A 5-year-old Staffordshire terrier exhibited slowly progressive signs of cerebellar disease, including nystagmus and dysmetria. After a 30-month course, the dog was euthanized. Grossly, the cerebellum was small and comprised only 5% of the brain weight. Histopathological examination of the brain documented diffuse degeneration. Purkinje cells were most depleted, but granular cells and the molecular layer of cerebellum were also depleted. The history and necropsy examination were evidence of late-onset primary cerebellar degeneration.

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Amphetamine and related drugs of abuse facilitate dopamine transmission in the striatum. This action is believed to underlie the increase in firing of striatal motor-related neurons after amphetamine administration in behaving rats. The present study extended this electrophysiological investigation to phencyclidine (PCP), a nonamphetamine psychomotor stimulant that acts primarily as a noncompetitive antagonist of N-methyl-D-aspartate (NMDA) glutamate receptors. Like amphetamine, PCP (1.0, 2.5, or 5.0 mg/kg) increased the activity of striatal motor-related neurons concomitant with behavioral activation. These effects were blocked by subsequent administration of either 1.0 mg/kg haloperidol or 20.0 mg/kg clozapine, typical and atypical neuroleptics, respectively. Dizocilpine (MK- 801), another noncompetitive NMDA antagonist, mimicked the effect of PCP. Collectively, these results indicate that amphetamine and NMDA antagonists exert comparable effects on striatal motor-related neurons, suggesting that the response of these cells to psychomotor stimulants is regulated by a dopaminergic-glutamatergic influence.

Physiatry alone was used to treat 3 large (30- to 40-kg [66 to 88 lb]) mature (6- to 9-year-old) dogs that were tetraparetic or tetraplegic. All 3 dogs had myelographic evidence of multiple chronic compressive extradural lesions of the caudal portion of the cervical spinal cord. All dogs improved substantially after a course of intensive physical treatment. For 2 dogs, an abbreviated treatment regimen was continued by the owners after the dogs were discharged. Both of these dogs regained and retained normal neurologic function. The other dog improved but was treated infrequently at home. That dog's signs recurred, and the dog was euthanatized. Persistent use of physical treatment for paralysis that results from conditions affecting the cervical spinal cord may be useful even without concurrent surgical or pharmacologic treatments.

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