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P1‐064: Can Rowland Universal Dementia Assessment Scale (RUDAS) be used in place of mini‐mental state examination (MMSE) for dementia screening in Thai geriatrics?
Author(s) -
Limpawattana Panita,
Tiamkao Somsak,
Sawanyawisuth Kittisak,
Thinkhamrop Bandit
Publication year - 2012
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2012.05.340
Subject(s) - dementia , mini–mental state examination , medicine , geriatrics , receiver operating characteristic , population , outpatient clinic , psychiatry , gerontology , physical therapy , disease , environmental health
the relationship between clinical course and CSF (A b and phosphorylated tau).Methods:We analyzed Apolipoprotein E (ApoE) genotype and b amyloid precursor protein (b APP) gene, examined MRI study and measured CSF A b 1-42, A b 1-40 and ptau-181 during the clinical course of the illness.Results:ApoE genotypewas e 4/e 4 homozygote. Aberrant high signal lesions in brain MRI appeared in right temporal lobe posterior lesion to occipital lobe in T2-weighted image and spread to other areas. Brain biopsy revealed A b deposits in vascular walls and numerous diffuse plaques in parenchymal areas. Initial corticosteroid therapy of betamethasone was effective to improve neurological symptoms of consciousness disturbance and motor deficits as well as MRI findings. After corticosteroid was stopped at 4 weeks, recurrence occurred and additional corticosteroid did not improve clinical symptoms and the patient progressed to a bed-ridden state and severe consciousness disturbance. Notably, CSF A b 1-42 and CSF A b 1-40 decreased while recurrent encephalopathy worsened. After intense deterioration, the patient became stable, and CSF A b 1-42 increased but was still at a very low level. Conclusions: This CAA encephalopathy case with ApoE e 4/e 4 homozygosity showed A b deposits in vascular walls and numerous diffuse plaques in parenchymal areas. This clinical course of the illness suggests that reduction of CSF A b 1-42 and A b 1-40 might be strongly related to deterioration of encephalopathy.