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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.
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