Effects of induced hypertension on transcranial Doppler ultrasound velocities in patients after subarachnoid hemorrhage

BACKGROUND AND PURPOSE: Transcranial doppler ultrasound (TCD) is used after subarachnoid hemorrhage to detect cerebral vasospasm and is often treated with induced hypertension. Cerebral autoregulation, however, may be disturbed in this population, raising the possibility that TCD velocities may be elevated by induced hypertension. To study this possibility, we performed continuous TCD monitoring of the middle cerebral artery during the induction and withdrawal of induced hypertension in patients after subarachnoid hemorrhage. METHODS: Twenty-eight patients were studied during the induction and withdrawal of hypertension using primarily phenylephrine. Continuous monitoring was performed on the middle cerebral artery with the highest flow velocity. Treatment was based on rising TCD velocities or clinical evidence for cerebral vasospasm. Mean arterial pressure and mean TCD velocities were recorded every minute. A change of > 15% from starting TCD values was considered significant. Cerebral autoregulation was calculated as a percentage of intact autoregulation. Patients were subsequently divided into groups of disturbed and intact autoregulation. RESULTS: In 10 of 19 patients (53%), TCD velocities changed by > 15% and paralleled changes in mean arterial pressure. This directly altered the TCD interpretation of the grade of vasospasm in 7 of 19 patients (36%). Three additional patients had smaller absolute changes in TCD velocities. No clinical difference could be identified between patients with disturbed and intact autoregulation. CONCLUSIONS: In patients with disturbed autoregulation after subarachnoid hemorrhage, induced hypertension can alter cerebral blood flow velocities. The level of autoregulation needs to be considered when interpreting TCD velocities in patients after subarachnoid hemorrhage.     

Hyperdynamic therapy: the nurse's role in the treatment of cerebral vasospasm

The onset of subtle diffuse ischemic neurological deficits often associated with cerebral vasospasm is a major cause of morbidity and mortality following aneurysmal subarachnoid hemorrhage. The exact etiology of cerebral vasospasm is unclear. Increasing intravascular volume, decreasing blood viscosity and inducing hypertension may help prevent or diminish neurological deficits from cerebral vasospasm by improving cerebral blood flow. An intensive multidisciplinary approach is necessary with the role of the neuroscience nurse being pivotal. An understanding of the subtle neurological changes suggestive of cerebral vasospasm and its effects leads to early recognition, and allows for rapid institution of therapy.     

Increased plasma concentration of adrenomedullin in patients with subarachnoid hemorrhage

Adrenomedullin (AM) is a potent hypotensive peptide originally identified in pheochromocytoma tissues. Impaired cardiovascular conditions, such as hypertension, myocardial infarction, and septic shock, stimulate production of AM. This study was performed to determine whether subarachnoid hemorrhage (SAH) altered plasma AM concentration. Plasma concentrations of AM in 17 patients with SAH were measured for 2 wk after the onset of SAH by AM-specific radioimmunoassay. Plasma concentrations of AM were increased in patients with SAH throughout the study period, compared with those in control subjects. Plasma concentrations of AM in patients classified as Hunt and Kosnik grade III or IV were significantly higher than those classified as Hunt and Kosnik grade I or II on the day of and the day after the onset of SAH. However, plasma concentrations of AM were unaffected by angiographic vasospasm. These findings suggest that plasma concentrations of AM are increased in patients with SAH and may reflect the severity of SAH. IMPLICATIONS: Adrenomedullin has been reported to affect the cerebral circulation. This study was performed to determine whether subarachnoid hemorrhage, a typical cerebrovascular disorder, altered plasma adrenomedullin concentrations. We found that plasma adrenomedullin concentrations increased in patients with subarachnoid hemorrhage, although no relationship was found between plasma adrenomedullin concentration and angiographic vasospasm. Plasma adrenomedullin concentration may reflect the severity of hemorrhage.     

