scholarly journals Stent-assisted angioplasty of cerebral arteries for the treatment symptomatic vasospasm

2021 ◽  
Vol 22 (4) ◽  
pp. 53-60
Author(s):  
M. Yu. Volodyukhin ◽  
N. G. Shaiakhmetov ◽  
A. G. Alekseev ◽  
V. I. Danilov
2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Anika Männer ◽  
Dominique Thomas ◽  
Marlies Wagner ◽  
Jürgen Konczalla ◽  
Helmuth Steinmetz ◽  
...  

Abstract Background and purpose Sphingosin-1-phosphate (S1P) plays a crucial role as a signaling molecule in the immune system and the vasculature. Previous studies suggested a role as a vasoconstrictor of cerebral arteries via the S1P3-Receptor. Cerebral vasospasm (VS) following aneurysmal subarachnoid hemorrhage (SAH) is a major cause of disability and poor neurological outcome. Early detection of vasospasm could facilitate the prevention of cerebral ischemia in SAH patients. The aim of this prospective case-control study was to characterize the dynamics of S1P in the cerebrospinal fluid (CSF) of patients with SAH in relation to hemorrhage volume, the occurrence of VS, and neurological outcome. Methods S1P levels in CSF of 18 control subjects and 18 SAH patients with placement of an external ventricular drainage (EVD) were determined by high sensitivity mass spectrometry from day 1 through 14 after SAH onset. Hemorrhage volume, development of asymptomatic vasospasm (aVS) and symptomatic vasospasm (sVS), and neurological outcome were correlated to day 1 S1P levels. Results The intrathecal S1P levels of SAH patients were higher than those of the control subjects, and correlated with hemorrhage volume. There was no significant difference in S1P levels between patients with aVS and those with sVS. S1P levels significantly correlated with neurological outcome on a sliding modified Rankin scale. Conclusion S1P levels were highest directly after placement of the EVD and correlated strongly with hemorrhage volume, which may be caused by the intrathecal clot and subsequent lysis of red blood cells, an important source of S1P. We did not detect a second peak of S1P release over the course of the intensive care period.


Neurosurgery ◽  
1989 ◽  
Vol 25 (3) ◽  
pp. 424-429 ◽  
Author(s):  
Stanley L. Barnwell ◽  
Randall T. Higashida ◽  
Van V. Halbach ◽  
Christopher F. Dowd ◽  
Charles B. Wilson ◽  
...  

Abstract We used intracerebral transluminal angioplasty to treat two episodes of symptomatic vasospasm in a patient recovering from an aneurysmal subarachnoid hemorrhage. The procedures were performed after medical therapies, intravascular volume expansion, and induced arterial hypertension failed to alleviate the patient's neurological condition. The first angioplasty, confined to the right middle cerebral and distal internal carotid arteries, took place more than 30 hours after the onset of left hemiplegia. Despite the subsequent discovery of a small parietal lobe infarct, it brought about a marked improvement in left motor function and may have also limited the spread of necrotic damage. The second angioplasty was necessitated when stenotic segments of the basilar and posterior cerebral arteries caused a 24-hour decline in the patient's mental status. Although delayed in relation to the onset of symptoms, it successfully reversed the patient's comatose state. The use of transluminal angioplasty for vasospasm is generally limited to cases where it can be performed shortly after the onset of neurological symptoms; delaying the procedure increases the risk of hemorrhage from reperfused areas of infarction. Our experience with this patient demonstrates that delayed angioplasty can improve vascular flow to ischemic territory, even after infarction, without complications and with resultant improvement in neurological function.


Neurosurgery ◽  
1981 ◽  
Vol 9 (6) ◽  
pp. 679-685 ◽  
Author(s):  
Shigeharu Suzuki ◽  
Eiji Sobata ◽  
Takashi Iwabuchi

Abstract The results of our previous experimental and clinical studies led us to the hypothesis that, in the pathogenesis of cerebral vasospasm, subarachnoid focal acidosis resulting from anaerobic changes of subarachnoid clots may be a factor upsetting the balanced synthesis of both thromboxane A2 and prostaglandin I2 from prostaglandin endoperoxides on the inner surface of cerebral arteries. Thus, there is a higher concentration of thromboxane A2, a prostanoid that causes arterial contraction and platelet aggregation. We tested the administration of trapidil, an antagonist and selective synthesis inhibitor of thromboxane A2, in a series of 20 cases for the prevention of cerebral vasospasm and cerebral ischemia after aneurysmal rupture. Vasospasm was demonstrated by angiography in 9 of these cases, but only 2 of the 9 showed mild signs of cerebral ischemia. Of the 20 patients, 15 were discharged from the hospital as cured and 3 had a neurological deficit at discharge. Our findings suggest the significance in symptomatic vasospasm of thrombus formation by platelet aggregation and the effectiveness of trapidil as a preventive.


