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Your search keyword '"Kochar DK"' showing total 4 results
Start Over Author "Kochar DK" Journal electromyography and clinical neurophysiology
4 results on '"Kochar DK"'

1. Study of motor and sensory nerve conduction velocities, late responses (F-wave and H-reflex) and somatosensory evoked potential in latent phase of intermittent acute porphyria.

Author

Kochar DK, Poonia A, Kumawat BL, Shubhakaran, and Gupta BK

Subjects
Adolescent, Adult, Electric Stimulation, Female, Humans, Male, Median Nerve physiopathology, Middle Aged, Porphyria, Acute Intermittent physiopathology, Reference Values, Evoked Potentials, Somatosensory physiology, H-Reflex physiology, Motor Neurons physiology, Porphyria, Acute Intermittent diagnosis, Reaction Time physiology, Sensory Receptor Cells physiology, Synaptic Transmission physiology
Abstract

Twenty-five patients of intermittent acute porphyria (IAP) in latent period were studied neurophysiologically by assessing motor and sensory nerve conduction velocities, late responses (F-wave and H-reflex) and somatosensory evoked potentials of median nerve and were compared with 15 age and sex matched control group. All the patients had at least one classical attack of IAP during which Watson Schwartz test was positive. None of them had any evidence of neurological defecit at the time of examination. Compared with the controls, patients of AIP had significantly slower motor and sensory conduction velocities of median nerve (P < 0.001) and it was more marked in the distal segment of the nerve. Nineteen out of 25 had one or the other abnormal neurophysiological parameter. Reduced nerve conduction velocity was not found to have any relation with age, sex or duration of the illness or number of attacks. Present study shows evidence of subclinical neuropathy in patients of intermittent acute porphyria in latent phase.

Published
2000

2. Brainstem auditory evoked potentials (BAEPs) and somatosensory evoked potentials (SEPs) in enteric encephalopathy (EE).

Author

Chauhan S, Kochar DK, Solanki BS, and Kumawat BL

Subjects
Acute Disease, Adolescent, Adult, Auditory Threshold physiology, Brain Diseases etiology, Brain Diseases metabolism, Coma etiology, Coma metabolism, Coma physiopathology, Delirium etiology, Delirium metabolism, Female, Humans, Malaria, Cerebral physiopathology, Male, Median Nerve physiopathology, Middle Aged, Movement Disorders etiology, Movement Disorders metabolism, Movement Disorders physiopathology, Neural Conduction physiology, Reaction Time physiology, Typhoid Fever metabolism, Brain Diseases physiopathology, Delirium physiopathology, Evoked Potentials, Auditory, Brain Stem physiology, Evoked Potentials, Somatosensory physiology, Typhoid Fever complications
Abstract

BAEPs and SEPs were studied in 25 patients of enteric encephalopathy in acute phase and the results were compared with 25 healthy control persons. In the study the important observations of BAEPs were delayed peak latency of wave III, wave V and delayed ILP I-V, and of SEPs was prolonged peak latency of N20. The electrophysiological evidence suggests metabolic cause for the coma and the SEP changes were similar to those observed in cerebral malaria reported earlier in this laboratory.

Published
1997

3. Somatosensory evoked potentials in cerebral malaria. A preliminary study.

Author

Kochar DK and Makkar RK

Subjects
Action Potentials physiology, Adult, Case-Control Studies, Female, Humans, Male, Median Nerve physiopathology, Neural Conduction physiology, Parietal Lobe physiopathology, Reaction Time physiology, Spinal Cord physiopathology, Evoked Potentials, Somatosensory physiology, Malaria, Cerebral physiopathology
Abstract

Somatosensory evoked potentials were recorded in patients of cerebral malaria by (R) median nerve stimulation. Important observations of this study were delayed absolute latency of N20, increased N13-N20 IPL i.e. central conduction time and distorted and dispersed waveforms of N9 and N20 peaks. The possible pathologic mechanism is discussed.

Published
1994

4. Somatosensory evoked potentials (SSEPs); sensory nerve conduction velocity (SNCV) and motor nerve conduction velocity (MNCV) in chronic renal failure.

Author

Makkar RK and Kochar DK

Subjects
Adult, Case-Control Studies, Female, Humans, Male, Median Nerve physiology, Parietal Lobe physiology, Peripheral Nervous System Diseases physiopathology, Reaction Time physiology, Spinal Cord physiology, Evoked Potentials, Somatosensory physiology, Kidney Failure, Chronic physiopathology, Motor Neurons physiology, Neural Conduction physiology, Neurons, Afferent physiology
Abstract

Somatosensory evoked potentials, sensory and motor nerve conduction velocity were studied in 25 patients of chronic renal failure and the results were compared with 15 healthy persons. The values more than +/- 3 S.D. were considered abnormal. SNCV was reduced in 11/25 patients; average reduction being 18 m/s (highly significant, p < 0.001); MNCV was reduced in 11/25 patients, average reduction being 20 m/s (highly significant, p < 0.001). Both SNCV and MNCV in same person were reduced in 6/25 patients. In SSEP N9, N13 and N20 were delayed in almost all the patients (highly significant, p < 0.001). Amplitude of N20 and N13 were reduced in 1 and 4 patients respectively but amplitude of N9 was normal. Out of different IPLS, Ebw-N9 was delayed in 5/25 patients (p < 0.9, insignificant); N9-N13 was delayed in 8/25 patients (p < 0.001, highly significant); N13-N20 was delayed in 1/25 patients (p < 0.01, significant). The evidence of these neurophysiological abnormalities collectively suggest the presence of central-peripheral axonopathy in this disease.

Published
1994

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