Changes in autonomic function as determined by ECG R-R interval variability in sandal, shoe and leather workers exposed to n-hexane, xylene and toluene

To clarify if autonomic nervous system effects might be associated with exposure to organic solvents, 30 sandal, shoe and leather workers exposed to n-hexane, xylene, and toluene, and 25 unexposed controls were examined using the coefficient of variation in electrocardiographic R-R intervals (CVRR), combined with the distribution of nerve conduction velocities (DCV). The C-CVRSA and C-CVMWSA (two component CVs of the CVRR reflecting parasympathetic and sympathetic activities, respectively) were also computed from component spectral powers using autoregressive spectral and component analyses. Concentrations of the metabolites of the solvents in urine samples taken in the morning before work were 0-3.18 (mean 1.39) mg/l for 2,5-hexanedione, 0.10-0.43 (mean 0.19) g/g creatinine (Cn) for methylhippuric acid, and 0.05-2.53 (mean 0.41) g/g Cn for hippuric acid. In the solvent workers, the CVRR and C-CVRSA were reduced significantly when compared with the unexposed controls. The faster velocities of the DCV as well as the sensory median nerve conduction velocity (SCV) were significantly slowed in the solvent-exposed workers. The SCV was significantly correlated with the CVRR and C-CVMWSA among the solvent workers. These data suggest that chronic exposure to some organic solvents may affect cardiac autonomic function (mainly, parasympathetic activity) in addition to faster myelinated fibers of the peripheral nerves. However, the absence of significant dose-effect relations among the solvent workers makes it difficult to definitively attribute the differences to specific solvent exposures.     

A central nerve conduction study in hypothyroidism: before and after thyroxine replacement

Employing a Nicolet CA 100 machine, 20 patients of primary hypothyroidism were selected for electrophysiological studies, including somato-sensory evoked potential (SSEP), brainstem auditory evoked potential (BAEP), and visual evoked potential (VEP), to assess the central nerve conduction before and after administration of the thyroid hormone. Before thyroxine replacement therapy, the latencies of N9, N13, and N20 in SSEP showed significant delay, while the central conduction time (CCT) merely had a tendency of prolongation. In BAEP, the peak and interpeak latencies delayed significantly. Additionally, the latency and amplitude of VEP also had significant difference between patients and controls. After thyroxine replacement, the SSEP, BAEP, and VEP studies revealed significant improvement, in correlation with clinical amelioration. In conclusion, the central nerve conduction would be affected in primary hypothyroidism and the improvement was usually the case, reflecting the clinical recovery after appropriate treatment. The electrophysiological study provides an objective method for monitoring the function of central nervous system in hypothyroidism before and after thyroxine treatment.     

Calcium disodium ethylenediaminetetraacetate-chelated lead as a predictor for subclinical lead neurotoxicity: follow-up study on gun-metal foundry workers

OBJECTIVES: To examine if chelated lead was a more predictive indicator of the subclinical effect of lead on conduction velocities of faster or slower nerve fibers as compared with blood lead (BPb). METHODS: Distribution of conduction velocities (DCV) in large myelinated fibers of the sensory median nerve was measured twice at a 1-year interval in 17 male gun-metal foundry workers with BPb concentrations of 22-59 (mean 40.2) microg/dl and a mobilization yield of lead into urine (MPb) by calcium disodium ethylenediaminetetraacetate of 0.15-2.09 (mean 1.19) mg/24 h for the 1st year and in 20 healthy males (controls). RESULTS: Yearly changes in the conduction velocities of faster fibers were significantly correlated with the corresponding change in MPb (P < 0.05) but not with that in BPb (P > 0.05). In ten workers showing an increase in MPb during the 1-year period (0.44 mg/24 h on average) the conduction velocities of faster fibers were decreased significantly, resulting in the values being significantly lower in all the workers combined than in the controls (P < 0.05). On the other hand, in the remaining workers, who showed a lesser extent of reduction in MPb (0.08 mg/24 h on average), the DCV did not change (P > 0.05). CONCLUSION: Chelated lead might be a more predictive indicator of the effect of lead on the conduction velocities of faster fibers than blood lead.     

