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Brain, Vol. 113, No. 5, 1251-1267, 1990
© 1990 Guarantors of Brain

research-article

HEREDITARY CEREBRAL HAEMORRHAGE WITH AMYLOIDOSIS—DUTCH TYPE

MAGNETIC RESONANCE IMAGING FINDINGS IN 7 CASES

J. HAAN1,, R. A. C. ROOS1, P. R. ALGRA2, J. B. K. LANSER3, G. T. A. M. BOTS4 and M. VEGTER-VAN DER VLIS5

1Department of Neurology, University Hospital Leiden, The Netherlands 2Department of Neuroradiology, University Hospital Leiden, The Netherlands 3Department of Neuropsychology, University Hospital Leiden, The Netherlands 4Department of Neuropathology, University Hospital Leiden, The Netherlands 5Department of Anthropogenetics, University Hospital Leiden, The Netherlands

Correspondence to: Correspondence to: Dr J. Haan, Department of Neurology, University Hospital, PO Box 9600, 2300 RC Leiden, The Netherlands.

The clinical history and magnetic resonance imaging (MRI) findings are presented of 7 patients with hereditary cerebral haemorrhage with amyloidosis—Dutch type (HCHWA-D). The diagnosis was based on clinical and genealogical data, was confirmed in 3 patients at autopsy and in 2 others by biopsy. Focal neurological signs, and at least some degree of global cognitive deterioration, were observed in all patients, with unequivocal dementia in 4. MRI showed haemorrhages and areas of gliosis and, to a variable extent, hyperintensity of the white matter in T2-weighted images. Neuropathological examination revealed a large recent haemorrhage together with residual lesions from previous haemorrhages or infarcts in all patients examined. The white matter lesions, present on MRI, turned out to be areas of ‘incomplete infarction’ with demyelination. It is concluded that (hereditary) amyloid angiopathy can lead to strokes, but also to subcortical ischaemic encephalopathy. Amyloid angiopathy should therefore be considered in the differential diagnosis of white matter lesions, found on CT or MRI, especially when patients present with a cerebral haemorrhage. The relationship between HCHWA-D and Alzheimer's disease, another disease with cerebral amyloid deposition and diffuse white matter involvement, is discussed.

Received May 4, 1989. Revised September 12, 1989. Accepted September 22, 1989.


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