, : 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
Chia-Cheng Chang, Hiroyuki Asada, Toshiro Mimura and Shinichi Suzuki
David J. Mikulis, Gregory Krolczyk, Hubert Desal, William Logan, Gabrielle deVeber, Peter Dirks, Michael Tymianski, Adrian Crawley, Alex Vesely, Andrea Kassner, David Preiss, Ron Somogyi and Joseph A. Fisher
. 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
Chia-Cheng Chang, Nobumasa Kuwana, Susumu Ito and Tadashi Ikegami
The responses of cerebral blood flow (CBF) and cerebrovascular reactivity (CVR) to administration of acetazolamide were investigated in 16 patients with dementia and ventriculomegaly to clarify the cerebral hemodynamics in patients with idiopathic normal-pressure hydrocephalus (NPH).
The mean CBF velocity in the whole brain was measured by the Patlak plot method by using technetium-99m hexamethylpropyleneamine oxime single-photon emission computerized tomography. The CVR values were obtained from the response to administration of 500 mg of acetazolamide and calculated as the percentage of change from the baseline mean CBF value. The mean CBF value was significantly reduced (p < 0.01) in six patients with (35.2 ± 5 ml/100 g/minute) and 10 patients without (33.5 ± 2.8 ml/100 g/minute) NPH compared with the age-matched normal controls (40.8 ± 3.2 ml/100 g/minute), showing no significant difference. The CVR was significantly impaired in patients with NPH (0.8 ± 1.7%; p < 0.001), whereas in patients without NPH preserved CVR (11.3 ± 3%) was demonstrated compared with the normal controls (14.7 ± 1.1%). In patients with NPH a significantly lower CVR (p < 0.001) was shown than in those without NPH. The CVR significantly increased (p < 0.001) after placement of a shunt in patients with NPH.
Reductions in both CBF and CVR may be diagnostic indicators of NPH in patients with dementia in whom ventriculomegaly is present. In patients with dementia and idiopathic NPH both reduced CBF and extremely impaired CVR are shown. The results of the present study suggest that ischemia due to the process of NPH is responsible for the reduction of CBF and manifestation of symptoms in patients with idiopathic NPH.
Giovanni Muscas, Christiaan Hendrik Bas van Niftrik, Jorn Fierstra, Marco Piccirelli, Martina Sebök, Jan-Karl Burkhardt, Antonios Valavanis, Athina Pangalu, Luca Regli and Oliver Bozinov
, 23 or cerebrovascular reactivity (CVR). 11 , 15 The application of intraoperative high-field MRI may deliver such information directly after the bypass anastomosis. By obtaining functional MRI blood oxygenation level–dependent (BOLD) volumes during repeated cycles of apnea, CVR can be measured at the brain tissue level. We previously reported the feasibility of intraoperative 3-T MRI BOLD-CVR and its preliminary application for neurovascular surgery. 6 The purpose of this study was to assess whether intraoperative BOLD-CVR can offer hemodynamic information at the
Fangyi Zhang, Shane M. Sprague, Farrokh Farrokhi, Matthew N. Henry, Minnette G. Son and Dennis G. Vollmer
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
Bo Voldby, Erna M. Enevoldsen and Finn T. Jensen
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
Wlodimierz Lewelt, Larry W. Jenkins and J. Douglas Miller
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
Jürgen Hamer, Ekhart Alberti, Siegfried Hoyer and Klaus Wiedemann
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
Kuniaki Ogasawara, Hirotsugu Yukawa, Masakazu Kobayashi, Chiaki Mikami, Hiromu Konno, Kazunori Terasaki, Takashi Inoue and Akira Ogawa
. 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