Magnetic auditory evoked fields: interhemispheric asymmetry

Magnetic auditory evoked fields (MAEFs) were recorded from the right (11 subjects) and the left (7 subjects) hemisphere following 128 click stimuli delivered to contralateral, ipsilateral and both (bilateral) ears. Right hemisphere MAEFs were of higher amplitude following contralateral, compared to ipsilateral, stimulation in 9 of 11 subjects; mean contralateral response amplitude was 135 +/- 33% (S.D) of ipsilateral response amplitude. Left hemisphere MAEFs were of higher amplitude following contralateral stimulation in 7 of 7 subjects; mean contralateral response amplitude was 145 +/- 44% of ipsilateral response amplitude. These observations are compatible with evidence that a majority of centripetal auditory input is crossed, and/or that contralateral auditory stimulation activates a larger area of cortex than does ipsilateral stimulation.     

R-R interval variation and the sympathetic skin response in the assessment of the autonomic nervous system in leprosy patients

OBJECTIVES: The aim of this study was to evaluate possible autonomic nervous system (ANS) dysfunction in leprosy patients with the sympathetic skin response (SSR) and the heart rate (R-R) interval variation (RRIV) measurements which are easy and reliable methods for evaluation of autonomic functions. MATERIAL AND METHODS: We studied 37 lepromatous leprosy patients (mean age: 38 +/- 17 years, range 23-62 years, 20 females and 17 males) and 35 age-matched healthy subjects (mean age: 34.19 +/- 12.74 years, range 24-48 years, 20 females and 15 males). Non-invasive bedside tests (orthostatic test, Valsalva ratio), R-R interval variation (RRIV) during at rest and deep breathing, the SSR latency and amplitude from both palms, and nerve conduction parameters were studied in all the subjects. RESULTS: The mean values of RRIV in leprosy patients during at rest [mean RRIV in patients, 17.42 +/- 8.64% vs controls, 22.71 +/- 3.77% (P < 0.05)] and during deep breathing [mean RRIV in patients, 21.64 +/- 9.08% vs controls, 30.70 +/- 5.99% (P < 0.005)] was significantly lower compared with the controls. The mean latency of SSR in leprosy patients [mean SSR latency in patients, 1.72 +/- 1.13 ms vs controls, 1.30 +/- 0.41 ms (P < 0.05)] was significantly prolonged compared with the controls. The mean amplitude of SSR in leprosy patients [mean SSR amplitude in patients, 0.54 +/- 0.57 microV vs controls, 1.02 +/- 0.56 microV (P > 0.05)] was smaller compared with the controls, but this difference was not significant. The mean Valsalva ratio in leprosy patients [mean in patients, 1.11 +/- 0.13 vs controls, 1.16 +/- 0.07 (P > 0.05)] was smaller compared with the controls, but not statistically significant. The mean difference of systolic and diastolic blood pressure between supine rest and during standing in leprosy patients were higher compared with the controls [mean systolic pressure in patients, 7 +/- 6 mmHg vs controls, 6 +/- 8 mmHg (P > 0.05) and mean diastolic pressure in patients, 3 +/- 3 mmHg vs controls, 3 +/- 2 mmHg (P > 0.05)], but they did not reach statistical significance. Furthermore, lower RRIV and the prolonged SSR latencies in leprosy patients were closely correlated to some parameters of sensorimotor nerve conduction and each other [median nerve distal latency and RRIV, r = -0.67 (P < 0.05), ulnar nerve distal latency and RRIV, r = -0.59 (P < 0.05), RRIV and SSR latency, r = -0.33 (P < 0.02)]. These data indicate that leprosy patients have the functional abnormalities of ANS. CONCLUSION: We conclude that combined use of these two tests, both of which can be easily and rapidly performed in the electromyogram (EMG) laboratory using standard equipment, allows separate testing of parasympathetic and sympathetic function, and are very sensitive methods in assessing of ANS function in peripheral neuropathy in leprosy patients.     

