Objective: In patients with hemifacial spasm (HFS), abnormal muscle responses (AMR) are frequently present. The objective of this study was to investigate whether the afferent input of AMR is mediated by antidromic fa...Objective: In patients with hemifacial spasm (HFS), abnormal muscle responses (AMR) are frequently present. The objective of this study was to investigate whether the afferent input of AMR is mediated by antidromic facial nerve stimulatio n or orthodromic trigeminal nerve stimulation. Methods: AMR in the orbicularis oris muscle were recorded in 28 patients with HFS. When AMR were present, they were recorded after subthreshold stimulation of the facial nerve and weak stimulation delivered to the skin. Results: AMR were recordable in 24 (86%) of the patients, and usually consisted of the early constant component (mean onset latency, 10.0 ms) and late variable component (35.3 ms), similar to R1 and R2 of the bli nk reflex. The early or late components of AMR, or both, were frequently elicite d after subthreshold stimulation of the facial nerve (43%)and skin stimulation (88%). Conclusions: AMR are likely to be mediated by trigeminal afferent inputs , rather than antidromic activation of the facial nerve, and are a type of trige minal reflex.展开更多
Background: Campylobacter jejuni enteritis is the most common antecedent infection in Guillain Barré syndrome (GBS). C. jejuni related GBS is usually acute motor axonal neuropathy (AMAN), but previous reports des...Background: Campylobacter jejuni enteritis is the most common antecedent infection in Guillain Barré syndrome (GBS). C. jejuni related GBS is usually acute motor axonal neuropathy (AMAN), but previous reports described many cases of the demyelinating subtype of GBS (acute inflammatory demyelinating polyneuropathy ) after C. jejuni infection. Objective: To investigate whether C. jejuni infection elicits AIDP. Methods: In 159 consecutive patients with GBS, antibodies against C. jejuni were measured using ELISA. Antecedent C. jejuni infection was determined by the strict criteria of positive C. jejuni serology and a history of a diarrheal illness within the previous 3 weeks. Electrodiagnostic studies were performed weekly for the first 4 weeks, and sequential findings were analyzed. Results: There was evidence of recent C. jejuni infection in 22 (14% ) patients. By electrodiagnostic criteria, these patients were classified with AMAN (n = 16; 73% ) or AIDP (n = 5; 23% ) or as unclassified (n = 1) in the first studies. The five C. jejuni positive patients with the AIDP pattern showed prolongedmotor distal latencies in two or more nerves and had their rapid normalization within 2 weeks, eventually all showing the AMAN pattern. In contrast, patients with cytomegalovirus or Epstein Barr virus related AIDP (n = 13) showed progressive increases in distal latencies in the 8 weeks after onset. Conclusion: Patients with C. jejuni related Guillain Barré syndrome can show transient slowing of nerve conduction, mimicking demyelination, but C. jejuni infection does not appear to elicit acute inflammatory demyelinating polyneuropathy.展开更多
Objective: To investigate the effects of hyperglycemia on axonal excitability in human diabetics. Diabetic nerve dysfunction is partly associated with the alt ered polyol pathway and Na+ K+ATPase activity, probably re...Objective: To investigate the effects of hyperglycemia on axonal excitability in human diabetics. Diabetic nerve dysfunction is partly associated with the alt ered polyol pathway and Na+ K+ATPase activity, probably resulting in a decrea se in the transaxonal Na+gradient and reduced nodal Na+currents. Methods:Thres hold tracking was used to measure the relative refractory periods (RPs) of media n motor axons in 58 diabetic patients, 45 normal subjects, and 12 patients with non diabetic axonal neuropathy. In diabetic patients, the relationship of RPs w ith hemoglobin A1c (HbA1c) levels was analyzed. Results: The mean RP was similar for diabetics and normal controls as a group, but was longer in patients with n on diabetic neuropathy than in normal controls (P=0.02). Diabetic patients with good glycemic control (HbA1c levels < 7%) had longer RPs than patients with po orer glycemic control and normal controls (P=0.01). RP was longest at the HbA1c level of 6%, gradually decreasing and reaching a plateau at the HbA1c level of 8 9%. Conclusions: Hyperglycemia shortens RPs, possibly because metabolic abno rmalities lead to reduced nodal Na+currents, and thereby to a lower inactivatio n of Na+channels when generating an action potential. Significance: RP measurem ents could provide new insights into the ionic pathophysiology of human diabetic neuropathy.展开更多
