I. Central nervous system
1. Removal and examination of the brain and the spinal cord
The goal for safe brain removal through an opened calvarium is to avoid mutilation via uncontrolled cuts. It is therefore recommended to observe standard techniques for calvarium removal. Several methods have been described to open the calvarium. The safe removal of the spinal cord is a challenging task but is manageable even under field condition. Guidelines are offered in Chapter 1, “The Equine Necropsy.” Sections of both sciatic nerves should be added to the routine central nervous system (CNS) tissue collection at necropsy.
2. Malformations
a. Hydrocephalus
Hydrocephalus is defined as excessive accumulation of cerebrospinal fluid (CSF) in ventricles resulting in compression atrophy of the neuropile. It is the consequence of obstruction to the path of CSF circulation. Hydrocephalus can be congenital or acquired.
Figure 3.1. Horse. Brain. Hydrocephalus. The caudal cerebral hemispheres are collapsed. An abscess obstructed the lateral apertures of the fourth ventricle.
b. Meningocele
This is a rare condition in the horse.
3. Degeneration
a. Equine leukoencephalomalacia (ELEM)
Substantial random necrosis of the white matter substance is the result of the consumption of moldy corn contaminated by Fusarium verticilloides (formerly F. moniliforme). Hay may also be contaminated with Fusarium. The major toxin involved is fumonisin B1. The toxin inhibits the enzyme ceramide synthase and interferes with the synthesis of sphingolipids. Clinical signs include dysphagia, ataxia, and blindness.
Figure 3.2. Horse. Brain. Leukoencephalomalacia. The frontal lobe unilaterally reveals massive malacia (cavitation).
Figure 3.3. Horse. Brain.Leukoencephalomalacia. Coronal sections are characterized by cavitations in the white matter substance.
Figure 3.4. Horse. Brain. Leukoencephalomalacia. There is evidence of loss of neuropile with disarray of neurofilaments, gliosis, and some mononuclear cell inflammation, including foamy macrophages. (H&E)
b. Nigropallidal encephalomalacia
Figure 3.5. Horse. Brain. Nigropallidal Encephalomalacia. The consumption of yellow star thistle (Centaurea solstitialis) and Russian knapweed (Centaurea (Reponticum) repens) results in bilateral symmetric malacia and yellow-tan discoloration in the substantia nigra and anterior globus pallidus. The toxic compounds are lactones and pyrones, effective in 30–90 days of eating the plant on a daily basis. The toxins have a dopaminergic effect and damage cell membranes. (Courtesy Dr. J. King, Cornell University.)
c. Cerebellar abiotrophy
The condition is defined as loss of organization of certain tissue substance of the cerebellum during fetal life and up to 6 months of age leading to progressive symmetric atrophy and occurs primarily in Arabian horses. The disorder can also be seen in Oldenburg horses, Miniature horses, and ponies. The determination of the weight correlation between cerebrum and cerebellum (reduced weight) and microscopic confirmation of deranged orientation of Purkinje cells and loss of granular cells in the cerebellum establish the specific diagnosis.
Figure 3.6. Horse. Cerebellum. Abiotrophy. Grossly, the reduction of the cerebellum may be subtle in some cases. The sulci between the vermis and the cerebellar hemispheres should not be present, and the cerebellum is reduced in weight when compared with the rest of the brain (less than 8% of the whole brain weight).
Figure 3.7. Horse. Cerebellum. Abiotrophy. The granular cell layer is hypocellular microscopically. (H&E)
Figure 3.8. Horse. Cerebellum. Abiotrophy. On higher magnification, the Purkinje cells are decreased and poorly aligned next to the granular cell layer. (H&E)
d. Grove poisoning
The plant Indigofera spicata (creeping indigo) produces indospicine, a liver and nervous tissue toxin. A single peptide, it inhibits protein synthesis as an antagonist to the amino acid arginine. When consumed by horses, the toxin induces hepatic encephalopathy and recumbence due to CNS involvement.
Figure 3.9. Horse. Brain. Grove Poisoning. There is microscopic evidence of gliosis and astrocytosis. (H&E)
e. Equine degenerative myelopathy (EDM)
Studies have implicated vitamin E deficiency and a possible breed and familial disposition (Morgan horse) to this disease. Copper imbalance has also been speculated to be involved in the pathogenesis. The disorder is associated with neuroaxonal dystrophy. The dystrophy is present in the cerebellum, brainstem, medulla oblongata, and spinal cord and is characterized by a histologic pattern of axonal loss and secondary demyelination.
Figure 3.10. Horse. Spinal Cord. Equine Degenerative Myeloencephalopathy (EDM). Axonal spheroids and neuroaxonal dystrophy. (H&E)
Figure 3.11. Horse. Hindquarter. Equine Degenerative Myeloencephalopathy (EDM). Atrophy of gluteal muscles, particularly evident on the right side.
f. Lower motor neuron disease (EMND)
This condition occurs sporadically in individual animals and rarely in outbreaks affecting the motor neurons located in the ventral horns of the spinal cord. Generalized weakness and coccygeal, triceps brachii, and femoral muscle neurogenic atrophy are clinical signs. The condition is responsive to treatment with vitamin E. An association with neurotoxins produced by blue-green algae or cyanobacteria has been hypothesized.
