The triple stimulation technique to study central motor conduction to the lower limbs.

OBJECTIVE: To quantify the percentage of motor units of a foot muscle that can be activated by transcranial magnetic stimulation (TMS) in normal subjects and patients. METHODS: We adapted the recently described triple stimulation technique (TST) for recordings from abductor hallucis (AH). Conventional motor evoked potentials (MEPs) of this muscle are usually small and variable in shape, because of an important temporal desynchronization of the TMS induced spinal motor neuron discharges. The TST allows 'resynchronization' of these discharges and thereby a quantification of the proportion of motor units activated by TMS. The lower limb (LL-) TST was applied to 33 sides of 18 normal subjects and 51 sides of 46 patients with multiple sclerosis, amyotrophic lateral sclerosis, or spinal cord disorders. RESULTS: In healthy subjects, the LL-TST demonstrated that TMS achieves activation of virtually all motor neurons supplying the AH. In 33 of 51 patient sides, abnormal LL-TST responses suggested corticospinal conduction failures of various degrees. The LL-TST was 2.54 times more sensitive to detect central conduction failures than the conventional LL-MEPs. Combining the LL-TST with TST of the upper limbs further increased the sensitivity to detect a conduction failure by 1.50 times. CONCLUSION: The LL-TST markedly improves the examination of corticospinal pathways.     

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.     

Correlates of disability in multiple sclerosis detected by transcranial magnetic stimulation

OBJECTIVE: To study the usefulness of corticospinally mediated excitatory responses and transcallosal inhibition (TI) elicited by transcranial magnetic stimulation (TMS) as a surrogate marker of disability in patients with different courses of MS. METHODS: Focal TMS of the motor cortex was performed in 118 patients with MS (96 with relapsing-remitting, 19 with primary progressive, and three with secondary progressive disease) who had an Expanded Disability Status Scale (EDSS) score between 0 and 6.5 and in 35 normal subjects. Central motor latencies (CML) and TI (onset latency, duration) were investigated. The Spearman rank correlation was used for statistical analysis. RESULTS: TMS disclosed prolonged CML in 52.5% and abnormal TI in 61% of the patients. In all patients the EDSS correlated with the frequency of abnormal TI (r = 0.58, p < 0.01) and abnormal CML (r = 0.51, p < 0.01). In patients with primary progressive MS (EDSS 1.5 to 6.5) the frequency of TI abnormalities correlated with EDSS (r = 0.65, p < 0.01) whereas CML did not. Delayed corticospinal responses in hand muscles always led to abnormal TI. CONCLUSIONS: The combination of central motor latencies and transcallosal inhibition evoked by transcranial magnetic stimulation yields objective data to estimate disease progression in MS as assessed by the EDSS.     

The clinical diagnostic utility of transcranial magnetic stimulation: report of an IFCN committee.

The review focuses on the clinical diagnostic utility of transcranial magnetic stimulation (TMS). The central motor conduction time (CMCT) is a sensitive method to detect myelopathy and abnormalities may be detected in the absence of radiological changes. CMCT may also detect upper motor neuron involvement in amyotrophic lateral sclerosis. The diagnostic sensitivity may be increased by using the triple stimulation technique (TST), by combining several parameters such as CMCT, motor threshold and silent period, or by studying multiple muscles. In peripheral facial nerve palsies, TMS may be used to localize the site of nerve dysfunction and clarify the etiology. TMS measures also have high sensitivity in detecting lesions in multiple sclerosis and abnormalities in CMCT or TST may correlate with motor impairment and disability. Cerebellar stimulation may detect lesions in the cerebellum or the cerebellar output pathway. TMS may detect upper motor neuron involvement in patients with atypical parkinsonism and equivocal signs. The ipsilateral silent period that measures transcallosal inhibition is a potential method to distinguish between different parkinsonian syndromes. Short latency afferent inhibition (SAI), which is related to central cholinergic transmission, is reduced in Alzheimer's disease. Changes in SAI following administration of cholinesterase inhibitor may be related to the long-term efficacy of this treatment. The results of MEP measurement in the first week after stroke correlate with functional outcome. We conclude that TMS measures have demonstrated diagnostic utility in myelopathy, amyotrophic lateral sclerosis and multiple sclerosis. TMS measures have potential clinical utility in cerebellar disease, dementia, facial nerve disorders, movement disorders, stroke, epilepsy, migraine and chronic pain.     

