Encephalomalacia:
- It may be defined as the degenerative changes of the brain. Changes comprises of demyelination, necrosis and edema.
- Degenerative changes of gray matter are known as polioencephalomalacia
- Degenerative changes of white matter are known as leukoencephalomalacia.
Etiology:
All species:
- Hepatic encephalopathy caused by alkaloid poisoning, hepatic arteriovenous anomaly, thrombosis of portal vein in horse
- Focal or diffuse lesion in axons or myelin of neuronal process
- Poisoning by organic mercurial, in some cases lead, selenium poisoning
- EHV-1 infections in horses
- Cerebellar cortical abiotrophy occurs in calves and lambs
Ruminants:
- BSE
- Plant poisons; Astralagus spp, Oxytropis spp, Swainsona spp, Vicia spp, Kochia scoparia
- Intoxication with toxin of Clostridium perfringens type D toxin
- Thiamine deficiency caused by Brackern fern poisoning, ingestion of mouldy corns and excess grain
- Sulphur toxicosis
- Antimetabolite of nicotinic acid causes encephalomalacia in sheep
- Neuronal dystrophy
- Inherited defect of Brown Swiss cattle known as weavers or degenerative myeloencephalopathy
- Swayback and enzootic ataxia caused by copper deficiency in lambs
- Prolonged parturition of calves causing cerebral hypoxia
- Ingestion of ammoniated forages
- Inherited neuronal degeneration in Angora goats
Horse:
- Feeding of mouldy corn infested with Fusarium monoliforme
- Feeding of yellow star thistle; Centaurea solstitialis
- Poisoning by bracken and horsetail causing a conditioned deficiency of thiamine
- Ischemic encephalopathy of neonatal maladjustment syndrome of foals
- EDM associated with vitamin E deficiency
Pigs:
- Mulberry heart disease
- Subclinical attacks of enterotoxemia
- Poisoning by organic arsenials and salt
Clinical Findings:
- Weakness in all four limbs
- Dullness or somnolence
- Blindness, ataxia
- Head pressing
- Circling
- Terminal coma
- In early stages of PEM in ruminants; muscle tremor, opisthotonus, nystagmus, convulsion
- In equine leukoencephalomalacia:
- Anorexia and depression
- Ataxia, circling, head-pressing
- Blindness
- Hyperaesthesia
- Agitation, delirium, recumbency, seizures and death
- Delayed retraction of tongue after extension
- In hepatotoxic form, icterus, swelling of lips and nose, petechiation, abdominal breathing and cyanosis.
Diagnosis:
- Physical and neurological examination of animal including assessment of gait, reflex
- Blood test to rule out infectious causes
- PM findings:
- Softening, cavitation and laminar necrosis of cortex may be visible
Treatment:
- PEM caused by thiamine deficiency can be corrected by administration of thiamine parenterally. Thiamine @10mg/kg, TID-QID, for cattle or small ruminants.
- If brain lesion is severe and treatment delayed, full recovery is not possible. Certain neurological signs remain within life time of affected animals.
- If there is no initial improvement, treatment course should be prolonged > 3 days.
- Reduction of cerebral edema can be attempted with administration of dexamethasone @ 1-2 mg/kg, IM or SC.
- Dietary supplementation of thiamine @3-10 mg/kg feed, for prevention of disease.
- In case of sulphur toxicosis, dietary sulphur should be reduced and drinking water containing high sulphur should be avoided.
- In case of toxicity by organic chemicals, appropriate measure for absorption of toxin should be adopted. Gastric lavage should be carried out to avoid further absorption of toxin.
- Salt intake should be reduced in case of salt poisoning.
- There is no specific therapy for equine leukoencephalomalacia. Feed infested with fungi should be removed immediately from feedlot.
- In case of agitation or delirium, sedation of animal is necessary for prevention of further injury.
- Activated charcoal and laxatives are administered to remove or flush out toxin from gastrointestinal tract.