Use of Anticoagulants, Electroencephalographic Monitoring, and Barbiturate Cerebral Protection in Carotid Endarterectomy

Neurosurgery ◽  
1981 ◽  
Vol 9 (1) ◽  
pp. 1-5 ◽  
Author(s):  
C. E. Gross ◽  
H. P. Adams ◽  
M. D. Sokoll ◽  
T. Yamada
Keyword(s):  
Cerebral Ischemia ◽  
Carotid Endarterectomy ◽  
Unique Feature ◽  
Treatment Protocol ◽  
Burst Suppression ◽  
Cerebral Protection ◽  
Eeg Monitoring ◽  
Specific Risk ◽  
Perioperative Anticoagulation ◽  
The Brain

abstract This paper describes a treatment protocol for threatened stroke in patients amenable to carotid endarterectomy. The protocol includes the use of perioperative anticoagulation, intraoperative electroencephalographic (EEG) monitoring, and hypertension or barbiturates to protect the brain against documented ischemia intraoperatively. The rationale and methods for protecting the patient from the threat of thromboembolism and cerebral ischemia during each of the periods of specific risk are discussed. The most unique feature of this protocol is the use of thiopental-induced EEG burst suppression for ischemia unresponsive to hypertension during carotid clamping, which has obviated the use of a potentially dangerous and cumbersome in-line arterial shunt.

EEG MONITORING FOR CEREBRAL ISCHEMIA DURING CAROTID ENDARTERECTOMY

1994 ◽  
Vol 81 (SUPPLEMENT) ◽  
pp. A215 ◽  
Author(s):  
R. M. CRAFI ◽  
T. J. Losasso ◽  
W. J. Perkins ◽  
M. R. Weglinski ◽  
F. W. Sharbrough
Keyword(s):  
Cerebral Ischemia ◽  
Carotid Endarterectomy ◽  
Eeg Monitoring

Perioperative Ischemic Complications of the Brain After Carotid Endarterectomy

Neurosurgery ◽  
2010 ◽  
Vol 67 (2) ◽  
pp. 286-294 ◽  
Author(s):  
Matthew O. Hebb ◽  
Joseph E. Heiserman ◽  
Kirsten P. N. Forbes ◽  
Joseph M. Zabramski ◽  
Robert F. Spetzler
Keyword(s):  
Cerebral Ischemia ◽  
Carotid Endarterectomy ◽  
Diffusion Weighted Imaging ◽  
Safe Procedure ◽  
Carotid Revascularization ◽  
Diffusion Weighted ◽  
Marginal Mandibular Nerve ◽  
Ischemic Complications ◽  
The Brain ◽  
Radiological Studies

Abstract BACKGROUND The potential morbidity of cerebral ischemia after carotid endarterectomy (CEA) has been recognized, but its reported incidence varies widely. OBJECTIVE To prospectively evaluate the development of cerebral ischemic complications in patients treated by CEA at a high-volume cerebrovascular center. METHODS Fifty patients with moderate or severe carotid stenosis awaiting CEA were studied with perioperative diffusion-weighted imaging of the brain and standardized neurological evaluations. Microsurgical CEA was performed by 1 of 2 vascular neurosurgeons. Radiological studies were evaluated by faculty neuroradiologists who were blinded to the details of the clinical situation. RESULTS Preoperative diffusion-weighted imaging studies were performed within 24 hours of surgery. A second study was obtained within 24 (92% of patients), 48 (4% of patients), or 72 (4% of patients) hours after surgery. Intraluminal shunting was used in 1 patient (2%), and patch angioplasty was used in 2 patients (4%). No patient had diffusion-weighted imaging evidence of procedure-related cerebral ischemia. Nonischemic complications consisted of postoperative confusion in an 87-year-old man with a urinary tract infection and a marginal mandibular nerve paresis in another patient. Radiological studies were normal in both patients. CONCLUSION CEA is a relatively safe procedure that may be performed with an acceptable risk of cerebral ischemia in select patients. The low rate of ischemic complications associated with CEA sets a standard to which other carotid revascularization techniques should be held. The current results are presented with a discussion of the senior author's preferred surgical technique and a brief review of the literature.

