Transcranial Doppler ultrasound studies of cerebral autoregulation and subarachnoid hemorrhage in the rabbit

1990 ◽  
Vol 73 (4) ◽  
pp. 601-610 ◽  
Author(s):  
Richard J. Nelson ◽  
Sheila Perry ◽  
Tony K. Hames ◽  
John D. Pickard
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Flow Velocity ◽  
Doppler Ultrasound ◽  
Transcranial Doppler ◽  
Cerebral Autoregulation ◽  
Time Course ◽  
Cerebrovascular Reactivity ◽  
Waveform Analysis ◽  
Content Type ◽  
Fine Print

✓ The authors describe a method for Doppler ultrasound recording of flow velocity in the basilar artery of normal rabbits and rabbits with experimental subarachnoid hemorrhage (SAH). With this transcranial Doppler (TCD) model, clinical assumptions regarding flow velocity/cerebral blood flow (CBF) relationships, autoregulatory responses, and Doppler spectral waveform analysis can be tested under controlled conditions and compared with established methods of CBF measurement (hydrogen clearance). The time course of changes in flow velocity following SAH (cerebral vasospasm) is successfully demonstrated using the experimental TCD method. There are significant differences in the flow velocity and CBF responses to hypercapnia, hypocapnia, and trimethaphan-induced hypotension which indicate that TCD cannot be considered a simple alternative to CBF measurement for the study of cerebrovascular reactivity and cerebral autoregulation.

A randomized trial of nicardipine in subarachnoid hemorrhage: angiographic and transcranial Doppler ultrasound results

1993 ◽  
Vol 78 (4) ◽  
pp. 548-553 ◽  
Author(s):  
E. Clarke Haley ◽  
Neal F. Kassell ◽  
James C. Torner ◽  
_ _
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Doppler Ultrasound ◽  
Transcranial Doppler ◽  
Transcranial Doppler Ultrasound ◽  
High Dose ◽  
Content Type ◽  
Central Registry ◽  
Significant Difference ◽  
Fine Print ◽  
Flow Velocities

✓ 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.

Cerebral hemodynamic impairment after aneurysmal subarachnoid hemorrhage as evaluated using transcranial Doppler ultrasonography: relationship to delayed cerebral ischemia and clinical outcome

2001 ◽  
Vol 95 (3) ◽  
pp. 393-401 ◽  
Author(s):  
Tõnu Rätsep ◽  
Toomas Asser
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Clinical Outcome ◽  
Transcranial Doppler ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Content Type ◽  
Unfavorable Clinical Outcome ◽  
Hemodynamic Impairment ◽  
Fine Print

Object. In this study the authors evaluated the relative role of cerebral hemodynamic impairment (HDI) in the pathogenesis of delayed cerebral ischemia and poor clinical outcome after aneurysmal subarachnoid hemorrhage (SAH). Methods. Cerebral hemodynamics were assessed daily with transcranial Doppler (TCD) ultrasonography in 55 consecutive patients with verified SAH. Hemodynamic impairment was defined as blood flow velocity (BFV) values consistent with vasospasm in conjunction with impaired autoregulatory vasodilation as evaluated using the transient hyperemic response tests in the middle cerebral arteries. A total of 1344 TCD examinations were performed, in which the evaluation of HDI was feasible during 80.9% and HDI was registered during 12% of the examinations. It was found that HDI occurred in 60% of patients and was frequently recorded in conjunction with severe vasospasm (p < 0.05) and a rapid increase of BFV values (p < 0.05). Detection of HDI was closely associated with the development of delayed ischemic brain damage after SAH (p < 0.05). Furthermore, because delayed ischemia was never observed in cases in which vasospasm had not led to the development of HDI, its occurrence increased significantly the likelihood of subsequent cerebral ischemia among the patients with vasospasm (p < 0.05). Detection of HDI was independently related to unfavorable clinical outcome according to Glasgow Outcome Scale at 6 months after SAH (p < 0.05). Conclusions. The results showed that HDI is common after SAH and can be evaluated with TCD ultrasonography in routine clinical practice. Detection of HDI could be useful for identifying patients at high or low risk for delayed ischemic complications and unfavorable clinical outcome after SAH.

Is routine transcranial Doppler ultrasound monitoring useful in the management of subarachnoid hemorrhage?

