ELECTROPHYSIOLOGICAL EVALUATION OF GENITO-SPHINCTERIC DYSFUNCTION IN MULTIPLE SYSTEM ATROPHY

Thirteen patients with multiple system atrophy underwent multimodality neurophysiological evaluation, including sphincteric needle electromyography (EMG), sacral reflexes, pudendal nerve terminal latency, pudendal (PSEPs) and tibialis posterior nerve somatosensory evoked potentials (TPSEPs), and perineal motor evoked potentials (PMEPs). EMG revealed denervation or neurogenic changes, with reduction in spontaneous tonic activity at rest and abnormal pudendal nerve terminal latency in 10 patients (76.9%); anal reflex was delayed in 7 patients (53.8%). TPSEPs scalp responses were clearly abnormal in 4 patients (30.7%), whereas PSEPs exhibited changes in 9 (69.2%): in 6 patients responses were delayed at lumbar level (46.2%), and in 5 over the scalp (38.4%). PMEPs showed an increase in latency with a mild prolongation of central motor conduction time (CMCT) in 2 cases (15.3%); 1 patient had prolonged latencies following both cortical and sacral stimulation, but a normal CMCT. Even if diagnostic yield is not improved using these investigations they provide evidence of multiple lesion sites other than Onuf's nucleus.­­     

Neurophysiological testing in anorectal disorders

The neurophysiological techniques currently available to evaluate anorectal disorders include concentric needle electromyography (EMG) of the external anal sphincter, anal nerve terminal motor latency (TML) measurement in response to transrectal electrical stimulation or sacral magnetic stimulation, motor evoked potentials (MEPs) of the anal sphincter to transcranial magnetic cortical stimulation, cortical recording of somatosensory evoked potentials (SEPs) to anal nerve stimulation, quantification of electrical or thermal sensory thresholds (QSTs) within the anal canal, sacral anal reflex (SAR) latency measurement in response to pudendal nerve or perianal stimulation, and perianal recording of sympathetic skin responses (SSRs). In most cases, a comprehensive approach using several tests is helpful for diagnosis: needle EMG signs of sphincter denervation or prolonged TML give evidence for anal motor nerve lesion; SEP/QST or SSR abnormalities can suggest sensory or autonomic neuropathy; and in the absence of peripheral nerve disorder, MEPs, SEPs, SSRs, and SARs can assist in demonstrating and localizing spinal or supraspinal disease. Such techniques are complementary to other methods of investigation, such as pelvic floor imaging and anorectal manometry, to establish the diagnosis and guide therapeutic management of neurogenic anorectal disorders.     

Clinical uro-neurophysiological investigation in multiple sclerosis

Subjective complaints of urinary dysfunction are common in multiple sclerosis patients. Uro-neurophysiological investigation, namely somatosensory evoked potentials (SEP) to stimulation of tibial and pudendal nerves, sacral reflex measurements and external anal sphincter electromyography (EMG) were employed in a group of 21 patients with mild to moderate multiple sclerosis and urinary symptoms. Tibial SEP showed abnormality in 86% and pudendal SEP in 48% of patients. Sacral reflexes were abnormal in 33% and external anal sphincter EMG showed abnormalities in 42% of patients (54% of women and 13% of men). Even in multiple sclerosis patients with urinary complaints tibial SEP seem to be more useful in evaluating nervous system dysfunction than pudendal SEP. On the other hand, abnormal pudendal SEP acconmpanied by normal tibial SEP may strengthen the suspicion of a conus lesion, the presence of which is some patients seems to be the cause of otherwise unexplained abnormalities of external anal sphincter EMG and sacral reflexes.     

Variability of cortically evoked motor responses in multiple sclerosis.

The calculated central motor conduction time (CMCT), onset latency variability (expressed as the mean consecutive difference; MCD) and amplitude (expressed as percentage of maximum peripheral M wave size) of electromyographic (EMG) responses in the first dorsal interosseous (FDI) muscle following magnetic motor cortex stimulation were investigated in 20 normal subjects and 21 patients with multiple sclerosis (MS). EMG responses were present in all patients studied. CMCT was prolonged (greater than 8.1 msec; the mean CMCT for normals plus 3 S.D.) in 19 out of 42 muscles (12 patients). Onset latency variability was increased (greater than 1.1 msec; mean plus 3 S.D. for normals) in 20 out of 42 muscles (14 patients). Maximal response amplitudes varied between 5% and 67% and were not significantly different from the normal group (range 16-64%). In 3 patients, increased onset latency variability was the only neurophysiological abnormality. Prolonged CMCT was the sole abnormal finding in only 1 patient. Abnormally large onset latency variability was associated with the clinical finding of both impaired fine finger movements and increased finger jerks. Abnormal CMCT was associated with increased finger jerks only. This study confirms the findings of prolonged CMCT in multiple sclerosis. The additional finding of abnormal variability in response latencies which correlates with the clinical signs suggests that this variability may also be a useful measure of pyramidal tract function.     

