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Cerebral amyloid angiopathy-related cognitive impairment: The search for a specific neuropsychological pattern
M Planton1, N Raposo1, J-F Albucher1
1Unité de neuropsychologie, département de neurologie, université de Toulouse, CHU de Toulouse, place du Docteur-Baylac, TSA 40031, 31059 Toulouse cedex 9, France; Inserm, université de Toulouse, Toulouse NeuroImaging Centre, place du Docteur-Baylac, 31024 Toulouse cedex 3, France.
Insights
Cerebral amyloid angiopathy (CAA) causes cognitive and psychiatric symptoms, often diagnosed after stroke or during dementia assessment. Research explores its unique impact on cognition, despite confounding factors like Alzheimer's disease.
Area of Science:
- Neurology
- Neuropsychology
- Pathology
Background:
- Cerebral amyloid angiopathy (CAA) is increasingly recognized in clinical settings, including stroke units, memory clinics, and emergency departments.
- Neuropsychological impairments, including deficits in perceptual speed, memory, attention, and executive function, have been documented in CAA patients.
- Psychiatric symptoms and the association between CAA and Alzheimer's disease (AD) are also noted, though comorbidities complicate assessment.
Purpose of the Study:
- To review the latest evidence on neuropsychological impairments in patients with Cerebral Amyloid Angiopathy (CAA).
- To discuss the potential emergence of a specific neuropsychological profile associated with CAA.
- To address the challenges in assessing CAA-specific symptoms due to confounding factors.
Main Methods:
- Literature review focusing on recent findings regarding neuropsychological deficits in CAA.
- Analysis of reported cognitive and psychiatric symptoms in CAA patients.
- Discussion of confounding factors and their impact on symptom characterization.
Main Results:
- Commonly reported neuropsychological deficits in CAA include impairments in perceptual speed, episodic and semantic memory, attention, and executive functions.
- Emerging evidence suggests potential psychiatric manifestations in CAA, such as personality changes and depression.
- The presence of comorbidities like small vessel disease, Lewy body disease, and AD complicates the precise characterization of CAA-related cognitive decline.
Conclusions:
- Cerebral amyloid angiopathy (CAA) is associated with a range of cognitive and psychiatric symptoms.
- Further research is needed to elucidate a specific neuropsychological profile for CAA and to disentangle its effects from comorbidities.
- Accurate assessment of CAA-related symptoms requires careful consideration of confounding factors.
Abstract:
Cerebral amyloid angiopathy is diagnosed in stroke units after lobar intracerebral hemorrhage. CAA can also be diagnosed in memory clinics when patients are referred for cognitive impairment assessment, and may be a reason for admission to emergency or neurology departments because of rapidly progressive cognitive or neurological decline, or a transient focal neurological episode. CAA may even be observed in older community-dwelling individuals. Neuropsychological impairment in CAA has been described over the past 20 years. The symptoms most commonly reported are perceptual speed, episodic memory, semantic memory, attention and executive function, and global cognitive impairments. Psychiatric symptoms, such as personality changes, behavioral disturbances and depression, have been more recently described. CAA is also a risk factor for the development of dementia, and its relationship with Alzheimer's disease has been demonstrated in post-mortem studies. Yet, despite the increase in literature on CAA-related cognitive and psychiatric symptoms, the specific characteristics of symptoms in CAA are difficult to assess because of the substantial prevalence of comorbidities such as small vessel disease due to high blood pressure, Lewy body disease and, of course, AD, all of which act as important confounding factors. Also, within the entity of CAA itself, the additive and perhaps synergistic effects of each lesion on cognition remain to be assessed. In the present paper, the focus is on the latest evidence of neuropsychological impairment observed in CAA patients, and the emergence of a possible specific neuropsychological profile due to CAA is also discussed.
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