Cerebrospinal fluid was taken but the pressure was not measured due to the dangers associated with a cysternal tap. Thus, swallowing epilepsy and vagal stimulation with syncope were not indicated. Induced swallowing by external palpation of the larynx did not precipitate hypotonia. Hypotonic episodes could not be initiated with the oculo-cardiac reflex. Electrocardiograms before and during the hypotonic episodes revealed no pronounced changes in heart rate. Otherwise routine physical, neurological, and laboratory workups were unremarkable. Upon physical examination we found the dog to be mildly overweight. It was noted that attacks consistently occurred when the dog was eating. The diet had consisted of liver, fish, cream and other table foods. There were no “personality” changes accompanying the onset of symptoms and previously trained responses such as “hand shaking” were normal. It had all vaccinations and seemed otherwise healthy. The dog was seen by several veterinarians and admitted to the University of Saskatchewan Veterinary Clinic in November 1972. In August, while taken on vacation, the dog acutely developed what the owners described as “drop attacks,” characterized by sudden onsets of weakness and falling, as if the dog were “fainting.” No abnormalities were then noted by the veterinarian or owner. The dog, a female toy poodle, was whelped in April of 1972 (litter of four two males) and purchased in June 1972 at 7 wk of age. We now report observations on a poodle which we have diagnosed as having the narcolepsy–cataplexy syndrome. These observations are of particular interest since major advances in the management and treatment of narcolepsy would certainly follow from studying animals afflicted with an analogous disease. However, there have recently been reports of narcoleptic-like conditions occurring in dogs (9, and Benjamin Hart, personal communication) and a cat ( 9). Furthermore, experimental induction of isolated narcoleptic symptoms in animals may be of only limited use as concluded by Mitler and Dement ( 11). Unfortunately such understanding is not likely to result from studies of human patient material in the forseeable future. As with other illnesses, a definitive approach to this serious and life-blighting illness will require understanding of the basic defect. At the present time treatments are only partially effective and eventually palliative. Narcolepsy is a life-long debilitating illness which afflicts between 100,000 and 150,000 Americans ( 1, 4). The condition may also be diagnosed by the presence of sleep onset REM-sleep episodes in clinical sleep recordings as reported by Rechtschaffen and Dement ( 12). Narcolepsy in human beings is a well-defined neurological condition characterized by the postpubertal onset of sleep attacks, sleep paralysis, hypnagogic hallucinations, and cataplexy ( 15– 18). The dog will be bred either with a littermate or a similarly afflicted male in an attempt to produce a population of afflicted dogs. The diagnosis of canine narcolepsy was further confirmed by two negative trials with neostigmine (ruling out myasthenia) and two positive trials with imipramine (cataplexy in human narcolepsy responds to imipramine treatment). These pathological manifestations are analogous to those characteristic of human narcolepsy.
Unambiguous sleep onset REM periods and cataplectic attacks were also observed.
During 41 hr of EEG, EOG, and EMG monitoring in conjunction with behavioral observation, the dog exhibited normal polygraphic wakefulness, slow-wave sleep and REM sleep. Presentation of food, water, or a plaything were the most frequent elicitors of attacks. However, such attacks could develop into complete cataplexy, causing postural collapse and areflexia, although extrinsic eye muscles and the muscles of respiration were spared. Observation indicated that attacks were frequently partial, involving only the neck musculature and hind legs. Physical examination disclosed no systemic factors to account for such atonic episodes. At approximately 4 mo of age, the dog presented cataplectic attacks. This report summarizes data on a female toy poodle which has a canine form of narcolepsy-cataplexy. No current treatment for this neurological disorder is satisfactory and a definitive approach to the disease requires an animal model of narcolepsy.
Narcolepsy in human beings is a life-long illness afflicting 100,000–150,000 Americans.
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