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.     

Frontal lobe atrophy and central motor conduction time in chronic alcoholics.

The central motor conduction time (CMCT) was investigated in 12 cases of chronic alcoholism with frontal lobe atrophy, 12 cases of chronic alcoholism without frontal lobe atrophy, and 12 age-matched healthy controls. The CMCT was significantly prolonged in the chronic alcoholics with frontal lobe atrophy as compared to the chronic alcoholics without frontal lobe atrophy and the healthy controls. A significant positive correlation was noted between the CMCT and the degree of frontal lobe atrophy. The CMCT may be prolonged in chronic alcoholics with frontal lobe atrophy.     

Corticospinal tract conduction block results in the prolongation of central motor conduction time in compressive cervical myelopathy.

OBJECTIVE: The objective of this study was to analyze corticospinal function in patients with compressive cervical myelopathy and to elucidate the mechanism underlying its prolonged central motor conduction time (CMCT). METHODS: Motor evoked potentials following transcranial magnetic stimulation (TMS) and peripheral conduction time in the ulnar and tibial nerves following electrical stimulation were measured from the abductor digiti minimi (ADM) and abductor hallucis (AH) muscles in 24 patients with compressive cervical myelopathy and used to calculate CMCT. Spinal cord evoked potentials (SCEPs) following transcranial electric stimulation were recorded intraoperatively from the C2-3 to C6-7 intervertebral levels. Correlations between prolonged CMCT and SCEP values were then estimated. RESULTS: The shorter/longer CMCT between the patients' right and left ADM and AH were 8.5+/-2.9/11.5+/-3.3 and 16.2+/-3.1/18.4+/-3.3 ms, respectively (mean+/-SD). The SCEPs amplitude at C6-7, compared to C2-3, was 25.7+/-21.0%. The attenuation of SCEP amplitude, but not latency, at C6-7 correlated significantly with CMCT prolongation. CONCLUSIONS: Our data support the view that CMCT prolongation is primarily due to corticospinal conduction block, rather than conduction delay. SIGNIFICANCE: Insight was provided into the mechanism of corticospinal dysfunction in compressive cervical myelopathy.     

Cognitive impairment and central motor conduction time in chronic alcoholics

The non-invasive technique of transcranial magnetic stimulation (TMS) was used in 62 chronic alcoholics to assess the functional status of descending motor pathways. The main aims of this study were: to investigate asymptomatic upper motor neuron dysfunction in alcoholics as well as to assess its relationship with parameters reflecting the intensity of exposure to alcohol; and to evaluate a possible relationship between central motor conduction time (CMCT) prolongation and neuropsychological measures of alcohol-related brain damage. Compared to control subjects, chronic alcoholics exhibited a significant prolongation of CMCT (23 out of 62 subjects). No significant correlation was found between CMCT prolongation and intensity and duration of abuse, presence of peripheral neuropathy, or brain atrophy on CT scans. Prolongation of CMCT from the upper limb correlated significantly with impairment of frontal skills on neuropsychological testing (p<0.01). These findings suggest that TMS may be a sensitive method for the detection in alcoholics of subtle neurological dysfunction, not confined to motor pathways.     

Central motor conduction time in patients with multifocal motor conduction block.

The finding of conduction block (CB) within short consecutive segments along a motor nerve is a key feature of multifocal motor neuropathy (MMN). Despite their different pathogenesis, this may be the only clinical difference between some cases of MMN and the pure spinal muscular atrophy form of motor neuron disease (MND). In 12 patients with distal atrophy and fasciculations and electrophysiological evidence of CBs in the upper limbs, we measured the peripheral and central motor conduction times (PMCT and CMCT) to hand muscles. We reasoned that patients with MMN should show an abnormally prolonged PMCT with normal CMCT, whereas an increased CMCT would suggest MND. All patients had delayed F-wave latency and increased PMCT. Three patients had increased CMCT. Follow-up showed little clinical and electrophysiological change in 7 of the 9 patients with normal CMCT, and a progressive motor deficit leading ultimately to death in 1 of the 3 patients with increased CMCT. This patient's electrophysiological follow-up showed a significant decrement of the compound motor action potential to both proximal and distal stimulation points, with disappearance of earlier CBs. Autopsy revealed loss of anterior horn cells and axons of the ventral root, and degeneration of large myelinated fibers. We conclude that determining the CMCT may help in differentiating MND from MMN. Persistence of a stable clinical picture over a span of at least 1 year and lack of electrophysiological signs of involvement of upper motor neurons should both be required before establishing the diagnosis of MMN even with electrophysiological evidence of CB.     

Comparison of direct and indirect measurements of the central motor conduction time in the monkey.

