Skin Sympathetic Nerve Activity Bursts Research Articles

Sympathetic toggled paroxysmal atrial fibrillation and recurrent premature atrial contractions in ambulatory patients

BackgroundAutonomic nerve activity is important in the mechanisms of paroxysmal atrial fibrillation (PAF). ObjectiveThe purpose of this study was to test the hypothesis that a single burst of skin sympathetic nerve activity (SKNA) can toggle on and off PAF or premature atrial contraction (PAC) clusters. MethodsSimultaneous recording of SKNA and electrocardiogram (neuECG) recording was performed over 7 days in patients with PAF. ResultsIn study 1, 8 patients (7 men and 1 woman; age 62 ± 8 years) had 124 episodes of PAF. An SKNA burst toggled both on and off PAF in 8 episodes (6.5%) (type 1), toggled on but not off in 12 episodes (9.7%) (type 2), and toggled on a PAC cluster followed by PAF in 4 episodes (3.2%) (type 3). The duration of these PAF episodes was <10 minutes. The remaining 100 episodes (80.6%) were associated with active SKNA bursts throughout PAF (type 4) and lasted longer than type 1 (P = .0185) and type 2 (P = .0027) PAF. There were 47 PAC clusters. Among them, 24 (51.1%) were toggled on and off, and 23 (48.9%) were toggled on but not off by an SKNA burst. In study 2, 17 patients (9 men and 8 women; age 58 ± 12 years) had <10 minutes of PAF (4, 8, 0, and 31 of types 1, 2, 3, and 4, respectively). There were significant circadian variations of all types of PAF. ConclusionA single SKNA burst can toggle short-duration PAF and PAC cluster episodes on and off. The absence of continued SKNA after the onset might have affected the maintenance of these arrhythmias.

Sympathetic toggled sinus rate acceleration as a mechanism of sustained sinus tachycardia in chronic orthostatic intolerance syndrome

The role of sympathetic nerve activity to maintain sinus rate acceleration remains unclear. The purpose of this study was to test the hypothesis that sustained (>30 seconds) sinus rate acceleration can be associated with either a sympathetic driven or a sympathetic toggled mechanism. We used a patch monitor to record skin sympathetic nerve activity (SKNA) and electrocardiogram over 24 hours. Study 1 included chronic orthostatic intolerance (OI) (n = 18), atrial fibrillation (n = 7), and asymptomatic normal control (n = 19) groups. Study 2 included 17 participants with chronic OI not treated with ivabradine, pyridostigmine, or β-blockers. While a majority of sinus rate acceleration was driven by persistent SKNA in study 1, some episodes were toggled on and off by SKNA bursts without persistent SKNA elevation. The sympathetic toggled sinus rate acceleration episodes were found in 7 of 18 participants with chronic OI (39%), 2 of 7 participants with atrial fibrillation (29%), and 6 of 19 normal control participants (32%) (P = .847) and were faster and longer in the chronic OI group than in other groups. In study 2, there were a total of 11 episodes of sinus rate acceleration that persisted for >200 seconds. Among these episodes, 6 (35%) were toggled on and off by SKNA bursts. Sustained sinus rate acceleration (may be toggled on or off) is associated with SKNA bursts in participants with chronic OI, participants with atrial fibrillation, and normal controls. Patients with OI had more frequent and longer episodes than did other groups.

Skin sympathetic nerve activity in patients with chronic orthostatic intolerance.

