Neuropsychological Similarities and Differences Between Amnestic Alzheimer's Disease and its Non-Amnestic Variants.

BACKGROUND: The neuropsychological recognition of early-onset Alzheimer's disease (AD) can be difficult because of non-amnestic variants such as logopenic variant primary progressive aphasia (lvPPA) and posterior cortical atrophy (PCA). OBJECTIVE: This study evaluated the similarities and differences between typical amnestic AD (tAD) and lvPPA and PCA on a screening neuropsychological battery. METHODS: We enrolled 51 patients meeting NIA-AA criteria for biomarker-supported AD (amnestic or non-amnestic) and having an age of onset of <65 years of age. Based on additional recommended clinical criteria for lvPPA and PCA, the early-onset AD patients were divided into three groups (28 tAD, 9 lvPPA, 14 PCA) of comparable age and dementia severity. We then analyzed their profiles on a focused, screening neuropsychological battery for early-onset AD. RESULTS: In addition to greater variance on the Mini-Mental State Examination, the lvPPA and PCA variants had episodic memory impairment that did not significantly differ from the memory impairment in the tAD patients. Despite differences on language and visuospatial tasks, they did not significantly distinguish the lvPPA and PCA from tAD. The lvPPA group, however, was distinguishable by worse performance on measures reflecting working memory (digit span forward, memory registration). CONCLUSIONS: On neuropsychological screening, all clinical early-onset AD subtypes may have memory impairments. Screening batteries for early-onset AD should also include measures of working memory, which is disproportionately decreased in lvPPA.

The utility of clinical criteria in patients with chronic traumatic encephalopathy.

BACKGROUND: Repetitive traumatic brain injury (TBI) is associated with chronic traumatic encephalopathy (CTE), a progressive neurodegenerative disorder characterized by Alzheimer-like changes in the brain. CTE has been defined through neuropathological findings among deceased athletes and others exposed to repetitive TBI, but to date there are no definitive clinical criteria for CTE. OBJECTIVE: To evaluate the utility of currently proposed clinical criteria for CTE and suggest improvements. METHODS: We describe two well-characterized patients referred for evaluation of CTE and apply the four major proposed criteria for CTE. These criteria were further assessed in a cohort of patients referred to a neurobehavior clinic with or without a history of TBI. RESULTS: Without a CTE biomarker, the current criteria were of limited utility when applied to the two patient and the Neurobehavior cohort. Six items were extracted as potentially improving the clinical diagnosis of CTE: length of exposure to head impacts, a progressive course, specific psychiatric symptoms, frontal-executive dysfunction, parkinsonism and tremors, and targeted findings on neuroimaging. CONCLUSIONS: The prevention and neurorehabilitation of CTE depends on clinical diagnosis, but, without a biomarker, the clinical diagnosis of CTE remains difficult. This report suggests that clinical criteria for CTE may be greatly improved with emphasis on several critical historical and clinical correlates of CTE.