Neural conduction velocity of the human auditory nerve: bipolar recordings from the exposed intracranial portion of the eighth nerve during vestibular nerve section

We measured the conduction velocity of the intracranial portion of the auditory nerve in 3 patients undergoing vestibular nerve section to treat Ménière's disease. The conduction velocity varied from patient to patient, with an average value of 15.1 m/sec. The latency of peak III of the brain-stem auditory evoked potentials (BAEPs) increased by an average of 0.5 msec as a result of exposure of the eighth nerve, and if that increase is assumed to affect the entire length of the auditory nerve (2.6 cm) evenly, then the corrected estimate of conduction velocity would be 22.0 m/sec. Estimates of conduction velocity based on the interpeak latencies of peaks I and II of the BAEP, assuming that peak II is generated by the mid-portion of the intracranial segment of the auditory nerve, yielded similar values of conduction velocities (about 20 m/sec).     

Nerve conduction velocity and H-reflex recovery in bipolar illness

Bipolar illness may be characterized by dysregulation and dysfunction of biologically active ions and ion pumps, respectively. In an effort to examine whether purported physiologic abnormalities may have functional counterparts, nerve conduction velocities (NCVs) and H-reflex recovery were examined in 7 acutely manic, 11 euthymic bipolar, 13 remitted schizophrenic, and 6 normal control individuals. All electrophysiologic tests were clinically normal. However, euthymic bipolar patients had significantly slower NCVs than either manic or normal individuals. Percent decrement of H-reflex recovery was nonsignificantly increased in manic versus euthymic bipolar subjects. Data analysis suggests lithium was not responsible for these changes. These data indicate that different mood states in bipolar illness are associated with alterations in electroneurophysiologic function.     

Peripheral motor and sensory nerve conduction studies in haemodialysis patients. A study of 54 patients

Peripheral motor and sensory nerve conduction velocities were studied prospectively in 54 chronic haemodialysis patients. The most sensitive parameters for the detection of polyneuropathy were the deep peroneal nerve motor conduction velocity, the sural nerve sensory conduction velocity and the H-reflex latency and H-index of the S1 roots. All patients examined were found to present at least one abnormal nerve conduction parameter. In the present study the side of the arteriovenous shunt had no statistically significant effect on the sensory and motor nerve conduction velocities in the upper extremities. There was a significant correlation between H-reflex latency and H-reflex index, and between H-reflex latency and sural nerve sensory conduction velocity.     

Adenylosuccinate synthetase of the yeast Saccharomyces cerevisiae: purification and properties

Motor and sensory nerve conduction velocities (MNCV and SNCV) were reduced in the sciatic nerve of rats after 4 weeks of untreated streptozotocin-induced diabetes, and declined further during the following 4 weeks. Treating diabetic rats with the novel peptide HP228 had no effect on the decline of MNCV after the first 4 weeks of diabetes but attenuated the decline in SNCV. HP228 treatment also prevented any further decline in MNCV or SNCV between weeks 4 and 8 of diabetes. Consequently, at the conclusion of the study, the nerve conduction velocities (NCVs) in treated rats were significantly (both P < .001) higher than in untreated diabetic rats. Reduced nerve homogenate Na+,K+-adenosine triphosphatase (ATPase) activity in diabetic rats was significantly (P < .05) increased by HP228 but remained significantly (P < .05) lower than in untreated controls. HP228 treatment also reduced nerve Na+,K+-ATPase activity of control rats compared with untreated controls (P < .05). There was no effect of HP228 on the hyperglycemia, nerve polyol accumulation, myo-inositol depletion, reduced nerve laser Doppler blood flow, thermal hypoalgesia, or reduced mean axonal caliber in diabetic rats or on any of these parameters in control rats. These data demonstrate that a novel peptide may protect against the slowing of nerve conduction in prolonged diabetes and that the mechanism of action is unrelated to aldose reductase inhibition, prevention of nerve ischemia, or axonal atrophy. HP228 may prove a potential therapeutic agent for the treatment of prolonged diabetic neuropathy.     

