Anaesthesia and the developing brain

Abstract

Increasing concern about the effect of anaesthesia on the infant and young child is being raised by healthcare practitioners, as well as the public. Immature neurons exposed to anaesthesia may lead to apoptosis and long-term neurobehavioural deficits in animals. The majority of anaesthetic agents work by influencing the gamma-aminobutyric acid or N-methyl-D-aspartate receptors and may induce animal neuroapoptosis. The search for neuroprotective strategies to reverse or counteract the effect of anaesthesia has not been very successful so far. Dexmedetomidine is an α 2 -adrenergic receptor and may have neuroprotective effects. Available human studies have failed to prove any long-term neurobehavioural deficiencies caused by anaesthetic exposure. Large international prospective studies are currently underway that may change the practice of paediatric and obstetric anaesthesiologists in the future.

Oxygen saturation profile in traumatic brain injury animal model after propofol administration

“…Propofol possesses neuroprotective effects attributed to its antioxidant activity and ability to decrease brain metabolic rate and it helps redistribute cerebral blood flow, suppress glutamate during ischemic events, and regulate apoptosis-associated proteins [10]. However, its effects on brain tissue following TBI, either neuroprotective or neurotoxic, are not fully understood [11][12][13][14][15]. In addition, apart from its neuroprotective effect, propofol can also cause respiratory depression, bronchospasm, laryngospasm, and apnea [16,17].…”