Transcranial Doppler: Does Addition of Blood to Agitated Saline Affect Sensitivity for Detecting Cardiac Right-to-Left Shunt?

BACKGROUND: Transcranial Doppler (TCD) with agitated saline has been shown to be an alternative for the detection of right-to-left shunts (RLS) with similar diagnostic accuracies as transesophageal echocardiography (TEE). It is hypothesized that the addition of blood to agitated saline increases the sensitivity of TCD for the detection of RLS. The aim of this meta-analysis was to determine whether agitated saline with blood increases the sensitivity of TCD for the detection of RLS compared to agitated saline alone and other contrast agents. METHOD: A systematic review of Medline, Cochrane, and Embase was performed to look for all prospective studies assessing intracardiac RLS using TCD compared with TEE as the reference; both tests were performed with a contrast agent and a maneuver to provoke RLS in all studies. RESULTS: A total of 27 studies (29 comparisons) with 1,968 patients met the inclusion criteria. Of 29 comparisons, 10 (35%) used echovist contrast during TCD, 4 (14%) used a gelatin-based solution, 12 (41%) used agitated saline, and 3 (10%) utilized 2 different contrast agents. The addition of blood to agitated saline improved the sensitivity of TCD to 100% compared to agitated saline alone (96% sensitivity, P = 0.161), echovist (94% sensitivity, P = 0.044), and gelatin-based solutions (93% sensitivity, P = 0.041). CONCLUSION: The addition of blood to agitated saline improves the sensitivity of TCD for the detection of RLS to 100% when compared to other conventional contrast agents; these findings support the addition of blood to agitated saline during TCD bubble studies.

Serum Uric Acid Is Associated with Cerebral White Matter Hyperintensities in Patients with Acute Lacunar Infarction.

BACKGROUND AND PURPOSE: The Effect of Cilostazol in Acute Lacunar Infarction Based on Pulsatility Index of Transcranial Doppler (ECLIPse) study showed a significant decrease in transcranial Doppler pulsatility index (PI) with cilostazol treatment after 90 days of acute lacunar infarction. The aim of this analysis was to perform a subgroup analysis of the ECLIPse study to explore the relationship between serum uric acid (UA) and the volume of white matter hyperintensities (WMH) in patients with acute lacunar infarction. METHODS: The ECLIPse was a multicenter, randomized, double-blind, placebo-controlled study conducted in Korea. For this subgroup analysis, WMH volume was measured for those subjects for whom FLAIR or T2-weighted images were available using semiautomated computerized software. RESULTS: Of the 203 patients in 8 hospitals in the ECLIPse study, 130 in 6 hospitals were entered for this subgroup analysis. The mean age was 64.7 ± 9.95 years, and 20.8% were women. The mean WMH volume was 11.57 cm(3) (.13 to 68.45, median 4.86) and mean serum UA was 5.2 mg/dL (1.5 to 8.9). Multiple linear regression analysis revealed that age (P < .001) and serum UA (P = .013) were significantly associated with WMH volume. Age-adjusted scatterplots showed that serum UA level was positively related to WMH volume in patients with acute lacunar infarction (r = 0.275, P = .003). CONCLUSIONS: This study showed that serum UA was associated with cerebral WMH in patients with acute lacunar infarction.

[Effect of TCM formula for promoting blood circulation to remove blood stasis on brainstem auditory evoked potential and Transcranial Doppler parameters in patients with sudden deafness].

OBJECTIVE: To observe the therapeutic effect of Xuefu Zhuyu Decoction (XZD) on patients with sudden deafness (SD). METHODS: Sixty patients with SD were treated with XZD, and the changes of brainstem auditory evoked potential (BAEP) and transcranial Doppler (TCD) parameters in them were detected before and after treatment and analyzed statistically. RESULTS: I, III and V waveform and peak latency (PL) of BAEP, velocity of vertebral basilar arterial blood flow and parameters of cerebral blood flow in SD patients were all improved to different levels after treatment with XZD. CONCLUSION: TCM formula for promoting blood circulation to remove blood stasis can improve BAEP and TCD parameters in SD patients; BAEP detection and TCD parameters can reflect nerve function and blood-supply state of internal ear and brain stem, and therefore are of great importance in guiding the clinical treatment and assessing the prognosis.

