UGHE Neurology Case - Complete Answers

Question 1: Top 3 Diagnoses and Why

Key point: CT head without contrast is the first-line imaging - it rules out hemorrhage immediately. If negative, the diagnosis shifts to ischemic stroke and time-to-treatment (tPA window) becomes urgent.

Question 2: Compare and Contrast Stroke Syndromes

Table A: Mechanism & Clinical Features

Table B: Presentation / Risk Factors / Associated Conditions (for the blank student table)

Question 3: Bell's Palsy vs. Stroke on Physical Exam

The Neuroanatomical Basis

• Stroke (Upper Motor Neuron lesion): Damages the cortex or internal capsule on one side. The forehead is spared because the intact opposite hemisphere can compensate. Weakness is confined to the lower face contralateral to the lesion. The patient can still wrinkle their forehead and raise their eyebrow on the weak side.
• Bell's Palsy (Lower Motor Neuron lesion): Damages CN VII (the facial nerve) itself, after it exits the facial nucleus. ALL branches are affected. Weakness involves the entire ipsilateral face - forehead AND lower face. The patient cannot raise the eyebrow or wrinkle the forehead on the affected side. Eye closure is also impaired (risk of corneal damage).

Quick Exam Comparison Table

Question 4: Artery Occlusion → Symptoms

4a. Behavior changes, left lower leg weakness → Anterior Cerebral Artery (ACA)

• The ACA supplies the medial surface of the frontal and parietal lobes (the "parasagittal" cortex) - this includes the motor and sensory homunculus for the leg.
• Left lower leg weakness → lesion in the right hemisphere (contralateral control).
• The frontal lobe is also the seat of executive function and personality; ACA strokes (especially bilateral or involving the anterior communicating artery) cause abulia, disinhibition, and personality/behavior changes.
• Arm and face are usually spared or minimally affected because they are represented more laterally (supplied by MCA).

4b. Vision loss → Posterior Cerebral Artery (PCA)

• The PCA supplies the occipital lobe (primary visual cortex, V1) and the inferior temporal lobe.
• Occlusion causes contralateral homonymous hemianopia (loss of the same half of the visual field in both eyes) because the visual cortex processes the contralateral visual field.
• It is the classic "stroke you can miss" - patients may not notice or just report "blurry vision." Always check visual fields formally.
• Source: Harrison's Principles, 22nd Ed.; Adams and Victor's Principles of Neurology: "occlusion of the posterior cerebral artery causes loss of vision in both eyes in the half of the retina on the opposite side."

4c. Headache, nystagmus, slurred speech → Basilar Artery (posterior circulation / vertebrobasilar)

• The basilar artery supplies the brainstem (pons, midbrain) and cerebellum via the AICA and PICA branches.
• Nystagmus - brainstem/cerebellar vestibular pathways.
• Dysarthria (slurred speech) - cranial nerve nuclei in the pons and cerebellar connections.
• Headache - common in posterior circulation strokes; severe headache + posterior signs should raise suspicion for basilar artery stroke or vertebral artery dissection.
• Additional posterior circulation signs: vertigo, diplopia, dysphagia, ataxia, crossed deficits (ipsilateral face + contralateral body), "locked-in syndrome" with basilar occlusion.

4d. Right facial droop, right arm weakness → Left Middle Cerebral Artery (MCA)

• The MCA supplies the lateral cortex including: motor strip (face, arm, hand > leg), sensory strip, and in the dominant hemisphere - language areas (Broca's area anteriorly, Wernicke's area posteriorly).
• Motor control is contralateral - so RIGHT face and arm weakness = LEFT hemisphere lesion.
• The face and arm are affected more than the leg because they are represented laterally on the cortex (MCA territory), while the leg is medial (ACA territory).
• This is exactly the presentation of the patient in this case: left MCA stroke causing right-sided face + arm weakness and aphasia.

Summary Table - Question 4

Labs and Tests When Symptoms Have Resolved: TIA Workup

Why the Workup Still Matters

1. Confirm it was vascular (rule out mimics)
2. Find the cause (cardiac? large vessel? small vessel? hematologic?)
3. Stratify risk and decide on admission vs. outpatient
4. Start secondary prevention immediately

The Full Workup

IMAGING (most urgent)

Key point from Tintinalli's: "positive findings on DWI have predictive value for subsequent early stroke risk in TIA patients, as does cervical vascular imaging by MRA."

CARDIAC WORKUP (critical in this patient - she has an irregular heart rhythm)

LABORATORY TESTS

• Hypercoagulability panel: Factor V Leiden, Prothrombin G20210A, protein C/S, antithrombin III, antiphospholipid antibodies (lupus anticoagulant, anticardiolipin)
• ESR/CRP (vasculitis)
• Blood cultures (if endocarditis suspected)
• Urine toxicology (cocaine in young patients)
• Sickle cell screen (if appropriate population)

ABCD2 Score - Risk Stratification Tool

Important caveat: The American College of Emergency Physicians (2016 guidelines) stated that ABCD2 alone should NOT be used to decide safe discharge - it is inadequate as a standalone risk stratification tool. Most high-risk TIA patients should be admitted.

Disposition Decision for This Patient

• ABCD2 score ≥ 4 (high risk)
• Irregular heart rhythm (likely AF) = high-risk embolic source
• Hypertension (chronic, inadequately controlled: BP 155/89)
• Symptoms lasted ~1 hour with both motor AND speech involvement
• Age 72

Labs and Tests When Symptoms Have Resolved: TIA Workup

What is happening now?

• ~10% stroke risk within 90 days after TIA
• 50% of those strokes occur within 48 hours of TIA onset
• 1 in 3 untreated TIA patients will have a stroke within 5 years

Imaging

From Bradley and Daroff's Neurology: "Patients with TIA and DW-MRI lesions are at greater early risk for experiencing a subsequent stroke than patients without a lesion."

Cardiac Workup

Blood Tests

ABCD2 Score - How Does This Patient Score?

Important caveat: The American College of Emergency Physicians (2016) states ABCD2 alone should not be used to discharge patients. It is a helpful tool but cannot independently confirm safety for outpatient management.

Disposition: Admit or Discharge?

1. ABCD2 score of 6 (high risk)
2. Likely atrial fibrillation (irregular heart rhythm = high-risk embolic source)
3. Symptoms lasted ~1 hour with both speech AND motor deficits
4. Age 72, uncontrolled hypertension
5. Needs urgent DWI-MRI, cardiac monitoring, and echocardiogram that cannot wait for outpatient

Immediate Treatment While Being Worked Up

• Dual antiplatelet therapy (aspirin + clopidogrel): start immediately in non-cardioembolic TIA. Pooled data from the POINT and CHANCE trials show dual therapy reduces major ischemic events vs. aspirin alone, with the greatest benefit in the first 21 days.
• If AF confirmed → switch to oral anticoagulation (DOAC preferred over warfarin) rather than antiplatelets - this is the most impactful secondary prevention step for cardioembolic TIA.
• High-intensity statin (e.g. atorvastatin 40-80 mg) regardless of baseline LDL.
• Blood pressure management: do not aggressively lower acutely; optimize long-term control.
• Carotid endarterectomy if ipsilateral carotid stenosis ≥70% found on imaging - most beneficial within 2 weeks of TIA.