Chapter 11 Neurophysiology of anaesthesia
2000; Elsevier BV; Linguagem: Inglês
10.1016/s1567-424x(09)70142-4
ISSN1567-424X
Autores Tópico(s)Epilepsy research and treatment
ResumoWhile recordings from brain slices or single cells can provide information about the effect of anaesthetics on receptors, cell membranes, and interactions of limited numbers of cells, they cannot resolve the problem of integration of the activity of different parts of brain. The rhythmic activity of electroencephalography (EEG) is assumed to reflect these integrative processes, and they are different in the awakened state, slow wave sleep, and rapid eye movement (REM) sleep. Numerous attempts have been made to estimate the depth of anaesthesia from EEG during the past decades. The problem with EEG has been its sensitivity to drug combinations used: although drug effect is clearly seen with all anaesthetics, all of them have their own unique impact on the EEG profile. The minimum alveolar concentration (MAC) of volatile anaesthetic causing inhibition of movement response to pain in 50% of cases does not require the brain: the values are similar when the spinal cord is disconnected from the brain. Therefore, a cortical measure (EEG) does not monitor activity of the spinal cord. Deepening anaesthesia with most general anaesthetics causes an increase of slow activity, which, finally, is abruptly suppressed, resulting in low amplitude mixed frequency activity. This abrupt change also involves a drop to a positive DC level, which is best seen in parietal leads.
Referência(s)