Chronic orthostatic intolerance (OI) is characterizedby the development of tachycardia and other symptomswhen assuming an upright body position. The purpose of this study was to test the hypothesis that skin sympathetic nerve activity (SKNA) bursts are specific symptomatic biomarkers in patients with chronic OI. We used an electrocardiogram monitor with a built-in triaxial accelerometer to simultaneously record SKNA and posture in ambulatory participants. Study 1 compared chronic OI (14 women and 2 men; mean age 35 ± 10 years) with reference control participants (14 women; mean age 31 ± 6 years). Study 2 included 17 participants with chronic OI (15 women and 2 men; mean age 39 ± 12 years) not yet treated with ivabradine, pyridostigmine, or β-blockers. In study 1, there were 124 episodes (8 ± 4 per participant) of postural changes, with 11 episodes (8.9%) associated with symptoms. In comparison, 0 of 104 postural changes (7 ± 3 per participant) in controls were symptomatic (P = .0011). In participants with chronic OI, the SKNA bursts associated with symptomshad higher burst frequencies, longer burst durations, and larger mean burst areas than did bursts during asymptomatic periods. However, SKNA bursts and tachycardia were asymptomaticin controls. We analyzed 110 symptomatic episodes in study 2 (6 ± 5 per participant). Among them, 98 (89.1%) followed at least 1 SKNA burst. In comparison, only 41 (37.3%) had heart rate exceed 100 beats/min 1 minute before symptom onset (P < .0001). SKNA bursts are a highly specific, albeit insensitive, symptomatic biomarker for chronic OI.

Skin Sympathetic Nerve Activity and the Short-Term QT Interval Variability in Patients With Electrical Storm.

Background: Skin sympathetic nerve activity (SKNA) and QT interval variability are known to be associated with ventricular arrhythmias. However, the relationship between the two remains unclear.Objective: The aim was to test the hypothesis that SKNA bursts are associated with greater short-term variability of the QT interval (STVQT) in patients with electrical storm (ES) or coronary heart disease without arrhythmias (CHD) than in healthy volunteers (HV).Methods: We simultaneously recorded the ECG and SKNA during sinus rhythm in patients with ES (N = 10) and CHD (N = 8) and during cold-water pressor test in HV (N = 12). The QT and QTc intervals were manually marked and calculated within the ECG. The STVQT was calculated and compared to episodes of SKNA burst and non-bursting activity.Results: The SKNA burst threshold for ES and HV was 1.06 ± 1.07 and 1.88 ± 1.09 μV, respectively (p = 0.011). During SKNA baseline and burst, the QT/QTc intervals and STVQT for ES and CHD were significantly higher than those of the HV. In all subjects, SKNA bursts were associated with an increased STVQT (from 6.43 ± 2.99 to 9.40 ± 5.12 ms, p = 0.002 for ES; from 9.48 ± 4.40 to 12.8 ± 5.26 ms, p = 0.016 for CHD; and from 3.81 ± 0.73 to 4.49 ± 1.24 ms, p = 0.016 for HV). The magnitude of increased STVQT in ES (3.33 ± 3.06 ms) and CHD (3.34 ± 2.34 ms) was both higher than that of the HV (0.68 ± 0.84 ms, p = 0.047 and p = 0.020).Conclusion: Compared to non-bursting activity, SKNA bursts were associated with a larger increase in the QTc interval and STVQT in patients with heart disease than in HV.

Sympathetic nerve outflow to skin in a case with dentatorubral-pallidoluysian atrophy

Dentatorubral-pallidoluysian atrophy (DRPLA) is an autosomal dominant neurodegenerative disorder characterized by slowly progressive cerebellar ataxia. Previously, autonomic symptoms or dysfunction have not been reported. To evaluate subclinical autonomic dysfunction regarding thermoregulatory function in SCA, we recorded sympathetic outflow to skin in a DRPLA patient confirmed by genetic analysis. We recorded skin sympathetic nerve activity (SSNA), which was elicited and recorded by using the microneurographical technique. In results, the resting frequency of SSNA bursts was very low (8.2 ± 0.4 bursts/min [institutional normal range: 20.8 ± 2.4 bursts/min]). However, acceleration of SSNA bursts induced by mental arithmetic stress was confirmed. The amplitude of reflex bursts induced by electrical stimuli was slightly low (9.6 ± 1.6 μV [institutional normal range: 10.9 ± 2.2 μV]), and the reflex latency was mildly prolonged (872 ± 23.7 msec [institutional normal range: 761.9 ± 51.7 msec]). These results suggest potentially central autonomic dysfunction in this patient with DRPLA. To our knowledge, this is the first report to record SSNA and confirm subclinical autonomic dysfunction in a case with DRPLA.

