HIPPOCAMPAL SCLEROSIS CONTRIBUTES TO DEMENTIA IN THE ELDERLY

Citation
J. Coreybloom et al., HIPPOCAMPAL SCLEROSIS CONTRIBUTES TO DEMENTIA IN THE ELDERLY, Neurology, 48(1), 1997, pp. 154-160
Citations number
23
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
00283878
Volume
48
Issue
1
Year of publication
1997
Pages
154 - 160
Database
ISI
SICI code
0028-3878(1997)48:1<154:HSCTDI>2.0.ZU;2-Y
Abstract
Objective: To assess the relevance of hippocampal sclerosis (HS) to de mentia in the elderly, Background: HS is a prominent pathologic findin g in some demented elderly, but the anatomic substrate and cognitive p rofiles of this dementia have not been well established. Design/Method s: An autopsy series, including dot-immunobinding assay to estimate ne ocortical synaptic density, of eight patients (three men, five women) with HS on whom extensive antemortem neuropsychological testing was av ailable. Results: Mean age at onset was 72.0 (+/-9.8) (range, 59 to 89 ) with a mean duration of symptoms of 6.5 (+/-2.9) years. Patients wer e only mildly impaired with a mean MMSE of 20.9 (+/-4.9) and a mean DR S of 103.1 (+/-12.5) at presentation. Cardiovascular disease was prese nt in 88%, with a mean Hachinski score of 3.4 (+/-2.2). No patient had a history of seizures. Sixty-three percent had depression or depressi ve symptoms. Neuropsychologically, most patients presented with promin ent memory and language deficits and became progressively demented. Ne uropathologically, isolated HS was a rare finding; many patients had e ither very mild or neocortical ''plaque only or plaque predominant'' A lzheimer's disease (AD) in addition to HS changes, Midfrontal neocorti cal synaptophysin counts were significantly reduced in all HS patients compared with controls (p = 0.0006). Conclusions: In the elderly, HS can be a neuropathologic substrate of dementia. Clinically, it can be associated with a course that is difficult to distinguish from AD alth ough cardiac disease and depression are frequent concomitants. Deterio ration of cognitive function in these subjects may relate to other pat hologic features such as neocortical synapse loss.