Carotid artery endarterectomy

Carotid artery endarterectomy

Carotid artery endarterectomy is widely used on the carotid artery of the neck as a way to reduce the risk of stroke, particularly when the carotid artery is narrowed by more than 70%. A carotid endarterectomy may itself cause a stroke at the time of operation.

Endarterectomy is also used as a supplement to a vein bypass graft to open up distal segments.

Pulmonary hypertension caused by chronic thromboembolic disease (CTEPH) may be amenable to pulmonary thromboendarterectomy of the pulmonary artery. This is a highly specialized procedure.


Carotid artery stenosis (CS) is a major cause of ischemic stroke. Treatment of CS consists of best medical treatment and carotid revascularization (CR), including carotid endarterectomy (CEA) and carotid artery stenting (CAS). Both CR techniques have their own procedural risks. Therefore, selection of the appropriate treatment for patients with CS is relatively complicated. Many studies and guidelines have reported the efficacy of each treatment for both symptomatic and asymptomatic patients. However, the results are still controversial, especially concerning the efficacy and safety of CEA and CAS 1).

Carotid endarterectomy is a surgical procedure to remove the atheromatous plaque material, or blockage, in the lining of an artery constricted by the buildup of soft/hardening deposits. It is carried out by separating the plaque from the arterial wall.

Atherosclerotic stenosis of the internal carotid artery causes 10–15% of all strokes. Carotid endarterectomy lowers the long-term risk of stroke in patients with symptomatic carotid artery stenosis 2) 3).

Carotid endarterectomy (CEA) is a common, well-developed surgical procedure.

Technique: Carotid endarterectomy is safe, effective, and durable, but can we make it better? 4).

Carotid artery endarterectomy indications.

Identifying patients at high risk for complications after CEA has proven challenging. Typically, the exclusion criteria from studies are cited, but in most cases, these are simply patients that were not included in the study because it was the investigators’ perception that these patients might be “high risk.” Therefore these risk factors are not validated. They are included here for completeness. NASCET and ACAS: age > 80 years, prior ipsilateral CEA, prior contralateral CEA within 4 months, prior neck XRT, tandem lesion larger than target lesion, other conditions that could cause symptoms (atrial fibrillation, prior stroke with persistent major deficit, valvular heart disease), major organ failure, uncontrolled hypertension or diabetes mellitus, and significant coronary artery disease 5) 6)

The SAPPHIRE Trial (Stenting and Angioplasty with Protection in Patients at High-Risk for Endarterectomy): patients with clinically significant cardiac disease (CHF, abnormal stress test, or need for open-heart surgery), severe pulmonary disease, contralateral carotid occlusion, contralateral laryngeal-nerve palsy, previous radical neck surgery or neck XRT, recurrent stenosis after endarterectomy, and age > 80 years 7).

The ARCHeR Trial (ACCULINK for Revascularization of Carotids in High-Risk patients) also included patients with tracheostomy, spinal immobility, and dialysis-dependant renal failure 8).

Most (but not all) surgeons monitor some parameter of neurologic function during carotid endarterectomy, and will alter technique (e.g. insert a vascular shunt) if there is evidence of hemodynamic intolerance of carotid clamping (only occurs in ≈ 1–4%).

  1. local/regional anesthesia: permits “clinical” monitoring of patient’s neurologic function 9) 10)

Disadvantages:

patient movement during procedure (often exacerbated by sedation and alterations in CBF), lack of cerebral protection from anesthetic and adjunctive agents. The only prospective randomized study found no di erence between local and general anesthesia 11). The multicenter, randomized controlled General Anesthesia versus Local Anesthesia (GALA) Trial 12) found no significant differences in the prevention of stroke, MI, or death for either anesthetic technique. Subgroup analysis showed trends (not statistically significant) favoring local anesthesia for perioperative death, event-free survival at 1 year, and patients with contralateral occlusion. Local anesthesia was associated with a significant reduction of shunt insertion 13).

A Cochrane Database Review found no evidence from randomized trials to favor either anesthetic technique 14)

  1. general anesthesia, possibly including barbiturates (thiopental boluses of 125–250 mg until 15– 30 second burst suppression on EEG, followed by small bolus injections or constant infusion to 15)

a) EEG monitoring

b) SSEP monitoring

c) measurement of distal stump pressure after CCA occlusion (unreliable), e.g. using a shunt if stump pressure <25 mm Hg

d) transcranial Doppler

e) near-infrared spectroscopy.


