Long-latency reflexes in contracted hand and foot muscles and their relations to somatosensory evoked potentials and transcranial magnetic stimulation of the motor cortex.

OBJECTIVE: The cortical relay time (CRT) for V2 of long-latency reflexes (LLRs) in the contracted thenar and short toe flexor muscles was studied. METHODS: LLRs and somatosensory evoked potentials (SEPs) were studied by electrical stimulation of the median or posterior tibial nerve. The CRT for V2 was calculated by subtracting the onset latency of cortical potentials in SEPs and that of motor evoked potentials (MEPs) by transcranial magnetic stimulation (TMS) from the onset latency of V2 in eight healthy subjects. RESULTS: The CRT for the thenar muscles was 11.4+/-0.9 ms (mean +/- SD), as the onset latency was 48.8+/-1.4 ms for V2, 16.0+/-1.2 ms for N20 and 21.3+/-1.1 ms for MEP, respectively. The CRT for the short toe flexor muscles was 3.0+/-1.3 ms, as the onset latency was 80.5+/-4.5 ms for V2, 35.3+/-1.8 ms for P38 and 42.2+/-2.0 ms for MEP, respectively. CONCLUSION: Significantly longer CRT for V2 for the thenar muscles (P<0.001, paired Student's t test) may indicate more synaptic relays as compared to that for the short toe flexor muscles.     

Changes in long-latency reflexes onset latencies across full-wave rectified and non-rectified recordings.

Electrically elicited long-latency reflexes (LLRs) were obtained from thenar muscles by either fully rectified or non-rectified raw recordings in 10 healthy volunteers. The LLR II onset latencies were significantly (P < 0.0001) delayed on rectified (mean +/- SD: 49.8+/-2.9 ms) compared to raw (45.3+/-2.3 ms) recordings, with a mean difference of 4.4 ms. These data show that, according to the recording technique employed, the LLR II onset latencies can change considerably. The possible implications on cortical relay time (CRT) calculation and the understanding of the intracortical connections physiology are discussed.     

Enhancement of motor cortical excitability in humans by non-invasive electrical stimulation appears prior to voluntary movement

The time course of facilitation of motor evoked potentials (MEPs) to transcranial electrical stimulation delivered at varying intervals near the onset of a voluntary ballistic movement was studied in 4 normal subjects. MEPs were recorded from the left thenar muscles to unifocal anodal stimulation of the right scalp overlying the hand motor area delivered every 8-10 sec. A click, occasionally associated with the scalp stimulation (P = 0.3-0.6), was the signal for the subject to make a brief thumb press on a piston at short latency. The timing of the scalp stimulus and the click was adjusted so that the former occurred approximately between 100 msec before and 100 msec after the onset of the voluntary movement signaled by the EMG in the thenar muscles. MEPs were not detected when the scalp was stimulated 80 msec or more before onset of voluntary movement and then appeared with increasing probability as the time interval before movement shortened. The amplitudes of MEPs in the 80-40 msec period preceding movement onset were small (less than 20% of maximum) and achieved maximum values 20 msec after movement onset.     

Motor and cortical sensory evoked potentials by magnetic stimulation

Motor evoked potentials (MEP) by magnetic stimulation on the scalp and the spinous processes of the 7th cervical (C 7) and 5th lumbar (L 5) vertebrae were studied in 20 normal subjects and 10 patients with the pyramidal tract lesions. The magnetic stimulator composed of two flat helical coils with mean inner diameters of 12.0 and 2.2 cm. The evoked muscle action potentials were recorded from the thenar muscle in the hand and abductor hallucis muscle in the leg. The mean peak latencies of MEP recorded from the thenar muscle were 22.1 +/- 1.7 and 12.8 +/- 0.9 msec at the stimulations on the scalp and C 7, respectively. The central motor conduction time (CMCT) between the cortex and C 7 was 9.1 +/- 1.1 msec. On the other hand, the peak latencies of MEP were 41.0 +/- 3.2 and 21.6 +/- 2.3 msec at the stimulations on the scalp and L 5, respectively. CMCT between the cortex and L 5 was 19.3 +/- 2.3 msec. The patients with pyramidal tract involvements showed delayed peak latencies or absent MEP. The cortical somatosensory evoked potentials (SEP) by the noninvasive magnetic stimulation on the levels of Th 10, Th 12 and L 5 spines, gluteus and ankle were studied in 20 normal subjects and 7 patients with neurological diseases. Cortical components P 2 and N 2 were recorded clearly in all normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Non-invasive evaluation of central motor tract excitability changes following peripheral nerve stimulation in healthy humans.

