Motor evoked potentials (MEPs) in lacunar syndromes.

Motor evoked potentials (MEPs) evoked in the biceps, thenar and tibialis anterior muscles by electrical stimulation of the scalp and of the spinal regions were recorded in 32 patients with focal deficits due to minor cerebral ischemia of the lacunar type and in a control group. Somatosensory evoked potentials (SEPs) to median nerve stimulation were also recorded. The central motor conduction times (CMCTs) and the threshold intensities for eliciting MEPs in the relaxed muscles were significantly increased on the affected side. Central motor conduction, for at least one muscle, was altered in 18 patients. MEP abnormalities were related to pyramidal signs (though they could be observed also in a patient without any motor impairment) and occurred independently of a specific clinical picture or a radiologically confirmed lacunar lesion. SEPs were less frequently altered than MEPs.     

The use of transcranial magnetic stimulation for monitoring descending spinal cord motor function.

This report describes our initial clinical experience using transcranial magnetic stimulation for monitoring spinal cord motor function during surgical procedures. Motor evoked potentials were elicited using a cap shaped coil placed on the scalp of 27 patients while recording peripheral motor responses (compound muscle action potentials--CMAPs) from the upper (N = 1) or lower limbs (N = 26). Wherever possible, cortical somatosensory responses (SEPs) were also monitored by electrically stimulating the left and right posterior tibial nerve (N = 25) or the median nerve (N = 1). The judicious choice of anesthetic regimens resulted in successfully obtaining motor evoked responses (MEPs) in 21 of 27 patients and SEPs in 26 of 27 patients. Single pulse TMS resulted in peripheral muscle responses having large variability, whereas, the variability of SEPs was much less. Criteria based on response variability for assessing clinically significant changes in both MEPs and SEPs resulted in two false negative predictions for SEPs and none for MEPs when evaluating postoperative motor function. We recommend monitoring both sensory and motor pathways during procedures where placing the spinal cord at risk of damage.     

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.     

Transcranial electrical motor evoked potentials as a prognostic indicator for motor recovery in stroke patients.

Transcranial electrical motor evoked potentials (MEP) were examined in 33 patients within three days after stroke. Normal values for MEP and motor central conduction time (CCT) were obtained in 46 healthy controls whose MEPs were evaluated during slight voluntary muscle contraction and at rest. Two months later 23 patients were re-examined clinically and electrophysiologically. Motor function change was correlated with MEP results. Two months after stroke the patients with normal or prolonged CCT had an improved motor function compared with those with absent CCT. MEP may be a valuable prognostic indicator in the acute stage of paralytic stroke for recovery of motor function.     

Motor potentials evoked by magnetic stimulation of the motor cortex in normal subjects and patients with motor disorders.

Motor evoked potentials (MEPs) elicited by magnetic coil stimulation of motor cortex were studied at rest and during maximum voluntary muscle contraction in 20 normal subjects and 42 patients with motor disorders. MEP parameters employed in this study included: onset latency, amplitude, MEP/M wave amplitude ratio and background EMG/MEP area ratio. Maximum voluntary contraction increased the amplitude of MEPs compared to the size of M waves elicited by peripheral nerve stimulation. A reduced MEP/M wave amplitude ratio had a higher correlation with pyramidal tract involvement than did a prolonged MEP onset latency. Analysis of MEP parameters may help in the differential diagnosis of cerebral infarction, ALS and cervical spondylotic radiculomyelopathy. The inhibitory period which follows MEPs during voluntary contraction was observed in all subjects; the mean duration in normal subjects was 126.6 +/- 29.5 msec. The mean duration of the inhibitory period in patients with cerebral infarction, ALS and cervical spondylotic radiculomyelopathy was 73.9 +/- 41.7 msec, 79.5 +/- 54.5 msec and 85.1 +/- 36.5 msec, respectively. These values were significantly shorter than in normal subjects.     

Facilitation and reciprocal inhibition by imagining thumb abduction.

