Yonekawa, Yasuhiro

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EDITORIALOuter diameter measured by 3D CISS MRIand quasi-Moyamoya diseaseYasuhiro YonekawaReceived: 21 August 2012 /Accepted: 22 August 2012 /Published online: 14 September 2012# Springer-Verlag 2012Outer diameter measured by 3D CISS MRI and quasi-Moyamoya diseaseThe interesting article by Kaku Y et al.: Outer diameternarrowing of the internal carotid artery and the middlecerebral arteries detected in Moyamoya disease detectedon 3D constructive interference in steady-state (CISS) MRimage…, shows us once more that:1. The pathology of Moyamoya disease, especially itspathological vessel walls, compared with those of othercerebrovascular diseases like atherosclerosis.One has to observe not only changes of the innerdiameter of the pathological vessels but also that of theouter diameter caused by remodeling of vascular walloriginating in the pathological process of a disease. Untilnow, we have paid attention only to the inner diameter,namely luminal stenosis or occlusion on the basis ofangiographical or MRI findings. The 3D-CISS MRI hasbeen revealed to be a good tool for measurement of theouter diameter to observe the latter process for instancechanges of vascular wall thickness due to its remodeling.2. The definition of Moyamoya disease and its differenti-ation from related diseases.The terminology Quasi-Moyamoya disease (<rui>Moyamoya disease in Japanese) could be found, so faras the author has searched around, initially in a chapterof the book Moyamoya disease edited by Prof. J Suzuki(one of finders of this disease and has coined the nameof “Moyamoya”) in 1983 [3]. Watanabe T and Suzuki Nclassified as “rui” Moyamoya disease which was how-ever out of diagnostic criteria of Moyamoya disease,including:a. Only one side corresponds with the criteria of Moya-moya disease (1) but the other side having normalvasculatures.b. Cases with one side or bilateral middle cerebral arteryMCA stenosis at the origin associated with Moyamoyavessels, however, combined with neither internal carotidartery ICA nor anterior cerebral artery ACA stenosesc. Combination with congenital malformation: AVM,primitive trigeminal arteryd. Associated with apparent basic disease such as: vonRecklinghausen disease, head trauma (mechanical vaso-constriction), fibromuscular dysplasia, tuberculous men-ingitis, atherosclerosis, post-irradiation, Fanconi’sanemia, sickle cell anemia, nonspecific arteritis, connec-tive tissue anomaly, cerebral angiitis due to leptospirosisAs you can follow, the definition of “rui” Moyamoya dis-ease thus inherits some confusion, while the definition of theresearch committee under the guideline (bilaterality of findingsof seno-occlusion at the terminal portion of the ICA and atproximal portion of the MCA and ACA combined with abnor-mal vasculatures Moyamoya at basal portion of the brain, andwithout any basic disease [1]) originally set in 1979 was farmore clear in separating Moyamoya disease from Moyamoyasyndrome having basic disease [1]. The name “rui” seems tohave changed into “quasi” at the time of the English edition ofthe above-mentioned book in 1986 published by Springer.The author of this editorial did not know, however,until quite recently that the research committee has nowincluded the terminology quasi-Moyamoya disease intothe diagnostic guideline in 2012 (originally in 2009 inJapanese) [2], so that this terminology can be usedequally to Moyamoya syndrome, which means thatquasi-Moyamoya disease also includes atherosclerosisbut excludes unilateral pathology without basic disease(above mentioned in “a”) namely probable Moyamoyadisease, and quasi-Moyamoya disease also includes theY. Yonekawa (*)University of Zurich,Haldenbachstrasse 18,Zurich 8091, Switzerlande-mail: yasuhiro.yonekawa@usz.chActa Neurochir (2012) 154:2159–2161DOI 10.1007/s00701-012-1495-xone with hyperthyroidism as shown in Fig. 1 and at-tached legends. The guideline excludes, by the way,AVMs, aneurysms, or congenital vascular anomaliessuch