Course Of Vasospasm Research Articles

The epidemiology of vasospasm in children with moderate-to-severe traumatic brain injury.

To gain a description of the prevalence and time course of vasospasm in children suffering moderate-to-severe traumatic brain injury. A prospective, observational study was performed. Children with a diagnosis of traumatic brain injury, a Glasgow Coma Score less than or equal to 12, and abnormal head imaging were enrolled. Transcranial Doppler ultrasound was performed to identify and follow vasospasm. Diagnostic criteria included flow velocity elevation more than or equal to 2 sd above age and gender normal values for the middle cerebral and basilar arteries. Additional criteria required for vasospasm diagnosis in the middle cerebral artery was a ratio of flow in the middle cerebral artery to extracranial internal carotid artery more than or equal to 3. None. Sixty-nine children were included. The prevalence of middle cerebral artery vasospasm in children with moderate traumatic brain injury (Glasgow Coma Score, 9-12) was 8.5% and was 33.5% in those with severe traumatic brain injury (Glasgow Coma Score, ≤ 8). The prevalence of basilar artery vasospasm in children with moderate traumatic brain injury was 3% and with severe traumatic brain injury was 21%. Mean time to onset of vasospasm was 4 days (± 2 d) in the middle cerebral arteries and 5 days (± 2.5 d) in the basilar artery. Mean duration of vasospasm in the middle cerebral artery was 2 days (± 2 d) and 1.5 days (± 1 d) in the basilar artery. Children in whom vasospasm developed were more likely to have been involved in motor vehicle accidents, had higher Injury Severity Scores, had fever at admission, and had lower Glasgow Coma Score scores. Good neurologic outcome (Glasgow Outcome Score Extended Pediatric version of ≥ 4) at 1 month from injury was seen in 76% of those with moderate traumatic brain injury without vasospasm and in 40% of those with vasospasm. In those with severe traumatic brain injury, good neurologic outcome was seen in 29% of those children without vasospasm and in 15% of those with vasospasm. Vasospasm occurs in a sizeable number of children with moderate and severe traumatic brain injury. Children in whom vasospasm developed were more likely to have been involved in a motor vehicle accident, had higher Injury Severity Scores, had fever at admission, and had lower Glasgow Coma scores than in those whom vasospasm did not develop. Based on these findings, we recommend aggressive screening for posttraumatic vasospasm in these patients. Future studies should establish the relationship between vasospasm and long-term functional outcomes and should also evaluate potential preventative or therapeutic options for vasospasm in these children.

The еffectiveness of simvastatin in treating vasospasm in patients with rupture of arterial cerebral aneurysms

Introduction. Vasospasm is a leading cause of disability and mortality in cases of arterial cerebral aneurysms rupture. The search for new methods of prevention and treatment still continues.Materials and methods. The study of the effectiveness of simvastatin in the prevention and treatment of vasospasm has been carried out. Spasm severity was assessed by transcranial Doppler, the level of C-reactive protein.Results. Decrease in the severity of arterial spasm and shortening of its regression term with simvastatin has been noted.Conclusions. The use of simvastatin in acute aneurysmal subarachnoid hemorrhage origin modifies the course of vasospasm, helps to prevent the development of critical vasospasm, reduces the activity of endothelial inflammation, reduces the duration of hospital stay.

Description of the Vasospasm Phenomena following Perimesencephalic Nonaneurysmal Subarachnoid Hemorrhage

Background. Perimesencephalic nonaneurysmal subarachnoid hemorrhage (PM-NASAH) is characterized by a benign course compared with aneurysmal SAH. While vasospasm (VS) after aneurysmal SAH is considered responsible for serious complications, VS post-PM-NASAH is not well documented. Our purpose was to characterize the incidence and course of VS among 63 patients—one of the largest databases of PM-NASAH patients with documented blood flow velocities in the literature. Methods. Data from 63 patients that were admitted with PM-NASAH from 2000 to 2012 and underwent transcranial Doppler tests to assess cranial vessel flow velocity was analyzed. Results. On average, the maximal flow velocity was measured on the 7th day after hemorrhage. Higher risk for VS was associated with younger age, female sex, and higher Hunt and Hess scores, a lower risk for patients treated with statins (P < 0.05). Using velocity thresholds for diagnosis of VS, 49.2% showed evidence of VS. This is the first description of blood flow velocities in PM-NASAH. VS average onset was on the 4th day, average cessation on day 15 after hemorrhage. No patients showed clinical manifestation of VS. Conclusions. VS post-PM-NASAH is not as rare as previously believed. However, its lack of clinical significance raises questions regarding the need for diagnosis and may suggest a less intensive treatment protocol.

