Delayed cerebral ischemia diagnosis

Delayed cerebral ischemia diagnosis

Local intraparenchymal neuromonitoring in the anterior cerebral artery/middle cerebral artery watershed area might detect the vast majority of delayed cerebral ischemias for all intracranial aneurysm locations, except for basilar artery aneurysms. In ACA and AcomA aneurysms, bilateral DCI of the ACA territory was common, and bilateral probe positioning might be considered for monitoring high-risk patients. Non-focal monitoring methods might be preferably used after BA aneurysm rupture 1).


Evaluating the proportion of the brain with critical hypoperfusion after SAH may better capture the extent of DCI than averaging CBF across heterogenous brain regions 2).

Early low CBF measurements and a high lactate and lactate to pyruvate ratio may be early warning signs of the risk of developing Delayed cerebral ischemia (DCI). The clinical value of these findings needs to be confirmed in larger studies 3).

Transcranial Doppler (TCD) and transcranial color-coded duplex sonography (TCCS) are noninvasive modalities that can be used to assess vasospasm. However, high flow velocity does not always reflect DCI.

Significant literature shows that perfusion computed tomography (CTP) can provide sufficient information on cerebral hemodynamics and effectively indicate delayed cerebral ischemia (DCI) before the development of infarction. Sun et al. aimed at performing a meta-analysis to provide a more full and accurate evaluation of CTP and CTP parameters in detecting DCI in patients with aneurysmal subarachnoid hemorrhage.

In the PubMed, MedLine, Embase and Cochrane databases analysis published from February 2005 to February 2013. The extraction of CTP parameters, including cerebral blood volume (CBV), cerebral blood flow (CBF), mean transit time (MTT), time to peak (TTP), interhemispheric ratios for CBV and CBF and interhemispheric differences for MTT and TTP. Pooled estimates of sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), diagnostic odds ratio (DOR) and the summary receiver-operating characteristic curve were determined.

Four research studies are met the inclusion criteria for the analysis. The pooled sensitivity, specificity, PLR, NLR and DOR of CTP for detecting the DCI were 82%, 82%, 4.56, 0.22 and 20.96, respectively. Through the evaluation of absolute CTP parameters, CBF and MTT showed diagnostic value for DCI, but CBF and TTP did not. Moreover, CBF ratio, MTT difference and TTP difference showed more diagnostic value than CBV ratio in DCI detection by the assessment of relative CTP parameters.

As a non-invasive and short time consuming screening method, CTP own a high diagnostic value for the detection of DCI after aneurysm rupture 4).

CTP maps were calculated with tracer delay-sensitive and tracer delay-insensitive algorithms and were visually assessed for the presence of perfusion deficits by two independent observers with different levels of experience. The diagnostic value of both algorithms was calculated for both observers.

Seventy-one patients were included. For the experienced observer, the positive predictive values (PPVs) were 0.67 for the delay-sensitive and 0.66 for the delay-insensitive algorithm, and the negative predictive values (NPVs) were 0.73 and 0.74. For the less experienced observer, PPVs were 0.60 for both algorithms, and NPVs were 0.66 for the delay-sensitive and 0.63 for the delay-insensitive algorithm.

Test characteristics are comparable for tracer delay-sensitive and tracer delay-insensitive algorithms for the visual assessment of CTP in diagnosing DCI. This indicates that both algorithms can be used for this purpose 5).


Whole-brain CT Perfusion (CTP) on Day 3 after aneurysmal subarachnoid hemorrhage (aSAH) allows early and reliable identification of patients at risk for delayed ischemic neurological deficits (DIND) and tissue at risk for delayed cerebral infarction (DCI) 6).


The association between alpha-delta ratio (ADR) on quantitative electroencephalography (EEG) and DCI has been reported in several previous studies, but their results are conflicting 7).