Characteristics of habituation of the sympathetic skin response to repeated electrical stimuli in man.

OBJECTIVES: To study the effect of repeating electrical peripheral nerve stimulation on latency, duration and amplitude of the sympathetic skin response (SSR). METHODS: SSRs were elicited in all limbs by median and peroneal nerves stimuli. In 10 subjects, 20 stimuli were applied at random time intervals (15-20 s). Another test was performed in 7 subjects using the same protocol, but switching the stimulation site every 5 or 10 stimuli without warning. RESULTS: The mean amplitude of right palmar response to right peroneal nerve stimulation decreased from 5.05+/-0.76 (SEM) mV at the first stimulus to 1.23+/-0.42 mV at the 20th stimulus (P<0.001). The latency did not change significantly (1473+/-82 to 1550+/-90 ms, P>0.1), while the duration increased (1872+/-356 to 3170+/-681 ms, P<0.001). Stimulation and recording at other sites showed similar trends. Changing the stimulation site failed to alter the adaptation process in terms of amplitude, latency or duration. CONCLUSIONS: Changes in amplitude and duration of the SSRs to repeated electrical stimuli can occur in presence of constant latency and appear to be independent of the source of sensory input. Peripheral sweat gland mechanisms may be involved in the loss of amplitude and increase in duration of the SSR during habituation.     

Sympathetic skin response and heart rate variability in patients with Huntington disease.

OBJECTIVE: To examine the autonomic nervous system functions in patients with Huntington disease. BACKGROUND: Although patients with Huntington disease frequently experience vegetative symptoms, it is not clear if there is dysfunction of the autonomic nervous system. METHODS: Sympathetic skin response (SSR) latency and amplitude from both palms and soles and R-R (heart rate) interval variation (RRIV) at rest and during the Valsalva maneuver were examined in 22 patients and 21 age-matched controls. Unified Huntington's Disease Rating Scale scores were determined in all the patients. RESULTS: Our data are reported as means +/- SEMs. The SSR latencies in patients (mean palm latency, 1835.8+/-110.7 milliseconds; mean sole latency, 2625.3+/-226.9 milliseconds) were prolonged compared with controls (mean palm latency, 1359.5+/-28 milliseconds [P<.01]); mean sole latency, 2038.1+/-44.9 milliseconds [P<.01]) and amplitudes in patients (mean amplitude, 1063.1+/-237.7 microV) were smaller compared with controls (mean amplitude, 1846.3+/-251.2 microV [P<.05]). The RRIV in patients both at rest (mean RRIV in patients, 3.7%+/-0.4% vs. controls, 9.7%+/-0.6% [P<.01]) and during the Valsalva maneuver (mean RRIV in patients, 6.3%+/-1.6% vs. controls, 14.5%+/-1.2% [P<.01]) was lower compared with controls. Furthermore, the prolonged SSR latencies, smaller amplitudes, and lower RRIV in patients compared with controls closely correlated with the various components of the Unified Huntington's Disease Rating Scale scores (total behavior score and SSR latency, R = 0.6 [P<.01]; total behavior score and SSR amplitude, R = -0.5 [P<.05]; total behavior score and RRIV, R = -0.4 [P<.05]; verbal fluency and SSR latency, R = -0.5 [P<.05]; verbal fluency and SSR amplitude, R = 0.5 [P<.05], verbal fluency and RRIV, R = 0.5 [P<.05]; total functional capacity and SSR latency, R = -0.6 [P<.01]; total functional capacity and SSR amplitude, R = 0.5 [P<.05]). CONCLUSION: These results suggest that there is autonomic nervous system dysfunction in patients with Huntington disease.     

Organization of auditory cortical areas in man.

