Hemispheric modulatory influences on skin resistance response latency: unilateral stimulation,bilateral recording

In order to evaluate the bilateral asymmetries in evoked electrodermal activity (EDA) and the use of EDA parameters as indices of relative hemispheric activation, skin resistance level (SRL), skin resistance response (SRR), and the SRR latency (L) were examined in 25 right-handed male subjects. We used bilateral recording with a unilateral stimulation (auditory click/patellar tendon tap) to assess the asymmetries of EDA variables related to the side of stimulation and to handedness. Although no significant asymmetry in C = SRRmax/SRL ratio was found, significant differences in latency were observed. Ipsilateral responses were 100 ms faster than contralateral responses for auditory stimulus, a result that can be explained in terms of contralateral delay of neuronal communication on EDA-l pathway. Response latency to reflex-motor activation was 60-100 ms shorter in the dominant hand, regardless of the stimulation site used. This result indicates that the reaction time of the EDA-2 pathway of the left hemisphere was shorter than the right for right-handed subjects. It is concluded that there is hemispheric asymmetry on EDA-2 pathway and that this asymmetry appears to be dependent on the preferred dexterity. These results have implications for the influence of both central and peripheral factors on EDA laterality and principally on laterality of response amplitude. Further, there is no single cortical mechanism modulating the asymmetries in the latency of this response.     

HEMISPHERIC MODULATORY INFLUENCE ON SKIN RESISTANCE RESPONSE LATENCY: UNILATERAL STIMULATION,BILATERAL RECORDING

In order to evaluate the bilateral asymmetries in evoked electrodermal activity (EDA) and the use of EDA parameters as indices of relative hemispheric activation, skin resistance level (SRL), skin resistance response (SRR), and the SRR latency (L) were examined in 25 right-handed male subjects. We used bilateral recording with a unilateral stimulation (auditory click/patellar tendon tap) to assess the asymmetries of EDA variables related to the side of stimulation and to handedness. Although no significant asymmetry in C = SRRmax/SRL ratio was found, significant differences in latency were observed. Ipsilateral responses were 100 ms faster than contralateral responses for auditory stimulus, a result that can be explained in terms of contralateral delay of neuronal communication on EDA-l pathway. Response latency to reflex-motor activation was 60-100 ms shorter in the dominant hand, regardless of the stimulation site used. This result indicates that the reaction time of the EDA-2 pathway of the left hemisphere was shorter than the right for right-handed subjects. It is concluded that there is hemispheric asymmetry on EDA-2 pathway and that this asymmetry appears to be dependent on the preferred dexterity. These results have implications for the influence of both central and peripheral factors on EDA laterality and principally on laterality of response amplitude. Further, there is no single cortical mechanism modulating the asymmetries in the latency of this response.     

Sympathetic skin response and cardiovascular autonomic function tests in Parkinson's disease and multiple system atrophy with autonomic failure.

The relationship between sympathetic skin response (SSR) and cardiovascular autonomic function tests (CVTs) was investigated in 15 patients with idiopathic Parkinson's disease (PD), 15 patients with clinical evidence of multiple system atrophy (MSA) with autonomic failure, and in 15 healthy control subjects. SSR was elicited by electrical stimulation of the right and left median nerves and simultaneously recorded on the palms of both hands. CVTs included the following sympathetic and parasympathetic tests: orthostatism, head-up tilt, cold pressor test, deep breathing, Valsalva maneuver, and hyperventilation. The SSR was normal in all patients with PD and control subjects but was abnormal or absent in all patients with MSA. For patients with MSA, SSR latency was significantly longer and amplitude was significantly smaller than that of patients with PD and control subjects. For patients with PD, SSR did not differ from that of control subjects. In these patients, SSR latency was significantly longer and SSR amplitude was smaller when the side with more marked motor symptoms was stimulated, both ipsilaterally and contralaterally to the side of stimulation. A statistically significant difference in SSR latencies and amplitudes was found between patients with PD and control subjects only when motor asymmetries were considered. CVTs showed severe sympathetic and parasympathetic hypofunction in patients with MSA, but not in patients with PD or control subjects. No correlation was found between SSR and CVTs that assess sympathetic function in patients and control subjects. SSR is indicated as an additional test for the evaluation of sympathetic degeneration in patients with MSA.     

