Polioencephalomalacia (PEM) literally means softening of the cerebrocortical grey matter distributed in a laminar (layered) pattern. It is also called cerebrocortical necrosis (CCN), laminar cortical necrosis or cortical necrosis. PEM is a sporadic disease caused by the overconsumption of simple carbohydrates, and the underconsumption of fiber; it occurs in cattle, sheep and goats, and was first seen in the 19th century when ruminants were fed the byproducts of sugar refining. Today PEM is most commonly seen in cattle at 6–18 months of age when fed concentrate rations. Sheep are usually affected at 2–7 months of age.
The lesion is associated with thiamine deficiency or a disturbance in thiamine metabolism. Ruminants are supplied with thiamine by synthetic activity of ruminal bacteria. PEM most commonly develops in cattle fed carbohydrate-rich and roughage-poor rations, which leads to subclinical lactic acidosis, and hence an alteration in ruminal microflora. Other mechanisms for disturbances in thiamine deficiency include:
- Production of inactive thiamine analogues
- Decreased thiamine absorption
- Increased faecal excretion of thiamine
Infection with Trypanosoma congolense can also cause focal PEM in the final stages of disease, likely due to ischemia from accumulation of parasites in the terminal capillaries of the brain.
Clinical signs of PEM are variable depending on the area of the cerebral cortex affected and may include head pressing, dullness, opisthotonos, central blindness, anorexia, muscle tremors, teeth grinding, trismus, salivation, drooling, convulsions, nystagmus, clonic convulsions, and recumbency. Early administration of thiamine may be curative, but if the lesion is more advanced, then surviving animals may remain partially blind and mentally dull.
- "Polioencephalomalacia: Introduction". The Merck Veterinary Manual. 2006. Retrieved 2007-07-10.
- Polioencephalomalacia: Disease Caused by a Deficiency of Thiamine at tvsp.org
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