Electrophysiological analysis of pudendal neuropathy following traction

Pudendal neuropathy is an unusual but important complication of orthopedic surgical procedures involving traction on the fracture table. We describe the clinical and electrophysiological features in six patients presenting with perineal sensory disorders and sexual dysfunction following surgical repair of femoral fracture, hip dislocation, or intra-articular foreign body, in which the traction table was used. All underwent electrophysiological recordings: bulbocavernosus muscle electromyography (EMG), measurements of the bulbocavernosus reflex latencies (BCRLs), somatosensory evoked potentials of the pudendal nerve (SEPPNs), sensory conduction velocity of the dorsal nerve of the penis (SCVDNP), and pudendal nerve terminal motor latencies (PNTMLs). Signs of denervation localized to the territory of the pudendal nerve were found in 3 patients, normal BCRL in 6, abnormal SEPPNs in 4, and abnormal SCVDNPs and PNTMLs in all cases. The outcome at 2-year follow-up was good, except in one patient with initially unrecordable PNTML. Perineal electrophysiological examination can thus confirm the pudendal neuropathy and give prognostic information.     

Mechanism of prolonged central motor conduction time in compressive cervical myelopathy.

OBJECTIVE: To investigate the mechanism of prolonged central motor conduction time (CMCT) in compressive cervical myelopathy, we compared the calculated CMCT following transcranial magnetic stimulation (TCM) and evoked spinal cord potentials (ESCPs) following transcranial electric stimulation (TCE). METHOD: Motor evoked potentials following TCM were recorded from abductor digiti minimi and abductor hallucis brevis muscles in 16 patients with compressive cervical myelopathy. CMCT was calculated by subtracting peripheral conduction time using peripheral nerve stimulation from MEP latency. ESCPs following TCE were recorded intraoperatively from posterior epidural space. RESULTS: CMCT was prolonged and significant attenuation of the ESCP amplitude following TCE was observed in all patients with cervical myelopathy. In 8 of 16 patients CMCT was significantly prolonged but ESCPs were recorded at the C6-7 level with normal negative peak latency. CONCLUSIONS: Prolonged CMCT may occur with only a minor amount of conduction slowing in the corticospinal tract in compressive cervical myelopathy. Impaired temporal summation of multiple descending potentials following TCM produced delays of motor neuron firing that contribute to the mechanism of prolonged CMCT.     

Magnetic brain stimulation: central motor conduction studies in multiple sclerosis

Central motor conduction (CMC) was evaluated in 32 normal subjects and 83 patients with multiple sclerosis, and the findings were correlated with clinical signs and evoked potential data. CMC time was obtained from the latency difference in responses from the abductor muscle of the little finger to magnetic stimulation of the motor cortex and electrical stimulation at the C-7/T-1 interspace. Mean CMC time in normal subjects was 6.2 msec (SD 0.86 msec), and amplitudes of responses to cortical stimuli were at least 18% of those obtained with stimuli at the wrist. CMC was abnormal in 60 patients with multiple sclerosis (72%); this correlated well with brisk finger flexor jerks (p less than 0.005). CMC was abnormal in 79% of patients with weakness of the abductor muscle of the little finger and in 54% with a normal muscle. Neurological examination was normal in 7 arms with abnormal CMC. Visual evoked potentials were abnormal in 67%, somatosensory evoked potentials in 59%, and brainstem auditory evoked potentials in 39% of those tested. For each procedure more subjects had abnormal CMC and normal evoked potentials than the reverse. The technique is of value for demonstrating and documenting central motor pathway lesions in multiple sclerosis, especially when physical signs are equivocal.     

Transcranial magnetic stimulation in pontine infarction: correlation to degree of paresis.