Average responses to clicks were recorded from the exposed human cortex of 19 adult patients during operation for the treatment of intracranial diseases. Auditory evoked responses were obtained from two areas. Short latency potentials were recorded on the superior surface of the temporal lobe corresponding to the transverse temporal gyri. These responses consisted of two positive waves P1 and P2 separated by a negative wave N1. P1 had a mean latency of 14-7+/-1-5 ms, N1 a mean latency of 19-1+/-2-6 ms and P2 a mean latency of 32-2+/-4-1 ms. Responses to stimulation of the contralateral ear were of higher amplitude than responses to stimulation of the ipsilateral ear. Responses of smaller amplitude and longer latency were obtained from the superior temporal gyrus and the upper lip of the sylvian fissure. These responses had a mean peak latency for P1 of 40-2+/-2-6 ms, for N1 of 62-5+/-12-5 ms and for P2 of 97-7+/-17-2 ms. It is concluded that the cortical auditory region of man may be subdivided in two major areas: an area on the supratemporal plane representing the primary auditory area or A1 and a region surrounding A1 which perhaps comprises two areas, one on the superior temporal gyrus and one on the upper bank of the sylvian fissure including frontal and parietal operculi.     

Influence of GAA expansion size and disease duration on central nervous system impairment in Friedreich's ataxia: contribution to the understanding of the pathophysiology of the disease.

OBJECTIVE: To verify if GAA expansion size could account for the severity of the central nervous system involvement in Friedreich's ataxia (FA). METHODS: Retrospective study of 52 FA patients (mean age 26.9+/-12.1 years; mean disease duration 10.6+/-7.6 years) homozygous for GAA expansion. Median nerve somatosensory evoked potentials (SSEPs) were available in 36 FA patients, upper limb motor evoked potentials (MEPs) to transcranial magnetic stimulation in 32, brainstem auditory evoked potentials (BAEPs) in 24, and visual evoked potentials (VEPs) in 34. N20, P100, MEP amplitude, SSEP and MEP central conduction time (CCT and CMCT), P100 latency and I-III and I-V interpeak latency, and a BAEP abnormality score were correlated with disease duration and GAA expansion size on the shorter (GAA1) and larger (GAA2) allele in each pair. RESULTS: The GAA1 size inversely correlated with the N20 amplitude (r = -0.49; P<0. 01). Disease duration directly correlated with CMCT (r = 0.57; P<0.01) and BAEP score (r = 0.61; P<0.01) and inversely with MEP (r = -0.40; P<0.05) and P100 amplitude (r = -0.39; P<0.05). CONCLUSIONS: Our data suggest that central somatosensory pathway involvement in FA is mainly determined by GAA1 expansion size. Vice versa, degeneration of pyramidal tracts, auditory and visual pathways seems to be a continuing process during the life of FA patients.     

Excitation and inhibition of marginal layer and interstitial interneurons in cat nucleus caudalis by mechanical stimuli

In cats anesthetized with urethane, the caudal medulla was stabilized in preparation for intracellular recording from interstitial neurons in the descending tract of the trigeminal nerve and from neurons in lamina I of nucleus caudalis. Glass micropipets (10-50 M ohms) were advanced from the surface to a maximum depth of 350 micrometer. When DC potential shifts occurred, it was found that mechanical stimuli to the face generated bursts of positive-going spikes, followed in some cases by inhibitory postsynaptic potentials (IPSPs). Subdermal electrical stimulation of the face in each receptive field almost always enabled the same neuron to be driven electrically. Recordings were classified as from primary afferent fibers or from interneurons. Primary fibers had a purely positive spike, with a latency varying by no more than 0.05 msec, and could follow stimulation at 500 Hz. The mean latency for the fibers was 1.87 +/- 0.06 msec (n=75), and their absolute refractory period was 0.42 +/- 0.02 msec (n=36). Recordings were classed as from interneurons if there was an IPSP or the latency was at least 4 msec, with a variation of latency of at lest 0.5 msec. Responses thought to be monosynaptically driven had a mean latency of 2.09 +/0 0.07 msec (n=32) and could follow pairs of stimuli at a mean minimum interval of 0.70 +/- 0.06 msec (n=20). Responses thought to be polysynaptically driven had a mean latency of 7.9 +/- 1.08 msec (n=49) and a mean interstimulus interval of 2.96 +/- 0.84 (n=20). Most responses were generated by brushing the face (n=87), some by pressure on the face (n=25), and a few by pinching the skin of the face (n=6). Interneuron responses were most commonly recorded in the first 200 micrometer of the descending tract, and this position was confirmed by the injection of pontamine sky blue and the examination of frozen sections. The recordings were thought to be from dendrites of marginal and interstitial cells or the somas of interstitial cells. The IPSPs which followed spike potentials could only follow stimuli at 10 Hz or less. The failure appeared to be at a primary afferent synapse upon an inhibitory interneuron. Collision tests between mechanically evoked and electrically evoked responses showed long-lasting inhibition of the response to electrical stimulation after collision. Presynaptic inhibition exerted on the primary afferent excitation was suggested as the explanation.     

