The most informative neurophysiological techniques available in the neurosurgical intensive care unit are electroencephalograph and somatosensory evoked potentials. Such tools, which give an evaluation of cerebral function in comatose patients, support clinical evaluation and are complementary to neuroimaging. They serve both diagnostic/prognostic and monitoring purposes. While for the former, discontinuous monitoring is sufficient, for the latter, to obtain increased clinical impact, continuous monitoring is necessary. To perform and interpret these examinations in the neurosurgical intensive care unit, both the technician and the neurophysiologist need specific training in the intensive care field. There is sufficient evidence to show that somatosensory evoked potentials are the best single indicator of early prognosis in traumatic and hypoxic-ischaemic coma compared to the Glasgow Coma Score, computed tomography scan and electroencephalograph. Indeed, somatosensory evoked potentials should always be combined with clinical examination to determine the prognosis of coma. Despite widespread use of somatosensory evoked potentials and their prognostic utility in acute brain injury, few studies exist on continuous somatosensory evoked potential monitoring in the intensive care unit. We carried out a pilot study of continuous electroencephalograph-somatosensory evoked potential monitoring in the neurosurgical intensive care unit (traumatic brain injury and intracranial haemorrhage, Glasgow Coma Score <9, intracranial pressure monitoring). All patients stable from a clinical and computed tomography scan point of view showed no significant somatosensory evoked potential modifications, while in the case of clinical deterioration (23%), somatosensory evoked potentials always showed significant modifications. While somatosensory evoked potentials correlated with short-term outcome, intracranial pressure showed a poor correlation. We believe neurophysiological monitoring is an ideal complement to the other parameters monitored in the neurosurgical intensive care unit. Whereas intracranial pressure is simply a pressure index, electroencephalograph-somatosensory evoked potential monitoring reflects to what extent cerebral parenchyma still remains metabolically active during acute brain injury.

Hypoxic-ischaemic (HI) encephalopathy is a severe complication of perinatal asphyxia and remains a frequent cause of a variety of brain disorders with long-term effects on the patients’ life. The associated brain damage is strongly related to the toxic action of excitatory amino acids, especially glutamate and aspartate. Lamotrigine is an anti-epileptic drug that blocks the voltage-gated sodium channels of the presynaptic neuron and inhibits the release of glutamate. In the present study a well-established model of perinatal asphyxia in 7-d-old rats was used to investigate the effect of lamotrigine on HI-induced damage to different hippocampal brain structures, since disruption of this brain area is thought to play a key role in schizophrenia and epilepsy. Therefore, a combination of ischaemia, induced by unilateral occlusion of the left common carotid artery, followed by exposure to a 1-h period of hypoxia, was carried out in neonatal 7-d-old rats. Immediately after the insult, lamotrigine was given i.p. The histological outcome in the hippocampus was conducted and the tissue levels of glutamate, aspartate, GABA, and glutamine in the same area were determined. A remarkable reduction of HI-evoked damaged neurons in most of the investigated hippocampal regions was noted after lamotrigine administration. Furthermore, lamotrigine decreased the asphyxia-induced hippocampal tissue levels of glutamate and aspartate. Immediately after perinatal asphyxia GABA levels were enhanced, while levels of glutamine were decreased. Lamotrigine administration did not affect either GABA or glutamine levels. These results suggest a neuroprotective effect of lamotrigine in this particular animal model of neonatal HI encephalopathy.

Background and objective Imbalance between cerebral oxygen supply and demand is thought to play an important role in the development of cerebral injury during cardiac surgery with cardiopulmonary bypass.

Methods We studied jugular bulb oxygen saturation, jugular bulb oxygen tension, arterial–jugular bulb oxygen content difference and oxygen extraction ratio in 20 patients undergoing warm coronary artery bypass surgery (34–37°C) with pH-stat blood gas management.

Results Only two patients showed desaturation (jugular bulb oxygen saturation <50%) at 5 min on bypass, and none from 20 min onwards. Multiple regression models were performed after using bypass temperature, mean arterial pressure, cerebral perfusion pressure, haemoglobin concentration and arterial carbon dioxide tension as independent variables, and arterial–jugular bulb oxygen content difference, jugular bulb oxygen saturation, oxygen extraction ratio and jugular bulb oxygen tension as individual dependent variables.

Conclusions We found that jugular bulb oxygen saturation, jugular bulb oxygen tension and oxygen extraction ratio are mainly dependent on arterial carbon dioxide tension, and arterial–jugular bulb oxygen content difference is dependent on arterial carbon dioxide tension and the bypass temperature. Our results suggest jugular bulb oxygenation is mainly dependent on arterial carbon dioxide tension during warm cardiopulmonary bypass.