Seiji Morii

Diagnostic significance of serum neuron-specific enolase and myelin basic protein assay in patients with acute head injury

BACKGROUND Neuron-specific enolase (NSE) and myelin basic protein (MBP) in the peripheral venous blood (PVB) have been reported to be sensitive markers for judging the prognosis of patients with head injury. However, to our knowledge, the levels of NSE and MBP in the internal jugular venous blood (IJVB) have never been studied. METHODS In 25 patients with acute head injury, blood samples were taken from the internal jugular vein and the peripheral vein at the same time before any medical or surgical procedure was performed. The levels of NSE and MBP in the both venous blood samples were measured. The time interval between injury and sampling was 1.5-8.0 hours (mean 4.3 hours). The levels of NSE and MBP in the IJVB were compared to those in the PVB. The relationship between the clinical outcome and the serum levels of those was evaluated. RESULTS The levels of NSE and MBP in the IJVB were almost equal to those in the PVB. The levels of NSE and MBP were significantly higher in the patients who died than in those who survived. In the survivors, the levels of NSE and MBP in the IJVB were 17.6 +/- 11.4 ng/ml and 1.4 +/- 1.5 ng/ml, whereas in the patients who died, both levels were elevated to 51.3 +/- 27.3 ng/ml (p < 0.005) and to 11.3 +/- 9.5 ng/ml (p < 0.01), respectively. CONCLUSIONS The assay of serum NSE and MBP levels provides a reliable laboratory indicator of the degree of brain damage and allows early prediction of the prognosis in patients with acute head injury.

The Mechanism of ICP Reducing Effect of Mannitol

The effect of mannitol to decrease raised ICP is well documented and mannitol is now widely used in clinical practice. However, the exact mechanism involved in the lowering of ICP still remains controversial, especially under the condition of vasogenic edema. The objective of this study is to reexamine and delineate the mechanism of the ICP reducing effect of mannitol, using the mathematical method to estimate the CSF dynamics and intracranial compliance (Marmarou 1975), the quantitative vasogenic edema model (Marmarou 1980), and specific gravimetric technique to measure the brain water content, without disturbing the semiclosed condition of the cranial cavity in cats.

Impaired Autoregulation in an Experimental Model of Chronic Cerebral Hypoperfusion in Rats

BACKGROUND AND PURPOSE To verify the hypothesis that impaired autoregulation may contribute to cerebral swelling or hemorrhage after a sudden recovery of perfusion pressure, we studied the chronic effects of cerebral hypoperfusion on the autoregulatory responses of the pial arterioles in situ. METHODS Eight to 12 weeks after a carotid-jugular fistula was created in rats, experiments were performed under alpha-chloralose and urethane anesthesia. Regional cerebral blood flow (rCBF) was determined by the hydrogen clearance method, and carotid pressure was measured. Using a closed cranial window, we determined the autoregulatory responses of the arterioles (30 to 50 microns) to both hypertension induced by norepinephrine and sudden fistula closure at various mean arterial pressures (MAPs). RESULTS rCBF on the fistula side was reduced by 27%. Carotid pressure was significantly lower than normal but was immediately increased by fistula closure. The pial arterioles showed marked elongation and enlargement. During induced hypertension, the arterioles in the fistula group started to dilate at an MAP lower than that of the control group (130 versus 180 mm Hg, respectively). The arterioles constricted when the fistula was occluded at normal MAP. However, when the fistula was occluded at an MAP higher than 130 mm Hg, the vessels dilated. CONCLUSIONS It was demonstrated that (1) chronic hypoperfusion induced impairment of the upper limit of autoregulation and (2) sudden fistula closure under hypertensive conditions caused vasodilation of the arterioles. These findings suggest that rapid restoration of perfusion pressure is possibly followed by a pressure breakthrough phenomenon in a chronically hypoperfused cerebrovasculature.

Moderate Hypothermia Reduces Hypotensive, But Not Hypercapnic Vasodilation of Pial Arterioles in Rats

Two types of acid—base strategies are available for the blood gas management of patients during hypothermia: alpha-stat and pH-stat management However, the more suitable strategy for therapeutic hypothermia is unclear. We studied the effects of hypothermia (30°C) and acid—base management on reactivity to hypercapnia and hypotension in rat pial arterioles, using a closed cranial window, The baseline diameter during hypothermia decreased in the alpha-stat (Paco2 was maintained at 35 mm Hg when measured at 37°C, n = 8), but not in the pH-stat (Paco2 was maintained at 35 mm Hg when corrected to the animals actual temperature, n = 7), Vasodilation induced by hypotension was significantly reduced in hypothermic groups compared with the normothermic group (n = 7), whereas responses to hypercapnia were preserved, Moreover, hypotensive vasodilation was more attenuated in the pH-stat, than the alpha-stat, management These findings show that moderate hypothermia and acid-base management alter cerebrovascular autoregulation.

Rapid enlargement of ventricles within seven hours after head injury.

We report a case of acute enlargement of the ventricles within 7 hours after head injury that was documented by repeated computerized tomography. It is suggested that the pathophysiological mechanism for this rapid enlargement of ventricles may be due to the raised intracranial pressure (ICP) that results from obstruction of cerebrospinal fluid pathways by subarachnoid hemorrhage, in addition to the elevation of ICP aggravated by frequent focal convulsive seizures.

Clinical Experience of 780 Cases of Postoperative ICP Monitoring

In our Institute, it is our routine to monitor the post-operative Intracranial Pressure (ICP) by the subdural balloon method in the treatment of neurosurgical patients who undergo intracranial surgery.

The effects of a carotid-jugular fistula on cerebral blood flow in the cat: An experimental study in the acute period

The purpose of the present study is to investigate the effects of feline carotid-jugular (CJ) fistula (Spetzlers model) on cerebral blood flow (CBF) in the acute period after creation of the fistula. Using laser-Doppler flowmetry, cortical CBF was measured on the fistula side of 11 cats. Temporary occlusion and opening of the fistula led to an immediate increase and decrease, respectively, in cortical CBF. However, CBF returned to baseline within 1 minute, on average. CO2 reactivity in the closed fistula was preserved. It is suggested that cerebral hemodynamic changes due to Spetzlers CJ fistula model are minimal in the acute period after fistulization.