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PS-2-5 Effect of bright light exposure on muscle sympathetic nerve activity in human
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Poster sesston 2. Microneurography
activity was digitized at 20 kHz after amplification and filtering. The E C G was digitized at 1 kHz. Single unit action potentials were detected by template-matching method, and were identified as sympathetic vasoconstrictor impulses from their pulse synchrony. Sympathetic spikes were observed in 32.5% of all heart beats at 0 °. The occurrence of spikes increased to 41.1% at 10°, and to 41.4% at 20 °. Thirteen units were accepted as single sympathetic efferents at 0 °, and 11 and 4 more units were detected at tilting from 0 ° to 10°, and from 10° to 20 °, respectively. The average of the minimum R-R interval that induced sympathetic spikes was 850.5 ms for 13 units at 0 °. The same 13 units fired at R-R interval of 822.6 ms at 10°, and 814.2 ms at 20 °. For 11 units that were recruited at 10 °, the minimum R-R interval was 853.7 ms at 10°, and shortened to 833.5 ms at 20 °, For 4 units that were recruited at 20 °, the minimum R-R interval was 881.2 ms, and longer than that of 24 other units. Recruitment of higher threshold units may be a possible mechanism of e n h a n c e m e n t of muscle sympathetic activity with head-up tilting.
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Effect of bright light exposure on muscle sympathetic nerve activity in human
Yasushi Saito 1, Tetsuo Shimizu i, Kazuo Mishima I Ken-ichi Takahashi 1, Yuji Takahashi 1, Susumu Kogawa z, Yuriko Ogawa 1, Yasuo Hishikawa J. 1Department of
Neuropsychiatry, Akita University School of Medicine, Japan; 2Aichi Prefecture Shiroyama Hospital, Japan It is well established that bright light has therapeutic effects on var-
ious kinds of neuropsychiatric disorder. However, the mechanism of the therapeutic action of bright light has not yet been fully elucidated. Niijima et al. (1992) found in rats that bright light exposure enhanced sympathetic outflow and suppressed vagal outflow. It is possib!e that similar modulations of the autonomic nerve system plays an important roles in the therapeutic effect of light in human. In this study, we examined the effect of bright light exposure on muscle sympathetic nerve activity (MSNA) recorded from the peroneal nerve in h u m a n with the use of microneurography. The subjects were 5 healthy males aged 32-41 years. The EEGs, EOGs, mental EMG, ECG, blood pressure and MSNA were simultaneously recorded. After the base line recording for 15 min under the room light (500 Lux), each subject was exposed to bright light (5000 Lux) for 20 min. After the bright light exposure, the same measurement under the room light was repeated for 15 rain. MSNA was expressed as burst rate (bursts/rain), burst incidence (bursts/100 heart beats) and total MSNA (sum of relative amplitude of MSNA bursts). After the bright light exposure, all parameters of MSNA were significantly increased as compared with those before the bright light exposure (P < 0.05, Wilcoxon). Blood pressure and heart rate didn't change significantly through out the study. This study first demonstrated that the bright light exposure enhances MSNA without significantly changing either blood pressure or heart rate.
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Antidromic activation of sensory fibres in proximal nerve lesions: microneurographic evidence R. Casale, M. Buonocore. "Clinica de/Lavoro" Foundation, Service of Clinical Neurophysiology, Rehabilitation Center of Montescano, Montescano (PV), Italy Foci ectopici with increased mechanosensitivity of sensory fibers are frequently seen in peripheral nerve lesions. Microneurography
has been reported to be able to record the antidromic activity of sensory fibers in humans therefore to evaluate the presence of an ectopic focus and establish the organic nature of sensory symptoms. This is the case report of a patient (male, 35 years old) whose presenting complaint was the onset of paraesthesia involving the ulnar side of the hand and forearm after performing specific movements. He had been referred to our Service as thoracic outlet syndrome. Electromyographic examination did not show any signs of lesion in the median and ulnar nerves. Microneurographic evaluation: after isolating a sensory funiculus from the ulnar nerve supplying an area of skin in the region affected by the paraesthesia, the patient was asked to perform some manoeuvres and following some of these (arm abduction, controlateral head rotation) a burst of activity could be recorded in the isolated nerve funiculus, with the concomitant appearance of the sensation of paraesthesia. These bursts of activity are attributable to antidromic stimulation of the sensory fibres in a proximal focus, probably localized at the level of the brachial plexus. This observation confirms how, in targeted cases, microneurography can be useful in the diagnosis of peripheral nerve lesions, permitting to prove both the presence of the ectopic focus and the organic nature of sensory symptoms.