Skin sympathetic nerve activity in patients with obstructive sleep apnea

Obstructive sleep apnea (OSA) is associated with increased cardiac arrhythmia and sudden cardiac death. We recently developed a new method (neuECG) to noninvasively measure electrocardiogram and skin sympathetic nerve activity (SKNA). The purpose of this study was to test the hypothesis that SKNA measured during sleep study is higher in patients with OSA than in those without OSA. We prospectively recorded neuECG and polysomnography in 26 patients undergoing a sleep study. Sleep stages were scored into rapid eye movement (REM), and non-REM sleep stages 1 (N1), 2 (N2), and 3 (N3). Average voltage of skin sympathetic nerve activity (aSKNA) and SKNA burst area were calculated for quantification. Apnea/hypopnea index (AHI) >5 per hour was used to diagnose OSA. There was a positive correlation (r = 0.549; P = .018) between SKNA burst area and the arousal index in OSA but not in the control group. aSKNA during sleep was 0.61 ± 0.09 μV in OSA patients (n = 18) and 0.53 ± 0.04 μV in control patients (n = 8; P = .025). Burst area was 3.26 (1.90-4.47) μV·s/min in OSA patients and 1.31 (0.67-1.94) μV·s/min in control (P = .047). More apparent differences were found during N2, when the burst area in OSA (3.06 [1.46-5.52] μV·s/min) was much higher than that of the control (0.89 [0.79-1.65] μV·s/min; P = .03). OSA patients have higher SKNA activity than control patients, with the most pronounced differences observed during N2. Arousal at the end of apnea episodes is associated with large SKNA bursts. Overlaps of aSKNA and SKNA burst area between groups suggest that not all OSA patients have increased sympathetic tone.

Left cardiac sympathetic denervation reduces skin sympathetic nerve activity in patients with long QT syndrome

Although left cardiac sympathetic denervation (LCSD) is an effective antiarrhythmic therapy for patients with long QT syndrome (LQTS), direct evidence of reduced sympathetic activity after LCSD in humans is limited. The purpose of this study was to assess skin sympathetic nerve activity (SKNA) in patients with LQTS undergoing LCSD. We prospectively enrolled 17 patients with LQTS who underwent LCSD between 2017 and 2019. SKNA recordings from the left arm (L-SKNA) and chest (C-SKNA) leads were performed before and after LCSD. Mean SKNA, burst activity, and nonburst activity of L-SKNA and C-SKNA were analyzed. The mean patient age was 21 ± 9 years (8 men 47%). The longest baseline corrected QT value was 497 ± 55 ms at rest and 531 ± 38 ms on exercise stress testing. Five patients (29.4%) had previous LQTS-triggered cardiac events including syncope, documented torsades de pointes, and ventricular fibrillation. In the 24 hours after LCSD, mean L-SKNA decreased from 1.25 ± 0.64 to 0.85 ± 0.33 μV (P = .005) and mean C-SKNA from 1.36 ± 0.67 to 1.05 ± 0.49 μV (P = .11). The frequency of episodes of SKNA bursts recorded from the left-arm lead (2.87 ± 1.61 bursts per minute vs 1.13 ± 0.99 bursts per minute; P < .001) and mean L-SKNA during burst (1.82 ± 0.79 μV vs 1.15 ± 0.44 μV; P < .001) and nonburst (1.09 ± 0.60 μV vs 0.75 ± 0.32 μV; P = .03) periods significantly decreased after LCSD, while the frequency of episodes of SKNA bursts recorded from the chest lead (P = .57) and mean C-SKNA during burst (P = .44) and nonburst (P = .10) periods did not change significantly. No arrhythmic events were documented after 11.9 months (range 3.0-22.2 months) of follow-up. LCSD provides an inhibitory effect on cardiac sympathetic activity by suppressing burst discharge as measured by SKNA.