A new perspective on the relationship between communication impairment and disempowerment following head injury in information exchanges

Transcranial doppler sonography is a diagnostic tool that allows the noninvasive study of intracranial circulation. In patients with aneurysmal subarachnoid hemorrhage, cerebral vasospasm is promptly diagnosed, even before clinical related symptoms. Feeding arteries of an arteriovenous cerebral malformation can be detected and their variations can be correlated to the treatment (neurosurgical and/or neuroradiological). When raised intracranial pressure (namely in head trauma), transcranial doppler sonography depicts vasospasm and/or typical variations of the waveforms, suggesting intracranial circulatory arrest.     

Hypocapnia and cerebral hypoperfusion in orthostatic intolerance

BACKGROUND AND PURPOSE: Orthostatic and other stresses trigger tachycardia associated with symptoms of tremulousness, shortness of breath, dizziness, blurred vision, and, often, syncope. It has been suggested that paradoxical cerebral vasoconstriction during head-up tilt might be present in patients with orthostatic intolerance. We chose to study middle cerebral artery (MCA) blood flow velocity (BFV) and cerebral vasoregulation during tilt in patients with orthostatic intolerance (OI). METHODS: Beat-to-beat BFV from the MCA, heart rate, CO2, blood pressure (BP), and respiration were measured in 30 patients with OI (25 women and 5 men; age range, 21 to 44 years; mean age, 31.3+/-1.2 years) and 17 control subjects (13 women and 4 men; age range, 20 to 41 years; mean age, 30+/-1.6 years); ages were not statistically different. These indices were monitored during supine rest and head-up tilt (HUT). We compared spontaneous breathing and hyperventilation and evaluated the effect of CO2 rebreathing in these 2 positions. RESULTS: The OI group had higher supine heart rates (P<0.001) and cardiac outputs (P<0.01) than the control group. In response to HUT, OI patients underwent a greater heart rate increment (P<0.001) and greater reductions in pulse pressure (P<0.01) and CO2 (P<0.001), but total systemic resistance failed to show an increment. Among the cerebrovascular indices, all BFVs (systolic, diastolic, and mean) decreased significantly more, and cerebrovascular resistance (CVR) was increased in OI patients (P<0.01) compared with control subjects. In both groups, hyperventilation induced mild tachycardia (P<0.001), a significant reduction of BFV, and a significant increase of CVR associated with a fall in CO2. Hyperventilation during HUT reproduced hypocapnia, BFV reduction, and tachycardia and worsened symptoms of OI; these symptoms and indices were improved within 2 minutes of CO2 rebreathing. The relationships between CO2 and BFV and heart rate were well described by linear regressions, and the slope was not different between control subjects and patients with OI. CONCLUSIONS: Cerebral vasoconstriction occurs in OI during orthostasis, which is primarily due to hyperventilation, causing significant hypocapnia. Hypocapnia and symptoms of orthostatic hypertension are reversible by CO2 rebreathing.     

A randomized trial of nicardipine in subarachnoid hemorrhage: angiographic and transcranial Doppler ultrasound results. A report of the Cooperative Aneurysm Study

Calcium antagonist drugs were proposed for use in patients with recent aneurysmal subarachnoid hemorrhage (SAH) because of their ability to block the effects of a wide variety of vasoconstrictor substances on cerebral arteries in vitro. It was suggested that these agents might, therefore, be useful in ameliorating cerebral vasospasm and its ischemic consequences which frequently complicate SAH. This hypothesis was tested in an arm of a randomized double-blind placebo-controlled trial of high-dose intravenous nicardipine in patients with recently ruptured aneurysms. Participating investigators were required to send selected copies of all admission and follow-up angiograms obtained between Days 7 and 11 following hemorrhage (the peak period of risk for vasospasm) to the Central Registry of the Cooperative Aneurysm Study for blinded interpretation and review for the presence and severity of angiographic vasospasm. In centers with transcranial Doppler ultrasound (TCD) capabilities, middle cerebral artery (MCA) mean flow velocities were measured and recorded. Angiograms obtained between Days 7 and 11 were available for 103 (23%) of 449 patients receiving nicardipine and 121 (26%) of 457 receiving placebo. There was a balance of prognostic factors for vasospasm between the groups. Fifty-one percent of placebo-treated patients had moderate or severe vasospasm on "Day 7-11 angiograms" compared to 33% of nicardipine-treated patients. This difference is statistically significant (p < 0.01). Sixty-seven (49%) of 137 placebo-treated patients examined with TCD between Days 7 and 11 had mean MCA flow velocities exceeding 120 cm/sec compared to 26 (23%) of 112 nicardipine-treated patients (significant difference, p < 0.001). These data suggest that high-dose intravenous nicardipine reduces the incidence and severity of delayed cerebral arterial narrowing in patients following aneurysmal SAH.     

