Wait for INR to fall to <1.7 naturally before considering thrombolysis*- The **half-life** of warfarin effects (especially factor II and X) is too long for the INR to normalize within the narrow **thrombolytic window**.- Delaying treatment would lead to **exceeding the 4.5-hour time limit**, resulting in irreversible brain tissue loss and permanent **neurological deficit**.*Proceed directly with alteplase as she is within the time window*- Administering **alteplase** when the INR is above 1.7 carries a high risk of **symptomatic intracranial hemorrhage**.- This approach violates standard **safety guidelines**; the INR must be corrected to **<1.7** before thrombolytic therapy can safely commence.
Question 95: A 52-year-old man with a history of chronic migraine presents to the neurology clinic having tried multiple preventive treatments without success. He experiences 12-15 headache days per month, of which 10 are migrainous. He has tried and failed adequate trials of propranolol, topiramate, and amitriptyline. He is considerably disabled by his headaches and has had to reduce his working hours. He does not overuse acute medications. Which treatment option would be most appropriate to consider next according to NICE guidance?
- A. Combination therapy with propranolol and topiramate
- B. Greater occipital nerve blocks with corticosteroid and local anaesthetic
- C. CGRP monoclonal antibody therapy (erenumab, fremanezumab, or galcanezumab)
- D. Sodium valproate 500 mg twice daily
- E. Botulinum toxin type A injections (Correct Answer)
Explanation: ***Botulinum toxin type A injections***- According to **NICE guidelines**, this is the recommended next step for patients with **chronic migraine** (≥15 headache days/month, of which 8 or more are migrainous) who have failed at least **three prior pharmacological preventives**.- The patient meets these criteria, including not having **medication overuse headache**, making botulinum toxin A the appropriate specific intervention for this clinical profile.*Combination therapy with propranolol and topiramate*- There is limited clinical evidence to support the **combination of two failed oral preventives** over switching to advanced therapies in chronic migraine.- **NICE guidance** prioritizes escalating to specialized treatments like Botulinum toxin type A rather than cycling through combinations of previously ineffective oral agents for refractory chronic migraine.*Greater occipital nerve blocks with corticosteroid and local anaesthetic*- While these may be used for **short-term relief** or as a bridge therapy, they are not typically recommended by **NICE** as a standard long-term **preventive strategy** for chronic migraine in this context.- They are more commonly utilized in the management of **cluster headaches**, specific neuralgias, or for acute exacerbations rather than as a primary long-term preventive for refractory chronic migraine after multiple drug failures.*CGRP monoclonal antibody therapy (erenumab, fremanezumab, or galcanezumab)*- Although these are indicated for chronic migraine after 3 drug failures, in the UK, they are traditionally positioned by **NICE technology appraisals** as an alternative or subsequent option to **Botulinum toxin type A**, depending on local commissioning policies and patient preference.- For this specific patient scenario with refractory chronic migraine after three oral preventives, **Botulinum toxin type A** is generally the established first-line injectable treatment in the pathway.*Sodium valproate 500 mg twice daily*- **Sodium valproate** is not recommended by **NICE** as a routine preventive treatment for migraine due to its side-effect profile, particularly **teratogenicity**, and the availability of more effective licensed alternatives.- Its use is strictly regulated, especially in patients of **childbearing potential**, and it does not precede specialized injectable therapies like Botulinum toxin type A in the current treatment algorithm.
Question 96: A 23-year-old woman presents to the Emergency Department following a witnessed seizure at work. Her colleague describes that she suddenly stopped talking mid-conversation, stared blankly ahead for about 30 seconds while smacking her lips, then seemed confused for a few minutes afterwards. She has no memory of the event. She has never had a seizure before and has no significant medical history. Neurological examination is now normal. What type of seizure has she most likely experienced?
- A. Generalised tonic-clonic seizure
- B. Absence seizure
- C. Focal seizure with impaired awareness (Correct Answer)
- D. Myoclonic seizure
- E. Atonic seizure
Explanation: ***Focal seizure with impaired awareness***- The sudden cessation of activity, blank stare, **lip smacking (automatism)**, 30-second duration, and subsequent **post-ictal confusion** with **amnesia** are classic features.- These events arise from a specific brain area, most commonly the **temporal lobe**, and involve a transient alteration or loss of consciousness. *Generalised tonic-clonic seizure*- These seizures involve an initial **tonic phase** (stiffening) followed by a **clonic phase** (rhythmic jerking) of all extremities.- They are characterized by a complete **loss of consciousness** and often result in injury, **tongue biting**, or incontinence, none of which were described. *Absence seizure*- Characterized by very brief episodes (typically 5-10 seconds) of **staring blankly** without automatisms, followed by immediate and full recovery.- These usually occur without **post-ictal confusion** or the complex motor automatisms like lip smacking observed in the patient. *Myoclonic seizure*- These are sudden, brief, shock-like **muscle jerks** that can affect one part of the body or be generalized.- They do not typically involve a **prolonged staring spell**, **impaired awareness**, or significant **post-ictal confusion**. *Atonic seizure*- Also known as "drop attacks," these involve an abrupt, sudden **loss of muscle tone**, causing the person to fall to the ground.- They do not present with **automatisms**, a prolonged staring period, or the post-ictal confusion described in this case.