Neurophysiologic studies of sensory gating in schizophrenia: Comparison of auditory and visual responses

Gating of visual and auditory evoked responses was assessed in chronic schizophrenic patients treated with neuroleptic drugs. Middle latency components of the visual evoked response (N90-P130) were recorded at the occiput after flash stimulus. Possible inhibitory mechanisms of sensory gating were assessed in a conditioning-testing paradigm by measuring the change in amplitude of response to a second stimulus, relative to the response to the first stimulus. Simultaneous electrooculograms were recorded to detect contamination of recordings by eye movement. Neither schizophrenic patients nor normal control subjects demonstrated significant suppression of visual evoked responses in the conditioning-testing paradigm. These results differed markedly from similar measurements of a middle latency component of the auditory evoked response (P50) recorded using the same conditioning-testing paradigm in these subjects. Normal controls showed significant decrements of the P50 response to the second auditory stimulus (mean decrement over 80%), whereas schizophrenic patients failed to show a significant decrement (mean less than 40%). This finding for auditory evoked responses replicated previous studies of normal and schizophrenic subjects. Multiple conditioning stimuli were substituted for the single conditioning stimulus used previously in an attempt to enhance gating of auditory responses, but suppression of the P50 test response did not increase in either normal or schizophrenics.     

Baroreflexes in patients with diabetes mellitus

We evaluated baroreflexes in 58 diabetic and 15 control subjects by determining the latency of response between the end of a Valsalva maneuver (VM) and points on the resultant blood pressure and heart rate (HR) response curves. Prolonged latencies indicative of sympathetic dysfunction were demonstrated in 44% to 88% of diabetic subjects. The results challenge the view that sympathetic dysfunction cannot be detected before parasympathetic abnormalities are manifest. Baroreflex latencies reflected sympathetic dysfunction early in the course of diabetes, sometimes in patients with normal HR responses to deep breathing and to a VM.     

Multisensory convergence at human temporo-parietal junction - epicortical recording of evoked responses.

OBJECTIVE: Previous lesion studies in patients and functional imaging studies in normal subjects have led to the notion that the temporo-parietal junction (TPJ) has an integrative function for multisensory inputs. However, its electrophysiological properties such as response latencies and distributions of responses to various stimulus modalities in humans have not been fully investigated. The aim of the study is to clarify this issue. METHODS: We recorded evoked potentials to different kinds of sensory stimuli including somatosensory, auditory and visual modalities in 6 patients with intractable partial epilepsy, who underwent chronic implantation of subdural electrodes in TPJ for presurgical evaluation. RESULTS: In 5 out of 6 subjects, at least one electrode located in TPJ for each subject showed a maximum somatosensory evoked response commonly to electric, passive joint motion and pain stimuli. These electrodes showed the maximum responses also to tone stimuli in all of 4 subjects studied, and to visual motion stimuli in 3 out of 5 subjects studied. The polarity was consistent regardless of the stimulus modality within each individual subject, although the anatomical location, polarity and latency varied among subjects. CONCLUSIONS: A small area in TPJ for each individual subject receives sensory information of multiple modalities possibly coming from different receptive sites, although the electrophysiological properties of the responses may vary among subjects. Significance: We confirmed the convergence of somatosensory, auditory and visual evoked responses at human TPJ.     

Skin nerve sympathetic activity reflex latency in Parkinson''s disease

Using a microneurographic method, skin nerve sympathetic activity (SSA) reflex latency was measured in 16 patients suffering from idiopathic Parkinson's disease (PD) and 11 age-matched normal subjects. The mean latency in patients with PD was significantly delayed (0.821 s, p less than 0.01), when compared with that in normal subjects (0.676 s). Reflex latency showed a significant positive linear correlation with arm length. By determining the SSA reflex latency, conduction velocities in post-ganglionic skin sympathetic nerve were measured indirectly. Averaged conduction velocities in PD and normal subjects, 1.76 m/s and 1.86 m/s, respectively, did not differ significantly (p greater than 0.1). This data suggests that the reflex pathway of SSA is disturbed in patients with PD and that the increased reflex latency is caused by a central/preganglionic delay.     

