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Effects of delayed, prolonged hypothermia on the pial vascular response after traumatic brain injury in rats

Yuji Ueda, Enoch P. Wei, Hermes A. Kontos, Eiichi Suehiro, and John T. Povlishock

N umerous investigators have shown dysfunction of the cerebral circulation after TBI. 17 Such dysfunction includes changes in cerebral blood flow, 16, 31 cerebrovascular reactivity, 13, 38 and cerebral autoregulation, 6, 11, 18 with the underlying assumption that these vascular abnormalities contribute to the brain's primary injury and/or its increased vulnerability to secondary insults such as hypoxia and hypotension. Because the onset of most secondary insults is typically delayed, this raises the opportunity for early therapeutic intervention to

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Short pressure reactivity index versus long pressure reactivity index in the management of traumatic brain injury

Erhard W. Lang, Magdalena Kasprowicz, Peter Smielewski, Edgar Santos, John Pickard, and Marek Czosnyka

at approximately 0.5–3 cycles per minute, which corresponds to a frequency of 0.008–0.05 Hz; 5 , 16 , 23 and 2) M waves, which occur at approximately 4–9 cycles per minute, which corresponds to a frequency of 0.07–0.15 Hz. 7 , 12 , 22 The 6 ventilatory cycles per minute ventilation test is a clinical tool to create an artificial stimulus for M-wave activity. 8 , 19 All clinical tests of cerebrovascular reactivity require a stimulus variable and a response variable. 1 , 3 , 10 , 15 , 32 The stimulus is classically an increase or decrease in ABP, which can be

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Altered cerebrovascular CO2 reactivity following subarachnoid hemorrhage in cats

Michael N. Diringer, Jeffrey R. Kirsch, Daniel F. Hanley, and Richard J. Traystman

mechanisms may contribute to ischemia. Cerebrovascular reactivity to CO 2 has been studied in both humans and animals. Yet, despite the large number of investigations performed to date, characterization of the phenomenon, the segments of vessels involved, and mechanisms responsible for the disturbance remains limited. The majority of studies in humans have tested the response to hypocarbia but not to hypercarbia, 5, 15, 40 or they have assessed CBF with spontaneous variations in arterial partial pressure of CO 2 (PaCO 2 ). 10, 16, 27 The two studies that evaluated

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The contribution of imaging in diagnosis, preoperative assessment, and follow-up of moyamoya disease

A review

Susanna Bacigaluppi, Amir R. Dehdashti, Ronit Agid, Timo Krings, Michael Tymianski, and David J. Mikulis

disease . AJNR Am J Neuroradiol 20 : 1836 – 1838 , 1999 50 Maeda M , Yagishita A , Yamamoto T , Sakuma H , Takeda K : Abnormal hyperintensity within the subarachnoid space evaluated by fluid-attenuated inversion-recovery MR imaging: a spectrum of central nervous system diseases . Eur Radiol 13 : 4 Suppl L192 – L201 , 2003 10.1007/s00330-003-1877-9 51 Mandell DM , Han JS , Poublanc J , Crawley AP , Stainsby JA , Fisher JA , : Mapping cerebrovascular reactivity using blood oxygen level-dependent MRI in patients with arterial

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Restoration of cerebrovascular responsiveness to hyperventilation by the oxygen radical scavenger n-acetylcysteine following experimental traumatic brain injury

Earl F. Ellis, Lyn Y. Dodson, and Richard J. Police

arachidonic acid metabolism by cyclooxygenase with concomitant formation of oxygen radicals. 17, 27 It has been well documented that oxygen radicals influence these abnormalities, since treatment of animals with indomethacin (which blocks the cyclooxygenase enzyme) or treatment with the free radical scavengers superoxide dismutase and catalase inhibit formation of the arteriolar abnormalities and maintain normal cerebrovascular reactivity to hyperventilation. 17, 27 Recent studies also show that, following acute pressor-induced arterial hypertension similar to the

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Brain tissue pressure: physiological observations in anesthetized cats

Fausto Iannotti, Julian T. Hoff, and Gerald P. Schielke

seven cats. No physiological manipulations were performed. After sacrifice the brains were examined for the presence of Evans blue dye extravasation. Water content was measured in the areas surrounding the TP needles. Cerebrovascular reactivity to changes in PaCO 2 and to changes in cerebral perfusion pressure (CPP) were evaluated after a steady state had been established for 1 hour in 11 cats. Ten percent CO 2 was added to the inspired air; rCBF was measured when PaCO 2 elevation was stable in six animals. Regional CBF was measured before and after the

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Intracranial Pressure: More Than a Number

Marek Czosnyka, Peter Smielewski, Ivan Timofeev, Andrea Lavinio, Eric Guazzo, Peter Hutchinson, and John D. Pickard

✓Many doctors involved in the critical care of head-injured patients understand intracranial pressure (ICP) as a number, characterizing the state of the brain pressure–volume relationships. However, the dynamics of ICP, its waveform, and secondarily derived indices portray useful information about brain homeostasis. There is circumstantial evidence that this information can be used to modify and optimize patients' treatment. Secondary variables, such as pulse amplitude and the magnitude of slow waves, index of compensatory reserve, and pressure–reactivity index (PRx), look promising in clinical practice. The optimal cerebral perfusion pressure (CPP) derived using the PRx is a new concept that may help to avoid excessive use of vasopressors in CPP-oriented therapy. However, the use of secondary ICP indices remains to be confirmed in clinical trials.

