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Discal cysts, which lie directly over intervertebral discs, are rare. Two old dogs with tetraparesis were referred to our facility. In both animals, magnetic resonance imaging revealed intraspinal extradural cystic mass lesions that were dorsal to degenerative intervertebral discs at the C3-C4 level. These lesions had low signal intensity on T1-weighted images, and high signal intensity on T2-weighted images. A ventral slot approach was used to perform surgical decompression, after which the symptoms improved remarkably. Discal cysts should be included in the differential diagnosis of dogs with cervical pain and tetraparesis. One effective treatment for discal cysts is surgical intervention.

A 12-year-old intact female llama was euthanized following acute onset of spastic tetraparesis and recumbency with inability to rise. Postmortem examination revealed caudal cervical spinal cord compression due to a mass within the ventral spinal canal arising from the C6-C7 intervertebral disk space and attached to an irregularly thickened annulus fibrosis. On histopathologic examination, the mass was composed of amorphous acellular basophilic to amphophilic material admixed with irregularly arranged collagen bundles. The amorphous material was metachromatic and contained multiple small foci of markedly vacuolated round cells, characteristic of origin from the nucleus pulposus. Severe necrosis of all white matter tracts with astrocytic reaction was present in the overlying spinal cord segment. Ascending and descending Wallerian degeneration and dissecting interstitial astrogliosis were present within white matter tracts above and below the lesion, respectively. The diagnosis was compressive myelopathy due to chronic extrusion of the nucleus pulposus of the C6-C7 intervertebral disk. To the authors' knowledge, this is the first report of intervertebral disk disease in a camelid.

Clinical and morphologic features of a progressive polyneuropathy in young mature Alaskan Malamutes are described. Clinical signs included progressive paraparesis, synchronous pelvic limb gait, exercise intolerance, hyperesthesia, hyporeflexia, muscle atrophy, and tetraplegia. Electromyographic testing revealed diffuse fibrillation potentials and positive sharp waves in limb muscles, especially in muscles below the elbow and stifle. Pathologic findings in skeletal muscles and peripheral nerves included neurogenic muscle atrophy, focal or diffuse loss of myelinated nerve fibers, myelinoaxonal necrosis, and variable demyelination or remyelination. Ultrastructural changes included axonal degeneration, presence of numerous Büngner bands, and denervated Schwann cell subunits. The nature and distribution of abnormal electrophysiologic and pathologic findings were suggestive of a distal sensorimotor polyneuropathy, which we have termed idiopathic polyneuropathy of Alaskan Malamutes to distinguish this condition from hereditary polyneuropathy of Norwegian Alaskan Malamutes, last described in 1982.

In a 7-year-old Doberman Pinscher with an atactic gait, neurologic examination revealed tetraparesis, conscious proprioceptive deficits, and rigid ventral flexion of the neck. Radiography and myelography revealed a ventral, extradural, dynamic compressive lesion between C6 and C7. Distraction decompression was performed, using cancellous bone screws and methylmethacrylate. After initial improvement, clinical signs recurred 2 weeks after surgery and progressed until the dog was euthanatized 6 weeks after surgery. Postmortem myelography revealed an extradural compressive lesion adjacent to the implant, between C5 and C6. Secondary compressive lesions induced by surgical or biomechanical alterations of the cervical portion of the spine may be complications of treatment of caudal cervical spondylomyelopathy.

An 18-month-old neutered male Rottweiler was examined because of slowly progressive spastic tetraparesis and ataxia. Signalment and clinical signs were suggestive of 2 neuronal degenerative diseases presumed to be inherited in young Rottweilers: leukoencephalomyelopathy and neuroaxonal dystrophy. Myelography revealed an extradural compression at the articulation of the second and third cervical vertebrae. At surgery, focal hypertrophy of the yellow ligament was observed to compress the spinal cord ventrally at that site.

A young cat had signs of tetraparesis that progressed to tetraplegia within a few weeks. Clinically, there was lower motor neuron disease with areflexia and muscle atrophy in all limbs. Degeneration of the motor neurons in the spinal cord was seen on histological examination. Ultrastructurally, the degeneration of nerve cells was characterized by abnormal proliferation of neurofilaments. These findings were compared to other motor neuron diseases and neurofibrillary accumulations in man and animals.