Efficacy of splinting and oral steroids in the treatment of carpal tunnel syndrome: a prospective randomized clinical and electrophysiological study

OBJECTIVE: To study the efficacy of splinting and oral steroids in the management of carpal tunnel syndrome (CTS). DESIGN: Prospective, randomized, open-label, clinical and electrophysiological study with 3-month follow-up. MATERIALS AND METHODS: Forty patients with CTS were randomly divided into splint group (N-20), wearing splint in neutral position for 4 weeks; and steroid group (N-20), who received oral prednisolone 20 mg/day for 2 weeks followed by 10 mg/day for 2 weeks. Clinical and electrophysiological evaluations were done at baseline and at 1-month and 3-month follow-up. Independent 't' test and paired 't' test were used for statistical analysis. OUTCOME MEASURES: Primary outcome measure was the symptom severity score and functional status score. Secondary outcome measures were median nerve sensory and motor distal latency and conduction velocity. RESULTS: At the end of 3 months, statistically significant improvement was seen in symptom severity score and functional status score in both groups (P<0.001). Median nerve sensory distal latency and conduction velocity also improved significantly in both the groups at 3 months. Improvement in motor distal latency was significant (P=0.001) at 3 months in steroid group, while insignificant improvement (P=0.139) was observed in splint group. On comparing the clinical and electrophysiological improvement between the two groups, except for the functional status score, there was no significant difference at 3-month follow-up. Improvement in functional status score was significantly more in steroid group (P=0.03). CONCLUSION: There was significant improvement in both groups, clinically as well as electrophysiologically, at 3 months. On comparing the efficacy of the two treatment methods, except for the functional status score, there was no significant difference between the two groups.     

Peripheral and central nervous system alterations in hypothyroidism: electrophysiological findings

The purpose of this study is to evaluate objectively the functional changes in the nervous system in hypothyroidism by different electrophysiological parameters and to determine the frequencies of these changes in patients with hypothyroidism. We enrolled 23 patients (17-64 years old, mean 38.2) with biochemical evidence of hypothyroidism, with thyroxine less than 4 microg/dl and thyrotropin above 4.5 mU/ml, and 200 age- and sex-matched normal subjects. Detailed clinical examination and electrophysiological measurements included electromyography, motor conduction velocity, visual-evoked potentials (VEPs), brainstem auditory-evoked potentials (BAEPs) and event-related potentials. Determinations of P300, Wechsler Adult Intelligence Scale (IQ) and electroencephalography (EEG) were performed. Of the hypothyroid patients 52% had peripheral nervous system (PNS) involvement. Entrapment neuropathy was the commonest (35%). Axonal neuropathy was recorded in 9% and myopathy was recorded in another 9%. The central nervous system (CNS) was affected in 78% of the cases. Significant prolongations of P100 latency of VEP, latency and interpeak latency of BAEPs of different waves of hypothyroid patients were compared to the control group. 52% had abnormal VEPs and BAEPs above the mean +/- 2 SD of the normal control group. Six patients (26%) had prolonged P300 latency while 16 patients had an IQ below 90. Eight patients (35%) had EEG changes. Diffuse slowing of background activity was the commonest. No significant correlation was observed between hormonal levels and the different electrophysiological parameters. Thus, the CNS is more vulnerable to the effect of hypothyroidism than the PNS. Therefore, we suggest performing electrophysiological studies in hypothyroid patients, even in the asymptomatic ones, early in the course of disease in order to detect the nervous system involvement.     

腕管综合征高频超声检测所见与电生理检查结果相关性研究

目的：探讨腕管综合征（CTS）患者高频超声检查正中神经结构改变与电生理结果的相关性，以作拟定临床治疗的参考。方法：对上肢麻木患者进行电生理检查，诊断为CTS后再进行高频彩超检查，重点测定受压正中神经最细处、最粗处的前后径，并计算最细处与最粗处之比。电生理主要检查正中神经运动传导末端潜伏期、波幅及感觉传导速度（SCV ）及波幅，对超声检查结果及电生理结果进行相关性分析。结果：SCV与直径的 Pearson相关性为0．850，呈高度相关性；运动末端潜伏期与直径的Pearson相关性为0．419，呈中度相关性；感觉传导波幅与超声所测直径的 Pearson相关性为0．220，为弱相关性；运动传导波幅与超声所测直径的 Pearson相关性为0．256，为极弱相关或无相关性；所有电生理数据与神经细粗比的 Pearson数据均低于0．2，为极弱相关或无相关性。结论：正中神经SCV与最细处直径呈高度负相关，运动末端潜伏期与最细处直径呈中度负相关，与正中神经解剖改变有关。     