Blunted response to systemic nitric oxide synthase inhibition in the cerebral circulation of patients with Type 2 diabetes.

AIMS: Diabetes is a major risk factor for stroke, but the mechanisms that impart the excess risk are unclear. Endothelial dysfunction, which has been demonstrated in the coronary and peripheral vasculature of diabetic patients, is an important early marker of vascular disease. However, the effect of diabetes on cerebrovascular endothelium has not been examined. We sought to investigate the effect of diabetes on basal cerebrovascular endothelial function as assessed by response to the nitric oxide synthase (NOS) inhibitor NG-monomethyl-L-arginine (L-NMMA). METHODS: Fourteen men with Type 2 diabetes and 15 age-matched male control subjects were recruited. The participants had no clinically evident vascular disease and were taking no vasoactive or lipid-lowering medication. Each received a single 15-min intravenous infusion of L-NMMA (0.8 mol/kg/min). Cerebral blood flow was assessed by colour Doppler imaging of the internal carotid artery (ICA) at 10-min intervals for 20 min prior to and following the infusion. Middle cerebral artery velocity (MCAv) was assessed by transtemporal Doppler ultrasound at the same time points. RESULTS: L-NMMA produced a mean reduction in ICA flow area under curve (AUC) in the control group of 12.8 +/- 17.8% compared with a 2.1 +/- 21.7% reduction in the group with diabetes (P < 0.05), indicating blunted basal cerebrovascular response to NOS inhibition in the diabetic group. There was no significant change in MCAv following L-NMMA in either group. Mean +/- sd MAP rose 6.4 +/- 4.2 mmHg in the control group vs. 8.8 +/- 3.5 mmHg in the diabetic group [P = not significant (NS)]. No adverse event or symptom was reported. CONCLUSIONS: Response to NOS inhibition is impaired in the cerebral circulation of patients with diabetes. This observation is consistent with the elevated cerebrovascular risk reported in this population, and may represent a future therapeutic target in stroke prevention.

Effect of oral administration of dotarizine on cerebrovasculature subjected to constriction followed by dilatation in rabbits.

In the study presented the effect of Dotarizine on blood flow velocity in cerebral arteries - in middle cerebral artery (MCA), and basilar artery (BA)- was investigated and compared utilising transcranial Doppler sonography during normoventilation, 15 min hyperventilation with subsequent 3 min anoxia in anaesthetized rabbits. In the Dotarizine treated group (12 rabbits) 25 mg/kg of Dotarizine dissolved in 0,25% agar was administered orally for five days twice daily. In the control group (9 rabbits) animals were fed with agar of the same concentration. The results revealed that decrease of flow velocity caused by hyperventilation and increase during anoxia were less pronounced in the Dotarizine treated group than in control group of animals. A difference between changes of flow velocity in MCA and BA during anoxia was found and the different reactivity of both vessels was established.

Vasoneuronal coupling in migraineurs after subcutaneous sumatriptan: a TCD study.

