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"Shivers" is a progressive equine movement disorder of unknown etiology. Clinically, horses with shivers show difficulty walking backward, assume hyperflexed limb postures, and have hind limb tremors during backward movement that resembles shivering. At least initially, forward movements are normal. Given that neither the neurophysiologic nor the pathologic mechanisms of the disease is known, nor has a neuroanatomic locus been identified, we undertook a detailed neuroanatomic and neuropathologic analysis of the complete sensorimotor system in horses with shivers and clinically normal control horses. No abnormalities were identified in the examined hind limb and forelimb skeletal muscles nor the associated peripheral nerves. Eosinophilic segmented axonal spheroids were a common lesion. Calretinin-positive axonal spheroids were present in many regions of the central nervous system, particularly the nucleus cuneatus lateralis; however, their numbers did not differ significantly from those of control horses. When compared to controls, calretinin-negative, calbindin-positive, and glutamic acid decarboxylase-positive spheroids were increased 80-fold in Purkinje cell axons within the deep cerebellar nuclei of horses with shivers. Unusual lamellar or membranous structures resembling marked myelin decompaction were present between myelin sheaths of presumed Purkinje cell axons in the deep cerebellar nuclei of shivers but not control horses. The immunohistochemical and ultrastructural characteristics of the lesions combined with their functional neuroanatomic distribution indicate, for the first time, that shivers is characterized by end-terminal neuroaxonal degeneration in the deep cerebellar nuclei, which results in context-specific hypermetria and myoclonus.

The clinical spectrum of shivers in horses is very variable in the degree or manifestation of signs. The diagnosis of a characteristic case of Shivers seldom presents a problem, however the signs of Shivers may be intermittent, occasional, or latent and very difficult to confirm. Shivers may be extremely difficult to detect in the early stages, and careful observation may be required before the diagnosis can be made. The disease primarily affects one or both hind limbs with or without tail elevation and trembling.

With progression of the disease, a gradual and progressive atrophy of the muscles of the thigh occurs, and this may progress to generalized muscle atrophy. Hindquarter weakness was present in 11 of 19 (58%) horses with shivers. Animals so affected sleep standing, and their front fetlocks and knees are bruised and disfigured by frequent half-falls. Affected horses frequently adopt an abnormal base-wide stance in the hind limbs. Excessive sweating has been noted in some cases.

Fibrotic myopathy results from scar tissue formation following injury to the semitendinosus and semimembranosus muscles. The gait is usually characterized by an abnormal slapping-type hindlimb gait with a lower arc of the limbs than seen with shivers or stringhalt. Horses with fibrotic myopathy can back normally. Adult Quarter horses are the most frequently affected breed.

Equine motor neuron disease (EMND) is clinically characterized by progressive weight loss despite a good appetite, symmetrical muscle wasting, muscle fasciculations, excessive sweating, tucked up abdomen, abnormal gait, excessive recumbency and an abnormally low head carriage. There are some similarities between the clinical signs of shivering and EMND. Bizarre stringhalt-like movement of a front or rear limb has been observed in some chronically affected EMND horses. Subacute to chronic EMND cases frequently have an abnormal elevation of their tail, lie down more frequently and have more muscle atrophy than a case of shivers.

Because Shivers is breed-related, there may be a genetic basis or predisposition for the disorder. Reports from past centuries suggest that shivers was prevented by breeding away from the con

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