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.

Reversible cerebral vasoconstriction syndrome

Reversible cerebral vasoconstriction syndrome

Reversible cerebral vasoconstriction syndrome (RCVS), AKA Call-Fleming syndrome, 1) a group of disorders sharing the cardinal clinical and angiographic features of reversible segmental multifocal cerebral vasoconstriction with severe headaches, focal ischemia, and/or seizures. May present as a hemorrhage restricted to a cortical sulcus

Epidemiology

RCVS has been reported to occur more frequently in women aged 20 to 50 years.

Etiology

Several mechanisms have been postulated involving transient deregulation of cerebral arterial tone, small vessel endothelial dysfunction, biochemical factors, hormonal deregulation, oxidative stress, and genetic predisposition. All these mechanisms and triggers are related with sympathetic over-activation which eventually produce vasoconstriction. RCVS is distinguished by acute severe recurrent thunderclap headaches with or without other neurological symptoms. However, the diagnosis can be challenging and most likely underdiagnosed requiring a high level of suspicion from the clinician 2).

Clinical features

Reversible cerebral vasoconstriction syndrome (RCVS) has emerged as the most frequent cause of thunderclap headache (TCH) in patients without aneurysmal subarachnoid hemorrhage, and as the most frequent cause of recurrent TCHs.

The typical TCHs of RCVS are multiple, recurring over a few days to weeks, excruciating, short-lived, and brought up by exertion, sexual activities, emotion, Valsalva maneuvers, or bathing, among other triggers. All these triggers induce sympathetic activation. In a minority of cases with RCVS, TCH heralds stroke and rarely death. Early diagnosis of RCVS in patients who present with isolated headache enables proper management and might reduce the risk of eventual stroke 3).

Outcome

Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by severe headache and diffuse segmental constriction of cerebral arteries that resolves spontaneously within a few months. Although manifestations of stroke are not included in diagnostic criteria of RCVS, it is known that some cases may be associated with stroke, including intracerebral hemorrhage, subarachnoid hemorrhage, or cerebral infarction.


Intracerebral hemorrhage is the most common vascular complication in hospitalized RCVS patients, resulting in longer hospitalizations with more invasive procedures and higher healthcare expenditure. However, overall outcomes are excellent regardless of types of ICH, with no inpatient mortality observed in patients with hemorrhagic RCVS. Female sex and middle to older age-group are associated with higher odds of ICH. 4).

Case series

162 patients with RCVS. Clinical, brain imaging, and angiography data were analyzed.

The mean age was 44±13 years, 78% women. Hemorrhages occurred in 43% including 21 patients with intracerebral hemorrhage (ICH) and 62 with convexal subarachnoid hemorrhage (cSAH). The frequency of triggers (eg, vasoconstrictive drugs) and risk factors (eg, migraine) were not significantly different between hemorrhagic and nonhemorrhagic RCVS or between subgroups (ICH versus non-ICH, isolated cSAH versus normal scan). Hemorrhagic lesions occurred within the first week, whereas infarcts and vasogenic edema accumulated during 2 to 3 weeks (P<0.001). Although all ICHs occurred before cSAH, their time course was not significantly different (P=0.11). ICH and cSAH occurred earlier than infarcts (P≤0.001), and ICH earlier than vasogenic edema (P=0.009). Angiogram analysis showed more severe vasoconstriction in distal versus proximal segments in all lesion types (ICH, cSAH, infarction, vasogenic edema, and normal scan). The isolated infarction group had more severe proximal vasoconstriction, and those with normal imaging had significantly less vasoconstriction. Multivariable analysis failed to uncover independent predictors of hemorrhagic RCVS; however, female sex predicted ICH (P=0.048), and angiographic severity predicted infarction (P=0.043).

ICH and cSAH are common complications of RCVS. Triggers and risk factors do not predict lesion subtype but may alter central vasomotor control mechanisms resulting in centripetal angiographic evolution. Early distal vasoconstriction is associated with lobar ICH and cSAH, and delayed proximal vasoconstriction with infarction 5).

Case reports

2018

Reversible Cerebral Vasoconstriction Syndrome Without Typical Thunderclap Headache Complicated by Intracranial Hemorrhage and Posterior Reversible Encephalopathy Syndrome:A Case Report 6).


Al-Mufti et al. from the Rutgers New Jersey Medical School, describe a case of medically refractory Reversible cerebral vasoconstriction syndrome (RCVS) that required treatment with intra-arterial (IA) verapamil and subsequent nimodipine, resulting in both angiographic and clinical improvement after failing to respond to hemodynamic augmentation.

They also supplement a description of the case with a review of other case studies and case series in which IA calcium channel blockers were used to treat RCVS. They propose that the case they outline demonstrates that neurointerventional management with IA verapamil is appropriate and effective as an early intervention of medically refractory RCVS.

Using PubMed and Google Scholar, they performed a search of the English language literature with several combinations of the keywords “intra-arterial”, “calcium channel blockers”, “reversible cerebral vasoconstriction syndrome”, “RCVS”, “nimodipine”, “verapamil”, “milrinone”, and “nicardipine” to identify studies in which RCVS was treated with IA calcium channel blockers.

They identified eight case studies and case series that met our inclusion criteria. Eighteen patients are encompassed in these eight studies.

IA administration of calcium channel blockers has been shown to return cerebral vessels to their normal caliber in patients with medically refractory RCVS. However, there are no randomized controlled trials of the treatment of RCVS, and further studies are needed to elucidate the optimal treatment protocol for medically refractory RCVS 7).