文摘Objective: In patients with hemifacial spasm (HFS), abnormal muscle responses (AMR) are frequently present. The objective of this study was to investigate whether the afferent input of AMR is mediated by antidromic facial nerve stimulatio n or orthodromic trigeminal nerve stimulation. Methods: AMR in the orbicularis oris muscle were recorded in 28 patients with HFS. When AMR were present, they were recorded after subthreshold stimulation of the facial nerve and weak stimulation delivered to the skin. Results: AMR were recordable in 24 (86%) of the patients, and usually consisted of the early constant component (mean onset latency, 10.0 ms) and late variable component (35.3 ms), similar to R1 and R2 of the bli nk reflex. The early or late components of AMR, or both, were frequently elicite d after subthreshold stimulation of the facial nerve (43%)and skin stimulation (88%). Conclusions: AMR are likely to be mediated by trigeminal afferent inputs , rather than antidromic activation of the facial nerve, and are a type of trige minal reflex.
文摘Background: Campylobacter jejuni enteritis is the most common antecedent infection in Guillain Barré syndrome (GBS). C. jejuni related GBS is usually acute motor axonal neuropathy (AMAN), but previous reports described many cases of the demyelinating subtype of GBS (acute inflammatory demyelinating polyneuropathy ) after C. jejuni infection. Objective: To investigate whether C. jejuni infection elicits AIDP. Methods: In 159 consecutive patients with GBS, antibodies against C. jejuni were measured using ELISA. Antecedent C. jejuni infection was determined by the strict criteria of positive C. jejuni serology and a history of a diarrheal illness within the previous 3 weeks. Electrodiagnostic studies were performed weekly for the first 4 weeks, and sequential findings were analyzed. Results: There was evidence of recent C. jejuni infection in 22 (14% ) patients. By electrodiagnostic criteria, these patients were classified with AMAN (n = 16; 73% ) or AIDP (n = 5; 23% ) or as unclassified (n = 1) in the first studies. The five C. jejuni positive patients with the AIDP pattern showed prolongedmotor distal latencies in two or more nerves and had their rapid normalization within 2 weeks, eventually all showing the AMAN pattern. In contrast, patients with cytomegalovirus or Epstein Barr virus related AIDP (n = 13) showed progressive increases in distal latencies in the 8 weeks after onset. Conclusion: Patients with C. jejuni related Guillain Barré syndrome can show transient slowing of nerve conduction, mimicking demyelination, but C. jejuni infection does not appear to elicit acute inflammatory demyelinating polyneuropathy.
文摘Objective: To investigate the effects of hyperglycemia on axonal excitability in human diabetics. Diabetic nerve dysfunction is partly associated with the alt ered polyol pathway and Na+ K+ATPase activity, probably resulting in a decrea se in the transaxonal Na+gradient and reduced nodal Na+currents. Methods:Thres hold tracking was used to measure the relative refractory periods (RPs) of media n motor axons in 58 diabetic patients, 45 normal subjects, and 12 patients with non diabetic axonal neuropathy. In diabetic patients, the relationship of RPs w ith hemoglobin A1c (HbA1c) levels was analyzed. Results: The mean RP was similar for diabetics and normal controls as a group, but was longer in patients with n on diabetic neuropathy than in normal controls (P=0.02). Diabetic patients with good glycemic control (HbA1c levels < 7%) had longer RPs than patients with po orer glycemic control and normal controls (P=0.01). RP was longest at the HbA1c level of 6%, gradually decreasing and reaching a plateau at the HbA1c level of 8 9%. Conclusions: Hyperglycemia shortens RPs, possibly because metabolic abno rmalities lead to reduced nodal Na+currents, and thereby to a lower inactivatio n of Na+channels when generating an action potential. Significance: RP measurem ents could provide new insights into the ionic pathophysiology of human diabetic neuropathy.