Peripheral nerve function during hyperglycemic clamping in healthy subjects

The influence of hyperglycemia with physiological hyperinsulinemia on peripheral nerve function was studied in 10 non-diabetic subjects. Blood glucose concentration was raised from 3.8 +/- 0.2 mmol/l (mean +/- SEM) to 17.1 +/- 1.4 mmol/l (mean +/- SEM) within 15 min and kept at this level for 120 min by intravenous glucose infusion. Sensory and motor nerve conduction velocity, and distal motor latency in the ulnar nerve were determined before, immediately after induction of hyperglycemia, and again after 120 min of hyperglycemia. Mean sensory nerve conduction velocity increased from 57.7 m/s to 59.5 m/s (P less than 0.005) immediately after induction of hyperglycemia, and after 120 min of hyperglycemia mean sensory nerve conduction velocity was 59.6 m/s (P less than 0.05). An insignificant increase was seen in motor nerve conduction velocity during hyperglycemia. Mean distal motor latency decreased from 3.1 ms to 3.0 ms (P less than 0.025) immediately after induction of hyperglycemia, and after 120 min of hyperglycemia distal motor latency was 2.9 ms (P less than 0.05). We conclude that short term hyperglycemia with physiological hyperinsulinemia seems to increase sensory nerve conduction velocity and decrease motor latency.     

Exclusive electrophysiological motor involvement in carpal tunnel syndrome.

OBJECTIVE: To define the frequency of exclusive electrophysiological motor involvement in carpal tunnel syndrome (CTS). METHODS: We reviewed the electrophysiological studies of 2727 consecutive hands with typical symptoms and signs of CTS and at least one abnormal test of the following: median distal motor latency (DML), digit two sensory conduction velocity (D2-SCV), segmental D2-SCV from wrist to palm, median-ulnar sensory latency difference from ring finger stimulation. RESULTS: Thirty-one hands (1.2%) had prolonged median DML ( > 4.4 ms) with normal SCV ( > 48 m/s). In 17 of 31 hands, segmental D2-SCV from wrist to palm or median-ulnar latency difference from ring finger stimulation were also performed with normal results in 8 hands, demonstrating a true exclusive electrophysiological motor involvement. CONCLUSIONS: In CTS, exclusive electrophysiological involvement of median motor fibers is rare. It may be related to preferential compression of the intraneural motor fascicles clumped superficially in the most volar-radial nerve quadrant or, more probably, to the fact that the recurrent thenar branch may exit the carpal tunnel through a separate ligamentous tunnel within the transverse carpal ligament where it may be preferentially or selectively compressed.     

Peripheral neuropathy associated with; plasma cell dyscrasia: a clinical and electrophysiological follow-up study

Thirteen patients with polyneuropathy associated with plasma cell dyscrasia had serial electrophysiological studies. Five patients with monoclonal IgG had motor and/or sensory symptoms of which 4 correlated with slow motor and sensory nerve conduction. The 4 patients with monoclonal IgM reactive with myelin-associated glycoprotein (MAG), had predominantly motor symptoms, demyelination in the nerve biopsy and slow motor and sensory nerve conduction. Four patients with monoclonal IgM without anti-MAG activity had mainly sensory symptoms, axonal neuropathy on nerve pathology and slow or absent sensory nerve conduction. After treatment with plasmapheresis and chemotherapy 9 patients improved clinically and 4 were unchanged. Criteria for electrophysiologic improvement were presence of sensory or motor responses that were absent before treatment, conduction velocity increased by more than 10 m/s and increase of amplitude by more than 100%. Electrophysiological studies showed improvement in 7, were unchanged in 4, and worse in 2. Sensory velocities in ulnar and sural nerves were significantly improved following treatment (P less than 0.002) and the same trend was noted for the sensory velocity in the median nerve (P less than 0.19). We conclude that nerve conduction studies in combination with clinical examinations are useful in documenting the effects of treatment in these neuropathies.     

