In 56 dogs and 1 cat a di ag no sis of sus pec ted fi bro car ti la gi nous em bo lism was made ba sed on the his to ry, the ty pi cal cli ni cal pre sen ta ti on and the ab sen ce of spe ci fic ab nor ma li ties on ra di og rap hy and my e log rap hy.None of the di ag no ses was con fir med by his top atho lo gi cal exa mi na ti on, sin ce none of the pa tients was eu tha ni zed at the time of di ag no sis.The ra py con si sted of sup por ti ve care with ad di ti o nal phy sio and/or hy dro the ra py in a quar ter of the ca ses.Short-and long-term re sults (more than 1 year af ter di ag no sis) were bet ter than ear lier re por ted.
Generalized myokymia and neuromyotonia (M/NM) in Jack Russell Terriers (JRTs) is related to peripheral nerve hyperexcitability syndrome in humans, a symptom complex resulting from diverse etiologies.Clinical and electrodiagnostic evaluation is used to narrow the list of possible etiological diagnoses in JRTs with M/NM.Nine healthy JRTs and 8 affected JRTs.A prospective study was conducted comparing clinical and electrophysiological characteristics in 8 JRTs affected by M/NM with 9 healthy JRT controls.All affected dogs except 1 had clinical signs typical of hereditary ataxia (HA). In 6 dogs, neuromyotonic discharges were recorded during electromyogram. Motor nerve conduction studies showed an axonal neuropathy in only 1 affected dog. Compared with controls, brainstem auditory-evoked potentials (BAEP) showed prolonged latencies (P<.05) accompanied by the disappearance of wave components in 3 dogs. Onset latencies of tibial sensory-evoked potentials (SEP) recorded at the lumbar intervertebral level were delayed in the affected group (P<.001). The BAEP and SEP results of the only neuromyotonic dog without ataxia were normal.The BAEP and spinal SEP abnormalities observed in JRTs with M/NM were associated with the presence of HA. Therefore, these electrophysiological findings presumably arise from the neurodegenerative changes characterizing HA and do not directly elucidate the pathogenesis of M/NM. An underlying neuronal ion channel dysfunction is thought to be the cause of M/NM in JRTs.
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