1)

Hurth H, Steiner J, Birkenhauer U, Roder C, Hauser TK, Ernemann U, Tatagiba M, Ebner FH. Relationship of the vascular territory affected by delayed cerebral ischemia and the location of the ruptured aneurysm in patients with aneurysmal subarachnoid hemorrhage. Neurosurg Rev. 2021 Mar 29. doi: 10.1007/s10143-021-01522-4. Epub ahead of print. PMID: 33782797.
2)

Jafri H, Diringer MN, Allen M, Zazulia AR, Zipfel GJ, Dhar R. Burden of cerebral hypoperfusion in patients with delayed cerebral ischemia after subarachnoid hemorrhage. J Neurosurg. 2019 May 31:1-8. doi: 10.3171/2019.3.JNS183041. [Epub ahead of print] PubMed PMID: 31151110.
3)

Rostami E, Engquist H, Howells T, Johnson U, Ronne-Engström E, Nilsson P, Hillered L, Lewén A, Enblad P. Early low cerebral blood flow and high cerebral lactate: prediction of delayed cerebral ischemia in subarachnoid hemorrhage. J Neurosurg. 2017 Jun 2:1-9. doi: 10.3171/2016.11.JNS161140. [Epub ahead of print] PubMed PMID: 28574309.
4)

Sun H, Zhang H, Ma J, Liu Y, Wang K, You C. Accuracy of computed tomography perfusion in detecting delayed cerebral ischemia following aneurysmal subarachnoid hemorrhage: a meta-analysis. Neurol India. 2013 Sep-Oct;61(5):507-12. doi: 10.4103/0028-3886.121922. PubMed PMID: 24262454.
5)

Cremers CH, Dankbaar JW, Vergouwen MD, Vos PC, Bennink E, Rinkel GJ, Velthuis BK, van der Schaaf IC. Different CT perfusion algorithms in the detection of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage. Neuroradiology. 2015 Jan 23. [Epub ahead of print] PubMed PMID: 25614332.
6)

Malinova V, Dolatowski K, Schramm P, Moerer O, Rohde V, Mielke D. Early whole-brain CT perfusion for detection of patients at risk for delayed cerebral ischemia after subarachnoid hemorrhage. J Neurosurg. 2015 Dec 18:1-9. [Epub ahead of print] PubMed PMID: 26684786.
7)

Yu Z, Wen D, Zheng J, Guo R, Li H, You C, Ma L. The predictive accuracy of alpha-delta ratio on quantitative electroencephalography for delayed cerebral ischemia in patients with aneurysmal subarachnoid hemorrhage: a meta-analysis. World Neurosurg. 2019 Feb 27. pii: S1878-8750(19)30493-0. doi: 10.1016/j.wneu.2019.02.082. [Epub ahead of print] PubMed PMID: 30825635.

Middle cerebral artery occlusion

Middle cerebral artery occlusion

Middle cerebral artery stenosis may lead to a middle cerebral artery stroke via three mechanisms:

(1) deep lacunar infarcts that develop when the exiting branch of the lenticulostriate artery is trapped within the thromboatheroma

(2) development of atheromatous ulceration with thrombosis and subsequent distal embolization

(3) hemispheric hypoperfusion caused by significant MCA obstruction and inadequate collateralization

Clinical

Complications

see Malignant middle cerebral artery territory infarction.


In these patients the clinical presentation usually starts with focal signs and progresses with a decline of consciousness until brainstem dysfunction is evident.

A shift of the ischemic tissue rather than intracranial hypertension is the most likely responsible for the initial decrease in consciousness 1) 2).

Several other satellite reactions are involved in an inexorable pathogenetic cascade, including disturbances of microvascular tone, endothelial cell swelling, and activation of platelets, leucocytes, and coagulation 3).

Diagnosis

Imaging studies are the mainstay for identification of people at higher risk for malignant infarction among the ischemic stroke population.

Perfusion computed tomography

Perfusion computed tomography of the brain is routinely performed for first and later controls. The earliest warning signs for developing malignant infarction include involvement of an area larger than 50% of the MCA territory and an infarct extending also to the anterior or posterior cerebral artery territories. A midline shift >10 mm, effacement of subarachnoid spaces, and attenuation of corticomedullary differentiation are also related to higher risk of severe deterioration 4), but they usually occur later, when a malignant syndrome is already in progress. The intravenous injection of contrast medium with elaboration of its distribution (perfusion-CT) entails higher diagnostic accuracy of ischemic areas and an even earlier detection of patients at higher risk. A drop in cerebral perfusion of more 66% is related to a likely malignant evolution 5).

