Progressive alteration of somatosensory evoked potential waveforms with lowering of cerebral tissue Po<sub>2</sub>in the rabbit

Colin, Fabienne; Bourgain, R.H.; Manil, Jacqueline

doi:10.3109/13813457809055940

Cited by 19 publications

(4 citation statements)

References 4 publications

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“…4 -5 Somatosensory evoked potential (SEP) is altered by systemic insults such as oligemia 6 -7 anemia, 8 intracranial hypertension, 9 and hypoxia. 10 The changes in superficially recorded waves during systemic oxygen deprivation 6 -8 -l0 are similar to those recorded when the cortical region (somatosensory cortex) is directly involved" and therefore may be as useful in quantitating the degree of insult in generalized insult as in localized insult.…”

Section: Discussionmentioning

confidence: 56%

Relationship of somatosensory evoked potentials and cerebral oxygen consumption during hypoxic hypoxia in dogs.

McPherson

Zeger

Traystman

1986

Stroke

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The effects of hypoxic hypoxia on cerebral hemodynamics and somatosensory evoked potential (SEP) were studied in 10 pentobarbital anestheteized dogs. Cerebral blood flow (CBF) was measured using the venous outflow technique and cerebral oxygen consumption (CMRO2) was calculated from the arterio-cerebro-venous oxygen difference times CBF. SEP was evaluated by percutaneous stimulation of an upper extremity nerve and was recorded over the contralateral somatosensory cortex. The latencies of the initial negative wave (N1), second positive wave (P2) and the amplitude of the primary complex (P1N1) were measured. Animals were breathed sequentially with oxygen concentrations of 21, 10, 6, 5, and 4.5% for five minutes each. Animals were returned to room air breathing when the amplitude of the SEP decreased to less than 20% of control and were observed for 30 minutes following reoxygenation. Severe hypoxia (4.5% O2) increased CBF to 200% of control, decreased CMRO2 to 45% of control, decreased amplitude and increased latency of SEP. Following reoxygenation, as CMRO2 increased toward control, latency of SEP decreased and amplitude increased and CBF returned to baseline within 30 min. During hypoxia and reoxygenation, the latencies of N1 and P2 and the amplitude of P1N1 were correlated with CMRO2 in individual animals. We conclude that changes in SEP amplitude and latency reflect changes in CMRO2 despite high CBF during rapidly progressive hypoxic hypoxia and following reoxygenation.

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Section: Discussionmentioning

confidence: 56%

Relationship of somatosensory evoked potentials and cerebral oxygen consumption during hypoxic hypoxia in dogs.

McPherson

Zeger

Traystman

1986

Stroke

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“…In fact, some authors report only latency changes during reduced oxygen intake [Deecke et al, 1976;Fowler and Lindeis, 1992;Lucertini et al, 1993], which should mainly indicate a prolonged impulse transmission time at the level of synapses. On the other hand, other data indicates only amplitude variations [Colin et al, 1978;Sohmer et al, 1982Sohmer et al, , 1989, that would rather suggest a decreased synchronism in neural discharge. Finally, in some papers, both latency and amplitude were affected by hypoxia [Kida and Imai, 1993;Sohmer et al, 1986a, b].…”

Section: Discussionmentioning

confidence: 94%

“…As a matter of fact, Sohmer et al [1986b] reported on cats that visual, somatosensory and vestibular evoked responses are not as sensitive to hypoxia as brainstem and cortical AEPs. On the contrary, in different animal models, Colin et al [1978] andMc Pherson et al [1986] detected changes in somatosensory evoked potentials. In man, visually and auditory evoked P300 responses are identically sensitive even to mild levels of hypoxaemia [Fowler and Prlic, 1995].…”

Section: Discussionmentioning

confidence: 99%

Human Auditory Steady-State Responses during Repeated Exposure to Hypobaric Hypoxia

