Cases reported "Alzheimer Disease"

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1/95. Selective sparing of verb naming in a case of severe Alzheimer's disease.

    A patient with severe Alzheimer's disease (AD) presented with a severe impairment in naming nouns but selective sparing of the naming of verbs. Her impairment in naming nouns was presented across a wide range of categories investigated. To our knowledge, this is the first case documenting the selective preservation of verb naming in a patient with AD. The implications for the notion of an intrinsic vulnerability of verb naming in AD and for the current knowledge of anatomical correlates of noun/verb processing are discussed.
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2/95. Progressive frontal gait disturbance with atypical Alzheimer's disease and corticobasal degeneration.

    OBJECTIVES: The clinical neuropsychological, neuroradiological, and neuropathological description of two patients presenting with a frontal gait disturbance. methods: Clinical case note review, neuropsychological assessment, functional imaging with (15)O(2) and (18)F-fluorodopa PET, and neuropathology. RESULTS: Both patients presented with frontal gait impairment and only later developed more widespread cognitive impairment. In both cases (15)O(2) PET disclosed focal hypometabolism in the medial frontal lobes and in one patient (18)F-fluorodopa uptake into the caudate and putamen was normal. The neuropathological examination in one patient showed Alzheimer's histopathology together with large swollen eosinophilic neurons characteristic of corticobasal degeneration, which were particularly prominent in the medial frontal lobes. CONCLUSION: Focal degeneration of the medial frontal lobes may present as an isolated gait disturbance and should be considered in the differential diagnosis of patients who present without an obvious structural abnormality on neuroimaging.
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ranking = 33.335227039306
keywords = cognitive impairment, impairment
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3/95. Early thalamic and cortical hypometabolism in adult-onset dementia due to metachromatic leukodystrophy.

    A case of early-onset adult dementia with family history of dementia is reported, characterised by neuropsychological deficits, suggesting frontal involvement, with mild non specific white matter abnormalities on CT scan. Familial Alzheimer's disease was suspected but the neuropathological diagnosis on brain biopsy was metachromatic leukodystrophy. 18FDG-PET revealed a very peculiar pattern of metabolic impairment in thalamic areas, in medial and frontopolar regions, and in occipital lobes. Neuropsychological follow-up showed relatively stable difficulties of long-term memory and signs of frontal lobe dysfunction, similar to those observed in subcortical dementias. MRI subsequently showed periventricular leukoencephalopathy. The brain metabolic pattern observed in that case of metachromatic leukodystrophy was quite different from that reported in other types of dementia.
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4/95. Posterior cortical atrophy variants of Alzheimer's disease.

    Posterior cortical atrophy (PCA) was first described by Benson in 1988 and, since then, has been regarded as a variant of Alzheimer's disease. We present 2 patients with symptoms suggestive of PCA and 2 patients with apraxia as the initial manifestation. Primary motor and sensory modalities were intact. Mild memory impairment was present early in the course of the disease and gradually worsened. Parieto-occipital atrophy was evident on brain MRI. HMPAO-SPECT demonstrated parieto-occipital hypoperfusion significantly different from the temporoparietal hypoperfusion usually described in senile dementia of the Alzheimer type. These findings suggest that HMPAO-SPECT can help in diagnosing atypical variants of Alzheimer's disease. We suggest that PCA represents two clinically related behavioral phenotypes: PCA with predominantly apraxia manifestations and PCA with predominantly visuospatial disturbances. Copyrightz1999S.KargerAG,Basel
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5/95. The impact of semantic memory impairment on spelling: evidence from semantic dementia.

    We assessed spelling and reading abilities in 14 patients with semantic dementia (with varying degrees of semantic impairment) and 24 matched controls, using spelling-to-dictation and single-word reading tests which manipulated regularity of the correspondences between spelling and sound, and word frequency. All of the patients exhibited spelling and reading deficits, except at the very earliest stages of disease. Longitudinal study of seven of the patients revealed further deterioration in spelling, reading, and semantic memory. The performance of both subject groups on both spelling and reading was affected by regularity and word frequency, but these effects were substantially larger for the patients. Spelling of words with exceptional (or more precisely, unpredictable) sound-to-spelling correspondences was most impaired, and the majority of errors were phonologically plausible renderings of the target words. reading of low frequency words with exceptional spelling-to-sound correspondences was also significantly impaired. The spelling and reading deficits were correlated with, and in our interpretation are attributed to, the semantic impairment.
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6/95. Anterior choroidal artery infarction presenting as a progressive cognitive deficit.

    PURPOSE: The authors describe a patient in whom neuroimaging using Tc-99m HMPAO SPECT, F-18 fluorodeoxyglucose (F-18 FDG) coincidence imaging, and magnetic resonance imaging (MRI) identified an anterior choroidal artery infarction. neuroimaging played a critical role in confirming this diagnosis, because the patient had symptoms of progressive cognitive decline and satisfied the National Institute of Neurological and Communicative Disorders and stroke-Alzheimer's disease and Related Disorders association criteria for Alzheimer's disease (AD). methods: Tc-99m HMPAO brain SPECT was performed using a triple-head gamma camera. F-18 FDG scanning was obtained 40 minutes after intravenous injection of 5 mCi F-18 FDG using a coincidence camera. A brain MRI scan was performed using a 1.5-Tesla scanner. RESULTS: Tc-99m HMPAO SPECT showed focal hypoperfusion to the right parahippocampal cortex. F-18 FDG coincidence imaging showed a more extensive reduction in glucose metabolism compared with SPECT. The MRI scan confirmed the presence of a small segmental choroidal artery infarction. The Tc-99m HMPAO and F-18 FDG scans were not consistent with AD. CONCLUSIONS: This case illustrates the value of the regional cerebral blood flow SPECT for evaluating memory impairment in the elderly. Decreased regional cerebral blood flow to the posterior temporoparietal region is consistent with AD, whereas regional cerebral blood flow diminution in a vascular territory is consistent with vascular dementia. In this case, the patient was clinically diagnosed with AD, and SPECT was performed to establish the baseline regional cerebral blood flow before the cholinesterase inhibitor donepezil was administered. An infarction was diagnosed on the regional cerebral blood flow brain SPECT scan, which was later confirmed by MRI. Infarctions of the parahippocampal cortex may resuft in memory impairment, which can appear clinically similar to AD.
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7/95. Alzheimer's disease due to an intronic presenilin-1 (PSEN1 intron 4) mutation: A clinicopathological study.