Skin sympathetic nerve activity and ventricular rate control during atrial fibrillation

The relationship between the ventricular rate (VR) during atrial fibrillation (AF) and skin sympathetic nerve activity (SKNA) remains unclear. The purpose of this study was to test the hypothesis that SKNA bursts accelerate VR during AF. We simultaneously recorded electrocardiogram and SKNA in 8 patients (median age 66.0 years [interquartile range {IQR} 59.0-77.0 years]; 4 men [50%]) with 30 paroxysmal AF episodes (all >10-minute long) and 12 patients (73.0 years [IQR 60.5-80.0 years]; 6 men [50%]) with persistent AF. The average amplitude of SKNA (aSKNA [μV]) during AF was analyzed in 1-minute windows and binned, showing 2 Gaussian distributions. We used the mean + 3SD of the first Gaussian distribution as the threshold that separates burst from baseline (nonburst) SKNA. All 1-minute aSKNA values above the threshold were detected, and the area between aSKNA and baseline of every 1 minute was calculated and added as burst area. VR was higher during SKNA bursts than during the nonburst period (103 beats/min [IQR 83-113 beats/min] vs 88 beats/min [IQR 76-101 beats/min], respectively; P = .003). In the highest quartile of the burst area during persistent AF, the scatterplot of maximal aSKNA and VR during each SKNA burst shows higher aSKNA and VR. The overall estimate of the correlation between maximal VR and aSKNA during bursts show a positive correlation in the highest quartile of the burst area (0.64; 95% confidence interval 0.54-0.74; P < .0001). SKNA bursts are associated with VR acceleration. These SKNA bursts may be new therapeutic targets for rate control during AF.

Skin sympathetic nerve activity and the temporal clustering of cardiac arrhythmias.

Simultaneous noninvasively recorded skin sympathetic nerve activity (SKNA) and electrocardiogram (neuECG) can be used to estimate cardiac sympathetic tone. We tested the hypothesis that large and prolonged SKNA bursts are associated with temporal clustering arrhythmias. We recorded neuECG in 10 patients (69 ± 10 years old) with atrial fibrillation (AF) episodes and in 6 patients (50 ± 13 years old) with ventricular tachycardia (VT) or fibrillation (VF) episodes. Clustering was defined by an arrhythmic episode followed within 1 minute by spontaneous recurrences of the same arrhythmia. The neuECG signals were bandpass filtered between 500-1000 Hz to display SKNA. There were 22 AF clusters, including 231 AF episodes from 6 patients, and 9 VT/VF clusters, including 99 VT/VF episodes from 3 patients. A total duration of SKNA bursts associated with AF was longer than that during sinus rhythm (78.9 min/hour [interquartile range (IQR) 17.5-201.3] vs. 16.3 min/hour [IQR 14.5-18.5], P = 0.022). The burst amplitude associated with AF in clustering patients was significantly higher than that in nonclustering patients (1.54 μV [IQR 1.35-1.89], n = 114, vs. 1.20 μV [IQR 1.05-1.42], n = 21, P < 0.001). The SKNA bursts associated with VT/VF clusters lasted 9.3 ± 3.1 minutes, with peaks that averaged 1.13 ± 0.38 μV as compared with 0.79 ± 0.11 μV at baseline (P = 0.041). Large and sustained sympathetic nerve activities are associated with the temporal clustering of AF and VT/VF. This study was supported in part by NIH grants R42DA043391 (THE), R56 HL71140, TR002208-01, R01 HL139829 (PSC), a Charles Fisch Cardiovascular Research Award endowed by Suzanne B. Knoebel of the Krannert Institute of Cardiology (TK and THE), a Medtronic-Zipes Endowment, and the Indiana University Health-Indiana University School of Medicine Strategic Research Initiative (PSC).

