Effect of age on sensory gating of the sleep state-dependent P1/P50 midlatency auditory evoked potential.

The P1/P50 midlatency auditory evoked potential is a sleep state-dependent waveform present during waking and rapid eye movement (REM) sleep and absent during slow-wave sleep. The P50 potential was studied in normal male and female subjects of various ages including post-pubertal adolescents (12-19 yrs), young adults (24-39 yrs), middle-aged adults (40-55 yrs) and older adults (55-78 yrs). There were no statistically significant differences in the mean peak amplitude or mean peak latency of the P50 potential between males and females or between age groups. Using a paired stimulus paradigm, the degree of sensory gating of the P50 potential was tested at three different interstimulus intervals (ISIs), 250, 500 and 1000 msec. There were no statistically significant differences in the sensory gating of the P50 potential between males and females. However, there was a significant decrease in sensory gating of the P50 potential in the adolescent group compared to each of the other age groups at the 250 msec ISI, but not at the 500 or 1000 msec ISI. These results suggest the presence of decreased sensory gating in normal adolescents compared to normal, older age groups.

Reduced sensory gating of the P1 potential in rape victims and combat veterans with posttraumatic stress disorder.

The P1 midlatency auditory evoked potential was studied in female rape victims with Posttraumatic Stress Disorder (PTSD) and compared to an age-matched female control group; and in male combat veterans with PTSD and compared to three groups of age-matched male control subjects. Sensory gating of the P1 potential was determined using a paired click stimulus paradigm in which the stimuli were presented at 250, 500 and 1000 msec interstimulus intervals (ISI). Results showed that sensory gating of the P1 potential was significantly decreased at the 250 msec ISI, and that there was a numerical, but not a statistically significant, decrease in sensory gating at the other intervals tested in both male and female PTSD subjects compared to all control groups. Since the P1 potential may be generated, at least in part, by the reticular activating system, dysregulation of sensory processing by elements of this system may be present in PTSD.

Disinhibition of the sleep state-dependent p1 potential in Parkinson's disease-improvement after pallidotomy.

We previously reported that the P1 or P50 midlatency evoked potential underwent decreased habituation or disinhibition in patients with Parkinson's Disease. This sleep state-dependent response appears to be generated by cholinergic elements of the reticular activating system. We attempted to determine if the decreased habituation or disinhibition of the P1 potential would be altered by bilateral pallidotomy. Twenty-three patients who met inclusion criteria for surgery underwent pre- and post-operative evaluation using a Modified United Parkinson's Disease Rating Scale (UPDRS) and P1 potential recordings. Decreased habituation of the P1 potential was determined using a paired stimulus paradigm in which click stimuli were presented at 250, 500 and 1000 msec interstimulus intervals (ISI). Pre-operatively, patients showed disinhibition of the P1 potential at the 250 msec ISI (60 37% vs. 21 20%) and 500 msec ISI (78 47% vs. 43 31%) compared to age-matched control subjects. Post-operatively, the same patients showed a significant improvement in habituation of the P1 potential at the same ISIs (250 msec 37 21%; 500 msec 43 32%). UPDRS scores for these patients pre-operatively were 59 18 and 24 11 post-operatively, resulting in a significant reduction in symptom severity. We conclude that bilateral pallidotomy resulted in a significant improvement in symptom ratings and reduced the disinhibition of the P1 midlatency evoked response.

Decreased habituation of midlatency auditory evoked responses in Parkinson's disease.

The P1 midlatency auditory evoked potential was studied in patients with Parkinson's disease and compared to that in age-matched controls. Habituation of the potential was determined by using a two-click stimulus paradigm in which the stimuli were presented at 250-, 500-, and 1,000-ms interstimulus intervals. Results showed that habituation of the P1 potential had a statistically significant decrease at the 250-ms and 500-ms interstimulus intervals in patients with Parkinson's disease compared to normal controls. The degree of decreased habituation was found to increase with severity of the disease such that stage 5 patients showed greater decreases in habituation compared to stage 4, as did stage 4 compared to stage 3. These findings may be explained by the presence of a dysregulation of sensory processing, possibly by elements of the reticular activating system, including the pedunculopontine nucleus, in Parkinson's disease.

Combat veterans with posttraumatic stress disorder exhibit decreased habituation of the P1 midlatency auditory evoked potential.

The current study used a paired stimulus paradigm to investigate the P1 midlatency auditory evoked potential in Vietnam combat veterans with posttraumatic stress disorder (PTSD) and three comparison groups: alcohol dependents, combat-exposed normals, and combat-unexposed normals. Compared to each comparison group, PTSD subjects exhibited significantly diminished habituation of the P1 potential. P1 potential habituation within the PTSD group, correlated significantly with intensity of PTSD reexperiencing symptoms, such as trauma-related nightmares and flashbacks. These findings are discussed as consistent with a sensory gating defect at the brainstem level in PTSD, and are further discussed in the context of other psychophysiological measures in PTSD and of P1 potential findings in psychiatric disorders other than PTSD.