Yasuharu Takeuchi

Effect of 35°C Hypothermia on Intracranial Pressure and Clinical Outcome in Patients With Severe Traumatic Brain Injury

BACKGROUND From 1994, we have used therapeutic hypothermia in patients with severe traumatic brain injury (Glasgow Coma Scale scores of 5 or less). In 2000, we altered the target temperature to 35 degrees C from the former 33 degrees C, as our findings suggested that cooling to 35 degrees C is sufficient to control intracranial hypertension, and that hypothermia below 35 degrees C may predispose patients to persistent cumulative oxygen debt. We attempted to clarify whether 35 degrees C hypothermia has the same effect as 33 degrees C hypothermia in reducing intracranial hypertension and whether it is associated with fewer complications and improved outcomes. METHODS We compared intracranial pressure (ICP) and biochemical parameters in the 30 patients treated with 35 degrees C hypothermia (January 2000 to June 2005) with those in the 31 patients treated with 33 degrees C hypothermia (July 1994 to December 1999). RESULTS Patient characteristics were similar in the two groups. The mean temperature during hypothermia was 35.1 +/- 0.7 degrees C in the 35 degrees C hypothermia group and 33.4 +/- 0.8 degrees C in the 33 degrees C hypothermia group. Mean ICP was controlled under 20 mm Hg during hypothermia in both the 35 degrees C hypothermia and 33 degrees C hypothermia groups. The incidence of intracranial hypertension and low cerebral perfusion pressure did not differ between the two groups. The 35 degrees C hypothermic patients exhibited a significant improvement in the decline of serum potassium concentrations during hypothermia and in the increment of C-reactive protein after rewarming. The mortality rate and the incidence of systemic complications tended to be lower in the 35 degrees C group. CONCLUSIONS Cooling patients to 35 degrees C is safe and the ICP reduction effects of 35 degrees C hypothermia are similar to those of 33 degrees C hypothermia.

Noninvasive evaluation of bone-forming activity within the calcified atherosclerotic lesions by Tc 99m HMDP scintigraphy.

The process of active calcium deposition as demonstrated by radiolabeled fluoride uptake has been recently proposed to be associated with high-risk plaques [(1)][1]. Similarly, the computed tomography (CT)-verified spotty calcification is associated with the plaques that have resulted in recent

Unusual hemodynamic stroke related to an accessory middle cerebral artery: The usefulness of fusion images from three-dimensional angiography

Background: Ischemic stroke associated with an anomaly of the middle cerebral artery (MCA) is a rare occurrence. The diagnosis is very difficult when there are steno-occlusive lesions associated with an accessory middle cerebral artery (AMCA). Case Description: A 77-year-old female with hypertension and hyperlipidemia experienced repeated transient ischemic attacks (TIAs) of motor aphasia and dysarthria. Although angiography showed only left intracranial occlusion, the fusion images of three-dimensional digital subtraction angiography (3-D DSA) showed complex steno-occlusive lesions and an AMCA related with the TIA. The cerebral blood flow (CBF) to the left frontal lobe was supplied by the AMCA, via the anterior communicating artery from the right internal carotid artery. The left temporal and parietal lobes were supplied by the stenotic MCA, via the left posterior communicating artery from the left posterior cerebral artery. Single-photon emission computed tomography showed a marked decrease in CBF to both the left frontal and temporal lobes. A left superficial temporal artery (STA)-to-left MCA double anastomosis was performed, in which each branch of the STA supplied branches of the AMCA and MCA. Conclusion: This is the first reported case of ischemic stroke in a patient with an AMCA. The exact diagnosis could be made only by using fusion images of 3-D DSA, which were useful for understanding the complicated CBF pattern and for the choice of recipient artery in bypass surgery.

Preoperative Embolization of Brain Tumor with Pial Artery or Dural Branch of Internal Carotid Artery as Feeding Artery

This study evaluated the clinical usefulness of preoperative embolization of the pial artery or dural branch of the internal carotid artery (ICA) for brain tumor. Subjects comprised 17 patients with large hypervascular brain tumors who underwent preoperative selective embolization. Micro-catheters (2- or 1.7-F) and shapeable hydrophilic micro-guide wires were used for pial artery (branching from the posterior or anterior cerebral artery) or ICA dural branch embolization. Embolization was performed under digital subtraction fluoroscopy with Polyvinyl alcohol (PVA) particles (150–250 mm) and/or liquid coil. Tumor resection was performed immediately or the day after embolization. Digital subtraction angiography (DSA) before and after endovascular devascularization, blood loss during tumor resection, and clinical outcome were evaluated. All endovascular procedures were technically successful. Post-embolization DSA revealed either a disappearance or a marked decrease of the tumor stain in all cases. Control of intraoperative bleeding was easily accomplished, and intraoperative blood loss was low. Preoperative particle embolization of the feeding artery from the cortical artery or ICA dural branch is safe and effective as adjuvant therapy before tumor resection.