The interval between muscle stretch and the onset of the long latency electromyographic responses (LLRs) has been theoretically fragmented into an afferent time (AT), taken at the peak of wave N20 of somatosensory evoked potentials and an efferent time (ET), calculated by means of magnetic transcranial stimulation (TCS), the two being separated by a cortical interval (CI). If this were the case, the afferent input should progressively 'energize' the sensorimotor cortex during the CI and change the excitability of cortico-spinal tracts. To investigate this, motor evoked potentials (MEPs) from thumb flexor muscles were recorded, whilst a conditioning stimulation of median or ulnar nerve randomly preceded (10-48 msec intervals) magnetic brain TCS. Nerve stimulation was adjusted to motor threshold and amplitudes of conditioned and test MEPs at different nerve-TCS interstimulus intervals were evaluated. Conditioned MEPs were significantly attenuated with nerve-TCS intervals between 16 and 20 msec for elbow and 20 and 22 msec for wrist stimulation. This was followed by MEP potentiation with nerve-TCS intervals corresponding to the sum of AT + CI (mean 23.2 msec, range 21.7-24.8). The onset latency of facilitated conditioned MEPs was about 1 msec briefer than that of test MEPs, but invariably longer than the latency of MEPs facilitated by a voluntary contraction. This protocol did not demonstrate amplitude facilitation of the segmental H reflex, corroborating the idea that the facilitated part of the conditioning nerve-TCS curve receives a transcortical loop contribution.     

Cortical magnetic stimulation in amyotrophic lateral sclerosis

Forty patients with ALS underwent cortical magnetic stimulation. Twelve had marked pseudobulbar signs; in these motor evoked potentials (MEPs) could not be elicited. Mean MEP latencies in the others, who had predominantly lower motor neuron signs, measured 23.3 +/- 2.1 msec (thenar), 18.7 +/- 5.3 msec (EDC), and 13.4 +/- 2.9 msec (biceps), respectively. These values were significantly longer (P greater than 0.001) compared with normal values (n = 35), which measured 20.2 +/- 1.6, 14.2 +/- 1.7, and 9.4 +/- 1.7 msec, respectively. MEP amplitude was often markedly reduced (less than 15% of the M wave) compared with a normal mean of 39.5 +/- 13.0%. Overall abnormal MEPs (delayed, absent, or reduced in amplitude) approached 100%. It is argued that measuring central motor delay, which was not significantly different in the patients compared with normals, is subject to error in ALS.     

A new indirect method for measuring spinal conduction velocity in man

A non-invasive, indirect method for measuring spinal cord mixed afferent-efferent conduction is described. The method is based upon eliciting late reflex responses labelled R1 and R2 from voluntarily contracting thenar and tibialis anterior muscles by preferentially stimulating median and common peroneal sensory nerve fibres. The mean onset latencies of R1 measured 27.5 msec and 30.6 msec recorded from hand and leg muscles respectively. R2 mean onset latencies measured 46.0 msec and 65.1 msec respectively. R1 has characteristics similar to an H-reflex. R2 is a long-loop reflex of unknown pathway assumed to involve similar circuits and rostral turn around points when elicited by both arm and leg stimulation. Mean spinal cord conduction time between the seventh cervical and fifth lumbar spinous processes, is given by (formula; see text) It measured 7.95 msec and the calculated mean conduction velocity was 57.9 +/- 5.7 m/sec.     