Both general anesthesia and local anesthesia are used in the University Hospital Pilsen for carotid endarterectomy (CEA). The decision as to which anesthetic technique to use during surgery is made individually.

The satisfaction of a group of 205 patients with regard to anesthesia used and their future preferences were evaluated prospectively through a questionnaire. The reasons for dissatisfaction were assessed.

CEA was performed under general anesthesia (GA) in 159 cases (77.6%) and under local anesthesia (LA) in 46 cases (22.4%). In the GA group, 148 patients (93.1%) were satisfied; 30 patients (65.2%) in the LA group were satisfied (p < 0.0001). The reason for dissatisfaction with GA were postoperative nausea and vomiting (7 patients), postoperative psychological alteration (3), and fear of GA (1). The reasons for dissatisfaction with LA were intraoperative pain (9 patients), intraoperative discomfort and stress (5), and intraoperative breathing problems (2). Of the GA group, 154 (96.9%) patients would prefer GA again, and of the LA group, 28 (60.9%) patients would prefer LA if operated on again (p < 0.0001). Overall, 172 patients (83.9%) would prefer GA in the future, and 33 patients (16.1%) would prefer LA.

Overall patient satisfaction with CEA performed under both GA and LA is high. Nevertheless, in the GA group, patient satisfaction and future preference were significantly higher. Both GA and LA have advantages and disadvantages for CEA. An optimal approach is to make use of both anesthetic techniques based on their individual indications and patient preference 16).

Post-op check

In addition to routine, the following should be checked:

  1. change in neurologic status due to cerebral dysfunction, including:

a) pronator drift(R/O new hemiparesis)

b) signs of dysphasia (especially for left-sided surgery)

c) mimetic muscle symmetry (assesses facial nerve function)

  1. pupil diameter and reaction (R/O stroke, Horner syndrome)

  2. severe H/A (especially unilateral) > may indicate hyperperfusion syndrome

  3. STA pulses (R/O external carotid occlusion)

  4. tongue deviation (R/O hypoglossal nerve injury)

  5. symmetry of lips (R/O weakness of lower lip depressors due to retraction of marginal mandibular branch of the facial nerve against mandible usually resolves in 6–12 wks, must differentiate from central VII palsy due to stroke)

  6. check for hoarseness (R/O recurrent laryngeal nerve injury)

  7. assess for a hematoma in operative site: note any tracheal deviation, dysphagia

A bovine placenta training model for CEA is inexpensive and readily available and closely resembles human carotid arteries. The model can provide a convenient and valuable simulation and practice addition for vascular surgery training 17).

Neurocognitive performance is used to assess multiple cognitive function, including motor coordination, before and after carotid endarterectomy (CEA).

Carotid artery endarterectomy complications.

Citation analysis on carotid endarterectomy has witnessed a marked shift in the publication trends from studying the outcome and complications to comparing carotid artery stenting with endarterectomy. This analysis is a good introductory article to physicians interested in this topic, as it summarizes the highly impactful articles and enlists the most-cited RCT on CEA 18).

Carotid artery endarterectomy case series


1)

Noiphithak R, Liengudom A. Recent Update on Carotid Endarterectomy versus Carotid Artery Stenting. Cerebrovasc Dis. 2016 Nov 30;43(1-2):68-75. [Epub ahead of print] PubMed PMID: 27898402.
2)

North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991; 325: 445–53.
3)

European Carotid Surgery Trialists’ Collaborative Group. Randomised trial of endarterectomy for recently symptomatic carotid stenosis: final results of the MRC European Carotid Surgery Trial (ECST). Lancet 1998; 351: 1379–87.
4)

Williamson RW, Spetzler RF. Carotid endarterectomy is safe, effective, and durable, but can we make it better? World Neurosurg. 2016 Jan 2. pii: S1878-8750(15)01794-5. doi: 10.1016/j.wneu.2015.12.087. [Epub ahead of print] PubMed PMID: 26752091.
5)

Nguyen LL, Conte MS, Reed AB, et al. Carotid endarterectomy: who is the high-risk patient? Semin Vasc Surg. 2004; 17:219–223
6)

Kang JL, Chung TK, Lancaster RT, et al. Outcomes after carotid endarterectomy: is there a high-risk population? A National Surgical Quality Improvement Program report. J Vasc Surg. 2009; 49:331–8, 339 e1; discussion 338-9
7)