Arousal electrical stimuli evoke sudomotor activity related to P300, and skin vasoconstrictor activity related to N140 in humans

ObjectiveArousal stimuli evoke bursts of skin sympathetic nerve activity (SSNA). SSNA usually contains sudomotor and vasoconstrictor neural spikes. The aim of this study was to elucidate which components of event-related potentials (ERPs) are related to sudomotor and vasoconstrictor responses comprising arousal SSNA bursts. MethodsWe recorded SSNA from the tibial nerve by microneurography, with corresponding sympathetic skin response (SSR), sympathetic flow response (SFR), and ERPs in 10 healthy subjects. Electrical stimulation of the median nerve was used to induce arousal responses. ERPs were classified by the occurrence of SSR and SFR. ResultsSSNA bursts followed by SSR were associated with larger P300 than SSNA bursts followed by no SSR. For N140, no difference in the amplitude was found between SSNA bursts with and without SSR. SSNA bursts followed by SFR were associated with larger N140 than SSNA bursts followed by no SFR. However, there were no differences in the amplitude of P300 between SSNA bursts with and without SFR. ConclusionsSudomotor and skin vasoconstrictor responses to arousal stimuli were differently associated with distinct ERP components. SignificanceThe possibility that sudomotor and skin vasoconstrictor activities comprising arousal SSNA reflect different stages of the cognitive process is suggested.

Active vasodilation by sympathetic outflow to limb skin in a patient with progressive aphasia

Despite considerable interest, a pure vasodilator response by skin sympathetic nerve activity (SSNA) bursts in human limbs has not been observed in previous studies. In a patient with progressive nonfluent aphasia, SSNA, sympathetic skin response, and skin blood flow were simultaneously recorded at rest and during electrical stimulation. There was a very low frequency of SSNA bursts at rest, and when electrical stimulation was delivered, reflex bursts of SSNA were always observed followed by a sympathetic skin response and an increase in skin blood flow. The reflex latency of SSNA was slightly prolonged and the mean amplitude of reflex SSNA bursts was lower after electrical stimulation, compared with the responses in healthy controls. We report for the first time that the active vasodilator component of cutaneous sympathetic activity in limbs was recorded without any vasoconstrictor component in a patient with progressive aphasia.

Reply to Young et al.

LETTERS TO THE EDITORReply to Young et al.Holly R. Middlekauff and Jeanie ParkHolly R. Middlekauff and Jeanie ParkPublished Online:01 May 2009https://doi.org/10.1152/japplphysiol.00017.2009MoreSectionsPDF (30 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat to the editor: We thank Drs. Young, Keller, Crandall, and Fadel (2) for their interest in our work (1), and their opinions regarding the impracticality of comparing skin sympathetic nerve activity (SSNA) between subjects in different groups. Since single SSNA bursts can include multiple small peaks, they ask, “Does a multiple peak burst represent one or more bursts?” In our study, such bursts were counted as one by the blinded investigator who analyzed all neurograms, thereby providing uniformity to burst quantification.Second, they correctly point out that the SSNA recordings may represent multiple fiber types and that any given neurogram may have varying contributions from each fiber type. They are concerned that in our multiunit recordings, we could miss the fiber type that potentially has elevated activity. Although this is true in theory, it is extremely unlikely. The SSNA neurogram is a random sample of total SSNA activity, and it is against the odds that during the 8 (or 16 total SSNA recordings if one includes healthy controls), we always missed the overactive skin fiber type. A more likely explanation for the absence of elevated SSNA in our recordings in end-stage renal disease patients is that it is not present.We invite Drs. Young, Keller, Crandall, and Fadel to review, once again, Fig. 1 in our paper. These representative neurograms lay to rest any real question whether SSNA is elevated in ESRD patients compared with healthy controls. In this case, a picture is truly worth a thousand words.REFERENCES1 Park J, Campese VM, Nobakht N, Middlekauff HR. Differential distribution of muscle and skin sympathetic nerve activity in patients with end-stage renal disease. J Appl Physiol 105: 1873–1876, 2008.Link | ISI | Google Scholar2 Young CN, Keller DM, Crandall CG, Fadel PJ. Comparing resting skin sympathetic nerve activity between groups: caution needed. J Appl Physiol; doi:10.1152/japplphysiol.91538.2008.Link | ISI | Google ScholarAUTHOR NOTESAddress for reprint requests and other correspondence: J. Park, Emory Univ., Renal Division, WMRB, 1639 Pierce Drive, Suite 338, Atlanta, GA 30322 (e-mail: [email protected]) Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation More from this issue > Volume 106Issue 5May 2009Pages 1753-1753 Copyright & PermissionsCopyright © 2009 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00017.2009History Published online 1 May 2009 Published in print 1 May 2009 Metrics

