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Electrophysiological Parameters (electrophysiological + parameter)
Selected AbstractsAcetyl-l-carnitine in the treatment of painful antiretroviral toxic neuropathy in human immunodeficiency virus patients: an open label studyJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2006Maurizio Osio Abstract Antiretroviral toxic neuropathy causes morbidity in human immunodeficiency virus (HIV) patients under dideoxynucleoside therapy, benefits only partially from medical therapy, and often leads to drug discontinuation. Proposed pathogeneses include a disorder of mitochondrial oxidative metabolism, eventually related to a reduction of mitochondrial DNA content, and interference with nerve growth factor activity. Carnitine is a substrate of energy production reactions in mitochondria and is involved in many anabolic reactions. Acetyl carnitine treatment promotes peripheral nerve regeneration and has neuroprotective properties and a direct analgesic role related to glutamatergic and cholinergic modulation. The aim of this study was to evaluate acetyl-l-carnitine in the treatment of painful antiretroviral toxic neuropathy in HIV patients. Twenty subjects affected by painful antiretroviral toxic neuropathy were treated with oral acetyl-l-carnitine at a dose of 2,000 mg/day for a 4-week period. Efficacy was evaluated by means of the modified Short Form McGill Pain Questionnaire with each item rated on an 11-point intensity scale at weekly intervals and by electromyography at baseline and final visit. Mean pain intensity score was significantly reduced during the study, changing from 7.35 ± 1.98 (mean ± SD) at baseline to 5.80 ± 2.63 at week 4 (p = 0.0001). Electrophysiological parameters did not significantly change between baseline and week 4. In this study, acetyl-l-carnitine was effective and well tolerated in symptomatic treatment of painful neuropathy associated with antiretroviral toxicity. On the contrary, no effect was noted on neurophysiological parameters. [source] Dorsal caudal tail and sciatic motor nerve conduction studies in adult mice: Technical aspects and normative dataMUSCLE AND NERVE, Issue 6 2010Robin H. Xia MD Abstract Mice provide an important tool to investigate human neuromuscular disorders. The variability of electrophysiological techniques limits direct comparison between studies. The purpose of this study was to establish normative motor nerve conduction data in adult mice. The dorsal caudal tail nerve and sciatic nerve motor conduction studies were performed bilaterally on restrained anesthetized adult mice. The means and standard deviations for each electrophysiological parameter were determined in normal mice. Data were compared with inflammatory demyelinating polyneuropathy mice to determine whether these parameters discriminate between normal and abnormal peripheral nerves. Normal adult mice had a distal latency of 0.89 (±0.17) ms and 0.75 (±0.09) ms, distal compound motor unit action potential amplitude of 13.2 (±5.9) mV and 28.1 (±8.3) mV, and conduction velocity of 74.6 (±9.0) m/s and 76.5 (±8.3) m/s, respectively. These data were validated by the finding of statistically significant differences in several electrophysiological parameters that compared normal and polyneuropathy-affected mice. A standardized method for motor nerve conduction studies and associated normative data in mice should facilitate comparisons of disease severity and response to treatment between studies that use similar models. This would assist in the process of translational therapeutic drug design in neuromuscular disorders. Muscle Nerve, 2010 [source] Bradykinin stimulates prostaglandin E2 production and cyclooxygenase activity in equine nonglandular and glandular gastric mucosa in vitroEQUINE VETERINARY JOURNAL, Issue 4 2008N. K. MORRISSEY Summary Reasons for performing study: There are few data available regarding regulation of prostaglandin (PG) generation by equine gastric mucosae and the role of the cyclooxygenase (COX) isoforms in their production. Objectives: To: 1) characterise and quantify PGE2 output in vitro; 2) examine the sensitivity of PGE2 production to exogenous bradykinin (BK) exposure; 3) determine the contribution of the COX-1 and COX-2 pathways to basal and BK-stimulated PGE2 production; and 4) measure if BK influences electrogenic ion transport in equine gastric mucosae in vitro. Methods: Full thickness gastric sheets were obtained from horses at post mortem, stripped of muscle layers and mounted in Ussing chambers. Tissues were exposed to bradykinin (BK, 0.1 ,mol/l) either alone, or following pretreatment with a selective COX-2 inhibitor (NS-398, 1 ,mol/l) or a nonselective COX inhibitor (piroxicam, 1 ,mol/l), or were untreated. Results: BK administration increased PGE2 output from the basolateral but not the apical faces of both tissue types. Piroxicam, but not NS-398, reduced basolateral PGE2 release below control