Yadav JS, Wholey MH, Kuntz RE, et al. Protected carotid-artery stenting versus endarterectomy in high- risk patients. N Engl J Med. 2004; 351:1493–1501
8)

Gray WA, Hopkins LN, Yadav S, et al. Protected carotid stenting in high-surgical-risk patients: the ARCHeR results. J Vasc Surg. 2006; 44:258–268
9)

Zuccarello M, Yeh H-S, Tew JM. Morbidity and Mortality of Carotid Endarterectomy under Local Anesthesia: A Retrospective Study. Neurosurgery. 1988; 23:445–450
10)

Lee KS, Courtland CH, McWhorter JM. Low Morbidity and Mortality of Carotid Endarterectomy Performed with Regional Anesthesia. J Neurosurg. 1988; 69:483–487
11)

Forssell C, Takolander R, Bergqvist D, et al. Local Versus Gen eral An esth esia in Carotid Surgery. A Prospect ive Randomized Study. Eur J Vasc Surg. 1989; 3:503–509
12) , 13)

Lewis SC, Warlow CP, Bodenham AR, Colam B, Rothwell PM, Torgerson D, Dellagrammaticas D, Horrocks M, Liapis C, Banning AP, Gough M, Gough MJ. General anaesthesia versus local anaesthesia for carotid surgery (GALA): a multicentre, randomised controlled trial. Lancet. 2008; 372:2132– 2142
14)

Rerkasem K, Rothwell PM. Local versus general anaesthesia for carotid endarterectomy. Cochrane Database Syst Rev. 2008. DOI: 1 0.1 002/1 465185 8. CD000126.pub3
15)

Spetzler RF, Martin N, Hadley MN, et al. Microsurgical Endarterectomy Under Barbiturate Protection: A Prospective Study. J Neurosurg. 1986; 65:63–73
16)

Mracek J, Kletecka J, Holeckova I, Dostal J, Mrackova J, Mork J, Priban V. Patient Satisfaction with General versus Local Anesthesia during Carotid Endarterectomy. J Neurol Surg A Cent Eur Neurosurg. 2019 Apr 29. doi: 10.1055/s-0039-1688692. [Epub ahead of print] PubMed PMID: 31035296.
17)

Belykh EG, Lei T, Oliveira MM, Almefty RO, Yagmurlu K, Elhadi AM, Sun G, Bichard WD, Spetzler RF, Preul MC, Nakaji P. Carotid Endarterectomy Surgical Simulation Model Using a Bovine Placenta Vessel. Neurosurgery. 2015 Jul 30. [Epub ahead of print] PubMed PMID: 26230044.
18)

Turki E, Almutairi OT, Modhi A, Mohammed B, Alturki AY. A bibliometric analysis on the most-cited publications on carotid endarterectomy throughout history. J Cerebrovasc Endovasc Neurosurg. 2021 Dec 2. doi: 10.7461/jcen.2021.E2021.03.010. Epub ahead of print. PMID: 34852422.

Plasma p-tau181

Plasma p-tau181

Frank et al. from the Boston University School of Medicine examined the ability of plasma hyperphosphorylated tau (p-tau)181 to detect cognitive impairment due to Alzheimer’s disease (AD) independently and in combination with plasma total tau (t-tau) and neurofilament light (NfL).

Plasma samples were analyzed using the Simoa platform for 235 participants with normal cognition (NC), 181 with mild cognitive impairment due to AD (MCI), and 153 with AD dementia. Statistical approaches included multinomial regression and Gaussian graphical models (GGMs) to assess a network of plasma biomarkers, neuropsychological tests, and demographic variables.

Plasma p-tau181 discriminated AD dementia from NC, but not MCI, and correlated with dementia severity and worse neuropsychological test performance. Plasma NfL similarly discriminated diagnostic groups. Unlike plasma NfL or t-tau, p-tau181 had a direct association with cognitive diagnosis in a bootstrapped GGM.

These results support plasma p-tau181 for the detection of Alzheimer’s disease dementia and the use of blood-based biomarkers for optimal disease detection 1).


Results suggest that in elderly individuals without dementia at baseline, plasma p-tau181 biomarkers were associated with greater memory decline and rates of clinical progression to dementia. Plasma p-tau181 improved prediction of memory decline above a model with currently available clinical and genetic data. While the clinical importance of this improvement in the prediction of memory decline is unknown, these results highlight the potential of plasma p-tau181 as a cost-effective and scalable Alzheimer’s disease biomarker 2)


Plasma p-tau231 is a promising novel biomarker of emerging AD pathology with the potential to facilitate clinical trials to identify vulnerable populations below the PET threshold of amyloid-β positivity or apparent entorhinal tau deposition. 3).