OBJECTIVE: The goal of the present study was to compare the indirect estimate of the central motor conduction time (CMCT) with direct measurement of the corticospinal conduction time between the motor cortex and cervical enlargement in macaque monkeys. METHODS: Responses to transcranial magnetic stimulation of the motor cortex were recorded from intrinsic hand muscles in adult macaque monkeys. The CMCT was calculated by subtracting the peripheral conduction time, measured with the F-wave method, from the latency of the motor evoked potentials (MEPs). In two monkeys, the actual conduction time between the motor cortex and cervical enlargement was measured directly by different invasive techniques. RESULTS: We found that the indirect calculation of CMCT overestimates the corticospinal conduction time to a significant extent. CONCLUSIONS: One possible source of error is an underestimate of the MEP peripheral conduction time. A collision test confirmed this hypothesis and showed that only a marginal proportion of the motoneurones that respond to a weak corticospinal input also participate in the F-wave. A more accurate estimate of the CMCT could be obtained by using the longest F-wave latency, rather than the shortest, to calculate the peripheral conduction time.     

Prolonged central motor conduction time of lower limb muscle in spinocerebellar ataxia 6.

We investigated the function of corticospinal tract in spinocerebellar ataxia 6 (SCA6) by measuring the central motor conduction time (CMCT). Motor evoked potentials (MEP) of tibialis anterior (TA) muscle were elicited by magnetic stimulation to motor cortex and spinal cord in 9 SCA6 patients and 10 normal height- and age-matched subjects. CMCT in lower limb of SCA6 patients (18.1+/-1.9 ms) was significantly prolonged than that of the normal subjects (15.0+/-1.0 ms) ((p < 0.001). The prolonged CMCT was well correlated with the duration of disease (p = 0.005), but MEP amplitudes and stimulation intensities were not significantly different. These results indicate that the corticospinal tract function is also impaired and correlate with the disease duration in SCA6.     

A double determination of central motor conduction time in the assessment of Hirayama disease

Objective

To investigate central motor conduction time (CMCT) in patients with Hirayama disease (HD) and to analyse the role of motor nerve root lesions in the pathogenesis of HD.

Sensorimotor central conduction time in comatose patients.

Motor evoked potentials (MEPs) following magnetic stimulation were recorded in 22 patients comatose as a result of head injury (13 cases), stroke (7 cases) or anoxia (2 cases). Somatosensory evoked potentials (SEPs) from median nerve were recorded as well in 19 cases in the same session. Thirteen patients died or remained vegetative (59.1%), 3 were severely disabled (13.6%) and 6 showed a good recovery (27.3%). MEPs were significantly related to the outcome; they appeared to be a more accurate prognostic indicator than the Glasgow Coma Scale (GCS). However, 1 out of 6 patients with bilaterally absent MEPs (16.7%) showed a good recovery. SEPs were significantly related to the outcome as well, but the combined use of SEP and MEP improved the outcome prediction, decreasing the rate of false negatives. Two patients had normal sensorimotor function, 13 a combined sensorimotor dysfunction, while 4 had a pure motor dysfunction. Our results suggest that SEPs and MEPs may improve the assessment of sensorimotor dysfunction in comatose patients. A significant relationship between MEPs and outcome appears to exist, but the assessment of MEP reliability requires further study.     

Age-dependent changes in central somatosensory conduction time.

The effects of aging on central somatosensory conduction time (CSCT) were examined using 125 neurologically healthy subjects aged 10-79 years. There was a mean overall increase in CSCT during the age span studied of 0.5 ms. However, the principal increase in CSCT did not appear to start until the end of the fourth decade, after which there was a steady incremental increase. There was little evidence of an abrupt stepwise increase in CSCT at any age. Age-dependent changes in asymmetry (right-left difference in CSCT) remained approximately constant until the end of the sixth decade. From the age of 60 years onwards, there was a small mean increase in asymmetry of 0.1 ms. Subjects were divided into six age groups and the upper limit of normal for both CSCT and asymmetry was defined for each.     

Significant correlation between corticospinal tract conduction block and prolongation of central motor conduction time in compressive cervical myelopathy

We examined the relationship between the CMCT and features of spinal cord evoked potentials (SCEPs) among 25 patients with compressive cervical myelopathy to elucidate the mechanism underlying the prolonged central motor conduction time (CMCT) in patients with compressive cervical myelopathy. CMCT values were calculated by measuring motor evoked potentials from the abductor digiti minimi muscles (ADMs) and abductor hallucis muscles (AHs) following transcranial magnetic stimulation and peripheral conduction times determined in the ulnar and tibial nerves. SCEPs following transcranial electrical stimulation were recorded intraoperatively from C2-3, C6-7 and T11-12. The shorter/longer CMCTs between the patients' right and left ADMs and AHs were 9.5+/-3.2/11.5+/-3.8 and 16.2+/-2.8/18.8+/-3.3 ms, respectively (mean+/-SD). The percentage ratio of the amplitude of the D-wave at C6-7 or T11-12 to that at C2-3 was 19.4+/-14.2 or 3.2+/-3.1%, respectively. The CMCT value was significantly correlated with the attenuation of SCEP amplitude, but not with SCEP latency both at C6-7 and T11-12, suggesting that CMCT prolongation is primarily due to corticospinal conduction block rather than conduction delay. Spinal motor neurons might need more time to fire in patients with compressive cervical myelopathy when corticospinal potentials, but not conduction, are attenuated, thereby resulting in prolonged CMCT.     

