Alzheimer's disease (AD) is associated with a loss of cholinergic neurons resulting in profound memory disturbances and irreversible impairment of cognitive function. The central cholinergic system is involved in the action of general anaesthetic agents. Anaesthetic modulation of cholinergic transmission has profound effects on brain function via a cascade of synaptic and postsynaptic events by binding both nicotinic and muscarinic receptors. During general anaesthesia, decrease in acetylcholine release and depression of cholinergic transmission facilitates the desirable effects of general anaesthetics, such as loss of consciousness, pain, voluntary movements and memory. From this point of view, patients with AD, characterized by a compromised neuronal transmission, represent particular cases in which the choice of anaesthesia drugs may have a negative effect on the postoperative outcome. A future challenge may be the identification of brain targets of general anaesthetics which do not expose patients to postoperative cognitive dysfunction, nor interfere with prognosis of brain degenerative disease.

The cholinergic system is one of the most important modulatory neurotransmitter systems in the brain. Alterations of the transmission communicators are accompanied by reduction of the cortical activity, which is associated with a learning and memory deficit. Down's syndrome is a pathological condition characterized by a high number of abnormalities that involve the brain. The cholinergic system is involved in alterations of the neurological system such as severe learning difficulties. To explain these alterations, important results are obtained from studies about murine trisomy 16 (animal model of Down's syndrome). The results obtained provide useful elements in the improvement of knowledge about the neurological and neurotransmissional alterations that are responsible for the neurobiological characteristics of Down's syndrome. These data potentially justify, in these patients, the therapeutic use of drugs that are principally administered to improve the severe learning difficulties of people with Alzheimer's disease, and suggest a trend which generates a hypothesis worthy of further exploration.

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With the stated dose (0.1 mg/kg) either it must have been necessary to assist ventilation to avoid desaturation while awaiting onset of adequate block for intubation, or intubation was performed without delay under conditions facilitated by the propofol bolus. I would regard neither approach as ideal in the obstetric patient.Although the authors wrote that neostigmine Ô2 mL' was given, I presume they meant 2 mg. Train-of-four neuromuscular stimulation was used, but, crucially, there is no documentation of a response (i.e. four twitches and absence of fade) that demonstrated complete reversal of neuromuscular block. I would be grateful if the authors would justify their choice of cisatracurium, and reassure me that their patients were fully reversed before extubation and the subsequent development of laryngospasm.

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