It is well known that motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) of the motor cortex are facilitated by voluntary muscle contraction. We evaluated the effects of imagination of movements on MEP latencies of agonist and antagonist muscles in the hand using TMS. Twenty-two healthy volunteers were studied. TMS delivered at rest and while imagining tonic abduction of the right thumb. MEPs were recorded in response to magnetic stimulation over the scalp and cervical spine (C7-T1), and central motor conduction times (CMCT) were calculated. MEPs were recorded from right abductor pollicis brevis muscle (APB) and adductor pollicis muscle (AP) simultaneously. Imagination of abduction resulted in a shortened latency of MEPs in the APB muscle, and a prolonged latency in the AP muscle. But the imagination caused no significant change in the latency of MEPs elicited by stimulation over the cervical spine. The changes of the CMCT may account for these latency changes with imagination of movement. These findings indicate that imagination of thumb abduction facilitates motoneurons of agonist muscle and has an inhibitory effect on those of antagonist muscle (reciprocal inhibition).     

Motor evoked potentials and central motor conduction: studies of transcranial magnetic stimulation with recording from the leg.

To determine central conduction times in the corticospinal pathways of humans using magnetic stimulation, we have developed a method for consistently recording conduction times between the motor cortex and the L4-5 level of the spinal cord. In 30 subjects, motor evoked potentials (MEPs) were recorded from the tibialis anterior muscle following contralateral motor cortex and peroneal nerve stimulation. In 18 of these subjects, the L4-5 intervertebral space was stimulated. The stimuli consisted of single, painless, short-duration magnetic pulses. In 12 subjects, measurements were made during voluntary ankle dorsiflexion, and during vibration of the TA tendon at rest. All subjects had measureable MEP latencies of 30.3 +/- 2.2 msec (mean +/- S.D.). The central motor conduction time (CMCT) was calculated using both a direct as well as an indirect method. The direct method in 18 subjects had a mean value of 16.2 +/- 1.7 msec, while the indirect method in all 30 subjects was 13.8 +/- 1.8 msec. No significant correlation of the CMCT was found with either age or height in these subjects. Ankle dorsiflexion significantly reduced the MEP latency and increased the amplitude, whereas vibration of the TA tendon significantly increased the amplitude alone. We conclude that MEPs may be consistently and painlessly measured in the lower extremity using magnetic stimulation in adults. Facilitation of the MEPs was produced more consistently by voluntary contraction than by vibratory stimulation of the tibialis anterior muscle tendon. Finally, CMCT was independent of both age and height in our study population.     

Somatosensory evoked potentials in chronic acquired demyelinating peripheral neuropathy

We recorded somatosensory evoked potentials (SEPs) over the scalp in eight patients with chronic acquired demyelinating peripheral neuropathy. They were obtained from 15 nerves in which sensory nerve action potentials (SNAPs) were absent or not more than 1 microV, but from which motor responses could be elicited. Motor and sensory (SEP-derived) conduction velocity was determined from the difference in response latency with wrist and elbow stimulation. In 11 nerves, afferent conduction velocity was slowed. In 10, there was relatively equal slowing in sensory and motor axons, whereas in 1 there was disproportionate slowing in afferent fibers. In four nerves, afferent conduction velocity was within the normal range despite slowing of motor conduction. We conclude that SEPs may be useful in evaluating peripheral sensory conduction in the absence of SNAPs, but can provide misleadingly normal data, presumably because of central amplification of an attenuated response arising from a few axons that conduct normally.     

Latency of motor evoked potentials to focal transcranial stimulation varies as a function of scalp positions stimulated.

