Occipital artery to middle cerebral artery bypass in pediatric moyamoya disease: rescue therapy after failed revascularization

Author(s):  
Akikazu Nakamura ◽  
Akitsugu Kawashima ◽  
Hugo Andrade-Barazarte ◽  
Takayuki Funatsu ◽  
Juha Hernesniemi ◽  
...  

OBJECTIVEPatients with pediatric moyamoya disease (PMMD) showing recurrent symptoms or decreased cerebral blood flow after initial revascularization therapy may require additional revascularization to improve their clinical condition. The authors evaluated the clinical and hemodynamic benefits of an occipital artery (OA)–middle cerebral artery (MCA) bypass for patients with PMMD who have undergone an initial revascularization procedure.METHODSThe authors retrospectively identified 9 patients with PMMD who had undergone OA-MCA bypass between March 2013 and December 2017, and who had received a previous superficial temporal artery–MCA bypass. The following clinical data were collected: initial revascularization procedure, symptoms (presence or recurrence), pre- and postoperative cerebral blood flow and cerebrovascular reactivity (CVR) changes, posterior cerebral artery (PCA) stenosis, PCA-related and nonrelated symptoms, and latest follow-up.RESULTSPreoperatively, all patients (n = 9) suffered non–PCA-related recurrent symptoms, and 4 had PCA-related symptoms. At 1-year follow-up, all patients with PCA-related symptoms showed complete recovery. Additionally, 8 (89%) patients with non-PCA symptoms experienced improvement. Only 1 (11%) patient showed no improvement after the surgical procedure. The mean pre- and postoperative CVR values of the MCA territory were 14.8% and 31.3%, respectively, whereas the respective mean CVR values of the PCA territory were 22.8% and 40.0%.CONCLUSIONSThe OA-MCA bypass is an effective rescue therapy to improve the clinical condition and hemodynamic changes caused by PMMD in patients who experience recurrent symptoms after initial revascularization.

1995 ◽  
Vol 80 (1) ◽  
pp. 64-70 ◽  
Author(s):  
Andreas Weyland ◽  
Heidrun Stephan ◽  
Frank Grune ◽  
Wolfgang Weyland ◽  
Hans Sonntag

1999 ◽  
Vol 91 (3) ◽  
pp. 677-677 ◽  
Author(s):  
Basil F. Matta ◽  
Karen J. Heath ◽  
Kate Tipping ◽  
Andrew C. Summors

Background The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram. Methods Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 micro/g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels. Results Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4+/-3 and 17+/-3% at 0.5 and 1.5 MAC sevoflurane; 19+/-3 and 72+/-9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P<0.05). All patients required phenylephrine (100-300 microg) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia. Conclusions In common with other volatile anesthetic agents, sevoflurane has an intrinsic dose-dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane.


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