Background: Diabetic peripheral polyneuropathy (DPN) is associated with a variety of symptoms. Nerve conduction studies (NCSs) are considered to be the gold standard of nerve damage assessments, but these studies are often dissociated from the subjective symptoms observed in DPN patients. Thus, the aim of the present study was to investigate the correlations between NCS parameters and neuropathic symptoms quantified using the Michigan Neuropathy Screening Instrument (MNSI). Methods: Patients with type 2 diabetes mellitus (T2DM) with or without symptoms of neuropathy were retrospectively enrolled. Demographic data, clinical laboratory data, MNSI score, and NCS results were collected for analysis; DPN was diagnosed based on the MNSI score (${\geq}3.0$) and abnormal NCS results. Pearson's correlation coefficients were used to evaluate the relationships between MNSI score and NCS variables. Results: The final analyses included 198 patients (115 men and 83 women) with a mean age of $62.6{\pm}12.7$ years and a mean duration of diabetes of $12.7{\pm}8.4$ years. The mean MNSI score was 2.8 (range, 0.0-9.0), and 69 patients (34.8%) were diagnosed with DPN. The MNSI score was positively correlated with the median motor nerve latency and negatively correlated with the median motor, ulnar sensory, peroneal, tibial, and sural nerve conduction velocities (NCVs). When the patients were categorized into quartiles according to MNSI score, peroneal nerve conduction velocity was significantly lower in the second MNSI quartile than in the first MNSI quartile (p = 0.001). A multivariate analysis revealed that the peroneal NCV was independently associated with MNSI score after adjusting for age, sex, and glycosylated hemoglobin A1c (HbA1c) levels. Conclusions: The present results indicate that a decrease in peroneal NCV was responsible for early sensory deficits in T2DM patients.
Small-fiber neuropathy (SFN) is a common clinical problems. The disorder is a generalized peripheral polyneuropathy that selectively involves small-diameter myelinated and unmyelinated nerve fibers. It is often idiopathic and typically presents with painful feet in patients over the age of 60. And autoimmune mechanisms are often suspected, but rarely identified. The clinical features consisted of painful dysesthesias and postganglionic sympathetic dysfunction, as well as reduced pinprick and temperature sensation. Although affected patients complain of neuropathic pain, this condition is often difficult to diagnose because of the few objective physical signs and normal nerve conduction studies. Diagnosis of SFN is made on the basis of the clinical features, normal nerve conduction studies, and abnormal specialized tests of small fiber function. These specialized studies include assessment of epidermal nerve fiber density as well as sudomotor, quantitative sensory, and cardiovagal testing. Unless an underlying disease is identified, treatment is usually directed toward alleviation of neuropathic pain.
Nerve conduction study (NCS) is an essential test for the diagnosis and follow-up of peripheral neuropathy. NCS can objectively quantify peripheral nerve function. NCS is affected by physiological factors such as height, age, body mass index, etc. Hence, the American Association of Neuromuscular & Electrodiagnosis Medicine (AANEM) is currently forming a Normal Data Task Force (NDTF) to present the normal value, but the number is significantly less. Currently, no research has been carried out on the correlation between nerve conduction speed and height and lower limb length in Koreans. Hence, this study sought to compare the nerve conduction velocity of the lower limbs according to the height and lower limb length. A total of 49 subjects were recruited. When the motor nerve conduction velocity and sensory nerve conduction velocity were compared according to the height and leg length, there was a statistically significant negative correlation of the peroneal and left tibial motor nerves with the height. Also, a statistically significant negative correlation was observed with the superficial peroneal sensory nerve and the sural nerve and the leg length. However, in this study, all the subject are in twentys age, whereas the NDTF is divided by age. Hence, additional studies involving subjects of various age groups are needed.
Among the various physiological factors that affect nerve conduction velocity (NCV), temperature is the most important. Because the influence of temperature is the most important source of error. It is known from animal experiments that conduction is eventually completely blocked at low temperatures, the myelinated A fibers being the first affected and the thin fibers of group C the last. Many studies showed that the NCV decreases linearly with lowering temperature within the physiological range. The distal motor latency increased by $0.2msec/^{\circ}C$ drop in temperature between $25^{\circ}C$and $35^{\circ}C$ in the median, ulnar and peroneal nerves. The temperature affect the neuromuscular transmission; The miniature endplate potential (MEPP) and endplate potential (EPP) are increase with increasing temperature. In myasthenia gravis, the reduction in the decremental response is observed following cooling. The lowering temperature make increase the amplitude of sensory compound action potential; make enlarge the surface area of compound muscle action potential with very little increase in amplitude; make diminish the fibrillation potential and increase the myotonia in needle electromyography (EMG). Because of these findings mentioned above, the skin temperature should be routinely monitored and controlled during nerve conduction tests and needle EMG and should be taken into account when interpreting the findings.
