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Neurologic Diagnosis
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Normal limb nerve conduction velocities are of the order of 40–70 m/s (see Table 1.5). Onset latencies are used, so conduction velocity measures the fastest conducting fibers in the nerve. Nerve conduction velocity is influenced by age and limb temperature. In infants, the motor conduction velocity is about one-half that of adults and increases to reach adult values at about 3–5 years. With advancing age conduction then slows. Cooling slows conduction by about 1.9 m/s/°C below normal temperature. Limb temperature must be known and controlled before NCS can be carried out and interpreted reliably. Cold hands and feet should be warmed before proceeding with NCS.
PMM2-CDG (Congenital disorders of glycosylation, type Ia)
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
The teenage years are dominated by progressive muscle atrophy and weakness, especially of the legs. This appears primarily to be due to lower motor neuron dysfunction. Nerve conduction velocity is reduced. Cerebellar ataxia and poor coordination continue. Skeletal deformities, kyphosis, scoliosis, and keel thorax appear to be consequences of muscle atrophy. The unusual fat pads may disappear during this period. Seizures occur in about 50 percent of patients, but frequency may decrease in adolescence. Hepatopathy may stabilize or disappear.
Skeletal Muscle Damage and Recovery from Eccentric Contractions
Published in Datta Sourya, Debasis Bagchi, Extreme and Rare Sports, 2019
It has been shown that ECCs cause histological damage in rats, not only in the myofibrils, the extracellular matrix, and the triads of the cytoplasmic membrane system (Piitulainen et al. 2008; Proske and Morgan 2001), but also in nerve fibers and cause thinning of myelin sheaths (Kouzaki et al. 2016). Kouzaki et al. (2016) reported that M-wave latency was delayed by 12% at 24 h and 24% at 48 h after 60 ECCs of the elbow flexors in women, which suggests musculocutaneous nerve impairment. However, a significant correlation was not observed between the delay in nerve conduction velocity and the decrease in muscle strength. Moreover, a study in which 60 isotonic ECCs were performed using a 40% MVC dumbbell demonstrated that the M-wave latency was delayed by 32% immediately after completion of the exercise (Ochi, Tsuchiya, and Yanagimoto 2017). However, in this study, the relationship between nerve conduction velocity and other muscle damage markers was not investigated. Thus, there are still several issues that need to be clarified with regard to the relationship between decreased nerve function due to ECCs and muscle damage. The studies on the effect of ECCs on nerve function are extremely limited and detailed studies using human subjects to investigate motor nerve conduction velocity are warranted. Moreover, investigations on sensory nerve function are necessary in the future.
Impact of occupational lead exposure on nerve conduction study data
Published in International Journal of Neuroscience, 2022
Tülin Aktürk, Gülay Çeliker, Hikmet Saçmacı
Nerve conduction studies were performed by the same neurologist using Nihon Kohden EMG device (model MEB-9400K, Tokyo, Japan), according to standard techniques. The sweep speed was set at 1 ms per division. The filter settings used a 20–2000 Hz bandpass for the sensory nerve studies and a 2–10,000 Hz bandpass for the motor nerve studies. Bipolar surface electrode recordings were used for motor and sensory nerve studies. The ground electrode was properly placed between the stimulator and the recording electrode. The temperature of the upper and lower extremities was kept at 32 °C or above. The recordings were obtained by supramaximal stimulation. All nerve conduction studies were carried out in a warm room at 26–28 °C. Nerve conduction studies were performed unilaterally on the non-dominantly side for each subject. Three features were measured in the nerves: distal latency, amplitude and nerve conduction velocity.
Slow progression of amyotrophic lateral sclerosis in a Chinese patient carrying SOD1 p.S135T mutation
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2022
Hanhui Fu, Kang Zhang, Xunzhe Yang, Libo Li, Liying Cui
Physical examination revealed no signs of cognitive impairment or bulbar palsy. Prominent atrophy was observed in her four limbs, more severe in the first dorsal interosseous muscles bilaterally. The Medical Research Council (MRC) grade of her right limbs was 2–3 and the left side was 4. Tendon reflexes were not elicited and bilateral pathological reflections were absent. No sensation disturbance was found. Nerve conduction velocity was normal. Needle electromyogram (EMG) revealed fibrillation and fasciculation potentials, as well as signs of neurogenic impairments in the cervical, thoracic, and lumbosacral segments. Routine hematological examinations, cerebrospinal fluid testing, brain and spinal cord MRI were unremarkable. Considering the long survival time that is different from the classical ALS phenotype, we conducted whole-exome sequencing (WES) for the patient and her family members. A missense mutation SOD1 c.404G>C, p.S135T was detected in this patient, but not in any other family members. (Figure 1(A,B)).
Comparison of nerve conduction velocity distribution methods by cold exposure and ischemia
Published in International Journal of Neuroscience, 2021
Kamil Savaş, Hilmi Uysal, Nazmi Yaraş
The assessment of peripheral nerve functions is essential in clinical neurophysiology in order to detect nerve conduction velocity (NCV) and conduction block at a subclinical stage [1, 2]. NCV studies are based on recording a compound action potential (CAP) from a peripheral nerve via surface or needle electrodes placed near the nerve bundle to calculate conduction velocity (CV), latency and duration. However, the information gained from clinical NCV studies generally applies to fast conducting fibers since they contribute more to CAP amplitude and duration than the slower ones. Consequently, no information is provided by current NCV methods with regard to slower conducting fibers or individual fiber groups. There is strong evidence to suggest that some diseases affect specific nerve groups. For example, diabetes mellitus [3] and uremic neuropathy [4] affect slower conducting sensory fibers earlier and more frequently than faster conducting sensory fibers. On this basis, the estimation of conduction velocity distribution (CVD) can provide a holistic comprehension of the pathophysiology of fibers affected by various neuropathies. It can also be used to monitor the efficacy of the applied treatment and healing process.