Cognitive effects of anxiety have been amply documented. Anxiety has been linked with an attentional bias toward threat, distractibility, and reductions in short-term memory (STM) capacity. These three functions have rarely been investigated jointly and permeability may account for some of the effects documented. In this experiment, we examine these three cognitive functions using one verbal and one visuospatial task. In the irrelevant speech paradigm, participants had to remember strings of letters while irrelevant neutral or threatening speech was presented. In the visuospatial sandwich paradigm, participants were asked to remember sequences of visuospatial targets sometimes presented within irrelevant distracters. We examined the links between state anxiety, worry, and indices of attentional bias toward threat, distractibility from neutral stimuli, and STM capacity. Results show that state anxiety was uniquely linked with impairments in STM while worry was more particularly related to distractibility, independently from permeability between the different cognitive functions. Attentional bias toward threat was linked with variance common to both anxiety and worry. An examination of clinical and non-clinical subgroups suggests that subjective threat perception and attentional bias toward threat are features that are particularly characteristic of clinical levels of anxiety. Our findings confirm the important links between anxiety and basic cognitive functions.

Clinical indications of amyloid imaging in atypical dementia remain unclear. We report a 68-year-old female without past psychiatric history who was hospitalized for auditory hallucinations and persecutory delusions associated with cognitive and motor deficits. Although psychotic symptoms resolved with antipsychotic treatment, cognitive and motor impairments remained. She further showed severe visuoconstructive and executive deficits, ideomotor apraxia, elements of Gerstmann’s syndrome, bilateral agraphesthesia and discrete asymmetric motor deficits. Blood tests were unremarkable. Structural brain imaging revealed diffuse fronto-temporo-parietal atrophy, which was most severe in the parietal regions. Meanwhile, FDG-PET suggested asymmetrical fronto-temporo-parietal hypometabolism, with sparing of the posterior cingulate gyrus. A diagnosis of possible corticobasal syndrome (CBS) was made. Amyloid-PET using the novel tracer NAV4694 was ordered, and revealed significant deposition of fibrillar amyloid (SUVR 2.05). The primary diagnosis was CBS with underlying Alzheimer pathology and treatment with a cholinesterase inhibitor was initiated. Determination of underlying pathological CBS subtype is not simple even when based on extensive investigation including clinical presentation, atrophy patterns on MRI, and regional hypometabolism on FDG-PET. By contrast, amyloid imaging quickly confirmed Alzheimer pathology, and allowed rapid initiation of treatment in this complex case with early psychiatric symptoms. This case study illustrates the clinical utility of amyloid imaging in the setting of atypical cases seen in a tertiary memory clinic.