What are the typical clinical manifestations and acute/secondary management for a lacunar infarct confined to the left external capsule in an older adult with hypertension and diabetes?

Lacunar Infarct of the Left External Capsule

Clinical Manifestations

A lacunar infarct confined to the left external capsule typically presents with pure motor hemiparesis affecting the right side of the body, without cortical signs such as aphasia, visual field defects, or neglect. 1

The external capsule contains motor fibers, and its involvement produces:

• Contralateral motor weakness (right-sided weakness from left external capsule lesion) without sensory deficits 1, 2
• Absence of cortical signs - no aphasia, despite left hemisphere involvement, which is the defining characteristic distinguishing lacunar syndromes from cortical strokes 1
• Possible ataxic hemiparesis if adjacent structures are involved 2, 3

The clinical presentation is paradoxical: favorable short-term prognosis but concerning long-term outcomes, with 85% survival at 2 years (highest among stroke subtypes) but increased risk of recurrent stroke, vascular death (~2% annually), and cognitive decline (20% after first lacunar stroke, >33% after recurrent events) 1, 4, 2, 5.

Acute Management

Immediate Assessment and Monitoring

Admit to an intensive care or stroke unit with neuromonitoring capabilities for the first 12-24 hours, as this is the highest-risk period for neurological deterioration. 6

• Perform hourly neurological assessments using Glasgow Coma Scale for the first 12-24 hours, as GCS changes within initial 12 hours predict worse 90-day functional outcomes 6
• Obtain non-contrast CT head immediately as first-line imaging, though it may be normal in up to 25% of acute lacunar infarcts initially 6
• Follow with MRI with DWI/ADC sequences within 24-48 hours if not performed emergently, as MRI is superior to CT for detecting acute lacunar infarcts 6

Thrombolytic Therapy Eligibility

Standard acute stroke protocols apply, including consideration for IV tissue plasminogen activator (tPA) if presenting within 4.5 hours 7. However, note that:

• Lacunar stroke patients have similar safety profiles with tPA compared to other stroke subtypes 7
• Symptomatic intracranial hemorrhage rates are approximately 5-7% 7
• Diabetes (present in 44.4% of lacunar infarct cases) does not contraindicate tPA and shows functional benefit 7, 1

Blood Pressure Management in Acute Phase

Do not aggressively lower blood pressure in the first 24 hours unless systolic BP >220 mmHg or diastolic >120 mmHg, or if thrombolytic therapy is planned. 7

• Small subsets of patients with large perfusion deficits may benefit from modest (10-20%) pharmacological elevation in systemic blood pressure, though this is not standard practice 7
• After the initial 24 hours, restart or initiate antihypertensive therapy targeting <130/80 mmHg 4

Diagnostic Workup

Complete the following within 24-48 hours 6:

• EKG, complete blood count, serum electrolytes, creatinine, fasting glucose, and lipid panel 6
• Transthoracic echocardiogram (TTE) to screen for structural heart disease and reduced ejection fraction 1
• Doppler ultrasonography of neck vessels to exclude >50% stenosis of relevant arteries, as this would reclassify the stroke as non-lacunar 1, 6
• Consider transcranial Doppler for cerebral vessel patency assessment 6

Critical pitfall: Do not assume a normal initial CT excludes significant infarction - up to 25% may be normal initially, necessitating MRI follow-up 6.

Secondary Prevention and Long-Term Management

Blood Pressure Control (Highest Priority)

Initiate combination therapy with diuretics plus ACE inhibitors targeting <130/80 mmHg, as hypertension is the primary modifiable risk factor for lacunar stroke. 4

• The PROGRESS trial demonstrated that perindopril plus indapamide reduced recurrent intracerebral hemorrhage by 63% (HR 0.37) 4
• Intensive BP lowering to systolic <130 mmHg reduces intracerebral hemorrhage risk by 60% (HR 0.37) in small vessel disease patients 4
• Target even more aggressive control (<130/80 mmHg) in diabetic patients, as diabetes is a strong determinant for multiple lacunar infarcts 4
• Reduce dietary salt to <2000 mg daily 4

Antiplatelet Therapy

Initiate aspirin 75-100 mg daily for secondary prevention. 4

• Antiplatelet drugs are the standard for lacunar infarct secondary prevention 1, 2
• Anticoagulation with heparin or low-molecular-weight heparins showed no benefit and increased bleeding complications in acute ischemic stroke trials, including lacunar subtypes 7

Lipid Management

Start statin therapy immediately regardless of baseline cholesterol levels (Class I, Level of Evidence A). 4

• The SPARCL trial demonstrated that lacunar infarct patients had absolute rates of recurrent stroke and major cardiovascular events as high as large-vessel atherothrombotic subgroups 4
• Statin therapy provides benefit across all ischemic stroke subtypes, including small-vessel disease (HR 0.85,95% CI 0.64-1.12) 1

Diabetes Management

Target HbA1c <7% with tight glycemic control, as diabetes is present in 44.4% of lacunar infarct cases and is an independent predictor of recurrent stroke. 1, 4

Monitoring and Follow-up

Schedule annual clinical follow-up to assess symptoms, functional status, medication adherence, and kidney function. 4

• Monitor for cognitive decline, as vascular cognitive impairment develops in 20% after first lacunar stroke and >33% after recurrent events 1
• Screen for silent lacunar infarcts (present in 10-30% of patients), which contribute to progressive cognitive decline 1
• Assess for chronic kidney disease, which increases recurrent stroke risk by 50% 4
• White matter hyperintensities are present in almost all older adults with hypertension and lacunar disease, though severity varies 1

Key Management Pitfall

Do not regard lacunar infarction as a benign disorder - while short-term mortality is low (3.3% at 90 days), long-term cardiovascular risk approaches 2% annually for MI and vascular death, with recurrent stroke rates similar to other ischemic stroke types 1, 4, 2, 5.