TRANSCRANIAL DOPPLER FOR PREDICTING DELAYED CEREBRAL ISCHEMIA AFTER SUBARACHNOID HEMORRHAGE

Transcranial Doppler (TCD) is widely used to monitor the temporal course of vasospasm after subarachnoid hemorrhage (SAH), but its ability to predict clinical deterioration or infarction from delayed cerebral ischemia (DCI) remains controversial. We sought to determine the prognostic utility of serial TCD examination after SAH. We analyzed 1877 TCD examinations in 441 aneurysmal SAH patients within 14 days of onset. The highest mean blood flow velocity (mBFV) value in any vessel before DCI onset was recorded. DCI was defined as clinical deterioration or computed tomographic evidence of infarction caused by vasospasm, with adjudication by consensus of the study team. Logistic regression was used to calculate adjusted odds ratios for DCI risk after controlling for other risk factors. DCI occurred in 21% of patients (n = 92). Multivariate predictors of DCI included modified Fisher computed tomographic score (P = 0.001), poor clinical grade (P = 0.04), and female sex (P = 0.008). After controlling for these variables, all TCD mBFV thresholds between 120 and 180 cm/s added a modest degree of incremental predictive value for DCI at nearly all time points, with maximal sensitivity by SAH day 8. However, the sensitivity of any mBFV more than 120 cm/s for subsequent DCI was only 63%, with a positive predictive value of 22% among patients with Hunt and Hess grades I to III and 36% in patients with Hunt and Hess grades IV and V. Positive predictive value was only slightly higher if mBFV exceeded 180 cm/s. Increased TCD flow velocities imply only a mild incremental risk of DCI after SAH, with maximal sensitivity by day 8. Nearly 40% of patients with DCI never attained an mBFV more than 120 cm/s during the course of monitoring. Given the poor overall sensitivity of TCD, improved methods for identifying patients at high risk for DCI after SAH are needed.

Spasm index in subarachnoid haemorrhage: consequences of vasospasm upon cerebral blood flow and oxygen extraction

A spasm index, defined as transcranial Doppler detected flow velocity in the middle cerebral artery divided by regional cortical cerebral blood flow (CBF), was used on 24 patients with subarachnoid haemorrhage (SAH). The aim was to estimate degree and time course of vasospasm, even in cases with great day-to-day variation in CBF, and correlate to CBF and oxygen extraction. All patients showed increase in spasm indices with peak index in the second or third week. The index seemed stable in spite of day-to-day fluctuations in CBF. Severe vasospasm were associated with poor clinical condition, reduced CBF (less than 30) and high AVDO2. The same picture could be seen with minor degree of vasospasm, probably, in some cases, due to high intracranial pressure. The results suggest that the spasm index is useful in monitoring patients with subarachnoid haemorrhage, and that severe vasospasm has a negative influence on clinical condition, CBF and oxygen extraction.