Does traumatic subarachnoid hemorrhage caused by diffuse brain injury cause delayed ischemic brain damage? Comparison with subarachnoid hemorrhage caused by ruptured intracranial aneurysms

OBJECTIVE: To examine whether traumatic subarachnoid hemorrhage (TSAH) caused by severe diffuse brain injury leads to delayed ischemic brain damage and secondary deterioration of outcome, as does aneurysmal subarachnoid hemorrhage (ASAH). METHODS: We examined 99 patients with diffuse brain injury with TSAH and 114 patients with ASAH. Computed tomographic (CT) findings, cerebral blood flow, and neurological outcomes were assessed during the acute and subacute phases and were compared between the two groups. RESULTS: The distribution of subarachnoid hemorrhage on the CT scans differed between the two groups. Unlike ASAH, TSAH was not limited to cisterns surrounding the circle of Willis but extended to supratentorial regions and interhemispheric fissures. Computed tomography-detected subarachnoid hemorrhage disappeared very early with TSAH and gradually with ASAH. In the ASAH group, mean cerebral blood flow decreased to 75% of normal during the acute phase and decreased a further 10% during the subacute phase. In the TSAH group, mean cerebral blood flow decreased to 85% of normal during the acute phase and increased slightly during the subacute phase. Neurological deterioration and in-hospital death peaked on Day 0 in association with TSAH and showed twin peaks in association with ASAH. The incidence of low-density areas on the CT scans was significantly higher with ASAH than with TSAH. All low-density areas on the CT scans of patients with ASAH corresponded to vascular territories, but low-density areas on the CT scans of patients with TSAH were rarely associated with vascular territories and contained deep-seated or gliding contusion types. CONCLUSION: The findings suggest that the incidence of vasospasm is low in association with TSAH and that the cause is different compared with ASAH. There is no evidence that the presence of TSAH in cases of diffuse brain injury leads to delayed ischemic brain damage and secondary deterioration of outcome.     

Transluminal angioplasty and intra-arterial papaverine for the treatment of cerebral vasospasm after ruptured arteriovenous malformations

BACKGROUND: This is the first report on the use of intra-arterial papaverine and percutaneous transluminal angioplasty in two patients with severe, symptomatic cerebral vasospasm who suffered ruptured arteriovenous malformations (AVMs). CASE DESCRIPTIONS: The source of hemorrhage was a venous aneurysm in the first case and a pedicular aneurysm of the distal posterior inferior cerebellar artery in the second case. In both cases, the AVMs were located in the superior vermis and there was minimal subarachnoid hemorrhage. The first patient underwent removal of the AVM before the period of cerebral vasospasm and the second patient underwent removal of the AVM after the cerebral vasospasm had resolved. The outcome was excellent in the first patient and poor in the second patient. CONCLUSION: Arteriovenous malformation with ruptured aneurysms may be at high risk for cerebral vasospasm even when there is minimal subarachnoid hemorrhage. We recommend early treatment of AVMs with ruptured pedicular, intranidal, or venous aneurysms to avoid rebleeding and to allow for aggressive treatment of cerebral vasospasm. The management of cerebral vasospasm after AVM rupture is discussed.     

