PubMed · 8423900
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
H J Blumenthal. 1993. Lacunes.. https://doi.org/10.1212/wnl.43.1_part_1.233
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Brain infarctions in patients with pseudoxanthoma elasticum (PXE) are thought to be associated with the damage of cerebral arteries injured by connective tissue change caused by PXE. We experienced 3 cases of PXE with lacunar brain infarction and evaluated the relationship between the damage of small penetrating arteries and PXE. All patients' diagnosis of PXE were confirmed by histological examination. They were a 47-year-old man and two women with 54 and 62 years of age old. All patients had pseudoxanthoma and angioid streaks and showed pyramidal tract signs. In addition, one patient presented Parkinsonism and another presented involuntary movement of the left lower extremities. None of these cases showed cortical symptoms. Brain CT and MRI revealed multiple lacuna in the areas of penetrating arteries, but their cerebral angiogram were almost normal. Severe small artery diseases, which cannot be attributable only to hypertension, were present. The relationship between such severe small artery disease and damage of the origin of small penetrating arteries caused by PXE was strongly suggested.
Explore the source record for details and available documents.
This article summarizes various concepts (Binswangers encephalopathy, multiinfarct-dementia, lacunar state, mixed dementia, dementia due to amyloid angiopathy or vasculitis) and classifications (DSM, ICD, ADDTC) on vascular dementia. It reviews historical, clinical, and diagnostic aspects (i.e. neuroradiology, SPECT, PET) as well as therapeutic approaches. The confusing nomenclature on vascular dementia is discussed, considering especially the non-convincing concept of multiinfarct-dementia that often has been misused as a synonym for vascular dementia. Multiinfarct-dementia is now restricted to a syndrome of vascular dementia due to several large vessels strokes. A current definition and classification of vascular dementia as suggested by NINDS-AIREN international workshop is described. It defines criteria consistent with the diagnosis of "possible", "probable" and "definite" vascular dementia based on clinical, radiologic and neuropathologic features. The criteria of "probable" vascular dementia include all the following: 1. the presence of dementia and cerebrovascular disease defined by focal signs on neurologic investigation and evidence of relevant cerebrovascular disease by brain imaging (multiple lacunae, extensive white matter lesions, multiple large-vessels infarcts or a strategically placed infarct) 2. A relationship between dementia and cerebrovascular disease (onset of dementia within 3 months following a recognized stroke; abrupt deterioration, stepwise progression). This classification of vascular dementia emphasises pathogenetic aspects and includes dementia resulting from small- and large-vessels disease as well as hypoperfusion, haemorrhagic dementia and dementia due to still unknown factors. Operational criteria for the frequent Binswangers encephalopathy--a prototype of vascular dementia--are presented. Thereby a basis for further research and discussion in this exciting area should have been formed.