Central Conduction Velocity Research Articles

Pain-Related Vertex Evoked Potentials. Comparison of Surface Electrical to Heat Stimulation.

Demonstration of nociceptive fiber abnormality is important for diagnosing neuropathic pain and small fiber neuropathies. This is usually assessed by brief heat pulses using lasers, contact heat, or special electrodes. We hypothesized that pain-related evoked potentials to conventional surface electrical stimulation (PREPse) can index Aδ afferences despite tactile Aß fibers coactivation. PREPse may be more readily used clinically than contact heat evoked potentials (CHEPS). Twenty-eight healthy subjects. Vertex (Cz-A1/A2) recordings. Electrical stimulation of middle finger and second toe with conventional ring, and forearm/leg skin with cup, electrodes. Contact heat stimulation to forearm and leg. Compression ischemic nerve blockade. PREPse peripheral velocities were within the midrange of Aδ fibers. N1-P1 amplitude increased with pain numerical rating scale graded (0-10) electrical stimulation (n = 25) and decreased with increasing stimulation frequency. Amplitudes were unchanged by different presentation orders of four stimulation intensities. PREPse N1 (∼130 milliseconds) and N2 (∼345 milliseconds) peaks were approximately 40 milliseconds earlier than that with CHEPS. PREPse and CHEPS N1-N2 interpeak latency (∼207 milliseconds) were similar. PREPse became unrecordable with nerve blockade of Aδ fibers. PREPse earlier N1 and N2 peaks, and similar interpeak N1-N2 latencies and central conduction velocities, or synaptic delays, to CHEPS are consistent with direct stimulation of Aδ fibers. The relation of vertex PREPse amplitude and pain, or the differential effects of frequency stimulation, is similar to pain-related evoked potential to laser, special electrodes, or contact heat stimulation. The relationship to Aδ was validated by conduction velocity and nerve block. Clinical utility of PREPse compared with CHEPS needs validation in somatosensory pathways lesions.

Trapezius Motor Evoked Potentials From Transcranial Electrical Stimulation and Transcranial Magnetic Stimulation: Reference Data, Characteristic Differences and Intradural Motor Velocities in Horses

Reason for Performing StudySo far, only transcranial motor evoked potentials (MEP) of the extensor carpi radialis and tibialis cranialis have been documented for diagnostic evaluation in horses. These allow for differentiating whether lesions are located in either the thoraco-lumbar region or in the cervical myelum and/or brain. Transcranial trapezius MEPs further enable to distinguish between spinal and supraspinal located lesions. No normative data are available. It is unclear whether transcranial electrical stimulation (TES) and transcranial magnetic stimulation (TMS) are interchangeable modalities.ObjectivesTo provide normative data for trapezius MEP parameters in horses for TES and TMS and to discern direct and indirect conduction routes by neurophysiological models that use anatomical geometric characteristics to relate latency times with peripheral (PCV) and central conduction velocities (CCV).MethodsTranscranial electrical stimulation-induced trapezius MEPs were obtained from twelve horses. TES and TMS-MEPs (subgroup 5 horses) were compared intra-individually. Trapezius MEPs were measured bilaterally twice at 5 intensity steps. Motoneurons were localized using nerve conduction models of the cervical and spinal accessory nerves (SAN). Predicted CCVs were verified by multifidus MEP data from two horses referred for neurophysiological assessment.ResultsMean MEP latencies revealed for TES: 13.5 (11.1–16.0)ms and TMS: 19.7 (12–29.5)ms, comprising ∼100% direct routes and for TMS mixed direct/indirect routes of L:23/50; R:14/50. Left/right latency decreases over 10 > 50 V for TES were: –1.4/–1.8 ms and over 10 > 50% for TMS: –1.7/–3.5 ms. Direct route TMS-TES latency differences were 1.88–4.30 ms. 95% MEP amplitudes ranges for TES were: L:0.26–22 mV; R:0.5–15 mV and TMS: L:0.9 – 9.1 mV; R:1.1–7.9 mV.ConclusionThis is the first study to report normative data characterizing TES and TMS induced- trapezius MEPs in horses. The complex trapezius innervation leaves TES as the only reliable stimulation modality. Differences in latency times along the SAN route permit for estimation of the location of active motoneurons, which is of importance for clinical diagnostic purpose. SAN route lengths and latency times are governed by anatomical locations of motoneurons across C2-C5 segments. TES intensity-dependent reductions of trapezius MEP latencies are similar to limb muscles while MEP amplitudes between sides and between TES and TMS are not different. CCVs may reach 180 m/s.

