Convincing evidence has shown that these calcium channels are involved in the persistence of pain ( 19). While their mechanisms of analgesia remain unknown, they are believed to decrease the release of glutamate, an excitatory neurotransmitter, via binding to the alpha2-delta subunit on voltage dependant calcium channels in the dorsal horn ( 17, 18). Gabapentin and Pregabalin (Lyrica, Pfizer), second generation antiepileptics, have shown promise for alleviating pain within the central nervous system ( 15, 16). Specific to the central nervous system, corticosteroids are thought to decrease the production of phospholipase A2 ( 11), a powerful regulator of inflammatory cascades, inhibit the expression of cytokines, and decrease the release of substance P ( 13, 14). Treatment was initiated with prednisone 0.5 mg/kg orally twice daily and gabapentin (Neurontin, Pfizer Canada, Kirkland, Quebec) 10 mg/kg orally 3 times daily. Magnetic resonance imaging (MRI) of the brain revealed CM with severe cerebellar crowding secondary to a caudal occipital malformation, kinking of the brainstem, caudal cerebellar herniation, occlusion of CSF passage through the foramen magnum, and SM affecting the cervical spinal cord ( Figure 1). The 2 following cases, recently presented to the Ontario Veterinary College Teaching Hospital, illustrate the variability in clinical signs that can be observed in dogs afflicted with CM/SM.Ī 3-year-old, spayed female CKCS was presented with a progressive 6-month history of mild paraparesis, cervical hyperesthesia, and frequent episodes of aggressively scratching at her neck and face. Occasionally, the presence of CM/SM is found as incidental findings while investigating another neurologic condition ( 11). Along with the CKCS breed, this condition has been reported in Pekingese dogs, Maltese terriers, miniature dachshunds, fox terriers, lhasa apsos, pomeranians, Yorkshire terriers, and a Samoyed dog ( 4, 8– 10). The incidence of CM in the CKCS breed is an estimated 95% and current studies suggest that SM is present in more than 50% of dogs with CM ( 7) with approximately 35% of affected dogs exhibiting clinical signs ( 2).
Recent data suggest that CM in the Cavalier King Charles spaniel (CKCS) is inherited ( 3, 7). Other documented etiologies causing SM in the dog include spinal trauma ( 4) and neoplasia in the region of the brainstem or foramen magnum ( 5, 6).
This malformation of the caudal fossa is known as a Chiari-like malformation (CM), a condition that appears similar to Chiari type I malformation in humans. A cause of SM in veterinary medicine is a reduced volume of the caudal fossa secondary to an inappropriately small occipital bone ( 2, 3).
Although the exact etiology and pathogenesis are unknown, SM is thought to develop secondary to an obstruction of cerebrospinal fluid (CSF) flow at the level of the foramen magnum ( 2). Syringomyelia (SM) is defined as a condition that results in the development of fluid-containing cavities within the parenchyma of the spinal cord as a consequence of abnormal cerebrospinal fluid movement through the foramen magnum ( 1).
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