1998 ◽  
Vol 88 (2) ◽  
pp. 272-276 ◽  
Author(s):  
Joanna M. Wardlaw ◽  
Ruth Offin ◽  
Graham M. Teasdale ◽  
Evelyn M. Teasdale
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Neurological Deficit ◽  
Transcranial Doppler ◽  
Controlled Trial ◽  
Positive Contribution ◽  
Content Type ◽  
Delayed Ischemic Neurological Deficit ◽  
Ultrasound Monitoring ◽  
The Impact ◽  
Fine Print

Object. In this prospective observational study, the authors assess the impact of routine transcranial Doppler (TCD) ultrasound monitoring on the diagnosis, management, and outcome of delayed ischemic neurological deficit complicating subarachnoid hemorrhage (SAH). Methods. Over a 10-month period 186 patients admitted to a regional neurosciences center were included in the study. Three times a week, routine TCD examinations performed by neuroradiographers made an important positive contribution to the diagnosis of delayed ischemic neurological deficit in 72% of patients with this complication and led to altered management for the benefit of the patient in 43%. In 9% of patients with recent SAH, it was believed that the outcome might have been better if the TCD result had been acted upon appropriately. The TCD results did not adversely influence management or outcome and were generally accurate when compared with those obtained on angiography. Conclusions. A routine TCD service provided by neuroradiographers is accurate and useful in diagnosing and managing elevated blood velocities and ischemic neurological deficit following SAH. In addition, it is possible that if the information gleaned from TCD findings was used more often in patient management, outcome might be improved; however, a randomized controlled trial is necessary to assess both these points definitively.

Time course of vasospasm in man

1978 ◽  
Vol 48 (2) ◽  
pp. 173-178 ◽  
Author(s):  
Bryce Weir ◽  
Michael Grace ◽  
John Hansen ◽  
Charles Rothberg
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Subarachnoid Space ◽  
Time Course ◽  
Content Type ◽  
Base Of Skull ◽  
Fine Print

✓ Measurements were made at eight predetermined positions on 627 sets of angiograms from 293 patients with aneurysms. A ratio between the sum of the vessel diameters in the subarachnoid space to the sum in the base of skull and neck was calculated and plotted against time. Vasospasm has its onset in man about Day 3 after subarachnoid hemorrhage, is maximal at Days 6 to 8, and is gone by Day 12. There is a tendency for patients in poor clinical grades to have more vasospasm. The patients with most vasospasm have a significantly higher mortality than those with the least.

Cerebrovascular reactivity to noradrenaline and serotonin following experimental subarachnoid hemorrhage

1980 ◽  
Vol 53 (4) ◽  
pp. 480-485 ◽  
Author(s):  
Ramiro D. Lobato ◽  
Jesús Marín ◽  
Mercedes Salaices ◽  
Fernando Rivilla ◽  
Javier Burgos
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Time Course ◽  
Contractile Response ◽  
Cerebral Arteries ◽  
Cerebrovascular Reactivity ◽  
Content Type ◽  
Experimental Subarachnoid Hemorrhage ◽  
6 Hydroxydopamine ◽  
Chronic Cerebral Vasospasm ◽  
Supersensitivity To Noradrenaline

✓ This study analyzes the time course of the changes induced by subarachnoid hemorrhage (SAH) in the sensitivity of cat cerebral arteries to noradrenaline and serotonin. Cerebral arteries displayed a supersensitivity to these amines, which was most marked 3 days after the experiment and then gradually disappeared. The supersensitivity to serotonin was greater and longer than the response to noradrenaline. The increased in the vascular contractile response induced by SAH was similar to that seen after superior cervical ganglionectomy or intracisternal injections of 6-hydroxydopamine. It is suggested that supersensitivity to noradrenaline and serotonin induced by SAH may be involved in the production of chronic cerebral vasospasm.