WS2.3. TMS: Clinical Application of MEPs

Transcranial magnetic stimulation (TMS) has utility for clinical assessment, studies of physiology, and therapy. There are a number of purposes in the clinic, particularly in regard to assessment of the corticospinal tract by central motor conduction velocity (CMCV). CMCV is obtained by getting the motor evoked potential (MEP) latency and subtracting the peripheral conduction time. Peripheral conduction time can be assessed with stimulation over the spine or with the F-wave technique. In situations such as multiple sclerosis and cervical myelopathy, central conduction time is prolonged. It can also be used to monitor corticospinal tract function during surgery. TMS can be useful in proving normal function in patients with functional paresis. Recently, it is also being investigated for evaluation of upper motor neuron function in patients with ALS. Excitability of the motor cortex in this circumstance is best assessed with threshold tracking. Another valuable use is for presurgical mapping to examine topography of functional cortex. This is most commonly done for motor function and language. Guidelines for optimal methodology for mapping have been published.

Central nervous system impairment detected by somatosensory evoked potentials in patients with Charcot-Marie-Tooth disease type 1A

Diseases related to peripheral myelin protein 22 (PMP22) have been implicated to involve the central nervous system (CNS). This study aimed to detect central nerve impairment using somatosensory evoked potentials (SSEPs) in patients with Charcot-Marie-Tooth disease (CMT) 1A. A total of 30 CMT1A patients and 26 healthy volunteers were included. Baseline characteristics, brain MRI and segmental SSEPs were collected from the participants. The peak latencies of N9, N13 and N20 were recorded, and central conduction velocity (CCT) was calculated and compared between groups. Significant differences were found in the peak latencies and amplitudes of N9, N13 and N20 between the two groups. CCT was significantly prolonged in the CMT group (7.05 ± 2.09 ms) compared to the control group (5.40 ± 1.79 ms) (p = 0.003). Six of 30 CMT patients had abnormal MRI signals, but no correlation with CCT was found. The central somatosensory pathway that carries SSEPs was impaired in CMT1A patients, which implies an important underlying role of PMP22 in the CNS.

Physiological properties of the lamina I spinoparabrachial neurons in the mouse.

Spinal cord lamina I neurons receiving dense input from nociceptors and projecting to the parabrachial area at the ponto-mesencephalic junction form the major ascending pain-related pathway in rodents. Lamina I spinoparabrachial (SPB) neurons have never been characterized in mice, despite the growing and extensive use of this species to understand the contribution of lamina I SPB neurons in chronic pain. The electrophysiological properties of lamina I SPB neurons recorded here in anaesthetized mice are comparable to those of rat or cat, forming a nociceptive and thermoreceptive pathway. It was confirmed 'on line' that lamina I SPB neurons that normally encode noxious stimuli can receive input from low threshold mechanoreceptors in certain conditions. The present work indicates that the study of lamina I SPB neurons in vivo could take advantage of the use of genetically modified mice. Ongoing studies investigating the role of lamina I projection neurons in the generation of chronic pain are mainly based on the use of genetically modified mice. However, lamina I projection neurons have never been physiologically characterized in this species. The present work aimed to fill this gap, and to assess the effect of spinal 'disinhibition' that may occur in chronic pain states on the responses of these neurons to light touch. Seventy lamina I spinoparabrachial (SPB) neurons were characterized in anaesthetized mice. These neurons showed low central conduction velocities (<12.4ms-1 ) and wide range of responses. Fifty-six neurons responded equally to noxious mechanical and thermal (heat) stimuli (16% responded consistently to light touch). Modality-specific neurons responded preferentially to thermal (cold) stimuli (n=10) and pinch (n=2), or specifically to heat (n=2). Spinal bicuculline and strychnine application induced responses to brush in half of the neurons tested, confirming directly the potential connection between low threshold mechanoreceptors and nociceptive-specific neurons, responsible for mechanical allodynia. Remarkably, the effect of the treatment was highly variable and apparently independent of the initial profile of the neurons. The present data confirm that mice lamina I SPB neurons have the expected characteristics to form a nociceptive and thermoreceptive pathway, but they constitute a highly heterogeneous group. The differential effect of spinal disinhibition observed here suggests that a subgroup of lamina I SPB neurons might be responsible for abnormal pain in pathological conditions, and emphasizes the importance of in vivo recording, a neglected approach.