Long-term hyperglycemia is related to peripheral nerve changes at a diabetes duration of 4 years. The Wisconsin Diabetes Registry

OBJECTIVE: To examine longitudinal hyperglycemia and peripheral nerve responses in a population-based incident cohort. RESEARCH DESIGN AND METHODS: A sample from an incident cohort of young people was comprehensively followed from diagnosis of IDDM. Participants were invited to submit blood samples three times per year for central testing of GHb. During their 4th year of diabetes, nerve conduction studies were performed on the median sensory and motor, peroneal motor, and sural sensory nerves. Relationships between mean GHb and nerve latencies, velocities, and amplitudes were explored. RESULTS: GHb was positively related to all nerve latencies and negatively related to all nerve velocities. The relationships between mean GHb and nerve conduction latencies and velocities differed by sex for the peroneal nerve latency (beta = 0.17 male subjects, beta = -0.01 female subjects; P < 0.001). Pubertal participants had lower velocities and longer latencies than prepubertal participants (beta = 0.37; P = 0.05 peroneal latency), after adjustment for GHb, height, and extremity temperature. Sensory and motor nerve amplitudes were related to GHb, and these relationships did not differ by sex. CONCLUSIONS: Our study indicates that sustained hyperglycemia is related to functional changes, at the minimum, in peripheral sensory and motor nerve conduction at a diabetes duration of 4 years. Our findings are consistent with a dying-back neuropathy, and there is some suggestion that chronic hyperglycemia may be more detrimental to nerves in male subjects than in female subjects.     

Treatment of hypertension in nondiabetic renal disease

To clarify whether long-term impaired glucose tolerance (IGT) is associated with dysfunction of peripheral and autonomic nerves, age-matched men with IGT and diabetes mellitus were followed prospectively for 12-15 years, when peripheral and autonomic nerve function was assessed. The patients comprised four subgroups: (1) 51 IGT subjects (duration of IGT at least 12-15 years); (2) 35 diabetic patients, with IGT 12-15 years ago, who later developed diabetes; (3) 34 diabetic patients, duration of diabetes at least 12-15 years; and (4) 62 age-matched non-diabetic control subjects. Mean age of the whole study population was 61 +/- 2 years (mean +/- SD), not different in the four groups. Peripheral nerve function tests included nerve conduction velocities, amplitudes, distal latencies, F-reflexes, and sensory perception thresholds for heat, cold, and vibration. Autonomic nerve function tests included the heart rate reaction during deep breathing (expiration to inspiration ratio) and to tilt (acceleration and brake indices). Despite 12-15 years of IGT, peripheral nerve function did not differ between IGT and control subjects, whereas autonomic nerve function deviated; an abnormal expiration to inspiration ratio (a sign of vagal nerve dysfunction) was significantly more common (15/51 versus 5/62; p < 0.01) in IGT than in control subjects. Diabetic patients (groups 2 and 3) showed lower conduction velocities (in general 2-4 m s-1 lower) than IGT and control subjects in all tested nerves. In conclusion, diabetes but not IGT, is associated with peripheral nerve dysfunction.     

A case of myelofibrosis that developed polycythemia vera following treatment with ranimustine and then acute myelogenous leukemia (M0)

Short latency somatosensory evoked potentials (SSEP) to median nerve stimulation recorded from post-Rolandic area and the surface of processus spinosus of Cvs at the same record time. To assess electrophysiologically functional status of central nervous system (CNS), SSEP were studied in 43 patients with ischemic heart disease (IHD); 18 cases of angina pectoris (AP group), 25 cases of old myocardial infarction (MI group), and 14 non-IHD controls (NC group). The N13, N20, P25 peak latencies (PLs) and the central conduction time (CCT, the peak latency between N13 and N20) in AP group or MI group were prolonged remarkably compared with NC group. Likewise, MI group showed significant prolongation of N20, P25 PLs and CCT compared to the AP group. Furthermore, in MI group, the N20 peak amplitude was significantly lowered; the subjects percentages of the N20 or P25 amplitude detraction more than 40 percent in one side and the P25 interextremital latency difference over 1 ms were significantly increased than those of the NC group. These results suggested the pathological changes of the somatosensory pathway from superior spinal cord or medulla oblongata to cerebral cortex primary sensory area in CNS in the IHD patients.     

NGF, cyclic AMP, and phorbol esters regulate oxytocin receptor gene transcription in SK-N-SH and MCF7 cells

In an initial study, the effects of galactose intoxication on nerve laser Doppler blood flow (NLDF) and nerve conduction velocity (NCV) were assessed after 1-16 weeks of galactose feeding in pentobarbital-anesthetized rats. NLDF was not significantly changed at any time point. NCV was significantly reduced after 16, but not 1 or 4, weeks of galactose feeding. In a second study, NLDF was not significantly changed by 4 weeks of galactose intoxication, but streptozotocin-diabetic NLDF was significantly reduced compared to both control (P<0.001) and galactose-intoxicated rats (P<0.05). Compared to control animals, sciatic motor NCV was significantly (P<0.001) reduced in the galactose group, while sciatic and saphenous sensory NCVs were not significantly changed. In the streptozotocin-diabetic rats, motor and sensory NCVs were all significantly reduced (P<0.001). In contrast to the NCV findings, mean caliber of myelinated axons in both the saphenous and sciatic nerves was reduced in galactose-intoxicated, but not streptozotocin-diabetic rats. The observed sequence of changes associated with these two models of diabetic neuropathy is not consistent with the proposed roles of ischemia and axonal dwindling in the reported nerve conduction deficits.     