Bilirubin as a cerebrospinal fluid marker of sentinel subarachnoid hemorrhage: a preliminary report in pigs

2004 ◽  
Vol 101 (6) ◽  
pp. 1026-1029 ◽  
Author(s):  
Chad J. Morgan ◽  
Gail J. Pyne-Geithman ◽  
Edward C. Jauch ◽  
Rakesh Shukla ◽  
Kenneth R. Wagner ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Time Course ◽  
Isotonic Saline ◽  
Bilirubin Concentration ◽  
Content Type ◽  
Arterial Blood ◽  
Potential Marker ◽  
Yorkshire Pigs ◽  
Fine Print

Object. A model of subarachnoid hemorrhage (SAH) in pigs was developed to investigate bilirubin concentration in cerebrospinal fluid (CSF) as a potential marker of sentinel SAH. Methods. Seven male Yorkshire pigs received a 250-µl injection of either whole autologous arterial blood (four animals) or isotonic saline (three animals) into the cisternae magna in an effort to produce volumetrically a model of sentinel SAH and a control injection model, respectively. Cerebrospinal fluid volumes of 100 µl were then collected from both the lumbar cistern and cisternae magna at 1 to 2-hour intervals for a total of 24 hours postinjection. The CSF was then tested for bilirubin. Mean concentrations of bilirubin (± standard deviation [SD]) obtained from the lumbar cistern 24 hours following the injection of blood or saline were 4.38 ± 1.04 µM in the SAH animals and 1.02 ± 0.05 µM in the controls. At 24 hours postinjection, mean concentrations (± SD) of cisternae magna bilirubin were 7.29 ± 1.33 ÉM and 1.33 ± 0.14 µM in the SAH animals and controls, respectively. In the SAH group, both the lumbar cistern and cisternae magna bilirubin concentrations differed significantly from baseline values 12 hours following SAH. Conclusions. Elevated concentrations of CSF bilirubin can be detected following a low-volume SAH, and the production of bilirubin occurred over a predictable time course. Twelve hours after hemorrhage, an elevated CSF bilirubin concentration was an indicator of hemolysis occurring in the subarachnoid spaces. The presence of bilirubin in CSF is a potential marker for differentiating SAHs from traumatic lumbar punctures in humans.

CO2 reactivity in arteriovenous malformations of the brain: a transcranial Doppler ultrasound study

1994 ◽  
Vol 80 (4) ◽  
pp. 624-630 ◽  
Author(s):  
Antônio A F. De Salles ◽  
Iñaki Manchola
Keyword(s):  
Carbon Dioxide ◽  
Doppler Ultrasound ◽  
Transcranial Doppler ◽  
Arteriovenous Malformations ◽  
Transcranial Doppler Ultrasound ◽  
Content Type ◽  
Control Subjects ◽  
Feeding Vessels ◽  
Carbon Dioxide Reactivity ◽  
Fine Print

✓ Arteriovenous malformations (AVM's) are congenital tangles of vessels that have a high blood flow through a low-resistance nidus. The vessels in the nidus may lack normal vasoreactivity in response to changes in PaCO2 or perfusion pressure (autoregulation). Arteriovenous malformation hemodynamics have been assessed based on the response of AVM feeding arteries to hypocapnia. Twenty-five AVM patients, aged 34 ± 11 years (mean ± standard deviation), were admitted to the Massachusetts General Hospital for proton-beam radiation therapy. Fourteen healthy volunteers aged 30 ± 7 years served as control subjects. Angiograms with calibrated markers permitting magnification correction were available for all patients. The limits of the middle cerebral artery, as determined by transcranial Doppler ultrasonography, were compared to measurements made on the angiograms. Hyperventilation was induced at a rate set by a metronome. Fixed bilateral Doppler probes allowed almost simultaneous sampling of two vessels. Volunteer control subjects were hyperventilated in two steps. The two PaCO2 step decreases were significant (mean resting PaCO2 40.6 ± 3.5 mm Hg, Step 1 level 29.4 ± 3.5 mm Hg and Step 2 level 23.8 ± 3.5 mm Hg; p < 0.01). These decreases induced a significant decrease in mean flow velocity (Vm) and an increase in the pulsatility index (p < 0.001). Mean carbon dioxide reactivity (%ΔVm/ΔPaCO2) was 2.74 ± 1.0 for Step 1 and 1.44 ± 1.8 for Step 2 (p < 0.003). The mean PaCO2 decrease in patients was from 39.5 ± 4.0 mm Hg to 27.0 ± 3.5 mm Hg. Carbon dioxide reactivity was 0.92 ± 1.12 for feeding vessels and 2.59 ± 1.78 for nonfeeding vessels (p < 0.001). Transcranial Doppler ultrasound and angiographic depth measurements correlated well. Hyperventilation induced significantly more hemodynamic changes in control and nonfeeding middle cerebral arteries than in feeding vessels. Impaired CO2 reactivity may help to identify AVM feeding vessels as well as the relative magnitude of the flow provided to the malformation.

