ABSTRACT
We present the longitudinal neurolinguistic, neuropsychological and neurologic follow-up of a 64 y.o. right-handed woman, who developed progressive apraxia of speech (PAOS), followed by peripheral agraphia then a left corticobasal syndrome (CBS). Neuroimaging (CT, MRI and FDG-PET) unequivocally showed progressive right hemispheric atrophy and hypometabolism. This particular evolution first confirms that PAOS is a phenotype of probable corticobasal degeneration (CBD). More importantly, this case underpins the neural organisation of motor planning processing in relation with speech, as well as graphic and limb praxis impairments, and constitutes a rare example of crossed-PAOS.
Subject(s)
Basal Ganglia Diseases/psychology , Neurodegenerative Diseases/psychology , Speech Disorders/psychology , Aged , Agraphia/etiology , Agraphia/psychology , Basal Ganglia/pathology , Basal Ganglia Diseases/complications , Basal Ganglia Diseases/pathology , Cerebral Cortex/pathology , Disease Progression , Female , Functional Laterality/physiology , Handwriting , Humans , Magnetic Resonance Imaging , Middle Aged , Neurodegenerative Diseases/complications , Neurodegenerative Diseases/pathology , Neuropsychological Tests , Positron-Emission Tomography , Psychomotor Performance/physiology , Speech Disorders/etiology , Speech Disorders/pathology , Tomography, X-Ray ComputedABSTRACT
OBJECTIVES: Studies of cognition in bipolar disorder (BD) have reported impairments in processing speed, working memory, episodic memory, and executive function, but they have primarily focused on young and middle-aged adults. In such studies, the severity of cognitive deficits increases with the duration of illness. Therefore, one would expect more pronounced deficits in patients with longstanding BD. The first aim of the present study was to determine the pattern and the magnitude of cognitive impairment in older euthymic BD patients. The second aim was to explore the interrelationship between these cognitive deficits and determine whether they reflect a single core impairment or the co-occurrence of independent cognitive deficits. METHODS: Twenty-two euthymic elderly BD patients and 22 controls, matched for gender, age, and education, underwent a comprehensive neuropsychological assessment. RESULTS: Compared to controls, BD patients had significantly reduced performance in processing speed, working memory, verbal fluency, and episodic memory, but not in executive function. Hierarchical regression analyses showed that verbal fluency and working memory impairments were fully mediated by changes in processing speed. This was not the case for the episodic memory dysfunction. CONCLUSION: The cognitive profile in older euthymic BD cases is similar to the one described in younger BD cohorts. Our results further suggest that impaired processing speed plays a major role in the cognitive changes observed in BD patients except for deficits in episodic memory, thus providing strong evidence that processing speed and episodic memory are two core deficits in elderly BD patients.
