Cluster Headache: Transcranial Doppler Ultrasound and rCBF Studies

Cephalalgia ◽  
1990 ◽  
Vol 10 (2) ◽  
pp. 87-94 ◽  
Author(s):  
Arve Dahl ◽  
David Russell ◽  
Rolf Nyberg-Hansen ◽  
Kjell Rootwelt
Keyword(s):  
Blood Flow ◽  
Cluster Headache ◽  
Glyceryl Trinitrate ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Transcranial Doppler ◽  
Statistical Significance ◽  
Transcranial Doppler Ultrasound ◽  
Normal Limits ◽  
Symptomatic Side

Transcranial Doppler and rCBF examinations were carried out in 25 cluster headache patients. Spontaneous and glyceryl trinitrate (nitroglycerin) provoked attacks were accompanied by a bilateral decrease in middle cerebral artery blood flow velocities. This decrease was more pronounced on the symptomatic side but the difference did not reach statistical significance. Mean hemispheric blood flow and rCBF were within normal limits during provoked attacks and similar to those found when patients were attack-free. During cluster periods middle cerebral artery velocities were significantly higher on the symptomatic side. Glyceryl trinitrate caused a bilateral middle cerebral artery velocity decrease which was significantly greater on the symptomatic side. Attacks provoked by glyceryl trinitrate appeared to begin when the vasodilatory effect of this substance was receding.

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.

Relationship between middle cerebral artery blood velocity and end-tidal PCO2 in the hypocapnic-hypercapnic range in humans

2003 ◽  
Vol 95 (1) ◽  
pp. 129-137 ◽  
Author(s):  
Kojiro Ide ◽  
Michael Eliasziw ◽  
Marc J. Poulin
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Transcranial Doppler ◽  
Transcranial Doppler Ultrasound ◽  
Blood Velocity ◽  
End Tidal ◽  
The Relationship ◽  
Peak Blood

This study examined the relationship between cerebral blood flow (CBF) and end-tidal Pco2 (PetCO2) in humans. We used transcranial Doppler ultrasound to determine middle cerebral artery peak blood velocity responses to 14 levels of PetCO2 in a range of 22 to 50 Torr with a constant end-tidal Po2 (100 Torr) in eight subjects. PetCO2 and end-tidal Po2 were controlled by using the technique of dynamic end-tidal forcing combined with controlled hyperventilation. Two protocols were conducted in which PetCO2 was changed by 2 Torr every 2 min from hypocapnia to hypercapnia ( protocol I) and vice-versa ( protocol D). Over the range of PetCO2 studied, the sensitivity of peak blood velocity to changes in PetCO2 (CBF-PetCO2 sensitivity) was nonlinear with a greater sensitivity in hypercapnia (4.7 and 4.0%/Torr, protocols I and D, respectively) compared with hypocapnia (2.5 and 2.2%/Torr). Furthermore, there was evidence of hysteresis in the CBF-PetCO2 sensitivity; for a given PetCO2, there was greater sensitivity during protocol I compared with protocol D. In conclusion, CBF-PetCO2 sensitivity varies depending on the level of PetCO2 and the protocol that is used. The mechanisms underlying these responses require further investigation.

scholarly journals Imaging transcranial Doppler ultrasound to measure middle cerebral artery blood flow: the importance of measuring vessel diameter

2020 ◽  
Vol 319 (1) ◽  
pp. R33-R42
Author(s):  
Catherine L. Jarrett ◽  
Katherine L. Shields ◽  
Ryan M. Broxterman ◽  
Jay R. Hydren ◽  
Soung Hun Park ◽  
...  
Keyword(s):  
Blood Flow ◽  
Middle Cerebral Artery ◽  
Doppler Ultrasound ◽  
Cerebral Artery ◽  
Transcranial Doppler ◽  
Transcranial Doppler Ultrasound ◽  
Vessel Diameter ◽  
Blood Velocity ◽  
Color Flow ◽  
Novel Approach

Cerebral blood flow (CBF) is commonly inferred from blood velocity measurements in the middle cerebral artery (MCA), using nonimaging, transcranial Doppler ultrasound (TCD). However, both blood velocity and vessel diameter are critical components required to accurately determine blood flow, and there is mounting evidence that the MCA is vasoactive. Therefore, the aim of this study was to employ imaging TCD (ITCD), utilizing color flow images and pulse wave velocity, as a novel approach to measure both MCA diameter and blood velocity to accurately quantify changes in MCA blood flow. ITCD was performed at rest in 13 healthy participants (7 men/6 women; 28 ± 5 yr) with pharmaceutically induced vasodilation [nitroglycerin (NTG), 0.8 mg] and without (CON). Measurements were taken for 2 min before and for 5 min following NTG or sham delivery (CON). There was more than a fivefold, significant, fall in MCA blood velocity in response to NTG (∆−4.95 ± 4.6 cm/s) compared to negligible fluctuation in CON (∆−0.88 ± 4.7 cm/s) ( P < 0.001). MCA diameter increased significantly in response to NTG (∆0.09 ± 0.04 cm) compared with the basal variation in CON (∆0.00 ± 0.04 cm) ( P = 0.018). Interestingly, the product of the NTG-induced fall in MCA blood velocity and increase in diameter was a significant increase in MCA blood flow following NTG (∆144 ± 159 ml/min) compared with CON (∆−5 ± 130 ml/min) ( P = 0.005). These juxtaposed findings highlight the importance of measuring both MCA blood velocity and diameter when assessing CBF and document ITCD as a novel approach to achieve this goal.

Effect of Nimodipine on Cerebrovascular Response to CO2 in Asymptomatic Individuals and Patients with Subarachnoid Hemorrhage: A Transcranial Doppler Ultrasound Study

Neurosurgery ◽  
1990 ◽  
Vol 27 (2) ◽  
pp. 247-251 ◽  
Author(s):  
Rolf W. Seiler ◽  
Arto C. Nirkko
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Transcranial Doppler ◽  
Doppler Ultrasonography ◽  
Transcranial Doppler Ultrasound ◽  
Initial Value ◽  
Ruptured Aneurysms ◽  
Ultrasound Study ◽  
Asymptomatic Individuals

Abstract The cerebrovascular response to CO2was evaluated by measuring relative changes in blood flow velocity within the middle cerebral artery by transcranial Doppler ultrasonography during normo-, hypo-, and hypercapnia. In seven patients without subarachnoid hemorrhage (five with unruptured arteriovenous malformations and two with aneurysms), the CO2vasoreactivity was tested on the side of the middle cerebral artery with normal flow velocities opposite the lesion. A baseline CO2reactivity test was obtained in each patient and then repeated under constant intravenous infusion of nimodipine, 2 mg/hr. Nine patients with ruptured aneurysms who were rated at Hunt and Hess Grades 1 or 2 were operated on within 1 to 3 days after the hemorrhage and treated with nimodipine, 2 mg/hr, given intravenously. In these patients. CO2vasoreactivity was tested during the second week after the hemorrhage, when the middle cerebral artery velocity was increased by at least 50% of the initial value or more. Nimodipine was then discontinued and, 48 hours later, when the middle cerebral artery velocity was still in the same range, CO2vasoreactivity was tested again. Two months later, after full recovery from the subarachnoid hemorrhage and normalization of the velocities, a third measurement of CO2reactivity was obtained as a baseline control. No significant effect of nimodipine on CO2vasoreactivity could be demonstrated in any of the test periods. In the second week after a subarachnoid hemorrhage, a significant reduction of the cerebrovascular response to CO2was found (P &lt; 0.005).

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