Electroencephalography and clinical neurophysiology
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Electroencephalogr Clin Neurophysiol · Feb 1991
The cause of increased pupillary light reflex latencies in diabetic patients: the relationship between pupillary light reflex and visual evoked potential latencies.
In 42 diabetic patients the relationship between the latency of the pupillary light reflex and the pattern reversal visual evoked potential (P100) was examined. Fifty-five percent of diabetic patients had pupillary light reflex latencies above the normal range. In 19% the visual evoked potentials were prolonged when compared to the normal range. ⋯ Increased VEP latencies showed no correlation with signs of cardiovascular autonomic neuropathy. We conclude that the afferent optic pathway can be affected in diabetic patients. However, prolongation of pupillary light reflex latency in diabetic patients is primarily due to an efferent pupillary defect and represents parasympathetic dysfunction.
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Electroencephalogr Clin Neurophysiol · Nov 1990
Effects of hypothermia on short latency somatosensory evoked potentials in humans.
Short latency somatosensory evoked potentials (SSEPs) elicited by median nerve stimulation were monitored in 14 adult patients undergoing cardiac surgery under cardiopulmonary bypass and induced hypothermia. SSEPs were recorded at 1-2 degrees C steps as the body temperature was lowered from 37 degrees C to 20 degrees C to determine temperature-dependent changes. Hypothermia produced increased latencies of the peaks of N10, P14 and N19 components, the prolongation was more severe for the later components so that N10-P14 and P14-N19 interpeak latencies were also prolonged. ⋯ On the other hand, more peripherally generated components, N10 and P14, were more resistant to the effect of hypothermia; P14 was always elicitable at 21 degrees C or above, whereas N10 persisted even below 20 degrees C. The amplitude of SSEP components had a poor correlation with temperature; there was a slight tendency for N10 and P14 to increase and for N19 to decrease with declining temperature. Because incidental hypothermia is common in comatose and anesthetized patients, temperature-related changes must be taken into consideration during SSEP monitoring under these circumstances.
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Electroencephalogr Clin Neurophysiol · Nov 1990
Temperature-dependent hysteresis in somatosensory and auditory evoked potentials.
Fourteen adult patients undergoing open heart surgery under induced hypothermia had median nerve, short-latency somatosensory evoked potentials (SSEPs) recorded during cooling (from 36 degrees C to 19 degrees C) and subsequent rewarming. Similar data on another group of patients who had brain-stem auditory evoked potentials (BAEPs) were also analyzed. Hypothermia produced increased latencies of the major SSEP and BAEP components and the latencies returned to normal with subsequent warming. ⋯ The temperature-latency regression curves were uniformly less steep during the warming phase compared to those during cooling. These findings suggest the existence of hysteresis in the relationship between temperature and EP latencies. The latencies at a given temperature below 30 degrees C depend on whether that temperature is reached during cooling or during warming.
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Electroencephalogr Clin Neurophysiol · Nov 1990
Somatosensory evoked potentials after median and tibial nerve stimulation in healthy newborns.
Cortical and spinal somatosensory evoked potentials (SEPs) have been recorded after median and tibial nerve stimulation in healthy newborns. Spinal SEPs were readily obtained and recorded in all but one neonates after stimulation of both nerves. ⋯ The mean feature of cortical SEPs was a negative wave (N27) for median nerve and a positive wave (P32) for tibial nerve. The present results demonstrate the feasibility of obtaining in the same baby, spinal and cortical SEPs after stimulation of median and tibial nerve, giving information on the functional integrity of central and peripheral somatosensory pathways which supply upper and lower limbs.
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Electroencephalogr Clin Neurophysiol · Jun 1990
Effect of partial sleep deprivation on sleep stages and EEG power spectra: evidence for non-REM and REM sleep homeostasis.
The effect of repeated partial sleep deprivation on sleep stages and sleep EEG parameters was investigated in young subjects. After 2 baseline nights (B1, B2) of 7.5 h, sleep was restricted for 2 nights (D1, D2) to the first 4 h of the habitual bedtime period. Two recovery nights (R1, R2) with 7.5 h sleep followed. ⋯ An enhancement of slow wave activity in REM sleep was present in D2. Power density in the frequency range of 13-16 Hz was reduced in non-REM sleep (R1), SWS (R2) and stage 2 (R1). The results show (1) that the moderate reduction of slow wave energy in the deprivation nights induces only a minor enhancement of slow wave activity during recovery sleep; and (2) that a REM sleep deficit gives rise to an immediate rebound when 'slow wave pressure' is low.(ABSTRACT TRUNCATED AT 250 WORDS)