    We describe 21 affected individuals from a kindred with early-onset autosomal dominant familial Alzheimer's disease caused by an intronic presenilin-1 mutation (in intron 4). Mean age at onset of symptoms was 37.4 years [95% confidence interval (CI): 36.6-38.2 years], mean age at death was 44.7 years (95% CI: 43.1-46.3 years) and mean duration of illness was 7.3 years (95% CI: 5.9-8.7 years). myoclonus and seizures were prominent features of this pedigree. In the four cases for whom neuropsychometric data were available, verbal memory impairment preceded visual memory deficits; naming was relatively preserved until late in the disease. One of these four cases underwent serial volumetric MRI scans demonstrating in vivo brain tissue loss of 3.9% (38.9 ml, annualized rate of atrophy: 1. 7%) over 22 months of follow-up. The four individuals who had necropsies demonstrated the neuropathological hallmarks of Alzheimer's disease. Apolipoprotein E (APOE) status was assessed in five individuals: the case with the youngest age at onset at 33 years of age was found to be homozygous epsilon4/epsilon4, > 1 SD below the mean age of onset for those of known APOE genotype (36.4 /- 2.3 years, mean /- SD), and > 2 SDs below the mean age of onset for the pedigree as a whole (37.4 /- 1.7 years, mean /- SD). APOE genotype may therefore modulate age at onset in this pedigree.
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8/95. Effects of individualized versus classical "relaxation" music on the frequency of agitation in elderly persons with Alzheimer's disease and related disorders.

    confusion and agitation in elderly patients are crucial problems. This study tested Gerdner's mid-range theory of individualized music intervention for agitation. An experimental repeated measures pretest-posttest crossover design compared the immediate and residual effects of individualized music to classical "relaxation" music relative to baseline on the frequency of agitated behaviors in elderly persons with Alzheimer's disease and related disorders (ADRD). Thirty-nine subjects were recruited from six long-term-care facilities in iowa. The sample consisted of 30 women and 9 men (mean age 82 years) with severe cognitive impairment. Baseline data were collected for 3 weeks. Findings from the Modified Hartsock music Preference Questionnaire guided the selection of individualized music. Group A (n = 16) received individualized music for 6 weeks followed by a 2-week "washout" period and 6 weeks of classical "relaxation" music. Group B (n = 23) received the same protocol but in reverse order. music interventions were presented for 30 minutes, two times per week. The Modified Cohen-Mansfield Agitation Inventory measured the dependent variable. A repeated measures analysis of variance with Bonferroni post hoc test showed a significant reduction in agitation during and following individualized music compared to classical music. This study expands science by testing and supporting a theoretically based intervention for agitation in persons with ADRD.
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ranking = 32.835227039306
keywords = cognitive impairment, impairment
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9/95. Failure at object identification improves mirror image matching.

    In a previous report ([5]: Davidoff J & Warrington EK. The bare bones of object recognition: implications from a case of object recognition impairment. Neuropsychologia 1999;37:279-92) the inability to differentiate between mirror images was recorded in a patient with excellent canonical view recognition. We now extend our investigation to a patient (JBA) with probable Alzheimer's disease in whom canonical view recognition was compromised. The reciprocal inhibition of two aspects of object processing are demonstrated in JBA. The patient's ability to detect mirror image rotations was dependent on her inability to identify the object. Paradoxically, her performance was more impaired for those stimuli that she was able to identify than those she was not.
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10/95. Presentation of amyloidosis in carriers of the codon 692 mutation in the amyloid precursor protein gene (APP692).

    Several mutations in the amyloid precursor protein (APP) gene may lead to either Alzheimer's disease or cerebral haemorrhage due to congophilic amyloid angiopathy (CAA). A single family is known in which both types of pathology are expressed because of a missense mutation at codon 692 of the APP gene (APP692). Here we describe the clinical and pathological expression of APP692 in eight patients with the mutation. Furthermore, 21 first-degree relatives with an a priori risk of 50% of being a carrier were tested for the APP692 mutation and studied for presymptomatic signs by neurological examination, neuropsychological testing and brain MRI. patients with APP692 presented with haemorrhage, dementia or both. The dementia in patients with the APP692 mutation was compatible with Alzheimer's disease both clinically and neuropathologically. Of the 21 healthy relatives at 50% risk, five carried the APP692 mutation. The presymptomatic carriers showed a subtle, non-significant impairment of cognitive function compared with relatives without APP692. A significant increase in the number of periventricular and subcortical white matter lesions at young age was seen in presymptomatic carriers (mean age 26.4 years). The findings of this study suggest that a single (genetic) mechanism may underlie the pathology of Alzheimer's disease and CAA. These diseases are manifested subclinically by white matter pathology. Further insight into the relationship between CAA and Alzheimer's disease may provide clues about the aetiology of Alzheimer's disease.
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