Histopathology of the brain vascular network in moyamoya disease.

Yamashita, Masanori; Oka, Kazunari; Tanaka, Keisei

doi:10.1161/01.str.14.1.50

Cited by 241 publications

(142 citation statements)

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“…In addition, a previous histopathological report described ruptured moyamoya vessels showing fibrin deposits in the wall, fragmented elastic laminae, attenuated media, microaneurysm formation, focal fibrin deposits, and marked attenuation of vessel wall thickness with diminution of the elastic lamina in patients with MMD. 31 Many researchers have reported that angiographic features related to hemorrhagic stroke in patients with MMD consist of anterior cerebral artery occlusion, cerebral aneurysms, and dilation of the anterior choroidal artery or posterior communicating artery. 8,17 In particular, microbleeds in deep and periventricular white matter have been reported as a probable predictor of subsequent intraventricular hemorrhage in pa- tients with MMD.…”

Section: Discussionmentioning

confidence: 99%

Association of apolipoprotein E gene polymorphism with small-vessel lesions and stroke type in moyamoya disease: a preliminary study

Jang

Huh

Lee

2016

JNS

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M oyaMoya disease (MMD) is a progressive cerebrovascular occlusive disorder consisting of bilateral stenosis or occlusion of the supraclinoid internal carotid artery (ICA) and its major branches, with net-like vessels in the area surrounding the circle of Willis. 27 Many studies have demonstrated a higher prevalence of asymptomatic cerebral microbleeds in patients with MMD compared with the normal population.11 In addition, a recent meta-analysis showed that a high incidence of asymptomatic cerebral microbleeds appeared to be correlated with the hemorrhagic onset type in patients with MMD.20 Kikuta et al. 12 identified the presence of multiple microbleeds as a predictor of subsequent hemorrhages in patients with MMD.abbreviatioNs APOE = apolipoprotein E; GRE = gradient-recalled echo; ICA = internal carotid artery; MMD = moyamoya disease; SVL = small-vessel lesion; T2WI = T2*-weighted imaging. obJective The present study was conducted to investigate whether microbleeds or microinfarcts are associated with apolipoprotein E (APOE) gene polymorphisms in patients with moyamoya disease (MMD), and if so, whether APOE gene polymorphisms are also associated with stroke type in patients with MMD. methods This cross-sectional, multicenter study included 86 consecutive patients with MMD who underwent T2*-weighted gradient echo or susceptibility-weighted MR imaging and 83 healthy control volunteers. Baseline clinical and radiological characteristics were recorded at diagnosis, and inter- and intragroup differences in the APOE genotypes were assessed. Multivariate binary logistic regression models were used to determine the association factors for smallvessel lesions (SVLs) and hemorrhagic presentation in patients with MMD. results There was no difference in APOE gene polymorphism and the incidence of SVLs between patients with MMD and healthy controls (p > 0.05). In the MMD group, 7 (8.1%) patients had microbleeds and 32 (37.2%) patients had microinfarcts. Microbleeds were more frequently identified in patients with hemorrhagic-type than in nonhemorrhagictype MMD (p = 0.003). APOE genotypes differed according to the presence of microbleeds (p = 0.024). APOE ε2 or ε4 carriers also experienced microbleeds more frequently than APOE ε3/ε3 carriers (p = 0.013). In the multivariate regression analysis in patients with MMD, microbleeds were significantly related to APOE ε2 or ε4 carrier status (OR 7.86;; p = 0.032) and cerebral aneurysm (OR 17.31; 95% CI 2.09-143.57; p = 0.008). Microinfarcts were independently associated with hypertension (OR 3.01; 95% CI 1.05-7.86; p = 0.007). Hemorrhagic presentation was markedly associated with microbleeds (OR 10.63; 95% CI 1.11-102.0; p = 0.041). coNclusioNs These preliminary results did not show a difference in APOE gene polymorphisms between patients with MMD and healthy persons. However, they imply that APOE gene polymorphisms may play certain roles in the presence of microbleeds but not microinfarcts in patients with MMD. A further confirmatory study is necessary to elucidate the effec...

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Section: Discussionmentioning

confidence: 99%

Association of apolipoprotein E gene polymorphism with small-vessel lesions and stroke type in moyamoya disease: a preliminary study

Jang

Huh

Lee

2016

JNS

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“…One fifth of the patients with MMD in Japan have haemorrhagic presentation. Haemorrhages can be due to breakdown of dilated friable perforating vessels that form the extensive basal collateral network (15). SAH in MMD is due to formation of pseudoaneurysm or microaneurysm (7).…”

Section: Discussionmentioning

confidence: 99%

Moyamoya disease associated with recurrent right thalamic haemorrhage and hydrocephalous: a case report.

Sinha¹,

Jain²,

Jagdhane³

et al. 2014

Turkish Neurosurgery

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Moyamoya disease, a rare chronic, progressive cerebrovascular disease leads to occlusion of intracranial internal carotid arteries and its proximal branches. We report a case of a 51-year-old female who presented with recurrent thalamic bleed and intraventricular haemorrhage nine years apart in the same territory. The first bleed was managed conservatively and second bleed led to development of hydrocephalus. The acute phase of the hydrocephalus was managed by external ventricular drainage and the final CSF diversion was managed by ventriculoperitoneal shunt. The definitive treatment could not be done to denial of consent from the patient. We present the case to highlight the role CSF diversion as a means of palliative treatment for the Moyamoya disease.KeywOrds: Moyamoya disease, Adult, Haemorrhage, Hydrocephalus, Ventriculoperitoneal shunt ÖZ Nadir, kronik ve progresif bir serebrovasküler hastalık olan Moyamoya hastalığı intrakraniyal internal karotid arterler ve proksimal dallarında tıkanmaya neden olur. Aynı bölgede dokuz yıl arayla nüks talamik ve intraventriküler kanamayla gelen 51 yaşında bir kadın hasta sunuyoruz. İlk kanama konservatif olarak izlenirken, ikinci kanama hidrosefali gelişmesine neden oldu. Hidrosefalinin akut fazı eksternal ventriküler direnajla tedavi edildi ve takiben ventrikülo-peritoneal şant uygulandı. Hasta olur vermediği için kesin tedavi yapılamadı. Olguyu moyamoya hastalığının palyatif tedavisi için beyin omurilik sıvısı (BOS) dolanımının rolünü vurgulamak üzere sunuyoruz.

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“…However, histopathological investigations have not revealed any evidence of active inflammation in the terminal portion of the internal carotid arteries (Hosoda, 1984;Yamashita et al, 1991). Since most histopathological examinations of this disease have only been conducted in adult bleeding cases, it remains unclear as to what kind of pathological changes exist in the most active state in younger aged patients.…”

Section: Discussionmentioning

confidence: 99%