O01	SYNCOPE AND THE BRAIN: SLAVE TO THE BLOOD PRESSURE, OR PRIMARY REGULATOR? B.D. Levine. Institute for Exercise and Environmental Medicine, Presbyterian Hospital and University of Texas Southwestern Medical Center, Dallas, TX Syncope ultimately occurs when cerebral perfusion is reduced below a critical level whereby there is inadequate delivery of oxygen and substrate to support neuronal metabolism. Under most circumstances, this occurs because of sudden hemodynamic collapse, and a resultant fall in perfusion pressure below the lower limit of autoregulation. However many patients describe symptoms in the upright position that could be attributed to cerebral hypoperfusion, despite a normal blood pressure. Moreover, some investigators report decreases in cerebral blood flow during orthostatic stress that may precede any hemodynamic deterioration, raising the possibility that a primary failure of autoregulation may precede and possibly even precipitate a secondary hemodynamic collapse. In this keynote address, the data for and against this hypotheses will be presented and a pathophysiological framework for the problem of syncope will be developed.
O02	Clinical Aspects of Cerebral Autoregulation D. W. Newell , R. Aaslid, Department of Neurological Surgery, University of Washington School of Medicine, Harborview Medical Center, Seattle, Washington Cerebral autoregulation is a mechanism which protects the brain against the effects of extreme blood pressure changes. The dynamics and the function of this mechanism can be evaluated using transcranial Doppler and arterial blood pressure recordings. Methods to evaluate the autoregulation function have included dynamic and static testing, and also evaluation of spontaneous fluctuations in blood pressure and blood flow velocity. Investigations using transcranial Doppler have revealed new knowledge regarding behavior of the system under normal conditions and also under the effects of anesthetic agents, changes in CO2, and other environmental influences. Alteration in autoregulatory function has also been studied in a variety of disease states including head injury, cerebrovascular occlusive disease, stroke, subarachnoid hemorrhage. The response under normal conditions, environmental influences, and in the setting of disease states will be discussed.
O03	INFLUENCE OF END-TIDAL CARBON DIOXIDE PRESSURE ON THE POSTURAL REDUCTION IN CEREBRAL BLOOD VELOCITY R.V. Immink, J. Gisolf, G.A. van Montfrans, J.J. van Lieshout Cardiovascular Research Institute Amsterdam, Academic Medical Centre, University of Amsterdam, The Netherlands Background: In the upright body position the cerebral blood flow is challenged by a reduction in mean arterial pressure at brain level (MAPbrain) and a reduction in end-tidal CO2 concentration (PetCO2). This study addressed the hypothesis that restriction of the postural fall in PetCO2 increases the transcranial Doppler-determined middle cerebral artery (MCA) mean blood velocity (Vmean) in the upright position. Methods: In 10 healthy young adults, the contribution of PetCO2 and posture on the MCA Vmean and systemic hemodynamic variables was evaluated by 5 min head-up tilting (HUT) at two levels of PetCO2. During free breathing (HUTFB), the postural fall in PetCO2 was unrestricted and during rebreathing (HUTRB) the postural fall in PetCO2 was restricted by the use of an expiratory CO2 rebreathing device. Results: Systemic hemodynamic responses to both tilts did not differ. As expected, after 1 min HUTFB, the reduction in PetCO2 was larger than during HUTRB (6.8±4.3 vs. 1.7±1.6 mmHg). This was also at 3 and 5 min, respectively, 6.6±5.1 vs. 3.1±1.4 mmHg and 6.3±4.8 vs. 2.3±0.8 mmHg (p<0.05). The reduction in MCA Vmean during HUTFB was larger (10±4 vs. 3±4 cm·s^-1;p<0.05) at 1 min, but not at 3 min (8±5 vs. 6±3 cm·s^-1) or at 5 min (7±5 vs. 6±4 cm·s^-1). The postural decline in MCA Vmean during the first 60 s of HUTFB was followed by a steady increase of 1.13 cm·s^-1·min^-1 (p<0.05). Conclusions: The postural fall in MCA Vmean is related to the PetCO2 in the first minute only. From then on, the 4 mm Hg difference in PetCO2 does not affect the MCA Vmean. This questions the contribution of the fall in PetCO2 to the reduction in MCA Vmean during prolonged orthostatic stress.
