Large Animal Neurology. Joe Mayhew

in young ruminants, neuroaxonal dystrophy in adolescent horses, or motor neuron disease in older horses.

       Metabolic diseases

      Many metabolic disorders such as hypocalcemia, hypomagnesemia, and ketoacidosis alter nervous tissue function, especially electrical transmission, when there are no morphologic lesions. Some cause degeneration of neurons and ultimately necrosis, often in selective areas of the CNS. These include hypoglycemia, hypoxia, and hepatoencephalopathy, the latter producing a striking hypertrophy and hyperplasia of astrocytes. Most are characterized by a lack of inflammation. The perinatal disease referred to as hypoxic and ischemic encephalopathy (Figure 4.10) also fits this category but is likely complex in its specific pathophysiology.

      Inherited, neuronal, metabolic disorders are often expressed as abiotrophy with selective, delayed neuroaxonal degeneration, or as lysosomal storage disease with an accumulation of metabolic products in macrophages and neurons. Other metabolic disorders result in hypomyelination or demyelination.

       Vascular lesions

      Interruption of the blood supply results in hemorrhagic or ischemic infarction and tissue necrosis (Figure 4.3), with neutrophilic and then monocytic phagocytosis of debris. Emboli and thrombi may be septic, parasitic, or fibrocartilaginous. More generalized infarction may occur with cardiopulmonary failure, disseminated clotting abnormalities, and septicemia. Hypertension, perhaps on a compartmental basis, may play a role in the vascular accidents associated with the neonatal hypoxic and ischemic encephalopathy seen most often in foals.³⁰

       Degenerative processes

      Many of these diseases that involve morphologic degeneration of CNS tissue are familial or hereditary and may be considered metabolic disorders. Of the remaining, most are of unknown origin, although hereditary, toxic, metabolic, nutritional, and viral factors are often suspected.

       Neoplasms and other tumors

With the exception of neurofibroma and lymphosarcoma in cattle, neoplasms involving nervous tissue are rare in domestic large animals. Neoplasms replace and compress nervous tissue, and both forms of intrusion often cause adjacent edema because of local vascular perturbations. Indeed, vascular compromise can result in considerable necrosis of CNS tissues as well as of the tumor itself. As a result of the space‐occupying effect and any associated edema, brain herniations occur with brain neoplasms just as they occur with cerebral abscesses and hematoma. These include herniations of the cingulate gyrus under the falx cerebri, the occipital lobes under the tentorium cerebelli, and the cerebellar vermis through the foramen magnum (Figures 4.8 and 4.10). All these tissue movements cause compression of parts of the brain. Primary CNS tumors are extremely rare in large animals, but can arise from meningeal, ependymal, choroidal, glial, and endothelial cell lines. Neuronal cell line neoplasms are even less frequently encountered. However, a proliferation of primitive neuroepithelial cells from the late developing brain sometimes occurs in young patients as a medulloblastoma. Ganglion and Schwann cell neoplasms occur in the PNS. Neoplasms involving the skull and vertebrae as well as metastatic neoplasms usually compress nervous tissue, the effects being identical to those of external injury. Lymphosarcoma probably is the most common neoplasm involving the brain and spinal cord in large animals, and probably it should be considered a primary tumor when it is in the epidural space and when it encompasses the peripheral nerves of cattle.

      There is an interesting group of neural tumors that include usually focal, disorganized proliferation of normal neural and other tissue elements in abnormal groupings or abnormal sites, collectively referred to as hamartomas.^31–33 These expansile tissue masses disrupt the function of adjacent neural tissues without usually causing tissue destruction.

       Idiopathic disorders

In many clinical neurologic syndromes such as self‐mutilation, no consistent gross or light microscopic findings exist. In some cases, a thorough search for lesions is not undertaken for various reasons. Biochemical, not morbid, lesions likely account for some of these syndromes. Other problems such as recurrent laryngeal neuropathy, stringhalt, and acquired equine polyneuropathy may be associated with consistent neuropathologic lesions, but the etiology is still uncertain. A further subcategory is diseases that involve impressive clinical syndromes and present impressive florid lesions and yet defy our understanding as to their biology. Such are the inflammatory disorders cumulatively expressed as granulomatous meningoencephalomyelitis (Figure 4.11). This latter, catch‐all diagnosis currently falls in the hinterland between infectious diseases as we know them, toxicities impacting on immune‐responsiveness, and neoplasms that allow cells and tissues to express their own varied, albeit unacceptable, phenotypes.

Figure 4.11 Granulomatous meningoencephalomyelitis (GME) is not common in horses but can present with fluctuant and progressive focal and multifocal signs related to brain and/or spinal cord disease, thus can result in syndromes akin to those seen with EPM caused by S. neurona in horses from the American continents. Small to coalescing lesions of granulomatous, nonsuppurative inflammatory lesions (arrows), sometimes focused around vessels in the white matter, can be seen grossly on this transverse section of forebrain at the level of the corona radiata and internal capsule from a horse with progressive behavioral and visual abnormalities suffering from GME.

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