Human auditory and somatosensory event-related potentials: effects of response condition and age

In order to develop an experimental paradigm for clinical application of cognitive event-related potentials we have recorded these potentials in a group of 27 healthy Japanese, aged 20-78 years, using all 4 stimulus/response combinations of auditory or somatosensory stimuli requiring a counting or button-press response. In an oddball paradigm we recorded N1 and P2 components to frequent auditory stimuli and P100, N150 and P200 components to frequent somatosensory stimuli. These components were also observed in the target responses for their respective modalities together with N2, P270, P3 and slow-wave components. P3 latency increased linearly with age for all 4 experimental conditions, although this increase was not statistically significant for the somatosensory stimulus/button-press response combination. The latency of P270 also increased significantly with age for the auditory stimulus/button-press response combination but did not do so in either of the counting response conditions. The principal difference between the latencies of ERPs to auditory compared with somatosensory stimuli was that P3 was significantly longer for somatosensory stimulation, although differences in task difficulty may have influenced this finding. With regard to amplitude, N2, P3 and slow-wave were all significantly more positive for somatosensory compared with auditory stimulation. The topography of P3 evoked by somatosensory stimuli was most predominant at central electrodes, whereas the auditory P3 was larger parietally. The button-press response was associated with potentials which were smaller in amplitude and shorter in latency than those associated with the count response. The button-press response had a marked effect on the amplitude of P3 recorded at the vertex and the central electrode contralateral to the moving finger.     

Sympathetic skin response evoked by laser skin stimulation

The objective of this study was to evoke sympathetic skin responses (SSRs) in healthy subjects using laser stimulation and to compare these responses with those induced by conventional electrical stimuli. Twenty healthy subjects were investigated. SSRs were obtained using electrical and laser stimuli delivered to the wrist controlateral to the recording site. The sympathetic sudomotor conduction velocity (SSFCV) was measured in 8 subjects by simultaneously recording the SSR from the hand and the axilla. The latency (L) of the laser-induced SSR (ISSR) was significantly longer than that of the electrically-evoked SSR (eSSR) (mean ISSRL= 1.7 +/- 0.145 ms, mean eSSRL= 1.56 +/- 0.14 ms, p<0.05). The amplitude (A) of the ISSR was lower than the eSSR amplitude (mean ISSRA = 1.31 +/- 0.26 mV, mean eSSRA = 2.59 +/- 0.49 mV, p<0.05). No significant difference between the ISSR and eSSR was observed in either the SSFCV or the variability and reproducibility parameters. Our findings show that SSRs can easily be induced by laser stimuli and that this method shares the technical limitations of conventional eSSRs.     