as primitive trigeminal artery as “basic” disease,what was still not the case at that time in the above-mentioned original paper of “rui” Moyamoya disease, ascan be seen in “c”. Differentiation of “basic disease orunderlying disease” from “concomitant or associateddisease” is not always easy. After all, terminology ofquasi-Moyamoya disease is considered still not to befree of confusion and not to have obtained generalacceptance.The original manuscript by Kaku et al. did not in-clude any mention of quasi-Moyamoya disease, so thatit was rather clear cut in differentiating findings of 3DCISS between Moyamoya disease and atheroscleroticcerebrovascular disease. Readers are, therefore, askednot to be confused with the final version, mentioningadditionally about hyperthyroidism, whose combinationbelongs also to quasi-Moyamoya disease or Moyamoyasyndrome, which includes also atherosclerosis as basicdisease.By the way, we also use from time to time theterminology Moyamoya angiopathy MMA [4, 5], inwhich all the clinico-pathology of Moyamoya disease,Moyamoya syndrome, and unilateral pathology are in-cluded. This concept has originated from the idea thatthe management–treatment of ischemia, epilepsy, orbleeding due to this entity can be performed on thebase of similar clinico-pathophysiology and not neces-sarily based on the etiology.Conflict of interest None.References1. Fukui M (1997) Members on the research committee on spontane-ous occlusion of the circle of Willis (Moyamoya disease) of theministry of Health and Welfare, Japan: Guidelines for the diagnosisand treatment of spontaneous occlusion of the circle of Willis(“moyamoya” disease). Clin Neurol Neurosurg 99(suppl 2):S238–S240Moyamoya angiopathy (MMA) Moyamoya disease (MMD) without basic disease ProbableMMD Moyamoya syndrome (MMS) (Quasi-Moyamoya disease) with basic disease* without basic diseasewith basic diseaseUnilateral pathologyBilateral pathology Fig. 1 Moyamoya disease, Moyamoya syndrome (quasi-Moyamoyadisease) and Moyamoya angiopathy *basic disease [1, 2]: atheroscle-rosis, autoimmune disease (systemic lupus erythematosus, antiphos-pholipid antibody syndrome, periarteritis nodosa and Sjögren’ssyndrome), meningitis, von Recklinghausen’s disease, brain tumors,Down’s syndrome, head injury, irradiation, hyperthyroidism, stenoce-phaly, Turner’s syndrome, Alagille syndrome, William’s syndrome,Noonan’s syndrome, Marfan’s syndrome, tuberous sclerosis,Hirschsprung’s disease, glycogen storage disease type 1, Prader-Willisyndrome, Wilms tumor, primary oxalosis, sickle cell disease, Fanco-ni’s anemia, spherocytosis, eosinophilic granuloma, type II plasmino-gen deficiency, leptospirosis, pyruvate kinase deficiency, proteinsomeone deficiency, protein C deficiency, fibromuscular hyperplasia,osteogenesis imperfecta, polycystic kidney, oral contraceptives, anddrug poisoning (cocaine, etc.)2160 Acta Neurochir (2012) 154:2159–21612. Research committee on the pathology and treatment of spontaneousocclusion of the circle of Willis (2012) Guidelines for diagnosis andtreatment of Moyamoya disease (Spontaneous occlusion of thecircle of Willis). Neurol Med Chir (Tokyo) 52:245–2663. Watanabe T, Suzuki N: “Rui”-Moyamoya (1983) in Suzuki J(ed):Moyamoya disease. Tokyo, Igaku-Shoin, pp 123–145 (Japan)4. Yonekawa Y, Takagi Y, Khan N☹ (2011) Adult Moyamoya disease.In: Winn HR (ed) Youmans Neurological Surgery. Elsevier, Vol 4,Chapter 356, pp 3689–36975. Yonekawa Y, Operative neurosurgery (2012) Personal view andhistorical backgrounds (9) Moyamoya angiopathy (MMA): Pasthistory and status presens. No Sjinkei Geka 40(1):67–87, in Jpn,Eng abstractThe authors is indebted to Ms. N. Matsuda (Igaku shoin) and Prof. Y.Takagi (Kyoto University) for helping to search references.Acta Neurochir (2012) 154:2159–2161 2161

Outer diameter measured by 3D CISS MRI and quasi-Moyamoya disease

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Outer diameter measured by 3D CISS MRI and quasi-Moyamoya disease

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