Fifteen cases of diffuse axonal injury(DAI) brought about by nonmissile head injury in humans are analyzed. All cases were subjected to comprehensive clinical studies such as measurement of cerebral blood flow by SPECT, continuous intracranial pressure monitoring and multimodality evoked potentials(MEPs). In the patients with DAI, a high incidence of low cerebral perfusion and abnormal MEPs. especially auditory evoked potentials, were found, with high incidence of high velocity traffic accident injury mechanism. On the other hand, a low incidence of increased intracranial pressure was found and dehydrating agents such as glycerol and mannitol did not exert a beneficial influence upon the clinical courses or the outcomes. The outcome of the patients with DAI depended upon the duration of coma and whether or not brain stem signs were noted.
Accidents, Traffic ; Axons ; Brain Stem ; Coma ; Craniocerebral Trauma ; Diffuse Axonal Injury* ; Evoked Potentials* ; Evoked Potentials, Auditory ; Glycerol ; Hand ; Humans ; Incidence ; Intracranial Pressure* ; Mannitol ; Perfusion ; Tomography, Emission-Computed, Single-Photon

Ischemia leads to a complex sequence of events culmination in the loss of functional integrity of the nervous system and, ultimately, in neuronal cell death. Intracellular accumulation of calcium ions following ischemia may alter protein kinase C(PKC) activity. But nature of change of the PKC activity depending on duration and degree of ischemia is not well understood. To understand the effect of the experimental focal ischemia on expression of PKC isozyme, we investigated the expression of PKC gamma, beta, alpha immunocytochemically and activities of cytochrome oxidase(CO) histochemically in focal ischemic brain of the rat. Two groups of focal ischemic infarction were produced in two groups of Sprague Dawley rats(200-300 gm) : Group I, Clip compression of left middle cerebral artery(MCA) for 10min and releases and sacrificed 48 hr later ; Group II, Electric coagulation of left MCA and killed 2-24 hr later. In the group I, CO activity and immunoreactivity(IR) for PKC gamma and beta were decreased generally in the left MCA territory, especially in layers II through IV of ischemic cortex. In the group II, decrease of CO activities and marked increase of three PKC isozyme IRs were noted in the layers I through IV. The isozymes displayed different localization in the control cortex, but the IRs of three isozymes markedly increased in the ischmic region, so that the difference among IR patterns disappeared. Although vacuolation and decrease of number of IR neuron were noted, there were remaining IR pyramidal neurons arounf vacuole in layers IV/V showing dense immuostaining in the cell body and apical dendrite. These results indicate that 10min acute ischemia inhibits activity of PKC gamma and beta and that prolonged ischemia longer than 2hr induces the expression of three PKC isozymes. Inhibition and possible induction of PKC are proposed to represent a critical step during ischemic neuronal injury.
Animals ; Brain ; Calcium ; Cell Death ; Cytochromes ; Dendrites ; Immunohistochemistry ; Infarction ; Ions ; Ischemia* ; Isoenzymes ; Neocortex* ; Nervous System ; Neurons ; Protein Kinase C* ; Protein Kinases* ; Rats* ; Vacuoles