We recorded motor evoked potentials (MEP) to transcranial magnetic stimulation from abductor pollicis brevis (APB), flexor carpi radialis (FCR), biceps brachii and deltoid muscles at rest and during slight voluntary activation. An 8-shaped coil connected to a Cadwell MES-10 magnetic stimulator was positioned over different scalp positions 1 cm apart. At least 24 stimuli were delivered at each location. Latencies of MEPs were compared with those obtained by electrical and magnetic stimulation during muscle activation. Progressively longer MEP latencies were obtained in 5 groups depending on the type and position of stimulation. The shortest latencies were obtained with (1) electrical stimulation during muscle contraction and (2) non-focal magnetic stimulation during muscle contraction; magnetic stimulation at rest produced longer latencies with stimulation of (3) an optimal position, (4) a suboptimal position, and (5) a non-optimal position. Mean latency differences between successive groups were 1.9, 2.0, 1.6, and 2.6 msec for APB. Similar latency differences were found for the other arm muscles. The results are compatible with the hypothesis that the different latencies evoked by stimulation at different scalp locations are determined by the summation at spinal motoneurons of excitatory postsynaptic potentials generated by successive numbers of I waves.     

Standardization of facilitation of compound muscle action potentials evoked by magnetic stimulation of the cortex. Results in healthy volunteers and in patients with multiple sclerosis.

To establish the importance of standardization of the facilitation of central motor conduction measured by magnetic stimulation we studied the effect of increasing voluntary muscle contraction on the central motor conduction time (CMCT) and motor evoked potential (MEP) amplitudes for 3 upper and 2 lower limb muscles. MEPs were elicited by magnetic stimulation of the cortex and the spinal roots. Muscle force was indirectly assessed from the integrated electrical muscle activity and expressed as the root mean square (RMS) and was varied from 0 to 40% of maximal activity. The central motor conduction time (CMCT) decreased during increasing muscle contraction, reaching constant values at approximately 10-20% RMSmax. Similarly, the increases of MEP amplitude tapered off at about the same RMS level. For each muscle an optimal RMS level was defined. The shortening of the CMCTs at the optimal RMS levels were: the brachial biceps, 3.4 msec; the radial carpal flexor of the wrist, 2.7 msec; the first dorsal interosseus muscle of the hand, 2.9 msec; the anterior tibial, 4.2 msec; and the abductor hallucis, 2.4 msec. The standardizing procedure was applied to 10 patients with multiple sclerosis. The stimulus thresholds were higher in these patients compared with those of the normals. Only the CMCT reduction of the BB was significantly larger (8.1 msec) than in the controls. Using standardized facilitation the diagnostic value of the amplitudes seems to be only a little less than that of the CMCTs.     

Modality-related scalp responses after electrical stimulation of cutaneous and muscular upper limb afferents in humans

To elucidate whether the selective electrical stimulation of muscle as well as cutaneous afferents evokes modality-specific responses in somatosensory evoked potentials (SEPs) recorded on the scalp of humans, we compared scalp SEPs to electrical stimuli applied to the median nerve and to the abductor pollicis brevis (APB) motor point. In three subjects, we also recorded SEPs after stimulation of the distal phalanx of the thumb, which selectively involved cutaneous afferents. Motor point and median nerve SEPs showed the same scalp distribution; moreover, very similar dipole models, showing the same dipolar time courses, explained well the SEPs after both types of stimulation. Since the non-natural stimulation of muscle afferents evokes responses also in areas specifically devoted to cutaneous input processing, it is conceivable that, in physiological conditions, muscle afferents are differentially gated in somatosensory cortex. The frontocentral N30 response was absent after purely cutaneous stimulation; by contrast, it was relatively more represented in motor point rather than in mixed nerve SEPs. These data suggest that the N30 response is specifically evoked by proprioceptive inputs.     

Neuromuscular consequences of prolonged hunger strike: an electrophysiological study.