Longitudinal conduction studies in hereditary motor and sensory neuropathy type 1

Motor conduction studies were performed serially in 10 patients, ages 10-62 years, with clinical and electrophysiological criteria of hereditary motor and sensory neuropathy type 1 (HMSN-1) over periods of 11-19 years. Median nerve conduction velocity (MNCV) and distal motor latency showed no significant change on serial studies. Mean median compound muscle action potential (CMAP) amplitude values, however, decreased 66% in 8 patients. Observed clinical progression in HMSN-1, over prolonged periods of time, was not associated with MNCV slowing. However, CMAP amplitude reduction, reflecting progressive axonal loss, correlated with clinical deterioration.     

Study on the latency difference between compound muscle and sensory nerve action potentials]

In motor nerve conduction studies compound muscle action potentials (CMAPs) appear later than sensory nerve action potentials (SNAPs). This time lag originates from the conduction delay at the distal motor axon, neuromuscular transmission time and muscle action potential induction time. To investigate the latency difference between CMAPs and SNAPs we studied 46 healthy individuals, 46 patients with diabetes mellitus and 33 patients with carpal tunnel syndrome, using the lumbrical and interossei recording method. In this method the recording active electrode was placed on the 2nd lumbrical muscle and the reference electrode on the proximal palmar aspect of the index finger. Supramaximal stimulation was given to the median or ulnar nerve trunk at 9-cm proximal to the recording active electrode. The CMAP from the 2nd lumbrical muscle (L) and the SNAP from the digital nerve (N) were recorded after median nerve stimulation, and the CMAP from the 2nd interossei muscles (I) was recorded after ulnar nerve stimulation. The residual latency, which is arbitrary defined as the latency difference (L-N) in this study, was 1.38 +/- 0.15 (mean +/- SD) msec in healthy individuals. About 1 msec of the residual latency is regarded as the time for neuromuscular transmission and the time to evoke muscle activities. Thus, the conduction delay at the distal motor axon was calculated as about 0.4 msec in healthy individuals. The residual latency was relatively constant in 29 diabetic patients without conduction delay across the carpal tunnel, which was defined by the latency difference (L-I) < or = 0.4 msec. Their sensory nerve conduction velocities (calculated from N latency) were always above 40 m/sec. On the other hand in diabetic patients with conduction delay across the carpal tunnel, which was defined by the latency difference (L-I) > 0.4 msec, the residual latency gradually increased as the sensory nerve conduction velocity decreased. Their sensory nerve conduction velocities were mostly less than 40 m/sec. The similar relationship was observed in patients with carpal tunnel syndrome without diabetes mellitus. We consider that the diabetic neuropathy alone doesn't cause the increase of the residual latency. Instead, severe conduction delay across the carpal tunnel decreases the N velocity and increases the residual latency. We can also regard the relationship between the latency difference (L-N) and N velocity as being in inverse proportion. Perhaps the increase of the residual latency was simply caused by the proportional decrease in the conduction velocity at the distal motor axon, not by the special mechanism concerning to the carpal tunnel syndrome. This paper presented the electrophysiological changes seen in the distal segment secondary to the proximal entrapment.     

Electrophysiological features of chronic inflammatory demyelinating polyradiculoneuropathy associated with IgG4 antibodies targeting neurofascin 155 or contactin 1 glycoproteins

ObjectiveChronic inflammatory demyelinating polyradiculoneuropathies (CIDP) with antibodies against neurofascin 155 (Nfasc155) or contactin-1 (CNTN1) have distinctive clinical features. Knowledge on their electrophysiological characteristics is still scarce. In this study, we are investigating whether these patients have specific electrophysiological characteristics.MethodsThe electrophysiological data from 13 patients with anti-Nfasc155 IgG4 antibodies, 9 with anti-CNTN1 IgG4 antibodies were compared with those of 40 consecutive CIDP patients without antibodies.ResultsAll the patients with antibodies against Nfasc155 or CNTN1 fulfilled the EFNS/PNS electrodiagnostic criteria for definite CIDP. There was no electrophysiological difference between patients with anti-CNTN1 and anti-Nfasc155 antibodies. Nerve conduction abnormalities were heterogeneously distributed along nerves trunks and roots. They were more pronounced than in CIDP without antibodies. Motor conduction velocity on median nerve <24 m/s or motor velocity on ulnar nerve <26 m/s or motor distal latency on ulnar nerve >7.4 ms were predictive of positive antibodies against the node of Ranvier with a sensitivity of 59% and a specificity of 93%.ConclusionsMarked conduction abnormalities may suggest the presence of positive antibodies against the node of Ranvier.SignificanceAnti-Nfasc155 and anti-CNTN1 antibodies target the the paranodal axo-glial domain but are associated with nerve conduction abnormalities mimicking a “demyelinating” neuropathy.     