According to the trigeminovascular model of pain in migraine, sterile neurogenic inflammation of dural vessels stimulates nociceptive fibres of the trigeminal nerve. Sumatriptan, a 5-HT1 receptor agonist, blocks this reaction and mediates vasoconstriction of meningeal arteries. However, it is uncertain, whether sumatriptan also has a vasoconstrictive effect on cerebral arteries, which may influence vasoneuronal coupling and induce secondary cerebral blood flow changes. We studied changes of cerebral blood flow velocity (CBFV) and the pulsatility index (PI) in the posterior cerebral artery (PCA) after stimulus activation before, 10 min and 30 min after subcutaneous application of 6 mg sumatriptan, in order to assess potential vasoactive effects on cerebral circulation. CBFV was recorded from both PCAs simultaneously in 27 migraineurs (twenty women, seven men, mean age 29 years), and arterial blood pressure (BP), heart rate (HR) and respiration rate (RR) were monitored. Although the mean diastolic blood pressure rose significantly from 75 mm Hg to 81 mm Hg (P<0.05) and systolic blood pressure and respiration rates remained constant, average CBFV values remained constant. Similarly, the relative increase of CBFV by visual stimulation, which is clearly higher compared to controls in other studies (55.0% before, 52.6% after 10 min, and 52.4% after 30 min), and absolute mean values for CBFV and PI did not change after visual stimulation. These results provide evidence against the hypothesis that sumatriptan produces vasoconstriction in the intracranial human arterial circulation as a potential risk of cerebral ischemia.

Transcranial Doppler evaluation of cerebral hemodynamics in migraineurs during prophylactic treatment with flunarizine.

Transcranial Doppler (TCD) recording was used to evaluate the mean flow velocity (MFV) and cerebrovascular reactivity to CO2 in 21 migraineurs during the interictal phase. Nine were affected by migraine with aura (MwA) and 12 by migraine without aura (MwoA). During each session the middle cerebral artery (MCA) flow velocity was examined in basal conditions, in hypocapnia after a 3-min period of hyperventilation, in basal conditions a second time, and in hypercapnia after breath-holding. The same procedure was followed in a group of 21 age- and sex-matched volunteers. Recordings were performed before (T1), during (T2), and after (T3) prophylactic treatment with flunarizine (10 mg/day for 2 months) to assess the possible effect of this drug on cerebral hemodynamics. In basal condition, increased MFV values were found in both MwA and MwoA patients. In MwA patients the reactivity index (RI) to hypocapnia was significantly increased in T1 (p < 0.05). This abnormal cerebrovascular reactivity disappeared during flunarizine treatment (T2) and in the post-therapy period (T3).

Transcranial Doppler directed dextran therapy in the prevention of carotid thrombosis: three hour monitoring is as effective as six hours.

BACKGROUND: Six hours' monitoring by transcranial Doppler (TCD) has been successful in directing Dextran therapy in patients at high risk of thrombotic stroke after carotid endarterectomy (CEA). OBJECTIVES: Is 3 h of routine monitoring as effective as 6 h in the prevention of early postoperative thrombotic stroke? DESIGN: Prospective, consecutive study in all patients with an accessible cranial window. METHODS: One hundred and sixty-six patients undergoing CEA underwent 3 h of postoperative monitoring by TCD. Any patient with > 25 emboli detected in any 10 min period or those with emboli that distorted the arterial waveform were commenced on an incremental infusion of dextran 40. RESULTS: The majority of patients destined to embolise will do so within the first 2 postoperative hours. Dextran therapy was instituted in nine patients (5%) and rapidly controlled this phase of embolisation although the dose had to be increased in three (33%). No patient suffered a postoperative carotid thrombosis but one suffered a minor stroke on day 5 and was found to have profuse embolisation on TCD; high dose dextran therapy was again instituted, the embolus count rate fell rapidly and he made a good recovery thereafter. Overall, the death and disabling stroke rate was 1.2% and the death/any stroke rate was 2.4%. CONCLUSION: Three hours of postoperative TCD monitoring is as effective as 6 h in the prevention of postoperative carotid thrombosis.

Reversal of severe cerebral vasospasm in three patients after aneurysmal subarachnoid hemorrhage: initial observations regarding the use of intraventricular sodium nitroprusside in humans.