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Intracerebral steal phenomenon associated with global hyperemia in moyamoya disease during revascularization surgery

Hideki Oshima, Yoichi Katayama, and Teruyasu Hirayama

Object. The collateral vessels in moyamoya disease appear to retain their ability to constrict during hypocapnia but not to dilate during hypercapnia. It has been claimed that hypercapnia, as well as hypocapnia, decreases the blood flow in regions perfused by collateral vessels, presumably because of intracerebral steal. If this holds true, the decrease in blood flow may be proportional to the global hyperemia in the brain. To establish appropriate hemodynamic control during revascularization surgery, the authors monitored the jugular bulb oxygen saturation (SjO2) intraoperatively, a method that could sensitively detect global hyperemia.

Methods. A total of 17 patients, most of whom presented with transient ischemic attacks or fluctuating neurological deficits, underwent intraoperative monitoring of their SjO2 and end-tidal carbon dioxide (ETCO2) after a state of anesthesia had been induced with isoflurane (Group 1) or propofol (Group 2). In eight of these patients, the regional cerebral blood flow (rCBF) of the collateral vessel territory was also monitored by laser Doppler flowmetry during the period of cortical exposure, and a total of 113 data sets (averaged values during 2.5-minute intervals) was collected. There was fluctuation in the ETCO2 levels ranging from 36 to 44 mm Hg. The mean SjO2 level was clearly greater (p < 0.01) in Group 1 (71.8 ± 2.2%) than in Group 2 (63.3 ± 2.1%). An episodic fall in rCBF was observed in association with a transient increase in SjO2. Such an event was not uncommon in Group 1 and there was a greater risk of rCBF decreasing when SjO2 exceeded a cutoff level of 76% (p < 0.01). This level could sometimes be reached at a broad range of ETCO2 readings (37–44 mm Hg). In Group 2, similar events sometimes occurred when SjO2 increased beyond 70%. However, this level could be reached only with a higher ETCO2 (42–44 mm Hg). The rCBF level was negatively correlated to SjO2 (p < 0.01), but not always to ETCO2, indicating that the episodic fall in rCBF was closely related to global hyperemia rather than the absolute level of hypercapnia.

Conclusions. The observed association between a fall in rCBF and global hyperemia supports the intracerebral steal hypothesis and indicates that it is prudent to avoid excessive global hyperemia. The optimal range of CO2 for isoflurane is more restricted than that for propofol, presumably because isoflurane induces hyperemia by itself. Monitoring of SjO2 appears to represent the most practical technique for detecting global hyperemia as well as global ischemia, both of which may cause ischemic complications in moyamoya disease.

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Pial arteriolar vessel diameter and CO2 reactivity during prolonged hyperventilation in the rabbit

J. Paul Muizelaar, Henk G. van der Poel, Zhongchao Li, Hermes A. Kontos, and Joseph E. Levasseur

✓ Hyperventilation reduces intracranial pressure (ICP) acutely through vasoconstriction, but its long-term effect on vessel diameter is unknown. In seven rabbits with a cranial window implanted 3 weeks earlier, the effect of prolonged hyperventilation on vessel diameter was studied. Anesthesia was maintained for 54 hours with a pentobarbital drip (1 mg/kg/hr). The pH, CO2, and HCO3 levels were measured in arterial blood and cisterna magna cerebrospinal fluid (CSF). The diameter of 31 pial arterioles was measured with an image splitter. After baseline measurements, pCO2 was reduced from 38 to 25 mm Hg and allowed to return to 38 mm Hg for 10 minutes every 4 hours.

There was an initial vasoconstriction of 13%, which progressively diminished by 3% every 4 hours. Thus, by the 20th hour, vessel diameters at a pCO2 of 25 mm Hg had returned to slightly above baseline values obtained at a pCO2 of 38 mm Hg. The temporary return of pCO2 to 38 mm Hg every 4 hours caused vasodilation: 12% at 4 hours, gradually increasing to 16% at 52 hours. Thus, at 52 hours, the vessel diameters were 105% of baseline at a pCO2 of 25 mm Hg and increased to 122% at a pCO2 of 38 mm Hg. Arterial pH had returned to baseline at 20 hours, and CSF pH had returned at 24 hours. Bicarbonate in blood and CSF remained decreased throughout the experiments. In three control experiments during which normocapnia was maintained, vessel diameter and pH and bicarbonate levels remained unaltered over the same period. The CO2 reactivity, tested by brief periods of hyperventilation every 4 hours, also did not change.

These results indicate that hyperventilation is effective in reducing cerebral blood volume for less than 24 hours and that it should be used only during actual ICP elevations. If used preventively, its effect may have worn off by the time ICP starts to rise for other reasons, and further decreases in pCO2 cannot be obtained. Moreover, the reduction in buffer capacity with lower bicarbonate renders the vessels more sensitive to changes in PaCO2. This could lead to more pronounced elevations in ICP during transient rises in PaCO2, such as during endotracheal suctioning in head-injured patients.

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Cerebral hemodynamics in patients with carotid artery occlusion and contralateral moderate or severe internal carotid artery stenosis

Fabrizio Vernieri, Patrizio Pasqualetti, Marina Diomedi, Patrizia Giacomini, Paolo M. Rossini, Carlo Caltagirone, and Mauro Silvestrini

R esults from several follow-up studies show a close correlation between impairment of cerebral hemodynamics in vascular territories distal to the site of CA occlusion and the risk of ipsilateral stroke. 8, 10, 29, 31–33 Besides supporting a reconsideration of the role of hemodynamic factors in the pathogenesis of stroke, 4, 5 this evidence also gives rise to the question of the opportuneness of extracranial—intracranial bypass surgery in patients with CA occlusion and exhausted cerebrovascular reactivity. 11 The surgical bypass procedure is considered very