Bilateral Testicular Leiomyosarcoma in a Stallion

Abstract

Brief communications The diagnosis of lower motor neuronopathy was based on the physical exam and histopathologic and electron microscopic findings, but the cause of these changes was not determined. Possible causes include heavy-metal intoxication, poisonous plant ingestion, viral infection, and nutritional imbalances. The localized distribution of the noninflammatory central nervous system lesions in the absence of other significant neuropathologic changes, such as Wallerian degeneration and the lack of significant axonal and myelin involvement, make these etiologies unlikely. However, not unlike other reported cases of neuronopathies, many of these causes could not be definitively confirmed or ruled out. Additionally, the cause of the esophageal, rumenal, and abomasal ulcers is not known. A direct relationship between these lesions and the spinal cord lesions could not be found, but these ulcers may be the result of an undetected infectious agent or mechanical trauma. A hereditary basis for the neuronopathy in this bull must also be considered because these lesions are very similar to hereditary neuronopathies previously reported in other bovine breeds and species. Hereditary canine spinal muscular atrophy of the Brittany Spaniel is characterized by similar localized neuronal swelling and ‘‘ghost cells’’ within the ventral gray matter horns of the spinal cord due to neurofilament accumulation in the perikarya. 2,6,7 The bundles of neurofilaments are the result of impaired transport, synthesis, or catabolism of cytoskeletal proteins and may be the underlying pathogenesis of neurofilament accumulation in this bull. 2,3,8 However, in Brittany Spaniels, unlike in the bull in this report, there are lesions in neurons within the brain stem (trigeminal motor and hypoglossal nuclei) and prominent muscular atrophy of the fore- and hind limbs. 2 Additionally, the intermediate phenotypic variant of canine spinal muscular atrophy is slowly progressive, whereas in this bull there was sudden onset with rapid progression, which may explain the lack of prominent spinal muscular atrophy. Additional hereditary lower motor neuronopathies have been described in Brown Swiss, horned Hereford, and Red Danish calves that had similar lesions within both the spinal cord and brain stem associated with skeletal muscle atro