Stimulation of motor tracts in multiple sclerosis.

Percutaneous electrical stimulation of the motor cortex was used to evaluate corticospinal conduction to upper-limb motoneurons in 29 patients with multiple sclerosis. Central motor conduction abnormalities were correlated with clinical signs and somatosensory evoked potentials. Muscle responses to cortical stimulation were altered in 20 patients. The most common abnormality was increased central motor conduction time; in two cases the responses to cortical stimulation were absent. Abnormalities were also present in patients with no clinical evidence of corticomotoneuron deficit. Alterations of muscle responses and of somatosensory evoked potentials were usually correlated, but may appear independently. Both testing methods are useful in the study of patients with multiple sclerosis.     

Transcranial magnetic stimulation of motor pathways directed to muscles supplied by cranial nerves in amyotrophic lateral sclerosis.

OBJECTIVES: In amyotrophic lateral sclerosis (ALS), transcranial magnetic stimulation (TMS) detects remarkable abnormalities of central motor circuits: cortical excitability threshold, silent period (SP) duration and intra-cortical inhibition. TMS directed to cranio-facial musculature was performed in ALS patients in order: (1) to document the neurophysiological involvement of motor central and peripheral cranial pathways by evaluating changes of threshold and SP; (2) to discover a possible correlation between the clinical picture and abnormal excitability properties. METHODS: Motor evoked potentials (MEPs) were recorded from masseter, genioglossus and orbicularis oris muscles of both sides in 25 ALS patients and 25 controls, in response to TMS delivered over the face M1 area and the vertex. RESULTS: TMS gave rise to two orders of responses: bilateral MEPs during contraction represented the central responses, and motor action potentials (MAPs) during rest represented the peripheral responses. MEPs were followed by SPs, which increased linearly with increasing TMS intensity (r=0.8). At least one of the analyzed parameters was abnormal in all patients: central abnormalities (increased active threshold, delayed MEPs, reduced SP) were found in 96% of patients, alone or combined with abnormalities of the MAPs (reduced area and/or prolonged latency). The reduction of SP was linearly related to the Norris score (r=0.95). CONCLUSIONS: Our study shows that TMS is able to detect the involvement of multiple cranial muscles in ALS. This finding offers often pre-clinical information about the disease picture. Therefore, it can be employed as a valuable means for early diagnosis.     

Motor neuron disease: usefulness of transcranial magnetic stimulation in improving the diagnosis.

Clinical upper motor neuron (UMN) involvement is sometimes difficult to detect in motor neuron disease (MND). For this reason we performed transcranial magnetic stimulation (TMS) to find out whether this technique may be useful in revealing signs of pyramidal tract impairment. Fifty-five MND patients, clinically divided into 22 amyotrophic lateral sclerosis (ALS), 18 ALS with probable UMN signs (ALS-PUMNS), 10 pure lower motor neuron syndrome (LMNS), and 5 progressive bulbar palsy (PBP), underwent standard TMS, recording from abductor digiti minimi and flexor allucis muscles. Prolongation of cortical motor evoked potential (MEP) latency and central conduction time (CCT) and absent MEP were considered as pathologic. ALS-PUMNS and LMNS patients were clinically reclassified after 1 year. TMS was abnormal in 95.4% of ALS, 72.2% of ALS-PUMNS, 50% of LMNS and 20% of PBP. Correlations between TMS parameters and both clinical signs of UMN involvement and disease severity were highly significant. TMS showed a high sensitivity, but lacked specificity. After 1 year, 11 patients among the ALS-PUMNS group were clinically reclassified as definite ALS: all of them had shown TMS abnormalities at the first examination. In conclusion, TMS provides important diagnostic information for an early prediction of ALS in those MND patients presenting with clinically equivocal UMN impairment.     

