Reactive proliferative vascular disorders of the CNS are poorly documented in veterinary medicine. Here, we describe widespread CNS hemangiomatosis in a 1-y-old female donkey with weakness, recumbency, and lifelong unthriftiness. Elevated serum creatine kinase and aspartate aminotransferase activities were consistent with skeletal muscle injury attributed to prolonged recumbency. Despite supportive care, the donkey remained unable to stand and was euthanized 5 d after presentation. Gross findings consisted of poor body condition and multiple gastric ulcers. Histologically, clusters of sometimes tortuous, redundant leptomeningeal and neuroparenchymal capillaries and small- to medium-sized arterioles and venules were present throughout the CNS. These changes were more pronounced in the spinal cord and cerebellum. Immunohistochemistry highlighted these vascular proliferations, with membranous labeling of endothelial cells for CD31 and cytoplasmic labeling for factor VIII-related antigen. Vascular myocytes had cytoplasmic labeling for smooth muscle actin. Although CNS development appeared undisturbed, other neuroparenchymal changes included Purkinje cell degeneration and necrosis with dendritic and axonal swelling and gliosis; white matter vacuolation and microgliosis (with occasional early, mildly vacuolated macrophages) of the ventral funiculi and the dorsal portion of the lateral spinal cord, cerebellum, and cerebrum; and white and gray matter vacuolation and gliosis of the thalamus and brainstem. Inflammatory cells within these areas had cytoplasmic labeling for ionized calcium-binding adaptor molecule 1. Moderate-to-severe skeletal muscle degeneration, atrophy, and fibrosis affected the dorsal sacrocaudal muscle. Our findings are consistent with congenital, widespread CNS hemangiomatosis.
Mendes et al. (Sun,) studied this question.