The Importance of Cerebral Ischemia during Carotid Endarterectomy

Neurosurgery ◽  
1991 ◽  
Vol 29 (5) ◽  
pp. 727-731 ◽  
Author(s):  
Edward Zampella ◽  
Richard B. Morawetz ◽  
Holt A. McDowell ◽  
H. E van Zeiger ◽  
Pamela D. Varner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Ischemia ◽  
Carotid Endarterectomy ◽  
Negative Correlation ◽  
Eeg Monitoring ◽  
Ipsilateral Hemisphere ◽  
133Xe Clearance ◽  
Eeg Changes ◽  
Xenon 133 ◽  
Electroencephalogram Eeg

Abstract The importance of cerebral ischemia produced by carotid clamping during carotid endarterectomy remains controversial. In an effort to determine the importance of cerebral ischemia during carotid endarterectomy. 369 patients undergoing 431 consecutive carotid endarterectomies were studied by Xenon-133 (133Xe) clearance and electroencephalogram (EEG) monitoring. None of the patients was shunted during the procedures. The severity of ischemia as indicated by 133 Xe clearance from the ipsilateral hemisphere during 20 to 30 minutes of carotid occlusion did not predict the appearance of complications in this group of patients (x2 = 1.417: P = 0.841). There was a highly significant relationship between the depth of cerebral ischemia as demonstrated by 133Xe clearance and the appearance of abnormalities on the EEG (x2 = 42.043, P < 0.0001). In the subgroup of patients developing abnormalities as shown by EEG. there was a negative correlation (x2 = 17.495; P < 0.002) between reduction in blood flow and the appearance of complications, in that the higher the blood flow during occlusion the more likely the patient developing EEG changes would develop complications.

scholarly journals Thiopentone Cerebral Protection under EEG Control during Carotid Endarterectomy

1986 ◽  
Vol 14 (1) ◽  
pp. 22-28 ◽  
Author(s):  
R. G. Hicks ◽  
D. R. Kerr ◽  
D. A. Horton
Keyword(s):  
Blood Pressure ◽  
Carotid Endarterectomy ◽  
Burst Suppression ◽  
Cerebral Protection ◽  
Brain Protection ◽  
Temporary Bypass ◽  
Neurological Morbidity ◽  
Eeg Changes

Seventy patients who underwent a total of 77 consecutive carotid endarterectomies were given thiopentone (mean dose 19 mg/kg) under EEG control for cerebral protection during the period of carotid clamping. This technique was used instead of elective insertion of a temporary bypass shunt in response to adverse EEG changes occurring after clamping. The EEG was monitored continuously throughout operation. The EEG burst-suppression pattern with electrically inactive periods of 30-60 seconds was taken as indicating a depth of barbiturate anaesthesia adequate to provide brain protection. Patients exhibited a drop in blood pressure during barbiturate administration: in most the pressure recovered spontaneously but in twenty operations metaraminol was needed to re-establish an adequate pressure before clamping. No adverse cardiological effects were associated with the administration of thiopentone or metaraminol. There was no mortality and no neurological morbidity in this series.

EEG MONITORING FOR CEREBRAL ISCHEMIA DURING CAROTID ENDARTERECTOMY (CEA): HOW MUCH IS ENOUGH?

1994 ◽  
Vol 6 (4) ◽  
pp. 301 ◽  
Author(s):  
R M Craft ◽  
T J Losasso ◽  
W J Perkins ◽  
M R Weglinski ◽  
F W Sharbrough
Keyword(s):  
Cerebral Ischemia ◽  
Carotid Endarterectomy ◽  
Eeg Monitoring

Cerebral protection from ischaemia during carotid endarterectomy

2020 ◽  
Vol 26 (1) ◽  
pp. 96
Author(s):  
A. N. Vachev ◽  
M. G. Prozhoga ◽  
O. V. Dmitriev
Keyword(s):  
Carotid Endarterectomy ◽  
Cerebral Protection

Exploring the Role of Remote Ischemic Preconditioning In Long Term Cognitive Impairment after Global Ischemia-Reperfusion-Induced Vascular Dementia in Mice

2020 ◽  
Author(s):  
Amteshwar Singh Jaggi
Keyword(s):  
Cognitive Impairment ◽  
Cerebral Ischemia ◽  
Vascular Dementia ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Remote Ischemic Preconditioning ◽  
Global Cerebral Ischemia ◽  
Cerebral Ischemic ◽  
The Brain