Electrodermal activity in patients with Parkinson's disease

Peripheral sympathetic activity was investigated in 25 Parkinson's disease (PD) patients and 27 healthy subjects by measuring the skin resistance level (SRL) and skin resistance response (SRR) at the palm of the hand during rest, auditory stimulation and patellar tendon tapping. Blood flow to the hand was also monitored. Normal responses were obtained from all the 27 healthy subjects with both stimuli. All but one of the 25 PD patients responded to sound, six patients failed to respond to patellar tendon tapping and one patient failed to respond to both stimuli. The SSRs (when detectable) of PD patients were always smaller in amplitude than those of normal subjects. It was also observed that while an electrodermal response was present, no vasomotor response could be elicited by either stimulus in some patients. The opposite was true in some other patients. When response latencies were evaluated, it was found that although the mean latency of the SRRs evoked by tendon tapping was shorter than the mean latency of responses to auditory stimuli in normal subjects, this was not the case in PD patients. SRR mean latency to patellar tendon tapping was significantly longer in PD patients compared with that in normal subjects. Mean latencies of responses to auditory stimuli were the same for both normal subjects and patients. The ratio of the SRR amplitude to SRL (i.e. relative change in SRL) during both types of stimulation was significantly smaller in PD patients than in normal subjects. All the above findings were also true when blood flow to the tissue was interrupted briefly. These findings support the conjecture that the abnormal peripheral sympathetic neural responses associated with PD may arise from a functional disorder in the basal ganglia that influence the efferent autonomic pathway, from impairment of the intermediolateral column of the spinal cord, and possibly from cognitive deficits.     

Ca2(+)-dependent adaptive properties in the solitary olfactory receptor cell of the newt

The time-dependent decay of the olfactory receptor potential was analyzed with a solitary cell preparation by using the whole-cell patch clamp technique. During prolonged stimulation by 10 mM N-amylacetate under standard conditions, 17 out of 63 isolated olfactory cells responded with slow depolarization. Of these 17 cells, response amplitudes in 14 cells ('phasic/tonic' response) gradually decayed within 9 s, with a half-decay time of 1.71 +/- 1.10 s (mean +/- S.D.). The relative amplitude (ratio of tonic component to peak amplitude, Vtonic/Vmax) was 0.29 +/- 0.10. The response decay was attributed to the inactivation of the odorant-activated conductance. The recovery after inactivation, which was determined with double pulse experiments, was dependent on the resting interval. The inactivation of the odorant-activated conductance was found to be observed only when the external medium contained Ca2+. In addition, it was found that the odorant-activated conductance was capable of permeating Ca2+ (PCa/PNa = 6.5), and a rise in the internal EGTA concentration (to 50 mM) inhibited the inactivation. These observations suggest that the decay of the olfactory response to prolonged stimulation is mediated by Ca2+ influx.     

Cognitive evoked potentials to anticipated oesophageal stimulus in humans: quantitative assessment of the cognitive aspects of visceral perception

Evoked potential studies provide an objective measure of the neural pathways involved with perception. The effects of cognitive factors, such as anticipation or awareness, on evoked potentials are not known. The aim was to compare the evoked potential response to oesophageal stimulation with the cortical activity associated with anticipation of the same stimulus. In 12 healthy men (23.5 +/- 4 years), oesophageal electrical stimulation (15 mA, 0.2 Hz, 0.2 msec) was applied, and the evoked potentials recorded using scalp electrodes. A computerized model of randomly skipped stimuli (4:1 ratio) was used to separately record the evoked potentials associated with stimulation and those associated with an anticipated stimulus. The electrical stimulus represented the nontarget stimulus and the skipped impulse the target (anticipatory) stimulus. This anticipatory evoked potential was also compared to auditory P300 evoked potentials. Reproducible evoked potentials and auditory P300 responses were elicited in all subjects. Anticipatory evoked potentials (peak latency 282.1 +/- 7.9 msec, amplitude 8.2 +/- 0.7 microV, P < 0.05 vs auditory P300 evoked potential) were obtained with the skipped stimulus. This anticipatory evoked potential was located frontocentrally, while the auditory P300 potential was located in the centro-parietal cortex. The anticipatory evoked potential associated with expectation of an oesophageal stimulus, although of similar latency to that of the auditory P300 evoked response, originates from a different cortical location. The recording of cognitive evoked potentials to an expected oesophageal stimulus depends on attention to, and awareness of, the actual stimulus. Anticipatory evoked potentials to GI stimuli may provide an objective electrophysiological tool for the assessment of the cognitive factors associated with visceral perception.     