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Microneurographic analysis of sweating disorders
Satoshi lwase 1, Tadaaki Mano 1, Junichi Sugenoya 2, Koji Yamamoto 3, Ken Murakami 3, Takehiko Ikeda l, Shigetaka Hakusui 4, Chihiro Miwa l, Yoshiki Sugiyama 1, Gen Sobue 5. l Department of Autonomic and Behavioral
Neurosciences, Research Institute of Environmental Medicine, Nagoya University, Japan; 2 Department of Physiology, 3 Department of lnternal Medicine IV, Aichi Medical University, 4 Department of Neurology, Nagoya Daini Red Cross Hospital; 5Department of Neurology, School of Medicine, Nagoya University, Japan The pathophysiology of the sweating disorders was analyzed by recording the sympathetic nerve activity from the skin nerve fascicle (skin sympathetic nerve activity, SSNA), which contains the sudomotor and the vasoconstrictor nerve activities, simultaneously with the skin potential change, the sweat rate by the ventilated capsule method, and the skin blood flow by the laser Doppler flowmetry. A tungsten microelectrode with a tip diameter of 1 #m, and impedance of 3 ~ 5 M ~ was inserted into the tibial, peroneal, or median nerves, and burst discharges from the postganglionic efferent sympathetic fibers were recorded. In patients with palmoplantar hyperhidrosis, resting activity of skin sympathetic nerve was moderately elevated, and the response of skin sympathetic nerve activity to mental stimuli and increase in ambient temperature was markedly enhanced. In anhidrosis, simultaneous recordings of skin sympathetic nerve activity, skin potential, and sweat rate determined that the lesions were estimated in the peripheral nerves, the sweat glands, or the sweat ducts. Resting SSNA in acquired idiopathic generalized anhidrosis (immune deposits in the sweat ducts), were markedly enhanced, and the responses to arousal stimuli showed normal SSNA reflex discharge, changes in skin potential, and reduction in skin blood flow, however, there was no response in sweat rate. Anhidrosis due to autonomic neuropathy demonstrated a low resting SSNA and lowered responses in SSNA reflex bursts, skin potential, sweat rate, and skin blood flow reduction. Hemihidrosis due to cervical cord lesion exhibited a lower resting SSNA in the affected side, whereas the response to arousal stimuli was normal. In the recovery stage, normalization
Poster sesston 2. Microneurography
activity was digitized at 20 kHz after amplification and filtering. The E C G was digitized at 1 kHz. Single unit action potentials were detected by template-matching method, and were identified as sympathetic vasoconstrictor impulses from their pulse synchrony. Sympathetic spikes were observed in 32.5% of all heart beats at 0 °. The occurrence of spikes increased to 41.1% at 10°, and to 41.4% at 20 °. Thirteen units were accepted as single sympathetic efferents at 0 °, and 11 and 4 more units were detected at tilting from 0 ° to 10°, and from 10° to 20 °, respectively. The average of the minimum R-R interval that induced sympathetic spikes was 850.5 ms for 13 units at 0 °. The same 13 units fired at R-R interval of 822.6 ms at 10°, and 814.2 ms at 20 °. For 11 units that were recruited at 10 °, the minimum R-R interval was 853.7 ms at 10°, and shortened to 833.5 ms at 20 °, For 4 units that were recruited at 20 °, the minimum R-R interval was 881.2 ms, and longer than that of 24 other units. Recruitment of higher threshold units may be a possible mechanism of e n h a n c e m e n t of muscle sympathetic activity with head-up tilting.
•2•
Effect of bright light exposure on muscle sympathetic nerve activity in human
Yasushi Saito 1, Tetsuo Shimizu i, Kazuo Mishima I Ken-ichi Takahashi 1, Yuji Takahashi 1, Susumu Kogawa z, Yuriko Ogawa 1, Yasuo Hishikawa J. 1Department of
Neuropsychiatry, Akita University School of Medicine, Japan; 2Aichi Prefecture Shiroyama Hospital, Japan It is well established that bright light has therapeutic effects on var-
ious kinds of neuropsychiatric disorder. However, the mechanism of the therapeutic action of bright light has not yet been fully elucidated. Niijima et al. (1992) found in rats that bright light exposure enhanced sympathetic outflow and suppressed vagal outflow. It is possib!e that similar modulations of the autonomic nerve system plays an important roles in the therapeutic effect of light in human. In this study, we examined the effect of bright light exposure on muscle sympathetic nerve activity (MSNA) recorded from the peroneal nerve in h u m a n with the use of microneurography. The subjects were 5 healthy males aged 32-41 years. The EEGs, EOGs, mental EMG, ECG, blood pressure and MSNA were simultaneously recorded. After the base line recording for 15 min under the room light (500 Lux), each subject was exposed to bright light (5000 Lux) for 20 min. After the bright light exposure, the same measurement under the room light was repeated for 15 rain. MSNA was expressed as burst rate (bursts/rain), burst incidence (bursts/100 heart beats) and total MSNA (sum of relative amplitude of MSNA bursts). After the bright light exposure, all parameters of MSNA were significantly increased as compared with those before the bright light exposure (P < 0.05, Wilcoxon). Blood pressure and heart rate didn't change significantly through out the study. This study first demonstrated that the bright light exposure enhances MSNA without significantly changing either blood pressure or heart rate.