levels in both tissue types. Both piroxicam and NS-398 pretreatment inhibited BK-stimulated PGE2 release. In separate experiments, BK was without effect upon electrophysiological parameters of tissues mounted in Ussing chambers. Conclusions: PGE2 is produced by the nonglandular and glandular equine gastric mucosae in vitro. Significantly more PGE2 is released basolaterally than apically. BK stimulated the production of PGE2 from the basolateral side of both tissue types. These findings suggest that COX-1 is a significant pathway for basal PGE2 production from the basolateral faces of both nonglandular and glandular equine gastric mucosae in vitro. Potential relevance: The identification of the cells responsible for basolateral PGE2 release, via both COX-1 and COX-2 pathways, under basal and BK-stimulated conditions requires further study. [source] Intramuscular AAV delivery of NT-3 alters synaptic transmission to motoneurons in adult ratsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2010Jeffrey C. Petruska Abstract We examined whether elevating levels of neurotrophin-3 (NT-3) in the spinal cord and dorsal root ganglion (DRG) would alter connections made by muscle spindle afferent fibers on motoneurons. Adeno-associated virus (AAV) serotypes AAV1, AAV2 and AAV5, selected for their tropism profile, were engineered with the NT-3 gene and administered to the medial gastrocnemius muscle in adult rats. ELISA studies in muscle, DRG and spinal cord revealed that NT-3 concentration in all tissues peaked about 3 months after a single viral injection; after 6 months NT-3 concentration returned to normal values. Intracellular recording in triceps surae motoneurons revealed complex electrophysiological changes. Moderate elevation in cord NT-3 resulted in diminished segmental excitatory postsynaptic potential (EPSP) amplitude, perhaps as a result of the observed decrease in motoneuron input resistance. With further elevation in NT-3 expression, the decline in EPSP amplitude was reversed, indicating that NT-3 at higher concentration could increase EPSP amplitude. No correlation was observed between EPSP amplitude and NT-3 concentration in the DRG. Treatment with control viruses could elevate NT-3 levels minimally resulting in measurable electrophysiological effects, perhaps as a result of inflammation associated with injection. EPSPs elicited by stimulation of the ventrolateral funiculus underwent a consistent decline in amplitude independent of NT-3 level. These novel correlations between modified NT-3 expression and single-cell electrophysiological parameters indicate that intramuscular administration of AAV(NT-3) can exert long-lasting effects on synaptic transmission to motoneurons. This approach to neurotrophin delivery could be useful in modifying spinal function after injury. [source] Hippocampal long-term depression as an index of spatial working memoryEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 5 2002Kazuhito Nakao Abstract Long-term potentiation (LTP), a form of synaptic plasticity in the hippocampus, is a cellular model for the neural basis of learning and memory, but few studies have investigated the contribution of long-term depression (LTD), a counterpart of LTP. To address the possible relationship between hippocampal LTD and spatial performance, the spatial cognitive ability of a rat was assessed in a spontaneous alternation test and, thereafter, LTD in response to low-frequency burst stimulation (LFBS) was monitored in the dentate gyrus of the same rat under anaesthesia. To enhance a divergence in the ability for spatial performance, some of the animals received fimbria,fornix (FF) transection 14 days before the experiments. LTD was reliably induced by application of LFBS to the medial perforant path of intact rats, while no apparent LTD was elicited in rats with FF lesions. The behavioural parameters of spatial memory showed a significant correlation with the magnitude of LTD. We found no evidence that the cognitive ability correlated with other electrophysiological parameters, e.g. basal synaptic responses, stimulus intensity to produce half-maximal responses, paired-pulse facilitation or paired-pulse depression. These results suggest that the magnitude of LTD in the dentate gyrus serves as a reliable index of spatial cognitive ability, providing insights into the functional significance of hippocampal LTD. [source] Characterization of the Acute Cardiac Electrophysiologic Effects of Ethanol in DogsALCOHOLISM, Issue 9 2007Guilherme Fenelon Background: Alcohol has been related to atrial fibrillation (holiday heart syndrome), but its electrophysiologic actions remain unclear. Methods: We evaluated the effects of alcohol in 23 anesthetized dogs at baseline and after 2 cumulative intravenous doses of ethanol: first dose 1.5 ml/kg (plasma level 200 mg/dl); second dose 1.0 ml/kg (279 mg/dl). In 13 closed-chest dogs (5 with intact autonomic nervous system, 5 under combined autonomic