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.     

Pattern electroretinography and visual evoked potentials in optic nerve diseases.

BACKGROUND: To evaluate transient pattern electroretinography (PERG) and pattern visual evoked potential (VEP) for the diagnosis, differential diagnosis and follow-up of optic nerve diseases. METHODS: Twenty-nine consecutive patients (14 female, 15 male) with the diagnosis of ischaemic optic neuropathy (n=14) and optic neuritis (n=15) were included in this study. Mean age of the patients with ischaemic optic neuropathy was 63.3+/-3.3 (60-78) years and the mean age of the patients with optic neuritis was 28.3+/-8.4 (19-43) years. In each patient ophthalmological examination and systemic evaluation were done and VEP and PERG were recorded. As a control group, VEP recordings of 35 healthy subjects were included. RESULTS: In the ischaemic optic neuropathy group (group 1), mean VEP amplitude (+/-SD) (1.96+/-0.95 microV) was found to be decreased significantly in the affected eyes in comparison to the control group and the unaffected eyes. The delay in latency (116.3+/-20.14 msec in the affected eyes compared with 101.31+/-6.19 msec in unaffected eyes) was statistically significant when compared with the healthy subjects. In the optic neuritis group (group 2), VEP amplitude was decreased (4.13+/-4.04 microV vs 6.97+/-3.35 microV and 6.97+/-4.43 microV) and latency was increased (122.59+/-20.09 msec vs 101.31+/-6.19 msec and 108.76+/-13.57 msec) in affected eyes significantly in comparison to the unaffected eyes and control group, respectively. Even though there were no significant differences for P50 latency and N95/P50 ratios between affected and unaffected eyes in both groups, N95 amplitude decreased significantly in the affected eyes of the ischaemic optic neuropathy patients and N95 latency was found to be decreased in optic neuritis patients. There was no correlation between VEP and PERG findings in both groups. CONCLUSION: VEP amplitude decreased significantly in ischaemic optic neuropathies while latency delay was more significant in patients with optic neuritis. PERG findings showed decreased N95 amplitude in ischemic optic neuropathy without associated latency changes.     

Sympathetic skin response: normal results in different experimental conditions.

(1) The sympathetic skin response (SSR) is a slow wave, generated in deep layers of the skin, resulting from reflex activation of the sudomotor sympathetic efferent fibres. The aim of this study was to define experimental conditions, best stimulation and recording procedures, and the criteria for validation of the responses. (2) Thirty normal subjects (aged 25-56) were tested. The stimulation was an electrical pulse train applied to the median nerve at the wrist, a binaural tone burst, or both simultaneously. Records were made with surface electrodes on hand and foot contralateral to the stimulated median nerve. (3) Response shape was most often biphasic in feet, biphasic or triphasic in hands. SSR amplitude was 3.1 +/- 1.8 mV in hands, 1.4 +/- 0.8 mV in feet. Normal mean onset latency was 1.5 +/- 0.08 sec for hand response, 2.05 +/- 0.10 sec for foot response. The mean conduction velocity along peripheral sympathetic nerve fibres was 1.40 +/- 0.14 m/sec in lower limbs. (4) Bimodal stimulation (burst + median) provided responses of larger amplitude. The influence of stimulation intensity was also investigated. A decrease in amplitude and lengthening of latencies were observed after 15-20 min of testing. (5) The criteria for validation of responses are discussed. The importance of central processing time in the response delay is pointed out. In good methodological conditions, SSR would appear to be a simple, effective means of assessing sympathetic sudomotor outflow in central and peripheral nervous system disorders.     