OBJECTIVE AND IMPORTANCE: The chronic delayed type of cerebral vasoconstriction that occurs after aneurysmal subarachnoid hemorrhage (SAH) is now the most important cause of mortality and neurological morbidity for patients who initially survive the rupture of cerebral aneurysms. Although intravascular volume expansion and cardiac performance enhancement have had a profound impact on the treatment of the chronic delayed type of cerebral vasoconstriction, this form of treatment is not tolerated by all patients and is unhelpful in some. A more specific and more reliable treatment for this condition has not been previously reported. Previous work in an animal model has demonstrated the efficacy of nitric oxide-donating compounds in reversing severe cerebral vasoconstriction when delivered to the adventitial side of the blood vessel. A clinical study was initiated after receiving approval from the United States Food and Drug Administration and the institutional review board. CLINICAL PRESENTATION: Three cases of prompt and substantial reversal of medically refractory vasospasm occurring after aneurysmal SAH in humans using an intrathecally administered nitric oxide donor and clinical, angiographic, and ultrasonographic documentation are presented. All patients developed severe vasospasm refractory to medical treatment 5 to 12 days after sustaining aneurysmal SAH. All patients manifested stupor of new onset (Glasgow Coma Scale score of 7) and new focal neurological deficit (hemiplegia). The condition was angiographically demonstrated in all cases. INTERVENTION: The patients were treated with intrathecally administered sodium nitroprusside, which caused the reversal of vasospasm, which was documented by angiography and transcranial Doppler ultrasonography up to 54 hours later and also by dramatic clinical improvement. Complications related to intracranial pressure elevation, changes in vital signs, and hemodynamic parameters were not observed during or after the procedures. Radiographic evidence of the reversal of vasospasm and brain ischemia was obtained. The clinical outcomes of the treated patients were excellent. All patients presented with hemiplegia and stupor that resolved or markedly improved (within several days, two patients; within 12 hours, one patient). All three patients were discharged and were living at home at the time of manuscript submission. CONCLUSION: These preliminary observations suggest that sodium nitroprusside delivered by an intrathecal route of administration may be a useful treatment for severe vasospasm complicating SAH in humans.

[Effect of drug-induced vasodilatation of basal brain arteries with nitroglycerin on blood flow velocity and volume flow in the middle cerebral artery]. / Einfluss medikamentöser Dilatation basaler Hirnarterien mittels Nitroglyzerin auf Strömungsgeschwindigkeit und Volumenfluss in der A. cerebri media.

AIM: The Müller-Casty flow index (FI) is recommended for use in transcranial Doppler sonography (TCD) to measure relative changes in volume flow. We examined the ability of the FI to assess the volume flow during diameter changes of basal cerebral arteries. METHOD: Nitroglycerin (NTG) was used to induce dilation of basal cerebral arteries without affecting cerebral blood flow. Transverse and sagittal sections of the middle cerebral artery (MCA) were obtained by magnetic resonance imaging (MRI) and blood flow velocities in the MCA were measured by TCD. The FI was calculated by multiplying Doppler shift frequency and signal power. RESULTS: NTG induced an increase of MCA-diameter in MRI. The mean FI remained approximately constant (-2.6 +/- 6%), while the mean blood flow velocity dropped significantly (-15 +/- 6%). CONCLUSION: The FI can be used to estimate volume flow in basal cerebral arteries even in case of diameter change.

Opposite effects of L-arginine and nitroglycerin on cerebral blood velocity: nitric oxide precursors and cerebral blood velocity.

Nitric oxide (NO), a gaseous molecule synthesized in the arteriolar endothelium from the amino acid L-arginine (L-arg), has been identified as the previously described Endothelium-Derived Relaxing Factor (EDRF): nitroderivatives such as nitroglycerin are known to induce vasodilation via NO release. The aim of this study was to evaluate by Transcranial Doppler (TCD) monitoring any changes in cerebral hemodynamics induced by both the infusion of L-arg and the sublingual administration of nitroglycerin in 20 healthy subjects. L-arg infusion induced a significant increase in blood velocity compared to the baseline value (mean +/- S.D. percent change = 18 +/- 8.71; p<0.0001 ) and a slight but significant decrease in Pulsatility Index. By contrast, nitroglycerin was able to cause a significant decrease in blood velocity (mean +/- S.D. percent change = 24.8 +/- 7.68; p<0.0001), while leaving Pulsatility Index unchanged. These data suggest that L-arg and nitroglycerin, both hypothesized to use NO as the final product at the vascular level, result in opposite blood velocity patterns within the cerebral circulation. This may be due to the particular type of artery and/or to the local endothelial environment whereby the released NO may act.