Aim: The aim of the present study is to explore the neuroprotective effects of remote ischemic preconditioning in long term cognitive impairment after global cerebral ischemia induced-vascular dementia in mice. Material and methods: The mice were subjected to global cerebral ischemia by occluding the bilateral common carotid arteries for 12 minutes followed by the 24 hours of the reperfusion. The remote ischemic preconditioning stimulus was delivered in the form of 4 cycles of ischemia/reperfusion for 5 minutes each. The cerebral ischemic injury induced-long term cognitive impairment-related learning and memory alterations was assessed using morris water maze, the motor performances of the animals were evaluated using rota-rod test and neurological severity score. The cerebral infract size of the brain were quantified using triphenyltetrazolium chloride staining. Results: Global cerebral ischemia causes long term memory impairment, decreases motor performances and increases the brain infract size in animals. The delivery of remote ischemic preconditioning stimulus significantly abolished the long-term cognitive impairment and ameliorates the motor performances as well as cerebral infract size in brain. Conclusion: The remote ischemic preconditioning mediates neuro protection against global cerebral ischemic injury induced long-term cognitive impairment.

DNA Damage and Repair in the Brain After Cerebral Ischemia

2001 ◽  
Vol 1 (6) ◽  
pp. 483-495 ◽  
Author(s):  
Bentham Science Publisher Philip K. Liu
Keyword(s):  
Dna Damage ◽  
Cerebral Ischemia ◽  
Dna Damage And Repair ◽  
The Brain

Minocycline inhibits mTOR signaling activation and alleviates behavioral deficits in the Wistar rats with acute ischemia stroke

2020 ◽  
Vol 19 ◽  
Author(s):  
Shengyuan Wang ◽  
Chuanling Wang ◽  
Lihua Wang ◽  
Zhiyou Cai
Keyword(s):  
Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Mammalian Target Of Rapamycin ◽  
Mtor Signaling ◽  
Acute Ischemia ◽  
Intragastric Administration ◽  
Underlying Mechanisms ◽  
Signaling Activation ◽  
The Brain ◽  
Minocycline Therapy

Background: Mammalian target of rapamycin (mTOR) has been evidenced as a multimodal therapy in the path-ophysiological process of acute ischemic stroke (AIS). However, the pathway that minocycline targets mTOR signaling is not fully defined in the AIS pathogenesis. This study is to aim at the effects of minocycline on the mTOR signaling in the AIS process and further discover the underlying mechanisms of minocycline involved in the following change of mTOR signaling-autophagy. Methods: Cerebral ischemia/reperfusion (CIR) rat animal models were established with the transient suture occlusion into middle cerebral artery. Minocycline (50mg/kg) was given by intragastric administration. The Morris water maze was used to test the cognitive function of animals. Immunohistochemistry and immunofluorescence were introduced for testing the lev-els of synaptophysin and PSD-95. Western blot was conducted for investigating the levels of mTOR, p-mTOR (Ser2448), p70S6, p-p70S6 (Thr389), eEF2k, p-eEF2k (Ser366), p-eIF4B (Ser406), LC3, p62, synaptophysin and PSD-95. Results: Minocycline prevents cognitive decline of the MCAO stroke rats. Minocycline limits the expression of p-mTOR (Ser2448) and the downstream targets of mTOR [p70S6, p-p70S6 (Thr389), eEF2k, p-eEF2k (Ser366) and p-eIF4B (Ser406)] (P<0.01), while minocycline has no influence on mTOR. LC3-II abundance and the LC3-II/I ratio were upregu-lated in the hippocampus of the MCAO stroke rats by the minocycline therapy (P<0.01). p62 was downregulated in the hippocampus from the MCAO stroke rats administrated with minocycline therapy(P<0.01). The levels of SYP and PSD-95 were up-regulated in the brain of the MCAO stroke rats administrated with minocycline therapy. Conclusion: Minocycline prevents cognitive deficits via inhibiting mTOR signaling and enhancing autophagy process, and promoting the expression of pre-and postsynaptic proteins (synaptophysin and PSD-95) in the brain of the MCAO stroke rats. The potential neuroprotective role of minocycline in the process of cerebral ischemia may be related to mitigating is-chemia-induced synapse injury via inhibiting activation of mTOR signaling.

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