Peer-reviewed veterinary case report
Signs and diagnosis of striatocapsular brain strokes in six dogs
By Rossmeisl, John H et al.·Published in Veterinary ophthalmology·2007·Department of Small Animal Clinical Sciences, United States·View original on PubMed →
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Original publication title: Presumed and confirmed striatocapsular brain infarctions in six dogs.
- Species:
- dog
Plain-English summary
A group of six dogs experienced sudden vision problems and weakness on one side of their bodies due to brain infarctions, which are areas of dead tissue caused by a lack of blood flow. The dogs showed signs like visual field deficits and difficulty with coordination. While some dogs had normal CT scans, MRI scans revealed brain lesions consistent with these infarctions. After treatment, the dogs showed improvements in behavior and movement, but some continued to have lingering sensory issues.
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Abstract
OBJECTIVE: To describe the clinical and diagnostic features of the canine sensorimotor syndrome caused by striatocapsular brain infarctions (SCI). ANIMALS STUDIED: Six dogs with diagnostic imaging or postmortem evidence of SCI. PROCEDURES: Medical records of dogs with SCI were retrospectively reviewed and the signalment, history, clinical signs, antemortem clinicopathologic test results, diagnostic imaging findings, case outcomes, and pathologic findings recorded. RESULTS: All dogs had an acute onset of nonprogressive homonymous visual field deficits and contralateral general proprioceptive (GP) deficits. Contralateral hemiparesis and facial hypalgesia were noted in 5/6 dogs. CT scans were normal in 2/4 dogs, and revealed poorly defined hypoattenuating lesions in the subcortical white matter in two dogs. MRI exams were performed in 5/6 dogs and revealed unilateral, variably sized, striatocapsular lesions consistent with nonhemorrhagic infarctions. Diagnostic imaging (6/6) and postmortem examinations (2/6) suggested that SCI resulted from lesions in the vascular territories of the rostral choriodal (6/6) and lenticulostriate arteries (2/6). Diseases predisposing to infarction were not identified in 5/6 dogs. Improvements in mentation, behavior, proprioceptive deficits, and hemiparesis were seen in surviving dogs, but persistent, symptomatic sensory deficits were noted during the follow-up period. CONCLUSIONS: SCI should be considered as a differential diagnosis for dogs with acute onset, nonprogressive homonymous hemianopia, contralateral GP deficits or hemiparesis, and facial hypalgesia. MRI is the preferred modality for the antemortem imaging diagnosis of SCI. Although partial recovery occurred in all surviving dogs, visual and facial sensory disturbances persisted.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/17204125/