Afferent excitation of human motor cortex as revealed by enhancement of direct cortico-spinal actions on motoneurones

Changes in motor cortex excitability induced by somatosensory afferences were evaluated in 5 subjects by testing how the short-latency cortico-spinal effects evoked by transcranial magnetic stimulation in flexor carpi radialis (FCR) motoneurones were influenced by volleys in median nerve afferent fibres. Transcranial magnetic stimulation induced two facilitatory peaks on FCR H reflex, the first at a conditioning-test interval of about −3 msec and the second at 0 msec, separated by a phase of inhibition. If an electric shock to the median nerve at the wrist, 0.8-1 × motor threshold (MT) for thenar muscles, preceded the cortical stimulus by 18–25 msec, an increase in size of both facilitatory peaks was observed. The increase was partly due to a direct action of the median nerve volley on motoneurones. When this contribution was subtracted, two peaks of additional facilitation resulted as the effect of combined conditioning. Additional facilitation was present even during the short-lasting phase ascribed to monosynaptic cortico-spinal excitation of motoneurones, i.e., the first millisecond of the earliest facilitatory peak. This result indicates that cortical responsiveness to magnetic stimulation had been enhanced by the peripheral stimulus. The time course of the excitability changes in motor cortex was compared with the cortical somatosensory evoked potentials (SEPs) induced by the same peripheral stimulus. Additional facilitation was present immediately after the N20 peak of SEPs and lasted 8–10 msec. Additional facilitation had the same threshold as N20 (0.6 × MT) and grew in parallel with it when grading the afferent stimulus up to 1 MT.     

The diagnostic significance of long-latency reflexes in multiple sclerosis

Reflexes of thenar muscles after median or radial superficial nerve stimulation have been investigated in both hands of 47 patients with probable or definite multiple sclerosis (MS) and compared with somatosensory evoked potentials (SEPs) to median nerve stimulation. A delay or absence of long-latency reflexes (LLRs) was found as pathological patterns. The results after median or radial superficial nerve stimulation were usually both pathologic or both normal except in cases with latencies at the upper limit of normal values. Pathological results of reflex testing were obtained in 61% of the patients with probable MS and in 79% of those with definite MS. Abnormal SEPs were found in 44% of the patients with probable MS compared to 62% with definite MS. All cases which had pathologic SEPs also had pathologic LLR. Hence, LLR testing detected more abnormalities than the routine median nerve SEP testing that has been used.     

Prolonged intracortical delay of long-latency reflexes: electrophysiological evidence for a cortical dysfunction in multiple sclerosis

Convincing evidence suggests that long-latency reflexes (LLRs) are capable of testing the transcortical sensorimotor reflex arch. By subtracting the sum of the latencies of N20 (afferent branch) and transcranially elicited motor evoked potentials (MEP; efferent branch) from the LLR II latency, the cortical relay time (CRT) can also be obtained, which is alleged to represent the time required for the cortical sensorimotor integration. The aim of the present study was to investigate if a cortical dysfunction occurs in multiple sclerosis (MS). Median nerve somatosensory evoked potentials (SEPs), MEPs and LLRs were recorded from the upper limbs of 23, not severely disabled MS patients in acute phases of the disease. Eighteen age and sex matched healthy volunteers served as controls. N20, MEP, LLR II latencies were measured, and the CRT was calculated for each limb. The statistical comparison between patients and controls was only weakly significant by taking into account conduction times along either the afferent (N20) or the efferent (MEP) pathways. On the contrary, it turned out to be considerably significant if both branches of the transcortical sensorimotor reflex arch, together with the intracortical pathway, were simultaneously tested by means of the LLRs. Moreover, the patients showed a significantly higher CRT compared with that found in the control subjects. These findings are consistent with a prolonged intracortical delay of LLRs in the MS group and suggest the occurrence of conduction velocity slowing and/or synaptic transmission impairment along the sensorimotor intracortical pathway in MS.     

