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Posterior cortical atrophy (PCA) is a rare neurodegenerative syndrome primarily affecting the parietal and occipital lobes. It is characterized by early deficits in visuospatial processing, numeracy, and literacy. The most common underlying pathology is Alzheimer’s disease (AD). PCA typically presents as a young onset form of dementia, with the majority of patients aged 50–65 years. The clinical presentation of PCA includes difficulties with visually and spatially complex tasks. Neuropsychological features include impairments in visuospatial and visuoperceptual processing. Neuroimaging studies show occipito-parietal atrophy and hypometabolism . There is limited evidence of a genetic component in PCAs. Pathologically, PCA is most commonly associated with AD. The consensus classification of PCA provides a framework for improved diagnosis and research. PCA shows overlap with other atypical AD presentations, and there is heterogeneity within the syndrome. The impact of PCA on everyday abilities and the subjective experience of individuals with PCA is not well understood. Management and support for PCA include pharmacological and nonpharmacological approaches .
This chapter reviews and contrasts the clinical and neuropsychological features of transient global amnesia (TGA) and transient epileptic amnesia (TEA). It discusses their pathophysiology and outlines an approach to the management of patients with transient amnesia. Attacks of TGA follow a wide variety of stresses, including strenuous exertion, sexual intercourse, immersion in water, pain and emotive events. Neuropsychological testing during attacks has confirmed that amnesia is much the most striking deficit in TGA, and is often the only impairment. In principle, the patchy impairment of remote memory which affects a high proportion of patients with TEA must have one of three explanations: failure to encode episodes into long-term memory, failure to consolidate and maintain such memories or failure to retrieve memories which have been successfully stored. TGA is a common and clearly defined clinical syndrome the aetiology of which remains obscure. Patients with TEA often benefit from anti-convulsant medication.
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