•
Antidromic activation of sensory fibres in proximal nerve lesions: microneurographic evidence R. Casale, M. Buonocore. "Clinica de/Lavoro" Foundation, Service of Clinical Neurophysiology, Rehabilitation Center of Montescano, Montescano (PV), Italy Foci ectopici with increased mechanosensitivity of sensory fibers are frequently seen in peripheral nerve lesions. Microneurography
has been reported to be able to record the antidromic activity of sensory fibers in humans therefore to evaluate the presence of an ectopic focus and establish the organic nature of sensory symptoms. This is the case report of a patient (male, 35 years old) whose presenting complaint was the onset of paraesthesia involving the ulnar side of the hand and forearm after performing specific movements. He had been referred to our Service as thoracic outlet syndrome. Electromyographic examination did not show any signs of lesion in the median and ulnar nerves. Microneurographic evaluation: after isolating a sensory funiculus from the ulnar nerve supplying an area of skin in the region affected by the paraesthesia, the patient was asked to perform some manoeuvres and following some of these (arm abduction, controlateral head rotation) a burst of activity could be recorded in the isolated nerve funiculus, with the concomitant appearance of the sensation of paraesthesia. These bursts of activity are attributable to antidromic stimulation of the sensory fibres in a proximal focus, probably localized at the level of the brachial plexus. This observation confirms how, in targeted cases, microneurography can be useful in the diagnosis of peripheral nerve lesions, permitting to prove both the presence of the ectopic focus and the organic nature of sensory symptoms.
•
Microneurographic analysis of sweating disorders
Satoshi lwase 1, Tadaaki Mano 1, Junichi Sugenoya 2, Koji Yamamoto 3, Ken Murakami 3, Takehiko Ikeda l, Shigetaka Hakusui 4, Chihiro Miwa l, Yoshiki Sugiyama 1, Gen Sobue 5. l Department of Autonomic and Behavioral
Neurosciences, Research Institute of Environmental Medicine, Nagoya University, Japan; 2 Department of Physiology, 3 Department of lnternal Medicine IV, Aichi Medical University, 4 Department of Neurology, Nagoya Daini Red Cross Hospital; 5Department of Neurology, School of Medicine, Nagoya University, Japan The pathophysiology of the sweating disorders was analyzed by recording the sympathetic nerve activity from the skin nerve fascicle (skin sympathetic nerve activity, SSNA), which contains the sudomotor and the vasoconstrictor nerve activities, simultaneously with the skin potential change, the sweat rate by the ventilated capsule method, and the skin blood flow by the laser Doppler flowmetry. A tungsten microelectrode with a tip diameter of 1 #m, and impedance of 3 ~ 5 M ~ was inserted into the tibial, peroneal, or median nerves, and burst discharges from the postganglionic efferent sympathetic fibers were recorded. In patients with palmoplantar hyperhidrosis, resting activity of skin sympathetic nerve was moderately elevated, and the response of skin sympathetic nerve activity to mental stimuli and increase in ambient temperature was markedly enhanced. In anhidrosis, simultaneous recordings of skin sympathetic nerve activity, skin potential, and sweat rate determined that the lesions were estimated in the peripheral nerves, the sweat glands, or the sweat ducts. Resting SSNA in acquired idiopathic generalized anhidrosis (immune deposits in the sweat ducts), were markedly enhanced, and the responses to arousal stimuli showed normal SSNA reflex discharge, changes in skin potential, and reduction in skin blood flow, however, there was no response in sweat rate. Anhidrosis due to autonomic neuropathy demonstrated a low resting SSNA and lowered responses in SSNA reflex bursts, skin potential, sweat rate, and skin blood flow reduction. Hemihidrosis due to cervical cord lesion exhibited a lower resting SSNA in the affected side, whereas the response to arousal stimuli was normal. In the recovery stage, normalization