Somatosensory evoked potentials during hypoxia and hypocapnia in conscious humans

PURPOSE: The objective of the study was to evaluate the effects of moderate hypoxia and hypocapnia on the latency and amplitude of cortical somatosensory evoked potentials (SSEPs) in conscious human subjects. METHODS: In ten volunteers the amplitude and latency of the cortical somatosensory evoked potentials were recorded during stimulation of the left posterior tibial nerve. Measurements of SSEPs and respiratory variables were made breathing ambient air, air containing a reduced oxygen percentage (17% O2, 14% O2 (n = 6) or 11% O2 (n = 10)), and again during voluntary hyperventilation breathing ambient air (PETCO2 = 20 mmHg, n = 10). RESULTS: Hypoxia (11% O2) caused mild stimulation of ventilation (P < 0.05) but had no effects on the latency or amplitude of the SSEP. Lesser degrees of hypoxia had no effects. Hyperventilation caused a small (2-4%) decrease) in the latency of the SSEP and an increase in the amplitude of the SSEP (P < 0.05). CONCLUSIONS: These findings in conscious subjects were consistent with previous observations in anaesthetized humans and anaesthetized dogs and show that the decrease in latency of the SSEP associated with hypocapnia is not due to changes in the depth of anaesthesia. These effects of hypocapnia may contribute to small variations in the latency of the SSEP when monitoring is performed during surgery, but are unlikely to be large enough to be of clinical concern.     

Hepatitis TT virus infection in high-risk groups

Aim of the present study was to evaluate the effect of acute hyperglycemia on peripheral nerve conduction measurements. Five healthy male volunteers aged 36-42 years underwent nerve conduction studies during hyperglycemia (blood glucose approximately 12 mmol/l) induced by intravenous infusion of glucose and maintained for 120 minutes. Peroneal motor and sural sensory nerve conduction velocities and amplitudes were measured from the right leg at 15 min intervals starting at 15 min before and continuing 30 min after glucose infusion. Data were analysed using paired t-test comparing measurements at each time point after the start of the infusion to the second control measurement immediately prior to the infusion. All nerve conduction velocities and amplitudes were similar before, during and after induced hyperglycemia. The results suggest that it is unnecessary to standardise blood glucose concentration during measurement of peripheral nerve functions.     

Intermediate nerve conduction velocities define X-linked Charcot-Marie-Tooth neuropathy families

Three genetic loci for the Charcot-Marie-Tooth (CMT) syndromes with slow motor nerve conduction velocities (hereditary motor and sensory neuropathy: HMSN type I) have been mapped to chromosomes 1 (CMT1B), 17 (CMT1A), and the X chromosome (CMTX). The clinical features of these three CMT subgroups are similar. To determine whether any clinical features distinguish CMTX families, the range of clinical findings and motor nerve conduction velocities were examined in two large CMTX families, the range of clinical findings and motor nerve conduction velocities were examined in two large CMTX families with CMTX proven by linkage to X-chromosome markers. CMTX males had more wasting and weakness than CMTX females or individuals with CMT1A. Patellar reflexes were more often retained in CMTX. Motor nerve conduction velocities were faster than in CMT1A. Intermediate-range median nerve conduction velocities were present in CMTX females (45 +/- 9 m/sec; range, 26 to 61 m/sec). These velocities were significantly faster than those for CMT1A females (22 +/- 8 m/sec, p < 0.0001). Median nerve conduction velocities in CMTX males (31 +/- 6 m/sec) were significantly slower than in CMTX females and faster than in CMT1A males (20 +/- 6 m/sec, p < 0.0001). The combination of slow conduction velocities in affected males (< 40 m/sec) and intermediate-range median motor conduction velocity results (> 40 m/sec) in affected or obligate carrier females is a useful distinguishing feature to separate CMTX from CMT1A, as intermediate conduction velocities are not present in autosomal-dominant dominant CMT1A families. This feature defines possible CMTX families for linkage studies. Families with no male-to-male inheritance of the syndrome, slow motor nerve conductions in affected males, and normal or intermediate-range conduction velocities in carrier females should be considered to be X-linked CMT families.     