Magnetic resonance imaging

Magnetic resonance imaging is another helpful exam, which in ischemic stroke can be used for prognostic purposes within few hours of clinical onset. Its sensitivity is higher than CT and it is more likely to show changes at earlier time points than CT scan. On diffusion weighted images (DWI) an ischemic area of at least 145 mL strongly predicts a massive cerebral infarction 6) 7).

It is straightforward that at final stages the pressure inside the skull of patients with large cerebral infarction is probably high. Anyway, a pressure increase limited to the infarcted and immediately adjacent areas could happen, leading to neurological worsening and even death despite no spread of intracranial hypertension 8).

Undisputed poor prognosis predictors as CT uncal herniation and anisocoria sometimes occur without an overall ICP raise is detected 9).

The measurement may also be influenced by the device used (solid-state or fluid-filled) as well as by its location (subdural, intraparenchymal, intraventricular; ipsilateral or contralateral to ischemia) 10).

Treatment

see Middle cerebral artery occlusion treatment.

Outcome

Malignant evolution is more common in younger patients 11).

Despite optimal medical management this condition may lead to death in 70–80% of cases 12) 13).

The criteria for surgical indication mean a selection of patients who likely will have less postoperative disabilities. Living with a severe neurological impairment may appear more acceptable in some cultures, and inhumane in others. A recent review anyway concluded that the vast majority of operated patients do not regret having undergone surgery 14).

The natural history of middle cerebral artery occlusion MCA occlusion has become increasingly important since the surgical option of EC/IC bypass surgery has been available.

The clinical course of 24 patients with angiographically-demonstrated occlusion of the MCA artery was reviewed. Eight patients presented with a major disabling stroke and five of these died during the acute phase of this ischemic event. The remaining 19 patients were followed for a mean of 54.2 months. There were five deaths in follow-up and two of these were due to subsequent strokes. Fourteen patients manifested a benign course: one of these had a further minor stroke and four had TIAs. Altogether, 3 strokes occurred during the follow-up period (2 fatal, 1 minor) and all were in the territory of the artery known to be occluded. Of those patients who survived their presenting ischemic event, 12 (63%) remained completely functional in terms of activities of daily living. MCA occlusion does not necessarily carry a poor prognosis with medial therapy alone and the role of bypass surgery hopefully will be clarified by the ongoing clinically randomized trial 15).

Case series

Encephaloduroarteriosynangiosis (EDAS) as a form of indirect revascularization has been recently proposed as a potentially promising alternative for patients with intracranial atherosclerotic disease (ICAD). The object of a study was to compare the prognostic roles between isolated EDAS and medical therapy in patients with atherosclerotic middle cerebral artery occlusion (MCAO).

From January 2014 to June 2017, 125 patients with atherosclerotic MCAO were enrolled in this prospective nonrandomized controlled cohort study. Patients who underwent EDAS (n = 60) were compared with those treated medically (n = 65). Early and late adverse events and functional outcomes including memory ability were compared between groups.

During 23.7 months of mean follow-up, rates of adverse events, including ischemic events in the territory of the qualifying middle cerebral artery (MCA), and death from any causes, were not significantly different in patients treated with EDAS and with medical therapy (6.7% vs. 12.3%; p=0.285). Landmark analyses revealed that at initial 6-month follow-up, there was no significant difference for adverse event rates, while the opposite finding was demonstrated for the subsequent period (EDAS 1/57 [1.7%] vs. medical management 7/64 [10.9%]; p=0.024). And the P value for the interaction between time (first 6 months vs. subsequent period) was 0.044. No significant differences were found with the respect to neural function status and cognitive ability.