blockade and 3 sham controls), electrophysiologic evaluation and monophasic action potential (MAP) recordings were undertaken in the right atrium and ventricle. In 5 additional dogs, open-chest biatrial epicardial mapping with 8 bipoles on Bachmann's bundle was undertaken. In the remaining 5 dogs, 2D echocardiograms and ultrastructural analysis were performed. Results: In closed-chest dogs with intact autonomic nervous system, ethanol had no effects on surface electrocardiogram and intracardiac variables. At a cycle length of 300 milliseconds, no effects were noted on atrial and ventricular refractoriness and on the right atrial MAP. These results were not altered by autonomic blockade. No changes occurred in sham controls. In open-chest dogs, ethanol did not affect inter-atrial conduction time, conduction velocity, and wavelength. Atrial arrhythmias were not induced in any dog, either at baseline or after ethanol. Histological and ultrastructural findings were normal but left ventricular (LV) ejection fraction decreased in treated dogs (77 vs. 73 vs. 66%; p = 0.04). Conclusion: Ethanol at medium and high doses depresses LV systolic function but has no effects on atrial electrophysiological parameters. These findings suggest that acute alcoholic intoxication does not directly promote atrial arrhythmias. [source] Abstracts of the 8th Meeting of the Italian Peripheral Nerve Study Group: 62JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2003C Briani Thalidomide seems to be effective in the treatment of cutaneous forms of lupus erythematosus refractory to other therapies. Peripheral neuropathy is the most severe side effect, but the incidence of neuropathy and its relation to thalidomide doses are still unclear. We prospectively monitored 12 patients treated with thalidomide for cutaneous lupus erythematosus in order to estimate the occurrence of side effects, particularly peripheral neuropathy. A total of 12 female patients, median age 38,6 years (range 26,56), with subacute or chronic cutaneous lupus erythematosus were considered. The patients were treated with low dose thalidomide (starting dose 100 mg, tapered to 50 mg/day or 50 mg alternative day) for up to 18 months. The average follow-up period was 8,6 months (range 2,18). Prior to, and regularly during treatment patients underwent neurological evaluation and electrophysiological study of at least 8 nerves in the 4 arms (ulnar, median, sural, peroneal nerves). At recruitment, one patient presented a sensory-motor peripheral neuropathy. Of the remaining 11 patients, six did not present electrophysiological evidence of neuropathy, one had a carpal tunnel syndrome and four showed slowing of ulnar nerve velocity at elbow. No patients developed neuropathy neither worsening of electrophysiological parameters during thalidomide treatment. The most common side effect was tremor, always reversible after withdrawing or reducing thalidomide. Paresthesias, somnolence, amenhorrea, constipation were also present. Only one patient had to stop the therapy for the occurrence, 10 days after taking 50 mg of thalidomide, of a severe, stabbing, "zoster-like" thoracic pain, which disappeared upon withdrawal of the drug. Started again on thalidomide, the symptoms reappeared and the patient definitely interrupted the therapy with benefit. All the 11 patients who continued on the therapy presented a significant improvement or remission of the cutaneous alterations. These preliminary data seem to indicate that low dose thalidomide is efficacious and tolerable for cutaneous lupus erythematosus. Peripheral neuropathy seems not to be a major side effect. A longer follow-up and the study of more patients are needed to confirm the results. [source] Dorsal caudal tail and sciatic motor nerve conduction studies in adult mice: Technical aspects and normative dataMUSCLE AND NERVE, Issue 6 2010Robin H. Xia MD Abstract Mice provide an important tool to investigate human neuromuscular disorders. The variability of electrophysiological techniques limits direct comparison between studies. The purpose of this study was to establish normative motor nerve conduction data in adult mice. The dorsal caudal tail nerve and sciatic nerve motor conduction studies were performed bilaterally on restrained anesthetized adult mice. The means and standard deviations for each electrophysiological parameter were determined in normal mice. Data were compared with inflammatory demyelinating polyneuropathy mice to determine whether these parameters discriminate between normal and abnormal peripheral nerves. Normal adult mice had a distal latency of 0.89 (±0.17) ms and 0.75 (±0.09) ms, distal compound motor unit action potential amplitude of 13.2 (±5.9) mV and 28.1 (±8.3) mV, and conduction velocity of 74.6 (±9.0) m/s and 76.5 (±8.3) m/s, respectively. These data were validated by the finding of statistically significant differences in several electrophysiological parameters that compared