reperfusion in diabetic nerve: Resistance for ischaemic conduction failure and prolonged conduction failure after reperfusion

reperfusion in diabetic nerve: Resistance for ischaemic conduction failure and prolonged conduction failure after reperfusion

e210 Japanese Society of Clincal Neurophysiology / Clinical Neurophysiology 118 (2007) e203–e212 26. Magnetic stimulation 28. Nerve conduction stud...

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e210

Japanese Society of Clincal Neurophysiology / Clinical Neurophysiology 118 (2007) e203–e212

26. Magnetic stimulation

28. Nerve conduction study

Slow frequency repetitive transcranial magnetic stimulation improves freezing gait—Y. Sawada 1, M. Tamaki 1, 1 2 1 K. Arasaki , K. Sudo ( Kanto Medical Center NTT-EC, Japan, 2 NTT Cyber-space laboratories, Japan)

Motor unit number estimation in spinal and bulbar muscular atrophy—A. Inaba, T. Yokota, H. Mizusawa (Tokyo Medical and Dental University, Japan)

Frozen gait is difficult phenomenon to be improved by physical therapy alone. We studied the effects of rTMS on frozen gait in 14 patients with parkinsonism during physical therapy using a gait analysis system. By this system, step length, step width, step duration and swing duration were analysed. Also foot pressure of heel, sole and big-toe were recorded separately. Forty stimulus of 90% of maximal output were applied at the frontal area of 6 patients with the frequency of 0.2 Hz in a day for one week. For excluding the placebo effect, stimulus were applied at the occipital area other 8 cases. These cases were given another one week rTMS on frontal area to find difference by stimulated site. The step length increased 60% or more in 5 cases, 30–60% in 5 cases and 0–30% in 6 cases each other. In the improved cases, difference was significant with P < 0.05. Improved cases showed smooth shift of weights from heel to big toe. Difference was not found between frontal and occipital stimulus site. The mechanism of these rTMS effect on frozen gait was not known yet. Further study is necessary to ascertain clinical effectiveness.

Objectives: To evaluate the number and size of the motor unit in patients with X-linked recessive spinal and bulbar muscular atrophy (SBMA). Subjects and methods: Eight patients with SBMA (44–67 years, duration of the illness: 2–30 years) were studied. The motor unit number estimation (MUNE) was performed by the multiple point stimulation (MPS). Ten single motor unit potentials (SMUP) were obtained from the first dorsal interosseous muscle using surface recording electrodes by the threshold electrical stimulation of the ulnar nerve around the wrist. The MUNE was calculated by dividing the negative peak area of the supramaximal CMAP by that of the averaged SMUP. Results: In SBMA, the MUNE decreased to 94 ± 59 (mean ± SD, range 32–187) as compared with the value of normal controls(288 ± 48, range 238–379). The averaged SMUP size in SBMA were increased to 212 ± 138 lV ms (normal controls: 107 ± 33 lV ms). As the disease progress, the MUNE tended to decrease and the averaged SMUP size increased. Conclusion: The MUNE might be one of the useful parameters for evaluating the motor unit loss in SBMA.

doi:10.1016/j.clinph.2007.06.046 doi:10.1016/j.clinph.2007.06.048

29. Nerve conduction study 27. Nerve conduction study Motor unit number estimates (MUNE) in amyotrophic lateral sclerosis (ALS)?: Comparison of the abductor pollicis brevis (APB) and abductor digiti minimi (ADM) muscles— S. Hirano, S. Kuwabara, S. Misawa, T. Hattori (Department of Neurology, Graduate School of Medicine, Chiba University, Japan)

Electrophysiological paradox to ischaemia/reperfusion in diabetic nerve: Resistance for ischaemic conduction failure and prolonged conduction failure after reperfusion— M. Baba 1, H. Nukada 2 (1 Hirosaki University, Japan, 2 University of Otago, New Zealand)

Objective: To investigate whether MUNE of APB or ADM is more sensitive or useful to evaluate the progression of ALS. Methods: In 26 patients with ALS, MUNE of both ADM and APB were measured, using the incremental method when MUNE was less than 10, or using the multiple point stimulation method when MUNE was 10 or more. Their outcomes were followed up. Results: MUNE (mean ± SD) was 25 ± 41 for APB and 41 ± 46 for ADM, significantly smaller than controls. Both the observation period and survival period were positively correlated with MUNE of both APB and ADM. MUNE of APB were less than 10 in 6 patients, all of whom had been intubated or deceased within 12 months from the first MUNE examination. Conclusion: MUNE of APB decreases more rapidly than that of ADM in ALS, suggesting preferential involvement of the thenar muscles. When performing MUNE in ALS patients, APBMUNE is more sensitive in predicting outcome, whereas ADMMUNE can be more appropriate to follow the disease course and may be a more useful parameter in clinical trial studies.

To investigate nerve conduction during ischaemic/reperfusion injury in diabetic nerve, transient near-complete ischameia of right hindlimb in STZ-diabetic (8–9 wk) rats was induced for 30 min, 1 h, 1 h 15 min, 1 h 30 min, 2 h, and 2 h 30 min by clipping major arteries. Nerve conduction study in sciatic-tibial nerves was carried out before and during ischaemia and after reperfusion, using near-nerve needles placed at sciatic notch, knee and ankle. CMAP was recorded by a needle inserting plantar muscles. Complete Ischemic conduction failure between ankle and thigh was noticed after 29.0 ± 8.2 min in controls and 45.0 ± 10.1 min in diabetic rats (mean ± SD, p < 0.02). In non-diabetic controls, CMAP reinstituted at the pre-ischaemic level within 10 min of reperfusion if ischaemia is within 2 h. In contrast, diabetic nerves showed prolonged conduction failure of axonal degeneration type after 2 h and 1 h 30 min of ischaemia. Following 1 h 15 min of ischaemia, diabetic nerve revealed prolonged conduction failure of axonal degeneration type in some and with delayed recovery in others. After 1-h ischaemia, delayed recovery was found in diabetic nerves. These abnormal recoveries could be restored after euglycaemia by insulin injection.

doi:10.1016/j.clinph.2007.06.047

doi:10.1016/j.clinph.2007.06.049