Brain Vasospasm After Head Injury

Object. The purpose of this prospective study was to evaluate the cumulative incidence, duration, and time course of cerebral vasospasm after traumatic brain injury (TBI) in a cohort of 299 patients. Methods. Transcranial Doppler (TCD) ultrasonography studies of blood flow velocity in the middle cerebral and basilar arteries (VMCA and VBA, respectively) were performed at regular intervals during the first 2 weeks posttrauma in association with 133Xe cerebral blood flow (CBF) measurements. According to current definitions of vasospasm, five different criteria were used to classify the patients: A (VMCA &gt; 120 cm/second); B (VMCA &gt; 120 cm/second and a Lindegaard ratio [LR] &gt; 3); C (spasm index [SI] in the anterior circulation &gt; 3.4); D (VBA &gt; 90 cm/second); and E (SI in the posterior circulation &gt; 2.5). Criteria C and E were considered to represent hemodynamically significant vasospasm. Mixed-effects spline models were used to analyze the data of multiple measurements with an inconsistent sampling rate. Overall 45.2% of the patients demonstrated at least one criterion for vasospasm. The patients in whom vasospasm developed were significantly younger and had lower Glasgow Coma Scale scores on admission. The normalized cumulative incidences were 36.9 and 36.2% for patients with Criteria A and B, respectively. Hemodynamically significant vasospasm in the anterior circulation (Criterion C) was found in 44.6% of the patients, whereas vasospasm in the BA—Criterion D or E—was found in only 19 and 22.5% of the patients, respectively. The most common day of onset for Criteria A, B, D, and E was postinjury Day 2. The highest risk of developing hemodynamically significant vasospasm in the anterior circulation was found on Day 3. The daily prevalence of vasospasm in patients in the intensive care unit was 30% from postinjury Day 2 to Day 13. Vasospasm resolved after a duration of 5 days in 50% of the patients with Criterion A or B and after a period of 3.5 days in 50% of those patients with Criterion D or E. Hemodynamically significant vasospasm in the anterior circulation resolved after 2.5 days in 50% of the patients. The time course of that vasospasm was primarily determined by a decrease in CBF. Conclusions. The incidence of vasospasm after TBI is similar to that following aneurysmal subarachnoid hemorrhage. Because vasospasm is a significant event in a high proportion of patients after severe head injury, close TCD and CBF monitoring is recommended for the treatment of such patients.

Dysfunction of nitric oxide synthases as a cause and therapeutic target in delayed cerebral vasospasm after SAH

Nitric oxide (NO), also known as endothelium-derived relaxing factor, is produced by endothelial nitric oxide synthase (eNOS) in the intima and by neuronal nitric oxide synthase (nNOS) in the adventitia of cerebral vessels. It dilates the arteries in response to shear stress, metabolic demands, pterygopalatine ganglion stimulation and chemoregulation. Subarachnoid hemorrhage (SAH) interrupts this regulation of cerebral blood flow. Hemoglobin, gradually released from erythrocytes in the subarachnoid space, destroys nNOS-containing neurons in the conductive arteries. This deprives the arteries of NO, leading to initiation of delayed vasospasm. But such vessel narrowing increases shear stress, which stimulates eNOS. This mechanism normally would lead to increased production of NO and dilation of arteries. However, a transient eNOS dysfunction evoked by an increase in the endogenous competitive NOS inhibitor, asymmetric dimethylarginine (ADMA), prevents this vasodilation. eNOS dysfunction has been recently shown to be evoked by increased levels of ADMA in cerebrospinal fluid (CSF) in response to the presence of bilirubin-oxidized fragments (BOXes). A direct cause of the increased ADMA CSF level is most likely decreased ADMA elimination owing to disappearance of ADMA-hydrolyzing enzyme [dimethylarginine dimethylaminohydrolase II (DDAH II)] immunoreactivity in the arteries in spasm. This eNOS dysfunction sustains vasospasm. CSF ADMA levels are closely associated with the degree and time course of vasospasm; when CSF ADMA levels decrease, vasospasm resolves. Thus, exogenous delivery of NO, inhibiting the L-arginine-methylating enzyme or stimulating DDAH II, may provide new therapeutic modalities to prevent and treat vasospasm. This paper will present results of pre-clinical studies supporting the NO-based hypothesis of delayed cerebral vasospasm development and its prevention by increased NO availability.

