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Bolus injections of lidocaine are commonly used during neuroanesthesia to prevent or treat ICP elevations caused by tracheal or painful stimuli. Lidocaine can also be employed in case of hard intracranial hypertension, when the usual therapy fails. With continuous perfusion, at high doses, of this agent, a state of lidocaine anesthesia can be induced which is more readily reversible than barbiturate anesthesia. A simultaneous anticonvulsant therapy is mandatory because of the well-known epileptogenicity of lidocaine. Closed cardiovascular monitoring is also needed to detect early signs of cardiotoxicity. Experimental works point to the effectiveness of i.v. lidocaine to prevent ischemic lesions secondary to a cerebral artery occlusion. This protective effect may result from some properties exhibited by lidocaine and not by thiopental: stabilisation of transmembrane ionic fluxes, inhibition of leucocytes intravascular sticking and tissular migration. So, i.v. lidocaine seems help to preserve or improve cerebral perfusion pressure and in cases when the latter decrease below the critical threshold, to protect against cerebral ischemia.

Ischemic cerebral edema frequently develops after aneurysm surgery and may lead to severe intracranial hypertension. Of prime importance are reducing the level of ICP and preserving oligemic areas from becoming infarcted. Besides correction of factors known to worsen intracranial hypertension, several therapeutics may be of value: external CSF drainage, perfusion of mannitol, induced arterial hypertension and use of anesthetic agents with cerebral vasoconstricting capability. Hyperventilation is not recommended. Arterial hypotension and hypovolemia certainly contribute to aggravate cerebral ischemia and must be corrected. Cerebral ischemia may be reduced by two specific approaches: by improving cerebral oxygen transport in ischemic areas using arterial hypertension and calcium blockers rather than hemodilution or hypervolemia; by reducing cerebral metabolic rates with heavy anesthesia under the cover of a complete cardiovascular monitoring. In view of the large heterogenicity in cerebral lesions and physiopathological stages, a therapeutical trial appears suitable in each individual case. Criteria allowing to know if any therapeutic, used alone or in association, is beneficial include increase in blood flow in ischemic areas, reduction of ICP level and normalizing of indices like CSF or venous jugular blood lactate.

From a study bearing upon 26 patients suffering from a cerebral circulatory insufficiency induced by a stenosis or a thrombosis, the writers analyse the part played by Hyperbare Oxygen in the neurologic evolution. The defining of the efficacy criteria enabled them to determine whenever this part was prevalent and obvious (that's to say in 20 p. 100 of the cases). However, in the other cases it was hard to decide whether Hyperbare Oxygen played any part. Only functional lesions are liable to benefit from this therapy which seems mainly useful to cover the period of circulatory adaptation at a time when supply circulations may come into play. The difficulty to appreciate the importance of supply circulations urges on to treat this type of patients early enough in a systematic way and all the more so as they are young.

The interest of neuroleptics in neurosurgery should be examined in the light of physiopathological and pharmacological data concerning cerebral circulatory autoregulation and intracranial pressure. The fairly favourable conclusions permit one to consider their wide use justified, especially, by the feeble hypnogenic effects, without any marked disturbance of the E.E.G., associated with an anticatecholaminergic and stabilizing effect on the autonomic nervous system. They therefore occupy a place of choice, in particular during induction of anesthesia in high risk patients, during operations requiring neurological or continuous E.E.G. investigations, in surgery of intracranial aneurysm and, finally, to obtain sedation and post-operative autonomic control.