Suppressed sympathetic skin response in Parkinson disease

The sympathetic skin response (SSR) was used to evaluate sympathetic sudomotor activity in Parkinson disease (PD) and the effects of antiparkinsonian medication on the disease. We recorded SSRs to electric and auditory stimulation in 58 untreated patients with PD and in 20 healthy controls. In addition to amplitude and latency measurements, we examined the number of SSRs evoked by a single stimulus and the response adaptation after repetitive stimuli. The patients with PD subsequently were randomized for administration of levodopa/carbidopa (n=19), bromocriptine (n=20), or selegiline (n=19) as their initial treatment. The measurement were repeated after 6 months of medication and after a washout period. SSR amplitudes were significantly lower in patients with PD than in the control subjects at baseline. The amplitude reduction was more pronounced in patients with high Unified Parkinson's Disease Rating Scale scores, in those with high tremor scores, and in those with PD symptoms that had lasted more than 1 year. The levodopa/carbidopa and bromocriptine treatments did not influence SSRs, although selegiline slightly decreased the amplitude. The synchronous responses after a single stimulus were often repetitive in the patients with PD than in the controls, although the response adaptation tendencies were similar. In conclusion, the degenerative process in PD involves the sudomotor system as reflected by the progressive suppression of SSR amplitudes with a correlation to PD symptom duration and clinical disability, whereas PD medications seems to have only minor effects. The changes in amplitude and the repetitiveness of SSRs with normal adaptation may be caused by deficits at several levels of the SSR reflex arch.     

The mismatch negativity and the P3a components of the auditory event-related potentials in autistic low-functioning subjects.

OBJECTIVE: In order to understand better the psychophysiological basis of auditory processing abnormalities in autism, we decided to study two automatic components of the auditory event-related potentials (ERPs): the mismatch negativity (MMN)--a component of the ERP which is recorded when, during repetitive auditory stimulation, rare changes are introduced--and the novelty-related P3a which is recorded as a response to unexpected novel events occurring in a sequence of repetitive stimuli. METHODS: Ten male subjects, mean age 12.3 years (SD 4.95), affected by autism and mental retardation were admitted to this study. All patients were also mentally retarded. Ten normal male subjects, mean age 12.2 years (SD 3.94), were used as controls. Auditory evoked potentials were recorded from 19 scalp electrodes (10-20 system), and stimuli were presented in sequences consisting of 2000 tones (70 dB, ISI=800 ms). Three types of stimuli were presented: (1) standard stimuli (1000 Hz tones, 80% of total stimuli), (2) deviant stimuli (1300 Hz tones, 10% of total stimuli), and (3) novel stimuli (complex and non-monotonal, 10% of total stimuli). To quantify the MMN, the evoked response to the standard tones was subtracted from the corresponding deviant stimulus response and its amplitude and latency at peak were measured over Fz, Cz and Pz; similarly, the P3a component of the ERP was obtained by subtracting the response to the standard tone from that to the novel stimuli and its amplitude and latency at peak were measured over Fz, Cz and Pz. Also, the amplitude and latency at peak for the N1 component of the auditory evoked potential obtained with the standard stimuli were measured over Fz, Cz and Pz. The correlation between age and MMN and P3a amplitude was also analyzed. RESULTS: N1 showed significantly shorter latencies in the autistic groups. MMN elicited by deviant stimuli, but not that elicited by novel stimuli, was found to be significantly larger in autistic children than in normal controls. P3a showed higher amplitude in autistic subjects than in normal controls during childhood; the opposite was observed during young adulthood. DISCUSSION: Our findings indicate that significant changes in ERPs can also be seen in non-cooperative individuals with autism and mental retardation, which might be different from the changes already reported for high-functioning autistic subjects and deserve further insight. These changes show developmental modifications that should be taken into consideration when analyzing data from autistic subjects.     

P3 after acoustic and somatosensory stimulation in patients with Huntington disease]

Sixteen Huntington patients (HD) (mean age 43.7 years) were studied and compared to 12 risk people for Huntington disease (HR) (mean age 31.2 years) and 25 normal people (mean age 33.2 years). A simple auditory or somatosensory paradigm was used requiring counting of the rare target stimulus. For the normal subjects, most of the recordings showed a slightly earlier latency for the P3 component of the ERPs with the auditory paradigm (P3A). For the HD, a clear P3 was observed in both modalities in 8 patients, in 5 cases no P3 for both stimuli and in 3 cases no P3 for the somatosensory paradigm (P3S) only. The mean value of the P3A latencies was increased compared to the normal control group and after the age effect correction. The mean value of the P3S is significantly more increased compared to the normal group and the "expected" value, according the P3A latencies. This dissociation is constant in all HD when the P3S is recorded and could be due to the fact that the endogenous component is also related to the stimulus modality (increased difficulty and/or subclinical abnormality in the somatosensory modality).     