Comparison between one- and two-hemorrhage models of cerebral vasospasm in rabbits

Injection of blood into the cisterna magna is one of the most frequently used methods to produce subarachnoid hemorrhage (SAH) models in animals. Although the two-hemorrhage model of vasospasm is frequently used in canine and rat models, most studies with rabbits only use the one-hemorrhage model. In the present study, we accomplished a side-by-side comparison between one- and two-hemorrhage models in rabbits. A total of 38 rabbits were randomly divided into three groups, i.e. control group ( n = 5), one ( n = 15)- and two ( n = 18)-hemorrhage model groups. The degree of cerebral vasospasm, the time course of cerebral vasospasm, the clinical behavior, and the residual amount of subarachnoid blood clots were measured on days 3, 5 and 7 after the establishment of the models. Compared with one-hemorrhage model, the time course of vasospasm in the two-hemorrhage model was more coincident with that observed in humans, produced more severe vasospasm after SAH, and had an acceptable low mortality. In conclusion, the two-hemorrhage model in rabbits is more appropriate than the one-hemorrhage model for the research on SAH or cerebral vasospasm, and thus can be used for the investigation of the mechanisms of and therapeutic approaches for cerebral vasospasm.

Dynamic Perfusion Computed Tomography in the Diagnosis of Cerebral Vasospasm

The aim of the study was to correlate absolute cerebral blood flow (CBF) and mean transient time (MTT) measured by dynamic perfusion computed tomographic (PCT) scanning with the clinical course, vasospasm severity, and perfusion abnormality in patients with cerebral vasospasm after aneurysmal subarachnoid hemorrhage. Forty-six patients with vasospasm after aneurysmal subarachnoid hemorrhage had 63 PCT images obtained during the course of vasospasm. All patients had transcranial Doppler measurements, 28 had an angiography study, and 38 had 99mTc single-photon emission computed tomographic imaging performed in conjunction with the PCT scan. The average minimal regional CBF (rCBF) and maximal regional MTT in patients with delayed ischemic deficit were significantly different in comparison with patients without delayed ischemic deficit (22.6 +/- 11.2 cm3/100 g/min versus 45.2 +/- 21.3 cm3/100 g/min, P < 0.001; 7.3 +/- 2.5 s versus 3.3 +/- 1.7 s, P < 0.05). The average minimal rCBF and maximal regional MTT in middle cerebral vascular territories in which severe middle cerebral artery vasospasm was measured by transcranial Doppler were significantly different in comparison with middle cerebral vascular territories in which no vasospasm was measured by transcranial Doppler (29.3 +/- 1.7 cm3/100 g/min versus 54.1 +/- 25.4 cm3/100 g/min, P < 0.01; 4.5 +/- 2.4 s versus 2.8 +/- 1.1 P < 0.001). The average minimal rCBF and maximal rMTT in vascular territories with estimated severe hypoperfusion on single-photon emission computed tomographic imaging were significantly different in comparison with values in vascular territories with unimpaired perfusion as estimated by single-photon emission computed tomographic imaging (18.9 +/- 6.9 cm3/100 g/min versus 54.2 +/- 23.4 cm3/100 g/min, P < 0.001, 0.001; 8.1 +/- 1.9 s versus 2.5 +/- 0.39 s, P < 0.001). The present study suggests that, in general, quantitative measurements of rCBF and regional MTT by PCT show high concordance rates with the clinical course, vasospasm severity, and hemodynamic impairments in patients with cerebral vasospasm aneurysmal subarachnoid hemorrhage.

Correspondence between the time course of cerebral vasospasm and the level of cerebral dopamine-β-hydroxylase in rabbits

The aim of the study was to explore whether the biphasic time course of the vasospastic response following experimental subarachnoid hemorrhage is associated with any concomitant changes in the amount of cerebral dopamine β-hydroxylase in the noradrenergic central nervous system. A single-hemorrhage animal model was used. Rabbits were sacrificed from day 1 to day 8 after subarachnoid hemorrhage. Intimal corrugation of the basilar artery and the amount of cerebral dopamine β-hydroxylase in the hypothalamus and brain stem were measured each day. Vasospastic changes occurred in the biphasic manner following subarachnoid hemorrhage. More profound vasospastic corrugation occurred in the acute phase, followed by a slightly less intense corrugation in the chronic phase (between days 5 and 8 after the subarachnoid hemorrhage). Simultaneously, a clear concomitant biphasic time course developed in the form of an increased amount of dopamine-β-hydroxylase in the noradrenergic nervous system of the rabbit hypothalamus and brain stem during the acute and chronic phases after the subarachnoid hemorrhage. Statistically significant correlation between basilar artery corrugation and the amount of dopamine β-hydroxylase was found. These results suggest the possible role of the central sympathetic system in the pathogenesis of vasospasm. At the same time, this study demonstrates the chronological similarity of the vasospastic development after subarachnoid hemorrhage in the animal experimental model with the human time course of vasospasm.