Question 97: Which clinical feature is part of the diagnostic criteria for dementia with Lewy bodies but NOT typically seen in early Alzheimer's disease?
- A. Progressive episodic memory impairment
- B. Recurrent complex visual hallucinations (Correct Answer)
- C. Language dysfunction and word-finding difficulties
- D. Impaired visuospatial skills
- E. Difficulty with executive functions
Explanation: ***Recurrent complex visual hallucinations***- These are a **core clinical feature** of Dementia with Lewy Bodies (DLB), typically described as well-formed, detailed, and appearing early in the disease process.- In contrast, visual hallucinations are usually a **late-stage manifestation** in Alzheimer’s Disease and are not part of its early diagnostic profile.*Progressive episodic memory impairment*- This is the **hallmark presenting symptom** of early Alzheimer’s disease due to early involvement of the **hippocampus**.- While memory loss occurs in DLB, it is often less prominent initially than **deficits in attention** or executive function.*Language dysfunction and word-finding difficulties*- These features, often referred to as **aphasia**, are common early markers of Alzheimer's disease as the pathology spreads to cortical areas.- While language may be affected in DLB, it is not a **discriminating core feature** used to differentiate it from other dementias.*Impaired visuospatial skills*- Visuospatial deficits occur in both conditions, but they tend to be **disproportionately severe** and earlier in DLB compared to early Alzheimer's.- Because this feature overlaps significantly in both diseases, it is not a reliable exclusive **diagnostic differentiator** for DLB over Alzheimer's.*Difficulty with executive functions*- Executive dysfunction (e.g., poor planning or multitasking) is a **non-specific finding** that can be seen in both DLB and Alzheimer's disease.- In DLB, these deficits are linked to **fluctuating cognition**, but they do not provide the specific diagnostic clarity that **hallucinations** offer.
Question 98: What is the mechanism of action of alteplase in acute ischaemic stroke?
- A. Directly inhibits platelet aggregation by blocking ADP receptors
- B. Blocks glycoprotein IIb/IIIa receptors on platelets
- C. Converts plasminogen to plasmin leading to fibrinolysis (Correct Answer)
- D. Inhibits thrombin and prevents fibrin formation
- E. Inhibits factor Xa in the coagulation cascade
Explanation: ***Converts plasminogen to plasmin leading to fibrinolysis*** - **Alteplase** is a recombinant **tissue plasminogen activator (tPA)** that restores blood flow by enzymatically dissolving existing thrombi. - It specifically catalyzes the conversion of **plasminogen** to **plasmin**, the enzyme responsible for degrading the **fibrin** meshwork of a clot, leading to **fibrinolysis**. *Directly inhibits platelet aggregation by blocking ADP receptors* - This mechanism describes **P2Y12 inhibitors** like **clopidogrel**, **prasugrel**, or **ticagrelor**. - These agents are **antiplatelet** drugs, primarily used to prevent new clot formation or growth, not to dissolve an established **fibrin clot** in acute stroke. *Blocks glycoprotein IIb/IIIa receptors on platelets* - This is the mechanism of action for **glycoprotein IIb/IIIa inhibitors** such as **abciximab**, **eptifibatide**, and **tirofiban**. - These drugs prevent the final common pathway of **platelet aggregation** by blocking the binding of **fibrinogen**, but they do not directly break down existing **fibrin clots**. *Inhibits thrombin and prevents fibrin formation* - This mechanism is characteristic of **anticoagulants** like **direct thrombin inhibitors** (e.g., **dabigatran**, argatroban) or the indirect action of **heparin** through **antithrombin**. - These agents are used to prevent new clot formation or propagation, but they are not **thrombolytics** designed to dissolve an existing **ischaemic stroke** clot. *Inhibits factor Xa in the coagulation cascade* - This is the primary mechanism for **direct oral anticoagulants (DOACs)** such as **rivaroxaban** and **apixaban**. - While they interfere with the **coagulation cascade** to prevent clot formation, they do not possess the **fibrinolytic** properties required for acute **reperfusion** in ischaemic stroke.
Question 99: A 67-year-old woman diagnosed with vascular dementia 2 years ago presents with her daughter who is concerned about capacity to manage finances. The patient has been making unusual purchases and has forgotten to pay bills. MMSE score is 20/30. She understands that she has memory problems but insists she can manage her money independently. She can describe what bills need to be paid but has repeatedly forgotten to pay them. What is the most appropriate approach to capacity assessment for financial decisions?
