Electroencephalograms During Hypoxia in Healthy Men

Rossen, Ralph

doi:10.1001/archneur.1961.00450180070008

Cited by 11 publications

(5 citation statements)

References 14 publications

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“…EEG recordings of cerebral hypoxia have been studied since the 1930s (39, 40) and it is well understood that neuronal activity is sensitive to changes in cerebral O 2 supply (41–43). In awake, resting, healthy humans, a slowing of EEG activity is generally observed in investigations under the condition of acute normobaric (44–46) and hypobaric hypoxia (47–49).…”

Section: Introductionmentioning

confidence: 99%

Acute and chronic hypoxia: implications for cerebral function and exercise tolerance

Goodall

Twomey

Amann

2014

Fatigue: Biomedicine, Health & Behavior

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Purpose To outline how hypoxia profoundly affects neuronal functionality and thus compromise exercise-performance. Methods Investigations using electroencephalography (EEG) and transcranial magnetic stimulation (TMS) detecting neuronal changes at rest and those studying fatiguing effects on whole-body exercise performance in acute (AH) and chronic hypoxia (CH) were evaluated. Results At rest during very early hypoxia (<1-h), slowing of cerebral neuronal activity is evident despite no change in corticospinal excitability. As time in hypoxia progresses (3-h), increased corticospinal excitability becomes evident; however, changes in neuronal activity are unknown. Prolonged exposure (3–5 d) causes a respiratory alkalosis which modulates Na+ channels, potentially explaining reduced neuronal excitability. Locomotor exercise in AH exacerbates the development of peripheral-fatigue; as the severity of hypoxia increases, mechanisms of peripheral-fatigue become less dominant and CNS hypoxia becomes the predominant factor. The greatest central-fatigue in AH occurs when SaO2 is ≤75%, a level that coincides with increasing impairments in neuronal activity. CH does not improve the level of peripheral-fatigue observed in AH; however, it attenuates the development of central-fatigue paralleling increases in cerebral O2 availability and corticospinal excitability. Conclusions The attenuated development of central-fatigue in CH might explain, the improvements in locomotor exercise-performance commonly observed after acclimatisation to high altitude.

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Section: Introductionmentioning

confidence: 99%

Acute and chronic hypoxia: implications for cerebral function and exercise tolerance

Goodall

Twomey

Amann

2014

Fatigue: Biomedicine, Health & Behavior

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“…8,9,16 Alterations in EEG activity also occur under hypoxic conditions, especially at an arterial oxygen saturation (SaO 2 ) ≤75% and oxygen tension (PO 2 ) ≤40 mmHg. 19 This occurs as neuronal activity in the brain is sensitive to changes in O 2 availability, [20][21][22] such that a depression of synaptic transmission occurs in neurones that may be non-resistant to hypoxia, leading to incoherent transmission between neurones. 19 Acute hypoxia also induces a decrease in a-activity at rest 23,24 and is associated with a suppression of a-activity across all cerebral hemispheres with increasing altitude (0-6000 m).…”

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confidence: 99%

Cerebrocortical activity during self‐paced exercise in temperate, hot and hypoxic conditions

Périard

Pauw

Zanow³

et al. 2017

Acta Physiologica

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“…Previous studies of the EEG during hypoxia or ischemia have reported initial increases of a and/or /3 activity followed by decrease of a activity with or without decrease of 13 activity. 10,13,23,24,37,42 In these previous studies, the initial increase of a and/or fl activity was transient and may have been missed in the present study since the EEG was recorded only during the final 10 minutes of each 30-minute experimental period. However, it seems unlikely that the decrease of ~ and/32 activity observed here was the result of hypoxic/ischemic cerebral damage since cerebral metabolites were not disturbed.…”

Section: Significance Of Current Findingsmentioning

confidence: 65%

Cerebral effects of hypocapnia plus nitroglycerin-induced hypotension in dogs

Artru

Wright.

Colley

1986

Journal of Neurosurgery

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This study examined the effect of hypocapnia (PaCO2 20 mm Hg) on cerebral metabolism and the electroencephalogram (EEG) findings in 12 dogs during nitroglycerin (NTG)-induced hypotension. Previous studies suggest that NTG is a more potent cerebral vasodilator than sodium nitroprusside or trimethaphan. It was speculated that combining hypocapnia with NTG-induced hypotension would cause less disturbance of cerebral metabolism and the EEG than the disturbances previously reported when hypocapnia was combined with hypotension induced by sodium nitroprusside or trimethaphan. All 12 dogs were examined at 1) normocapnia with normotension; 2) hypocapnia with normotension; and 3) hypocapnia combined with NTG-induced hypotension to mean arterial blood pressure (MABP) levels of 60, 50, and 40 mm Hg. In six dogs the cerebral metabolic rate of oxygen was determined, and the EEG was evaluated using compressed spectral analysis. Brain tissue metabolites were calculated in the other six dogs. During normotension, hypocapnia caused no deterioration of cerebral metabolism or of the EEG. Hypocapnia combined with NTG-induced hypotension caused a decrease of the power of the alpha and beta 2 spectra of the EEG at MABP's of 60 mm Hg or less. At an MABP of 40 mm Hg, brain tissue phosphocreatine and the cerebral energy charge decreased, while the brain tissue lactate:pyruvate ratio increased. Thirty minutes after restoration of normocapnia with normotension, cerebral metabolites returned to initial values, but the power of the EEG alpha and beta 2 spectra was decreased compared to baseline values. The cerebral metabolic disturbances and EEG alterations seen here with hypocapnia plus NTG-induced hypotension were similar to those previously reported with hypocapnia plus sodium nitroprusside-induced hypotension, and less than those previously reported with hypocapnia plus trimethaphan-induced hypotension. For hyperventilated patients, administration of NTG may be a better hypotensive treatment than trimethaphan, but similar in effect to sodium nitroprusside.

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Electroencephalograms During Hypoxia in Healthy Men

Cited by 11 publications

References 14 publications

Acute and chronic hypoxia: implications for cerebral function and exercise tolerance

Acute and chronic hypoxia: implications for cerebral function and exercise tolerance

Cerebrocortical activity during self‐paced exercise in temperate, hot and hypoxic conditions

Cerebral effects of hypocapnia plus nitroglycerin-induced hypotension in dogs

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