In the long-term, isolated EDAS can be considered effective and safe for patients with atherosclerotic MCAO, whereas it may need additional medical therapy support in the short-term 16).

Case reports

A 69-year-old with right hemiparesis and global aphasia. Perfusion computed tomography imaging revealed ischemic penumbra in the middle cerebral artery territory. Angiography showed left middle cerebral artery occlusion. Mechanical thrombectomy with one pass was performed, and successful recanalization was obtained. Embolic material was retrieved; it contained tumor fragments with atypical keratinizing squamous cell carcinoma. Contrast computed tomography imaging indicated tumor invasion into the superior vena cava, and contrast transcranial Doppler indicated the presence of a right-to-left shunt after the Valsalva maneuver. They diagnosed the patient with acute ischemic stroke of large vessel occlusion due to venous invasion of esophageal carcinoma via a right-to-left shunt. This is the first case of embolic occlusion resulting from an extracardiac tumor via a right-to-left shunt. Contrast transcranial Doppler potentially detects right-to-left shunts in patients who cannot undergo transesophageal echocardiography 17).

References

1)

Frank JI. Large hemispheric infarction, deterioration, and intracranial pressure. Neurology. 1995;45(7):1286–1290.
2) , 9)

Schwab S, Aschoff A, Spranger M, Albert F, Hacke W. The value of intracranial pressure monitoring in acute hemispheric stroke. Neurology. 1996;47(2):393–398.
3)

del Zoppo GJ, Mabuchi T. Cerebral microvessel responses to focal ischemia. Journal of Cerebral Blood Flow & Metabolism. 2003;23(8):879–894.
4)

Lam WWM, Leung TWH, Chu WCW, Yeung DTK, Wong LKS, Poon WS. Early computed tomography features in extensive middle cerebral artery territory infarct: prediction of survival. Journal of Neurology, Neurosurgery & Psychiatry. 2005;76(3):354–357.
5)

Hofmeijer J, Algra A, Kappelle LJ, van der Worp HB. Predictors of life-threatening brain edema in middle cerebral artery infarction. Cerebrovascular Diseases. 2008;25(1-2):176–184.
6)

Krieger DW, Demchuk AM, Kasner SE, Jauss M, Hantson L. Early clinical and radiological predictors of fatal brain swelling in ischemic stroke. Stroke. 1999;30(2):287–292.
7)

Kasner SE, Demchuk AM, Berrouschot J, et al. Predictors of fatal brain edema in massive hemispheric ischemic stroke. Stroke. 2001;32(9):2117–2123.
8)

Poca MA, Benejam B, Sahuquillo J, et al. Monitoring intracranial pressure in patients with malignant middle cerebral artery infarction: is it useful? Journal of Neurosurgery. 2010;112(3):648–657.
10)

Carhuapoma JR, Qureshi AI, Bhardwaj A, Williams MA. Interhemispheric intracranial pressure gradients in massive cerebral infarction. Journal of Neurosurgical Anesthesiology. 2002;14(4):299–303.
11) , 13)

Hacke W, Schwab S, Horn M, Spranger M, de Georgia M, von Kummer R. ‘Malignant’ middle cerebral artery territory infarction: clinical course and prognostic signs. Archives of Neurology. 1996;53(4):309–315.
12)

Wijdicks EFM, Diringer MN. Middle cerebral artery territory infarction and early brain swelling: progression and effect of age on outcome. Mayo Clinic Proceedings. 1998;73(9):829–836.
14)

Rahme R, Zuccarello M, Kleindorfer D, et al. Decompressive hemicraniectomy for malignant middle cerebral artery territory infarction: is lifeworth living? Journal of Neurosurgery. 2012;117(4):749–754.
15)

Moulin DE, Lo R, Chiang J, Barnett HJ. Prognosis in middle cerebral artery occlusion. Stroke. 1985 Mar-Apr;16(2):282-4. PubMed PMID: 3975967.
16)

