Ischemic Stroke Involving a Perforating Artery in a Bitch

CASE REPORT

Abstract

Background: Cerebrovascular accidents arise from an interruption in cerebral blood flow and lead to neurological deficits associated with either infarction or hemorrhage. In dogs, ischemic infarcts result from obstructive events that impair cerebral perfusion and may appear as territorial or lacunar lesions. These infarcts are typically linked to embolic processes of diverse origins and concomitant diseases that influence their pathogenesis. This study aims to correlate clinical manifestations with the pathological lesions identified in a bitch diagnosed with a perforating artery ischemic stroke.
Case: A 5-year-old Shih Tzu bitch presented with hyperacute neurological signs that began 6 days earlier, initially characterized by nystagmus and sialorrhea, and later progressing to epileptic seizures. Physical and neurological examinations revealed obtundation, non-ambulatory tetraparesis, right-sided head turn and pleurothotonus, unresponsive anisocoria, deficits in menace response and nasal sensation, and absence of proprioception in all limbs, indicating a lesion involving the forebrain and brainstem. Clinicopathological evaluation demonstrated normocytic normochromic anemia, neutrophilia, and mild hyperproteinemia. Magnetic resonance imaging identified an amorphous intra-axial hyperintense area on T2-weighted and FLAIR sequences involving the left thalamus and midbrain, with mild mass effect, consistent with infarction. Due to the guarded prognosis and lack of clinical improvement, euthanasia was elected. Cerebrospinal fluid (CSF) analysis was within normal limits. Gross neuropathology revealed thalamic-mesencephalic areas of malacia, and histopathology confirmed liquefactive necrosis with vacuolization, tissue rarefaction, gitter cell infiltration, and hemorrhage. Renal degeneration and necrosis were also observed. The definitive diagnosis was ischemic cerebrovascular accident due to occlusion of the right perforating artery.
Discussion: The patient was younger than the age range typically reported for canine cerebrovascular accidents, which are more commonly observed in older dogs. The membranous glomerulonephritis identified suggested a protein-losing nephropathy, a condition associated with hypercoagulability and microthrombus formation, which may have contributed to ischemic infarction through occlusion of the right perforating artery. The elevated creatine kinase level was attributed to prolonged recumbency. The hyperacute neurological signs, including seizures, depressed mentation, postural reaction deficits,
anisocoria, head turn, and pleurothotonus, were consistent with lesions affecting the thalamus, diencephalon, and midbrain. Magnetic resonance imaging revealed T1-weighted hypo-intensity and T2-weighted and FLAIR hyperintensity, corresponding to previously described features of ischemic infarction. The hyperacute onset and non-progressive course supported the diagnosis of ischemic stroke involving the right perforating artery.Gross neuropathological examination revealed areas of malacia with pronounced gitter cell infiltration, findings consistent with cerebral ischemia. This case demonstrates that ischemic stroke, although less common in young animals, should remain a differential diagnosis in patients presenting with hyperacute neurological deficits and highlights the value of targeted diagnostic investigations for etiologic determination.
Keywords: Cerebrovascular accident; perforating artery; midbrain; encephalomalacia.