Transcranial magnetic stimulation was performed in 20 patients with pontine infarction who had initially some degree of hemiparesis. Only patients with a well defined lesion on magnetic resonance imaging that was appropriate for the neurological signs were included. Recordings were made from the abductor pollicis brevis muscle (APB) bilaterally. The degree of hand paresis was estimated clinically and related to the following parameters: central motor conduction time (CMCT), interside latency difference of total latency, and amplitude ratio of affected to unaffected side. Increasing degree of paresis was associated with increasing latency parameters and decreasing amplitude ratio. In the four patients with severe paresis a low amplitude response could be evoked and CMCT was delayed by up to 10 ms. When the paresis had resolved at the time of transcranial magnetic stimulation CMCT was normal. However, amplitude ratio was less than 100% in all but one patient, with most of the values ranging between 40% and 60%, which indicates a subclinical pyramidal tract lesion. Median nerve sensory evoked potentials (SEP) and related interside latency difference to amplitude ratio N20/P25 were also recorded. In contrast to TCMS, decreased amplitude ratio of SEP was not associated with delayed latency. Clinically, the mild degree of and good recovery from paresis in ventral pontine infarction was remarkable.     

Correlation between disability and transcranial magnetic stimulation abnormalities in patients with multiple sclerosis

Multiple sclerosis (MS) is an idiopathic inflammatory demyelinating disorder of the central nervous system. Clinical evaluation, MRI, cerebrospinal fluid testing and evoked potentials (EP) are among the available methods utilized for disease diagnosis and monitoring. To date, no surrogate markers have been established to assess disease evolution and progression. The aim of this study is to assess motor evoked potentials (MEP) of MS patients by transcranial magnetic stimulation (TMS) and investigate the possible correlations between TMS abnormalities and disability in the patient group, which includes a subgroup with no apparent pyramidal tract dysfunction. A total of 131 clinically definite MS patients were included in the study. Motor responses to TMS stimulation were recorded. Absent values, decreases in amplitude, prolongation of latency and central motor conduction time (CMCT) were considered as abnormal. A total of 109 (83%) patients displayed abnormal MEP amplitude, 68 (52%) displayed MEP latency, and 64 (49%) displayed CMCT abnormalities. Abnormal CMCT, latency and amplitude results were correlated with Expanded Disability Status Scale scores (p < 0.001). Our results indicate that TMS-EP in MS patients is correlated with disability, and that these findings may support the role of EPs in predicting disability even in subclinical presentations.     

The significance of delayed long-loop responses to ankle displacement for the diagnosis of multiple sclerosis

The present study compares the results of sensory evoked potentials after stimulation of the tibial nerve with measurements of short (M1), medium (M2) and long-loop latency (M3) responses of leg muscles in 42 patients suffering from multiple sclerosis. EMG responses were elicited by a movable platform which was tilted in pitch toe-up around the subject's ankle joint. The short latency response of the triceps surae muscle was nearly always normal in latency. The M2 response was lacking in about 30% of the patients and 10% of normals. The long latency response (M3) in the antagonistic anterior tibial muscle was significantly delayed (beyond 162 msec = AM + 2.5 S) in 69% of the patients. The delayed M3 response was found to indicate demyelination as reliably as the delayed somatosensory evoked potential (66% of the patients). The frequency of coincident results in the entire group was 86%. Additional information is gained in cases where SEPs are normal, but M3 is delayed (7%). Furthermore, patients lacking P40 of the SEP still exhibit M3 responses, the latency of which may be measured (24%). The results favour the assumption that M3 is mediated by a supraspinal pathway.     

Epidurally recorded spinal cord evoked potentials in patients with cervical myelopathy and normal central motor conduction time measured by transcranial magnetic stimulation.

OBJECTIVE: Use epidural recording of evoked spinal cord potentials (ESCPs) to investigate the pathology of cervical spondylotic myelopathy (CSM) in patients with normal central motor conduction time (CMCT) in upper and lower limbs. METHODS: A total of 75 patients with CSM were studied. All patients were examined before surgery for motor evoked potentials (MEPs) following transcranial magnetic stimulation (TMS). They were also evaluated during surgery by epidurally recorded ESCPs following stimulation of the median nerve, brain and spine. RESULTS: Seven patients (9%) showed normal CMCT in upper and lower limbs upon TMS examination. Only the ESCPs following median nerve stimulation (MN-ESCPs) were abnormal in these patients. In 5 of the 7 patients, a marked block in conduction of MN-ESCPs was observed at the C3-4 intervertebral level. The remaining two patients showed attenuation in the amplitude of MN-ESCPs at mid-cervical levels. CONCLUSIONS: We present 7 cases of CSM with negative CMCT findings. From the MN-ESCP results, we surmise that the pathology of CSM with normal CMCT is due predominantly to dysfunction of sensory systems involved in the upper limbs. SIGNIFICANCE: Examination by TMS is useful in the diagnosis of CSM but the possibility of negative CMCT findings upon TMS must be borne in mind. Multi-functional evoked spinal cord responses demonstrate that lesions in the sensory system are the major underlying pathology.     

