What is acute thalamic lacunar infarction?

Acute Thalamic Lacunar Infarction

Acute thalamic lacunar infarction is a small subcortical stroke (<1.5 cm diameter) occurring in the thalamus, caused primarily by small vessel disease affecting the penetrating arteries that supply the deep brain structures. 1, 2

Definition and Pathophysiology

• Lacunar infarcts are subcortical strokes measuring <1.5 cm in diameter on CT or MRI without evidence of cortical involvement, primarily caused by small vessel disease affecting penetrating arteries deep in the brain. 1, 2

• The pathophysiology differs from other stroke subtypes: lacunar infarcts are generally not caused by atherosclerosis but rather by a distinct arteriopathy of small vessels, often related to chronic hypertension or diabetes. 2, 3

• When specifically involving the thalamus, these infarcts affect the territory of thalamic perforating arteries, with the inferolateral artery being the most commonly implicated arterial territory (85.2% of cases). 4

Clinical Presentation

Patients with acute thalamic lacunar infarction typically present with sensory disturbances (most common) or motor symptoms, rather than the complete Dejerine-Roussy syndrome. 4, 5

Common presenting symptoms include:

• Sensory disturbances affecting the contralateral side (present in the vast majority of cases) 5
• Limb weakness or pure motor hemiparesis 4
• Hemiataxia (less common) 5
• Rare manifestations include involuntary movements such as hemi-chorea 6

The clinical presentation depends on which thalamic nuclei are affected:

• Prominent sensory symptoms occur when the pulvinar and ventral posterior thalamic nucleus are involved 5
• Motor symptoms predominate when adjacent nuclei such as ventral lateral or lateral posterior nuclei are affected 5

Diagnostic Approach

Diagnosis requires neuroimaging (CT or MRI) showing a small (<1.5 cm) subcortical infarct in the thalamus, with MRI being more sensitive than CT for detecting acute lacunar infarcts. 7, 1, 2

• MRI with diffusion-weighted imaging (DWI) is the preferred modality for detecting acute thalamic lacunar infarction, as it can identify small acute ischemic lesions that may be missed on CT. 7, 4, 6

• CT head without contrast can detect stroke mimics and is an option for initial imaging, though it is relatively insensitive for acute small infarcts. 7

• Potential sources of cardioembolism and ipsilateral large-artery stenosis should be excluded to confirm the diagnosis of lacunar stroke rather than other stroke subtypes. 1, 2

• SPECT imaging may demonstrate perfusional asymmetry in the affected thalamus, which can correlate with clinical symptoms. 6

Risk Factors and Etiology

Hypertension is the predominant risk factor, present in approximately 88.9% of patients with pure thalamic infarcts. 4

Additional risk factors include:

• Diabetes mellitus (44.4% of cases) 4
• Hyperlipidemia (37% of cases) 4
• Smoking history (particularly in men: 60%) 4
• Excessive alcohol consumption (particularly in men: 46.7%) 4

Based on TOAST classification, the vast majority (85.2%) of pure thalamic infarcts are due to small vessel occlusion (SVO), with only rare cases attributable to large artery atherosclerosis. 4

Prognosis and Long-term Outcomes

Among stroke subtypes, patients with small-artery (lacunar) occlusion have the highest survival rate at 85% at 2 years, making this the most favorable stroke subtype prognostically. 1, 2, 3

Important prognostic considerations:

• Most patients experience good functional recovery when risk factors are controlled 4
• Thalamic pain syndrome develops in a significant proportion of patients (approximately 59% in one series), which can severely interfere with social activities in some cases 5
• Stroke recurrence occurs in approximately 26% of patients during long-term follow-up 4
• Cognitive deficits may persist, including problems with attention, concentration, executive function, and memory retrieval, particularly with right thalamic lesions affecting intralaminar nuclei 8
• Deaths are more commonly related to other comorbidities (cancer, multi-organ failure) rather than the stroke itself in elderly patients 4

Management

Standard acute stroke management protocols apply, with antiplatelet drugs used for secondary prevention. 1

Critical management considerations:

• Aggressive control of vascular risk factors (particularly hypertension and diabetes) is essential to prevent recurrence 4
• Long-term monitoring for development of thalamic pain syndrome is warranted, as this complication can significantly impact quality of life 5