Quantitative measures of sympathetic skin response in diabetes: relation to sudomotor and neurological function.

The sympathetic skin response (SSR) at the foot to a deep inspiration was measured in 68 randomly selected diabetic patients and 46 age matched normal subjects and compared with other quantitative measures of neurological and sudomotor function. SSR was obtained in all but three diabetic patients. The upper limit of normal for the onset latency was 2202 ms and the lower limit for the amplitude of the first wave 92 microV. Ten diabetic patients had measurable but prolonged latencies, and 11 had measurable but low amplitudes. There were no significant associations between latency, height, and age, but in insulin dependent patients there was a significant diminution of response amplitude with increasing duration of diabetes. Latency was weakly associated with Marstock thermal thresholds, respiratory RR variation, and common peroneal nerve conduction velocity. SSR amplitude was associated with the density of pilocarpine activatable sweatspots in the same region of the foot. Patients with abnormal latencies were significantly older and had reduced thermal sensation than those with normal latencies. Median coefficients of variation for repeat testing in diabetic patients were 9% for latency and 13% for amplitude. The test is objective and reproducible, but latency measurements reflect conduction in a long multineuronal pathway and are not purely a measure of peripheral C fibre function; amplitude measurements reflect the density of spontaneously activable sweat glands and are therefore a valid measure of peripheral sympathetic activity, though they depend more on temperature than do latencies (mean change over the range 32-34 degrees C; 8.5% degrees C for amplitude, -2.5%/degrees C for latency).     

The influence of external timing cues upon the rhythm of voluntary movements in Parkinson''s disease.

The ability of patients with Parkinson's disease (PD) and healthy subjects to synchronise finger tapping, produced by rhythmic wrist movements, with auditory signals of target frequencies (range 1-5 Hz) and to sustain such rhythms following sudden withdrawal of auditory cues was studied. Healthy subjects were able, in the presence of auditory cues, to duplicate target frequencies accurately over the range investigated both in terms of mean tapping rate and in regularity of tapping. PD patients were less accurate under these conditions and on average tended to tap too rapidly at the lower (1-3 Hz) target frequencies and too slowly at the highest (5 Hz) target frequency. In addition, the variability of their tapping rhythms was generally greater. Healthy subjects were able to sustain tapping rhythms well following suppression of auditory signals. By contrast, withdrawal of external timing cues resulted in marked impairment of the patients' rhythm generation. At lower frequency targets (1-3 Hz) patients' tapping rates increased over rates which were already elevated in the presence of external cues. Conversely, at higher target frequencies (4-5 Hz), the average tapping rate tended to decline further from previously depressed levels. The accuracy of almost all patients fell outside the normal range. Two patterns of tapping errors were found. The first was hastening of tapping which was most evident at intermediate target frequencies. The second was faltering which occurred mainly at the higher target frequencies. These forms of behaviour may result from inherent abnormalities of internal rhythm generation since they occurred both in the presence and absence of external timing signals. Overall, our findings are consistent with the view that the basal ganglia have a role in the internal cueing of repetitive voluntary movements.     

Event-related potentials in response to 3-D auditory stimuli

To evaluate auditory spatial cognitive function, age correlations for event-related potentials (ERPs) in response to auditory stimuli with a Doppler effect were studied in normal children. A sound with a Doppler effect is perceived as a moving audio image. A total of 99 normal subjects (age range, 4–21 years) were tested. In the task-relevant oddball paradigm, P300 and key-press reaction time were elicited using auditory stimuli (1000 Hz fixed and enlarged tones with a Doppler effect). From the age of 4 years, the P300 latency for the enlarged tone with a Doppler effect shortened more rapidly with age than did the P300 latency for tone-pips, and the latencies for the different conditions became similar towards the late teens. The P300 of auditory stimuli with a Doppler effect may be used to evaluate auditory spatial cognitive function in children.     

Auditory and visual event-related perturbations in the 40 Hz auditory steady-state response.