Transcranial Doppler echo contrast studies using different colour processing modes.

OBJECTIVES: To study the effects of different colour imaging modes on the contrast-medium-enhanced image of the intracranial cerebral arteries. METHODS: Twelve healthy volunteers were studied transcranially after administration of 10 ml BY963 successively with Power Doppler (p-TCCS) and with colour Doppler frequency imaging mode (f-TCCS) in a randomized order. RESULTS: The latency time (mean+/-SD) from the injection until the signal enhancement in the middle cerebral artery was 17.1+/-5.8 s for p-TCCS and 17.8+/-4 s for f-TCCS, and the duration of the optimal diagnostically useful signal enhancement was 44.2+/-8.2 s and 40.2+/-12.6 s respectively. CONCLUSIONS: Based on the measured parameters, both imaging modes were of equal value. Theoretical differences in sensitivity of the two methods play no particular role facing the immense signal enhancement after echo contrast application.

The safety and efficacy of cyclosporine A in the prevention of vasospasm in patients with Fisher grade 3 subarachnoid hemorrhages: a pilot study.

OBJECTIVE: To evaluate the safety and any potential effect of cyclosporine A (CycA) in preventing cerebral vasospasm. METHODS: Nine patients with Fisher Grade 3 subarachnoid hemorrhages were studied. After a loading dose of 7.5 mg/kg of CycA was administered every 12 hours for two doses, enteral treatment with CycA was started within 72 hours of the onset of the subarachnoid hemorrhage. Whole blood CycA levels were titrated to maintain levels of 50 to 400 ng/kg. Transcranial doppler ultrasonography was performed daily. Middle cerebral artery velocities were used to assess the degree of vasospasm. Angiography was performed to confirm the vasospasm in symptomatic patients, or it was performed if transcranial doppler ultrasonograms were unobtainable. Patients were treated with a standard pharmacological regimen of nimodipine. Induced hypertension, hemodilution, and hypervolemia were instituted at the discretion of the neurosurgical team. Intra-arterial papaverine was infused into the vasospastic vessels of three recalcitrant patients. Outcome was assessed at 6 months with the Glasgow Outcome Scale. RESULTS: All the patients displayed evidence of vessel narrowing, which was disclosed by transcranial doppler ultrasonography or angiography. Five patients developed ischemic deficits, two were treated with intra-arterial papaverine, and three died of complications secondary to vasospasm. No significant hepatic, renal, or infectious complication developed as a result of the administration of CycA. CONCLUSIONS: CycA proved safe to use but failed to prevent the development of cerebral vasospasm or delayed ischemic deficits in patients considered at high risk.

Changes in transcranial Doppler flow velocity waveform following inhibition of nitric oxide synthesis. Experimental study in anaesthetised rabbits.

BACKGROUND: Analysis of the transcranial Doppler blood flow velocity (FV) waveform is used clinically to detect changes in cerebral haemodynamic profile. Such changes may be initiated both by alterations in microvascular resistance and in the tone of the cerebral arteries. METHODS: The role of endothelial mechanisms was investigated using inhibition of NO synthesis by systemic administration of NG-nitro-L-arginine methyl ester (L-NAME, 6 mg/kg) followed by simultaneous monitoring of both basilar artery FV and cerebrocortical microcirculation (laser Doppler flowmetry, LDF) in anaesthetised, ventilated rabbits over 60 minutes. RESULTS: Arterial blood pressure (AP) increased significantly (p < 0.01) above baseline level in the second minute following L-NAME and remained elevated until the end of experiment. Time average mean and systolic FV decreased immediately following L-NAME injection, with the statistically significant (p < 0.01) decrease from the third minute. Diastolic FV did not show such radical changes. LDF exhibited a slow decrease with time becoming significantly lower than baseline (p < 0.01) at 50 min. CONCLUSION: A gradual decrease in cortical microcirculation preceded by a rapid reaction recorded in the TCD waveform implies that an increase in the tone of the great cerebral arteries is the predominant phenomenon seen during the acute phase of NO synthase inhibition.