Objectives : Although the diagnosis of hereditary neuropathy with liability to pressure palsies (HNPP) is important for correct prognostic evaluation and genetic counseling, the diagnosis is frequently missed or delayed. Our main aim on undertaking this study was to characterize the electrodiagnostic features of HNPP. Material and Methods : Clinical, electrophysiologic and molecular studies were performed on Korean HNPP patients with 17p11.2 deletion. The results of electrophysiologic studies were compared with those of Charcot-Marie-Tooth disease type 1A (CMT1A) patients carrying 17p11.2 duplication. Results : Eight HNPP (50 motor, 39 sensory nerves) and six CMT1A (28 motor, 16 sensory nerves) patients were included. The slowing of sensory conduction in nearly all nerves and the distal accentuation of motor conduction abnormalities are the main features of background polyneuropathy in HNPP. In contrast to CMT1A, where severity of nerve conduction slowing was not different among nerve groups, HNPP sensory nerve conduction was more slowed in the median and ulnar nerves than in the sural nerve (p<0.01), and DML was more prolonged in the median nerve than in the other motor nerves (p<0.01). TLIs were significantly lower in HNPP than in the normal control and CMT1A patients for the median and ulnar nerves (p<0.01), and were also significantly reduced for the peroneal nerve (p<0.05) compared with those of the normal controls. Conclusion : The distribution and severity of the background electrophysiologic abnormalities are closely related to the topography of common entrapment or compression sites, which suggests the possible pathogenetic role of subclinical pressure injury at these sites in the development of the distinct background polyneuropathy in HNPP.
Although various criteria on the diagnosis of diabetic neuropathy are applied from trial to trial, being tailored in concert with its purpose, the utmost evidences of the diagnosis are subjective symptoms and objective signs of neurologic deficit. The application and interpretation of auxiliary electrophysiological test including nerve conduction study (NCS) should be made on the context of clinical pictures. The evaluation of the functions of small, thinly myelinated or unmyelinated nerve fibers has been increasingly stressed recently with the advent of newer techniques, e.g., measurement of intraepidermal fiber density, quantitative sensory testing, and autonomic function test. And the studies with those techniques have shed light to the nature of the evolution of diabetic neuropathy. The practical application of these techniques to the diagnosis of diabetic neuropathy in the individual patients, however, should be made cautiously due to several shortcomings: limited accessibility, wide overlapping zone between norm and abnormality with resultant unsatisfactory sensitivity and specificity, difficulty in performing subsequent tests, unproven quantitative correlation with clinical deficit, and invasiveness of some technique. NCS, as an extension of clinical examination, is still the most reliable electrophysiological test in evaluating neuropathy and gives the invaluable information about the nature of neuropathy, whereas the newer techniques need more refinement of the procedure and interpretation, and the accumulation of large scaled data of application to be considered as established diagnostic tools of peripheral neuropathy.
Background: Sciatic nerve injury due to intramuscular injection (SNIII) is still a health problem. This study aimed to determine whether there is a correlation between neuropathic pain and electrodiagnostic findings in SNIII. Methods: Patients whose clinical and electrodiagnostic findings were compatible with SNIII participated in this retrospective cohort study. Compound muscle action potential (CMAP) and sensory nerve action potential (SNAP) amplitudes of the sural, superficial peroneal, peroneal, and tibial nerves were graded from 1 to 4. Leeds assessment of neuropathic symptoms and signs scale (LANSS) was applied to all patients. Results: Forty-eight patients were included in the study, 67% of whom had a LANSS score ≥ 12. Sural SNAP amplitude abnormalities were present in 8 (50%) out of 16 patients with a LANSS score < 12, and 28 (87.5%) out of 32 patients with a LANSS score ≥ 12, with significant differences between the groups (P = 0.011). There was a positive correlation between the LANSS score and the sural SNAP amplitude grading (P = 0.001, r = 0.476). A similar positive correlation was also found in the LANSS score and the tibial nerve CMAP amplitude grading (P = 0.004, r = 0.410). Conclusions: This study showed a positive correlation between the severity of tibial nerve CMAP/sural SNAP amplitude abnormality and LANSS score in SNIII. Neuropathic pain may be more common in SNIII patients with sural nerve SNAP amplitude abnormality.