Preliminary Measurement of Intraoperative Sympathetic Nerve Activity Using Microneurography and Laser Doppler Flowmetry During Surgical Resection of Suprasellar Tumors

Intraoperative microneurography (enabling direct measurement of sympathetic outflow) and laser Doppler flowmetry were used to measure skin sympathetic nerve activity (SSNA) and skin blood flow (SBF) as indicators of hypothalamic damage during resection of 12 suprasellar tumors, 6 craniopharyngiomas, 4 meningiomas, 1 pituitary adenoma, and 1 germ cell tumor. SSNA was measured from a tungsten microelectrode inserted into the peroneal nerve, and SBF was measured from the foot innervated by the peroneal nerve. SBF reduction was induced by nociceptive procedures and non-nociceptive procedures before tumor exposure, on exposed tumors, and directly on the hypothalamus. SSNA could be reliably recorded in only 4 patients because of technical difficulties. In these patients, SSNA bursts appeared, followed by SBF reduction. The number of SSNA bursts was 37% to 100% of the number of SBF reduction events. Various surgical procedures involving painful stimuli or mechanical stress on the hypothalamus induced SSNA bursts and SBF reduction. The present findings suggest that SSNA and SBF can be used to detect sympathetic nerve activity, as an indicator of hypothalamic function, during neurosurgical procedures.

Sympathetic sudomotor and vasoconstrictive neural function in patients with Parkinson's disease

To evaluate sympathetic sudomotor and vasoconstrictive neural function in Parkinson's disease (PD), we simultaneously recorded sympathetic skin response (SSR) and skin blood flow (SVR; skin vasomotor reflex), as well as skin sympathetic nerve activity (SSNA) measured in peroneal nerves by microneurography, comparing 12 patients with idiopathic PD with 16 healthy controls. Resting SSNA frequency (8.8 ± 4.3 bursts/min) was significantly lower in PD patients than in controls ( p < 0.01). Frequency increases in response to performing mental arithmetic were slightly smaller in PD patients than in controls. PD patients exhibited normal SSNA reflex latencies compared with controls. Although no significant relationship was found between resting SSNA frequency and disease duration or degree of disability, a significantly negative correlation between increases in SSNA with mental arithmetic and PD duration was observed. Occurrence of SSR and SVR following SSNA bursts induced by electrical stimuli was reduced in PD ( p < 0.05). In patients with PD, sympathetic sudomotor and vasoconstrictive neural function was decreased at rest, but SSNA reflex latencies in the legs were nearly normal. Since responses of peripheral target organs may be impaired, both central and peripheral factors may contribute to autonomic symptoms in PD.

Skin sympathetic neuroeffector response is attenuated dose-dependently by systemic prostaglandin E1 injection in humans

