CNS Involvement in GBS: Brainstem Auditory Evoked Potential

systema nervosum centrale Involvement in GBS Brainstem Auditory evoked PotentialBRAINSTEM AUDITORY elicited POTENTIAL AS AN INDEX OF systema nervosum centrale DEMYELINATION IN GB SYNDROMEDr. Smita Singh*, Dr. Nitesh Mishra**, Dr. Shraddha Singh, Dr. Sunita Tiwari addictGuillain-Barr Syndrome (GBS) is an acute, frequently severe and fulminant polyradicular neuropathy that is autoimmune in nature. GBS manifest as rapidly evolving atomic number 18flexic motor paralysis with or without arresting disturbances. It of importly involves circumferential vile system and autonomic anxious system. There are obsolete evidences about the involvement of central nervous system ( central nervous system) in GBS. The main objective of the orbit was to assess the CNS involvement in GBS use the Brainstem Auditory elicited Potential (BAEP). The piece of work was conducted in the clinical neurophysiology lab in the department of physiology, CSMMU Lucknow. Study group involved 26 subjects (n=26 ) having GBS and moderate group involved 30 typical subjects (n=30). BAEPS were recorded by Neuroperfect- electromyogram 2000 EMG/NCV/EPsytem. The data so obtained were subjected to compend using statistical Package for Social Sciences (SPSS) Version 13.0. There was signifi dismisst increase in PIII PV peak latencies and PI-PIII PI-PV interpeak latencies in twain left and safe ear in the take aim group, which showed the CNS involvement in GBS which can be assessed using BAEP.Key words Guillain-Barr Syndrome, Central Nervous System, Brainstem Auditory elicited PotentialINTRODUCTIONGuillain-Barr Syndrome (GBS) is an acute, frequently severe and fulminant polyradicular neuropathy that is autoimmune in nature. GBS manifest as rapidly evolving areflexic motor paralysis with or without sensory disturbances. The usual pattern is asc obliterateing paralysis i.e. weakness begins in distal limbs but rapidly advances to affect the proximal muscle functions. Lower cranial braces ar e usually involved causing bulbar weakness and difficulty with handling secretions and maintaining airways. Deep Tendon Reflexes (DTR) usually disappears with in initiatory few days of onslaught. Bladder dysfunction if present is usually transitory1.In severe themes of GBS autonomic involvement is leafy vegetable. Usual feature are passing of vasomotor control with wide fluctuation in blood pressure, postural hypotension and cardiac dysrhythmias. Pain is another common feature of GBS near common is deep aching pain in weakened muscles.GBS shows mainly 2 types of pathophysiology, demyelinating stochastic variable and axonal devolution. Basis of demyelinating form is conduction block, which results in voiced paralysis and sensory disturbances. Reco truly is possible as remyelination occurs. Axonal degeneration shows slow rate of recovery and results in greater degree of eternal rest disability.CSF shows albuminocytological dissociation that is elevated CSF protein level (100- 1000gm/dl) without accompanying pleocytosis. CSF usually remains normal when duration of disease is less than 48 hours. CSF protein level increases at the end of first week of illness.Electrodiagnostic features are mild or absent in early stages and lag behind clinical evolution. Demyelinating form shows lengthy distal latencies, slow conduction velocities, conduction block and temporal dispersion of mixed legal action authorisation. Axonal form shows decrease amplitude of compound action voltage without conduction retardation and prolongation of latencies.There are several(prenominal) clinical, pathologic and electrophysiologic evidences that have established that GBS affects predominantly the peripheral nervous system. focal demyelination of the Schwann cell derived myelin has been described. Neuropathologic and electrophysiologic evidences for involvement of central nervous system are rare.There are few studies2, 3, 4, 5, which have been performed to explore the involvemen t of CNS in GBS. However, there exists no study in the Indian milieu regarding the like.The present study is an effort to explore the CNS involvement in GBS by measuring audile evoked potentials. This test evaluates the integrity of auditive (Brainstem Auditory Evoked Potential) pathway by measuring evoked potentials.Evoked potentials are recorded as electronic impulses by surface electrodes attached to the scalp. A computer extracts these low amplitude impulses from background brain cast activity and averages the signals from repeated stimuli.Brainstem auditory evoked potentials, produced by delivering get hold ofs to the ear, and befriend to locate auditory lesions and evaluate brainstem integrity.MATERIAL METHODSThe study was conducted in the clinical neurophysiology lab in the department of physiology, CSMMU Lucknow. The subjects of study group were selected from neurology, pedology and medicine department of CSMMU Lucknow and selection of the subjects of study group ha d been done on the basis of detailed history, though clinical examination, laboratory investigations and clinically proved cases of GBS. Normal healthy controls were selected after through clinical examination and it was see to it that they do not have any apparent clinical illness that may affect the evoked potentials.Clearance from the institutional ethical commissioning was obtained written informed consent had been taken from the entire subjects study and control group. The study was conducted on clinically diagnosed cases of GBS of twain sexes.The subjects were diagnosed on the basis of history, clinical examination, and typical CSF profile (albuminocytological dissociation) and electrophysiological evidences of demyelination.Subjects having prior neurological illness, apparent hearing and optical impairment, AFP due to another cause were excluded from the study group.All the subjects of study and control group were tested under similar laboratory conditions. Subjects were condition sufficient time to relax rapport had been established so that they live comfortable and cooperate during investigationRecordings