normal and polyneuropathy-affected mice. A standardized method for motor nerve conduction studies and associated normative data in mice should facilitate comparisons of disease severity and response to treatment between studies that use similar models. This would assist in the process of translational therapeutic drug design in neuromuscular disorders. Muscle Nerve, 2010 [source] Clinical and electrophysiological parameters distinguishing acute-onset chronic inflammatory demyelinating polyneuropathy from acute inflammatory demyelinating polyneuropathyMUSCLE AND NERVE, Issue 2 2010Annie Dionne MD Abstract Up to 16% of chronic inflammatory demyelinating polyneuropathy (CIDP) patients may present acutely. We performed a retrospective chart review on 30 acute inflammatory demyelinating polyneuropathy (AIDP) and 15 acute-onset CIDP (A-CIDP) patients looking for any clinical or electrophysiological parameters that might differentiate AIDP from acutely presenting CIDP. A-CIDP patients were significantly more likely to have prominent sensory signs. They were significantly less likely to have autonomic nervous system involvement, facial weakness, a preceding infectious illness, or need for mechanical ventilation. With regard to electrophysiological features, neither sural-sparing pattern, sensory ratio >1, nor the presence of A-waves was different between the two groups. This study suggests that patients presenting acutely with a demyelinating polyneuropathy and the aforementioned clinical features should be closely monitored as they may be more likely to have CIDP at follow-up. Muscle Nerve, 2010 [source] Clinical Significance of the Atrial Fibrillation Threshold in Patients with Paroxysmal Atrial FibrillationPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2001KEIJI INOUE INOUE, K., et al.: Clinical Significance of the Atrial Fibrillation Threshold in Patients with Paroxysmal Atrial Fibrillation. AF threshold and the other electrophysiological parameters were measured to quantify atrial vulnerability in patients with paroxysmal atrial fibrillation (PAF, n = 47), and those without AF (non-PAF, n = 25). Stimulations were delivered at the right atrial appendage with a basic cycle length of 500 ms. The PAF group had a significantly larger percentage of maximum atrial fragmentation (%MAF, non-PAF: mean ± SD = 149 ± 19%, PAF: 166 ± 26%, P = 0.009), fragmented atrial activity zone (FAZ, non-PAF: median 0 ms, interquartile range 0,20 ms, PAF: 20 ms, 10,40 ms, P = 0.008). Atrial fibrillation threshold (AF threshold, non-PAF: median 11 mA, interquartile range 6,21 mA, PAF: 5 mA, 3,6 mA, P < 0.001) was smaller in the PAF group than in the non-PAF group. Sensitivity, specificity, and positive predictive value of electrophysiological parameters were as follows, respectively: %MAF (cut off at 150%, 78%, 52%, 76%), FAZ (cut off at 20 ms, 47%, 84%, 85%), AF threshold (cut off at 10 mA, 94%, 60%, 81%). There were no statistically significant differences between the non-PAF and PAF groups in the other parameters (effective refractory period, interatrial conduction time, maximum conduction delay, conduction delay zone, repetitive atrial firing zone, wavelength index), that were not specific for PAF. In conclusion, the AF threshold could be a useful indicator to evaluate atrial vulnerability in patients with AF. [source] Objective assessment of neurotoxicity while shifting from carbamazepine to oxcarbazepineACTA NEUROLOGICA SCANDINAVICA, Issue 5 2004B. Clemens Objectives , Objective assessment of non-overt neurotoxicity of carbamazepine (CBZ) vs oxcarbazepine (OXC) in patients with difficult-to-treat partial epilepsy, who were resistant to CBZ treatment and were converted from CBZ monotherapy to OXC monotherapy. Material and methods , Therapeutically equivalent doses (150 mg OXC for every 100 mg CBZ) were compared in 20 adult patients. Neurological investigation, conventional and spectral EEG analysis, brainstem auditory evoked responses (BAER) were carried out in both treatment conditions. EEG and BAER data of 20 age-matched healthy controls helped interpretation. Primary target variables (electrophysiological parameters) were evaluated blindly. Results , There were no significant differences between treatment conditions concerning the neurological condition, lack of clinically evident neurotoxicity, seizure frequency and EEG spike frequency. OXC treatment was characterized by less delta, theta, and alpha power, more beta power, and significantly greater mean alpha frequency (P = 0.03 and 0.05 for the left and right occipital leads, respectively), than CBZ treatment. Interpeak latencies were prolonged in the CBZ condition as compared with normals (P = 0.01) and OXC (P = 0.02). Conclusion , In this cohort of patients substitution of OXC for CBZ was associated with significant normalization of electrophysiological parameters, indicating decreasing neurotoxicity while shifting from CBZ to OXC monotherapy. [source] |