The effects of salient auditory and visual 'foreground' stimuli on responses to 'background' probe stimuli were investigated. The foreground stimuli were given at long and aperiodic intervals and required a discriminative judgment. Simultaneously, evoked potentials were obtained in response to background probe auditory stimuli presented in a continuous train at about 40/sec. The 40 Hz steady-state rhythm (SSR) evoked under such conditions was extracted using digital averaging and filtering techniques and examined continuously for evidence of change in latency or amplitude during the period surrounding the foreground stimulus. Within the first 200-300 msec after the onset of an acoustic foreground stimulus the latencies of individual peaks in the rhythm were momentarily reduced by a mean of 5.5 msec. A shift in the 40 Hz rhythm was also seen following visual foreground stimuli, although the shift was about one-third that following acoustic stimuli. A latency shift of comparable magnitude was not produced by deliberate manipulation of intensity or signal-to-noise ratio of the stimuli used to evoke the rhythm. The latency shift response is discussed in terms of a transient period of sensory facilitation during orienting or alerting associated with the foreground stimuli.     

Adductor T reflex abnormalities in patients with decreased patellar reflexes

The adductor reflex (AR) is a tendon reflex that has various features that differ from other tendon reflexes. This reflex was tested in different disorders presenting with diminished patellar reflexes such as diabetic lumbosacral radiculoplexus neuropathy (DLRPN), L2–L4 radiculopathy, and distal symmetric diabetic neuropathy (diabetic PNP). The AR and crossed‐AR (elicited by tapping the contralateral patellar tendon) were recorded using concentric needle electrodes. Additionally, the patellar T reflex (vm‐TR) and vastus medialis H reflex (vm‐HR) were recorded using surface electrodes. AR was recorded in only one out of eight patients with DLRPN, but it was recorded in 21 out of 22 patients with L2–L4 radiculopathy (95.5%). Of these reflexes, only AR showed prolonged latency in the L2–L4 radiculopathy group. The latencies of AR, vm‐TR, and vm‐HR were prolonged in patients with diabetic PNP. We conclude that AR can be useful in the differential diagnosis of some lower motor neuron disorders that present with patellar reflex disturbance. Muscle Nerve 40: 264–270, 2009     

Visual-evoked potentials to onset of chromatic red-green and blue-yellow gratings in Parkinson's disease never treated with L-dopa.

The differential dysfunction of chromatic and achromatic visual pathways in early Parkinson's disease (PD) was evaluated by means of visual-evoked potentials (VEPs) recorded in 12 patients (mean age 60.1 +/- 8.3 years; range 46 to 74 years) in the early stages of PD and not yet undergoing treatment with L-dopa, and in 12 age-matched controls. Visual stimuli were full-field (14 deg) equiluminant red-green (R-G), blue-yellow (B-Y), and black-white (B-W) sinusoidal gratings of two cycles per degree, presented in onset (300 milliseconds)--offset (700 milliseconds) mode, at two contrast (K) levels (90% and 25%). The VEP mean latencies were significantly more delayed in PD patients than in controls for chromatic than for luminance stimuli, in particular for B-Y stimuli of low contrast (K90%: B-W = 6.6 milliseconds, R-G = 3.34 milliseconds, B-Y = 15.48 milliseconds; K25%: B-W = 7.8 milliseconds, R-G = 14.8 milliseconds, B-Y = 28.9). Latencies of chromatic VEPs were more variable that achromatic VEP latencies in both normal subjects and PD patients. Therefore, the frequency of latency abnormalities (within 30%) was not significantly different for the three visual stimuli. Our results show that, in addition to achromatic VEPs, chromatic VEPs are impaired in early PD patients not yet undergoing L-dopa therapy, indicating an acquired color deficiency in these patients. The greater delay for the B-Y VEPs suggests a higher vulnerability of visual blue-cone pathway in the early stages of the disease. However, the overall sensitivity of chromatic VEPs in detecting early visual impairment in PD is comparable with that of achromatic VEPs.     

Human short-latency auditory responses obtained by cross-correlation

Short-latency auditory responses were obtained by cross-correlation of continuous, pseudorandom noise stimuli with averaged scalp potentials from adults with normal hearing. Responses were recorded for spectrum levels of 14-74 dB for noise bandwidths from 800 to 6000 Hz. At the lowest intensity level of broadband noise, all 10 subjects showed replicable cross-correlation functions (CCFs), which were characterized by prominent positive peaks at delays (latencies) of 5-7 msec. Male subjects exhibited longer delays than females. Delay (latency) increased with decreasing stimulus intensity. Very early responses (less than 2 msec) attributable to cochlear microphonic, which were prominent in earlier work on guinea pigs, were not well seen in these human data. CCFs for responses to band-limited stimuli and off-line derivation of band-limited CCFs for responses evoked by broadband stimuli both showed that this technique is most sensitive to frequency-following behavior at low frequencies (less than 800 Hz). However, definite phase-locked responses to even the highest passband (3100-6200 Hz) were seen. These results support the use of the CCF technique as an efficient method of frequency-specific assessment of the auditory system.     