Prevalence of risk factors in spontaneous intracerebral hemorrhage and aneurysmal subarachnoid hemorrhage

OBJECTIVE: To evaluate whether differences exist in the occurrence of modifiable risk factors between aneurysmal subarachnoid hemorrhage and spontaneous intracerebral hemorrhage, since these stroke subtypes have frequently been combined in epidemiological studies and labeled hemorrhagic stroke. DESIGN: Cross-sectional survey. SETTING: Helsinki University Central Hospital in Helsinki, Finland. PATIENTS: One hundred fifty-six consecutive patients with spontaneous intracerebral hemorrhage aged 16 to 60 years (96 males and 60 females) and 281 patients with aneurysmal subarachnoid hemorrhage (145 males and 136 females) who were admitted to an emergency department. MAIN OUTCOME MEASURES: Prevalence of several health habits, previous diseases, and medication of patients with spontaneous intracerebral hemorrhage were compared with that of patients with subarachnoid hemorrhage using multiple logistic regression. RESULTS: Hypertension (odds ratio [OR], 2.6; 95% confidence interval [CI], 1.6-4.3), diabetes mellitus (OR, 26.4; 95% CI, 3.1-221.6), alcohol intake within the preceding week (for 1-150 g of alcohol: OR, 2.0; 95% CI, 1.1-3.6; for 151-300 g of alcohol: OR, 1.7; 95% CI, 0.8-3.8; and for > 300 g of alcohol: OR, 4.4; 95% CI, 2.1-9.1), and anticoagulant treatment (OR, 21.8; 95% CI, 2.3-207.3) were all significantly more common, but current cigarette smoking (OR, 0.3; 95% CI, 0.2-0.5) was less common in patients with intracerebral hemorrhage than in those with subarachnoid hemorrhage simultaneously after adjustment for sex, age, and body mass index. In males, hypertension (OR, 2.3; 95% CI, 1.1-4.5) and alcohol intake (for > 300 g/wk: OR, 5.8; 95% CI, 2.2-15.7) were more common, but current smoking (OR, 0.2; 95% CI, 0.1-0.4) was less common in patients with intracerebral hemorrhage than in those with subarachnoid hemorrhage after adjustment for age, body mass index, and diabetes mellitus. In females, hypertension (OR, 2.9; 95% CI, 1.4-5.8) and anticoagulant treatment (OR, 10.0; 95% CI, 1.0-100.2) were more common in patients with intracerebral hemorrhage after adjustment for age and body mass index. In univariate statistics, patients with intracerebral hemorrhage were also older, more often had previous symptoms of cerebral ischemia, and had higher values for body mass index and gamma-glutamyltransferase than did those with subarachnoid hemorrhage. CONCLUSIONS: Hypertension, diabetes mellitus, anticoagulant treatment, and amount of alcohol taken within 1 week seem more commonly to be associated with intracerebral hemorrhage than with subarachnoid hemorrhage, which is, however, associated more frequently with cigarette smoking.     

Local overexpression of thrombomodulin for in vivo prevention of arterial thrombosis in a rabbit model