Zhang Q, Li Y, Tong H, Wu X, Wang Y, Ge W, He C, Liu R, Yu S. Comparison of therapeutic efficacy between isolated encephaloduroarteriosynangiosis and medical treatment in patients with atherosclerotic middle cerebral artery occlusion. World Neurosurg. 2018 Jun 20. pii: S1878-8750(18)31272-5. doi: 10.1016/j.wneu.2018.06.057. [Epub ahead of print] PubMed PMID: 29935318.
17)

Araki S, Maekawa K, Kobayashi K, Sano T, Yabana T, Shibata M, Miya F. Tumor Embolism Through Right-to-Left Shunt Due to Venous Invasion of Esophageal Carcinoma. J Stroke Cerebrovasc Dis. 2020 Sep 30;29(12):105352. doi: 10.1016/j.jstrokecerebrovasdis.2020.105352. Epub ahead of print. PMID: 33010722.

Superficial temporal artery to middle cerebral artery bypass for moyamoya disease complications

Superficial temporal artery to middle cerebral artery bypass for moyamoya disease complications

see Superficial temporal artery to middle cerebral artery bypass complications.

The Japan Adult Moyamoya study reported 1) 9.4% of complications in 84 cases reported.


Cerebral hyperperfusion syndrome (CHS) is a common complication after direct bypass surgery in patients with Moyamoya disease (MMD).

Although the main potential complications associated with this treatment are cerebral hyperperfusion and cerebral ischemia, the adverse impacts of revascularization surgery remain unclear.

Transient neurological symptoms are frequently observed during the early postoperative period after direct bypass surgery for moyamoya disease.

Hyperperfusion syndrome is believed to be the cause.


Abnormal signal changes in the cerebral cortex can be seen in postoperative MR images.

MR perfusion and Single photon emission computed tomography (SPECT) are well known imaging studies to evaluate hemodynamic change between prior to and following superficial temporal artery (STA)-middle cerebral artery (MCA) anastomosis in moyamoya disease. But their side effects and invasiveness make discomfort to patients.


Since preventive measures may be inadequate, Yang et al. assessed whether the blood flow difference between the superficial temporal artery (STA) and recipient vessels (△BF) and the direct perfusion range (DPR) are related to CHS.

They measured blood flow in the STA and recipient blood vessels before bypass surgery by transit-time probe to calculate △BF. Perfusion changes around the anastomosis before and after bypass were analyzed with FLOW 800 to obtain DPR. Multiple factors, such as △BF, DPR, and postoperative CHS, were analyzed using binary logistic regression.

Results: Forty-one patients with MMD who underwent direct bypass surgery were included in the study. Postoperative CHS symptoms occurred in 13/41 patients. △BF and DPR significantly differed between the CHS and non-CHS groups. The optimal receiver operating characteristic (ROC) curve cut-off value was 31.4 ml/min for ΔBF, and the area under the ROC curve (AUC) was 0.695 (sensitivity 0.846, specificity 0.500). The optimal cut-off value was 3.5 cm for DPR, and the AUC was 0.702 (sensitivity 0.615, specificity 0.750).

Postoperative CHS is caused by multiple factors. △BF is a risk factor for CHS while DPR is a protective factor against CHS 2).

References

1)

Miyamoto S, Yoshimoto T, Hashimoto N, Okada Y, Tsuji I, Tominaga T, Nakagawara J, Takahashi JC; JAM Trial Investigators. Effects of extracranial-intracranial bypass for patients with hemorrhagic moyamoya disease: results of the Japan Adult Moyamoya Trial. Stroke. 2014 May;45(5):1415-21. doi: 10.1161/STROKEAHA.113.004386. Epub 2014 Mar 25. PMID: 24668203.
2)

Yang D, Zhang X, Tan C, Han Z, Su Y, Duan R, Shi G, Shao J, Cao P, He S, Wang R. Intraoperative transit-time ultrasonography combined with FLOW800 predicts the occurrence of cerebral hyperperfusion syndrome after direct revascularization of Moyamoya disease: a preliminary study. Acta Neurochir (Wien). 2020 Oct 2. doi: 10.1007/s00701-020-04599-w. Epub ahead of print. PMID: 33006072.
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