The study of Karikari et al. adds significant weight to the growing body of evidence in the use of plasma p-tau181 as a non-invasive diagnostic and prognostic tool for AD, regardless of clinical stage, which would be of great benefit in clinical practice and a large cost-saving in clinical trial recruitment. 4)


O’Connor et al. investigated the timing of p-tau181 changes using 153 blood samples from 70 individuals in a longitudinal study of familial AD (FAD). Plasma p-tau181 was measured, using an in-house single-molecule array assay. We compared p-tau181 between symptomatic carriers, presymptomatic carriers, and non-carriers, adjusting for age and sex. We examined the relationship between p-tau181 and neurofilament light and estimated years to/from symptom onset (EYO), as well as years to/from the actual onset in asymptomatic subgroup. In addition, we studied associations between p-tau181 and clinical severity, as well as testing for differences between genetic subgroups. Twenty-four were presymptomatic carriers (mean baseline EYO -9.6 years) while 27 were non-carriers. Compared with non-carriers, plasma p-tau181 concentration was higher in both symptomatic (p < 0.001) and presymptomatic mutation carriers (p < 0.001). Plasma p-tau181 showed considerable intra-individual variability but individual values discriminated symptomatic (AUC 0.93 [95% CI 0.85-0.98]) and presymptomatic (EYO ≥ -7 years) (AUC 0.86 [95% CI 0.72-0.94]) carriers from non-carriers of the same age and sex. From a fitted model, there was evidence (p = 0.050) that p-tau181 concentrations were higher in mutation carriers than non-carriers from 16 years prior to estimated symptom onset. Our finding that plasma p-tau181 concentration is increased in symptomatic and presymptomatic FAD suggests potential utility as an easily accessible biomarker of AD pathology. 5).


1)

Frank B, Ally M, Brekke B, Zetterberg H, Blennow K, Sugarman MA, Ashton NJ, Karikari TK, Tripodis Y, Martin B, Palmisano JN, Steinberg EG, Simkina I, Turk KW, Budson AE, O’Connor MK, Au R, Goldstein LE, Jun GR, Kowall NW, Stein TD, McKee AC, Killiany R, Qiu WQ, Stern RA, Mez J, Alosco ML. Plasma p-tau181 shows stronger network association to Alzheimer’s disease dementia than neurofilament light and total tau. Alzheimers Dement. 2021 Dec 2. doi: 10.1002/alz.12508. Epub ahead of print. PMID: 34854549.
2)

Therriault J, Benedet AL, Pascoal TA, Lussier FZ, Tissot C, Karikari TK, Ashton NJ, Chamoun M, Bezgin G, Mathotaarachchi S, Gauthier S, Saha-Chaudhuri P, Zetterberg H, Blennow K, Rosa-Neto P; Alzheimer’s Disease Neuroimaging Initiative. Association of plasma P-tau181 with memory decline in non-demented adults. Brain Commun. 2021 Jun 14;3(3):fcab136. doi: 10.1093/braincomms/fcab136. PMID: 34222875; PMCID: PMC8249102.
3)

Ashton NJ, Pascoal TA, Karikari TK, Benedet AL, Lantero-Rodriguez J, Brinkmalm G, Snellman A, Schöll M, Troakes C, Hye A, Gauthier S, Vanmechelen E, Zetterberg H, Rosa-Neto P, Blennow K. Plasma p-tau231: a new biomarker for incipient Alzheimer’s disease pathology. Acta Neuropathol. 2021 May;141(5):709-724. doi: 10.1007/s00401-021-02275-6. Epub 2021 Feb 14. PMID: 33585983; PMCID: PMC8043944.
4)

Karikari TK, Benedet AL, Ashton NJ, Lantero Rodriguez J, Snellman A, Suárez- Calvet M, Saha-Chaudhuri P, Lussier F, Kvartsberg H, Rial AM, Pascoal TA, Andreasson U, Schöll M, Weiner MW, Rosa-Neto P, Trojanowski JQ, Shaw LM, Blennow K, Zetterberg H; Alzheimer’s Disease Neuroimaging Initiative. Diagnostic performance and prediction of clinical progression of plasma phospho-tau181 in the Alzheimer’s Disease Neuroimaging Initiative. Mol Psychiatry. 2021 Feb;26(2):429-442. doi: 10.1038/s41380-020-00923-z. Epub 2020 Oct 26. PMID: 33106600.
5)