of BAEPSBAEPS were recorded by Neuroperfect- EMG 2000 EMG/NCV/EPsytem. The EPs were recorded with disc electrode from standard scalp location.Electrode were placed at solar apex (Cz, reference electrode) ,ipsilateral and contralateral mastoid process (Ai and Ac active electrode) and os frontale (Fz, ground electrode) after proper cleaning the scalp or tegument site with alcohol followed by EEG conducting pasteFor recording 2000 click stimuli at the rate of 11Hz/sec with duration of .1 ms were delivered at 70 dB. The other ear was masked by pure white illegitimate enterprise at 40 dB. This click generated by passing 0.1 ms determine pulses trough shielded headphone. Electrical impedance was kept less than 5 kilo ohm.Peak latencies of all the flaps I., II, III, IV and V and interpeak latencies of I-III,II-V and I-V were determined for both ri ght and left ears separately.STATISTICAL ANALYSISThe data so obtained were subjected to analysis using Statistical Package for Social Sciences (SPSS) Version 13.0. The data has been shown as meanSD, to compare the difference between the normal and healthy controls t test for independent samples has been carried out. The confidence limit of the study was kept at 95%, hence a p value less than 0.05 denoted statistically significant difference.RESULTSTable 1 Peak Brainstem Auditory Evoked Potentials for Left chastise Ears ** pTable 2 Inter-peak latencies for BAEP for Left Right Ears * PDISCUSSIONGuillian Barre syndrome (GBS) is regarded as a predominantly motor neuropathy with transient or absent sensory features. Although the central nervous system is seldom involved, GBS associated with CNS, manifestations has been described in children by Okumura et. al (2002)6. and in adults by Maier H et. al. (1997)3, and Muller HD et. al.(2003)4Maier H et. al. (1997)3 acknowledged histopathol ogical changes in CNS of GBS endurings. He open up infiltration of macrophages microglial cells and/or lymphocyte in different areas of central nervous system. Spinal cord and brainstem shows lymphocytic infiltration and microglial activation.Histopathological feature of CNS involvement is besides observed by Muller HD et. al. (2003)4 in form of the cellular infiltration of spinal cord though not very significant and elicited CNS involvement in GBS occur, though rare. There are few studies which had demonstrated CNS (changes) lesion in GBS on neuroimaging.Nadkarni N et. al. (1993)7 observe MRI conclusion of CNS white upshot lesion in patient of GBS who had developed symptoms of optic neuritis after plasmapharesis. These findings suggest there may be possibility of same antigenic mechanism of pathogenesis in CNS as well as peripheral nervous system.Okumura et. al. (2002)6 reported the clinical feed in and electrophysiological and neuroimaging of a patient of GBS associated wit h CNS lesion. He found mild slowing of background activities without paroxysmal discharge in electroencephalogram (EEG), mildly prolonged N2 latency with abnormal waveform in VEPs. BAEPs were unremarkable. In magnetic sonorousness imaging (MRI) there were multiple lesions in cortex and sub-cortex in the right occipital lobe and in the deep white liaison in both frontal lobes. Despite all these lesions there was no evident CNS manifestation in the case.This implies that an association of CNS involvement in patients with GBS could be under estimated because almost lesions can be clinically silent.The present study was an effort to evaluate central nervous system involvement in patients of GBS in Indian population because there is no study regarding the same performed in the India.In the view of known pathologic involvement of most proximal portion of peripheral establishments in GBS, the most promising cause of these BAEP abnormalities is focal demyelination of Schwann cell deriv ed myelin sheath that covers the extramedullary portion of the auditory nerves.Prolongation I-III IPL indicative of lesion in the auditory nerve to medullary crossroads or lower pons around superior olive trapezoid body. The prolongation of I-V IPL suggests the abnormality of conduction of auditory signals from the proximal auditory nerve to the mesencephalon via pons.The findings of the study of BAEPs are comparable and show similarity with the results of study done by Zgorzalewicz M et. al. (2003)8 except there is an additional finding of IPL III-V prolongation in our study.In the study done by Schiff JA et. al. (1985)9 had in any case found prolonged I-III inter peak latencies (IPL) in five of half dozen patients of GBS and I-V IPL in two of six patients, these results are comparable with the present study. Ropper AH et. al. (1986)10 also find the BAEP abnormality in the form of I-III and III-V IPL prolongation in patients of GBS, though that was not clinically significant.Wh ereas Nelson KR et. al. (1988)11, find the BAEPs abnormality in patients of GBS as prolongation of wave II latency and total absence of BAEM wave form in the early stage of disease and with the complaints of sudden onset of deafness, hearing improved with the recovery and BAEP abnormality of conduction block was replaced as a prolongation of wave I latency. After convalescent geological period BAEPs become normal. In present study there was no case present as similar complaint and BAEPs finding.Topcou M et. al. (1993)12 had performed evoked potential study in patients of GBS and found BAEPs and VEPs values were abnormal in some patients during early course of illness, though the values were not statistically significant.Wong V et. al. (1997)13 had found BAEPs abnormality in Miller Fischer syndrome (MFS), a variant of GBS. His findings of BAEPs abnormalities suggest proximal auditory nerve and brainstem involvement.CONCLUSIONThus it can be concluded from our study that though often ignored, the central nervous system demyelination does occur in Guillain-Barr Syndrome (GBS) and the same can be assessed using evoked potentials like Brainstem Auditory Evoked Potentials (BAEP).REFERENCESHarrisons Principle of sexual medicine, 15th ed. 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