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Clinical and electrophysiological characterization of myokymia and neuromyotonia in Jack Russell terriers

An Vanhaesebrouck (UGent) , Iris Van Soens (UGent) , L Poncelet, Luc Duchateau (UGent) , Sofie Bhatti (UGent) , Ingeborgh Polis (UGent) , Seppe Diels (UGent) and Luc Van Ham (UGent)
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Abstract
Background: 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. Objective: Clinical and electrodiagnostic evaluation is used to narrow the list of possible etiological diagnoses in JRTs with M/NM. Animals: Nine healthy JRTs and 8 affected JRTs. Methods: A prospective study was conducted comparing clinical and electrophysiological characteristics in 8 JRTs affected by M/NM with 9 healthy JRT controls. Results: 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. Conclusions and Clinical Importance: 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.
Keywords
EVOKED-POTENTIALS, MOTOR UNIT-ACTIVITY, PERIPHERAL-NERVE HYPEREXCITABILITY, Potassium channels, Hereditary ataxia, MACHADO-JOSEPH-DISEASE, Electrodiagnostics, Dog, SPINAL-CORD, GENERALIZED MYOKYMIA, FRIEDREICHS ATAXIA, NORMAL DOGS, STIMULATION, SCA3

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Chicago
Vanhaesebrouck, An, Iris Van Soens, L Poncelet, Luc Duchateau, Sofie Bhatti, Ingeborgh Polis, Seppe Diels, and Luc Van Ham. 2010. “Clinical and Electrophysiological Characterization of Myokymia and Neuromyotonia in Jack Russell Terriers.” Journal of Veterinary Internal Medicine 24 (4): 882–889.
APA
Vanhaesebrouck, A., Van Soens, I., Poncelet, L., Duchateau, L., Bhatti, S., Polis, I., Diels, S., et al. (2010). Clinical and electrophysiological characterization of myokymia and neuromyotonia in Jack Russell terriers. JOURNAL OF VETERINARY INTERNAL MEDICINE, 24(4), 882–889.
Vancouver
1.
Vanhaesebrouck A, Van Soens I, Poncelet L, Duchateau L, Bhatti S, Polis I, et al. Clinical and electrophysiological characterization of myokymia and neuromyotonia in Jack Russell terriers. JOURNAL OF VETERINARY INTERNAL MEDICINE. 2010;24(4):882–9.
MLA
Vanhaesebrouck, An, Iris Van Soens, L Poncelet, et al. “Clinical and Electrophysiological Characterization of Myokymia and Neuromyotonia in Jack Russell Terriers.” JOURNAL OF VETERINARY INTERNAL MEDICINE 24.4 (2010): 882–889. Print.
@article{1235162,
  abstract     = {Background: 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.
Objective: Clinical and electrodiagnostic evaluation is used to narrow the list of possible etiological diagnoses in JRTs with M/NM.
Animals: Nine healthy JRTs and 8 affected JRTs.
Methods: A prospective study was conducted comparing clinical and electrophysiological characteristics in 8 JRTs affected by M/NM with 9 healthy JRT controls.
Results: 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 {\textlangle} .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 {\textlangle} .001). The BAEP and SEP results of the only neuromyotonic dog without ataxia were normal.
Conclusions and Clinical Importance: 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.},
  author       = {Vanhaesebrouck, An and Van Soens, Iris and Poncelet, L and Duchateau, Luc and Bhatti, Sofie and Polis, Ingeborgh and Diels, Seppe and Van Ham, Luc},
  issn         = {0891-6640},
  journal      = {JOURNAL OF VETERINARY INTERNAL MEDICINE},
  keyword      = {EVOKED-POTENTIALS,MOTOR UNIT-ACTIVITY,PERIPHERAL-NERVE HYPEREXCITABILITY,Potassium channels,Hereditary ataxia,MACHADO-JOSEPH-DISEASE,Electrodiagnostics,Dog,SPINAL-CORD,GENERALIZED MYOKYMIA,FRIEDREICHS ATAXIA,NORMAL DOGS,STIMULATION,SCA3},
  language     = {eng},
  number       = {4},
  pages        = {882--889},
  title        = {Clinical and electrophysiological characterization of myokymia and neuromyotonia in Jack Russell terriers},
  url          = {http://dx.doi.org/10.1111/j.1939-1676.2010.0525.x},
  volume       = {24},
  year         = {2010},
}

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