Evidence for impaired cortical inhibition in schizophrenia using transcranial magnetic stimulation

BACKGROUND: Cortical inhibition (CI) deficits have been proposed as a pathophysiologic mechanism in schizophrenia. This study employed 3 transcranial magnetic stimulation (TMS) paradigms to assess CI in patients with schizophrenia. Paired-pulse TMS involves stimulating with a lower-intensity pulse a few milliseconds before a higher-intensity pulse, thereby inhibiting the size of the motor evoked potential produced by the higher-intensity pulse. In the cortical silent period paradigm, inhibition is reflected by the silent period duration (ie, the duration of electromyographic activity cessation following a TMS-induced motor evoked potential). Transcallosal inhibition involves stimulation of the contralateral motor cortex several milliseconds prior to stimulation of the ipsilateral motor cortex, inhibiting the size of the motor evoked potential produced by ipsilateral stimulation. METHODS: We measured CI using these 3 paradigms in 15 unmedicated patients with schizophrenia (14 medication-naive and 1 medication-free for longer than 1 year) (13 were in the transcallosal inhibition paradigm), 15 medicated patients with schizophrenia (11 taking olanzapine, 1 risperidone, 1 quetiapine, 1 methotrimeprazine + perphenazine, 1 quetiapine + loxapine), and 15 healthy controls. RESULTS: Unmedicated patients demonstrated significant CI deficits compared with healthy controls across all inhibitory paradigms whereas medicated patients did not (at all inhibitory intervals, paired-pulse TMS: controls = 59.9%, medicated = 44.3%, unmedicated = 28.7%; cortical silent period: controls = 55.0 milliseconds, medicated = 60.4 milliseconds, unmedicated = 39.7 milliseconds; transcallosal inhibition: controls = 33.6%, medicated = 23.7%, unmedicated = 10.4%; P<.05). CONCLUSIONS: These results suggest that schizophrenia is associated with deficits in CI and that antipsychotic medications may increase CI.     

Transcranial magnetic stimulation: applications in neurology

INTRODUCTION: Transcranial magnetic stimulation (TMS) was first applied to assess conduction time along the corticospinal tract, namely by recording motor evoked potentials. STATE OF ART: At present, TMS techniques include cortical excitability and mapping studies using single or paired-pulse paradigms on the one hand, and repetitive TMS to induce cortical plasticity and to modify brain function on the other hand. TMS is a valuable, non-invasive tool in the diagnosis and the pathophysiological assessment of cortical dysfunction involved in various neurological diseases (multiple sclerosis, myelopathy, amyotrophic lateral sclerosis, movement disorders, epilepsy, stroke). PERSPECTIVES AND CONCLUSION: In the near future, repetitive TMS could have therapeutic applications in neurology (epilepsy, stroke rehabilitation program) as is already the case in some psychiatric diseases. However, most of the new indications for treatment with cortical stimulation will be based on surgically-implanted neuromodulation procedures.     

Increased cortical excitability with longer duration of Parkinson's disease as evaluated by transcranial magnetic stimulation

Transcranial Magnetic Stimulation (TMS) was used to evaluate the cortical excitability and central motor pathways in Parkinson's disease (PD) and correlate with severity and duration of disease. 19 cases of PD and 13 controls were enrolled. The threshold intensity (TI), cortical latency (CL), central conduction time (CCT), motor evoked potential amplitude (MEP) obtained with TMS were correlated with Hoehn and Yahr and duration of disease. The threshold intensity (TI) was significantly lower in patients of PD than controls. The TI in patients with PD was 53.16-/+8.4% patients and 67.1-/+21.6% in controls (p<0.05). This strongly correlated with duration of disease, TI being lower in patients with disease duration more than 5 years. There was no difference in the other TMS parameters - CL, CCT, MEP between patients and controls. Our study revealed increased excitability in PD which was related to longer duration of disease.     

Effect of discharge desynchronization on the size of motor evoked potentials: an analysis.