Are There Abnormalities in Peripheral and Central Components of Somatosensory Evoked Potentials in Non-Specific Chronic Low Back Pain?

Chronic low back pain (CLBP) was shown to be associated with longer reflex response latencies of trunk muscles during external upper limb perturbations. One theoretical, but rarely investigated possibility for longer reflex latencies might be related to modulated somatosensory information processing. Therefore, the present study investigated somatosensory evoked potentials (SEPs) to median nerve stimulation in CLBP patients and healthy controls (HC). Latencies of the peripheral N9 SEP component were used as the primary outcome. In addition, latencies and amplitudes of the central N20 SEP component, sensory thresholds, motor thresholds and nerve conduction velocity were also analyzed in CLBP patients and HC. There is a trend for the CLBP patients to exhibit longer N9 latencies at the ipsilateral Erb’s point compared to HC. This trend is substantiated by significantly longer N9 latencies in CLBP patients compared to normative data. None of the other parameters showed any significant difference between CLBP patients and HC. Overall, our data indicate small differences of the peripheral N9 SEP component; however, these differences cannot explain the reflex delay observed in CLBP patients. While it was important to rule out the contribution of early somatosensory processing and to elucidate its contribution to the delayed reflex responses in CLBP patients, further research is needed to find the primary source(s) of time-delayed reflexes in CLBP.

Acute changes in soleus H-reflex facilitation and central motor conduction after targeted physical exercises

We tested the acute effect of exercises targeted simultaneously at cortical and brainstem circuits on neural transmission through corticobulbar connections. Corticobulbar pathways represent a potential target for rehabilitation after spinal cord injury (SCI), which tends to spare brainstem circuits to a greater degree than cortical circuits. To explore this concept, able-bodied volunteers (n=20) underwent one session each of three exercises targeted at different nervous system components: treadmill walking (spinal locomotor circuits), isolated balance exercise (brainstem and other pathways), and multimodal balance plus skilled hand exercise (hand motor cortex and corticospinal tract). We found that short-interval soleus H-reflex facilitation increased after one session of balance and multimodal exercise by 13.2±4.0% and 8.3±4.7%, and slightly decreased by 1.9±4.4% after treadmill exercise (p=0.042 on ANOVA across exercise type). Increases in long-interval H-reflex facilitation were not significantly different between exercises. Both balance and multimodal exercise increased central motor conduction velocity by 4.3±2.6% and 4.5±2.8%, whereas velocity decreased by 4.3±2.7% after treadmill exercise (p=0.045 on ANOVA across exercise type). In conclusion, electrophysiological transmission between the motor cortex and spinal motor neurons in able-bodied subjects increased more following one session of balance exercise than treadmill exercise.