Power spectral analysis of heart rate variation in diabetic patients with neuropathic foot ulceration

OBJECTIVE: To evaluate the relationship between diabetic autonomic neuropathy and diabetic neuropathic foot ulceration, we used power spectral analysis (PSA) of heart rate variation, which provides the accurate simultaneous quantification of parasympathetic and sympathetic activities, to assess autonomic function in diabetic patients. RESEARCH DESIGN AND METHODS: We studied 55 NIDDM patients including 10 diabetic patients without neuropathy, 23 diabetic patients with neuropathy and no history of foot ulceration, and 22 diabetic patients with neuropathic foot ulceration. We performed PSA of 100 R-R intervals at rest and analyzed the results by fast Fourier transformation. RESULTS: The low frequency (LF) power, which reflects sympathetic activity, and the high frequency (HF) power, which reflects parasympathetic (vagal) activity, were inversely correlated with the duration of diabetes and the fasting plasma glucose (FPG) levels. By multiple regression analysis, the FPG remained with significant influence on both LF and HF powers. The LF and HF powers were positively correlated with motor nerve conduction velocity (MCV) and sensory nerve conduction velocity (SCV) in the upper and lower limbs and the coefficient of variation of R-R intervals. The LF and HF powers were significantly reduced in patients with neuropathy and patients with foot ulceration compared with patients without neuropathy. Although the median MCV and SCV were similar between diabetic patients with neuropathy and patients with foot ulceration, both the LF and HF powers were significantly decreased in patients with foot ulceration compared with patients with neuropathy. There was no difference in the value of the LF:HF ratio, an index of sympathovagal balance, among three subgroups. We observed a positive correlation between LF and HF power in all subjects; however, the LF and HF powers were not correlated in the subgroups of patients with foot ulceration. CONCLUSIONS: These results showed that diabetic patients with neuropathic foot ulceration have a greater impairment in spectral indexes of autonomic activity obtained by PSA than patients with neuropathy and no history of foot ulceration, whereas no difference was present in nerve conduction velocities.     

Determination of hydroperoxides and structures by high-performance liquid chromatography with post-column detection with diphenyl-1-pyrenylphosphine

OBJECTIVE: The aim of this meta-analysis was to review the existent evidence on the effectiveness of tolrestat in the treatment of diabetic peripheral neuropathy. RESEARCH DESIGN AND METHODS: Individual patient data on 738 subjects from the three randomized clinical trials published on this topic were analyzed using changes in motor nerve conduction velocities (NCVs) as endpoints. Nerves investigated included median, ulnar, tibial, and peroneal. RESULTS: The pooled analysis of NCV taken as a continuous measurement showed a significant treatment effect, the magnitude of this benefit being approximately equal to 1 m/s for all the nerves investigated. When looking at the proportion of patients experiencing a loss of NCV of at least 1 or 2 m/s in at least two out of the four nerves investigated, it emerged that treatment reduced by > 40% the risk of such outcomes after adjusting for patients' characteristics. The odds ratios relative to the placebo group were 1.82 (1.30-2.52) and 1.70 (1.15-2.48) for a decrease of 1 and 2 m/s, that is, placebo-treated patients have an 82 and 70% increased risk for a loss of nerve function of 1 and 2 m/s, respectively. No statistically significant difference in treatment effect emerged after stratification according to baseline motor NCV and glycated hemoglobin levels. CONCLUSIONS: After a treatment duration ranging between 24-52 weeks, patients treated with tolrestat had a reduced risk for developing nerve function loss compared with placebo-treated patients. Future long-term trials are needed to evaluate the impact of the treatment on more clinically meaningful endpoints such as the development of foot complications.     

