Hubert L. Rosomoff

Resuscitation from severe brain trauma

Severe traumatic brain injuries are extremely heterogeneous. At least seven of the secondary derangements in the brain that have been identified as occurring after most traumatic brain injuries also occur after cardiac arrest. These secondary derangements include posttraumatic brain ischemia. In addition, traumatic brain injury causes insults not present after cardiac arrest, i.e., mechanical tissue injury (including axonal injury and hemorrhages), followed by inflammation, brain swelling, and brain herniation. Brain herniation, in the absence of a mass lesion, is due to a still-to-be-clarified mix of edema and increased cerebral blood flow and blood volume. Glutamate release immediately after traumatic brain injury is proven. Late excitotoxicity needs exploration. Inflammation is a trigger for repair mechanisms. In the 1950s and 1960s, traumatic brain injury with coma was treated empirically with prolonged moderate hypothermia and intracranial pressure monitoring and control. Moderate hypothermia (30 degrees to 32 degrees C), but not mild hypothermia, can help prevent increases in intracranial pressure. How to achieve optimized hypothermia and rewarming without delayed brain herniation remains a challenge for research. Deoxyribonucleic acid (DNA) damage and triggering of programmed cell death (apoptosis) by trauma deserve exploration. Rodent models of cortical contusion are being used effectively to clarify the molecular and cellular responses of brain tissue to trauma and to study axonal and dendritic injury. However, in order to optimize therapeutic manipulations of posttraumatic intracranial dynamics and solve the problem of brain herniation, it may be necessary to use traumatic brain injury models in large animals (e.g., the dog), with long-term intensive care. Stepwise measures to prevent lethal brain swelling after traumatic brain injury need experimental exploration, based on the multifactorial mechanisms of brain swelling. Novel treatments have so far influenced primarily healthy tissue; future explorations should benefit damaged tissue in the penumbra zones and in remote brain regions. The prehospital arena is unexplored territory for traumatic brain injury research.

Meningioma Induced by Thorium Dioxide

THORIUM dioxide (Thorotrast) was introduced as a contrast medium for cerebral angiography by Egas Moniz et al.1 in 1931. Its instillation into the subarachnoid space and ventricles for encephalomyelography was described in the following year by Radovici and Meller.2 , 3 This contrast medium, containing thorium, with a half-life of 1.4 X 1010 years, was employed extensively for many years, despite the potential hazard from subsequent lifelong radiation. Its use has been almost completely abandoned, however, since its implication in the pathogenesis of a variety of carcinomas, sarcomas and endotheliomas.4 , 5 The present report provides an additional example of tumor formation in the .xa0.xa0.

Isolated Intraspinal Extradural Tuberculosis

TUBERCULOMAS of the central nervous system are not common occurrences. In a series of 5344 patients with known pulmonary tuberculosis, there was but 1 case.1 Among a group of 38,510 patients admitt...