後脛骨神経刺激による末梢伝導速度・脊髄伝導速度・中枢伝導速度の測定と臨床応用

後脛骨神経刺激による末梢伝導速度・脊髄伝導速度・中枢伝導速度の測定と臨床応用

脳幹聴覚誘発電位の中枢伝導時間延長が手がかりとなり，Ｃｘ３２に新規の遺伝子変異が確認されたＣＭＴＸ１の成人男性例

CMTX1, the second most common type of inherited hereditary motor and sensory neuropathy (HMSN), is associated with mutations of the gene for the gap junction protein connexin 32 (Cx32). In this condition, central conduction velocity is known to be delayed, presumably because mutated Cx32 is expressed in oligodendrocytes. A 45-year-old man presented with a 5-year history of progressive gait disturbance due to leg muscle weakness. The family history revealed that the mother had also progressive gait disturbance in her early 40s, and the younger sister could not walk faster than before at the age of 41. On neurological assessment, the patient exhibited pes cavus, distal muscle atrophy and weakness, and absence of the knee and ankle jerks. Touch sensation was impaired in the both feet. Motor and sensory nerve conduction velocities were reduced to 30-36 m/s with mild temporal dispersion. Sural nerve biopsy revealed diffuse loss of large myelinated fibers with the remaining large and intermediate nerve fibers being frequently surrounded by a thin myelin sheath. Onion bulb formation was only occasional and mild in degree. His hearing acuity was normal on pure-tone audiometry, but BAEP test demonstrated prolonged central conduction time (-I wave 1.8 milliseconds, I-V wave 6.4 milliseconds). The BAEP findings prompted us to choose Cx32 gene to analyze first to find a novel mutation of two (A and T) base pairs deletion at codons 277 and 278 (Met93fs). Thus, the present case indicates that Cx32 gene mutation should be targeted first in case of HMSN with abnormal BAEP.

Motor Potentials by Magnetic Stimulation in Periventricular Leukomalacia

Periventricular leukomalacia is characterized by damage to the brain's white matter and impairments in motor function. Motor-evoked potentials by transcranial magnetic stimulation evaluate corticospinal tract function. We analyzed alterations in motor-evoked potentials in newborns with periventricular leukomalacia. Thirty infants (aged 4.37 +/- 1.1 months mean +/- S.D.) were divided into three groups: 10 healthy, and 10 with focal and 10 with diffuse periventricular leukomalacia. Potentials recorded in the right abductor pollicis brevis of healthy infants indicated a total motor conduction time of 26.3 +/- 2.4 ms, central motor conduction time of 17.0 +/- 2.6 ms, and central motor conduction velocity of 12.3 +/- 2.2 m/s. In the tibialis anterior, total motor conduction time was 27.4 +/- 2.6 ms; central motor conduction time was 16.7 +/- 2.8 ms, and central motor conduction velocity was 25.2 +/- 3.4 m/s. In the focal periventricular leukomalacia and diffuse periventricular leukomalacia groups, an increase in central motor conduction time and a decrease in central motor conduction velocity (P < 0.05) were evident, without differences between the two groups. Motor-evoked potentials in periventricular leukomalacia revealed an increase in central motor conduction time and a decrease in central motor conduction velocity, without differences between diffuse and focal types.

Spinothalamic lamina I neurones selectively responsive to cutaneous warming in cats.

1. In order to further characterize the role of lamina I as the source of central ascending neural pathways for thermoreception and thermoregulation, experiments were performed on anaesthetized cats to determine the quantitative response characteristics of warming-specific lumbosacral spinothalamic lamina I neurones. 2. We identified 10 neurones out of 474 that were selectively excited by cutaneous warming (Warm cells). Their thresholds were all in the range 35-37 degrees C at a baseline of 34.5 degrees C, and their discharge linearly encoded the temperature of graded, innocuous warming stimuli with a sensitivity of 2.1 Hz x degrees C(-1). 3. The stimulus-response function of the Warm cells plateaued at temperatures that were in the noxious heat range. 4. The Warm cells were distinguished from other classes of spinothalamic lamina I neurones by their peripheral inputs, central conduction velocities and level of ongoing activity. 5. The discharge of Warm cells compares well with the known human psychophysics of warm sensibility, and these neurones are likely to be crucial to discriminative thermoreception. Additionally, a role in thermoregulation, a defining feature of mammalian homeostasis, is suggested.

Spinothalamic lamina I neurons selectively sensitive to histamine: a central neural pathway for itch.

