Interpretation of Tiny Hypodense Basal Ganglia Lesion on CT Six Days Post-Transient Neurological Event
This tiny hypodense area in the left basal ganglia most likely represents a chronic lacunar infarct rather than an acute ischemic lesion, given the absence of mass effect, the six-day delay in imaging, and the complete resolution of symptoms. 1
Key Imaging Features Favoring a Chronic Lesion
The lack of mass effect or surrounding edema strongly suggests a chronic lacunar infarct, because acute infarcts typically produce cytotoxic edema that leads to sulcal effacement and tissue swelling visible on CT. 1
Acute basal ganglia infarcts usually manifest as loss of gray-white differentiation and diffuse hypodensity of the caudate or lentiform nucleus, rather than as a tiny, well-demarcated hypodense focus. 1
Small areas of hypodensity in the basal ganglia are commonly observed in chronic vascular disease and represent old lacunar infarcts from small penetrating artery occlusion. 2
Why This is Unlikely to Represent the Acute Event
Non-contrast CT significantly underestimates acute ischemia in the first 6 hours after symptom onset, and the scan can appear completely normal in up to 25% of patients with acute cerebellar infarction. 1
The shortest delay for visibility of a hypodense area from acute infarction is approximately 17-19 hours, but at 27 hours densities may still be normal. 3
The clinical presentation—a brief 15-minute episode of altered orientation without motor or sensory deficits—is more consistent with a transient ischemic attack (TIA) than with a stroke that would produce a visible acute infarct. 1
Critical Diagnostic Considerations
This Finding Requires Further Vascular Workup
The presence of even a small chronic lacunar infarct indicates underlying cerebrovascular disease and warrants investigation for stroke risk factors and large vessel disease. 4
Small subcortical infarctions can result from either small-vessel disease (true lacunar infarction) or large-vessel disease (lacunar-like infarction), and distinguishing between these has significant management implications. 4
Patients with lacunar-like infarcts from large-vessel disease have a higher rate of progressive stroke compared to those with pure lacunar infarcts from small-vessel disease. 4
Recommended Next Steps
Obtain MRI with diffusion-weighted imaging (DWI) to definitively determine if there was any acute ischemia associated with the transient event, as DWI detects acute ischemia within minutes with high sensitivity and specificity. 1
Perform vascular imaging (CT angiography or MR angiography) to evaluate for large-vessel stenosis or occlusion that could explain the clinical event and guide secondary prevention strategies. 1
Almost all patients with acute ischemic lacunar syndromes have acute lesions on diffusion-weighted MRI within 3 days after stroke onset, so the absence of acute findings would confirm this is an incidental chronic lesion. 5
Common Pitfalls to Avoid
Do not assume the hypodense lesion explains the transient neurological event without advanced imaging, as CT has poor sensitivity for acute ischemia and this lesion likely predates the recent symptoms. 1
Do not dismiss the clinical event as insignificant simply because CT shows only a tiny chronic lesion—TIA is a medical emergency requiring urgent evaluation and secondary stroke prevention. 1
Remember that the basal ganglia are supplied by short, straight lenticulostriate arteries that transmit high blood pressure directly to end-arterioles, making this region particularly vulnerable to both acute and chronic small vessel disease. 6