Central and peripheral conduction times in multiple sclerosis

Somatosensory evoked potentials (SEPs) were recorded simultaneously from the cervical spine and scalp in 25 normal subjects and 105 patients with established or suspected multiple sclerosis (MS) using median nerve stimulation. The normal latency of the main peak of the cervical SEP (N14) following median nerve stimulation at the wrist was 13.7 +/- 0.8 msec. The peak latency of the first cortical event of the scalp SEP (N20) was 19.1 +/- 0.9 msec. The difference in these latencies (N20 -- N14) reflects a conduction time between the dorsal column nuclei and cortex. It measured 5.45 +/- 0.7 msec. The conduction times between the wrist and Erb's point and Erb's point and N14 measured 8.6 +/- 0.7 msec and 5.1 +/- 0.6 msec respectively. There was a 68.6% overall incidence of abnormalities of N14, N20 or (N20 -- N14) in the patients. This incidence was over 80% in definite and early probable or latent MS, 68.2% in progressive spinal MS and 40.0% in suspects. SEPs were also simultaneously recorded from the lower thoracic spine (T12) and scalp in a different group of 25 normal subjects using tibial nerve stimulation. The latency of the thoracic SEP (N21) was 21.4 +/- 1.5 msec and that of the first cortical event of the scalp SEP (P40) was 38.6 +/- 2.2 msec. The difference in these latencies (P40 -- N21) which reflects conduction between T12 and the cortex measured 17.2 +/- 1.7 msec. Conduction between the ankle and popliteal fossa was 7.0 +/- 0.65 msec and between the popliteal fossa and N21, it was 14.5 +/- 1.1 msec. All of a small group of MS suspects showed abnormality of P40 or (P40 -- N21).     

Age-related changes in muscle fatigue resistance in humans

OBJECTIVE: The goal of this study was to compare the relative contributions from the muscle and the central nervous system to muscle fatigue resistance in aging. METHODS: Each subject carried out 90 s of sustained maximal voluntary isometric contraction (MVC) of the thumb using the thenar and forearm thumb muscles. Contractile capacity of the thenar muscles was assessed through tetanic stimulation of the median nerve. Interpolated doublets delivered during an MVC represented the overall voluntary activation level while transcranial cortical stimulation with an electromagnetic stimulator was used to assess motor output upstream from the corticomotoneuronal pathway. RESULTS: Nine elderly subjects [four females and five males, 70+/-9 years old (mean+/-SD)] and 10 younger subjects (five females and five males, 30+/-6 years old) were tested. After the fatiguing exercise, the elderly group's MVC declined by 29% as opposed to 47% in the younger group (p<0.01). The elderly group's greater fatigue resistance was accounted for by increased fatigue resistance at the muscle level as well as in the central nervous system. At least some of the decline in the central motor drive was upstream from the corticomotoneuronal pathway. CONCLUSION: The higher muscle fatigue resistance in the elderly group was attributable to differences in both the peripheral and central nervous systems.     

Influence of isoflurane anesthesia on motor evoked potentials elicited by transcortical,brainstem, and spinal root stimulation