We found a class of lamina I spinothalamic tract (STT) neurons selectively excited by iontophoretic histamine. The responses of this class of neurons parallel the pure itching sensation this stimulus elicits in humans, and match the responses of peripheral C-fibers that have similar selectivity. These neurons have distinct central conduction velocities and thalamic projections, indicating that they constitute a unique subset of STT neurons. These findings can explain why a lesion of the lateral STT disrupts itch along with pain and temperature sensations. Our findings provide strong evidence that itch is subserved by specific neural elements both peripherally and centrally.

Distribution and latency of muscle responses to transcranial magnetic stimulation of motor cortex after spinal cord injury in humans.

Noninvasive transcranial magnetic stimulation (TMS) of the motor cortex was used to evoke electromyographic (EMG) responses in persons with spinal cord injury (n = 97) and able-bodied subjects (n = 20, for comparative data). Our goal was to evaluate, for different levels and severity of spinal cord injury, potential differences in the distribution and latency of motor responses in a large sample of muscles affected by the injury. The spinal cord injury (SCI) population was divided into subgroups based upon injury location (cervical, thoracic, and thoracolumbar) and clinical status (motor-complete versus motor-incomplete). Cortical stimuli were delivered while subjects attempted to contract individual muscles, in order to both maximize the probability of a response to TMS and minimize the response latency. Subjects with motor-incomplete injuries to the cervical or thoracic spinal cord were more likely to demonstrate volitional and TMS-evoked contractions in muscles controlling their foot and ankle (i.e., distal lower limb muscles) compared to muscles of the thigh (i.e., proximal lower limb muscles). When TMS did evoke responses in muscles innervated at levels caudal to the spinal cord lesion, response latencies of muscles in the lower limbs were delayed equally for persons with injury to the cervical or thoracic spinal cord, suggesting normal central motor conduction velocity in motor axons caudal to the lesion. In fact, motor response distribution and latencies were essentially indistinguishable for injuries to the cervical or thoracic (at or rostral to T10) levels of the spine. In contrast, motor-incomplete SCI subjects with injuries at the thoracolumbar level showed a higher probability of preserved volitional movements and TMS-evoked contractions in proximal muscles of the lower limb, and absent responses in distal muscles. When responses to TMS were seen in this group, the latencies were not significantly longer than those of able-bodied (AB) subjects, strongly suggestive of "root sparing" as a basis for motor function in subjects with injury at or caudal to the T11 vertebral body. Both the distribution and latency of TMS-evoked responses are consistent with highly focal lesions to the spinal cord in the subjects examined. The pattern of preserved responsiveness predominating in the distal leg muscles is consistent with a greater role of corticospinal tract innervation of these muscles compared to more proximal muscles of the thigh and hip.

A study of central and peripheral nerve conduction in patients with primary hypothyroidism: the effects of thyroxine replacement.

Somato-Sensory Evoked Potential (SSEP) and Peripheral Nerve Conduction (PNC) studies were performed in twenty patients with primary hypothyroidism to elucidate the changes of central and peripheral nervous systems in hypothyroid state and the effects of thyroxine replacement. Before thyroxine replacement therapy, eleven patients had significantly delayed SSEP (prolonged latencies of N9, N13, or N20), and only three patients had prolonged central conduction time (between N13 and N20). PNC abnormalities with decreased conduction velocity and diminished amplitudes were found in fourteen patients. After thyroxine treatment, both SSEP and PNC studies demonstrated significant improvement and paralleled the clinical neurological amelioration. The central and peripheral conduction velocities returned to normal limits, while the abnormality in amplitude still persisted. There were also discrepancies between SSEP and PNC studies in both the abnormality pattern and the recovery potential. Our observations may suggest: firstly, both the SSEP and PNC studies may be useful, alternative tools in monitoring the neurological disorders in hypothyroidism; and secondly, the pathogenesis of central and peripheral nervous dysfunction in hypothyroidism may be via different mechanisms.

Physiological identification of morphologically distinct afferent classes innervating the cristae ampullares of the squirrel monkey.