Multimodality evoked potentials in progression of metachromatic leukodystrophy

A 2-yr-3-mo-old girl with metachromatic leukodystrophy (MLD) was examined using serial multiple electrophysiological procedures. Sensory nerve conduction velocity was delayed earlier and more severely than motor nerve conduction velocity. Visual evoked potentials (VEPs) showed prolonged latency of wave IV. Auditory brainstem responses (ABRs) showed prolonged latency of waves I and V, and the I-V interval. As to the interpeak latency of somatosensory evoked potentials (SEPs), the P9-P14 and the P14-N20 intervals were prolonged on admission. Two months later, both intervals were more prolonged, but the prolongation of the P9-P14 interval was the most prominent. The demyelination in our case may have started in the cerebral white matter, progressed to the peripheral nerves, and at last via the spinal root reached the brainstem. An electrophysiological follow-up study may be valuable in the understanding of the progressive pathological changes and in the evaluation of therapeutic measures.     

Digital vibration syndrome: neuro-physiologic study in 17 patients

Studies were carried out on 17 male workers with clinical vibration disease who had been working with different vibrating tools (compressed-air hammers, chain-saws, rock drills, grinders) for 2 to 39 years. Their neurophysiological results were compared with those of 20 healthy men (control group). Median motor nerve conduction velocity (NCV) between elbow and wrist was significantly reduced and motor distal latency (DL) significantly longer in 43% cases. A distinct decrease of the conduction velocity of distal (finger-wrist) median sensory fibers (in 56% of cases) as well as reduced amplitude of the sensory evoked potential (62% of cases) were found. EMG showed alterations only in patients with NCV abnormalities. These electrophysiological findings point to distal axonal as well as to demyelination damage. The results, which are discussed in relation to previously published work in this field and according to a pathogenetic hypothesis of this syndrome, allowed us to draw practical conclusions for the neurophysiological examination of patients with vibration disease.     

感觉性共济失调型格林-巴利综合征3例临床与电生理

目的 :了解感觉性共济失调型格林 -巴利综合征的临床与电生理特点。方法 :观察临床及电生理表现 ,测定了正中神经、尺神经、腓神经末端潜伏期 ,运动神经传导速度 ,运动诱发波幅 ;感觉神经传导速度 ,感觉诱发波幅。结果 :临床表现 :1.急性起病。 2 .病前有感染史。 3.感觉减退或消失、感觉性共济失调。 4.脑脊液蛋白细胞分离。电生理检查 :1.感觉神经传导速度减慢。 2 .感觉神经诱发波幅降低或缺失。结论 :临床及电生理特点可作为感觉性共济失调型格林 -巴利综合征的诊断标准之一。     

Proximal axonal changes after peripheral nerve injury in man

Peripheral nerve injury leads to changes in the proximal axon. Traumatic nerve injuries in humans were investigated to characterize such electrophysiological changes. Mixed nerve conduction studies (MNCS) and motor conduction studies (MCS) were performed proximal to the injury. Control values were obtained from the uninjured limb. Median (n = 24) and ulnar (n = 35) nerve injuries were studied. The injured nerves had significant mixed nerve action potential (MNAP) amplitude reductions (median: P < 0.0001; ulnar: P < 0.0001). The majority of the MNAP amplitude reductions were severe and early. There was slowing in the mixed nerve conduction velocity (MNCV) (median: P = 0.09; ulnar: P = 0.04) and motor conduction velocity (MCV) (median: P = 0.046; ulnar: P = 0.005). Axonal loss appears to play a significant role in producing the MNCS changes observed, and its early occurrence is noteworthy. Proximal MCV reduction could be secondary to the effects of injury as well as collateral sprouting of uninjured axons. Proximal axonal changes may have an impact on recovery.     

Refractory period impairment in sural nerves of diabetics

Polyneuropathy is a frequent complication in diabetics. In a non-selected group of 65 diabetics, 30 patients had clinical signs of neuropathy. These patients had more significant changes in electrophysiological parameters than patients without clinically evident polyneuropathy. Significant reduction of sural nerve conduction velocity was observed in 16 of 30 patients with and in 4 of 35 diabetics without clinical signs of polyneuropathy. Additional information was obtained when paired stimuli were applied and the test response latency was measured. Stimulus intervals of 3 ms gave the highest quota of information about involvement of the sural nerve. Significant prolongation of the test response in paired stimulation at intervals of 3 ms was found in 21 of 30 patients with clinically apparent diabetic polyneuropathy and in 16 of 35 diabetics without clinical signs of polyneuropathy.     