OBJECTIVES: The purpose of this study was to determine the electrophysiological consequences of neuromuscular and central nervous system involvement in a group of patients presented with the neurological complications of a long-term hunger strike (HS). METHODS: Motor and sensory nerve conduction (NCV), F wave, somatosensory evoked potential (SEP) and motor evoked potential (MEP) studies were performed in 12 male and 3 female patients (mean age: 29.4) following HS. RESULTS: All patients whose weight loss was 11-31 (mean: 22.8) kg after 69-day HS, had neurological findings consistent with Wernicke's encephalopathy or Wernicke-Korsakoff syndrome. Abnormally prolonged latency and/or low amplitude sensory nerve action potentials were found in 7 patients. The amplitudes of compound muscle action potentials were significantly reduced in ulnar, median and tibial motor NCV studies as compared to the controls. F waves elicited by median nerve stimulation at wrist and muscle responses evoked by cervical and lumbar magnetic stimulation had significantly prolonged latencies. MEPs recorded from the lower extremities showed a slight prolongation in central conduction times. The cortical response latencies were prolonged in tibial SEPs. CONCLUSIONS: The most prominent finding in this patient group was the low amplitude of CMAPs elicited in motor NCV studies which was concluded to be resulted from the reversible muscular changes. The other electrophysiological findings suggested that peripheral nerves and long central nervous system pathways were also mildly involved.     

Central motor tract propagation in man: studies with non-invasive, unifocal, scalp stimulation

Motor-evoked potentials (MEPs) to unifocal, anodal scalp stimulation have been recorded in 45 healthy volunteers from proximal and distal upper limb muscles. Optimal responses were obtained through a pericranial cathode consisting of 6 or more regularly spaced, interconnected plaques whose impedance was carefully balanced with that of a 0.8-cm2 stimulating anode on the scalp. Individual rectangular pulses with threshold intensity (70-86 mA) 100-200 microseconds in duration, with rise-decay times shorter than 50 microseconds resulted more efficient in eliciting individual MEPs in the target muscle. The foci of maximal response for hand and shoulder muscles were localized. The scalp-to-cervical cord conduction time along the motor tracts governing the hand muscles was 5.21 +/- 0.42 ms. This index was highly correlated with the subject's height and stable in time when repeatedly tested. Collision between orthodromically and antidromically propagated motor impulses was obtained by simultaneous stimulation of scalp and median nerve at wrist. Response facilitation was achieved by means of prestimulus voluntary contraction of the target muscle, continuous vibration of its tendon or scalp stimulation with paired shocks. Facilitation of MEPs was obtained by prestimulating the ipsilateral motor cortex 8-24 ms before the stimulation of the one contralateral to the target muscle. This was considered at least in part mediated by transcallosal connections. An efferent volley secondary to scalp stimulation was recorded for the nerve trunk with the near-nerve technique. Segmental and suprasegmental mechanisms underlying MEP facilitation provoked by phasic and tonic contractions of the target muscle have been investigated.     

Differences between the effects of three plasticity inducing protocols on the organization of the human motor cortex

Several experimental protocols induce lasting changes in the excitability of motor cortex. Some involve direct cortical stimulation, others activate the somatosensory system and some combine motor and sensory stimulation. The effects usually are measured as changes in amplitude of the motor-evoked-potential (MEP) or short-interval intracortical inhibition (SICI) elicited by a single or paired pulses of transcranial magnetic stimulation (TMS). Recent work has also tested sensorimotor organization within the motor cortex by recording MEPs and SICI during short periods of vibration applied to single intrinsic hand muscles. Here sensorimotor organization is focal: MEPs increase and SICI decreases in the vibrated muscle, whilst the opposite occurs in neighbouring muscles. In six volunteers we compared the after effects of three protocols that lead to lasting changes in cortical excitability: (i) paired associative stimulation (PAS) between a TMS pulse and an electrical stimulus to the median nerve; (ii) motor practice of rapid thumb abduction; and (iii) sensory input produced by semicontinuous muscle vibration, on MEPs and SICI at rest and on the sensorimotor organization. PAS increased MEP amplitudes, whereas vibration changed sensorimotor organization. Motor practice had a dual effect and increased MEPs as well as affecting sensorimotor organization. The implication is that different protocols target different sets of cortical circuits. We speculate that protocols that involve repeated activation of motor cortical output lead to lasting changes in efficacy of synaptic connections in output circuits, whereas protocols that emphasize sensory inputs affect the strength of sensory inputs to motor circuits.     

Examination of the descending pathway to the external anal sphincter and pelvic floor muscles by transcranial cortical stimulation.