"Threshold-level" multipulse transcranial electrical stimulation of motor cortex for intraoperative monitoring of spinal motor tracts: description of method and comparison to somatosensory evoked potential monitoring

Numerous methods have been pursued to evaluate function in central motor pathways during surgery in the anesthetized patient. At this time, no standard has emerged, possibly because each of the methods described to date requires some degree of compromise and/or lacks sensitivity. OBJECT: The goal of this study was to develop and evaluate a protocol for intraoperative monitoring of spinal motor conduction that: 1) is safe; 2) is sensitive and specific to motor pathways; 3) provides immediate feedback; 4) is compatible with anesthesia requirements; 5) allows monitoring of spontaneous and/or nerve root stimulus-evoked electromyography; 6) requires little or no involvement of the surgical team; and 7) requires limited equipment beyond that routinely used for somatosensory evoked potential (SSEP) monitoring. Using a multipulse electrical stimulator designed for transcranial applications, the authors have developed a protocol that they term "threshold-level" multipulse transcranial electrical stimulation (TES). METHODS: Patients considered at high risk for postoperative deficit were studied. After anesthesia had been induced and the patient positioned, but prior to incision, "baseline" measures of SSEPs were obtained as well as the minimum (that is, threshold-level) TES voltage needed to evoke a motor response from each of the muscles being monitored. A brief, high-frequency pulse train (three pulses; 2-msec interpulse interval) was used for TES in all cases. Data (latency and amplitude for SSEP; threshold voltage for TES) were collected at different times throughout the surgical procedure. Postoperative neurological status, as judged by evaluation of sensory and motor status, was compared with intraoperative SSEP and TES findings for determination of the sensitivity and specificity of each electrophysiological monitoring technique. Of the 34 patients enrolled, 32 demonstrated TES-evoked responses in muscles innervated at levels caudal to the lesion when examined after anesthesia induction and positioning but prior to incision (that is, baseline). In contrast, baseline SSEPs could be resolved in only 25 of the 34 patients. During surgery, significant changes in SSEP waveforms were noted in 12 of these 25 patients, and 10 patients demonstrated changes in TES thresholds. Fifteen patients experienced varying degrees and durations of postoperative neurological deficit. Intraoperative changes in TES thresholds accurately predicted each instance of postoperative motor weakness without error, but failed to predict four instances of postoperative sensory deficit. Intraoperative SSEP monitoring was not 100% accurate in predicting postoperative sensory status and failed to predict five instances of postoperative motor deficit. As a result of intraoperative TES findings, the surgical plan was altered or otherwise influenced in six patients (roughly 15% of the sample population), possibly limiting the extent of postoperative motor deficit experienced by these patients. CONCLUSIONS: This novel method for intraoperative monitoring of spinal motor conduction appears to meet all of the goals outlined above. Although the risk of postoperative motor deficit is relatively low for the majority of spine surgeries (for example, a simple disc), high-risk procedures, such as tumor resection, correction of vascular abnormalities, and correction of major deformities, should benefit from the virtually immediate and accurate knowledge of spinal motor conduction provided by this new monitoring approach.     

Effects of head-up tilting on vagal nerve activity in man

OBJECTIVES: To evaluate the contribution of the vagal nerve activity in the cardiovascular postural adaptation, effects of decremental head-up tilting (90 degrees, 64 degrees, 53 degrees, 44 degrees, 37 degrees, 30 degrees, 24 degrees, 17 degrees, 12 degrees, 6 degrees and 0 degree) on time- and frequency-domain heart rate variability variables were analyzed in healthy young female. BACKGROUND: During head-up tilting, a hydrostatic venous pooling in the extremities occurs owing to gravity. To pump up the blood toward the upper body, the sympathetic nerve activity has been shown to play an important role. So, to date, few studies evaluated the effects of vagal nerve activity to stabilize the cerebral blood flow during head-up tilting. METHODS: Eight young female volunteers (age, 23.3 +/- 0.8 years; mean +/- SD) were evaluated. The electrocardiogram (ECG) by bipolar chest leads was recorded continuously during procedures, and the bed was tilted at 0.1 interval of sine function of tilting angle from upright position (90 degrees) to supine position (0 degree). The time domain measurements of cycle length variability (co-efficient of variance in percent for R-R intervals [CVRR], number of differences between adjacent R-R intervals that are > 50ms [RR50]) and the frequency domain measurements of low (0.08 to 0.15Hz, LF), high (0.15 to 0.40Hz, HF) and total (0.08 to 0.40, TF) power were performed to assess the cardiac sympathetic and vagal nerve activity. RESULTS: The CVRR showed no significant change during decremental head-up tilting, whereas the RR50 and the square root of HF power, more specific indices of cardiac parasympathetic tone, showed significant negative linear correlations to the sine of the tilting angle. In markers of cardiac sympathetic tone, there were significant positive correlations between the sine of the tilting angle and the normalized LF power or the LF-to-HF power ratio (LF/HF). CONCLUSION: These findings suggest that, in healthy young female, not only cardiac sympathetic nervous system but also cardiac vagal nervous system respond linearly to the change in body axis component of gravity, and they may contribute reciprocally and coordinately to cardiovascular postural adaptation.     