O04	The relationships between flow in the internal Carotid artery and collateral function in the circle of Willis. M.Fouladiun, J.Holm, R.Volkmann, H.Zachrisson. Dept.of Surgery and Clinical Physiology. Sahlgrenska University Hospital, Göteborg, Sweden Background: Large multicenter studies have shown that carotid surgery reduces the risks for stroke in patients with symptomatic severe carotid artery stenosis. The grading of the stenosis in these studies depended on selective carotid angiography, a method that is seldom used nowadays. Carotid ultrasound has shown a good correlation to angiography and is often used in these cases. A good collateral function increases the intracerebral blood pressure and can affect the blood flow through the carotid artery stenosis and therefore the estimation of the degree of stenosis. The aim of the present study was to try to find relations between degree of the stenosis and the collateral function in the circle of Willis. Methods: The maximal systolic and diastolic velocities were determined in the internal carotid artery (ICA) with Duplex ultrasound. The function of the anterior communicating artery and the blood flow velocity in the middle cerebral artery were estimated with transcranial Doppler (TCD) with and without proximal compression of the common carotid artery. Material: The results of the carotid Doppler and TCD were examined retrospectively.658 studies of 357 patients (age 67 range 39-89 years) were evaluated. Results: Spontaneous collateral flow compensation in the circle of Willis as a marker of hemodynamic significant stenosis was seen (with few exceptions) only in stenosis of 70% or more. Low ICA flow velocity despite high-grade carotid artery stenosis was seen in 10 % of the patients. Conclusion: Spontaneous collateral flow in the circle of Willis indicates a carotid artery stenosis of >70%. Data about collateral function can influence the estimation of the degree of carotid artery stenosis. TCD-examination should therefore be included in investigation of patients with suspicion of symptomatic carotid artery stenosis.
O05	carotid intima media thickness asymmetry in an untreated uncomplicated hypertensive population SA Rodríguez Hernandez^2, MP van Boxtel^1, AA Kroon^2, WH Mess^2, J Lodder^2, J Jolles^1, PW de Leeuw^2. EURON^1, CARIM^2 and University Hospital Maastricht, The Netherlands Background: For the determination of intima media thickness (IMT) usually the average of several measurements in the left and right common carotid artery is calculated. How-ever, it is not known whether differences exist between both carotid arteries. The present study assesses the concordance between the IMT of the left and right carotid artery. Methods: We studied the IMT of both carotid arteries in 102 untreated uncomplicated hypertensives. We measured the IMT of the posterior wall of the left and right common carotid artery at 1 cm proximal to the bulb from an anterolateral and posterolateral view (SONOS 5500; Agilent-Philips; linear array transducer, 3-11 MHz). The enddiastolic B-mode images were analyzed offline with an automated edge-tracking method (M'ath, version 2.0.1; Metris, France). The average IMT was measured over a length of 10 mm, and the mean of both the anterolateral and posterolateral view were calculated and used for further analysis. Also, the lumen diameter was measured. Additionally, flow velocity indices were derived (syst, diast, pulsatility index[PI], resistance index [RI]) from the Doppler spectrum. Results: Age (yrs) 56 ± 11 Sex (m/f) 61/41 BMI, kg/m^2 29 ± 6 Clinic SBP (mmHg) 165 ± 7 Clinic DBP(mmHg) 94 ± 8 Left IMT (mm) 0,752 ± 0,11 Right IMT (mm) 0,717 ± 0,11* *t-test paired samples p<0,001 There was no left right difference of the lumen diameter or velocity parameters. Conclusions: Our data demonstrate that in the investigated population the carotid IMT is significantly lower on the right side. It is proposed that this is related to the anatomical differences between the left and right arteries branching off the aortic arch. Whether these findings have consequences for the formation of atherosclerosis and/or cerebral complications remains to be determined.
