Abstract

Abstract : A 5-year-old, castrated male, Maltese was presented with history of acute flaccid paralysis. The dog waspresented with sudden loss of muscle tone and involuntary movements of hind limbs. Neurologic examination revealedreduced postural reaction in the bilateral hind limbs. MRI of brain showed moderate hydrocephalus, but otherexamination results were normal. Based on the characteristic episodes and examination results, canine cataplexy wassuspected. Treatment was initiated with clomipramine as cataplexy control. Clinical signs resolved with 3-monthmedication. This case demonstrates therapeutic diagnosis of cataplexy. To the author’s knowledge, this is the first reportof cataplexy treating with clomipramine.Keywords : cataplexy, clomipramine, narcolepsy Cataplexy in dogs is relatively rare disease and manifestsitself as sudden weakness of muscle tone, often triggered bypositive emotional stimuli [5]. In genetically narcolepticDoberman puppies, the mean age of onset of cataplexy isabout 9 weeks, and female has more severe cataplexy thanmales [9]. Most of narcolepsy, which is sleep disorder, dogs experi-ence clinical signs of cataplexy [2]. Two different pathophys-iology mechanisms are involved in cataplexy and narcolepsy.Mutation in the hypocretin-receptor-2 gene causes the famil-ial type [7, 8, 10]. This type is inherited autosomal recessivetransmission and onset is young age (≤ 6 months) [10]. Theother is sporadic type caused by loss of the hypocretinligand, which is an excitatory peptide neurotransmitter madein the hypothalamus [4]. Onset of age is wide range as com-pared with familial type [10]. In human medicine, generalized cataplexy causes com-plete collapse of patients, whereas partial cataplexy affectsonly the face, voice or arms. In severe cases, respiratory andextraocular muscles could be attacked [6]. In veterinary med-icine, cataplexy attack may be affect all muscles or restrictedto head, trunk or certain limbs [4]. According to the previousreports [4], most cataplexy attacks initiated in the hind legsand affected bilateral.This report describes therapeutic diagnosis and successfuluse of clomipramine in the treatment of dog with cataplexy.A 5-year-old, castrated male, Maltese dog was presented tohistory of flaccid paralysis 1 to 2 times a week. The dog fellto the ground completely atonic, and bilateral hind limbsmoved involuntary. There was no loss of consciousness. Thisneurological signs observed 2 months prior to the presenta-tion, and episode lasted a few seconds to 2 min. A severeepisode also occurred with loss of consciousness, elicited byexcitement. Previous administration of nonsteroidal antin-flammatory drug (Firocoxib, Previcox; Merial, France) bythe referring veterinarian for pain control didn’t improve theclinical signs. Physical examination revealed intermittenthind limbs weakness when physical manipulation of bothpatellar (grade I/IV medial patellar luxation), but no otherabnormalities were found. The hemogram showed stress leu-kogram (21,030/µL, reference range, 6,000~17,000/µL), andserum chemistry profiles were within normal limits. Therewere no remarkable abnormalities in the thoracic, abdominaland accurately positioned hind limb radiographs. Electrocar-diography was also examined for exclusion of possibility ofcardiogenic episode, and result had no remarkable findings.To rule out myasthenia gravis and neurologic sign inducedby canine distemper virus infection, laboratory examinationswere performed, and acetylcholine receptor antibody concen-tration was within reference range (0.02 nmol/L, referencerange 0.0~0.6 nmol/L), and canine distemper polymerase chainreaction (PCR) of cerebrospinal fluid (CSF) sample result wasnegative. Result of food-elicited cataplexy test (FECT) foridentifying cataplexy was not revealed unusual outcome. Onneurologic examination, the dog presented reduced posturalreaction in the bilateral hind limbs, and this result could besuspected lesion of 4th lumbar vertebra to 3rd sacral verte-bra. However, lumbosacral region was normal at magnetic

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