Posterior Cerebral Artery Territory Infarcts in the New England Medical Center Posterior Circulation Registry

Yamamoto, Yasumasa; Georgiadis, Alexandros; Chang, Hui-Meng; Caplan, Louis R.

doi:10.1001/archneur.56.7.824

Cited by 146 publications

(132 citation statements)

References 22 publications

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“…35,93 Cardiogenic embolism (nϭ32 [41%]) and embolism from the ECVA, ICVA, and basilar artery (nϭ25 [32%]) were the most common sources of embolism, while 8 (10%) were categorized as cryptogenic embolism. 93 Intrinsic PCA disease was present in only 7 patients (9%). Vasoconstriction due to migraine and coagulopathies accounted for 9% of PCA territory infarcts.…”

Section: Vascular Occlusive Lesionsmentioning

confidence: 99%

Posterior Circulation Ischemia: Then, Now, and Tomorrow

Caplan

2000

Stroke

172

103

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know and appreciate where we are now and where we are going in the future, it is essential to know where we have been. We cannot afford to relive and repeat the history of stroke every several decades. Posterior circulation stroke represents a microcosm of stroke in general. In this presentation I first review the development of ideas regarding brain and posterior circulation ischemia and its recognition and treatment. I then share some recent data from a large prospective registry of patients with posterior circulation ischemia. Finally, I look ahead to reflect on what I believe should be the future directions for research and for the care of patients with posterior circulation disease.Patients who present to physicians and hospitals with symptoms that suggest posterior circulation ischemia are handled differently from patients who have symptoms that suggest anterior circulation disease in the great majority of medical facilities in the United States and in the world. A patient who has an attack of dizziness with diplopia and ataxic gait usually has a brain image but seldom has vascular or cardiac investigations. A diagnosis of "vertebrobasilar insufficiency" (VBI) is often made, and physicians then debate whether or not to treat with warfarin-type anticoagulants, and, if so, for how long and at what intensity. In contrast, a patient who has right-hand weakness and aphasia is usually evaluated and treated quite differently at the very same facilities. Brain imaging, cardiac investigations, noninvasive vascular tests of the carotid and intracranial anterior circulation with the use of extracranial and transcranial ultrasound and/or MR angiography (MRA) and CT angiography, and catheter angiography are often pursued, depending on the local technological capabilities and experience of the treating physicians. An effort is made to identify the etiology and mechanism of the ischemia. Treatment is then chosen among a variety of possibilities (including carotid artery surgery, angioplasty, anticoagulants, and antiplatelet aggregants) depending on the nature, location, and severity of the occlusive disease and the mechanism of ischemia.Why should anterior and posterior circulation ischemia be handled so differently? Does this schizophrenic approach make sense? After all, the internal carotid artery and its branches and the vertebral (VA) and basilar arteries (BA) and their branches are just a few inches apart; they are made of the same coats and look the same under the microscope except for size. These vessels carry the same blood under the same blood pressure. The diseases that affect the blood vessels in the 2 circulations are the same. Do stroke mechanisms really differ between the 2 circulations? How did this differing approach originate, and does it continue to make sense today? These are some questions that I will attempt to answer as I review the development of ideas about posterior circulation ischemia and as I report recent data. Development of IdeasHerein I review how knowledge about the posterior circulation ...

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Section: Vascular Occlusive Lesionsmentioning

confidence: 99%

Posterior Circulation Ischemia: Then, Now, and Tomorrow

Caplan

2000

Stroke

172

103

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“…Ayrıca çeşitli serilerde PSA enfarkt sıklığı %5 ile %25 arasında değişen oranlarda bildirilmiştir (7)(8)(9). Kalkarin, temporooksipital, parietooksipital ve temporal arter sulama alanında oluşan kortikal PSA enfarktları tüm PSA enfarktlarının 2/3'ünü oluştururken kombine PSA enfarktları (derin+kortikal) çeşitli serilerde %5-38,5 oranında bildirilmiştir (1,2,6,8,10).…”

Section: Discussionunclassified

“…Etiyolojiye bakıldığında serimizde en sık kardiyoemboli (%47,3) gözlenmiş olup gruplar arasında (grup 1-%45,7, grup 2-%50) anlamlı istatistiksel farklılık gözlenmedi. Önceki çalışmalar ile karşılaştırıldığında kardiyoemboli sıklığı Arboix (%21,6), Lee (%20) ve Kumral'a (%17) göre daha sık, Ntaios'a (%52,9) göre daha az ve Yamamota (%41) ile benzer oranda idi (7)(8)(9)(18)(19)(20). Ayrıca KaE grubunda Ntaios'a benzer şekilde kortikal PSA enfarkt üstünlüğünü saptadık (20).…”

Section: Discussionunclassified

“…Ayrıca KaE grubunda Ntaios'a benzer şekilde kortikal PSA enfarkt üstünlüğünü saptadık (20). Daha önce yapılmış çalışmalarda EPSAH sıklığı %1,7 ile %16 aralığında değişen oranlarda gözlenirken çalışmalara konvansiyonel MR veya MRA dahil edilmesi ile bu oranın (%18,5, %30, %43,6, %49,6, %50,6) arttığı görülmektedir (7)(8)(9)12,19,21). Serimizde ikinci sıklıkta gözlediğimiz EPSAH (%21,1) grubunda 12 hastanın 7'sinde kortikal PSA, 5'inde PSA+ enfarktı mevcuttu.…”