Figure 3.12. Horse. Spinal cord. Lower Motor Neuron Disease (EMND). There is neuronal chromatolysis. The neurons are swollen and have lost the nucleus. No inflammation is present. (H&E)
g. Cervical stenotic compressive myelopathy
Also known as “wobbler” syndrome, this is a disorder of young fast-growing thoroughbred and standardbred horses and is associated with the vertebrae of the cervical spinal cord. Compression of the cervical spinal cord from either narrowing of the epidural space or instability result in neuroaxonal degeneration (Wallerian degeneration) of ascending (above the lesion) and descending (below the lesion) nervous spinal tracts with clinical manifestations of lameness and ataxia. There are two forms: the static form affecting C5-C6 vertebrae and the dynamic stenotic form affecting C3-C4 vertebrae. Osteochondrosis of the articular facets is another differential cause as are healed fractures of vertebral facets. Thorough evaluation for vertebral dysplastic predisposing lesions necessitates disarticulation of affected vertebrae.
Figure 3.13. Horse. Cervical Vertebrae. Stenotic Myelopathy. There is evidence of severe stenosis of the spinal canal.
Figure 3.14. Horse. Cervical Vertebrae. Stenotic Myelopathy. Disarticulated vertebrae with focal narrowing of the spinal canal on left.
Figure 3.15. Horse. Cervical Vertebrae. Instability. Narrowing of the spinal canal results during flexion of the neck.
Figure 3.16. Horse. Spinal Cord (“Wobbler”). Neuroaxonal Degeneration (Wallerian Degeneration). There is microscopic evidence of axonal swelling, loss of myelin, and the presence of gitter cells. (H&E)
Figure 3.17. Horse. Articular Facets, Vertebrae. Osteochondrosis. There is evidence of crevices in the articular cartilage and asymmetry of articular facets.
Figure 3.18. Horse. Spinal Cord. Cervical Myelopathy. The condition is characterized by asymmetric narrowing of the dorsolateral spinal canal resulting in unilateral compression atrophy of the spinal cord.
h. Postanesthetic myelopathy
In young heavy breed horses undergoing surgery in dorsal recumbency, hypotension induced by anesthesia (halothane) and increased pressure on the caudal vena cava by large abdominal, possibly impacted organs may lead to ischemic neuroaxonal degeneration and polycavitation of the spinal cord. Asymmetric or possibly symmetric lesions of malacia can be anywhere in the spinal cord.
Figure 3.19. Horse. Spinal Cord. Hemorrhage, malacia, and cavitations are present on cut section affecting mainly the gray matter, but also white matter substance. Differential diagnosis: Fibrocartilagenous embolism from the nucleus pulposus to the vessels of the cervical intumescence of the spinal cord via ventral spinal artery. Seen in large equine breeds. (Courtesy Dr. A. Hattel, Pennsylvania State University.)
Figure 3.20. Horse. Spinal Cord. Microscopically myelomalacia is evident. (H&E) (Courtesy Dr. A. Hattel, Pennsylvania State University.)
4. Inflammation
a. Viral
i. Rabies.
A zoonotic disease affecting the CNS of many mammalian species is caused by a neurotropic RNA rhabdovirus. The clinical signs in affected horses are extremely variable. Both vicious and paralytic forms may occur. The virus reaches the CNS by retrograde axonal transport from bite wounds. Grossly, there may be a rare mild hemorrhage on the meningeal surface. The disease can be controlled by vaccination.
Figure 3.21. Horse. Brain. Rabies. Grossly, the appearance of the brain is usually unremarkable.
Figure 3.22. Horse. Brain. Rabies. The microscopic changes are perivascular lymphocytic polioencephalomyelitis indicative of viral etiology. (H&E)
Figure 3.23. Horse. Brain. Rabies. There is lymphocytic trigeminal ganglionitis. (H&E) (Reprinted with permission from Equine Infectious Diseases, Selon-Long, Figure 19.11, Page 189, Copyright Elsevier, 2007.)
Figure 3.24. Horse. Brain. Rabies. The finding of magenta intracytoplasmic inclusion bodies, the so-called Negri bodies (arrows), is conclusive evidence for the diagnosis of rabies. (H&E)
Figure 3.25. Horse. Cerebellum. Rabies. Viral antigen is demonstrated in the cytoplasm of Purkinje cells and cells of the granular cell layer by indirect immunohistochemistry. (IHC) (Reprinted with permission from Equine Infectious Diseases, Selon-Long, Figure 19.8, Page 188, Copyright Elsevier, 2007.)
Charts A and B. Distribution of Rabies-Induced Encephalomyelitis in Equine Brain and Spinal Cord. (Courtesy Dr. Carlo Cantile, Pisa University.)
It has been suggested that cervical spinal cord and adjacent brainstem are optimal tissue regions for rabies testing in the horse.
ii. Equine alpha viral encephalomyelitis.
Eastern equine encephalitis (EEE), Western equine encephalitis (WEE), and Venezuelan equine encephalitis (VEE) strains have been described for this family of Togaviridae, all arthropod-borne viruses. They primarily affect the gray matter substance of the brain and spinal cord inducing a polioencephalomyelitis. In the southeastern part of the United States, EEE is very prevalent. High fever is a hallmark clinical sign of EEE together with CNS disturbances such as depression and dementia. The virus initially spreads hematogenously to the bone marrow, lymph nodes, muscle and connective tissue, followed by a secondary cycle within the CNS. The virus has affinity to neurons, glial cells, cardiocytes, smooth muscle cells, and fibroblasts in the renal interstitium. The disease can be controlled by vaccination. Alphaviruses are a public health consideration in that they are transmitted to people via mosquitoes (e.g., Culiseta sp. and Culex sp.) and are listed as bioterror agents.
Figure 3.26. Horse. Brain. EEE. On rare occasions, cases of EEE exhibit diffuse hyperemia of the meningeal surface.
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