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Cortical Visual Loss
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
The prognosis varies with the cause: patients with infarction can recover with time, while those with posterior cortical atrophy slowly worsen. Recovery can be dissociated, with ocular motor deficits improving but not attentional abnormalities (415). Little is known about treatment: cognitive and perceptual rehabilitation may improve visual function and reaching (424).
Dementia
Published in Henry J. Woodford, Essential Geriatrics, 2022
The accumulation of beta-amyloid plaques (also called neuritic plaques) within the brain appears to be a key component of the pathogenesis of AD.40 It has been termed the ‘amyloid cascade'. However, trials aiming to reduce amyloid deposition have failed to produce beneficial effects.41 It may be that amyloid build-up is simply the ‘smoke' and a different pathological process is the actual ‘fire'. The genetic links listed above all seem to enhance the accumulation of amyloid proteins. Secondary pathological changes include tau protein hyperphosphorylation (to form neurofibrillary tangles), inflammation and lipid peroxidation. The net result is neuron death in specific brain areas. The parietal and temporal lobes are most frequently affected, although variants involving other brain areas have been described. One of these is ‘posterior cortical atrophy', which presents with predominant visuospatial difficulties, such as reading, recognising objects and judging distances.
The experience of living with young onset dementia
Published in Marjolein de Vugt, Janet Carter, Understanding Young Onset Dementia, 2021
Few studies have studied the phenomenology of different diagnoses from the perspective of those with the condition, but some have explored subjective experiences of posterior cortical atrophy (PCA; Harding et al., 2018), behavioural-variant frontotemporal dementia (bvFTD; Griffin et al., 2016) and primary progressive aphasia (PPA; Douglas, 2014).
Posterior cortical atrophy: clinical, neuroimaging, and neuropathological features
Published in Expert Review of Neurotherapeutics, 2023
John Best, Marianne Chapleau, Gil D. Rabinovici
Posterior Cortical Atrophy is a progressive neurodegenerative syndrome characterized by impairment of higher-order visual processing in the setting of progressive atrophy of the parietal and occipital lobes. Initial symptoms are typically visual, including problems reading, driving, and navigating. Other parietal lobe functions including dyspraxia, features of Balint’s and Gerstmann’s syndromes, and subtle language features can also occur early in the disease course. Diagnosis is often delayed due to limited public and clinician awareness of the disorder. Insight is typically preserved throughout much of the course of the illness. Underlying pathology is most commonly AD but can also be caused by DLB, CBD, and less commonly prion disease or frontotemporal lobar degenetration with TDP type A inclusions. There is an overlapping genetic risk with typical AD risk genes, though the association of APOE ε4 genotype with PCA is weaker than its association with amnestic AD. Preliminary evidence potentially implicates novel genetic risks in genes related to visual system development and function.
Differential effects from cognitive rehabilitation and high-definition tDCS in posterior cortical atrophy: A single-case experimental design
Published in Neuropsychological Rehabilitation, 2022
Christine Sofka Dugas, Elena Keltner-Dorman, John Hart Jr.
Posterior cortical atrophy (PCA) is an atypical variant of Alzheimer’s disease (AD) and is a progressive neurodegenerative condition characterized by localized atrophy of the occipitoparietal regions of the brain (Crutch et al., 2017). Generally, patients diagnosed with PCA present with cognitive deficits affecting visuospatial processing with relatively preserved declarative memory, executive functions, and linguistic skills in the initial stages (Crutch et al., 2012). Some visuospatial deficits that are commonly observed in PCA include spatial neglect (Behrmann et al., 2004; Corbetta et al., 2000), simultagnosia (Friedman-Hill et al., 2003), alexia, visual agnosia (Crutch et al., 2012), impaired spatial navigation (Ciaramelli et al., 2010), and/or dyscalculia (Delazer et al., 2006).
A case of ALS with posterior cortical atrophy
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2019
Tanja C. W. Nijboer, Bram Nitert, Henk-Jan Westeneng, Leonard H. Van Den Berg, Michael A. van Es
Here, we report an ALS patient with unusual cognitive deficits, which would meet the diagnostic criteria for the posterior cortical atrophy (PCA) clinicoradiologic syndrome. PCA is a syndrome characterized by deficits in higher-order visual processing and features consistent with aspects of Gerstmann and Balint syndromes but with relatively preserved episodic memory in the early stages. The most common pathology underlying PCA is Alzheimer Disease (AD) and is therefore also considered an atypical form of AD (2). Although rare alternative underlying pathologies such as corticobasal degeneration, Lewy body disease, and prion disease have been reported (3). To our knowledge, this is the first report of PCA in ALS.