1,721,142 research outputs found
Monitoring cognitive changes: psychometric properties of six cognitive tests
No full textObjectives. Repeated neuropsychological assessments are often used to monitor change in cognitive functioning over time. Thus, knowledge about the reliability and stability of neuropsychological tests and the effects of age and IQ is of paramount importance. In this study we document, for six cognitive tests: test-retest reliabilities, practice effects, reliable change (RC) indices corrected for practice, and the impact of premorbid IQ and age.
Design. A sample of 188 normal adults (aged 40-70 years) were administered, on two occasions, one or more of the following tests: the Graded Naming Test (GNT), the Silhouettes Test, two tests of verbal fluency, the Modified Wisconsin Card Sorting Test, and a new test of speed and attention (the Symbol Digit Test). There was a I month interval between assessments. At first assessment, all participants were administered the revised National Adult Reading Test (NART).
Results. The test-retest reliability of the tests ranged from very good (the GNT and Silhouettes Test) to moderate (verbal fluency tests and Symbol Digit Test) and to poor (Modified Card Sorting Test). Significant, although modest, practice effects were found on all tests. RC indices were generally large except for the Graded Naming Test and the Silhouettes Test. Premorbid IQ scores significantly correlated with performance on all the tests, the exception being semantic fluency. Age only correlated with the Silhouettes Test and the new Symbol Digit Test. Neither NART IQ nor age correlated with practice effects.
Conclusion. The psychometric properties of the GNT and Silhouettes Test indicated that they are useful tools for monitoring even small cognitive changes. In contrast, the verbal fluency tests and the new Symbol Digit Test are only suitable for monitoring large changes in performance. The Modified Card Sorting Test is an unreliable tool for monitoring 'executive' functions
Effect of donepezil on transcranial magnetic stimulation parameters in Alzheimer's disease
Full text linkIntroduction: There is a need for a reliable, noninvasive biomarker for Alzheimer's disease (AD). We assessed whether short-latency afferent inhibition (SAI), a transcranial magnetic stimulation paradigm that assesses cholinergic circuits of the brain, could become such a biomarker.
Methods: Nineteen patients with AD underwent four SAI testing sessions. The timing of their usual donepezil dose was altered to create different cholinergic states for each session. This was compared to the SAI results from 20 healthy subjects.
Results: SAI was not able to distinguish the different cholinergic states assessed in our study. There appeared to be a diurnal variation in cholinergic function in the control group, which was not present in the AD cohort.
Discussion: SAI does not appear to have a role in diagnosis and assessment of AD patients. The loss of diurnal variation, however, warrants further investigation as it may provide further biochemical insights about AD
Neologistic jargon aphasia and agraphia in primary progressive aphasia
No full textThe terms 'jargon aphasia' and 'jargon agraphia' describe the production of incomprehensible language containing frequent phonological, semantic or neologistic errors in speech and writing, respectively. Here we describe two patients with primary progressive aphasia (PPA) who produced neologistic jargon either in speech or writing. We suggest that involvement of the posterior superior temporal-inferior parietal region may lead to a disconnection between stored lexical representations and language output pathways leading to aberrant activation of phonemes in neologistic jargon. Parietal lobe involvement is relatively unusual in PPA, perhaps accounting for the comparative rarity of jargon early in the course of these diseases. (C) 2008 Elsevier B.V. All rights reserved
Survival in Alzheimer disease
No full textWe thank Dr Lesser for his comments. We agree that deaths in older populations with AD are often from comorbid conditions, and we would not wish to overinterpret the limited survival data from this study. We also accept that determining symptom onset is an inexact science. However, we would suggest that in this small cohort the disease course of about a decade cannot be considered an aggressive one. Since publication of our study, 2 additional subjects have died 8.9 and 16.8 years after onset thereby increasing the mean time from onset to death to 9.4 years. We agree, however, that further study is required to resolve these issues and in particular to assess genetic factors that may influence the rate of disease progression. Although findings in familial AD may not necessarily generalize to sporadic disease, the study of early-onset pedigrees affords the opportunity to assess progression with fewer confounds of comorbidity
A decade of prediagnostic assessment in a case of Familial Alzheimer's disease: tracking progression from asymptomatic to MCI and dementia
No full textTracking progression from pre-MCI to dementia: a decade of pre-diagnostic assessment in a case of Familial Alzheimer's disease
No full textThe neuropsychology of variant CJD: a comparative study with inherited and sporadic forms of prion disease
No full textObjective: To assess cognitive function in variant Creutzfeldt-Jakob disease (vCJD). We describe the neuropsychological profiles of 10 cases and compare these data with cross sectional data obtained from patients with histologically confirmed sporadic CJD and cases with inherited prion disease with confirmed mutations in the prion protein gene.
