Alzheimer's disease: with apraxia
50 year old presents with a one year history of short term memory difficulty. On examination, he was unable to imitate meaningless hand gesture, copy a shape-drawing and recognize visual objects on the left side.
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Precuneus atrophy, right more than left. Reduced posterior perfusion bilaterally on ASL.
Mild frontoparietal atrophy. Small gliosis on left frontal lobe. Mild scattered hyperintensities on FLAIR. Equivocal subtle hippocampal atrophy.
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Hypometabolism posteriorly with right parietotemporal and bilateral precuneus predominance.
Apraxia is the inability to execute a higher-order motor, visual or speech function in the absence of primary weakness, sensory or cerebellar deficits. Major areas of praxis examination include visual, oro-bucco-lingual, gait, ideomotor, ideational, constructional and callosal. Other forms of apraxia also exist (e.g. dressing apraxia & limb-kinetic). Traditionally, motor apraxia is conceptualised into three component ideational(e.g. loss of concept), ideomotor (e.g. loss of transition between concept and motor action) and limb-kinetic (e.g. disruption of smooth transition of motor action. Some regard this as not a 'true' apraxia).
The concept of apraxia and its determination remain imprecise. Apraxia examination, for example, has several components: elicitation (e.g. verbal vs. visual command), contexts of action (e.g. formal testing, naturalistic observation, with or without objects), and types of gesture (e.g. transitive vs intransitive, meaningful vs. meaningless)1. In research settings, a few apraxia instruments have been used to ensure more consistent findings2,3. At its essence, the concept of praxis lies in between the constituents of the semantic-concept component of action and the kinetic-spatial component of control.
Left parietal lobe has been frequently correlated in various apraxia studies. However, the underlying neural correlate is more likely due to an aberration within the parietal network or connectivity, as opposed to an isolated structural lesion, when considering the multiple elements in apraxia 4,5.
The patient presents with left-sided visual (inability to imitate meaningless hand gesture) and constructional apraxia (reduced ability to copy the left side of his drawing), which suggest impairment in the right parietal lobe. These clinical findings correlate with the precuneal (right more than left) atrophy. The hypometabolism in the precuneus, and parietotemporal area, is demonstrated in the FDG-PET study. The patient is ambidextrous. The visuoconstructional impairment supports the right parieto-occipital impairment. The radiological findings and cerebrospinal fluid testing (amyloid B1-42/p-tau ratio 4) support the diagnosis of young onset Alzheimer's disease.
Apraxia seemed to be more prevalent in certain types of dementia, particularly those with parietal lobe involvement. Such dementia may include some Alzheimer's dementia spectrum (e.g. amnestic type, posterior cortical atrophy and logopaenic type) and the subcortical dementia spectrum (e.g. corticobasal degeneration, primary non-fluent aphasia, dementia with Lewy Body) 6,7,8. Apraxia in Alzheimer's disease can also present in the absence of significant amnesia, and some suggest a separate neurodegenerative clinical entity of primary progressive apraxia9. In practice, such patients may present with a deterioration in their daily function, as opposed to forgetfulness.
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