Posttraumatic vasospasm: the epidemiology, severity, and time course of an underestimated phenomenon: a prospective study performed in 299 patients

The purpose of this prospective study was to evaluate the cumulative incidence, duration, and time course of cerebral vasospasm after traumatic brain injury (TBI) in a cohort of 299 patients. Transcranial Doppler (TCD) ultrasonography studies of blood flow velocity in the middle cerebral and basilar arteries (VMCA and VBA, respectively) were performed at regular intervals during the first 2 weeks posttrauma in association with 133Xe cerebral blood flow (CBF) measurements. According to current definitions of vasospasm, five different criteria were used to classify the patients: A (VMCA > 120 cm/second); B (VMCA > 120 cm/second and a Lindegaard ratio [LR] > 3); C (spasm index [SI] in the anterior circulation > 3.4); D (VBA > 90 cm/second); and E (SI in the posterior circulation > 2.5). Criteria C and E were considered to represent hemodynamically significant vasospasm. Mixed-effects spline models were used to analyze the data of multiple measurements with an inconsistent sampling rate. Overall 45.2% of the patients demonstrated at least one criterion for vasospasm. The patients in whom vasospasm developed were significantly younger and had lower Glasgow Coma Scale scores on admission. The normalized cumulative incidences were 36.9 and 36.2% for patients with Criteria A and B, respectively. Hemodynamically significant vasospasm in the anterior circulation (Criterion C) was found in 44.6% of the patients, whereas vasospasm in the BA-Criterion D or E-was found in only 19 and 22.5% of the patients, respectively. The most common day of onset for Criteria A, B, D, and E was postinjury Day 2. The highest risk of developing hemodynamically significant vasospasm in the anterior circulation was found on Day 3. The daily prevalence of vasospasm in patients in the intensive care unit was 30% from postinjury Day 2 to Day 13. Vasospasm resolved after a duration of 5 days in 50% of the patients with Criterion A or B and after a period of 3.5 days in 50% of those patients with Criterion D or E. Hemodynamically significant vasospasm in the anterior circulation resolved after 2.5 days in 50% of the patients. The time course of that vasospasm was primarily determined by a decrease in CBF. The incidence of vasospasm after TBI is similar to that following aneurysmal subarachnoid hemorrhage. Because vasospasm is a significant event in a high proportion of patients after severe head injury, close TCD and CBF monitoring is recommended for the treatment of such patients.

High-dose methylprednisolone prevents vasospasm after subarachnoid hemorrhage through inhibition of protein kinase C activation

We have previously shown that the inflammatory process after subarachnoid hemorrhage causes vasospasm. The efficacy of methylprednisolone by suppression of the inflammatory process has been reported, although pharmacological mechanisms have not been clarified. The purpose of this study was to investigate the pharmacological mechanism of methylprednisolone on vasospasm. Using the 'two-hemorrhage' canine model, progression of angiographic vasospasm was assessed in nontreated and treated groups with methylprednisolone. Methylprednisolone 10 mg kg-1 was injected i.v. after the first injection of blood, and the same dose was injected every 12 h until day 7. Protein kinase C (PKC) activity of canine basilar arteries in both groups was measured during the course of vasospasm. In the isometric tension study, the effect of methylprednisolone on tensions induced by phorbol 12-myristate 13-acetate (PMA), or high-K+ solution, was also evaluated. Methylprednisolone significantly reduced severity of vasospasm. In the treated group, PKC activity was not enhanced compared with the nontreated group at any point. Methylprednisolone inhibited tonic tension induced by PMA, but not that induced by high-K+ solution. We conclude that methylprednisolone prevents severity of vasospasm through inhibition of PKC activation, but does not work as a Ca2+ channel blocker. [Neurol Res 2002; 24: 215-222]

Cerebrospinal fluid membrane-bound tissue factor and myelin basic protein in the course of vasospasm after subarachnoid hemorrhage