O’Connor A, Karikari TK, Poole T, Ashton NJ, Lantero Rodriguez J, Khatun A, Swift I, Heslegrave AJ, Abel E, Chung E, Weston PSJ, Pavisic IM, Ryan NS, Barker S, Rossor MN, Polke JM, Frost C, Mead S, Blennow K, Zetterberg H, Fox NC. Plasma phospho-tau181 in presymptomatic and symptomatic familial Alzheimer’s disease: a longitudinal cohort study. Mol Psychiatry. 2020 Jul 14. doi: 10.1038/s41380-020-0838-x. Epub ahead of print. PMID: 32665603.

Parasagittal Meningioma Differential Diagnosis

Parasagittal Meningioma Differential Diagnosis

see also Meningioma Differential Diagnosis.


Intracerebral schwannoma 1) 2) 3) 4).

Extra-axial ependymoma 5) 6).

Fibrous histiocytoma 7).

Rosai-Dorfman disease 8).


A 14-year-old female mosaic for the de novo p.R108H pathogenic variant in the PIK3CA gene was found to have a large tumor involving the superior sagittal sinus with mass effect on the motor cortex most consistent with a parafalcine meningioma. She underwent surgical resection with pathology demonstrating a venous malformation. PIK3CA pathogenic variants have been identified in nonsyndromic extracranial venous and lymphatic malformations as well in brain tumors, including glioma and meningioma. However, PIK3CA variants have not previously been identified in purely intracranial venous malformations. This distinction is relevant to treatment decisions, given that mTOR inhibitors may provide an alternative option for noninvasive therapy in cases of suspected venous malformation 9).


1)

Li M, Mei J, Li Y, Tao X, Hong T. Intracerebral schwannoma mimicking meningioma: case report. Can J Neurol Sci. 2013 Nov;40(6):881-4. PubMed PMID: 24257236.
2)

Ma L, Yang SX, Wang YR. Intracerebral schwannoma mimicking parasagittal meningioma. J Craniofac Surg. 2013 Nov;24(6):e541-3. doi: 10.1097/SCS.0b013e31828601bf. PubMed PMID: 24220461.
3)

Bristol RE, Coons SW, Rekate HL, Spetzler RF. Invasive intracerebral schwannoma mimicking meningioma in a child. Childs Nerv Syst. 2006 Nov;22(11):1483-6. Epub 2006 Sep 22. PubMed PMID: 17021734.
4)

Takei H, Schmiege L, Buckleair L, Goodman JC, Powell SZ. Intracerebral schwannoma clinically and radiologically mimicking meningioma. Pathol Int. 2005 Aug;55(8):514-9. PubMed PMID: 15998381.
5)

Singh V, Turel MK, Chacko G, Joseph V, Rajshekhar V. Supratentorial extra-axial anaplastic ependymoma mimicking a meningioma. Neurol India. 2012 Jan-Feb;60(1):111-3. PubMed PMID: 22406799.
6)

Salunke P, Kovai P, Sura S, Gupta K. Extra-axial ependymoma mimicking a parasagittal meningioma. J Clin Neurosci. 2011 Mar;18(3):418-20. doi: 10.1016/j.jocn.2010.04.042. Epub 2011 Jan 13. PubMed PMID: 21236682.
7)

Tsutsumi M, Kawano T, Kawaguchi T, Kaneko Y, Ooigawa H, Yoshida T. Intracranial meningeal malignant fibrous histiocytoma mimicking parasagittal meningioma–case report. Neurol Med Chir (Tokyo). 2001 Feb;41(2):90-3. PubMed PMID: 11255634.
8)

Kattner KA, Stroink AR, Roth TC, Lee JM. Rosai-Dorfman disease mimicking parasagittal meningioma: case presentation and review of literature. Surg Neurol. 2000 May;53(5):452-7; discussion 457. Review. PubMed PMID: 10874144.
9)

Filippidis A, Lidov H, Al-Ibraheemi A, See AP, Srivastava S, Orbach DB, Fehnel KP. Intracranial venous malformation masquerading as a meningioma in PI3KCA-related overgrowth spectrum disorder. Am J Med Genet A. 2021 Dec 2. doi: 10.1002/ajmg.a.62570. Epub ahead of print. PMID: 34854542.
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