[Transcranial Doppler ultrasound: effects of intravenous anesthetics in neurosurgical patients]. / Transkranielle Dopplersonographie: Effekte intravenöser Anästhetika bei neurochirurgischen Patienten.

AIM: Although adverse effects on cerebral blood flow have been reported, intravenous anaesthetic and sedative agents are often used in neurosurgical patients. Monitoring of these effects by transcranial Doppler sonography remains a questionable procedure as long as the cross-sectional area of the insonated basal cerebral arteries is unknown. This study should evaluate the effects of thiopental, propofol, midazolam and alfentanil on flow velocities and "vessel cross-sectional area" (proportional to the reflected Doppler signal power) measured by transcranial Doppler sonography. METHOD: 19 patients with severe cerebral lesions (Glasgow Coma Scale < 6) were investigated. They were hyperventilated and sedated with fentanyl and flunitrazepam. The Doppler probe was fixed to the temporal bone and focussed to the middle cerebral artery of the more severely lesioned side. Baseline values of flow velocities and vascular cross-sectional area were measured. If routine nursing procedures required a deeper degree of sedation, either thiopental 2.5 mg/kg, propofol 1 mg/kg, midazolam 0.075 mg/kg or alfentanil 0.025 mg/kg were injected intravenously over 30 s. Further measurements were made 60, 120 and 300 s after start of the injection. Mean +/- SD were calculated, statistical evaluation was performed by analysis of variance and paired t-tests using the Bonferroni correction (p < 0.05). RESULTS: The injected agents induced significant decreases of the mean value of flow velocities; the "vessel cross-sectional area" remained unaltered. In some patients paradoxical increases of v were observed. CONCLUSION: The results indicate that intravenous anaesthetic agents are not likely to influence the cross-sectional area of the major basal cerebral arteries. Therefore TCD seems to be a valid tool to monitor the effects of these agents on the cerebral circulation of neurosurgical patients. This is probably of prognostic and therapeutic value.

The haemodynamic effect of transcranial Doppler-guided high-dose nimodipine treatment in established vasospasm after subarachnoid haemorrhage.

Eleven patients (7 females) with aneurysmal subarachnoid haemorrhage (SAH) and transcranial Doppler (TCD) signs of vasospasm during prophylactic intravenous nimodipine treatment (2 mg/h) were treated with TCD-guided high-dose (4 mg/h) intravenous nimodipine. The patients were followed clinically and with serial TCD investigations. Increasing nimodipine to high-dose treatment led to a reduction of the abnormally elevated mean flow velocities (FV) in all patients. There was also a reversal of clinical signs of delayed ischaemia. In one patient, repeated computer tomographic (CT) investigations revealed a reversal of ischaemic changes. Reduction of nimodipine from 4 to 2 mg/hr resulted in a return to abnormally elevated mean FV as well as a return of clinical signs of cerebral ischaemia. The outcome was favourable in 82% of the patients and there was no mortality or vegetative survival. No patient deteriorated clinically due to vasospasm during treatment with high-dose nimodipine. The individual effect of nimodipine treatment can be monitored by the use of serial TCD investigations. TCD-guided high-dose nimodipine treatment appears to be an effective treatment in SAH patients developing vasospasm despite prophylactic standard dose treatment. The data give support for a direct vascular effect of nimodipine on cerebral vasospasm.