No marker that predicts accurately the time of occurrence of cerebral vasospasm due to subarachnoid hemorrhage (SAH) has been reported. In the present study, membrane-bound tissue factor (mTF) and myelin basic protein (MBP) concentrations in cerebrospinal fluid (CSF) were evaluated as a predictor of the time of occurrence of cerebral vasospasm. The mTF and MBP concentrations were measured in the CSF from 28 patients with SAH due to ruptured aneurysm. Serial assays were performed from day 4 to day 14 after SAH. CSF mTF and MBP concentrations from days 5 to 9 correlated with the volume of cerebral infarction due to vasospasm and outcome three months after SAH. From the serial assays, CSF mTF measurements predicted the time of occurrence and severity and irreversibility of symptoms due to vasospasm. In conclusion, CSF mTF is predictive of the occurrence and the recovery of cerebral vasospasm, while CSF MBP is only an indicator of severity of brain damage due to vasospasm. [Neurol Res 2001; 23: 715-720]

Perioperative management of aneurysmal subarachnoid hemorrhage: Part 2. Postoperative management.

Perioperative management of aneurysmal subarachnoid hemorrhage: Part 2. Postoperative management.

A review of cerebral vasospasm in aneurysmal subarachnoid haemorrhage

The possible mechanisms by which calcium antagonists are effective in the management of cerebral vasospasm are discussed. They number seven: relaxation of spastic arteries or prevention of spasm; opening up of collateral channels; neuronal protection at the membrane level; intracellular actions in neurones or vascular cells; alterations of blood rheology; antimitogenic effects; and improved fluid management of patients. A number of more minor actions may also be involved. It is likely that more than one mechanism is involved in their protective effect, especially at different periods in the time course of vasospasm.

Posttraumatic cerebral arterial spasm: transcranial Doppler ultrasound, cerebral blood flow, and angiographic findings

Thirty patients admitted after suffering closed head injuries, with Glasgow Coma Scale scores ranging from 3 to 15, were evaluated with transcranial Doppler ultrasound monitoring. Blood flow velocity was determined in the middle cerebral artery (MCA) and the intracranial portion of the internal carotid artery (ICA) in all patients. Because proximal flow in the extracranial ICA declines in velocity when arterial narrowing becomes hemodynamically significant, the extracranial ICA velocity was concurrently monitored in 19 patients. To assess cerebral perfusion, cerebral blood flow (CBF) measurements obtained with the intravenous 133Xe technique were completed in 16 patients. Vasospasm, designated as MCA velocity exceeding 120 cm/sec, was found in eight patients (26.7%). Severe vasospasm, defined as MCA velocity greater than 200 cm/sec, occurred in three patients, and was confirmed by angiography in all three. Subarachnoid hemorrhage (SAH) was documented by computerized tomography in five (62.5%) of the eight patients with vasospasm. All cases of severe vasospasm were associated with subarachnoid blood. The time course of vasospasm in patients with traumatic SAH was similar to that found in patients with aneurysmal SAH; in contrast, arterial spasm not associated with SAH demonstrated an uncharacteristically short duration (mean 1.25 days), suggesting that this may be a different type of spasm. A significant correlation (p less than 0.05) was identified between the lowest CBF and highest MCA velocity in patients during the period of vasospasm, indicating that arterial narrowing can lead to impaired CBF. Ischemic brain damage was found in one patient who had evidence of cerebral infarction in the territories supplied by the arteries affected by spasm. These findings demonstrate that delayed cerebral arterial spasm is a frequent complication of closed head injury and that the severity of spasm is, in some cases, comparable to that seen in aneurysmal SAH. This experience suggests that vasospasm is an important secondary posttraumatic insult that is potentially treatable.

The course of vasospasm following subarachnoid haemorrhage in rats. A vertebrobasilar angiographic study.

The course of vasospasm following subarachnoid haemorrhage in rats was studied using vertebrobasilar angiography. Wistar and Sprague Dawley rats were compared with respect to vasospastic response after bleeding. A more pronounced vasospasm was found in Sprague Dawley rats. In order to avoid a possible toxic effect on the contrast medium, only one angiogram per animal was initially performed. However, a comparison with the results obtained in a separate series of non-challenged animals demonstrated a difficulty due to high variability in basilar artery size in the latter group. Therefore, vasospasm can be more readily shown if multiple angiograms are used in the same animal so that the vasospasm can be expressed as a percentage of the initial diameter of the basilar artery. It was found that multiple angiograms are well tolerated when non-ionic contrast media are used.

