Large Animal Neurology. Joe Mayhew
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Figure 4.9 Septic thromboemboli can lodge in any vessel in the CNS but will often arrive via the major carotid supply and thus seed the forebrain as was the case with this foal suffering from Aspergillus sp. superinfection after neonatal sepsis and abdominal surgery. The necrotic inflammatory lesions seen on this transverse section of the fresh forebrain and midbrain (arrows) are particularly in gray matter that usually has a greater blood supply than white matter.
Protozoa and amoeba
Encysted protozoal forms may be associated with little cellular reaction. With dividing forms such as Sarcocystis sp. merozoites, there is often severe necrosis with hemorrhage and inflammation comprised of lymphocytes and macrophages, sometimes neutrophils, eosinophils, and multinucleated giant cells. Amoeba usually only invades the CNS following massive exposure via portals such as the olfactory turbinates. These agents also take advantage of immunocompromised states.
Helminth and arthropod parasites
Penetration of the CNS by fly larvae (myiasis) and roundworms (nematodiasis) is usually accidental and random, whereas invasion by some nematodes and tapeworm cysts (coenurosis) is part of the respective life cycles. In the natural host, minimal damage may result. In unnatural hosts, however, massive tissue destruction, hemorrhage, protein exudate, and an influx of neutrophils and macrophages with variable numbers of eosinophils and giant cells occur. Such parasites can arrive in the CNS through natural foramina or via the blood supply. Subsequent meanderings can be tortuous and surprisingly may simply separate the tissues without causing much inflammation. Also, parasites can leave the CNS after creating devastation.
Immune mechanisms
Type I, anaphylactic immune responses in the CNS are rare, partly because the CNS is a relatively privileged site, somewhat isolated from the immune system. Cytotoxic, autoimmune, type II reactions directed against natural or altered antigens such as myelin do occur in the CNS and PNS, causing nonsuppurative encephalitis or neuritis, respectively. Antigen–antibody complex, type III mediated vasculitis occurs in the CNS in some diseases, and, like other forms of vasculitis, CNS damage results more from infarction than from inflammation. The latter can be neutrophilic, lymphocytic, or mixed.
Prion agents
The transmissible spongiform encephalopathies or prion diseases are caused by novel infectious agents that do not incite a detectable immune response in the host. Generally, they are endemic diseases of low incidence, have a prolonged incubation period, and are uniformly fatal. Although evidence of the infectious agent can usually be detected in several peripheral tissues, particularly those of the lymphoreticular system, pathological lesions are confined to the nervous system. The lesions consist of vacuolation of neurons, neuronal loss, astrocytosis and microglial activation, and accumulation of protease‐resistant, self‐propagating forms of the host‐encoded protein PrP, termed PrPSc. In some cases, accumulations of PrPSc as amyloid plaques and scrapie‐associated fibrils occur in the brain.
Injury causing only loss of function is referred to as concussion in the brain, spinal shock in the spinal cord and neurapraxis in the PNS.
Physical and chemical disorders
Concussion, with loss of function, is only the mildest effect of CNS trauma, whereas contusion or bruising and laceration with tissue disruption cause morphologic lesions with degrees of cell death, hemorrhage, edema, and neutrophil and macrophage infiltration. Microglial then astrocytic activation, proliferation, and hypertrophy all occur in adjacent viable tissue. The site of major tissue damage may not be directly related to the site of traumatic impact on the calvaria or vertebral column. Parenchymal and subarachnoid bleeding is common, but subdural and epidural hematoma formation is less frequent in domestic animals than in man. Hematomas, cerebral abscesses and other space‐occupying lesions, create local pressure and edema that can cause brain swelling and herniation of parts of the brain (Figures 4.7, 4.9, and 4.10).30 Destroyed tissue is removed by activated microglia, but if it is more extensive, it is removed by infiltrating monocytic macrophages. This results in pools of lipid‐laden macrophages with net‐like cytoplasm—gitter cells. Such large lesions may heal to form an astroglial scar, but more so a fluid‐filled cavity lined by astrocytes. Secondary neuronal fiber degeneration will occur along fiber tracts that are separated from their cell bodies by the injury.
Figure 4.10 This is a caudal view of the occipital lobes and section through the midbrain of a neonatal foal that suffered birth asphyxia and demonstrated bizarre behavior and somnolence prior to developing intractable seizures. Diffuse forebrain swelling that resulted from the cerebral neuronal necrosis caused by the asphyxia is evident by the herniated ventral portions of the occipital lobes of the cerebrum (arrows). Additionally, softening and necrosis (malacia) is present in both rostral colliculi (arrowheads) that likely also resulted from the effects of oxygen deprivation on these sensitive regions of gray matter.
Heat, cold, chemicals, and ionizing irradiation can cause immediate cell death with massive vascular breakdown and tissue infarction. Some delayed effects, particularly on the maintenance of myelin, may be noted with irradiation.
Toxic diseases
Some toxins such as cyanide interfere with oxygen transport. Water and salt intoxications directly alter osmolality of cells, interrupting many metabolic functions associated with swelling or shrinking cells. Lesions, if present, are usually symmetrical, often diffuse and usually end with tissue necrosis, sometimes with subsequent brain swelling (Figure 4.8). Some plant (e.g., yellow star thistle) and microbial (e.g., Clostridium perfringens type D) toxins produce extremely selective and focal lesions, suggesting that they are mediated by selective neurotransmitter disruption or more likely by selective vascular derangements.
Some such as botulinum toxins affect neurotransmission directly while others like lolitrem‐B in perennial ryegrass staggers interfere with membrane ion channels resulting in an acquired channelopathy.
And finally, other toxins interfere with (macro)molecular biosynthesis as occurs with corynetoxins in annual ryegrass toxicity disrupting glycoprotein synthesis, and fumonisins in equine leukoencephalomalacia/moldy corn poisoning disrupting sphingolipid metabolism.
Nutritional diseases
Starvation and disorders associated with inadequate vitamin A, vitamin D, calcium, and phosphorus intake can be associated with vertebral fractures. Thiamine deficiency can cause cerebrocortical neuronal necrosis in ruminants, hemorrhagic necrosis of white matter in felidae and axonal degeneration in horses. Lesions of cell death tend to be symmetrical with nutritional diseases. Of course, dietary imbalances involving calcium, phosphorus, vitamin A, vitamin D, copper, etc., can result in neurocrania and vertebral defects that impinge on CNS and PNS structures asymmetrically, especially when secondary trauma plays a role.
Antioxidant failure effects various syndromes depending on age, and species especially. Thus, as exemplified by vitamin E deficiency, this