Intra-arterial infusion of papaverine combined with intravenous administration of high-dose nicardipine for cerebral vasospasm.

The clinical effect of combination therapy with high doses of intravenous nicardipine and intra-arterial infusion of papaverine on symptomatic vasospasm after subarachnoid haemorrhage (SAH) was analysed retrospectively. In 66 of 122 patients who underwent early aneurysm surgery between 1990 and 1993, the intracranial haemodynamics were documented by transcranial Doppler (TCD) ultrasonography. 33 of these 66 patients received high dose nicardipine intravenously (Group I); the other 33 patients were not treated with calcium antagonists (Group II). Symptomatic vasospasm occurred in 6 Group I patients (18%) and in 13 (39%) in Group II patients. All 19 symptomatic patients received an intra-arterial infusion of papaverine; 15 patients (79%) responded well to this therapy and the symptoms were reversed quickly. Although the mean flow velocity (MFV) was not different between the two groups, it was reduced significantly after papverine infusion. Our retrospective analysis suggests that symptomatic vasospasm can be treated effectively with the combination of intravenous high dose nicardipine and intra-arterial infusion of papaverine, and that the correct timing of the infusions is crucial.

[Effect of halothane anesthesia on cerebral blood flow velocity in children]. / Einfluss der Halothan-Anästhesie auf zerebrale Blutflussgeschwindigkeiten bei Kindern.

The effects of halothane on the cerebral circulation were studied in 23 children during general anaesthesia. Blood flow velocity in one middle cerebral artery was recorded continuously by transcranial Doppler sonography. Furthermore arterial blood pressure, pulse rate, endtidal CO2partial pressure and endtidal halothane concentration were recorded. Mean flow velocities/mean arterial blood pressures were 79 cm x s-1/65 mmHg; 86 cm x s-1/61 mmHg; 78 cm x s-1/54 mmHg and 67 cm x s-1/48 mmHg with 1; 1.5; 2 and 2.5 per cent endtidal halothane concentrations, respectively. Endtidal CO2-partial pressure and pulse rate remained constant throughout the study. The higher cerebral blood flow velocities seen with 1.5 per cent halothane compared with 1 per cent can be explained by an increase in cerebral blood flow. The lower cerebral blood flow velocities and arterial blood pressure with 2.5 per cent halothane compared with 1.5 per cent indicate impaired cerebral autoregulation. However, cerebral blood flow appeared to be sufficient even with low arterial blood pressures.

[The value of various transcranial color doppler tests for determining cerebrovascular reserve capacity]. / Wertigkeit verschiedener TCD-Tests zur Ermittlung der zerebrovaskulären Reservekapazität.

One of the techniques for the assessment of the cerebrovascular reserve capacity is the so-called "breath-holding" test. In order to minimise haemodynamic changes following deep inspiration the patients should hold their breath at the end of a normal inspiration. We studied three different ways (breath holding following normal inspiration [NI], deep inspiration [DI], hyperventilation [HV]), of performing this test in 20 healthy volunteers. The acetazolamide test was taken as a reference. The mean flow velocity (FVmean) in the middle cerebral artery was recorded continuously using a TCD monitoring system. Blood pressure, cardiac output and heart rate were measured simultaneously. Breath holding after deep inspiration resulted in longer apnoea (DI: 68.1 +/- 24.1 s; NI: 44.8 +/- 18.4 s; p < 0.01), produced the highest increase of FVmean (DI: +72.2 +/- 29.8%; NI: +69.2 +/- 29.0%) and was the least inconvenient to the patients. Following HV apnoea was longest (93.0 +/- 33.5 s; p < 0.01), but resulted in the lowest increase of FVmean were not significant. A significantly lower increase of FVmean (44.2 +/- 13.4%, p < 0.01 resp.) could be observed after intravenous injection of 1 g acetazolamide. There were no significant haemodynamic changes in any case. Thus, this bedside test does not appear to be influenced by variations in breath holding.