In 26 neurologically normal patients and 9 healthy volunteers EMG responses after transcranial cortical stimulation (TCCS) were recorded from the external anal sphincter (EAS), the anterior tibial muscle (TA), the bulbocavernosus muscle (BC) and the rectus abdominis muscle (RA). Electrical TCCS was used in 29 subjects and magnetic TCCS in 6 subjects. Response patterns in the different muscles in relation to the strength of the stimulus were analyzed. It was found that the response patterns related to the strength of stimulation differed totally between the TA and the EAS. When the stimulus strength was increased stepwise, a response with a latency of 31.9 +/- 2.5 msec was first recorded in the TA, followed at higher strength by a secondary response with a latency of approximately 100 msec. In contrast, a response with a latency of 105.5 +/- 23.9 msec was first recorded in the EAS. The latency of this response gradually shortened with increasing stimulus strength until a response with a constant latency of 36.1 +/- 6.1 was obtained. In some subjects the response pattern in the BC was similar to that in the TA, and in others it was similar to that in the EAS. Responses in the TA, RA and EAS were all facilitated during voluntary contraction of the EAS. Both responses in the TA and in the EAS were facilitated by voluntary contraction of the TA. During voluntary contraction of the TA an inhibitory period was always recorded, while in the EAS no inhibitory periods were observed during either contraction or relaxation. The hypothesis that the fastest cortico-motoneuronal pathway to the EAS is polysynaptic is proposed.     

Brain excitability and long latency muscular arm responses: non-invasive evaluation in healthy and parkinsonian subjects.

Thirty healthy and 35 volunteers affected by Parkinson's disease (PD) were examined. Long latency responses (LLRs) and short latency somatosensory evoked potentials (SEPs) after median nerve stimulation were respectively recorded from forearm flexor muscles, and from 19 scalp electrodes, during relaxation (condition 1), light and maximal muscle contraction (conditions 2 and 3). Linear interpolation of SEPs was performed to produce isopotential colour maps. Latencies and amplitudes of the V1-V2 component in LLR, as well as of parietal, central and frontal scalp SEPs were analysed in the 3 experimental conditions. Highly significant inverse correlation matched the frontal SEP to the LLR V2 component amplitudes, both in healthy and in PD subjects. However, the V2 component--which in the former group was reliably identifiable only in condition 3--was presented in conditions 1 and 2 in a high percentage of PD subjects who also showed an abnormally reduced frontal SEP during complete relaxation. Excitability changes of brain motor areas induced by a sensory input were tested as follows: the motor cortex was transcranially stimulated (TCS) by magnetic pulses with an intensity 10% below (A) or above (B) the threshold for twitch elicitation during complete relaxation of forearm muscles; TCS was randomly preceded (range 14-32 msec) by a shock to the median or ulnar nerve at the elbow with identical characteristics as for LLR elicitation. An initial epoch of 'inhibition' followed by a peak of 'facilitation' of the amplitude of motor responses to TCS was observed when conditioning stimuli to the median nerve preceded TCS by 14-20 and by 24-32 msec, respectively. Contrary to normals, conditioning stimulation of the median nerve did not significantly influence the excitability threshold to TCS in those parkinsonians with depressed frontal N30.     