OBJECTIVE: Motor evoked potentials (MEPs) after transcranial magnetic brain stimulation (TMS) are smaller than CMAPs after peripheral nerve stimulation, because desynchronization of the TMS-induced motor neurone discharges occurs (i.e. MEP desynchronization). This desynchronization effect can be eliminated by use of the triple stimulation technique (TST; Brain 121 (1998) 437). The objective of this paper is to study the effect of discharge desynchronization on MEPs by comparing the size of MEP and TST responses. METHODS: MEP and TST responses were obtained in 10 healthy subjects during isometric contractions of the abductor digiti minimi, during voluntary background contractions between 0% and 20% of maximal force, and using 3 different stimulus intensities. Additional data from other normals and from multiple sclerosis (MS) patients were obtained from previous studies. RESULTS: MEPs were smaller than TST responses in all subjects and under all stimulating conditions, confirming the marked influence of desynchronization on MEPs. There was a linear relation between the amplitudes of MEPs vs. TST responses, independent of the degree of voluntary contraction and stimulus intensity. The slope of the regression equation was 0.66 on average, indicating that desynchronization reduced the MEP amplitude on average by one third, with marked inter-individual variations. A similar average proportion was found in MS patients. CONCLUSIONS: The MEP size reduction induced by desynchronization is not influenced by the intensity of TMS and by the level of facilitatory voluntary background contractions. It is similar in healthy subjects and in MS patients, in whom increased desynchronization of central conduction was previously suggested to occur. Thus, the MEP size reduction observed may not parallel the actual amount of desynchronization.     

Transcranial magnetic stimulation in Beh?et's disease: a cross-sectional and longitudinal study with 44 patients comparing clinical, neuroradiological, somatosensory and brain-stem auditory evoked potential findings.

OBJECTIVES: To compare neurological involvement in Beh?et's disease as documented by transcranial magnetic stimulation (TMS) with clinical, neuroradiological, somatosensory (SEP) and auditory evoked potential (BAEP) findings. METHODS: Forty-four patients were studied over an 8 year period. Nine patients had follow-up studies done. TMS central motor conduction (CMC) studies to upper and lower limb muscles, brain magnetic resonance imaging (MRI), SEP, and BAEP testing were conducted. RESULTS: Thirty-nine patients had CMC slowing, decreased amplitude or absent motor evoked potentials (MEP); 5 of these patients were neurologically normal. Concordance of TMS results, clinical deficits, and MRI findings occurred in 36 of the 39 patients. SEP and BAEP testing proved non-complementary to MEP. Generally, follow-up studies revealed faster CMC and higher MEP amplitude. However, in two patients the CMC time to one target muscle became prolonged with diminished MEP amplitude over a period of 1.5-3 years. CONCLUSIONS: TMS can be useful in detecting and quantifying motor tract dysfunction in Beh?et's disease and provides functional information complementary to imaging studies. TMS is more sensitive than either SEP or BAEP. Our longitudinal studies suggest that TMS studies may be valuable in monitoring disease activity or therapeutic response.     

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.     

Lower extremity motor evoked potentials in multiple sclerosis

Transcranial magnetic stimulation was performed on 25 patients with definite multiple sclerosis. Motor evoked potentials were recorded from the anterior tibial muscle. Central motor conduction time was calculated using the equation (F + M-1)/2 by stimulation of the common peroneal nerve. Motor evoked potentials were capable of detecting subclinical pyramidal tract lesions in multiple sclerosis. In patients with multiple sclerosis, the incidence of abnormality of motor and somatosensory evoked potentials was similar. Central motor conduction time was correlated with overall and pyramidal tract subscores on the Kurtzke Disability Status Scale and the Scripps Neurological Rating Scale. Central motor conduction time abnormalities correlated best with the presence of a Babinski's sign but also correlated significantly with weakness and hyperreflexia.     