Effects of laserneedle stimulation in the external auditory meatus on brainstem and very early auditory evoked potentials in humans

OBJECTIVES: For the first time, brainstem auditory evoked potentials (BAEP) and very early auditory evoked potentials (EAEP) were investigated in 23 volunteers (mean age: 26.5 +/- 3.6 years) under resting conditions and during continuous and frequency modulated (2 Hz) laser stimulation in the external auditory meatus. METHODS: Using a new ear adapter, the outer region of the auditory canal was stimulated with laser light (685 nm, 4 x 30-40 mW, duration: 10 minutes). RESULTS: The EAEPs were significantly changed during continuous (p=0.019), as well as frequency modulated (p=0.014) laser stimulation compared with control measurements. DISCUSSION: Physiologic alterations of inner ear mechanism such as extra-cerebral changes in conductance or stimulation-dependent depolarization processes in extra-cerebral regions of the auditory system could be possible explanations for the significant difference in measurement parameters.     

Electrophysiological observations on the human pudendo-anal reflex.

A reproducible electrophysiological technique is described to determine the latency of reflex contraction of the external anal sphincter in response to stimulation of the dorsal genital nerve: the pudendo-anal reflex. This was studied in 38 asymptomatic control subjects and 20 women with neurogenic faecal incontinence, supplemented by determination of the mean motor unit potential duration (MUPD) of the external anal sphincter and anorectal manometry. The reflex latency in the control group was 38.5 +/- 5.8 (SD) ms and appeared to be independent of age or sex. Three patients with faecal incontinence had absent reflexes; the remainder showed significant prolongation of latency (56 +/- 12.2 SD ms) and diminution of amplitude. MUPD was prolonged in incontinence and showed significant correlation with the corresponding reflex latency determination (tau = 0.56, p less than 0.001). The latency of this polysynaptic spinal reflex hence provides a reliable index of neuropathy of the external anal sphincter.     

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.     

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.     

Neuropeptide-induced cytosolic Ca2+ transients and phosphatidylinositol turnover in cultured human retinal pigment epithelial cells.

Neuropeptide-induced mobilization of cytosolic free Ca2+ concentration ([Ca2+]i) and phosphatidylinositol (PI) turnover in cultured human retinal pigment epithelial (RPE) cells were studied and their temporal relationship was compared. After RPE cells were loaded with fura-2/AM, [Ca2+]i was analyzed using a digital imaging microscopy system. Bombesin-related peptides which include bombesin, neuromedin B, and neuromedin C induced significant [Ca2+]i transients in RPE cells, whereas other neuropeptides, neuropeptide Y, vasoactive intestinal polypeptide (VIP), and substance P were not effective to produce [Ca2+]i transients. The percentage of reactive cells which showed positive [Ca2+]i transients induced by bombesin-related peptides was around 50%. Bombesin (1 microM) showed a peak concentration of 663 +/- 27.0 nM (mean +/- S.E.M., n = 61), neuromedin B (1 microM), 327 +/- 28.7 nM (mean +/- S.E.M., n = 38), and neuromedin C (1 microM), 357 +/- 22.7 nM (mean +/- S.E.M., n = 32). Ca2+ transients occurred within 30 s and lasted less than 5 min after the application of the neuropeptides. Chelation of the extracellular Ca2+ by EGTA significantly shortened the total time of [Ca2+]i transients induced by the above. The measurements of phosphoinositides in RPE cells revealed that neuropeptide-induced PI turnover was as quick as [Ca2+]i transients. Inositol biphosphate (IP2) and inositol triphosphate (IP3) in RPE cells showed transient increases at 15 s after the stimulation by bombesin-related peptides. These data show that changes in [Ca2+]i and PI turnover are directly linked and both are important in the signal transduction system of bombesin-related peptides in RPE cells. The data also suggest that bombesin-related peptides may play some possible roles in RPE cells.