A series of head-injured patients, in coma, were treated with hyperbaric oxygen (OHP) at 2.5 atm. Cerebral blood flow (CBF), cerebral metabolic rates of oxygen (CMRO2), glucose (CMRGL), and lactate (CMRL act), and various cerebrospinal fluid (CSF) parameters were measured before and 2 h after the treatment. Pre-OHP and post-OHP average values of arterial blood and CSF lactate, and CMRL act were higher than normal, while CBF, CMRO2 and CSF oxygen pressure (PO2) were lower. CBF tended to increase after OHP in some patients and to decrease in others. This discrepancy and the conflicting results of the literature can be tentatively explained in assuming that there is a different effect of OHP on normal brain circulation as compared to impaired brain circulation. Changes of cerebral metabolic rates were inconsistent and did not relate to changes of CBF, except with repeated studies of the same patient. A correlation was found between the variations of CMRGL and those of arterial blood and CSF glucose content. CSF PO2, CSF acid-base balance, and CSF lactate content did not vary, and arterial PO2 showed a consistent fall. In two patients who were neurologically improved after OHP exposure, the CBF and metabolic changes were not the same.

The advantages of the sitting position for neurosurgery of the posterior fossa are evident and universally admitted. However, respiratory and haemodynamic consequences make this position uncommon and even exceptional for the old patient whose existing physiological cardiovascular and pulmonary disturbances may result in greater risks. In this study, the complications observed during and after surgery in twenty-two patients over 65 years are analysed. These patients underwent functional neurosurgical procedures in sitting position. According to the results, old age does not appear to be an absolute contra-indication of the sitting position for this type of surgery.

Forty-five patients in deep coma resulting from head injury were treated with pentobarbital in doses adjusted to maintain serum barbiturate levels between 15 and 25 mg/l and short burst suppression phases on EEG. Brain death occurred in 20%. The overall mortality rate was 60%, no death being attributable to treatment; 24% of the patients were able to resume active life. Patients with non-reactive pupils during the early phase of coma were compared with patients of similar ages and neurological symptoms non treated with pentobarbital. In treated patients the incidence of brain death was reduced by 50% and the mortality rate by 25% (p less than 0.05), without increase in deaths from intercurrent complications and in severe sequelae among survivors.

Isolation procedures were adopted after usual measures failed to control hospital-acquired infection in a neurological ICU. All patients with an intubation or a tracheostomy were treated in individual rooms following the rules of strict isolation. The circulation of contaminated equipments was strictly isolated from the rest of the ICU. The efficacy of this isolation policy was aasessed by comparing the rates of hospital-acquired infections during the year before and the year after its adoption. The rates of pulmonary infections and venous catheters infections were significantly reduced (p less than or equal to 0.001). The rates of septicemias and urinary infections were relatively unaffected. The mortality caused by nosocomial infections showed a 64% fall (p less than 0.001) which accounted for a 29% reduction in the overall mortality (p less than 0.05). The average stay in the ICU was shortened by 20% and antibiotics consumption declined by 64% leading to substantial savings of money. The activity of the ICU as reflected by the number of admitted patients was unaffected.

Coagulation of the Gasserian ganglian is currently recommended in the treatment of trigeminal neuralgia due to the slight risks that it presents. It is accompanied by brief but intense periods of pain which necessitate the need of an Anaesthetist. As well as we have been able to verify in the course of sixty-two of these procedures, a discontinuous narcosis obtained by reiterated injections of propanidid presents a satisfying solution. It permits the neurological examinations, which need absolute cooperation of the patient, before each new coagulation to be accomplished in good conditions.

60 patients were included in a prospective study to evaluate the effectiveness of hyperbaric oxygenation (OHP) as a treatment of head injury coma. They were assigned to nine subgroups according to age, level of consciousness and eventual neurosurgical procedure, and then selected randomly for OHP or standard therapy. OHP was administered in one or several series of daily exposure at 2.5 ATA. However, the OHP therapy protocol was to be interrupted in 11 cases developing pulmonary, hyperoxic, or infectious complications. Overall mortality and mean duration of coma in survivors were not different in both groups, indicating that OHP was either ineffective or too intermittently applicated. Analysis of results in subgroups revealed that, in one subgroup (18 patients), the rate of recovered consciousness at 1 month was significantly higher when OHP was used. These patients were under 30 and had a brain stem contusion without supratentorial mass lesion. The view is defended that, besides its toxic action on the normal nervous tissue, OHP can counteract edema and ischemia in the zones of brain injuries.