Anorectal functions in patients with spinal cord injury

We wished to establish anorectal functions in patients with spinal cord lesions, related to the level of lesion and its completeness. We also wished to determine the value of neurophysiological tests for completeness of transsections in comparison with manometry and visceral sensory testing. In 32 patients (31.5 +/- 14.1 years, 25 males) with spinal trauma, completeness of transsection was assessed clinically. In 16 of these patients (30 +/- 15.6 years, nine males), a neurological work-up included recording of somatosensory evoked potentials (SEP) and motor evoked potentials (MEP) from the pudendal nerve within the first week after trauma. Also, anal sphincter EMG and pudendal nerve terminal motor latency (PNTML) were assessed. All patients also underwent conventional anorectal manometry and visceral sensory testing. Of all 32 patients, 15 were judged as 'complete' based on their clinical signs. Of those 16 tested neurologically, seven were labelled 'complete' since no MEP or SEP were detectable; one had pudendal SEP and MEP present, while SEP were present but delayed (47.0 +/- 8.8 msec) in the remaining patients. In four of these patients, also MEP were recorded (27.9 +/- 5.2 msec) and normal. PNTML was present in 12/16 patients independent of the completeness of lesion, and was rated normal in nine and delayed in three patients. EMG was normal in five, and pathological in 11 cases. In 5/15 cases of those judged as 'complete' (in 3/7 evaluated neurologically), visceral sensory testing revealed a minimal threshold for rectal perception of distension of 44 mL (range: 10-130), which sometimes was also perceived as urge to defecate. In a further case, manometry showed major voluntary action of the anal sphincter. These patients had lesions at all levels of the spinal column, ranging from cervical (C4,C6,C7) via thoratical (2 x T7,T8,T12) to lumbar segments. Anorectal function testing, and specifically visceral sensory testing may be superior to neurological assessment of 'completeness' of spinal cord lesions. It may be that visceral afferent pathways others than spinothalamic tract are involved in rectal perception that are less accessible to conventional neurophysiological diagnostic work-up.     

Bulbocavernosus reflex latencies and somatosensory evoked potentials after pudendal nerve stimulation in the diagnosis of impotence

Summary The bulbocavernosus reflex (BCR) was examined in 39 normal potent men and in 252 patients with impaired potency of varying aetiology. For BCR evaluation minimum, maximum and mean latencies, the temporal dispersion in ten successive responses, together with minimum and maximum side differences from simultaneous recordings of the left and right bulbocavernosus muscles were determined. Pathological findings were deteced in 125 patients. Somatosensory evoked potentials (SSEPs) recorded from the scalp after stimulation of the penile dorsal nerves and the terminal branches of the pudendal nerve were investigated in 30 controls and in 246 patients. An abnormal SSEP was found in 63 patients.     

Neurophysiological studies in acute transverse myelitis

A systematic evaluation of anterior horn cell, motor and sensory pathways is possible by electromyography (EMG), motor (MEPs) and somatosensory (SEPs) evoked potentials, respectively, which may provide valuable information on acute transverse myelitis (ATM). In a prospective hospital-based study, EMG, MEP and SEP studies were carried out on admission and after 3 months in 39 patients with ATM. All the patients also underwent detailed clinical evaluation, and spinal magnetic resonance imaging (MRI) was performed in 28. Outcome was defined at the end of 3 months as poor, partial or complete recovery on the basis of functional status. Spinal MRI revealed hyperintense signal changes in T2 extending for two segments to the entire spinal cord. Central motor conduction time to tibialis anterior (CMCT-TA) was more frequently abnormal (90%), followed by tibial SEP (77%). CMCT to abductor digiti minimi (ADM) was abnormal in 30% and median SEP in 15% of patients. Evidence of denervation on EMG was present in 51% of patients. The CMCT-TA improved in 48% patients and tibial SEP in 32%. Median SEP improved in all patients, and CMCT-ADM remained prolonged in two. At 3 months 2 patients had died, and 18 had poor, 10 partial and 9 complete recovery. CMCT was correlated with miscle power, tone, reflec and MRI changes. Patients' outcome of was correlated with CMCT, SEP and EMG. These results are consistent with pronounced involvement of dorsal region of spinal cord in ATM. MEP is more frequently abnormal than SEP. Received: 31 August 1999 / Received in revised form: 12 June 2000 / Accepted: 28 June 2000     