O06	Dynamic cerebral autoregulation disturbances correlate with severity of brain trauma M. Müller, Bianchi O, Stock C, Schwertfeger K University hospital, Saarland University, Homburg/Saar, Germany Background: Head injured patients run a high risk of secondary brain ischemia associated with or due to cerebral autoregulation (CA) failure. To prevent such events a non-invasive continuous monitoring system is lacking. We investigated whether assessment of phase shift as an index of CA might be a useful candidate for such purposes. Method: Cerebral blood flow velocity (V) in the MCA and arterial blood pressure (BP) were recorded simultaneously over 6 minutes, and the phase shift between V and BP at 0.1 Hz was calculated by means of transfer function analysis. Recordings were performed in 33 normal subjects under normo- and hypocapnic conditions to generate normative data. 27 patients with severe head trauma (GCS <8) underwent serial follow up investigations of phase shift and CT scanning during the first 8 days after trauma allowing a comparison between phase shift and CT scanning in a total of 115 instances. Traumatic lesions (in the MCA territory) on CT scan were classified in to: 0, no lesion; 1, small lesion (diameter < 3 cm); 2, large lesion (diameter >3 cm). At each instance, the patients were classified into being normocapnic or hypocapnic. Results: Normative phase shift was 78°±28 in normocapnia, and 101°±25 in hypocapnia. In the trauma patients, CA was classified disturbed when phase shift was below the 2SD-limit (22° in normocapnia, 51° in hypocapnia). A disturbed CA was significantly (p<0.01) more frequent in the CT group 2 (19 out of 42) compared to group 0 (7/44) and 1 (5/29). Conclusion: Phase shift changes correlate with the severity of injured brain tissue. As an index of CA it seems a promising tool for continuous long term monitoring of CA dynamically. Grants: BMBF 01 K0 9707, DFG Mü 1433/4-1
O07	Improvement in the Transcranial Doppler Parameters of Hypertensive Patientes after treatment with an AngiotensinI-Converting Enzyme inhibitor Anamarija Mrđen General Hospital Neurology, ZADAR, Croatia BACKGROUND: This study was designed to demonstrate the cerebral hemodynamic changes related to hypertension using transcranial doppler sonography. METHOD: To investigate the effects of antihypertensive drug and to demonstrate the hemodynamic changes related to hypertension 75 stroke free hypertensive patientes asigned to be treated with an angiotensin I converting enzyme inhibitir cilazapril and 20 with beta blocker atenolol for 6 months.Because of corellation in hemodynamic changes occuring in long standing patientes we mesured the flow velocitiies/FV/ and Gosling resistance index / PI / of MCA with EME TC 2000 before and 6 months of administration drugs in two different groups:the patientes with shorter duration of hypertension and longer duration / less then 5 years and more then 5 years /. RESULTS: There occure significantly changes in hemodynamic parametars /p-0,039 in first group treated with cilazapril/hypertension less then 5 years/ in FV and p-0,001 in PI.Second group of patientes treated with cilazapril/hypertension longer then 5 years/ FV p-0,014 and PI p- 0,013.This differences where not observed in patients who took atenolol.In the first group /duration of hypertension less then 5 years/ FV p-0,73,PI p-0,22 and in the second group /hypertension more then 5 years/ FV p-0,46 PI p- 0,85. CONCLUSION:Transcranial doppler sonography can be a sensitive tool in the investigation of vascular imparment caused by hypertension and folow up hypertensive patientes. Considering all this facts the ACE inhibitors with their caracteristics can contribute not only in hypertension treatment but also in prevention of cerbrovascular diseases.