1989 ◽  
Vol 71 (5) ◽  
pp. 654-660 ◽  
Author(s):  
David W. Newell ◽  
Joseph M. Eskridge ◽  
Marc R. Mayberg ◽  
M. Sean Grady ◽  
H. Richard Winn

✓ Angioplasty of narrowed cerebral arteries was performed in 10 patients who became symptomatic from vasospasm following subarachnoid hemorrhage. This procedure was accomplished with a microballoon catheter via percutaneous transfemoral insertion. Patients were selected for treatment if they had delayed neurological deficits due to vasospasm which were not responsive to hypervolemic hypertensive therapy. Eight patients (80%) showed sustained improvement in neurological function following the procedure. In two patients transcranial Doppler ultrasound recordings were obtained which revealed decreased mean blood flow velocities following angioplasty. Two patients died, one from an aneurysmal rebleed, and one secondary to diffuse vasospasm. There was one case of delayed stroke 6 weeks following the procedure. The overall results of this series indicate that in selected cases percutaneous balloon angioplasty can offer marked improvement to patients with ischemic deficits due to vasospasm following subarachnoid hemorrhage.


2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S520-S520
Author(s):  
Petter Vikman ◽  
Lars Edvinsson

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S557-S557
Author(s):  
Takeshi Kondoh ◽  
Seiji Nakajima ◽  
Akitsugu Morishita ◽  
Haruo Yamashita ◽  
Eiji Kohmura ◽  
...  

2008 ◽  
Vol 35 (S 01) ◽  
Author(s):  
E Leinisch ◽  
F Schlachetzki ◽  
C Müller ◽  
U Bogdahn ◽  
W Jakob ◽  
...  

1979 ◽  
Vol 42 (02) ◽  
pp. 603-610 ◽  
Author(s):  
J H Adams ◽  
J R A Mitchell

SummaryThe ability of potential anti-thrombotic agents to modify platelet-thrombus formation in injured cerebral arteries in the rabbit was tested. Low doses of heparin were without effect, while higher doses produced variable suppression of white body formation but at the expense of bleeding. Aspirin did not inhibit white body formation but another non-steroid anti-inflammatory agent, flurbiprofen was able to do so, as was the anti-gout agent, sulphinpyrazone. Magnesium salts both topically and parenterally, suppressed thrombus formation and increased the concentration of ADP which was required to initiate thrombus production at minor injury sites.


2019 ◽  
Vol 91 (7) ◽  
pp. 29-34 ◽  
Author(s):  
M M Tanashyan ◽  
A L Melikyan ◽  
P I Kuznetsova ◽  
A A Raskurazhev ◽  
A A Shabalina ◽  
...  

Myeloproliferative disorders (MPD) are accompanied by a high proportion of thrombotic complications, which may lead to cerebrovascular disease (CVD). Aim. To describe MRI-findings in patients with Ph - negative MPD and evaluate any cerebrovascular disease. Materials and methods. We included 104 patients with Ph - negative MPD (age varied between 20 and 58) with clinical correlates of cerebrovascular pathology. Results. Brain MRI showed post - stroke lesions in 20% of patients (7 hemispheric infarcts due to thrombotic occlusion of one of the large cerebral arteries, 14 - cortical infarcts). 37 patients (36%) had vascular cerebral lesions. Cerebral venous sinus thrombosis occurred in 5 patients - in 7% (n=3) of patients with polycythemia vera and 5% (n=2) - in patients with essential thrombocythemia. The incidence of vascular cerebral lesions was associated with higher levels of the following: erythrocyte, platelet count, fibrinogen, and with the decrease in fibrinolytic activity, as well. Conclusion. The pioneering results of the study include the description and analysis of brain MRI-findings in patients with Ph - negative MPD. The underlying mechanisms of cerebrovascular pathology in these patients are associated with certain blood alterations (particularly, hemorheology) which present a major risk factor.


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