Neurotoxicity of Anesthetics

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Abstract
The major and most obvious manifestation of a toxic effect of either a local or a general anesthetic is CNS irritability. When this progresses to frank seizures, a marked increase in the rate of cerebral metabolism is known to occur. Delivery of adequate O2 to the brain by an increase in blood flow becomes critical and is the usual compensatory response. Assuming such a response is possible and ventilation is adequate, there is no evidence of neurologic damage due to seizures. With repeated seizures and inadequate ventilation, brain damage will occur. Seizures produced by local anesthetics are perhaps more life-threatening because the patient may not be as closely monitored and loss of airway is more likely. When seizures are produced by general anesthetics, treatment usually consists of simply decreasing the inspired concentration and correcting any hypocapnia. With local anesthetics, an abrupt decrease in brain concentration is not possible and some kind of pharmacologic CNS depression is necessary. In this regard, prevention and treatment were improved by the use of diazepam. Other toxic effects of local anesthetics on neural tissue are difficult to demonstrate and assuming use of proper concentrations, must be rare. CNS toxicity of general anesthetics other than seizures is also difficult to demonstrate and is speculative. General anesthesia produced by inhalational agents cannot be equated with that produced by i.v. administration of barbiturates. Despite the clinical syndrome of barbiturate intoxication, it seems clear that CNS toxicity secondary to an overdose of barbiturates consists of an exaggerated pharmacologic depression, which is totally reversible by adequate supportive measures. Gross overdoses of volatile anesthetics can produce, in addition to pharmacologic CNS depression, a direct toxic effect on cerebral metabolic pathways.