Acute Ischemic Stroke (Lacunar Infarction)
This patient has suffered an acute lacunar stroke affecting the sensorimotor pathways, most likely in the posterior limb of the internal capsule or thalamus, given the sudden onset, distal-predominant motor and sensory loss without cortical signs, and his vascular risk factors of diabetes and hypertension. 1
Immediate Diagnostic Workup
Obtain urgent brain MRI with diffusion-weighted imaging (DWI) to confirm acute lacunar infarction and exclude hemorrhage, large vessel stroke, or other structural pathology. 2, 3
- If MRI is unavailable or contraindicated, perform non-contrast CT immediately to exclude hemorrhage, though CT may miss acute lacunar infarcts in the first 24-48 hours 1
- MRI with DWI is superior for detecting small subcortical infarcts and can differentiate acute from chronic lesions 3
- Look specifically for restricted diffusion in the posterior limb of internal capsule, corona radiata, or thalamus—the typical locations for pure sensorimotor stroke 4, 5
Understanding the Clinical Presentation
This presentation is consistent with a sensorimotor lacunar syndrome, one of the five classical lacunar syndromes that results from occlusion of a single penetrating artery supplying the deep brain structures 1:
- Distal-predominant weakness (power 0 below elbow, 4- at elbow and shoulder) indicates involvement of the corticospinal tract fibers that are somatotopically organized with hand representation more prominent 1
- Complete sensory loss in the same distribution suggests involvement of adjacent sensory pathways in the posterior limb of internal capsule or thalamus 4, 5
- Absence of cortical signs (no aphasia, neglect, visual field defects, or loss of consciousness) excludes cortical stroke 1
- Absence of cranial nerve involvement excludes brainstem stroke 5
- No radicular pain excludes peripheral nerve or spinal cord pathology 2
Critical Risk Factor Assessment
Diabetes and hypertension are the two most important risk factors for lacunar stroke, and their coexistence dramatically increases risk of small vessel disease. 1, 6, 7
- Hypertension is present in 70-80% of patients with lacunar infarction 1
- Diabetes accelerates small vessel arteriopathy and increases lacunar stroke risk 2-3 fold 6, 7
- The combination of diabetes and hypertension creates a synergistic effect on microvascular damage 6, 7
Differential Diagnosis to Exclude
While lacunar stroke is most likely, urgently exclude:
- Hemorrhagic stroke or hemorrhagic transformation - requires immediate CT or MRI to rule out, as management differs completely 2, 3
- Large vessel stroke with minimal cortical signs - MRI/MRA will identify this and may change acute management options 3
- Spinal cord pathology (cervical myelopathy, cord infarction) - the distal-predominant pattern and absence of sensory level makes this less likely, but MRI spine should be considered if brain imaging is negative 2
- Peripheral nerve pathology (brachial plexopathy, multiple mononeuropathies) - the sudden onset, complete sensory loss, and absence of radicular pain make this unlikely 2
Acute Management Protocol
If presenting within 4.5 hours of symptom onset and imaging excludes hemorrhage:
- Assess eligibility for intravenous thrombolysis (tPA) immediately 1
- Check blood glucose, as hypoglycemia can mimic stroke and must be corrected before thrombolysis 8
- Lacunar strokes are eligible for thrombolysis if within the time window, though benefit may be less pronounced than for large vessel occlusions 1
Immediate supportive care:
- Maintain blood pressure permissively elevated (allow up to 220/120 mmHg) in acute phase unless thrombolysis is planned 1
- Initiate antiplatelet therapy (aspirin 325 mg) within 24-48 hours if thrombolysis not given 1
- Monitor for neurological deterioration, as 20-40% of lacunar strokes show early progression 1
Secondary Prevention Strategy
Lacunar stroke requires aggressive long-term management despite appearing "minor," as it carries high risk of recurrence, dementia, and death in the long term. 1
- Blood pressure control to <130/80 mmHg is essential, as hypertension is the dominant modifiable risk factor 6, 7
- Start ACE inhibitor or ARB as first-line antihypertensive, given proven benefit in diabetic patients with vascular disease 6
- Initiate high-intensity statin therapy regardless of baseline cholesterol, as statins reduce recurrent stroke risk in lacunar patients 1
- Long-term antiplatelet therapy with aspirin or clopidogrel 1
- Optimize diabetes control with target HbA1c <7% to reduce microvascular progression 6
Prognosis and Follow-Up
Lacunar strokes show a paradoxical clinical course: 1
- Short-term prognosis is favorable - low early mortality (2-3%) and good functional recovery in 60-70% of patients 1
- Long-term prognosis is concerning - 5-year stroke recurrence rate of 25-30%, increased dementia risk, and progressive white matter disease 1
- Asymptomatic progression of small vessel disease is typical, requiring ongoing monitoring with repeat imaging at 3-6 months 1
Critical Pitfalls to Avoid
- Do not dismiss this as a "minor stroke" - lacunar infarcts require the same aggressive secondary prevention as large vessel strokes due to high long-term morbidity 1
- Do not delay neuroimaging - acute stroke protocols require imaging within 25 minutes of arrival to assess thrombolysis eligibility 2, 3
- Do not assume the diagnosis without imaging - 5-10% of suspected lacunar strokes have alternative diagnoses on MRI 3
- Do not undertreated blood pressure - achieving target <130/80 mmHg is critical but often requires 2-3 antihypertensive agents 6