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Transcranial Doppler sonography in chronic paroxysmal hemicrania
1Department of Neurology, University Hospital of Trondheim, Norway.
Insights
Transcranial Doppler sonography revealed reduced cerebral blood flow velocity during chronic paroxysmal hemicrania (CPH) attacks. Patients with CPH showed slightly altered cerebral vasomotor reactivity compared to healthy controls.
Area of Science:
- Neurology
- Vascular Neurology
- Neuroimaging
Background:
- Chronic paroxysmal hemicrania (CPH) is a rare headache disorder.
- The underlying pathophysiology, particularly vascular involvement, remains incompletely understood.
Purpose of the Study:
- To investigate cerebral blood flow dynamics and vasomotor reactivity in patients with CPH using transcranial Doppler (TCD) sonography.
Main Methods:
- Three CPH patients and nine healthy controls underwent TCD sonography.
- Cerebral blood flow velocities (MCA, ACA) were measured during spontaneous CPH attacks.
- Cerebral vasomotor reactivity (VMR) was assessed via induced hyperventilation and end-tidal PCO2 changes.
Main Results:
- Middle cerebral artery velocity (VMCA) and anterior cerebral artery velocity (VACA) decreased bilaterally during CPH attacks.
- VMCA reduction occurred early in the attack, preceding significant hyperventilation.
- CPH patients exhibited slightly reduced VMR in MCA, posterior cerebral artery, and symptomatic ACA compared to controls.
Conclusions:
- These findings suggest abnormal cerebral vascular reactivity in individuals with CPH.
- TCD sonography may offer insights into the vascular mechanisms of CPH.
Abstract:
Three patients with chronic paroxysmal hemicrania (CPH) (1 M, 2 F) and 9 healthy controls (8 M 1 F) were studied with transcranial Doppler (TCD) sonography. One patient who was studied during the spontaneous attacks hyperventilated markedly. Middle cerebral artery velocity (VMCA) was measured in the first attack, and anterior cerebral artery velocity (VACA) in the second attack, respectively. VMCA and VACA decreased bilaterally during attack. VMCA started to decrease at an early stage of the attack, i.e. prior to the major hyperventilation that was observed during the attack. VACA on the symptomatic side decreased less than that on the other side (P < 0.05). Cerebral vasomotor reactivity (VMR) was expressed as the percentage change in mean blood flow velocity as a function of end-tidal PCO2 (PETCO2) reduction induced by voluntary hyperventilation (delta V/delta PETCO2). In the 3 patients, a slightly lowered VMR was observed in the MCA and posterior cerebral artery on both sides, and in the ACA on the symptomatic side (P > 0.05) in comparison with controls. These observations may imply an abnormal vascular reactivity in CPH.