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Anæsthesia for Neuroradiological Investigations

In patients with normal cerebrospinal fluid (CSF) pathways, the volatile anesthetic agents halothane, trichloroethylene and methoxyflurane have been shown to produce small increases in CSF pressure (McDowall et al. 1966), but significantly greater increases in CSF pressure are produced in those with intracranial spaceoccupying lesions (Jennett et al. 1969, Fitch et al. 1969). In this latter group of patients, it was noted that the increases in CSF pressure occurred on top of a base-line pressure (under unsupplemented nitrous oxide-oxygen anmsthesia) which was not greatly elevated above normal values. Many of these patients were therefore in the 'compensated' phase of tumour growth, but the administration of a volatile anesthetic resulted in a very great increase in intracranial pressure because of the compressed state of the intracranial contents. It was suggested that these increases in intracranial pressure might be of clinical importance in several ways (Fitch & McDowall 1969) as, for example, by lowering cerebral perfusion pressure, by producing pressure gradients within the skull or by producing intracerebral stealing of blood from ischemic to normal areas of brain. The present study was designed to explore the second of these possibilities, namely that gradients of pressure could be produced between separate intracranial compartments during the administration of volatile anuesthetic agents in the presence of an intracranial space-occupying lesion. Methodology Five unselected mongrel dogs with artificiallyinduced intracranial space-occupying lesions were studied. Anesthesia was inducedwith thiopentone sodium (25 mg/kg) and maintained with 70% nitrous oxide and 30% oxygen, halothane being added during the surgical preparation. The animals were intubated and ventilation was controlled under suxamethonium-induced muscle paralysis. The temporal muscles were reflected on both sides of the skull, and two burr holes were made, one on either side. A thin-walled loose balloon, for the measurement of supratentorial intracranial pressure, was inserted through one burr hole so as to lie subdurally over the frontal cortex. The burr hole on the opposite side of the skull admitted a second balloon which acted as the artificial space-occupying lesion and could be expanded by a constant infusion pump. This second balloon lay extradurally and was so placed that it overlay the parietal cortex in all the experiments. Finally, a catheter was positioned in the cisterna magna for the measurement of posterior fossa pressure. All measurements were made electronically, the following parameters being recorded: arterial blood pressure, central venous pressure, supratentorial and infratentorial pressure, ECG, EEG and pupil size. After control measurements, including the effect of 1 0% halothane on the intracranial pressure in the uncompressed state, had been obtained, the constant infusion pump was started. This pump was so adjusted that it inflated the extradural balloon with glycerol at a rate of 1 ml per 20 minutes. At the end of each 20 minute period, the pump was stopped and 1-0% halothane administered for 10 minutes. The halothane was then discontinued and the pump restarted. This procedure was repeated throughout each experiment, except the first one, in which the pump was allowed to run continuously.