normal perfusion pressure breakthrough
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2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Manuel Revuelta ◽  
Alvaro Zamarrón ◽  
Jose Fortes ◽  
Gregorio Rodríguez-Boto ◽  
Raquel Gutiérrez-González

Abstract Loss of cerebral autoregulation in normal perfusion pressure breakthrough (NPPB) phenomenon has been reported in other Central Nervous System diseases such as neonatal intraventricular haemorrhage. Several studies have demonstrated that low-dose indomethacin prevents this latter condition. A previous rat model was used to resemble NPPB phenomenon. Study animals were distributed in 4 groups that received 3 doses of indomethacin at different concentrations prior to fistula occlusion 60 days after its creation. Control animals received saline solution. Intracranial pressure (ICP) increased in all groups following fistula creation, whereas mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) decreased as a manifestation of cerebral hypoperfusion and intracranial hypertension. The administration of indomethacin was associated with raised MAP and CPP, as well as decreased ICP. Sodium fluorescein extravasation was slight in study animals when comparing with control ones. Histological analysis evidenced diffuse ischaemic changes with signs of neuronal apoptosis in all brain layers in control animals. These findings were only focal and slight in study animals. The results suggest the usefulness of indomethacin to revert, at least partially, the haemodynamic effects of NPPB phenomenon in this experimental model, as well as to reduce BBB disruption and histological ischemia observed in absence of indomethacin.


Neurocirugía ◽  
2020 ◽  
Vol 31 (5) ◽  
pp. 209-215
Author(s):  
Juan Manuel Revuelta ◽  
Álvaro Zamarrón ◽  
José Fortes ◽  
Gregorio Rodríguez-Boto ◽  
Jesús Vaquero ◽  
...  

2020 ◽  
Vol 31 (5) ◽  
pp. 209-215
Author(s):  
Juan Manuel Revuelta ◽  
Álvaro Zamarrón ◽  
José Fortes ◽  
Gregorio Rodríguez-Boto ◽  
Jesús Vaquero ◽  
...  

2017 ◽  
Vol 3 (4) ◽  
pp. 220-223 ◽  
Author(s):  
Zongyu Xiao ◽  
Xiaojuan Chen ◽  
Kunzheng Li ◽  
Zhengping Zhang

Calcified chronic subdural hematoma (CCSDH) is a rare disease that accounts for approximately 0.3%–2.7% of all chronic subdural hematomas (CSDHs). The clinical features of CCSDH are very similar to those of noncalcified CSDH and include headache, decreased alertness, weakness, numbness, gait disturbance, seizures, memory impairment, confusion, and unconsciousness. All symptomatic CCSDH should be treated surgically. Majority of these patients recover well following surgery. In this report, we present the case of a patient with CCSDH who developed severe cerebral edema following its removal, necessitating decompressive craniectomy. Although there were no abnormal findings in laboratory blood tests, and no signs of brain herniation or epilepsy was found the following day after surgery, the patient's family refused all treatment and a postoperative brain computed tomography (CT) scan. The patient was discharged and died at home. Cerebral hematoma and normal perfusion pressure breakthrough (NPPB) may cause severe cerebral edema following the total removal of a CCSDH.


2014 ◽  
Vol 38 (3) ◽  
pp. 399-405 ◽  
Author(s):  
Leonardo Rangel-Castilla ◽  
Robert F. Spetzler ◽  
Peter Nakaji

2014 ◽  
Vol 37 (4) ◽  
pp. 559-568 ◽  
Author(s):  
Raquel Gutiérrez-González ◽  
Alvaro Pérez-Zamarron ◽  
Gregorio Rodríguez-Boto

2013 ◽  
Vol 20 (1) ◽  
pp. 46-56
Author(s):  
Aurelia Mihaela Sandu ◽  
Mircea Radu Gorgan

Abstract Background: Giant arteriovenous malformations (AVMs) are congenital lesions, with nidus sizing more than 6 cm. According to Spetzler-Martin scale, grade V AVMs have a nidus larger than 6 cm in diameter, profound venous drainage and are located in eloquent areas. Method: We report a case of a 39 years old woman, with giant left frontal AVM, grade V Spetzler-Martin, who was admitted for generalized seizures, with onset 32 years ago, refractory to full dose antiepileptic polytherapy, which severely impaired the patient’s quality of life. Results: The patient underwent surgery and we performed total resection of the AVM. We emphasize on surgical technique, intraoperative difficulties and outcome. Conclusions: Surgery is the therapy of choice in AVMs, because it provides cure of the lesion, and is the only treatment capable of preventing hemorrhage and controlling seizures. Management in grade V AVMs is challenging, because of their large size, multiple dilated arterial feeders from anterior and posterior circulation and external carotid arteries, high blood flow, vascular steel from the surrounding brain, enlarged draining veins, profound venous drainage and location in eloquent area. Giant AVMs with high flow nidus, causing a great degree of vascular steel in the surrounding brain, with hypoperfusion of normal parenchyma may develop early normal perfusion pressure breakthrough. Total resection in grade V AVMs can be performed with minimal transient morbidity and favorable outcome. Total resection permits control of intractable seizures with reduced dose of antiepileptic therapy.


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