Cerebrovascular Reactivity in Migraineurs as Measured by Transcranial Doppler

Cephalalgia ◽  
1990 ◽  
Vol 10 (2) ◽  
pp. 95-99 ◽  
Author(s):  
T Darrell Thomas ◽  
Gary J Harpold ◽  
B Todd Troost
Keyword(s):  
Blood Flow ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Doppler Ultrasound ◽  
Cerebral Artery ◽  
Transcranial Doppler ◽  
Blood Flow Velocity ◽  
Transcranial Doppler Ultrasound ◽  
Cerebrovascular Reactivity ◽  
Artery Blood Flow

Transcranial Doppler ultrasound is a relatively new diagnostic modality which allows the non-invasive assessment of intracranial circulation. A total of 10 migraine patients were studied and compared to healthy controls without headaches. Migraineurs during the headache-free interval demonstrated excessive cerebrovascular reactivity to CO2, evidenced by an increase in middle cerebral artery blood flow velocity of 47% ± 15% compared to 28% ± 14% in controls ( p = 0.026). Differences between the two study groups revealed no significant decrease in middle cerebral artery blood flow velocity with hypocapnia. However, the differences between middle cerebral artery blood flow velocity during hyperventilation and CO2 inhalation were significantly different ( p = 0.004) comparing migraineurs and controls. Instability of the baseline blood flow velocities was also noted in migraineurs during the interictal period. Characteristics which may allow differentiation of migraineurs from other headache populations could possibly be obtained from transcranial Doppler ultrasound flow studies.

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

1992 ◽  
Vol 77 (4) ◽  
pp. 575-583 ◽  
Author(s):  
Neil A. Martin ◽  
Curtis Doberstein ◽  
Cynthia Zane ◽  
Michael J. Caron ◽  
Kathleen Thomas ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Doppler Ultrasound ◽  
Transcranial Doppler ◽  
Transcranial Doppler Ultrasound ◽  
Arterial Spasm ◽  
Content Type ◽  
Closed Head ◽  
Extracranial Ica ◽  
Fine Print

✓ 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 113Xe 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 < 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.

Chronic cerebral vasospasm after large subarachnoid hemorrhage in monkeys

1982 ◽  
Vol 57 (2) ◽  
pp. 224-232 ◽  
Author(s):  
Francisco Espinosa ◽  
Bryce Weir ◽  
Donald Boisvert ◽  
Thomas Overton ◽  
William Castor
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Ct Scan ◽  
Cerebral Vasospasm ◽  
Time Course ◽  
Neurological Status ◽  
Clinical Situation ◽  
Content Type ◽  
Cranial Ct ◽  
Chronic Cerebral Vasospasm ◽  
Fine Print

✓ The authors have developed a model of chronic cerebral vasospasm analogous to the clinical situation, by inducing a large subarachnoid hemorrhage (SAH) in monkeys. With this model, the size of the SAH apparent on the first computerized tomography (CT) scan was correlated with the incidence and severity of cerebral vasospasm that developed. Indices monitored for up to 21 days after SAH included cranial CT scan, cerebral blood flow, vessel caliber, and neurological status. The 18 monkeys studied for 48 hours or more were divided into two groups according to the size of the SAH on CT scan. Vasospasm was more common in the group with large SAH. In this group, on Days 0, 7, and 14, the incidence of vasospasm was significantly higher than at other times (p < 0.001, p < 0.01, and p < 0.05, respectively), and the percentage reduction in vessel caliber was significantly greater than in the group with small/medium SAH (Day 7, p < 0.02; Days 0 and 14, p < 0.05). Delayed neurological deficit developed in two monkeys with large SAH. Apathy was noted from Day 17 to Day 21 in one, and unsteadiness and drowsiness were noted on Days 4 and 5 in the other. Overall, the incidence, degree, and time course of vasospasm reflected the size of the hemorrhage.

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