Transcranial magnetic stimulation (TMS) in movement disorders]

Transcranial magnetic stimulation (TMS) has been used to study several aspects of movement disorders: central motor conduction time (CMCT), electromyographic (EMG) silence evoked by TMS, reset of tremor rhythm by TMS, GABAergic inhibitory interneuronal function of the motor cortex studied with paired-pulse TMS. In this communication, We briefly summarize results of paired-pulse TMS in movement disorders. NORMAL SUBJECTS: A subthreshold conditioning stimulus over the motor cortex reduced the size of EMG responses to a succeeding suprathreshold test stimulus given to the same motor cortex. This inhibition is considered to be an inhibitory effect on the motor cortex because the same conditioning stimulus has no influence on H-reflexes or electrical cortical responses. Pharmacological effects on this inhibition suggested that it is mediated by GABAergic inhibitory systems in the motor cortex. PATIENTS: The cortical inhibition was reduced in cortical myoclonus, which is consistent with the notion that the studied effect is mediated by GABAergic systems. The inhibition was disturbed in focal dystonia, whereas normal inhibition was elicited in Segawa's disease. Reduced inhibition was seen in Parkinson's disease (PD), whereas normal inhibition in essential tremor. Normal inhibition was evoked in all patients with chorea. Abnormal inhibition in basal ganglia disorders must reflect damaged movement selection in the motor cortex secondary to the primary lesion in the basal ganglia. This abnormality occurs in some movement disorders and does not occur in the others, which indicates different pathomechanisms for involuntary movements. It is conspicuous that normal inhibition was evoked in Segawa's disease even though the patients had dystonia.     

Sensitivity of transcranial magnetic stimulation of cortico-bulbar vs. cortico-spinal tract involvement in Amyotrophic Lateral Sclerosis (ALS)

Background An upper motor neuron (UMN) lesion in amyotrophic lateral sclerosis (ALS) is often difficult to identify because clinical signs may be discrete or masked by severe simultaneous LMN lesions. We compared the diagnostic sensitivity of transcranial magnetic stimulation (TMS) to cranial muscles and limb muscles in the detection of UMN lesions. Design We investigated corticobulbar and corticospinal tract function to the tongue/orofacial muscles and abductor digiti minimi/tibial anterior muscles with TMS in 51 patients with ALS to compare the diagnostic yield in the detection of UMN dysfunction. An UMN lesion was assumed when the following were found: the peripheral conduction time and amplitude of the M-wave were within the normal range, the response to cortical stimulation was absent, the TMS evoked/M-wave amplitude ratio was reduced, and the central motor conduction time or the interside difference was delayed (> mean+2.5 SD). Results On the basis of these criteria a UMN lesion to the orofacial muscles was identified in 24 patients (47 %), to the tongue in 27 (53 %), and to the upper and lower limbs in 13 (25 %) and 22 patients (43 %), respectively. Combined abnormalities from all sites increased the diagnostic yield to 39 patients (76 %). TMS of the limb muscles confirmed a UMN lesion in only 15 (54 %) of the 28 patients with clinically confirmed UMN involvement. This number increased to 23 patients (82 %) if tongue and orofacial muscles were taken into acount. Conclusion Our results indicate the early and in most cases subclinical corticobulbar tract involvement of the central motor pathways to the orofacial muscles and tongue in ALS. TMS of the tongue and orofacial muscles had a higher sensitivity in identifying UMN lesions than that of the upper and lower limbs. Received: 13 December 2000, Received in revised form: 15 March 2001, Accepted: 1 April 2001     

Impairment of callosal and corticospinal system function in adolescents with early-treated phenylketonuria: a transcranial magnetic stimulation study