Data from 213 cases of simultaneous carotid endarterectomy and coronary artery bypass grafting (CEN/CABG) were analyzed (1980-1996). There were 154 males (72.3%), and 59 females (27.7%), (mean age: 65. 6 years, range: 42-83). One hundred and thirty-two patients (62.0%) had angina, 58 (37.2%) had myocardial infarction, and 23 (10.8%) had congestive heart failure. Symptomatic cerebrovascular disease was present in 89 patients (41.7%). One hundred and twenty-two patients (57.2%) had three-vessel coronary artery disease, 41 (19.2%) had left main disease, and 27 (12.6%) had a low ejection fraction (ejection fraction /=75% diameter reduction) stenosis was present in 168 (78.8%) of the operated carotid arteries. The contralateral internal carotid artery was severely stenosed or occluded in 35 patients (16.4%). The hospital mortality rate was 5. 6% (12 patients). The cause of death was cardiac in ten patients (4. 6%), and neurologic in two (1%). Eleven patients (5.1%) developed a stroke postoperatively; eight strokes were ipsilateral to the operated artery, and six were permanent. Myocardial infarction occurred in five patients (2.3%). Independent predictors of early mortality were age >62 years, hypertension, and postoperative stroke (p < 0.05). Male sex was the only independent predictor of neurologic morbidity (p < 0.05). Late follow-up data were obtained for 163 (81.0%) patients (mean: 54.8 months, range: 1-168). Four (9. 3%) out of the 43 late deaths were attributed to strokes. There were three (1.8%) late ipsilateral strokes, and five (3.1%) contralateral strokes. The 5- and 10-year survival probabilities were 75 +/- 4%, and 52 +/- 6.9%. The freedom from late ipsilateral neurologic morbidity at 5 and 10 years were 97 +/- 1.7% and 90 +/- 4.0%, respectively. Taken together, the results indicate that combined carotid endarterectomy and coronary artery bypass grafting can be performed safely in this high-risk group of patients. Excellent long-term freedom from stroke can be expected.     

Amount of subarachnoid blood and vasospasm: current aspects. A transcranial Doppler study

Subsequent to admission after aneurysmal subarachnoid haemorrhage (SAH), 120 patients (74 women and 46 men) underwent microsurgical clipping of a total of 158 cerebral aneurysms within 96 hours after the bleed. Their mean age was 46 (20-91) years. Computed tomography (CT) findings were graded according to the modified Fisher scale and all patients had daily transcranial doppler (TCD) recordings of their basal cerebral arteries. In 19% of SAH was grade I on CT, in 44% grade II and in 37% grade III. The rate of patients who developed severe vasospasm as documented by TCD (mean blood flow velocities exceeding 160 cm/s on 2 or more consecutive days) was 39% for grade I patients, 26% for grade II patients and 34% for patients with SAH grade III on the initial CT. There was no difference in the rate of occurrence of severe vasospasm, when the patients were split into 2 groups according to the time of performance of the initial CT scan-within 24 hours, and 48-80 hours after SAH, respectively. It is concluded that the amount of subarachnoid blood on the initial CT scan should no longer be used as the indicator for occurrence and severity of the multifactorial entity vasospasm.     

Neuroradiologic diagnosis and treatment of vasospasm

For survivors of aneurysmal subarachnoid hemorrhage, cerebral vasospasm significantly contributes to its morbidity and mortality by causing delayed ischemic neurological deficit. Noninvasive evaluation with computed tomography, transcranial doppler and single photon emission computerized tomography helps guide clinical decisions. Endovascular therapy of symptomatic vasospasm with balloon angioplasty and to a lesser extent with intraarterial papaverine infusion has emerged as an important treatment adjunct to neurosurgical medical and operative management. Early and aggressive treatment with balloon angioplasty has resulted in sustained clinical improvement in about two-thirds of patients suffering from neurological deficits attributable to vasospasm. Encouraging long-term clinical and transcranial artery damage following angioplasty. Despite balloon angioplasty's 2% to 5% peri-procedure mortality rate, it remains under used.     

