Читать книгу Large Animal Neurology - Joe Mayhew - Страница 102

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.