Unilateral watershed infarction

Case contributed by Samah Al-Obaidi
Diagnosis certain


Acute history of dysphasia. Known case of hypertension.

Patient Data

Age: 55 years
Gender: Male

Multiplanar brain MRI revealed scattered T2/FLAIR hyperintense foci in the left cerebral hemisphere distributed in the centrum semiovale, subcortical white matter, insular cortex and periventricular region, showing diffusion restriction.

T2WI revealed absent signal void in the petrous and cavernous portions of the left ICA which is confirmed by the cerebral MRA study.

Diffuse brain atrophy.

Infratentorial structures are unremarkable.

Signs of chronic maxillary sinusitis. 

Case Discussion

Watershed infarcts occur at the border zones between major cerebral arterial territories as a result of hypoperfusion.

There are two patterns of border zone infarcts:

  1. Cortical border zone infarctions CWS
    Infarctions of the cortex and adjacent subcortical white matter located at the border zone of ACA/MCA and MCA/PCA. It may be embolic if isolated and less frequently due to hemodynamic compromise.

  2. Internal border zone infarctions IWS
    Infarctions of the deep white matter of the centrum semiovale and corona radiata at the border zone between lenticulostriate perforators and the deep penetrating cortical branches of the MCA or at the border zone of deep white matter branches of the MCA and the ACA. These are caused mainly by arterial stenosis or occlusion.

  • Bilateral watershed infarcts happen mainly due to severe systemic hypotensive crises.

  • On the basis of their radiological appearance, IWS infarcts have been divided into confluent and partial infarcts. Confluent infarcts correspond to large cigar-shaped infarcts alongside the lateral ventricle, whereas partial IWS infarcts may appear either as a single lesion or in a chain-like (or “rosary-like”) pattern in the CSO (centrum semiovale). However, partial IWS infarcts sometimes are difficult to distinguish from lacunar, medullary, or striatocapsular infarcts, as well as from leukoaraiosis. The latter, however, affects in a diffuse way the periventricular white matter bilaterally as it represents chronic diffuse white matter ischemia. Partial IWS infarct and leukoaraiosis may, however, coexist, particularly in the elderly. Regarding medullary infarcts, they correspond to small, immediately subcortical infarcts caused by occlusion of medullary arteries arising from the pial plexus. They are generally smaller and more superficial than partial IWS infarcts, but IWS and white matter medullary infarcts have been sometimes lumped together as so-called subcortical white matter infarcts because of the difficulty in distinguishing between them.

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