ABSTRACT
Objectives: To analyze the hemodynamic characteristics of dysplastic posterior cerebral artery with transcranial Doppler ultrasonography (TCD) and to investigate the diagnostic value of TCD. Methods: Fifty-two patients with posterior cerebral artery P1 segment (PCA-P1) dysplasia screened by MRA and TCD were selected. The hemodynamic changes before and after the carotid compression test were observed, and compared with 52 healthy subjects without abnormal blood vessels (control group). Results: Circled digit oneThe blood flow velocity of 52 patients with PCA-P1 dysplasia on the dysplasia was 55 ± 8 cm/s on the dysplastic side, which was significantly lower than that of 60 ± 6 cm/s in the control group (P < 0.01). After compressing the ipsilateral common carotid arteries (CCAs) respectively, the velocity of PCA-P1 on the dysplastic sides was 192 ± 25 cm/s, and it was significantly higher than 96 ± 14 cm/s in the control group (P < 0.01). The ratio of velocity in patients with dysplasia before and after the compression test (after Vp/before Vp) was 3.52 ± 0.53, and it was significantly higher than 1.60 ± 0.17 in the control group (P < 0.01). Circled digit twoAfter compressing the ipsilateral CCAs respectively, the end-diastolic flow velocity and the ratio before compression (after Vp/before Vp) was 4.48 ± 1.28, and it was significantly higher than 1.61 ± 0.25 in the control group (P < 0.01). Circled digit threePCA-P1 pulsatility index (PI) on the dysplastic sides was 1.00 ± 0.22, and it was significantly higher than 0.78 ± 0.09 in the control group (P < 0.01). There was significant difference (P < 0.01). Circled digit fourOf the 52 patients, the flow spectrum of 28 patients showed high-resistance changes and the flow spectrum of 24 patients was normal. Before and after compressing the ipsilateral CCAs, the ratio of high-resistance spectrum group compared to that before compressing (after Vd/before Vd) was 5.3 ± 1.1, and it was significantly higher than 3.5 ± 0.6 in normal blood flow spectrum group. There was significant difference (P < 0.01). However, there was no significant difference between after VP/before VP and the normal blood flow spectrum group. ©Dysplasia in PCA-P1 was suspected in 39 cases by TCD, and 32 of them were confirmed with MRA. The positive coincidence rate was 82.1%, 17 of them showed high-resistance flow spectrum, and 16 had dysplasia in PCA-P1 confirmed by MRA. The positive coincidence rate was 94.1%. Conclusion: TCD in combination with blood flow spectrum shape may initially diagnose the dysplasia in PCA-P1 according to the changes of hemodynamic parameters of PCA-P1 before and after the CCA compression test.
ABSTRACT
Objective: To analyze the hemodynamic characteristics in detecting of anatomic variations of anterior cerebral artery (ACA) and anterior communicating artery (ACoA) with transcranial Doppler (TCD). Methods: Sixty-two patients with anatomic variations of ACA or ACoA (patient group) and 48 healthy subjects without variation (control group) diagnosed by magnetic resonance imaging (MRA) and TCD were selected. The hemodynamic changes in extracranial and intracranial vessels in both groups were detected by TCD. Results: Circled digit oneForty-eight patients with unilateral hypogenesis of ACA-A1 in the patient group. The blood flow velocity of ACA-A1 on the hypogenetic sides was 61±16 cm/s, it was significantly lower than 86±15 cm/s in the control group; the blood flow velocity of ACA-A1 on the thick sides was 125±12 cm/s, and it was significantly higher than that in the control group (all P <0.01). The blood flow velocity on the thin sides was about 1/2 of that on the thick sides. Circled digit twoAfter pressing the contralateral CCA, the blood flow velocity of bilateral ACA-A1 increased to various degrees. The ratio of peak systolic blood flow velocity on the thin sides was 3.10±0.50, and it was significantly higher than 1.93± 0.24 in the control group. The ratio on the thick sides was 1.33 + 0.11. It was significantly lower than that in the control group. There was significant difference (P < 0.01). The ratio on the thin sides was more than two times of that on the thick sides. Circled digit threeNine patients with unilateral absence of ACA-A1, the blood flow velocity of contralateral ACA-A1 was 131±17 cm/s, and it was significantly higher than that of the control group and the ipsilateral MCA blood flow velocity. The blood flow velocity of the extracranial internal carotid artery in 57 patients on the thin or absence sides of ACA-A1 was 47±11 cm/s, and it was significantly lower than 60±13 cm/s on the contralateral sides (P < 0.01). Circled digit fourThe blood flow signals in 5 patients with the absence of ACoA were disappeared after compressing the ipsilateral CCA and ACA respectively. Conclusion: According to the hemodynamic changes before and after the bilateral ACA Queckenstedts test, and in combination with the assistant indices such as blood flow velocity of extracranial internal carotid artery, blood flow signal intensity, and blood flow distribution, TCD may primarily detect the significant variation of ACA or ACoA.
ABSTRACT
Objectives: To analyze the hemodynamic characteristics in patients with unilateral hypogenesis of anterior cerebral artery (ACA) using transcranial Doppler ultrasonography (TCD) and to discuss the diagnostic value of it. Methods: Twenty-eight patients with unilateral hypogenesis of ACA were confirmed by TCD and magnetic resonance angiography (MRA). The characteristics of hemodynamic changes were observed in hypogenetic side and contralateral anterior cerebral artery A1 segment (ACA-A1) before and after compression of the common carotid artery. They were also compared with 28 normal controls. Results: The blood flow velocity of the hypogenetic side ACA-A1 (62 ± 17) cm/s of the 28 patients was significantly lower than that of the control group [(87 ± 15) cm/s; P < 0. 01]; the blood flow velocity of the contralateral ACA-A1 (123 ± 13) cm/s was significantly higher than that of the control group (P < 0.01). The average blood flow velocity of the hypogenetic side ACA-A1 was almost half of the contralateral ACA-A1. After compressing the common carotid arteries respectively, the blood flow velocity of the hypogenetic side ACA-A1 increased for several times (3.0.8 ± 0.51), and it was significantly higher than that of the control group (1.97 ± 0.25; P < 0.01); the blood flow velocity of the contralateral side ACA-A1 increased for several times (1.35 ± 0.11), and it was significantly lower than that of the control group (P < 0.01); the average blood flow velocity of the hypogenetic side ACA-A1 was more than 2 times of the contralateral ACA-A1. Conclusion: Accordin g to hemodynamic changes before and after compression of the common carotid artery, together with the signal strength of blood flow, and the distribution of blood flow, TCD may defect unilateral hypogenesis of ACA.