Methods: Patients referred to the Specialist Cognitive Disorders Clinic at the National Hospital for Neurology and Neurosurgery and the National Prion Clinic at St Mary’s Hospital, London for further investigation of suspected CJD were recruited into the study. The neuropsychological test battery evaluated general intelligence, visual and verbal memory, nominal skills, literacy skills, visual perception and visuospatial functions, and visuospatial and executive function.
Results: The results indicate that moderate to severe cognitive decline is a characteristic feature of vCJD. Specifically, verbal and visual memory impairments and executive dysfunction were pervasive in all disease groups. Nominal skills were impaired in variant and sporadic CJD, significantly so when compared with the inherited prion disease group. Perceptual impairment was less frequent in the vCJD group than in the sporadic and inherited groups.
Conclusion: This study confirms the occurrence of generalised cognitive decline in patients with vCJD. Although decline in cognitive function ultimately affects all domains, there is a suggestion that some components of visual perception may be spared in vCJD. The results also suggest that nominal function may be preserved in some cases with inherited prion disease
A second family with familial AD and the V717L APP mutation has a later age of onset
No full textFour mutations have been reported at the 717 codon of the amyloid precursor protein (APP), with valine substituted by isoleucine, glycine, phenylalanine, and leucine. While several families with the isoleucine substitution have been described, the other substitutions have been reported in only one family each worldwide.
A family with the V717L APP mutation has been previously reported,1 with a mean age at onset of 38 years (range 35 to 39), based on four affected family members, and a mean age at death of 46 years (range 40 to 50). We have identified a second family with a later mean age at onset of 50 years (range 48 to 57) and mean age at death of 61 years (range 57 to 68)
Mapping the onset and progression of atrophy in familial frontotemporal lobar degeneration
No full textBACKGROUND:
Frontotemporal lobar degeneration (FTLD) may be inherited as an autosomal dominant disease. Studying patients "at risk" for developing FTLD can provide insights into the earliest onset and evolution of the disease.
METHOD:
We carried out approximately annual clinical, MRI, and neuropsychological assessments on an asymptomatic 51 year old "at risk" family member from a family with FTLD associated with ubiquitin-positive and tau-negative inclusion bodies. We used non-linear (fluid) registration of serial MRI to determine areas undergoing significant regional atrophy at different stages of the disease.
RESULTS:
Over the first 26 months of the study, the patient remained asymptomatic, but subsequently developed progressive speech production difficulties, and latterly severe orofacial dyspraxia, dyscalculia, frontal executive impairment, and limb dyspraxia. Regional atrophy was present prior to the onset of symptoms, and was initially centred on the left dorsolateral prefrontal cortex and the left middle frontal gyrus. Latterly, there was increasing asymmetric left frontal and parietal atrophy. Imaging revealed excess and increasing global atrophy throughout the study. Neuropsychological evaluation revealed mild intellectual impairment prior to the onset of these clinical symptoms; frontal executive and left parietal impairment subsequently emerged, culminating in widespread cognitive impairment. Fluid registered MRI allowed the emerging atrophy patterns to be delineated.
CONCLUSION:
We have demonstrated the onset and progressive pattern of in vivo atrophy in familial FTLD using fluid registered MRI and correlated this with the clinical features. Fluid registered MRI may be a useful technique in assessing patterns of focal atrophy in vivo and demonstrating the progression of degenerative diseases
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