No abstract

No abstract

Background: The neurophysiological examination provides valuable pathophysiological information for the diagnosis, prognosis, and therapy of patients with polyneuropathy (Fuglsang-Fredriksen A., Pugdahl K. Clin Neurophysilogy 122: 440-455, 2011). Nerve conduction study (NCS) is the most objective and reliable measure of peripheral nerve function and is considered the gold standard for the diagnosis of most neuropathies. Aim of the study: To evaluate the clinical usefulness of nerve conduction study (NCS) in the differentiation between axonal and demyelinating polyneuropathies. Methods: In the present study, 125 patients with polyneuropathy were studied ranging age from 9 to 79 years. Thirtysix patients were classified as axonal polyneuropathy, 23 patients as demyelinating, and 9 as mixed, while 57 patients were classified as neuropathic. Nerve conduction study (NCS) and electromyography (EMG) were performed using Nihon Kochden electromyography machine with surface recording and stimulating electrodes. Results: There is statistically significant linear correlation between reduction in sensory nerve action potential (SNAP) amplitude and decrease in sensory conduction velocity (SCV) of median and ulnar nerves. Also, there is statistically significant inverse correlation between reduction in compound motor action potential (CMAP) amplitude and increase in distal motor latency (DML). There is statistically significant linear correlation between reduction in compound motor action potential (CMAP) amplitude and decrease in motor conduction velocity (MCV). There is statistically significant linear correlation between reduction in compound motor action potential (CMAP) amplitude and decreased grade of power in both axonal and demyelinating polyneuropathy; statistically significant linear correlation was found between decrease in conduction velocity and decrease in grade of power. Conclusion: The present study demonstrates significant correlation between amplitude reduction and conduction slowing in demyelinating as well as axonal polyneuropathy.

No abstract

Background: It's though that mitochondrial dysfunction is participated in multiple sclerosis (MS) pathogenesis. Serum lactate and uric acid levels are biochemical markers related to mitochondrial dysfunction. Aim of work: to assess mitochondrial dysfunction in sufferers with MS through investigating lactate and uric acid serum levels. Subjects and Methods: This case carried out on 32 patients with MS and 20 safe controls matched by age and sex. Patients have been diagnosed with MS in keeping with McDonald Criteria 2017. Both participants underwent a careful history taking, thorough general and neurological exam and evaluation of serum lactate and uric acid. Using the expanded disability status scale (EDSS), the degree of impairment in sufferers with MS became assessed and fatigue became evaluated the usage of the fatigue severity scale (FSS). Results: Patients had significantly higher serum lactate levels when relative to controls (40.7 ± 18.1 versus 20. 1 ± 5.8 mg/dl, p=0.001). There were no statistically relevant variations among patients and controls regarding serum uric acid levels (4.9± 1.1 versus 5.3 ± 1.2 mg/dl, p=0.337). Correlation analysis showed significantly inverse correlation among levels of serum lactate andEDSS (r=-0.124, p=0.016) and FSS (r=-0.504, p=0.003). Conclusion: Serum lactate but not serum uric acid is elevated in MSpatients. It was associated with EDSS and FSS.