Section: Discussionunclassified

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Mechanisms, clinical features and risk factors for stroke in the posterior cerebral artery infarcts

Aydın¹,

Borucu²,

Pazarcı³

et al. 2015

tnd

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Bulgular: Otuz beş hasta (%61) PSA kortikal dal enfaktüsü geçirirken, 22 hastada (%39) kortikal ve derin PSA besleme alanında enfarkt saptandı. Etyolojiye bakıldığında her iki grupta da kardioembolizmin (n=27, %47) daha sık olduğu saptandı. Bunu sırayla entrensek PSA hastalığı (n=12, %21), proksimal arter hastalığı (n=10, %17), kriptojenik emboli (n=8, %15) izledi. İnme başlangıcında hastaların %52 baş ağrısı gösterdi. Hastaların %78'inde görme alanı bozuklukları, %54'ünde motor semptomlar, %24'ünde duysal semptomlar mevcuttu.Sonuç: PSA kortikal ve derin sulama alanındaki enfarktlarda kardiyojenik emboli ve entrensek PSA hastalığının daha sık olduğu düşünüldü. PSA kortikal dal enfarktı olanlar ile derin ve kortikal dal enfarktı olanlar arasında etyoloji ve risk faktörleri açısından anlamlı istatistiksel değişiklik saptanmadı. (Türk Nöroloji Dergisi 2015; 21:49-54) Anah tar Ke li me ler: Posterior serebral arter, akut serebral enfarktüs, etyoloji Objective: The objective of our study was to investigate the association between the infarcts in the cortical and deep posterior cerebral artery (PCA) perfusion area and the mechanisms of stroke, their clinical features and risk factors. Materials and Methods:Fifty seven patients who suffered strokes first time and have infarcts in the PCA perfusion area and admitted to our Neurology Clinics between January 2002 and August 2007 were included in this study. Subjects were divided in two groups as cortical branch infarct group and deep (thalamus) + cortical branch group. Patients were evaluated in four etiologic clusters; 1. Occlusion in the posterior cerebral artery or its branches. 2. Occlusion proximal to the posterior cerebral artery. 3. Cardio-embolic reasons. 4. Cryptogenic embolism group. All patients had cranial CT, MRI, neck Doppler USG, MRA or DSA, transesophageal or trans-thoracic echocardiography, hematologic and vasculytic investigations. Risk factors in all patients were recorded.

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“…However, reports of migratory cardioembolic events that occlude penetrating vessel ostia are reported, but their involvement is typically greater than 1 cm in parenchymal size. Cardioembolic stroke affecting the posterior circulation accounts for ≤25% of posterior circulation ischemic events in some registries [18][19][20][21][22][23][24][25][26].…”

Section: Evaluation Of Patients At Risk For Cardioembolic Strokementioning

confidence: 99%

Prevention of Cardioembolic Stroke

Freeman

Aguilar

2011

Neurotherapeutics

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Cardiac causes of ischemic stroke lead to severe neurological deficits from large intracranial artery occlusion compared to small vessel ischemic stroke. The most common cause of cardioembolic stroke is atrial fibrillation (AF), which has an increasing incidence with age. AF stroke trials demonstrate that anti-coagulation is superior to anti-platelet therapy in terms of ischemic stroke prevention. Recently, warfarin was compared with dabigatran, an oral, direct thrombin inhibitor, and was found to be at least equally effective in reducing ischemic stroke with less intracranial bleeding risk. Future research is investigating other direct thrombin inhibitors as potential alternatives to warfarin, which has a narrow therapeutic index, requires frequent blood monitoring, has multiple drug interactions, and a higher rate of intracranial bleeding. Other causes of cardioembolic stroke include myocardial infarction, left ventricular thrombus, reduced ejection fraction, valvular abnormalities, and endocarditis. Patent foramen ovale is a common finding on echocardiograms in patients with and without stroke (up to 20% of the population), and it is a controversial source of cryptogenic stroke. The best way to prevent cardioembolic stroke remains early detection and treatment of AF, and treating the underlying stroke mechanism. Cardiac magnetic resonance imaging is an emerging technology and reveals some sources of cardiac embolism missed by echocardiography, and might provide an additional diagnostic tool in investigating cardioembolic stroke.

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Posterior Cerebral Artery Territory Infarcts in the New England Medical Center Posterior Circulation Registry

Abstract: The great majority of pure PCA and PCA+ territory infarcts are caused by cardiac or intra-arterial embolism. Intrinsic PCA disease, vasoconstriction, and coagulopathy are less common causes of infarction.

Cited by 146 publications

References 22 publications

Posterior Circulation Ischemia: Then, Now, and Tomorrow

Posterior Circulation Ischemia: Then, Now, and Tomorrow

Mechanisms, clinical features and risk factors for stroke in the posterior cerebral artery infarcts

Prevention of Cardioembolic Stroke

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