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Brain, Vol. 123, No. 9, 1850-1862, September 2000
© 2000 Oxford University Press

Striatocapsular haemorrhage

Chin-Sang Chung1, Louis R. Caplan4, Yasumasa Yamamoto5, Hui Meng Chang6, Soo-Joo Lee1, Hee-Jung Song1, Hye-Seung Lee1, Hyun-Kil Shin2 and Kyung-Moo Yoo3

1 Departments of Neurology in Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, 2 Soonchunhyang University Hospital, Chunan and 3 Koshin University Hospital, Pusan, Korea, 4 Beth-Israel-Deaconess Hospital, Harvard Medical School, Boston, USA, 5 Kyoto Second Red Cross Hospital, Kyoto, Japan and 6 Singapore General Hospital, Singapore

Correspondence to: Chin-Sang Chung, MD, Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 ILWON-dong, Kangnam-ku, Seoul, Korea 135-710 E-mail: cschung{at}smc.samsung.co.kr

Haemorrhages in the striatocapsular area, or striatocapsular haemorrhages (SCHs), have been regarded as a single entity, although the area is composed of several functionally discrete structures that receive blood supply from different arteries. We analysed the morphological and clinical presentations of 215 cases of SCHs according to a new classification method we have designed on the basis of arterial territories. SCHs were divided into six types: (i) anterior type (Heubner's artery); (ii) middle type (medial lenticulostriate artery); (iii) posteromedial type (anterior choroidal artery); (iv) posterolateral type (posteromedial branches of lateral lenticulostriate artery); (v) lateral type (most lateral branches of lateral lenticulostriate artery); and (vi) massive type. The anterior type (11%) formed small caudate haematomas, always ruptured into the lateral ventricle, causing severe headache, and mild contralateral hemiparesis developed occasionally. The outcome was excellent. The middle type (7%) involved the globus pallidus and medial putamen, frequently causing contralateral hemiparesis and transient conjugate eye deviation to the lesion side. About 50% of the patients recovered to normal. The posteromedial type (4%) formed very small haematomas in the posterior limb of the internal capsule and presented with mild dysarthria, contralateral hemiparesis and sensory deficit, with excellent outcome in general. The posterolateral type (33%) affected the posterior half of the putamen and posterior limb of the internal capsule and presented with impaired consciousness and contralateral hemiparesis with either language dysfunction or contralateral neglect. The outcome was fair to poor but there were no deaths. The lateral type (21%) formed large elliptical haematomas between the putamen and insular cortex. Contralateral hemiparesis with language dysfunction or contralateral neglect developed frequently but resolved over several weeks. The clinical outcome was relatively excellent except when the haematoma size was very large. The massive type (24%) formed huge haematomas affecting the entire striatocapsular area. Marked sensorimotor deficits and impaired consciousness, ocular movement dysfunctions including the `wrong-way' eyes were observed quite frequently. The outcome was very poor with a case fatality rate of 81%. The clinico-radiological presentations suggested its origin was the same as the posterolateral type.


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