Feeding a meal in the hospital elicited a cataplectic event characterized by buckling of the hind limbs and drooping of the neck, followed quickly by complete collapse to the floor. Abnormalities were not detected on thoracic radiographs, abdominal radiographs, or abdominal ultrasound. The neurologic evaluation was normal other than moderate pain elicited on palpation of the caudal cervical and mid-lumbar spine, consistent with suspected concurrent IVDD. On presentation, the dog was moderately overweight (BCS 7/9) but otherwise had a normal physical examination. Hand-feeding one kibble at a time with vigorous petting prevented collapse episodes although the dog still staggered and became drowsy during feeding. Robaxin, West-Ward Pharmaceuticals Corp., Eatontown, NJĪnd failed to improve. Metacam, Boehringer Ingelheim Vetmedica, Inc., Ridgefield, CT The dog was treated for suspected intervertebral disk disease (IVDD) with meloxicam 1 1 Thoracic radiographs showed collapsed intervertebral disk spaces at T11-12 and T12-13 but were otherwise normal. Two weeks before admission, the referring veterinarian performed a CBC and serum biochemical profile, which were both within normal limits. The dog was also described to be more lethargic and have drooped eyelids since the onset of episodes. The collapse episodes only occurred while eating and were characterized by a sudden fall to the floor with a quick recovery and return to eating (see supplemental video). Since the onset of signs, every meal was associated with a single collapse episode except one meal, which was associated with two episodes. The owners reported that the collapse episodes occurred 30–40 seconds after the initiation of feeding, which was twice daily. These findings suggest that disruptions in downstream signaling of hypocretin secondary to an intracranial mass effect might result in narcolepsy-cataplexy in dogs and that brain MRI should be strongly considered in sporadic cases of narcolepsy-cataplexy.Ī 6-year-old male neutered Dachshund was referred to the University of Tennessee Veterinary Medical Center's Internal Medicine Service for an acute onset of collapsing while eating of 20 days’ duration. Nine months after SRT, the dog developed clinical hyperadrenocorticism, which was successfully managed with trilostane.
The Dachshund underwent stereotactic radiotherapy (SRT), which resulted in reduction in the mass and coincident resolution of the cataplectic attacks. The dog was also negative for the hypocretin receptor 2 gene mutation associated with narcolepsy in Dachshunds, ruling out familial narcolepsy. Cerebral spinal fluid hypocretin-1 levels were normal, indicating that tumor effect on the ventral lateral nucleus of the hypothalamus was not the cause of the dog's narcolepsy-cataplexy. A 6-year-old male neutered Dachshund had presented for acute onset of feeding-induced cataplexy and was found to have a pituitary macrotumor on magnetic resonance imaging (MRI).
In this report, a pituitary mass is described as a unique cause of narcolepsy-cataplexy in a dog. Familial narcolepsy secondary to breed-specific mutations in the hypocretin receptor 2 gene and sporadic narcolepsy associated with hypocretin ligand deficiencies occur in dogs.
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