Takenobu Murota

The effect of intravenous lidocaine on experimental brain edema and neural activities

A series of experiments was conducted to clarify the effect of intravenous administration of lidocaine on brain water content, local cerebral blood flow (lCBF), and neural recovery in brain injury induced by exposure of the cats cerebral surface to the air. The injury produced ischemia and edema in the cortex and white matter without direct damage of the cortex. Lidocaine (3.0 mg/kg) was given intravenously for 30 minutes immediately after air exposure and thereafter at the rate of 2 mg/kg/hour. Twelve hours after exposure, lidocaine significantly suppressed cortical ischemia and edema; however, it had no effects in the white matter. The electrophysiologic activities of the cortex and white matter which were assessed by the direct cortical response and somatosensory evoked response were significantly preserved by lidocaine compared with nontreated animals. The results of this experiment demonstrate that intravenous lidocaine has a significant beneficial effect on cortical ischemia and electrophysiologic activities of the cortex and white matter in injured brain.

Prediction and evaluation of brainstem function by auditory brainstem responses in patients with uncal herniation

Serial measurements of auditory brainstem-evoked responses (BERs) were conducted in 15 patients with supratentorial mass lesions. Significant prolongation of the latency of wave V BERs, which originates in the inferior colliculus, occurred when the intracranial pressure (ICP) approached 30 mmHg. In four of five patients whose BERs were measured before pupillary changes, a significant lengthening of wave V latency was observed prior to clinical manifestation of uncal herniation. These results suggest that immediate medical or surgical decompression of ICP should be performed when ICP approaches 30 mmHg with significant prolongation of wave V latency.

Effect of External Decompression on Cerebral Venous System Occlusion

Decompressive craniectomy (external decompression) is available for patients with uncontrollable intracranial hypertension. However, some authors have reported that external decompression has no beneficial effects due to edema enhancement [1]. We have developed a new experimental model of cerebral venous system occlusion [8]. The venous occlusion in this model led to intracranial hypertension. In this study, we investigated the effect of decompressive craniectomy on the cerebral circulation and cerebral edema in this model.

Experimental Study on Cerebral Venous Circulatory Disturbance

It is well known that the disturbance of cerebral venous circulation, such as resulting from dural sinus thrombosis or occlusion of large cerebral veins or dural sinus during surgery, often leads to brain swelling which causes neurological deficits. However, the pathophysiology of venous circulatory disturbance is poorly understood because of difficulties in making standardized experimental models. In this study, the authors have developed a new experimental model and studied the pathophysiology of cerebral venous circulatory disturbance using this model.

Auditory Brain Stem Responses in Uncal Herniation

The authors have reported that in patients with uncal and central herniation, lengthening of the latency and deterioration of the wave form of the auditory brain stem response (BER) wave V, which originates in the inferior colliculus, correlated well with a rostrocaudal neurological impairment after pupillary change (Nagao et al. 1983). In this study, further investigations were carried out on whether or not the changes in BER wave V are related to the development of uncal herniation before pupillary changes and to obtain objective parameters, with which to assess the effectiveness of medical decompression of ICP in the stage of uncal herniation, manifested by pupillary change (Plum and Posner 1980).

Effects of methylprednisolone on cortical neural activity, blood flow, and water content in air exposure-induced cerebral edema

The correlation of changes in cortical neuron activity with water content and local cerebral blood flow was investigated in cats with brain edema produced by air exposure. The further effect of high-dose methylprednisolone on these factors was studied. Six hours after exposure of the brain surface to air, the water content of the white matter significantly increased. The local blood flow of the cortex and white matter significantly decreased with significant suppression of cortical neural activity (direct cortical response), indicating that ischemia was responsible for neural suppression. A single, large dose of methylprednisolone (30 mg/kg, i.v.) at the beginning of air exposure significantly reduced brain edema of the cortex and white matter 12 h after air exposure and improved the local blood flow of the cortex. Methylprednisolone also caused a remarkable improvement in cortical neural activity. This steroid effect on cortical neural function may play a role in the rapid neurologic improvement observed with their use in addition to the effect on brain edema.

Effects of Glycerol on Cerebral Blood Flow and Neural Function in Patients with Intracranial Space Occupying Lesions

Hyperosmolar agents are often administered to obtain a rapid decrease in elevated intracranial pressure (ICP). Numerous workers have reported the effects of glycerol but little is known about its actions on cerebral circulation in the area of peritumoral edema and neural function. This study was undertaken to elucidate the effect of glycerol on regional cerebral blood flow (rCBF) and neural function in patients with intracranial space occupying lesions.