Chronic dysimmune demyelinating polyneuropathy: a clinical and electrophysiological study of 93 patients.

OBJECTIVES--To identify clinical, electrophysiological, and immunological characteristics of chronic immune demyelinating polyneuropathy to define for each group the appropriate therapeutic strategies. METHODS--The clinical and electrophysiological data and the response to treatment of 93 patients with an acquired chronic dysimmune demyelinating polyneuropathy (CDDP) studied over a period of 10 years were reviewed. Two groups were identified: group 1, comprising 64 patients with an idiopathic CDDP, of whom 13 had serum monoclonal or polyclonal gammopathy without detectable antibodies directed against the "myelin associated glycoprotein" (MAG), and group 2, comprising 29 patients with an IgM monoclonal gammopathy of undetermined significance (MGUS) with antibodies binding to the MAG. RESULTS--Group 1 patients had either a progressive or relapsing course. The relapsing course had more pronounced distal slowing of motor conduction velocity. In group 1, there were no significant clinical or electrophysiological differences between patients with or without gammopathy. Patients with anti-MAG antibody (group 2) differed significantly from group 1 patients, especially on the basis of electrophysiological results. They had a more pronounced slowing of peroneal motor nerve conduction velocity, a lower frequency of conduction block, and a distal accentuation of conduction slowing, distinguishing them from those with idiopathic CDDP, Charcot-Marie-Tooth polyneuropathy type 1A, and control subjects. CONCLUSION--The idiopathic CDDP group is heterogeneous with probably different subgroups. Patients with IgM MGUS polyneuropathy and anti-MAG antibodies have characteristics which distinguish them significantly from other CDDP and suggest different immune mechanisms and responses to treatment.     

Cold elbow syndrome: spurious slowing of ulnar nerve conduction velocity

Low temperature decreases nerve conduction velocity (NCV). The across-elbow segment of the ulnar nerve is superficial and may be particularly susceptible to decreased temperature. We evaluated patients without clinical ulnar neuropathy at the elbow (UNE) but with isolated slowing of the across-elbow ulnar NCV (normal group), and patients with clinical and electrodiagnostic findings of UNE (UNE group). All subjects had ulnar motor nerve studies completed before and after warming. The mean across-elbow NCV was 43.4 m/s and 48.6 m/s (P < 0.0001) in the normal group, and 37.4 m/s and 37.7 m/s (P = 0.90) in the UNE group, before and after warming, respectively. There was no change in the forearm segment NCV in either group. Seventeen of 32 subjects in the normal group had completely normal studies after warming. No patients with UNE developed normal across-elbow NCV with warming. Low temperature slows across-elbow ulnar NCV in normal subjects without impact on the forearm segment. Warming of the elbow improves across-elbow ulnar NCV in normals, but does not reverse the abnormalities in patients with UNE. Elbow warming should become a routine part of ulnar nerve conduction studies, especially when there is isolated conduction slowing in the across-elbow segment.     

Electrophysiological Characteristics of the Pediatric Femoral Nerve and Their Use in Clinical Diagnosis

ObjectiveTo explore the electrophysiological characteristics of the pediatric femoral nerve at different ages.MethodsSurface electrodes were used to detect femoral nerve conduction in 163 healthy children aged 0-14 years recruited to this study and divided into six age groups. Based on the range of normal values obtained, the diagnosis of 22 patients with suspected femoral nerve injury was confirmed.ResultsWe obtained normal values for pediatric femoral nerve motor and sensory conduction in all age groups, including proximal and distal compound muscle action potential latencies, proximal compound muscle action potential amplitude and duration, motor conduction velocity, F-wave latency, and sensory conduction velocity. We measured proximal compound muscle action potential in all children in all age groups. The manifestation of femoral nerve injury in the 22 patients was primarily a clear decrease or absence of compound muscle action potential amplitude or a lengthened latency. Electromyographs revealed that 104 muscle parts were involved in the nerve function, in which 59 parts were found to be abnormal (56.73%).ConclusionsThe development of pediatric femoral nerve mainly began after 1 years old and continued to 14 years old. The proximal latency and compound muscle action potential amplitude of the pediatric femoral nerve have clinical value. Detection of the femoral nerve is important in the diagnosis of lower limb monoplegia, especially for acute flaccid paralysis associated with nonpolio enterovirus infection.     

