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, : Cerebral ischemia and white matter edema in experimental hydrocephalus: a combined in vivo MRI and MRS study . Brain Res 757 : 295 – 298 , 1997 3 Chang CC , Kanno H , Yamamoto I , Kuwana N : Cerebrovascular reactivity to acetazolamide in alert patients with cerebral infarction: usefulness of first-pass radionuclide angiography using 99mTc-HMPAO in monitoring cerebral haemodynamics . Nucl Med Commun 22 : 1119 – 1122 , 2001 4 Chang CC , Kuwana N , Ito S , Ikegami T : Impairment of cerebrovascular reactivity in patients with normal

. Fig. 5. Case 1. Cerebrovascular reactivity maps obtained before EMDS (upper) and 5 (center) and 7 (lower) months after EMDS. Yellow/red/orange values indicate positive reactivity with yellow being the highest (see scale with CVR values as indicated). Blue and pale blue mark negative reactivity with pale blue being most negative. Black arrows indicate improved CVR in the immediate vicinity of the flap, which is marked by the presence of a surgical clip artifact ( red asterisk , artifact is also seen on adjacent images). The artifact is more prominent on

I t is well established that CBF decreases significantly following TBI in clinical patients 19, 43 and in experimental animal models. 3, 6, 17, 19, 44 Clinically, cerebrovascular reactivity to hypercapnia has also been shown to be impaired, especially during the acute stage following severe head injury. 8, 13, 20 In animal studies, there is evidence that hypercapnic cerebral vasodilation is either attenuated or abolished depending on the degree of injury in different TBI models. 17, 20, 21, 34, 44 Recently, authors of reports have suggested that

than those in Grades III and IV. 12 A few human studies have suggested a correlation between defective cerebrovascular reactivity and cerebral vasospasm 7, 11, 14 and raised intracranial pressure. 7 We have previously reported that regional cerebral blood flow (rCBF) and cerebral metabolic rate of oxygen (CMRO 2 ) are decreased following SAH, and that this decrease correlates with the degree of angiographic vasospasm. 34 In the present study, we have investigated the cerebral autoregulation and the CO 2 reactivity in patients with recent SAH, with special

increments. The data should be interpreted in the light of knowledge of prior episodes of hypoxia and hypercapnia. Control cats had a stable CBF despite the reduction of MABP to 60 mm Hg. At this point, CBF fell in one animal that had been spontaneously hypertensive. In the remaining cats, CBF fell in a pressure-passive manner after the reduction of MABP to 40 mm Hg. All control animals had preserved cerebrovascular reactivity to hypoxia and to hypercapnia. The responsiveness of CBF to hypoxia and hypercapnia in the mild trauma group was only slightly depressed, and

cerebral tissue compliance. One major factor in cerebral bulk compliance seems to be cerebrovascular reactivity. In the presence of decreased cerebrovascular resistance, arterial hypertension will lead to an increase of the cerebral pulse amplitude and thus must exert a very unfavorable influence on the ICP. It has been shown that in intracranial hypertension the undamped transmission of raised systemic blood pressure to the dilated cerebral vascular bed favors the propagation of brain edema. 21, 22, 32, 34 Furthermore, it has been demonstrated in animal preparations

. Cerebral Blood Flow Measurements Cerebral blood flow was assessed using 123 I-IMP SPECT scanning, which was performed with the aid of a ring-type scanner (Headtome-SET 080; Shimadzu Corp., Kyoto, Japan) before CEA and both immediately and 3 days after the procedure. Cerebrovascular reactivity to acetazolamide was also measured for evaluation of the patient's cerebral hemodynamic reserve before CEA. The preoperative 123 I-IMP SPECT study was performed longer than 1 month after the last ischemic event and 7 to 10 days before the CEA. The 123 I-IMP SPECT study was