Gonsales et al., present an unusual case of an 18-year-old female who developed RCVS after embolization of a dural arteriovenous fistula with onyx embolic material. A cerebral angiogram was performed and verapamil was administered intra-arterially demonstrating slight improvement of the constricted vessels with clinical improvement. The patient was maintained on oral verapamil during hospitalization. At 7-month follow-up, the patient was neurologically stable and a cerebral angiogram demonstrated no signs of vasoconstriction.

Endovascular procedures are a rare trigger for the development of RCVS and may be misdiagnosed. Prompt recognition of symptoms and diagnosis with treatment are necessary to reduce the risk of stroke. The management should follow the premise of discontinuing precipitating drugs and administering CCBs 8).

2016

A 19-year-old woman had a thunderclap headache, followed by left hemiparesis and left homonymous hemianopsia. Laboratory tests showed no signs of infection and immunological test results were unremarkable. MRI revealed a cerebral infarction in the right posterior cerebral artery territory, and digital subtraction angiography(DSA)showed right posterior cerebral artery stenosis on day 2. The first follow-up DSA demonstrated an irregular, bead-like appearance on day 9, but the stenotic lesion returned to normal on day 21. Reversible cerebral vasoconstriction syndrome should be suspected in cases of rapid resolution of symptoms 9).

2014

Ishi et al. present three cases of RCVS associated with various types of stroke, and then review the literature. Case 1:A 49-year-old woman presented with a headache followed by left hemiparesis and dysarthria. One month before the onset, she was transfused for severe anemia caused by uterus myoma. CT images revealed intracerebral hemorrhages in the right putamen and right occipital lobe. Angiography revealed multiple segmental constrictions of the cerebral arteries. One month after the onset, these vasoconstrictions improved spontaneously. Case 2:A postpartum 38-year-old woman who had a history of migraine presented with thunderclap headache. Imaging revealed a focal subarachnoid hemorrhage in the right postcentral sulcus and segmental vasoconstriction of the right middle cerebral artery. One week after the onset, this vasoconstriction improved spontaneously. Case 3:A 32-year-old woman who had a history of migraine presented with headache followed by left homonymous hemianopsia. Imaging revealed a cerebral infarction of the right occipital lobe and multiple constrictions of the right posterior cerebral artery. These vasoconstrictions gradually improved spontaneously 10).

References

1)

Call GK, Fleming MC, Sealfon S, et al. Reversible cerebral segmental vasoconstriction. Stroke. 1988; 19:1159–1170
2) , 8)

Gonsales D, das Gracas F, Santos R, Aguilar-Salinas P, Hanel RA. Reversible Cerebral Vasoconstriction Syndrome as an Unusual Complication of a Dural Arteriovenous Fistula treated with Onyx Embolization. World Neurosurg. 2018 May 8. pii: S1878-8750(18)30931-8. doi: 10.1016/j.wneu.2018.04.211. [Epub ahead of print] PubMed PMID: 29751188.
3)

Ducros A, Wolff V. The Typical Thunderclap Headache of Reversible Cerebral Vasoconstriction Syndrome and its Various Triggers. Headache. 2016 Apr;56(4):657-73. doi: 10.1111/head.12797. Epub 2016 Mar 26. Review. PubMed PMID: 27015869.
4)

Patel SD, Topiwala K, Saini V, et al. Hemorrhagic reversible cerebral vasoconstriction syndrome: A retrospective observational study [published online ahead of print, 2020 Sep 7]. J Neurol. 2020;10.1007/s00415-020-10193-y. doi:10.1007/s00415-020-10193-y
5)

Topcuoglu MA, Singhal AB. Hemorrhagic Reversible Cerebral Vasoconstriction Syndrome: Features and Mechanisms. Stroke. 2016 Jun 7. pii: STROKEAHA.116.013136. [Epub ahead of print] PubMed PMID: 27272485.
6)

Miki K, Takemoto K, Morishita T, Kouzaki Y, Irie Y, Iwaasa M, Abe H, Inoue T. [Reversible Cerebral Vasoconstriction Syndrome Without Typical Thunderclap Headache Complicated by Intracranial Hemorrhage and Posterior Reversible Encephalopathy Syndrome:A Case Report]. No Shinkei Geka. 2018 Dec;46(12):1111-1115. doi: 10.11477/mf.1436203877. Japanese. PubMed PMID: 30572309.
7)

Al-Mufti F, Dodson V, Wajswol E, El-Ghanem M, Alchaki A, Nuoman R, Thabet A, Sutherland A, Roychowdhury S, Hidalgo A, Gupta G. Chemical angioplasty for medically refractory reversible cerebral vasoconstriction syndrome(). Br J Neurosurg. 2018 Sep 12:1-5. doi: 10.1080/02688697.2018.1479512. [Epub ahead of print] PubMed PMID: 30207193.
9)

Koh M, Tsuboi Y, Fukuda O. [A Case of Juvenile Cerebral Infarction due to Reversible Cerebral Vasoconstriction Syndrome]. No Shinkei Geka. 2016 Nov;44(11):965-969. Japanese. PubMed PMID: 27832620.
10)

Ishi Y, Sugiyama T, Echizenya S, Yokoyama Y, Asaoka K, Itamoto K. [Reversible cerebral vasoconstriction syndrome associated with stroke: three case reports]. No Shinkei Geka. 2014 Feb;42(2):129-36. Japanese. PubMed PMID: 24501186.
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