Sparky's shaking again: Seizures in young dogs (Proceedings)
Seizure disorders in young animals pose different considerations as to etiology and therapeutic decisions compared to adult dogs. Congenital, developmental, metabolic, toxic, infectious and inflammatory causes should be considered more likely in younger dogs and puppies. Seizures are the manifestation of abnormal synchronous electrical activity in the brain and are the most common neurological disorder in dogs. Seizures may be categorized as generalized, when whole body involvement is present or partial, when a portion of the body is affected. Consciousness is unimpaired during simple partial seizures and is altered during complex partial seizures. A pre ictal period prior to the seizure and a post ictal period lasting minutes to hours after the seizure are common with generalized seizures. Pre and post ictal signs may include anxiety, attention seeking, panting and pacing. The recognition of seizures can sometimes be difficult as vestibular episodes, dyskinesias and syncopal episodes can appear seizure like. A thorough history should be gathered including potential for toxin exposure, familial history, previous events, activity during onset, time of onset, duration of the event, elimination during the event, and interictal behavioral or gait changes. In puppies information regarding birth, litter mates, suckling and weight gain is also important. CBC, serum chemistry and urinalysis should be done on all dogs presenting for seizures. Hypoglycemia should be ruled out in all puppies. Bile acid testing is important in all puppies and small breed dogs.
Portosystemic shunts (PSS) often cause episodic encephalopathic signs such as mentation changes, ataxia, blindness and seizures. Other signs include vomiting, anorexia, PU/PD, decreased weight, hematuria and stranguria. Pre and post prandial bile acids are often over 100 and 200 µmol/L. Ammonium biurate or uric acid crystalluria is common.1 Confirmation of PSS may be done via abdominal ultrasound or nuclear scintigraphy. Therapy includes a low protein diet, antibiotics, lactulose and surgical ligation/constriction. Anticonvulsant therapy is indicated if seizures are present or perioperatively as post operative generalized seizures are associated with a poor prognosis.1 The mechanism of hepatic encephalopathy has been unclear. Possible causes include hyperammonemia, altered tryptophan synthesis and metabolism, false neurotransmitter synthesis, alterations in amino acid neurotransmitters and increased cerebral concentrations of an endogenous benzodiapine.2
A metabolic defect causing L-2 Hydroxyglutaric aciduria has recently been recognized in Staffordshire Bull Terriers3 and the West Highland White Terrier.4 Clinical signs include seizures, ataxia, stiff gait, decreased mentation and head tremors. Signs occur from 4 months to 7 years of age, but are often identified less than 1 year of age. Organic acid analysis of urine, CSF and plasma are abnormal in affected dogs. MR imaging identified bilaterally symmetric, diffuse hyperintensity on T2 imaging in the gray matter throughout the brain. No known effective treatment is known at this time, other than symptomatic anticonvulsant therapy. Dietary therapy may be of benefit. Cobalamin therapy may be beneficial in methylmalonic aciduria in people.3 A 6 month old Cavalier King Charles Spaniel was reported to have seizures secondary to a hexanoylglycine aciduria. L-Carnitine therapy is recommended in people with medium- chain acyl CoA dehydrogenase deficiency and thus may be of benefit for hexanoylglycine aciduria.5Hydrocephalus is an increase in CSF volume and should be considered in toy and brachiocephalic breeds. A domed shaped head or persistent fontanelle may be present. Most commonly, stenosis of the mesencephalic aquaduct is present. CSF accumulates rostral to the obstruction and cerebral cortical atrophy occurs. Ventricular dilatation can lead to tearing of ependymal cells and periventricular diverticula. Hydrocephalus may also result secondary to neoplasia or infection obstructing CSF flow. Clinical abnormalities may not be present. Loss of cortical neurons can lead to cerebral signs and seizures. Vestibular and cerebellar signs can be seen. Diagnosis is made via cranial MRI or CT scan. Ultrasound through a persistent fontanelle may also be used in diagnosis. CSF analysis is important to rule out concurrent inflammatory or infectious disorders. Recurrent seizures should be treated with anticonvulsant therapy. If seizures are refractory to anticonvulsant therapy, or if addition neurological abnormities are present medical or surgical therapy may be considered. Glucocorticoids decrease CSF production and may be beneficial if periventricular edema is present. Prednisone starting at 0.5 mg/kg PO BID may be given with tapering to the lowest effective dose. Omeprazole also decreases CSF production and may be of benefit. Acetazolamide, a carbonic anhydrase inhibitor may be of benefit. Surgical placement of a ventriculoperitoneal shunt is considered for dogs with progressive signs not responsive to medical therapy. Success with shunting is variable. Potential complications include infection, occlusion, and shunt migration. The need for surgical revision is not uncommon.6