Peripheral nervous system involvement in human and experimental chronic American trypanosomiasis

An electrophysiological and histological study of the muscle and the peripheral nervous system (PNS) was carried out in chronic human American trypanosomiasis (Chagas' disease) and in an experimental Chagas' disease (Chd) mouse model. Altogether 995 patients with chronic Chd and 261 mice, experimentally infected with RA and CA-I parasite strains, were investigated. Results were compared with matched controls. Techniques employed in humans were: clinical assessment, conventional electromyography (EMG), estimated number of motor units, motor and sensory nerve conduction velocities, repetitive nerve stimulation and muscle and sural nerve biopsies. In mice conventional EMG, sciatic nerve conduction time, sciatic nerve action potential amplitude, in vitro miniature end-plate potentials (MEPPs) and end-plate potentials (EPPs) recordings, muscle, nerve and spinal cord histology and identification of cell phenotypes within the inflammatory infiltrates were the employed procedures. Out of 511 patients submitted to clinical examination, 52 disclosed signs and symptoms of mixed peripheral neuropathy. By employing electrophysiological techniques, it could be shown that about 30% of the investigated patients had one or more of the following features: diminished interference pattern, most of the remainder motor unit potentials being (MUPs) polyphasic; reduced number of functional motor units in the thenar, hypothenar, soleus and/or edb muscles; slow sensory and motor nerve conduction velocities; low sensory action potential amplitude and impairement of neuromuscular transmission. In mice, MUPs duration and amplitude were increased at later stages of the infection, nerve conduction was slow, nerve action potentials were of low amplitude, mepps were of low amplitude and double epps were frequently found. Muscle histology in humans with chronic Chd showed type I and type II grouping, atrophic angular fibers and targetoid muscle fibers. In mice perivascular mononuclear cells infiltrates, small round fibers, muscle fibers necrosis, atrophic angular fibers, type II muscle fibers grouping and grouped muscle fibers atrophy were found. Sural nerve samples showed segmental and paranodal demyelination and axonal loss. The same features were observed in mice nerves, also in this model mononuclear cells infiltrates at the nerve, dorsal root ganglia and meninges surrounding the spinal cord were observed. Muscle and nervous tissues infiltrates were mainly composed of T lymphocytes with predominance of CD8 or CD4 subsets according to the parasites strain employed for infecting the animals. These findings suggest that the skeletal muscle and the PNS may be involved in chronic American trypanosomiasis.     

Contrasting effects of treatment with omega-3 and omega-6 essential fatty acids on peripheral nerve function and capillarization in streptozotocin-diabetic rats

Essential fatty acid metabolism is impaired by diabetes mellitus and this may be important in the aetiology of peripheral nerve dysfunction. The effects of gamma-linolenic acid (omega-6) and fish oil (omega-3) alone, and in combination, on nerve function and capillarization were examined in 2-month streptozotocin-diabetic rats. Diabetes resulted in approximately 15% and 23% decreases in saphenous sensory and sciatic motor nerve conduction velocities, respectively (p < 0.001). Motor and sensory conduction velocities were in the non-diabetic range after both preventive and reversal omega-6 treatment of diabetic rats (p < 0.001). No significant changes occurred in omega-6 treated non-diabetic rats. Preventive omega-3 treatment was largely ineffective. Reversal treatment with a combination of omega-6 and omega-3 fatty acids was marginally effective and improved motor (p < 0.05), but not sensory conduction velocity. In vitro measurement of sciatic nerve resistance to hypoxic conduction failure in diabetic rats revealed a 56% increase in the time taken for the compound action potential amplitude to be reduced by 80% (p < 0.01) compared to non-diabetic rats. This was partially prevented by omega-6 treatment (29% increase, p < 0.01). Reversal omega-6 treatment had a lesser effect (37% increase, p < 0.05 compared to untreated diabetic rats). omega-3 treatment had no significant effect on conduction failure time. Sciatic endoneurial capillary density increased by 11% with preventive omega-6 treatment (p < 0.05), but was unaffected by reversal omega-6 and by omega-3 treatments.(ABSTRACT TRUNCATED AT 250 WORDS)