Abstract

Electrical stimulation over the motor cortexl base ofthe skulll and cervical spine motor roots was performed in 9 male rats (41 0 ± 86 g) before and after induction with isoflurane at 7 MAC concentration. The mean latency and amplitude of descending spinal evoked potential (OSEP) from spinal cord and motor evoked potentials (MEPs) from forearm muscles obtained after motor cortexl brainsteml and cervical root stimulations were calculated and compared. The electrical current intensity to elicit the MEPs after corticall brainsteml and spinal roots stimulation were 23.4 ± 7.61 7.0 ± 3.71 and 7.4 ± 0.8 mAl respectively. The brainstem stimulation activated descending motor pathways with a latency midway between that produced by electrical stimulation over the motor cOrtexI and by electrical stimulation over the cervical enlargements. The latency difference between cortical (8.8 ± 3.2 msec) and brainstem (5.7 ± 7.2 msec) stimulation was 3.7 ± 2.3 msec in all forearm extensor muscles. The latency difference between cervical (3.6 ± 0.9 msec) and brainstem stimulation (5.7 ± 7.2 msec) was 2.3 ± 7.7 msec for the same musclesl suggesting the brainstem stimulation activates the descending motor neurons at the level of cervicalmedullary junction. The amplitudes were 789 ± 7471 672 ± 3541 and 765 ± 389 µV for corticall brainsteml and cervical root stimulations. The inhalation anesthesia isoflurane at 7MAC (7.2%) completely abolished the cortical and brainstem MEPs within minutesl while the MEPs elicited by direct stimulation of the cervical spinal roots remained unchanged. Our results indicate synaptic-dependent MEPs elicited at motor cortex or brainstem levels are highly sensitive to isoflurane anesthesia. [Neural Res 1998; 20: 555-558]     

Somatosensory evoked potentials in the term newborn.

Median nerve somatosensory evoked potentials (SEPs) were recorded from surface electrodes in 40 healthy term infants (range 36.5-43 weeks postmenstrual age). Electrical stimulation at 5 Hz was used, averaging the response to several runs of 1024 stimuli to each median nerve, bandpass 10-3000 Hz, sweeptime 100 msec. Identifiable potentials were collected over the cervical cord on all runs in all 40 infants and from the cortex in at least some runs in 39 out of 40 infants. The cervical response showed little variation and consisted of a clear negative wave with up to 3 peaks, mean latency of the largest 10.2 +/- 0.7 msec, followed by a positive deflection. The cortical response was very variable in form and latency between infants and to a lesser degree within infants. Four types of cortical wave form were found, symmetrical, asymmetrical, plateau and M shaped, of increasing complexity. In 11% of trials the response was absent or indistinct but could usually be uncovered by alteration in stimulus frequency or intensity. In the whole group, the mean latency for N1 was 30.0 +/- 6.8 msec and for the central conduction time 19.8 +/- 6.5 msec. Significant differences were found between the 4 cortical wave forms in the main variables measured, which gave support for form S being the most primitive and form M the most mature response.     

Motor evoked potentials of subjects over 70 years of age with and without recurrent falls.

Motor evoked potentials (MEPs) of 83 elderly (79+/-4 years) subjects, 43 with recurrent falls and 40 without, and of 31 healthy young (42+/-9 years) subjects were measured from thenar (and hypothenar) and tibialis anterior muscles. Forty-four of the aged subjects without overt neurological diseases were used as controls. Absolute latencies from the cortex to the target muscles as well as the latency differences from the cortex to the level of the fifth lumbar vertebra (LV) were longer in the aged than in the young, but the latency difference from the cortex to the brachial plexus was shorter. The cortical, brachial plexus and lumbar (LV) latencies were all dependent on height as well as age. The latency differences from the cortex to the plexus or LV were not height-dependent but were age-dependent. The thenar MAXMEP/CMAP ratio was significantly higher in hands with thenar atrophy (in 30% of the aged subjects) than without; thenar atrophy thus excludes the use of this parameter in about one-third of the aged subjects. There were no significant differences in the MEP latencies or amplitudes of the recurrent fallers and the non-fallers. Subjects having more frequent falls, however, tended to have lower amplitudes of MEPs in the lower extremities.     