Cerebral hemorrhage in Sneddon syndrome

INTRODUCTION: Sneddon syndrome is the association of livedo retricularis and cerebrovascular lesions. It is a vasculopathy of vessels of small and medium calibre which affects young people and is of unknown origin. It is often associated with arterial hypertension and repeated ischemic cerebrovascular accidents which lead to intellectual deterioration. CLINICAL CASE: We describe a 49 year old man who, from the age of 23, had had repeated transient or established episodes compatible with ischemic cerebrovascular accidents. These were followed by various neurological sequelae and by intellectual deterioration. Finally he died of a cerebral hemorrhage whilst on anticoagulant treatment with Synthron. We show the neuroimaging findings (CT, MR and angiography) and the neuropathological studies (cerebral hemorrhage, fibrosis of the intima of the vessels of the circle of Willis, absence of inflammation, bilateral unsymmetrical leukoencephalopathy of the cerebral hemispheres and multiple cortical infarcts). CONCLUSION: We wish to draw attention to the occurrence of this complication, its possible relationship to the vasculopathy mentioned, bursting of one of the arteries of the revascularization complex, arterial hypertension or anticoagulant treatment, and also to add one more case to the few described as having hemorrhage and neuropathology in Sneddon syndrome.     

Failure of platelet angiotensin II binding to predict pregnancy-induced hypertension

OBJECT: Nimodipine therapy has become a standard component of the treatment regimen used in patients with aneurysmal subarachnoid hemorrhage (SAH). Its prescribed use at 60 mg every 4 hours for 21 days is based on reputable, randomized prospective studies. However, because only 20 to 30% of patients with SAH suffer clinical cerebral vasospasm, it is clear that most patients do not actually need the drug. Of course, this fact is not evident until several treatment days have passed. It is common practice, without well-documented consequences, to terminate nimodipine therapy before 21 days in certain clinical circumstances. The aim of this study was to evaluate the effectiveness of abbreviating the duration of nimodipine treatment in the setting of a good-grade aneurysmal SAH. METHODS: A retrospective clinical review was made of 90 consecutive patients who experienced a Hunt and Hess Grade I through III aneurysmal SAH and were treated with nimodipine for 15 days or less. CONCLUSIONS: None of the patients studied suffered a delayed neurological deficit as a result of the abbreviated course of nimodipine.     

Surgical outcome of anterior communicating artery aneurysms

During a 6-year period, 65 consecutive patients who had undergone anterior communicating artery aneurysmal surgery were reviewed at a follow-up examination from 6 to 78 months (mean 35 months) after operation. On admission 69% of cases had a good Hunt and Hess scale (grades I to II) and 31% a poor grade (grades III to V). The degree of subarachnoid hemorrhage (SAH) was determined by Fisher's grade. Sixteen (25%) patients were classified in grades I and II. Forty-six percent of cases had pre-existing hypertension. Early surgery (within the first three days after the bleeding) was performed in 17% of cases. Intraoperative rupture of aneurysm occurred in six (9.2%) patients. Symptomatic cerebral vasospasm was diagnosed in 14 (22%) cases, but only 8 (12%) had evidence of low density on the computerized tomographic scan. Hydrocephalus developed in 16 (25%) cases and 10 needed ventriculoperitoneal shunting. The outcome was determined using the activity of daily life. Sixty-five percent of the patients made a good recovery and 13.8% died. The significant poor prognostic factors included a poor pre-operative grade of the Hunt and Hess scale, the presence of symptomatic cerebral vasospasm, and the Fisher's SAH grade of greater than II. Other factors which apparently were not related to the outcome included age, sex, timing of surgery, history of hypertension, intraoperative rupture, and the development of hydrocephalus.     

Cerebral vascular smooth muscle potassium channels and their possible role in the management of vasospasm

One of the promising therapeutic uses of the potassium channel openers is in the management of cerebral vasospasm, a prolonged vasoconstriction of major cerebral arteries which follows aneurysmal subarachnoid haemorrhage. In this review, we first summarize the properties of potassium channels in cerebral vascular smooth muscle. Calcium-activated and ATP-dependent potassium channels are the major potassium channels identified in the cerebrovascular smooth muscle and both are believed to play a role in the regulation of cerebrovascular smooth muscle tone. The calcium-activated potassium channels can be activated by depolarization, by elevation of internal calcium and by some vasodilators. Some neuropeptides and potassium channel openers open the ATP-dependent potassium channels and produce vasodilation. We then review the effects of both synthetic and endogenous potassium channel openers in the cerebrovascular system, discuss their efficacy in the management of models of cerebrovascular spasm, and outline the clinical promise of these agents.     

