Striatocapsular infarct

Striatocapsular infarcts, also known as basal ganglionic capsular infarcts or lenticulostriate infarcts, are uncommon infarcts involving the caudate nucleusputamen, and anterior limb of the internal capsule without any involvement of the cortex, caused by either a complete or partial proximal MCA occlusion.

Striatocapsular infarcts are uncommon, but also likely under-recognized, with one landmark series reporting 11 cases out of a stroke registry containing 1,600 patients 1.

Risk factors are thought to be more akin with those of thromboembolic cortical ischemic stroke rather than those of lacunar infarction, with hypertension, smoking, hypercholesterolemia, carotid stenosis, and atrial fibrillation being important risk factors 2-4.

Although there is a variable clinical presentation, classically patients with striatocapsular infarcts, in the acute phase, exhibit both cortical (e.g. aphasia, sensory neglect or extinction, apraxia) and subcortical (e.g. upper limb hemiparesis, dysarthria) neurological signs, despite the cortex not being directly involved in the infarction 1-4. The underlying mechanisms for these cortical signs being present in this subcortical striatocapsular infarction are unfortunately not well understood, but are thought to be due to decreased, but not absent, cortical blood flow, as discussed below 1-4.

Striatocapsular infarcts are defined as infarcts involving the caudate nucleusputamen, and anterior limb of the internal capsule that are at least 30 mm in length and 10 mm in width, without involvement of the overlying cerebral cortex 1-4. Although they occur in a similar area to lacunar infarcts, and have previously been described as ‘giant lacunes’ or ‘super lacunes’ 1, they are not only larger than Miller Fisher’s lacune definition 5, but also have a different pathogenesis and clinical phenotype 1-4.

These infarcts are caused by one of two mechanisms, most often thromboembolic in etiology 1-4:

However unlike cortical infarcts that may also be due to MCA occlusion, the overlying cortex is not involved in striatocapsular infarcts 1-4. This is likely either due to either collateral circulation via transcortical and transdural anastomoses, or the partial MCA occlusion still allowing the MCA to be patent enough to supply blood to the cortex 1-4.

Prominent features seen on cross-sectional imaging include:

  • infarction of the caudate nucleus, putamen, and anterior limb of the internal capsule 1-4
  • a characteristic ‘comma’ (or 'lentiform' or 'triangular') shape that is initially hypodense on CT or have increased diffusion signal on DWI 3,6,7 (see ischemic stroke for radiographical temporal progression of such lesions) 
  • no evidence of acute cortical ischemia 1-4, although there may be cortical hypoperfusion evident on perfusion studies 8
  • at least 30 mm in length and 10 mm in width in size 3, although it is not certain how widely accepted these specific measurements are

In addition to initial CT or MRI, it may be useful to perform CT angiography and carotid Doppler ultrasound, as well as other components of the stroke etiology work-up that would be normally performed for a cortical ischemic stroke of likely thromboembolic origin 7.

The term was coined by Peter Bladin and Samuel Berkovic, Australian neurologists, in their 1984 seminal paper 1.

Stroke and intracranial haemorrhage
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Article information

rID: 53883
Synonyms or Alternate Spellings:
  • Lenticulostriate infarct
  • Striatocapsular infraction
  • Basal ganglionic capsular infarct
  • Basal ganglionic capsular infarction
  • Basal ganglia capsular infarct
  • Basal ganglia capsular infarction
  • Basal ganglionic infarct
  • Basal ganglionic infarction
  • Lenticulostriate infarction

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Cases and figures

  • Figure 1: region of infarct (purple)
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  • Case 1: classic comma-shaped infarct
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  • Figure 2: anatomy of the basal ganglia
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  • Case 2: encephalomalacia
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  • Case 3
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  • Case 3: angiogram showing M1 occlusion
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