Abnormalities of central motor conduction in Parkinson''s disease

The new technique of magnetic stimulation was used to measure amplitude of the motor evoked potential (MEP) recorded from abductor digiti minimi whilst stimulating at the head, and motor conduction time (MCT) between head and neck. Bilateral studies were made in 12 normal subjects and 56 patients with Parkinson's disease. The amplitudes of the MEPs were were significantly larger (P < 0.05) in the patients (mean 1.6 mV, SD 1.4) compared with the normal subjects (mean 0.9 mV, SE 0.6). MCTs were significantly shorter (P < 0.001) in patients (mean 8.1 ms, SD 1.3) compared with the normal subjects (mean 9.4 ms, SD 1.2). Although the pathophysiological basis of these changes has not been determined, they provide objective measurements which may be clinically valuable in monitoring therapy.     

Central motor conduction time in Parkinson's disease

Central motor conduction time (CMCT) was analysed in 11 patients with Parkinson's disease and 10 age matched healthy controls. CMCT was measured during muscle relaxation, muscle contraction and in patients with Parkinson's disease before and 1 h after intravenous infusion of L-dopa (0.25%, 20 ml). Although the CMCT during muscle contraction did not differ significantly between Parkinson's disease and healthy controls, the CMCT during muscle relaxation was significantly shorter in Parkinson's disease than in healthy controls. The CMCT during muscle relaxation in Parkinson's disease was significantly longer after intravenous infusion of L-dopa than before, but the CMCT during muscle contraction did not differ significantly before and after intravenous infusion of L-dopa. The CMCT during muscle contraction was significantly shorter than the CMCT during muscle relaxation in healthy controls. However, in Parkinson's disease, the CMCT did not differ significantly between muscle relaxation and contraction. We consider that the central motor conduction pathway during muscle relaxation in Parkinson's disease is modified to be similar to that during muscle contraction in healthy subjects.     

Noninvasive measurement of central sensory and motor conduction

Potentials evoked by median and peroneal nerve stimulation were digitally filtered between 300 and 2,500 Hz to measure early latency components and assess sensory cord conduction velocity. Short (R1) and long (R2) latency reflex responses were recorded from contracting thenar and tibialis anterior muscles. R1 is considered a spinal reflex akin to the H-reflex. Clinical evidence suggests that R2 involves a reflex arc with turnaround at the motor cortex. Sensory-motor cord velocity was derived from the latencies of R1 and R2. The method can be used to compare peripheral and central sensory conduction or conduction in central sensory and motor pathways.     

F responses and central motor conduction in multiple sclerosis

Two electrophysiological investigations were used to study 18 patients with multiple sclerosis--F wave characteristics including amplitude, persistence and frequency, which can provide a measure of motoneurone excitability, and magnetic stimulation of the cortex, which enables measurement of conduction along central motor pathways. There was an increase in the mean amplitude and persistence of the F response in patients with abnormal central motor conduction (CMC), although no correlation between the degree of abnormality of CMC and increase in F response amplitude was found. Increase in mean amplitude and persistence of the F response were also found in patients with normal CMC but clinical evidence of a UMN disorder (spasticity and/or weakness); there was no correlation, however, between any single F response characteristic and any particular clinical sign. CMC appears to be the preferred test for detecting subclinical motor lesions in MS: of the patient sides with normal clinical examination, 36% showed abnormal CMC, whereas 23% showed abnormal F responses.     

Prolonged cortical relay time of long latency reflex and central motor conduction in patients with spinocerebellar ataxia type 6.

OBJECTIVE: Spinocerebellar ataxia type 6 (SCA6) is a neurodegenerative disorder characterized by a slowly progressive ataxia and dysarthria. Anatomically. SCA6 was said to affect only the cerebellum. However, ithasbeen argued that SCA6 may involve widespread regions of the brain. This study was designed to investigate the electrophysiological functions of the central nervous system in patients affected with SCA6. METHODS: Nine patients with SCA6 and 10 normal, age-matched control subjects were included in the study. The motor evoked potentials, somatosensory evoked potentials, and long latency reflex (LLR) of the hand muscle were measured to evaluate the functions of the central nervous system. RESULTS: Significantly delayed LLR, as well as prolonged cortical relay time (CRT) and central motor conduction time (CMCT) of the hand muscle, were noted in the patients with SCA6. CONCLUSIONS: The prolongation of CMCT andCRT suggested that SCA6 disturbed the functions of the corticospinal tract and the transcortical polysynaptic pathways from the sensory to motorcortices. It seems likely that the CNS dysfunction caused by SCA6 is not limited to the structures that are anatomically abnormal. Furthermore, the prolongation of CMCT alone does not seem to suffice to differentiate between various types of autosomal dominant cerebellar ataxias. Molecular analysis is indispensable for the diagnosis of different genetic types of SCA.