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Differentiating cognitive impairment due to corticobasal degeneration and Alzheimer disease.
Day, Gregory S; Lim, Tae Sung; Hassenstab, Jason; Goate, Alison M; Grant, Elizabeth A; Roe, Catherine M; Cairns, Nigel J; Morris, John C.
Afiliación
  • Day GS; From the Charles F. and Joanne Knight Alzheimer Disease Research Center (G.S.D., T.S.L., J.H., A.M.G., E.A.G., C.M.R., N.J.C., J.C.M.), Department of Neurology (G.S.D., T.S.L., J.H., C.M.R., N.J.C., J.C.C.), Division of Biostatistics (E.A.G.), and Department of Pathology and Immunology (N.J.C.), Was
  • Lim TS; From the Charles F. and Joanne Knight Alzheimer Disease Research Center (G.S.D., T.S.L., J.H., A.M.G., E.A.G., C.M.R., N.J.C., J.C.M.), Department of Neurology (G.S.D., T.S.L., J.H., C.M.R., N.J.C., J.C.C.), Division of Biostatistics (E.A.G.), and Department of Pathology and Immunology (N.J.C.), Was
  • Hassenstab J; From the Charles F. and Joanne Knight Alzheimer Disease Research Center (G.S.D., T.S.L., J.H., A.M.G., E.A.G., C.M.R., N.J.C., J.C.M.), Department of Neurology (G.S.D., T.S.L., J.H., C.M.R., N.J.C., J.C.C.), Division of Biostatistics (E.A.G.), and Department of Pathology and Immunology (N.J.C.), Was
  • Goate AM; From the Charles F. and Joanne Knight Alzheimer Disease Research Center (G.S.D., T.S.L., J.H., A.M.G., E.A.G., C.M.R., N.J.C., J.C.M.), Department of Neurology (G.S.D., T.S.L., J.H., C.M.R., N.J.C., J.C.C.), Division of Biostatistics (E.A.G.), and Department of Pathology and Immunology (N.J.C.), Was
  • Grant EA; From the Charles F. and Joanne Knight Alzheimer Disease Research Center (G.S.D., T.S.L., J.H., A.M.G., E.A.G., C.M.R., N.J.C., J.C.M.), Department of Neurology (G.S.D., T.S.L., J.H., C.M.R., N.J.C., J.C.C.), Division of Biostatistics (E.A.G.), and Department of Pathology and Immunology (N.J.C.), Was
  • Roe CM; From the Charles F. and Joanne Knight Alzheimer Disease Research Center (G.S.D., T.S.L., J.H., A.M.G., E.A.G., C.M.R., N.J.C., J.C.M.), Department of Neurology (G.S.D., T.S.L., J.H., C.M.R., N.J.C., J.C.C.), Division of Biostatistics (E.A.G.), and Department of Pathology and Immunology (N.J.C.), Was
  • Cairns NJ; From the Charles F. and Joanne Knight Alzheimer Disease Research Center (G.S.D., T.S.L., J.H., A.M.G., E.A.G., C.M.R., N.J.C., J.C.M.), Department of Neurology (G.S.D., T.S.L., J.H., C.M.R., N.J.C., J.C.C.), Division of Biostatistics (E.A.G.), and Department of Pathology and Immunology (N.J.C.), Was
  • Morris JC; From the Charles F. and Joanne Knight Alzheimer Disease Research Center (G.S.D., T.S.L., J.H., A.M.G., E.A.G., C.M.R., N.J.C., J.C.M.), Department of Neurology (G.S.D., T.S.L., J.H., C.M.R., N.J.C., J.C.C.), Division of Biostatistics (E.A.G.), and Department of Pathology and Immunology (N.J.C.), Was
Neurology ; 88(13): 1273-1281, 2017 Mar 28.
Article en En | MEDLINE | ID: mdl-28235814
ABSTRACT

OBJECTIVE:

To identify clinical features that reliably differentiate individuals with cognitive impairment due to corticobasal degeneration (CBD) and Alzheimer disease (AD).

METHODS:

Clinical features were compared between individuals with autopsy-proven CBD (n = 17) and AD (n = 16). All individuals presented with prominent cognitive complaints and were evaluated annually with semistructured interviews, detailed neurologic examinations, and neuropsychological testing.

RESULTS:

Substantial overlap was observed between individuals with dementia due to CBD and AD concerning presenting complaints, median (range) duration of symptoms before assessment (CBD = 3.0 [0-5.0] years, AD = 2.5 [0-8.0] years; p = 0.96), and median (range) baseline dementia severity (Clinical Dementia Rating Sum of Boxes CBD = 3.5 [0-12.0], AD = 4.25 [0.5-9.0], p = 0.49). Subsequent emergence of asymmetric motor/sensory signs, hyperreflexia, gait abnormalities, parkinsonism, falls, urinary incontinence, and extraocular movement abnormalities identified individuals with CBD, with ≥3 discriminating features detected in 80% of individuals within 3.1 years (95% confidence interval 2.9-3.3) of the initial assessment. Individuals with CBD exhibited accelerated worsening of illness severity and declines in episodic memory, executive functioning, and letter fluency. Semiquantitative pathologic assessment revealed prominent tau pathology within the frontal and parietal lobes of CBD cases. Comorbid AD neuropathologic change was present in 59% (10 of 17) of CBD cases but did not associate with the clinical phenotype, rate of dementia progression, or dementia duration.

CONCLUSIONS:

CBD may mimic AD dementia early in its disease course. Interval screening for discriminating clinical features may improve antemortem diagnosis in individuals with CBD and prominent cognitive symptoms.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Ganglios Basales / Corteza Cerebral / Enfermedades Neurodegenerativas / Enfermedad de Alzheimer / Disfunción Cognitiva Tipo de estudio: Observational_studies / Qualitative_research / Risk_factors_studies Límite: Aged / Aged80 / Female / Humans / Male / Middle aged Idioma: En Revista: Neurology Año: 2017 Tipo del documento: Article
Texto completo
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Ganglios Basales / Corteza Cerebral / Enfermedades Neurodegenerativas / Enfermedad de Alzheimer / Disfunción Cognitiva Tipo de estudio: Observational_studies / Qualitative_research / Risk_factors_studies Límite: Aged / Aged80 / Female / Humans / Male / Middle aged Idioma: En Revista: Neurology Año: 2017 Tipo del documento: Article