Transcranial magnetic stimulation: role in the evaluation of disability in multiple sclerosis

BACKGROUND: In patients with multiple sclerosis (MS), transcranial magnetic stimulation (TMS) has shown significant prolongation of central motor conduction time (CMCT). Abnormal CMCT may reflect sub-clinical involvement of motor pathways and correlate with clinical motor disability. OBJECTIVE: To determine the diagnostic yield of TMS in MS and the possible correlation of TMS abnormalities with clinical disability. MATERIALS AND METHODS: Thirty patients with clinically definite MS presenting in acute relapse or with progressive disease course and 30 healthy controls were evaluated. TMS parameters evaluated included threshold intensity, motor evoked potentials (MEP) amplitudes and latencies and CMCT. Reassessment studies were done after three months. STATISTICAL ANALYSIS: Student t-test, Mann-Whitney U test and Spearman's rank correlation test were used to assess the relationships. RESULTS: Patients with MS had significantly higher threshold intensities, prolonged CMCT and reduced MEP amplitudes as compared to controls. Abnormalities in at least one parameter were observed in 86.7% of patients. When inter-side asymmetries in MEP latency and/or in CMCT were considered, the diagnostic yield increased to 96.7%. The diagnostic yield was 74.7% for visual evoked potentials, 13.3% for brainstem auditory evoked response and 10% for cerebrospinal fluid oligoclonal band. One MS patient without pyramidal or cerebellar dysfunction had prolonged CMCT. CMCT abnormalities correlated significantly with the degree of pyramidal signs, limb ataxia, intention tremor, dysdiadokokinesia and overall cerebellar score. In patients who had clinical improvement, follow-up studies showed improvement in CMCT parameters. CONCLUSION: TMS is a highly sensitive technique to evaluate cortico-spinal conduction abnormalities in MS that may have no clinical correlate and in monitoring the course of the disease. The effects of cerebellar dysfunction on TMS results need further evaluation.     

Neurophysiological evaluation of central-peripheral sensory and motor pudendal fibres

Extensive neurophysiological investigations were carried out in 18 healthy volunteer subjects, and 6 patients with neurological disease. The tests consisted of spinal and scalp somatosensory evoked potentials (SEPs) to stimulation of the dorsal nerve of penis/clitoris, motor evoked potentials (MEPs) from the bulbocavernosus muscle (BC) and anal sphincter (AS) in response to scalp and sacral root stimulation, and measurement of sacral reflex latency (SRL) from BC and AS. In the control subjects, the mean sensory total conduction time (sensory TCT), as measured at the peak of the scalp P40 wave was 40.9 msec (range: 37.8-44.2). The mean sensory central conduction time (sensory CCT = spine-to-scalp conduction time) was 27.0 msec (range: 23.5-30.4). Transcranial brain stimulation was performed by using a magnetic stimulator both at rest and during voluntary contraction of the examined muscle. Sacral root stimulation was performed at rest. Motor total conduction times (motor TCT) to BC and AS muscles were respectively 28.8 and 30.0 msec at rest, and 22.5 and 22.8 msec during contraction. Motor central conduction times (motor CCT) to sacral cord segments controlling BC and AS muscles were respectively 22.4 and 21.2 msec at rest, and 15.1 and 12.4 msec during contraction. The mean latencies of SRL were respectively 31.4 msec in the bulbocavernosus muscle and 35.9 msec in the anal sphincter. Combined or isolated abnormalities of SEPs, MEPs and SRL were found in a small group of patients with neurological disorders primarily or secondarily affecting the genito-urinary tract.     

Central motor conduction to upper and lower limbs after magnetic stimulation of the brain and peripheral nerve abnormalities in 20 patients with Friedreich''s ataxia

Central motor conduction time (CMCT) to thenar and soleus muscles was measured after magnetic stimulation of the cortex in 20 cases of Friedreich's ataxia (FA) and was abnormal in all. CMCT values were related to disease duration and disability. The amplitude of CMAP after cortex stimulation was severely reduced in the most disabled patients. Reduction in amplitude of the nerve evoked potentials was related neither to disease duration nor grade of disability. These results suggest that clinical worsening in FA is mainly due to progressive central motor pathway involvement. CMCT study is a better index of disease progression than peripheral nerve examination. Abnormalities in CMCT may be the third electrophysiological diagnostic criterion in FA, after reduced amplitude of nerve action potentials and absent H reflex.     