Cortical relay time for long latency reflexes in patients with definite multiple sclerosis

BACKGROUND: Long latency reflexes (LLR) include afferent sensory, efferent motor and central transcortical pathways. It is supposed that the cortical relay time (CRT) reflects the conduction of central transcortical loop of LLR. Recently, evidence related to the cortical involvement in multiple sclerosis (MS) has been reported in some studies. Our aim was to investigate the CRT alterations in patients with MS. METHODS: Upper extremity motor evoked potentials (MEP), somatosensory evoked potentials (SEP) and LLR were tested in 28 patients with MS and control subjects (n=22). The patients with MS were classified according to the clinical form (relapsing-remitting [R-R] and progressive groups). The MS patients with secondary progressive and primary progressive forms were considered as the "progressive" group. CRT for LLR was calculated by subtracting the peak latency of somatosensory evoked potentials (SEP) and that of motor evoked potentials (MEP) by transcranial magnetic stimulation from the onset latency of the second component of LLR (LLR2) (CRT = LLR2 - [MEP latency + N20 latency]) RESULTS: Cortical relay time was calculated as 7.4 +/- 0.9 ms in control subjects. Cortical relay time was prolonged in patients with MS (11.2 +/- 2.9 ms) (p<0.0001). The latencies of LLR, MEP and SEP were also prolonged in patients with MS. Cortical relay time was not correlated with disease severity and clinical form in contrast to other tests. CONCLUSIONS: Our findings suggested that CRT can be a valuable electrophysiological tool in patients with MS. Involvement of extracortical neural circuits between sensory and motor cortices or cortical involvement due to MS may cause these findings.     

Projection of thenar muscle afferents to frontal and parietal cortex of human subjects.

There is some controversy about the projection of muscle afferents from the human upper limb to cerebral cortex and about their contribution to somatosensory evoked potentials. In 8 normal volunteers, the somatosensory projections of muscle and cutaneous afferents from the hand were recorded at 21 scalp sites, using a non-cephalic reference. Low-threshold thenar muscle afferents were selectively activated by intramuscular microstimulation. In addition, the averaged data for the projections were mapped for each individual. In each subject a focal parietal negativity was detected over the contralateral parietal cortex at a mean latency of 20.8 msec (S.D. 1.15 msec) following stimulation of thenar muscle afferents. The amplitude of the parietal 'N20-P25' was relatively small (mean 0.49 microV, range 0.18-1.56 microV). A small focal positivity was detected, maximal over contralateral frontal cortex at 22.8 msec (S.D. 2.05 msec) but recorded bilaterally. In all subjects subcortical positive waves (P9 and P14) were defined for the muscle afferent volley. This pattern of cortical activity was similar to that for the projection from the digital nerves of the index finger. For the cutaneous input the latency of the parietal 'N20' was 21.7 msec (S.D. 1.17 msec) and of the frontal 'P22' was 24.2 msec (S.D. 3.09 msec). The amplitude of the parietal 'N20-P25' was larger for the cutaneous projection (mean 1.59 microV; range 0.65-4.28 microV).     

Cortical generators of somatosensory evoked potentials to median nerve stimulation

In 12 patients with intractable partial seizures, chronically implanted subdural electrodes were used to define the relationship of the epileptogenic focus to cortical functional areas. Cortical somatosensory evoked potentials (SEPs) to median nerve stimulation were recorded from these electrodes. The initial cortical positivity, postrolandic primary cortical potential (PCP), was recorded in all 12 patients with a mean latency of 22.3 +/- 1.6 msec. A potential of opposite polarity, prerolandic PCP, was defined in nine patients with a mean latency of 24.1 +/- 2.7 msec. The latency of the postrolandic PCP was 1.61 +/- 1.59 msec shorter than the prerolandic PCP (p less than 0.01, paired t test). The maximum amplitude postrolandic PCP was 2.1 times larger than the maximum prerolandic PCP (p less than 0.02, paired t test). The phase reversal of the SEPs was compared with the position of the rolandic fissure (RF) defined by electrical stimulation. This study shows that the latency and amplitude characteristics of post- and prerolandic PCPs are significantly different and give support to the concept that they are produced by different generators; and cortical SEPs are helpful in locating the RF.     

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.