The transcranial activation and the conduction properties of corticospinal and callosal neurons were investigated in 12 early-treated adolescents (aged 17.3, SD 3.5 years; range 14–27 years) with phenylketonuria (PKU) by focal transcranial magnetic stimulation (fTMS) of the motor cortex. The patients had no functionally relevant motor disturbances in daily life or on clinical testing. Corticospinally mediated excitatory (response thresholds, amplitudes, central motor latencies) and inhibitory [duration of postexcitatory inhibition (PI)] effects of fTMS were investigated in contralateral hand muscles. Transcallosal inhibition (TI) (onset latency, duration, transcallosal latency) of tonic electromyographic (EMG) activity was tested in ipsilateral muscles. Peripheral motor latencies were determined for responses elicited by magnetic stimulation over cervical nerve roots. Ten normal subjects served as controls. Since in all PKU patients, central and peripheral motor latencies were normal, no neurophysiological indication of a demyelination of corticospinal or peripheral motor fibres was found. However, cortical thresholds of corticospinally mediated responses were increased (52.1, SD 11.6% versus 35.0, SD 7.4% of maximum stimulator output; P < 0.05; n = 24 hands) and their amplitudes reduced (2.9, SD 1.4 mV versus 6.1, SD 1.5 mV, P < 0.05). The duration of PI was shortened (132, SD 53 ms versus 178, SD 57 ms; P < 0.05). TI was absent in 37.5% of the investigated hands or tended to be weak. When TI was present, its onset latencies (38.0, SD 3.6 ms versus 34.7, SD 3.3 ms) and transcallosal latencies were prolonged (18.5, SD 3.8 ms versus 14.8, SD 3.2 ms), while its duration was normal. These abnormal excitatory and inhibitory effects of fTMS suggest a reduced susceptibility of cortical excitatory and inhibitory neuronal structures compatible with a loss of neurons or a rarefication of their dendrites. Received: 1 December 1997 Received in revised form: 13 March 1998 Accepted: 27 April 1998     

The diagnostic value of motor evoked potentials.

OBJECTIVE: To assess the diagnostic usefulness of motor evoked potentials (MEPs) and to identify the optimal method for calculating the central conduction time. The test results were evaluated in a prospective study of 1023 neurological patients. METHODS: We evaluated the correlation between clinical and electrophysiological findings, the accuracy, the sensitivity, the percentage of subclinical abnormalities and the false negative rates of MEPs in different neurological disorders. In patients with lower motor neuron involvement, we compared the central conduction time calculated as the difference between the latency of the cortical and magnetic root stimulation responses with that calculated using the F-wave method. RESULTS: The agreement index between electrophysiological and clinical findings was 87%. The overall accuracy of the test was 0.97. The higher sensitivity values were demonstrated in spinal cord disorders (0.85), hereditary spastic paraplegia (0.80) and motor neuron diseases (0.74). The higher percentages of subclinical abnormalities were found in motor neuron disorders (26%) muscular diseases (24%), multiple sclerosis (13.5%) and spinal cord diseases (12.5%). The higher false negative rates were found in sylvian stroke (0.36) and hereditary spastic paraplegia (0.16). Central conduction study using magnetic paravertebral stimulation but not using the F-wave method, resulted in 12% and 10% of false positive values in lower limb multiradiculopathies and in neuropathies, respectively. CONCLUSIONS: MEPs represent a highly accurate diagnostic test. MEP clinical value is maximum in motor neuron, muscle and spinal cord diseases. In patients with lower motor neuron involvement, the gold standard for central conduction determination is the F-wave method.     

Corticomotor organisation and motor function in multiple sclerosis

Our objective was to determine whether there are changes in the corticomotor map for the hand in multiple sclerosis, and whether these changes correlate with indices of motor function and measures of corticomotor conduction or excitability. Transcranial magnetic stimulation (TMS) maps, motor evoked potential (MEP) latency and amplitude, motor threshold and EDSS and Purdue-pegboard measurements were made in 26 subjects with relapsing-remitting multiple sclerosis. Correlations were sought between these measurements using the Pearson product-moment correlation with a level of significance of p = 0.05 (two-tailed). Map displacement was positively correlated with MEP latency (p = 3 x 10(-4)) and EDSS (p = 0.007), and negatively correlated with Purdue score (p = 4 x 10(-4)). Purdue scores correlated with all MEP parameters (latency, p = 4 x 10(-10); threshold, p = 4 x 10(-6); amplitude, p = 0.003). We conclude that motor reorganisation is associated with impaired corticomotor conduction and may reflect a process of neural plasticity associated with axonal demyelination in MS. An understanding of motor function in MS should incorporate models of both axonal demyelination and conduction deficits as well as neural plasticity.