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Electrophysiological Features (electrophysiological + feature)
Selected AbstractsElectrophysiological features in the distinction between hereditary demyelinating and chronic acquired demyelinating neuropathiesJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2004F Poglio We carried out an electrophysiological retrospective study in 55 patients with chronic demyelinating acquired and hereditary neuropathies. Alterations of motor nerve conduction velocities (MNCV), distal motor latencies (DML), conduction blocks (CB) and compound muscle action potential (CMAP) were compared, considering the whole number of nerves for each disease. MNCV, DML, CB and CMAP were considered suggestive of demyelination when meeting the American Academy of Neurology (AAN) criteria. Abnormally slow MNCV was found respectively in the 46% of all the CMTX female nerves studied, in the 56.5% of CMTX males, 84% of CMT1A, 74% CIDP and 70% of MAG-PNP. Prolonged DML was observed in the 25% of the CMTX female nerves studied, in the 49.5% of CMTX males, 81% of CMT1A, 63% of CIDP and 71% of MAG-PNP. Moreover, CB were quite often evidenced in CIDP and MAG-PNP nerves (respectively in 48% and 29%) and rarely in hereditary neuropathies. Finally, we observed CMAP reduction in the 45% of all the CMTX female nerves studied, in the 50% of CMTX males, 63% of CMT1A, 49% of CIDP and 60% of MAG-PNP. A well-characterized pattern generally allows an electrophysiological distinction between CMT1A, CMTX males, MAG-PNP on one side and CIDP and CMTX females on the other side. A clear electrodiagnostic distinction result is often hard between CMTX males and MAG-PNP and between CIDP and CMTX females. [source] Rhythmic hippocampal slow oscillation characterizes REM sleep in humansHIPPOCAMPUS, Issue 6 2001Róbert Bódizs Abstract Hippocampal rhythmic slow activity (RSA) is a well-known electrophysiological feature of exploratory behavior, spatial cognition, and rapid eye movement (REM) sleep in several mammalian species. Recently, RSA in humans during spatial navigation was reported, but systematic data regarding human REM sleep are lacking. Using mesio-temporal corticography with foramen ovale electrodes in epileptic patients, we report the presence of a 1.5,3-Hz synchronous rhythmic hippocampal oscillation seemingly specific to REM sleep. This oscillation is continuous during whole REM periods, is clearly observable by visual inspection, and appears in tonic and phasic REM sleep episodes equally. Quantitative analysis proved that this 1.5,3-Hz frequency band significantly differentiates REM sleep from waking and slow-wake sleep (SWS). No other frequency band proved to be significant or showed this high rhythmicity. Even in temporo-lateral surface recordings, although visually much less striking, the relative power of the 1.5,3-Hz frequency band differentiates REM sleep from other states with statistical significance. This could mean that the 1.5,3-Hz hippocampal RSA spreads over other cortical areas in humans as in other mammals. We suggest that this oscillation is the counterpart of the hippocampal theta of mammalian REM sleep, and that the 1.5,3-Hz delta EEG activity is a basic neurophysiological feature of human REM sleep. Hippocampus 2001;11:747,753. © 2001 Wiley-Liss, Inc. [source] Idiopathic Left Ventricular Arrhythmias Originating Adjacent to the Left Aortic Sinus of Valsalva: Electrophysiological Rationale for the Surface ElectrocardiogramJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2010TAKUMI YAMADA M.D. IVT Arising Adjacent to the Left Sinus of Valsalva.Background: Idiopathic ventricular arrhythmias (VAs) may be amenable to catheter ablation within or adjacent to the left sinus of Valsalva (LSOV). However, features that discriminate these sites have not been defined. The purpose of this study was to determine the electrocardiographic and electrophysiological features of VAs originating within or adjacent to the LSOV. Methods and Results: We studied 48 consecutive patients undergoing successful catheter ablation of idiopathic VAs originating from the left coronary cusp (LCC, n = 29), aortomitral continuity (AMC, n = 10) and great cardiac vein or anterior interventricular cardiac vein (Epi, n = 9). A small r wave, or rarely an R wave, was typically observed in lead I during the VAs and pacing in these regions. An S wave in lead V5 or V6 occurred significantly more often during both the VAs and pacing from the AMC than during that from the LCC and Epi (p < 0.05 to 0.0001). For discriminating whether VA origins can be ablated endocardially or epicardially, the maximum deflection index (MDI = the shortest time to the maximum deflection in any precordial lead/QRS duration) was reliable for VAs arising from the AMC (100%), but was less reliable for LCC (73%) and Epi (67%) VAs. In 3 (33%) of the Epi VAs, the site of an excellent pace map was located transmurally opposite to the successful ablation site (LCC = 1 and AMC = 2). Conclusions: The MDI has limited value for discriminating endocardial from epicardial VA origins in sites adjacent to the LSOV probably due to preferential conduction, intramural VA origins or myocardium in contact with the LCC. (J Cardiovasc Electrophysiol, Vol. 21, pp. 170-176, February 2010) [source] Role of activity-dependent mechanisms in the control of dopaminergic neuron survivalJOURNAL OF NEUROCHEMISTRY, Issue 2 2007Patrick P. Michel Abstract Dopaminergic neurons that constitute the nigrostriatal pathway are characterized by singular electrical properties that allow them to discharge in vivo spontaneously in a spectrum of patterns ranging from pacemaker to random and bursting modes. These electrophysiological features allow dopaminergic neurons to optimize the release of dopamine in their terminal fields. However, there is emerging evidence indicating that electrical activity might also participate in the control of dopaminergic neuron survival, not only during development, but also in the adult brain, thus raising the possibility that alterations in ionic currents could contribute actively to the demise of these neurons in Parkinson disease. This review focuses on the mechanisms by which activity-dependent mechanisms might modulate dopaminergic cell survival. [source] Novel MPZ Mutation In A Sporadic CMT PatientJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2001E Bellone Mutations in the gene for the major structural protein component of peripheral nerve myelin, myelin protein zero (MPZ), are associated with some forms of hereditary neuropathies such as Charcot-Marie-Tooth disease type 1B (CMT1B), Dejerine-Sottas syndrome (DSS) and congenital hypomyelinating neuropathy (CHN). The common pathological characteristics of these allelic disorders are severe demyelination and remyelination of peripheral nerves. Recently, MPZ mutations were also found in patients with the axonal form of CMT neuropathy (CMT2). We studied a patient with negative familiar history and clinical and electrophysiological features of Charcot-Marie-Tooth disease: distal muscle weakness and atrophy, foot deformities (pes cavus), and severely reduced nerve conduction velocities in the motor and sensory nerves. The sural nerve biopsy showed marked loss of myelinated fibers, few onion bulbs, and a high percentage of fibers showing excessive myelin outfoldings. DNA analysis excluded CMT1A duplication by Southern blot and by pulsed field gel electrophoresis methods. SSCP analysis of all six exons of MPZ revealed a shift band in exon 2 in the patient's DNA. No such difference was detected in normal controls. Direct sequencing disclosed a G , A transition at nucleotide position 181. This base substitution predicts the replacement of aspartic acid with asparagine at codon 61. A mutation at the same codon (but different amino acid replacement) was recently identified in a family with the axonal type of CMT, in which the disease was autosomal dominantly inherited. This finding provides further confirmation of the role of MPZ gene in peripheral neuropathies and suggests that MPZ coding region mutations may account for a considerable number of CMT cases which do not involve DNA duplication on 17p11.2-p12. This research was partially supported by a MURST and an Ateneo grant to FA, by a Ministero della Sanitŕ grant to PM. Our laboratory is a member of the European Charcot-Marie-Tooth Consortium co-ordinated by Prof. Christine Van Broeckhoven. [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] | |||||||||||||