In an older patient with vascular risk factors who has an MRI showing a subacute infarct in the right thalamus and right basal ganglia, Fazekas grade I cerebral microangiopathy and minimal hemispheric atrophy, what is the likely diagnosis and what acute and secondary stroke‑prevention management should be initiated?

Subacute Lacunar Infarct with Cerebral Small Vessel Disease

This patient has suffered a subacute lacunar infarct in the right thalamus and basal ganglia, with underlying cerebral small vessel disease (Fazekas grade I microangiopathy), and requires immediate initiation of aggressive blood pressure control targeting <130/80 mmHg, antiplatelet therapy with aspirin, high-intensity statin therapy, and comprehensive vascular risk factor modification to prevent recurrent stroke and cognitive decline. 1, 2, 3

Diagnosis

The MRI findings confirm a subacute lacunar infarct affecting the right thalamus and basal ganglia, representing occlusion of a penetrating artery supplying these deep brain structures. 4, 5 The presence of Fazekas grade I white matter changes and minimal atrophy indicates underlying cerebral small vessel disease (cerebral microangiopathy), which is the pathophysiological substrate causing both the acute infarct and chronic white matter injury. 2, 6, 7

Key Diagnostic Features

• Acute symptomatic lesions in the thalamus and basal ganglia affect major motor and sensory tracts, which explains why these particular small vessel lesions presented with acute stroke symptoms rather than remaining clinically silent. 5
• Fazekas grade I microangiopathy represents early chronic microvascular ischemic changes with myelin loss, axonal damage, and gliosis in deep white matter regions. 2
• The combination of acute lacunar infarct plus white matter hyperintensities confirms the diagnosis of cerebral small vessel disease, most commonly caused by lipohyalinosis from chronic hypertension and diabetes. 6, 7

Acute Management

Immediate Antiplatelet Therapy

• Initiate aspirin 75-81 mg daily immediately for secondary stroke prevention, as this is first-line antiplatelet therapy after lacunar infarct. 3

Blood Pressure Management (Critical Priority)

• Target systolic blood pressure <130/80 mmHg using diuretics and/or an ACE inhibitor as the optimal regimen for preventing recurrent stroke and cardiovascular events. 3
• Patients with lacunar stroke treated to SBP <130 mmHg versus 130-140 mmHg experience 63% fewer intracerebral hemorrhages, making aggressive BP control essential. 3
• The relationship between blood pressure and vascular cognitive impairment is linear down to at least 100/70 mmHg, so lower pressures continue to provide benefit. 2

Lipid Management

• Initiate high-intensity statin therapy (e.g., atorvastatin 40-80 mg daily) targeting LDL cholesterol <100 mg/dL, as statin therapy is recommended for all patients with cerebrovascular disease unless contraindicated. 3, 8

Secondary Prevention Strategy

Comprehensive Vascular Risk Factor Control

Blood Pressure:

• Intensive systolic blood pressure control to <120 mmHg in patients >50 years with baseline systolic >130 mmHg reduces mortality, cerebrovascular events, and dementia/cognitive impairment by 0.4-0.7% absolute risk reduction per year. 2
• Hypertension is the strongest modifiable risk factor for progression of cerebral small vessel disease and poor cognitive performance. 2

Diabetes Management:

• Target HbA1c <7% with multifactorial intensive treatment addressing hyperglycemia, hypertension, dyslipidemia, and microalbuminuria, as diabetes increases vascular cognitive impairment risk by 20-40%. 2, 3

Lifestyle Modifications:

• Immediate smoking cessation is mandatory, as tobacco use increases intracerebral hemorrhage risk and stroke risk returns to baseline within 5 years of quitting. 2, 3
• Limit alcohol intake to ≤2 drinks per day, as frequent alcohol use elevates blood pressure and hemorrhage risk. 3
• Recommend a diet low in saturated fat and cholesterol. 3

Cognitive Screening and Monitoring

• Perform formal cognitive testing focusing on executive function and processing speed, as these domains are most affected by white matter changes and lacunar infarcts. 2, 3
• The prevalence of cognitive impairment is approximately 20% after a first stroke and exceeds one-third with recurrent strokes. 3
• Screen systematically for neuropsychiatric symptoms including depression, anxiety, and apathy using validated tools, as these frequently coexist with cerebral small vessel disease. 2

Prognostic Considerations

• The highest recurrence risk occurs in the first year, making immediate and aggressive risk factor modification essential rather than delaying intervention. 3
• Age, vascular risk factors, high nocturnal blood pressure, and severity of cerebral small vessel disease at onset have significant prognostic implications for death (mainly cardiovascular), recurrent stroke, and cognitive decline. 4
• The presence of moderate-to-severe white matter hyperintensities indicates diffuse arteriopathy and is independently associated with hypertension and impaired renal function. 3

Recommended Diagnostic Workup

Neuroimaging

• The initial MRI has already characterized the infarct and detected white matter lesion burden, providing important prognostic information. 3
• Ensure the MRI protocol included diffusion-weighted imaging (DWI), FLAIR, and susceptibility-weighted imaging (SWI) or gradient-echo (GRE) to comprehensively assess for acute ischemia, white matter hyperintensities, and microbleeds. 2

Additional Testing

• Check estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio, as impaired renal function independently predicts worse outcomes and indicates systemic small vessel disease. 3
• Consider vascular imaging (CTA or MRA) if there is clinical suspicion for large vessel stenosis, though this is not routinely required for typical lacunar infarcts. 1

Long-term Management and Follow-up

• Schedule periodic visits (at minimum annually) for monitoring blood pressure control, medication adherence, and cognitive function. 3
• Repeat brain MRI every 2-3 years or sooner if clinical decline occurs to assess progression of white matter disease and detect new silent infarcts. 2
• Consider referral to cognitive neurology if cognitive decline is detected on screening. 2

Critical Pitfalls to Avoid

• Do not delay risk factor modification while awaiting symptom progression; proactive, aggressive control of blood pressure and other vascular risks is essential for preventing further brain injury, as the highest recurrence risk is in the first year. 2, 3
• Do not assume all cognitive deficits are solely due to vascular pathology; mixed Alzheimer's disease pathology is common in older adults with cerebral small vessel disease and should be considered. 2
• Do not underestimate the long-term prognosis; while lacunar infarcts were historically regarded as benign, recent studies show increased risk of death (mainly cardiovascular), recurrent stroke, and dementia several years after the initial event. 4