Transbasal approaches to aneurysms of the vertebro-basilar junction.

The most difficult aneurysms to be surgically treated are those of the vertebro-basilar junction area. This is due to their deep location and the proximity of brain stem and cranial nerves. Recently, new transbasal surgical approaches have been developed in order to realize a shorter and more direct access. Clival lesions, such as neoplasms, angiomas, and aneurysms, can now be safely faced through these routes. In this paper, we report our recent experience in transbasal approaches for the management of six consecutive patients, with aneurysms in this area. In four of these patients, the initial treatment consisted of an attempt at endovascular aneurysm obliteration using the Guglielmi Detachable Coil system, whereas, in the other two patients (basing on age, aneurysm size and neurological conditions), surgery was considered as the treatment of choice. Unfortunately, the endovascular treatment failed in all cases, and all patients had to be eventually operated on. In all cases, surgical clipping was performed through the combination of a transmastoid (asterional) approach with the suboccipital lateral approach. By this route, in all cases, parent arteries proved well delineated, the aneurysms could always be correctly clipped. Good long-term results were achieved in all cases but one. When surgery is to be performed, the importance of a thorough wide exposure of the whole vertebro-basilar junction area, as well as the importance of having multiple accesses to the lesion, cannot be overemphasized.

Alterations of protein kinase C in rat hippocampus following traumatic brain injury.

Calcium-dependent excitotoxic processes contribute significantly to pathologic responses to traumatic brain injury (TBI). TBI causes neuronal depolarization and excessive excitatory neurotransmitter release, which may lead to increases in intracellular calcium levels. However, responses of calcium-dependent enzymes such as protein kinase C (PKC) following TBI are poorly understood. Since PKC plays an important role in signal transduction and maintenance of normal neuronal function, we investigated changes in PKC activity and protein levels following fluid percussion brain injury in rats. We observed a 23.1% increase in PKC activity 1 h postinjury and 80.7% increase in PKC activity 3 h postinjury. There was no statistically significant change in PKC activity 5 min and 24 h after injury. PKC immunolabelling studies detected a significant increase in PKC levels in membrane fractions 3 h but not 1 h after injury. Thus PKC activation is transiently increased following TBI and may play an important role in pathophysiologic responses to TBI.