Endothelial injury following experimental subarachnoid hemorrhage in rats: effects on brain blood flow

BACKGROUND: The leading cause of death and disability in patients suffering from aneurysmal subarachnoid hemorrhage (SAH) is cerebral vasospasm, a persistent, progressive, and often irreversible constriction of cerebral arteries. A wide array of pathological changes occur in cerebral arteries following SAH, with endothelial injury being the earliest and most consistent one. Since intact endothelium modulates many reflexes that influence vascular tone, damage to them may represent a significant contributor to cerebral vasospasm. METHODS: Changes in local cerebellar blood flow (LCBF) and pathological alterations in major cerebral arteries were studied and compared in rats at various time intervals following SAH. SAH induced by the subarachnoid injection of 0.3 ml of whole blood. Sham rats received a subarachnoid injection of 0.3 ml of isotonic saline. RESULTS: Except for an immediate but transient decrease, LCBF remained unchanged over a 3 day period following saline injection. Likewise, there were no pathological alterations in cerebral arteries of saline-injected rats. In contrast, the subarachnoid injection of whole blood produced significant changes in both LCBF and cerebral arteries. Within 30 minutes post-blood injection, LCBF became significantly decreased and remained so for 4 hours. However, within 24 hours, LCBF had returned to control levels where it remained for 3 days. Endothelial injury was observed in the basilar and middle cerebral arteries from 30 minutes through 4 hours, the same periods in which LCBF was significantly reduced. Within 24 hours, the time period in which LCBF had rebounded to control ranges, cerebral arteries showed no evidence of endothelial damage and resembled control cells. CONCLUSION: The results indicate a direct correlation between changes in LCBF and the structural integrity of endothelial cells in the early stages following SAH. The lack of chronically depressed LCBF (after 1 day) may be related to the quick structural repair of endothelium.     

Transcranial Doppler in vertebrobasilar vasospasm after subarachnoid hemorrhage

OBJECTIVE: The primary objective of this study was to assess the incidence of vertebrobasilar vasospasm after subarachnoid hemorrhage (SAH) by means of transcranial Doppler ultrasonography and to evaluate the clinical significance of this phenomenon. The secondary objective was to analyze the different factors influencing the development, the severity, and the duration of vertebrobasilar vasospasm. METHODS: Fifty-seven patients with traumatic SAH and 44 patients with spontaneous SAH were evaluated and monitored by means of transcranial Doppler ultrasonography. Vasospasm of the anterior and middle cerebral arteries was defined by mean flow velocities (FVs) exceeding 120 cm per second and at least three times the FV of the internal carotid artery. Vasospasm of the basilar and vertebral arteries was defined by a mean FV exceeding 60 cm per second. RESULTS: Vasospasm of the anterior or middle cerebral arteries was found in 27 patients and was associated with vertebrobasilar spasm in 20 patients. FVs in anterior circulation vessels were neither related to the cause of the SAH nor did they correlate with the outcome. Forty-six patients (45.5%) had FVs exceeding 60 cm per second and 25 (24.8%) had FVs exceeding 85 cm per second. In 10 of these patients, direct or computed tomographic angiography showed arterial narrowing involving the vertebrobasilar system, whereas in 21 more patients, computed tomography disclosed a cerebral infarction involving the vertebrobasilar vascular territory. Vertebral artery FVs in this group were twice that of the ipsilateral carotid artery. Vertebrobasilar vasospasm was significantly more frequent after head injury, although it was not related to the type of intracranial lesion or the Glasgow Coma Scale score at admission. It did correlate, however, with outcome (P < 0.0001) and with the intensity of SAH (P < 0.0001). Delayed neurological deterioration occurred in 14 patients and was significantly more frequent in patients with basilar artery FVs above 85 cm per second (P < 0.001). Prognosis, however, could not be reliably predicted by FVs in the basilar artery, even when an FV of 110 cm per second was chosen for prediction criterion. CONCLUSION: These results suggest that vertebrobasilar vasospasm is more common than previously thought, especially in association with head injury, with which it may significantly contribute to brain stem ischemic lesions and therefore justify specific therapeutic measures.     

