One of the factors limiting the accuracy of the 15O steady-state method for the measurement of regional cerebral blood flow and oxygen metabolism is the requirement that a constant arterial blood concentration be maintained over long periods. A new method has been developed to correct for the variation of the arterial concentration in the C15O2 and 15O2 steady-state inhalation technique. The time course of the arterial activity is obtained by multiple sampling over the study period. The same 15O model as is used in the steady-state method is employed but is solved without assuming equilibrium. Look-up tables are generated to relate flow and oxygen extraction fraction to tissue activity, and from them the regional parameters are estimated. Theory and simulation studies suggest that substantial improvement in accuracy can be obtained with no increase in statistical error. The validity of the method was checked experimentally by making repeated measurements in the same subject after perturbing the gas delivery. The conventional steady-state method showed significantly larger deviations in repeat measurement than did the new method. Thus, it is concluded that the proposed method is superior.
Summar y : A practical method has been developed that, using II COZ and positron emission tomography (PET), computes and maps (a) "effective pH" (pH,), a weighted average of intra-and extracellular pH, and (b) "clearance" (K\), product of blood flow and llCOZ ex traction. This method, together with measurements of ce rebral blood flow (CBF) and oxygen extraction fraction (OEF), was applied to 12 patients with cerebral ischemia or stroke. The regional K\ was positively correlated with CBF (n = +0.78). The k\/CBF ratio, representing the extraction fraction ratio of llCOZ to H/50, was nega tively correlated with CBF (r = -0.54), suggesting that I leoz extraction decreases as flow increases. In five acute stroke patients within 2 days of onset, the injured cortex had lower CBF (20.6 mi/min/IOO g), higher OEF Brain pH is tightly regulated by physicochemical buffering, by metabolic breakdown and production of acids, and perhaps by active transport of H + or HC03 -. Such tight control is necessary at least in part because of the pH dependence of the activity of several enzymes involved in energy metabolism and Received March 13, 1989; revised June 5, 1989; accepted June 8, 1989 Address correspondence and reprint requests to Dr. N. M. Alpert at Division of Nuclear Medicine, Massachusetts General Hospital, Fruit Street, Boston , MA 02 114, U.S.A.Abbreviations used: ANOVA, analysis of variance; CBF, ce rebral blood flow; CBV, cerebral blood volume; CMR02 , cere bral metabolic rate of 02; CSF, cerebrospinal fluid; CT, com puted tomography; DMO, 5,5-dimethyl-2,4-oxazolidinedione; FWHM, full width at half-maximum; GLM , General Linear Model; OEF, oxygen extraction fraction; OM, orbitomeatal; PET, positron emission tomography; ROI, region of interest; TIA, transient ischemic attack. 859(78. 1 %), and lower pH, (6.96) than the contralateral cor tex (CBF = 41.4 mi/min/IOO g, OEF = 53.3%, pH, = 7.00), suggesting intracellular acidosis with intact cell membranes. In three stroke patients 5-8 days after onset, the injured cortex had higher CBF (60.9 mllmin/IOO g), lower OEF (32.0%), and higher pH, (7. 12) than the con tralateral cortex (CBF = 45.3 ml/min/IOO g, OEF = 58.0%, pH, = 7.06), which suggested an increase in ex tracellular volume compartment reflecting loss of cell membrane integrity. This method provides information on the regional tissue acid-base status and cell membrane integrity, which may be prognostic of tissue viability. Ke y Words: Brain pH-Positron emission tomography \\ COz-Stroke-Cerebral acid-base status-Hydrogen ion concentration .
Introduction This report is the first of a traumatic intracranial arteriovenous malformation (AVM) identified with the use of ultrasound imaging. This case study involves a 49-year-old man with a traumatic intracranial arteriovenous malformation that was identified using transcranial imaging and spectral analysis studies. Methods Transcranial ultrasonic imaging with spectral analysis was performed, using a 2.5MHz hand-held probe identified the traumatic AVM. Correlated follow-up testing was conducted using magnetic resonance angiography and computed tomography scan. Results were correlated with ultrasound findings. Results Bilateral middle cerebral and anterior cerebral arteries were identified revealing normal waveforms and velocities. Left posterior cerebral artery could not be insonated or visualized whereas the right posterior cerebral artery revealed normal waveforms and velocities. A single area of “jet” flow was in the distal internal carotid artery (in the area of carotid cavernous sinus). A peak systolic velocity of 318 cm/sec and an end diastolic velocity of 152 cm/sec were identified in the “jet,” which is consistent with the clinical suspicion of an AVM. The magnetic resonance angiography demonstrated normal right internal carotid, middle cerebral, and anterior cerebral arteries. On the left, there was diffusion of signal in the region of the cavernous sinus. This flow signal extended anteriorly and laterally into the region of the lateral orbit. Also, a second channel of flow appeared extending up into the middle cerebral artery territory, suggesting some retrograde venous flow. Findings reported were consistent with AVM of the carotid artery at the cavernous sinus. Conclusion This report represents with the first reported incidence of diagnosis of traumatic AVM of intracranial vessels. Duplex scanning should be considered if concern exists for such an entity as it appears capable of actually identifying this pathology.
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