To clarify the effects of prostaglandin E1 (PGE1) on the vasoconstrictive responses, we compared the correlation between the amplitude of integrated skin sympathetic nerve activity (SSNA) and per cent reduction in skin blood flow (SBF) before and after the infusion of lipo PGE1 and placebo (bolus one-shot infusion, single blind study), and constant rate infusion of PGE1 (10 and 50 ng kg−1 min−1 by infusion pump, dose-dependency study) in ten healthy men. SSNA was recorded microneurographically from the median nerve simultaneously with SBF by laser Doppler flowmetry at the index fingertip. The measurement was conducted 30 min after injection of lipo PGE1 or placebo, and during the drip infusion of 10 and 50 ng kg−1 min−1 of PGE1 with maneuvers to enhance SSNA. The resting and activated skin blood flow were not significantly different between 10 ng lipo PGE1 and placebo administration, and between baseline and 10, 50 ng kg−1 min−1 of PGE1 injection. The vascular response, defined as the slope of regression line between logarithm of amplitude of integrated SSNA bursts and the reduction in SBF, was significantly suppressed by injection of lipo PGE1 as compared with that by placebo. It was also decreased dose-dependently by the constant rate infusion of PGE1 (10 and 50 ng kg−1 min−1). We concluded that the intravenous injection of PGE1 attenuates vasoconstrictive responses to SSNA, and analysis of the relations between SSNA and vasoconstrictive response, i.e. the neuroeffector response, is suggested to be an important tool to assess the drug effect.

Skin sympathetic nerve activity and event-related potentials during auditory oddball paradigms

Skin sympathetic nerve activity (SSNA) from the tibial nerve and event-related brain potentials (ERPs) were recorded simultaneously during auditory oddball paradigms with a counting task in 10 healthy subjects to elucidate the relationships between the autonomic nervous system and the cognitive process. After the target tones, SSNA bursts were observed more frequently than after the non-target tones. Moreover, the amplitudes of SSNA bursts elicited after the target tones were higher than those elicited after the non-target tones. However, when subjects ignored the series of tones, there was no significant difference between the incidence of SSNA bursts after rare tones and frequent tones. The P300 latencies for the target trials with SSNA bursts were shorter than those for the target trials without SSNA bursts. The average ERP wave forms for the target trials with SSNA bursts showed larger positive deflection in the early part of the P300 component than those for the target trials without SSNA bursts. We conclude that SSNA is generated in relation to the conscious cognitive process, as well as to the reactive automatic process to changes in repeating stimuli. The early part of the P300 component, possibly P3a, may be related to the mechanisms that generate SSNA.

Possible mechanism of anhidrosis in a symptomatic female carrier of Fabry's disease: an assessment by skin sympathetic nerve activity and sympathetic skin response

Fabry's disease, X-linked alpha-galactosidase deficiency, features a variety of autonomic abnormalities including anhidrosis. In this study, we measured the skin sympathetic nerve activity (SSNA), skin potential and sweat rate in a symptomatic female carrier to investigate the underlying pathophysiology of anhidrosis. The basal activity and responsiveness of SSNA were both fairly well preserved, although slightly reduced compared with the control levels. However, sweating was completely absent, despite the normal skin potential change in response to SSNA bursts. These results suggest that anhidrosis in Fabry's disease is a result of sweat gland dysfunction as well as abnormal SSNA.

Heat-induced finger vasoconstriction controlled by skin sympathetic nerve activity

Finger blood flow (BF) and skin sympathetic nerve activity (SSA) to the glabrous side of the hand were measured during immersion of the hand in a water bath in which temperature (Tw) was raised every 10 min by steps of 2 degrees C from 35 or 37 to 41 degrees C. The experiments were conducted during the summer in rooms in which ambient temperature was 28-32 degrees C or 35 degrees C. The nine healthy male subjects were wearing summer clothes. Finger BF through vessels located deep in the skin was measured by using laser-Doppler flowmetry (ALF-2100, Advance). With the use of a tungsten microelectrode SSA was recorded directly from the median nerve at the wrist or antecubital fossa of the tested arm. With finger vessels already dilated at Tw of 35 or 37 degrees C, finger BF decreased, with a concomitant increase in the SSA bursts as Tw rose to 39-41 degrees C. We confirmed in one subject that anesthetic blockade of the median nerve at the site proximal, but not distal, to the recording site blocked responses to the step rise in Tw in the SSA bursts and in finger BF. From these results we conclude that, with the subject in a warm state, blood vessels of the finger respond to local heating with vasoconstriction, and this finger vasoconstriction is evoked reflexively, largely through the increased sympathetic outflow to the resistance vessels of the finger.