Cerebrovascular reactivity in hypertensive patients: a transcranial Doppler study

PURPOSE: We studied the usefulness of transcranial Doppler sonography for assessing changes in vasoreactivity in patients with hypertension and the hemodynamic consequences of hypertension. METHODS: The study group comprised 25 patients with chronic severe hypertension and 25 age- and sex-matched healthy subjects. Cerebrovascular reserve capacity was assessed by transcranial Doppler recording of the blood flow velocity in both middle cerebral arteries before and 5, 10, 15, and 20 minutes after intravenous injection of 1 g of acetazolamide (Diamox). Blood pressure, blood gases, and other blood parameters were also measured before and after acetazolamide injection. The sizes of the left atrium, left ventricle, and aortic root were measured by echocardiography and correlated with the vasoreactivity after acetazolamide injection. RESULTS: After acetazolamide injection, no significant changes in blood pressure were observed in either group. The mean blood flow velocity in the middle cerebral arteries of hypertensive patients (60.8 +/- 2.6 cm/sec) was not significantly different from that of controls (58.8 +/- 1.9 cm/sec) before acetazolamide injection. Ten minutes after acetazolamide injection, the percentage change in blood flow velocity was significantly lower in the hypertensive group (36.2 +/- 4.5%) than in the controls (52.6 +/- 3.7%). A significant negative correlation (p < 0.05) between decreased vasoreactivity and increased size of the left atrium and aortic root was observed. CONCLUSIONS: Vasoreactivity decreases in hypertensive patients without neurologic deficits or computed tomography abnormalities. Enlargement of the left atrium correlates well with the severity of the impairment in vasoreactivity. Transcranial Doppler sonography can be a sensitive tool in the investigation of vascular impairment caused by hypertension and in the follow-up of hypertensive patients.     

Cerebral blood flow and the response to acetazolamide during the acute, subacute, and chronic stages of aneurysmal subarachnoid hemorrhage

Cerebral blood flow (CBF) and response to acetazolamide were measured during the acute, subacute, and chronic stages after aneurysmal subarachnoid hemorrhage and correlated with symptomatic vasospasm and clinical outcome in 45 patients who underwent early clipping of ruptured cerebral aneurysms, of whom 18 had symptomatic vasospasm and 27 did not. Xenon-enhanced computed tomography was used to measure CBF in both groups during the acute, subacute, and chronic stages, defined as days 0-4, 5-20, and > or = 21, respectively. Vasoresponse was assessed by the CBF increase in response to 1 g of acetazolamide administered after the baseline CBF study, except in the subacute stage of patients with symptomatic vasospasm. Outcome was scored based on activities of daily living 2-3 months after subarachnoid hemorrhage. CBF values and the response to acetazolamide were preserved during the acute stage but CBF values fell considerably below control values during the subacute stage in patients with vasospasm. The regions with flow values below 15 ml/100 g/min subsequently converted to infarction and the regions with those above 19 ml/100 g/min remained intact without infarction. During the chronic stage, low CBF persisted, but the response to acetazolamide was higher than that of the control group. Outcome scores were good and fair. CBF values were normal during all stages in patients without vasospasm. The response to acetazolamide fell transiently during the subacute stage. All outcome scores were excellent. In conclusion, the CBF informations soon after the onset of symptomatic vasospasm are useful to predict a reversibility of ischemic brain tissue and a final outcome. We suggest that vasospasm may cause a pathological or ischemic insult to brain tissue during the subacute stage, and the brain may remain metabolically depressed thereafter, leading to a poor outcome. Even clinically asymptomatic patients may suffer mildly vasospastic or ischemic conditions during the subacute stage.