Cerebral vasospasm evaluated by transcranial Doppler ultrasonography at different intracranial pressures

The present study evaluates the interdependence of clinical stage, cerebral vasospasm, intracranial pressure (ICP), and transcranial Doppler ultrasonographic parameters. The mean flow velocity of blood in the middle cerebral artery and the index of cerebral circulatory resistance as a measure of the peripheral vascular flow resistance were determined in 76 patients with spontaneous subarachnoid hemorrhage. The ICP was measured using an epidural transducer in 41 patients. There was no case in which both high ICP and a high mean flow velocity were observed simultaneously. The investigations led to the following conclusions. 1) In patients with a resistance index of less than 0.5, changes in the mean flow velocity seem to reflect sufficiently the actual severity and time course of vasospasm. 2) During the time course of vasospasm, an increase in the resistance index above values of 0.6 with a simultaneously decreased mean flow velocity indicates a rise in ICP rather than a reduction in vasospasm. 3) With a pronounced increase in ICP, evaluation of the severity and time course of vasospasm by transcranial Doppler ultrasonography based solely upon the mean flow velocity can lead to false-negative results.

The correlation between immunological reaction in the arterial wall and the time course of the development of cerebral vasospasm in a primate model

To investigate the role of immunological reactions in the development of cerebral vasospasm after subarachnoid hemorrhage (SAH), the authors studied the correlation between immune/inflammatory reactions in the arterial wall and the time course of vasospasm in primates. Twenty monkeys were divided into four groups of 5 animals each: 1) a control group of sham-operated animals, 2) animals subjected to angiography 3 days after the induction of SAH (3-day SAH), 3) animals subjected to angiography 7 days after SAH (1-week SAH), and 4) animals subjected to angiography 7 and 14 days after SAH (2-week SAH). To induce SAH, the main cerebral arteries on the right were dissected free of the arachnoid, and an autologous blood clot was placed around the arteries. To evaluate vasospasm, all animals underwent a baseline angiogram before SAH; angiography was repeated at different intervals in each group, as outlined above. Histopathological changes and the deposition of the immunoglobulin IgG in the arterial wall were evaluated immunohistochemically in each group. The cerebral arteries on the side of the clot showed evidence of mild vasospasm (-24.6% reduction) on the angiogram performed on Day 3, severe vasospasm (-51.7%) on Day 7, and mild vasospasm (-12.8%) on Day 14. The infiltration of inflammatory cells was most marked in the spastic arterial wall in the 1-week SAH group. In the 2-week SAH group, severe myonecrosis and intimal disruption were observed, even in the vessels that showed only mild vasospasm, and the inflammatory reactions had almost abated.(ABSTRACT TRUNCATED AT 250 WORDS)

The Timing of Surgery and Vasospasm

The relationship of time of surgery and vasospasm is influenced by three factors: (1) the time course of vasospasm, (2) the effectiveness of clot removal at surgery, and (3) the choice of medical management to prevent rebleeding and to treat vasospasm. Data to date demonstrate that angiographic vasospasm and vasospasm-related deficits occur in the period from 4 to 14 days after subarachnoid hemorrhage. Surgical intervention in the period of risk for vasospasm is associated with higher morbidity and mortality rates. Morbidity and mortality rates are lowest following surgery in patients who have delayed surgery; however, morbidity and mortality rates for overall management are equivalent for patients with early surgery because of vasospasm and rebleeding in patients waiting for delayed surgery. The surgical removal of the clot may be accomplished in only a limited number of patients, and most series do not reflect a large change in vasospasm occurrence following early surgery. Changes to more aggressive medical therapy in terms of prevention or reversal of ischemia from vasospasm rendered after the aneurysm is clipped and rebleeding is prevented have been initiated during the past decade. The effectiveness and safety of these treatments may play an important future role in the choice of time of surgery and the relationship of time of surgery to vasospasm-related deficits.