Nerve conduction in the Guillain-Barré-Strohl syndrome

Summary Fifty cases of the Guillain-Barré-Strohl syndrome were investigated clinically and electrophysiologically—20 in the acute phase, and 30, as a matter of followup, many years after. The sural nerve was biopsied in six cases. There was no evident correlation between clinical symptoms and slowing of motor and sensory conduction. Nerve conduction velocity became slower after the beginning of clinical improvement. The electrophysiological abnormalities concerned both sensory and motor fibers despite the frequent absence of clinical sensory manifestations. The so-called long nerves were involved earlier and more markedly than the so-called short nerves. Conduction velocity and distal latency were equally affected. A slight electrophysiological defect was noticeable even many years after the acute phase of the syndrome, in completely symptoms free patients. Some correlation existed between conduction velocity changes and histological findings.This work was supported by grant from the Polish Academy of Sciences No. 10.4.2.02     

Conduction velocity changes in peripheral nerves in the acute stage of the Guillain-Barre syndrome

In 20 cases of acute Guillain-Barré syndrome (including 4 recurrent cases the conduction velocity was measured in the nerves: facial, axillary, musculocutaneous, peroneal, sural and ulnar (motor and sensory). In the long nerves the maximal as well as minimal conduction velocity was determined. At the peak of development of clinical manifestations all electrophysiological parameters differed from the normal values, in particular, significant changes were found in long nerves (complete parallelism was found between the velocity of conduction and end latency). In the first stage of regression of clinical manifestations the electrophysiological parameters continued to show an increased abnormalities, only later they approached the normal values. Sensory conduction was disturbed in an equal degree as the motor conduction despite absence of clinical sensory disturbances. In recurrent cases slowing down of conduction was much more striking and persisted also during remission. In all studied cases independently of the character and course of the disease there was no correlation between the clinical state and the changes in the determined electrophysiological parameters.     

Subclinical lesions of peripheral nervous system in multiple sclerosis patients

BACKGROUND AND PURPOSE: In the last years the presence of peripheral nervous system (PNS) lesions has been noted in patients with multiple sclerosis (MS). The frequency and degree of PNS damage reported by many authors differ among publications, so does the type of PNS lesions. The aim of our study was to perform an electrophysiological evaluation of the peripheral nervous system in patients with a definite diagnosis of multiple sclerosis and without any clinical signs of peripheral neuropathy. MATERIAL AND METHODS: 110 patients were included in the study, comprising 70 people with a definite diagnosis of multiple sclerosis and 40 people without any symptoms of organic nervous system lesion serving as a control group. During neurologic examination of MS patients the degree of disability measured by EDSS scale, the duration of the disease as well as number of relapses were assessed. A "disease progression factor" was calculated by dividing a number of relapses by disease duration in years. Patients with common etiologies for peripheral neuropathy such as diabetes, renal insufficiency, thyroid gland dysfunction, proliferative disorders etc. were excluded from the study. Orthodromic motor conduction and late responses (F wave) in median, ulnar, peroneal and tibial nerves as well as sensory conduction in median, ulnar (orthodromic) and sural (antidromic) nerves were evaluated. RESULTS: There was electrophysiological evidence of peripheral nervous system lesions in at least one nerve in 52 (74.2%) MS patients. In 30 patients (42.8%) more than one peripheral nerve was lesioned. There were more significant differences noted during the examination of sensory nerves. Sensory amplitudes in all of the sensory nerves examined were significantly lower than in control group. Furthermore we observed slow sensory conduction velocities and prolonged sensory latencies in ulnar and sural nerves. There were significant differences between the two groups of patients concerning motor conduction too: prolonged distal latency in tibial and sural nerves, prolonged F wave latency in median, peroneal and tibial nerves, low motor amplitude in ulnar and peroneal nerves, low motor conduction velocity in ulnar nerve -- all noted in MS patients. We found no correlation between conduction parameters and the patients' age, disease duration, number of relapses and disease progression degree. CONCLUSIONS: We found out that subclinical peripheral nervous system abnormalities are very frequent in MS patients. We noted both sensory and motor nerve lesions of a demyelinating-axonal character. Sensory abnormalities were more pronounced than motor ones. There was no correlation between the degree of PNS lesions and the patients' age and/or progression of multiple sclerosis.