Lucertini¹,

Verde²,

Santis³

2002

Audiol Neurotol

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This study was aimed at evaluating the time course of auditory steady-state response (SSR) variations during two consecutive exposures to hypobaric hypoxia. Six normal subjects were examined in a hypobaric chamber at ground level. Then, they climbed to a simulated altitude of 17000 ft (5182 m), where SSRs were recorded after 6, 12, 18, 24 and 30 min. Thereafter, they breathed 100% O₂ and SSRs were recorded after 2 min of reoxygenation. A second exposure to hypoxia followed, with SSR recordings after 6 and 12 min. Finally, the subjects returned to ground level for recovery recording. A phase shift of SSR sinus wave was observed at the beginning of both exposures to hypoxia, although in the first recording (i.e. at 6 min) during the first exposure, the result was not statistically significant. A slight SSR phase shift was still detectable on return to ground level. The central acoustic pathway involved in SSR genesis was probably the area which was found to be most sensitive to hypoxia, compared to other parts of the auditory apparatus (e.g. the cochlea). This data could suggest an impairment of compensation mechanisms when consecutive exposures to hypoxia are performed.

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“…[65] Severe progressive hypoxia is associated with a decrease in SSEP amplitude and increase in latency ultimately leading to complete loss of cortical SSEPs. [66] Cortical SSEPs are more sensitive than spinal and subcortical responses, presumably because the latter are more tolerant of hypoxia than cerebral cortex, because of their lower metabolic rate. [67] Early response to ischaemia or hypoxia can manifest as a transient increase in SSEP amplitude (injury potential) before amplitude decreases and latency is prolonged.…”

Section: Non-anaesthetic Intra-operative Factors Affecting Evoked Potmentioning

confidence: 99%

Anaesthetic considerations for evoked potentials monitoring

Bithal

2014

Journal of Neuroanaesthesiology and Critical Care

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Intra-operative neurophysiologic monitoring (IONM) under anaesthesia has achieved popularity because it helps prevent/ minimize neurologic morbidity from surgical manipulations of various neurologic structures. Neurologic functions in an anaesthetised patient can be monitored either by electroencephalography (EEG) or by evoked potentials. Whereas, EEG is difficult to analyse, evoked potentials, in contrast, are easy to interpret, they are either present or absent, delayed or not delayed, with normal or abnormal wave. The goal of IONM is to identify changes in nervous system function prior to irreversible damage. Many factors need consideration when selecting an anaesthetic regimen for intra-operative monitoring of evoked potentials. The very pathophysiological condition or the potential risks of the contemplated surgical procedure, which require evoked potentials monitoring, may place constraints on anaesthetic management as well. With the availability of numerous anaesthetic techniques, an appropriate plan for managing both anaesthesia and IONM in a patient should be organised. It is extremely essential not to alter the pharmacological state of the patient to avoid any changes in the recording of evoked responses. While an anaesthesiologist may alter plans for a patient in order to facilitate IONM, monitoring team too, sometimes may be required to modify plans for monitoring when a particular anaesthetic agent or technique is strongly indicated or contraindicated. At times, compromise may be required between an anaesthesia technique and a monitoring technique. To serve patients’ best interest, it is critical to have a team approach and good communication among the neurophysiologist, anaesthesiologist and surgeon.

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Progressive alteration of somatosensory evoked potential waveforms with lowering of cerebral tissue Po₂in the rabbit

Cited by 19 publications

References 4 publications

Relationship of somatosensory evoked potentials and cerebral oxygen consumption during hypoxic hypoxia in dogs.

Relationship of somatosensory evoked potentials and cerebral oxygen consumption during hypoxic hypoxia in dogs.

Human Auditory Steady-State Responses during Repeated Exposure to Hypobaric Hypoxia

Anaesthetic considerations for evoked potentials monitoring

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Progressive alteration of somatosensory evoked potential waveforms with lowering of cerebral tissue Po2in the rabbit

Cited by 19 publications

References 4 publications

Relationship of somatosensory evoked potentials and cerebral oxygen consumption during hypoxic hypoxia in dogs.

Relationship of somatosensory evoked potentials and cerebral oxygen consumption during hypoxic hypoxia in dogs.

Human Auditory Steady-State Responses during Repeated Exposure to Hypobaric Hypoxia

Anaesthetic considerations for evoked potentials monitoring

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Progressive alteration of somatosensory evoked potential waveforms with lowering of cerebral tissue Po₂in the rabbit