- A. She lacks capacity as she has a diagnosis of dementia and MMSE <24/30
- B. She has capacity as she can describe what needs to be done even though she forgets to do it
- C. Capacity should be assessed specifically for the financial decisions in question using the two-stage test (Correct Answer)
- D. Arrange formal neuropsychological testing before determining capacity
- E. She lacks capacity because she has failed the functional test by not paying bills
Explanation: ***Capacity should be assessed specifically for the financial decisions in question using the two-stage test***- Capacity is **decision-specific** and **time-specific**; a diagnosis of vascular dementia does not automatically imply a lack of capacity for all tasks.- The **two-stage test** involves identifying an impairment of the mind and then determining if that impairment prevents the patient from understanding, retaining, weighing, or communicating information regarding that **specific decision**.*She lacks capacity as she has a diagnosis of dementia and MMSE <24/30*- A diagnosis of dementia or a specific **MMSE score** cannot be used to automatically assume a lack of capacity under the **Mental Capacity Act**.- Capacity must be presumed unless proven otherwise through a functional assessment, regardless of **cognitive screening** results.*She has capacity as she can describe what needs to be done even though she forgets to do it*- Being able to describe a task does not equate to having capacity if the patient cannot **retain** the information or **use/weigh** it to execute the decision.- Memory impairment that leads to a consistent failure to follow through on financial obligations may indicate a lack of the **retention** element of the functional test.*Arrange formal neuropsychological testing before determining capacity*- While **neuropsychological testing** provides detailed data on cognitive deficits, it is an adjunct and not a prerequisite for a clinical capacity assessment.- The legal assessment of capacity is a **clinical judgment** based on the functional test and does not require specialized formal testing in most routine cases.*She lacks capacity because she has failed the functional test by not paying bills*- Making "unwise decisions" or failing to perform a task (like paying bills) is not, by itself, evidence of a **lack of capacity**.- The assessment must determine if the **impairment of mind** (vascular dementia) is the direct cause of the inability to understand, retain, or weigh the specific information required to manage finances.
Question 100: A 42-year-old woman presents with right-sided weakness that developed over 20 minutes and has now completely resolved after 45 minutes. She has no past medical history and takes no regular medications. Examination is entirely normal. Blood pressure is 128/78 mmHg, heart rate is 72 bpm and regular. ECG shows sinus rhythm. Blood glucose is 5.4 mmol/L. She is a non-smoker with BMI of 24. According to current guidelines, what is the most appropriate acute management?
- A. Reassure and arrange outpatient neurology review within 2 weeks
- B. Aspirin 300 mg and clopidogrel 300 mg, then arrange CT head within 7 days
- C. Admit for observation and start aspirin only after CT excludes haemorrhage
- D. Aspirin 300 mg immediately and arrange urgent specialist assessment within 24 hours (Correct Answer)
- E. Start aspirin 75 mg and arrange MRI brain as an outpatient
Explanation: ***Aspirin 300 mg immediately and arrange urgent specialist assessment within 24 hours***- This presentation is highly suggestive of a **Transient Ischaemic Attack (TIA)**, which requires immediate antiplatelet therapy. NICE guidelines recommend **aspirin 300 mg** stat for suspected TIA to reduce immediate stroke risk.- **Urgent specialist assessment** within **24 hours** is crucial for further risk stratification (e.g., ABCD2 score), investigation (e.g., carotid Doppler, brain imaging), and initiation of long-term secondary prevention.*Reassure and arrange outpatient neurology review within 2 weeks*- Reassurance is inappropriate given the significant **short-term stroke risk** following a TIA, especially within the first 48 hours.- Waiting **two weeks** for neurological review is dangerously delayed; guidelines mandate assessment within 24 hours for most TIAs.*Aspirin 300 mg and clopidogrel 300 mg, then arrange CT head within 7 days*- While **dual antiplatelet therapy (DAPT)** with aspirin and clopidogrel can be used after TIA, it's typically initiated after **specialist assessment** and confirmation of diagnosis, not as an initial emergency step before any imaging.- Waiting **7 days for a CT head** is too long; brain imaging (CT or MRI) and carotid imaging are required much sooner to identify the cause and guide further management.*Admit for observation and start aspirin only after CT excludes haemorrhage*- For suspected TIA, **aspirin** should be started immediately based on clinical grounds, without waiting for a CT scan to exclude haemorrhage, unless there are atypical features suggesting haemorrhage. The risk of delay outweighs the very low risk of haemorrhage in a TIA.- Formal **admission** is not universally required for all TIAs, especially those with low ABCD2 scores, but urgent assessment remains paramount.*Start aspirin 75 mg and arrange MRI brain as an outpatient*- The acute loading dose for aspirin in suspected TIA is **300 mg**, not the lower 75 mg maintenance dose, which would be insufficient for immediate antiplatelet effect.- Relying solely on an **outpatient MRI** without immediate clinical assessment and initiation of acute management delays critical intervention during the period of highest stroke risk.
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