Lenticulostriate Lesion Symptoms
Lenticulostriate lesions primarily cause motor deficits, sensory deficits, and cognitive dysfunction, with the severity and specific manifestations depending on lesion size and whether there is associated cortical involvement. 1
Core Clinical Manifestations
Motor and Sensory Deficits
- Hemiparesis is the most common motor manifestation, with severity dependent on damage to the upper part of the posterior limb of the internal capsule 1
- Hemisensory loss frequently accompanies motor deficits, forming part of the classic "HHH" syndrome (hemiparesis, hemihypesthesia, hemianopsia) when lesions are larger 2
- Isolated motor or sensory deficits can occur with smaller, more distal lesions 3
Cognitive and Language Impairments
- Mild aphasia may occur with pure lenticulostriate infarcts, characterized by prominent expressive and lexicosemantic task impairments 4
- More severe aphasia patterns (such as Broca's aphasia) only occur when there is associated cortical involvement not visible on CT but detectable on MRI 4
- Cognitive dysfunction is a recognized feature, though specific patterns depend on lesion laterality and extent 1
Lesion Size Determines Clinical Heterogeneity
Distal and Small Lesions (ds-SSSI)
- Most often associated with severe white matter hyperintensities as the underlying pathology 3
- Tend to produce milder, more focal deficits 3
Distal and Large Lesions (dl-SSSI)
- Higher rate of concurrent atherosclerotic disease including coronary heart disease 3
- More extensive neurological deficits due to larger territory involvement 3
Critical Distinction: Pure vs. Mixed Lesions
The presence or absence of cortical involvement is the most critical factor determining symptom severity and complexity. 4
Pure Lenticulostriate Infarcts (MRI-confirmed)
- Mild aphasia with expressive and lexicosemantic impairments 4
- Motor and sensory deficits proportional to lesion size 1
- Absence of hemineglect, gestural apraxia, and anosognosia 4
Mixed Lesions (with cortical involvement)
Important Clinical Pitfalls
- CT scans may miss associated cortical lesions that are visible on MRI, leading to underestimation of expected deficits 4
- Do not assume a lacunar syndrome based solely on CT findings; MRI is superior for detecting mixed lesions 4
- The concept of lacunar infarctions relating purely to lipohyalinosis is often proposed without adequate evidence; cardiac embolism is the principal mechanism 1
- Lenticulostriate arteries are terminal vessels without anastomoses, making them susceptible to hemorrhagic transformation 1
Functional Prognosis
- Functional outcome (measured by Barthel Index, length of stay, nursing home placement) does not differ significantly between cortical, subcortical, or mixed lesion locations when patients present with HHH deficits 2
- Prognosis depends primarily on the intensity of damage to the upper part of the posterior limb of the internal capsule rather than whether the lesion is purely subcortical or mixed 1
- Recovery patterns are similar across anatomic groups when initial deficit severity is comparable 2