1. Semicircular-canal afferents in the squirrel monkey were characterized by their resting discharge, discharge regularity, sensitivity to galvanic currents delivered to the ear (beta *), the gain (g2Hz), and phase lead (phi 2Hz) of their response to 2-Hz sinusoidal head rotations, and their antidromic conduction velocity. Discharge regularity was measured by a normalized coefficient of variation (CV*); the higher the CV*, the more irregular the discharge. g2Hz and phi 2Hz were expressed relative to angular head velocity. 2. These physiological measures were used in an attempt to discern the discharge properties of the three morphological classes of afferents innervating the crista. Presumed bouton (B) fibers were identified as slowly conducting afferents. Presumed calyx (C) fibers were recognized by their irregular discharge and low rotational gains. The remaining fibers were considered to be dimorphic (D) units. Single letters (B, C, and D) are used to emphasize that the classification is based on circumstantial evidence and may be wrong for individual fibers. Of the 125 identified fibers, 13 (10%) were B units, 36 (29%) were C units, and 76 (61%) were D units. 3. B units were regularly discharging D units ranged from regularly to irregularly discharging. C units were the most irregularly discharging afferents encountered. The mean resting discharge for the entire sample was 74 spikes/s. Resting rates were similar for regularly discharging B and D units and higher than those for irregularly discharging C and D units. 4. Except for their lower conduction velocities, the discharge properties of B units are indistinguishable from those of regularly discharging D units. Many of the discharge properties of B and D units vary with discharge regularity. There is a strong, positive relation when beta *, g2Hz, or phi 2Hz is plotted against CV*. For beta * or phi 2Hz, C units conform to the relation for B and D units. In contrast, values of g2Hz for C units are three to four times lower than predicted from the relation for the other two classes. 5. Internal (axon) diameters (dp) of peripheral vestibular-nerve fibers were estimated from central antidromic conduction velocities. Thick fibers (dp > or = 49 microns) were irregularly discharging, mostly C units. Medium-sized fibers (dp = 1.5-4 microns) included regular, intermediate, and irregular D units, as well as C units. Thin fibers (dp < or = 1.5 microns) were defined as B units.(ABSTRACT TRUNCATED AT 400 WORDS)

Corticospinal projections to upper limb motoneurones in humans.

1. Magnetic stimulation was applied over the motor cortex in forty-five normal human subjects and peristimulus time histograms (PSTHs) of the discharges of single motor units were used to record changes in the firing probability of individual spinal motoneurones of contralateral upper limb muscles. Recordings were obtained from 153 motor units from fourteen upper limb muscles. 2. For the majority of motor units the initial effect was a short latency facilitation. The estimated central conduction velocities and the rise times of the underlying excitatory postsynaptic potentials (EPSPs) were compatible with monosynaptic facilitation by a fast corticospinal pathway. In some motor units the initial effect was a short latency inhibition. Other units showed no statistically significant changes in firing probability. The proportion of the tested motor units in each of these categories depended on the muscle. All of the sampled units of first dorsal interosseous (1DI) showed short latency facilitation, as did the majority of units in the forearm and the biceps brachii. More than half of the sampled motor units of triceps brachii and deltoid showed either no effect or were inhibited. 3. To compare the net short latency actions of the neurones activated by magnetic stimulation on various motoneurone pools, the magnitude of the short latency facilitation or inhibition in a given motor unit was normalized to the magnitude of the short latency facilitation in the 1DI motor unit of the same subject at the same stimulus intensity, and these data were pooled for a number of subjects. 4. 1DI motoneurones received strong net facilitation (estimated mean EPSP amplitude 2.9 +/- 0.2 mV), the motoneurones of forearm muscles and biceps brachii received weaker net facilitation and triceps brachii and deltoid received no net effect. 5. It is concluded that the short latency corticospinal projections to upper limb motoneurones in humans have a distinct pattern which is similar to that in other primates.