Neurophysiological study in Pelizaeus-Merzbacher disease

The neurophysiological characteristics of Pelizaeus-Marzbacher disease (PMD) were studied in four Japanese patients aged between 5 and 13 years. Pendular spontaneous nystagmus was always recorded with a frequency between 2.5 and 4 Hz, and abnormal saccades with an almost twofold prolongation in onset time and 50% decrease in velocity were noted. Brainstem auditory evoked potentials consistently demonstrated severely altered waves II to V, following a normal wave I, despite normal hearing acuity. Somatosensory evoked potentials (SEPs) were always absent between brainstem components and early cortical responses. Late cortical components of SEPs and visual evoked potentials with significantly prolonged latencies were recorded in the three younger cases having normal sensory and visual acuity (N35 of SEP, 73.1 ± 2.1 ms; N75 of VEP, 129.0 ± 12.7 ms; mean ± S.D.), while these peaks were absent in the oldest case having the most severe handicap. In motor evoked potentials (MEPs), R1 of blink reflex with significantly prolonged latency (14.9 ± 1.48 ms) was always obtained, and no subsequent R2 was elicited. Magnetic transcortical stimulation elicited no MEPs of the thenar even in the facilitating condition on voluntary contraction despite mild weakness of the thenar, while normal MEPs were always elicited on cervical stimulation. These electrophysiological findings were consistent with extensive conduction slowing involving the brainstem to the cerebrum, which seemed to be accompanied by conduction block in motor systems rather than sensory systems. Although each of the results was not specific, in combination they suggested the characteristics of diffuse brain dysmyelination in PMD.     

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 somatosensory evoked potentials in Autosomal Dominant Hereditary Spastic Paraparesis (ADHSP) linked to chromosome 2p, SPG4

The aim of our study was to evaluate Motor Evoked Potentials (MEPs) and cortical excitability, using Transcranial Magnetic Stimulation (TMS) as well as short latency Somatosensory Evoked Potentials (SEPs) in Autosomal Dominant Hereditary Spastic Paraparesis (ADHSP) patients. MEPs were recorded from upper and lower limb muscles in 12 patients (7 m and 5f) affected by ADHSP with spastin mutation (SPG4). We measured: (i) motor threshold (MTh); (ii) total motor conduction time (TMCT); (iii) direct and indirect central motor conduction time (d-CMCT and i-CMCT) calculated by subtracting from the cortical latency those obtained on magnetic spinal stimulation (d-PMCT) and via the F-wave method (i-PMCT); (iv) MEP amplitude (MEP/Mmax ratio%) and (v) duration of the cortical silent period (CSP). Latency, amplitude and persistence of the F-wave obtained with electrical nerve stimulation were also considered; H reflex was also tested from lower extremities. SEPs were recorded from spine and scalp sites following median and posterior tibial nerve stimulation; conventional latency and amplitude measurements were performed. In a comparison with the control group, the MTh recording from lower limbs was significantly higher (67.5 +/- 7.7% versus 52.5 +/- 6.9%), MEPs were absent in one case and showed reduced amplitude in the remainders (22.9 +/- 12.6% versus 66.3 +/- 25.9% of M wave); TMCT resulted to be abnormal (36.5 +/- 3.9 ms versus 27.1 +/- 1.4 ms) and d-CMCT as well as i-CMCT were significantly prolonged (23.1 +/- 3.5 ms versus 13.8 +/- 1.3 ms; and 20.1 +/- 3.4 ms versus 10.6 +/- 1.3 ms, respectively). The CSP, which was normal from the hands, was significantly shortened from the legs and correlated with spasticity scoring (Ashworth scale). Cortical SEPs from lower limbs were abnormal in all cases, whereas SEPs by stimulation of median nerves were normal; F-wave parameters from upper limbs showed no abnormalities, whereas an increased persistence was detected from lower limbs; H reflex amplitudes resulted larger compared with controls. Moreover, shortening of the CSP, being correlated with the Ashworth scale, can be considered an electrophysiological marker of spasticity that seems to arise from impairment of the supraspinal or intracortical inhibitory pathways with an additional contribution of increased segmental motor neuron excitability. These data prove the existence of comparable neurophysiological abnormalities in ADHSP with spastin mutation (SPG4) when long ascending and descending pathways are involved.     

Intrarectal ground electrode improves the reliability of motor evoked potentials recorded in the anal sphincter

Motor evoked potentials (MEPs) can be recorded in the external anal sphincter in response to magnetic stimulation of the cerebral cortex or sacral roots. However, the magnitude of the stimulus artifact may alter the reliability of anal MEP recording. An intrarectal ground electrode substantially reduces stimulus artifact and technical failure, improving MEP latency determination to sacral root stimulation in particular.