Sympathetic skin response (SSR) is abnormal in multiple sclerosis

As the function of the autonomic nervous system is often compromised in multiple sclerosis (MS), different standardized tests are used to detect disseminated abnormalities in cardiovascular autonomic functions. Sympathetic skin response (SSR), a slow wave generated in deep layers of the skin, is induced by reflex activation of sudomotor sympathetic efferent fibers. SSR was studied in 70 patients classified into different categories according to the diagnostic criteria for MS. We also obtained pattern reversal visually evoked potentials and brainstem auditory evoked potentials as well as somatosensory evoked potentials (by median and posterior tibial nerve stimulation). SSR was abnormal in 66 patients (94.2%), including abnormal foot latency with normal hand latency in 30 (42.8%), delayed foot and hand latencies in 30 (42.8%), and no response in 6 (8.6%). The percentages of SSR abnormalities were similar in the different patient categories. Pathological SSR were more common than abnormal evoked potentials in suspected and probable MS. SSR appears to be a simple and effective means of assessing sympathetic sudomotor outflow disturbances in MS, providing a valuable addition to current electrophysiological procedures for the detection of MS lesions.© 1995 John Wiley &Sons, Inc.     

Postpartum lumbosacral plexopathy limited to autonomic and perineal manifestations: clinical and electrophysiological study of 19 patients

The objective was to describe perineal electrophysiological findings and to determine their diagnostic value in a type of lumbosacral plexopathy after vaginal delivery, which only involves the lower part of the plexus (S2-S4). Consecutive female patients referred to an outpatients' urodynamic clinic were the source. Nineteen previously healthy women, 13 multiparae and six para 1, were investigated. Mean age was 33.7 (SD 5.4) (range 28-41) years. All of them presented with urinary (stress incontinence 14, dysuria five), anorectal (faecal incontinence eight, dyskesia one), or sexual dysfunctions (hypoorgasmia or anorgasmia six) after vaginal delivery. No associated lower limb sensory or motor deficits were noted. All the patients had electrophysiological recordings (bulbocavernosus muscle EMG, measurements of the bulbocavernosus reflex latencies (BCRLs), somatosensory evoked potentials of the pudendal nerve (SEPPNs), and pudendal nerve terminal motor latencies (PNTMLs)). Cystometry and urethral pressure profile (UPP) were performed in the 14 patients with stress urinary incontinence. Perineal electrophysiological examination disclosed signs of denervation in the perineal muscles in all the cases, prolonged BCRLs in 17/19, and abolished BCRLs in 2/19, abnormal SEPPN in 1/19, and normal PNTMLs in all the patients. Urodynamic investigations disclosed low urethral closure pressure for age (< 50 cm H(2)O) in half of the patients. In conclusion, Lower postpartum lumbosacral plexopathy is evoked when perineal sensory disturbances whether or not associated with urinary or faecal incontinence persist after a history of a difficult vaginal delivery. Electrophysiological investigations precisely identify the site of the lesion and demonstrate distal innervation integrity.     

Quantification of Uhthoff's phenomenon in multiple sclerosis: a magnetic stimulation study.

OBJECTIVE: To quantify temperature induced changes (=Uhthoff phenomenon) in central motor conduction and their relation to clinical motor deficits in 20 multiple sclerosis (MS) patients. METHODS: Self-assessment of vulnerability to temperature and clinical examination were performed. We used motor evoked potentials to measure central motor conduction time (CMCT) and applied the triple stimulation technique (TST) to assess conduction failure. The TST allows an accurate quantification of the proportion of conducting central motor neurons, expressed by the TST amplitude ratio (TST-AR). RESULTS: Temperature induced changes of TST-AR were significantly more marked in patients with prolonged CMCT (P=0.037). There was a significant linear correlation between changes of TST-AR and walking velocity (P=0.0002). Relationships were found between pronounced subjective vulnerability to temperature and (i) abnormal CMCT (P=0.02), (ii) temperature induced changes in TST-AR (P=0.04) and (iii) temperature induced changes in walking velocity (P=0.04). CMCT remained virtually unchanged by temperature modification. CONCLUSIONS: Uhthoff phenomena in the motor system are due to varying degrees of conduction block and associated with prolonged CMCT. In contrast to conduction block, CMCT is not importantly affected by temperature. SIGNIFICANCE: This is the first study quantifying the Uhthoff phenomenon in the pyramidal tract of MS patients. The results suggest that patients with central conduction slowing are particularly vulnerable to develop temperature-dependent central motor conduction blocks.