ABSTRACT
BACKGROUND: The contingent negative variation (CNV) reflects neuronal activities related to sensorimotor integration and motor planning or execution and is probably originated from the frontal-subcortical circuit. The aim of this study is to investigate the neurophysiologic changes in uremia and the effect of hemodialysis to them by utilizing the CNV test. METHODS: Fifteen right-handed healthy subjects and 12 patients with end stage renal disease (ESRD) were studied. CNV was recorded from Fz, Cz, and Pz referenced to linked ear lobes by using an S1 (click)-S2 (flashes)-key press paradigm. The amplitude of initial CNV (iCNV) was calculated as the average amplitude of 550~750 msec after S1. The amplitude of late CNV (lCNV) was calculated as the average amplitude between 200 msec before S1 and S2. The test was repeated for the patients group at the time of pre- and post-hemodialysis. Neuropsychological measurements, the trail making test (TMT) and mini-mental state score (MMSE), were conducted at the time of each test. RESULTS: Both the mean amplitudes of iCNV and lCNV at the vertex (Cz) were significantly lower in the patient group than those in the control group (p<0.05). The MMSE score and TMT were also significantly different between the patient and control group (p<0.05). There was no significant correlation between the values of neuropsychological tests and the parameters of CNV. Both iCNV and lCNV were not significantly different between the pre- and post-dialysis test. CONCLUSIONS: It appears that CNV negativity in uremia reflects dysfunctions in the frontal-subcortical circuit. In addition, hemodialysis seems to have no significant effect on it in patients with ESRD.
Subject(s)
Humans , Contingent Negative Variation , Ear , Evoked Potentials , Kidney Failure, Chronic , Neurons , Neuropsychological Tests , Renal Dialysis , Trail Making Test , UremiaABSTRACT
BACKGROUND: For the early detection and prevention of diabetic neuropathy, it is important to identify subclinical diabetic neuropathies. A routine nerve conduction study often fails to detect the early stages of neuropathy. The purpose of this study is to evaluate the clinical usefulness of electrophysiological indexes including the residual latency(RL), terminal latency index (TLI) and modified F ratio (MFR) in detecting early diabetic neuropathy with no objective clinical or electrophysiological abnormalities. METHODS: A nerve conduction study of the upper/lower limbs was investigated in 38 subclinical diabetic neuropathy patients with normal nerve conduction studies (group I), 35 clinical diabetic neuropathy patients with normal nerve conduction studies (group II) and 31 normal controls. RL, TLI and MFR were calculated and compared among the groups. RESULTS: Compared with the control group, the MFR of the lower limbs and TLI of both the upper/lower limbs were significantly decreased in both group I and II (p<0.05). RL was increased in both groups, but the difference was not statistically significant. Comparing the indexes between group I and II, there was no significant difference. CONCLUSIONS: RL, TLI and MFR are useful indexes for reflecting distal conduction slowing especially in slowly progressing polyneuropathies such as diabetic neuropathy. The results also suggest that electrophysiological changes veiled in a routine nerve conduction study were present before the clinical manifestations.
Subject(s)
Humans , Diabetic Neuropathies , Extremities , Lower Extremity , Neural Conduction , PolyneuropathiesABSTRACT
No abstract available.
Subject(s)
Central Nervous System Neoplasms , Cerebral Ventricle Neoplasms , LymphomaABSTRACT
No abstract available.
Subject(s)
Colitis, Ulcerative , Polyneuropathies , Ulcer , VasculitisABSTRACT
BACKGROUND: Motor conduction slowing in diabetic distal symmetrical polyneuropathy (DSP) generally exceeds that in distal axonal polyneuropathy. Additional mechanisms secondary to axonal injury may contribute towards this slowing. However, clinical and pathophysiological significances of motor conduction slowing have been rarely discussed. The purpose of this study is to evaluate the clinical and pathophysiological significance of conduction slowing in DSP. METHODS: We analyzed motor conduction studies of 39 patients with symptomatic painful DSP and 24 patients with asymptomatic painless DSP. Motor conduction studies of 39 patients with amyotrophic lateral sclerosis (ALS) were used as controls for the amplitude-dependent slowing of conduction. Percentages of normal limits were calculated for the compound muscle action potential amplitude (CMAP), distal motor latency (DL), and conduction velocity (CV), and converted to a square root (SQRT) form. The changes of SQRT-DL or SQRT-CV according to SQRT-CMAP changes were plotted and analyzed. RESULTS: Regression analysis showed that DL and CV were amplitude-dependent in both painless DSP and ALS. The changes of DL and CV in painful DSP did not show amplitude-dependency except DL in the lower extremities. CONCLUSIONS: This data supports the hypothesis that the mechanism of slowing is similar in both painless DSP and ALS and results from the loss of large, fast-conducting fibers. Lack of amplitude-dependency of conduction slowing in painful DSP may reflect the combined axonal and demyelinating changes, possibly due to inflammation.