[Pain caused by ephaptic transmission occurring in the recovery phase of diabetic vascular mononeuropathy was effectively suppressed with L-threo-3,4-dihydroxyphenyl-serine].
A 59-year-old man with an 8-years history of diabetes mellitus had an acute onset of sharp pain in the anterior part of right lower leg. One month later, the pain changed to deep dull nature in the deeper site of the peroneal region. The pain increased, when he stood up, walked, and stayed in the cold room and decreased by rest. It was more painful in the evening than in the morning. The first sharp pain was thought to be caused by ischemia due to diabetic vascular neuropathy. The next dull pain was considered to be originated from ephaptic transmission between sympathetic efferent fibers to group IV and afferent ones from the skeletal muscle. The latter dull pain was selectively suppressed by nerve block when it became effective to the branch of deep peroneal nerve to extensor digitorum longus muscle. The hypothesis of ephaptic transmission was supported by meaningful decrease of muscle sympathetic activity detected by microneurography before and after the dosage of L-DOPS, which effectively suppressed the pain as well as other alpha-stimulant, midodrine hydrochloride. We concluded that the ephaptic pain caused by muscle sympathetic activity could be suppressed by the vasoconstrictive drugs through the mechanism of baroreflex control.
Ohshima
F
F
Department of Neurology, Yokohama Rousai Hospital.
Kunimoto
M
M
Inoue
K
K
D000316:Adrenergic alpha-Agonists / Q000627:therapeutic use; D017704:Baroreflex / Q000502:physiology; D003929:Diabetic Neuropathies / Q000150:complications / Q000503:physiopathology*; D015103:Droxidopa / Q000627:therapeutic use*; D006801:Humans; D007866:Leg; D008297:Male; D008875:Middle Aged; D008879:Midodrine / Q000627:therapeutic use; D018482:Muscle, Skeletal / Q000294:innervation*; D009619:Nociceptors / Q000503:physiopathology; D010146:Pain / Q000188:drug therapy* / Q000209:etiology*; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D009435:Synaptic Transmission / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000627:therapeutic use
D000316:Adrenergic alpha-Agonists; D014662:Vasoconstrictor Agents; D008879:Midodrine; D015103:Droxidopa