Cortical somatosensory evoked potentials in spinal cord injury patients

The amplitude and latency of somatosensory evoked potentials (SEPs) in healthy subjects depend on intensity of stimulation. The effect of this parameter on SEPs in patients with neurologic disorders has not been systematically studied, although it could have a profound impact if SEPs are to be used for prognostication. We have compared the latency and amplitude of SEPs in healthy subjects and patients with spinal cord injury (SCI). Stimulation intensity was standardized at two different biologically calibrated levels. Cortical SEPs in patients with SCI showed greater decrease in latency and increase in amplitude with increased intensity of stimulation in comparison to healthy subjects. These phenomena were observed in the majority of patients with incomplete SCI who subsequently showed improvement in cortical SEPs. We observed situations in which the SEP was absent with the usual intensity of stimulation and present only with the stronger stimulation intensity. Furthermore, SEP latencies often changed dramatically with different intensities of stimulation, potentially making any calculation of central conduction velocity meaningless without precise standardization of stimulation. These findings demonstrate a necessity for a biological calibration of stimulation intensity to improve the repeatability of SEPs. We suggest the use of two different standardized intensities of stimulation for SEP studies in SCI patients, one of which should be stronger than the intensity presently recommended.

Motor and somatosensory evoked potentials in hereditary spastic paraplegia.

Motor evoked potentials (MEPs) from the arms and legs to transcranial stimulation of the motor cortex and somatosensory evoked potentials (SSEPs) from stimulation of the nerves of the arms and legs, were recorded in 11 patients with hereditary spastic paraplegia. Electrophysiological abnormalities were found to be distributed differently among the systems examined; the longer the pathway, the higher the incidence and severity of impairment. MEPs from the leg were either absent or clearly reduced or prolonged in all patients. Eight patients showed abnormal cortical SSEPs on stimulation of the leg (absent or reduced responses in four, slowed central conduction velocity in seven), but only two of these patients had abnormal MEPs from the arm (absent responses). Cortical SSEPs on stimulation of the median nerve were reduced in two patients. Mean values of amplitude and central conduction velocity for MEPs and SSEPs from the leg were significantly different between patients and controls. Such differences were not found for either MEPs or SSEPs from the arm. This distribution of abnormalities, which suggests a differential involvement of the spinal pathways, parallels the reported pathological pattern in which degeneration of axons is more common and severe in the motor and sensory fibres supplying the leg.

Quantification of motor pathways to the pelvic floor in humans

The motor innervation of the pelvic floor plays a major role in defecation disorders such as fecal incontinence. It consists of central motor pathways and peripheral nerve fibers. Transcranial magnetoelectric stimulation of the brain and magnetoelectric stimulation of the lumbosacral motor roots were performed in 10 healthy volunteers. Motor evoked potentials were recorded from the external anal sphincter. This procedure allowed differentiation between a predominantly central and a solely peripheral component of the motor innervation of the external and sphincter. To compare these recordings with well-established data, motor evoked potentials were also recorded from the anterior tibial muscle. The central motor conduction time was 20.9 +/- 2.4 ms to the external anal sphincter and 14.8 +/- 2.3 ms to the anterior tibial muscles. Central motor conduction velocities were 40.7 +/- 5.2 and 55.5 +/- 7.6 m/s, respectively. This showed that conduction in the central fibers to the external anal sphincter was significantly slower than in those to the anterior tibial muscle. We conclude 1) that magnetoelectric stimulation allows differentiation between central and peripheral portions of the motor innervation of the pelvic floor, and 2) that central motor pathways innervating the pelvic floor differ significantly in their physiological properties from those innervating limb muscles.

Influence of Magnetic Resonance Imaging on Evoked Potentials and Nerve Conduction Velocities in Humans

The authors investigated the influence of a 1.0-T magnetic field of a magnetic resonance (MR) imaging device, as well as the possible effects of the changing magnetic field and the RF field, on somatosensory, visual, and auditory evoked potentials and on peripheral nerve conduction velocities. The neural potentials outside and inside the static magnetic field were recorded before and after MR imaging. The measured latencies before and after MR imaging were within the normal range for healthy volunteers. The magnetic field did not significantly alter central or peripheral conduction velocities.