Excess of pyridoxine, in contrast to other nutrients, may result in neuropathy. Case reports are sparse, and little is known about the clinical and electrophysiological findings. Eight patients with pyridoxine-induced neuropathy were investigated, and a review of the literature was undertaken. Nerve conduction studies showed axonal sensory or sensorimotor polyneuropathy. And the blood levels of vitamin B6 were markedly elevated. After discontinuation of vitamin supplements, all patients showed no significant improvement in clinical and electrophysiological findings. Supplementation with pyridoxine at doses greater than 50 mg/day for extended durations may be harmful and should be discouraged.
Background: Acute brachial plexitis is an acute idiopathic inflammatory disease affecting brachial plexus, which is characterized by initial severe pain in shoulder followed by profound weakness of affected arm. This is a retrospective study to evaluate the clinical and electrophysiological profile of acute brachial plexitis. Methods: Sixteen patients with acute brachial plexitis were sampled. The electrodiagnostic studies included motor and sensory nerve conduction studies (NCSs) of the median and ulnar, sensory NCSs of medial and lateral antebrachial cutaneous nerves, and needle electromyography (EMG) of selected muscles of upper extremities and cervical paraspinal muscles. The studies were performed on both sides irrespective of the clinical involvement. Results: In most of our patient, upper trunk was predominantly affected (14 patients, 87.50%). Only two patients showed either predominant lower trunk affection or diffuse affection of brachial plexus. All had an acute pain followed by the development of muscle weakness of shoulder girdle after a variable interval ($7{\pm}8.95$ days). Ten patients (62.50%) had severe disability. In NCSs, the most frequent abnormality was abnormal lateral antebrachial cutaneous sensory nerve action potentials (SNAPs). On needle EMG, all the patients showed abnormal EMG findings in affected muscles. Conclusions: In this study, pain was the presenting feature in all patients, and the territory innervated by upper trunk of the brachial plexus was most frequently involved. The most common NCS abnormality was abnormal SNAP in lateral antebrachial cutaneous nerve. Our findings support that the electrodiagnostic test is useful in localizing the trunk involvement in acute brachial plexitis.
Inferior alveolar nerve dysfunction may be the result of trauma, disease, or iatrogenic injury. Inferior alveolar nerve injury is inherent risk in endodontic therapy, orthognathic surgery of the mandible, and extraction of mandibular teeth, particularly the third molars. The sensory disturbances of inferior alveolar nerve associated with such injury have been well documented clinical problem that is commonly evaluated by several clinical sensory test including Tinels sign, Von Frey test(static light touch detection), directional discrimination, two-point discrimination, pin pressure nociceptive discrimination, and thermal test. These methods used to detect and assess inferior alveolar nerve injury have been subjective in nature, relying on the cooperation of the patients. In addition, many of these techniques are sensitive to differences in the examiners experience and skill with the particular technique. Data obtained at different times or by different examiners are therefore difficult to compare. Prior experimental studies have used electro diagnostic methods(sensory evoked potential) to objectively evaluate inferior alveolar nerve after nerve injury. This study was designed with inferior alveolar nerve of rabbit. Several types of injury including mind, moderate, severe compression and perforation with 19 gauze, 21 gauze needle and 6mm, 10mm traction were applied for taking the sesory evoked ppterntial. Latency and amplitude of injury rabbit inferior alveolar nerve were investigated with sensory evoked potential using unpaired t-test. The results were as follows : 1. Intensity of threshold (T1) was $128{\pm}16{\mu}A$ : latency, $0.87{\pm}0.07$ microsecond : amplitude, $0.4{\pm}0.1{\mu}V$ : conduction velocity, 23.3 m/s in sensory evoked potential of uninjured rabbit inferior alveolar nerve. 2. Rabbit inferior alveolar nerve consists of type II and III sensory nerve fiber. 3. Latency was increased and amplitude was decreased in compression injury. The more injured, the more changed in latency and amplitude. 4. Findings in perforation injury was similar to compression injury. Waveform for sensory evoked potential improved by increasing postinjured time. 5. Increasing latency was prominent in traction injury rabbit inferior alveolar nerve. 6. In microscopic histopathological findings, significant degeneration and disorganization of the internal architecture were seen in nerve facicle of severe compression and 10mm traction group. From the above findings, electrophysiological assessment(sensory evoked potential) of rabbit injured inferior alveolar nerve is reliable technique in diagnosis and prognosis of nerve injury.
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