Temporal characteristics of tapping responses in healthy subjects and in patients who sustained cerebrovascular accident

Tapping responses were recorded in a group of patients who sustained lesions from cerebrovascular accidents and from an age-matched group of healthy subjects. In each experiment the stimuli were an auditory signal, a flash, or a light touch on the arm, delivered either at random intervals or at fixed time intervals of 1, 2, 3, or 4 s. The tapping response was done with each hand separately (first experiment) or with each hand alternately (second experiment). Healthy subjects, 'predicted' the stimuli (response time less than 150 ms), when the 'preferred' fixed time interval was used. One group of patients (n = 3), did not predict the stimuli at the preferred fixed intervals when tapping was done with the hand related to the involved hemisphere. The second group of patients (n = 3) did not predict the stimuli when tapping was done with either hand.     

Sensory gating-out and gating-in in normal and schizophrenic participants

In contrast to sensory gating, the brain's ability to re-respond to relevant stimuli and the potential differences between healthy and schizophrenic participants have not been studied in great detail. Here, we explore what auditory paradigms are useful to measure this re-responding ability. Evoked potentials (EPs) were obtained from the Cz channel using 3 paired stimulus paradigms (pairs with equal stimuli {PE}, the second stimulus being lower {PL} or higher {PH} in frequency) and 2 short-train paradigms in which 5 identical stimuli were followed by a lower frequency stimulus (train lower {TL}) or higher frequency stimulus (train higher {TH}). Data were collected from 17 healthy control participants (NC) and 17 age and gender-matched patients with schizophrenia (SZ). Up to 4 data sets obtained on 4 different days were available for each participant. Ensemble averages were computed for each session, from which the P50, N100, and P200 latencies and amplitudes were obtained. No significant differences in amplitude or latency of the various EP components were found between the responses to the second stimulus obtained with the 5 paradigms. Neither did the responses to the fifth and sixth stimuli differ for the TL and TH paradigm, with the exception of the N100 latency of the fifth stimulus, which was longer for TH than TL for NC. Healthy participants had larger amplitudes and shorter latencies than the patients with schizophrenia for the responses to the first stimuli, with the latency differences continuing for the fifth and sixth response. Also, the amplitude and latency of the first response was larger than for the second response in both populations. In conclusion, none of the paradigms studied here, with the employed parameters, are useful to measure the re-responding ability of the brain. Also, the shorter latencies for the repeated stimulus suggest that the neural mechanism underlying attenuation of repeated stimuli is of a facilitating nature.     

The effect of posture on the normal and pathological auditory startle reflex.

The effect of posture on the EMG pattern of the normal auditory startle reflex was investigated. The startle response to an unexpected auditory tone was studied in eleven normal subjects when standing, and in six normal subjects when sitting relaxed or tonically plantar flexing both feet. Reflex EMG activity was recorded in the tibialis anterior and soleus about twice as frequently when standing, than when sitting relaxed. In addition, the median latencies to onset of reflex EMG activity in the tibialis anterior and soleus were about 40 and 60 ms shorter during standing, than when sitting relaxed. No short latency EMG activity was recorded in the calf muscles during tonic plantar flexion of the feet, while sitting. The effect of posture on the EMG pattern of the pathological auditory startle reflex was studied in five patients with hyperekplexia. In three patients the latency to onset of reflex EMG activity in the tibialis anterior was shorter when standing, than when sitting relaxed. The EMG pattern of the reflex response to sound was studied in detail in two of these patients and consisted of up to three successive components. The expression of each EMG component depended on the postural set of the limbs. In particular, a distinct short latency component was found in posturally important muscles following auditory stimulation. This short latency component was not recorded when sitting relaxed. It is concluded that the EMG pattern of the physiological and pathological auditory startle response is not fixed, but may change with the postural stance of the body. This finding supports the theory that the normal startle reflex and the abnormal startle reflex in hyperekplexia have a common brainstem origin.