Neuropsychological profile of dementia with Lewy bodiespsy_283
|
|
- Arron Perry
- 5 years ago
- Views:
Transcription
1 doi: /j x PSYCHOGERIATRICS 2009; 9: REVIEW ARTICLE Neuropsychological profile of dementia with Lewy bodiespsy_283 Haruhiko ODA, Yasuji YAMAMOTO and Kiyoshi MAEDA Division of Psychiatry, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan Correspondence: Dr Haruhiko Oda, Division of Psychiatry, Kobe University Graduate School of Medicine, Kusunoki-cho, Chuou-ku, Kobe, Hyogo , Japan. Received 1 September 2008; accepted 30 September This review article was presented by the author in Symposium of the 23rd annual meeting of Japanese Psychogeriatric Society in Kobe, June Key words: Alzheimer disease, attentional dysfunction, dementia with Lewy bodies, memory, visuospatial impairment. Abstract Dementia with Lewy bodies (DLB) accounts for 10 25% of all dementia cases in clinical populations and is considered to be the second most common degenerative dementia in elderly people after Alzheimer s disease (AD). Dementia with Lewy bodies is characterized by the presence of cognitive, psychiatric, and motor symptoms. Although the neuropsychological profiles of patients with DLB often differ from those of patients with AD, the diagnostic sensitivity, specificity, and predictive values of these profiles remain largely unknown. The present paper reviews the neuropsychological profiling of DLB and attempts the neuropsychological differentiation of DLB from AD. INTRODUCTION Dementia with Lewy bodies (DLB) is considered the second most common form of neurodegenerative dementia after Alzheimer s disease (AD). Considerable attention has focused on discrimination between DLB and AD. Originally, DLB was defined as a clinicopathologic entity with a specific constellation of clinical features, and a descriptive approach was proposed to assess its neuropathology. 1 From a pathological standpoint, DLB is a common disorder of a-synuclein metabolism and is characterized by the development of abnormal cytoplasmic inclusions, called Lewy bodies, throughout the brain. A Lewy body is composed of a-synuclein associated with other proteins, such as ubiquitin, neurofilament protein, and ab crystallin. Lewy bodies were first seen and linked to Parkinson s disease ( paralysis agitans ) in 1912 by the neurologist Frederic Lewy. 2 Lewy bodies appear as spherical masses that displace other cell components. There are two morphological types of Lewy bodies, brain stem and cortical. A brain stem Lewy body is an eosinophilic cytoplasmic inclusion that consists of a dense core surrounded by a halo, approximately 10 mm in diameter, of radiating fibrils, the primary structural component of which is a-synuclein. Hematoxylin and eosin staining is not sufficient for the detection of cortical Lewy bodies and is not capable of detecting Lewy neurites. Lewy did not ascribe neurobehavioral significance to Lewy bodies initially observed in postencephalitic parkisonian patients in Okazaki et al. described two patients with parkinsonism and dementia with cortical Lewy body like eosiophilic inclusions in Although these inclusion bodies lacked the distinctive halo of brain stem Lewy bodies, this group of investigators made an association between these cerebral inclusions and dementia. In 1976, Kosaka et al. reported an autopsied case with progressive dementia and parkinsonism, the neuropathologic features of which were the widespread presence of Lewy bodies thoroughout the central nervous system as well as Alzheimer s changes. 4 In 1978, Kosaka described three cases with distribution of cortical Lewy bodies. 5 In 1984, Kosaka et al. proposed the term diffuse Lewy body disease (DLBD). 6 Based on the concept of DLBD, the term DLB was proposed by the consortium on DLB international workshop. 1 Recently DLB, Parkinson disease (PD), and PD with dementia (PDD) have been identified as being part of the spectrum of Lewy body disease. 7 There are four subtypes of DLB: a neocortical type (nearly equal DLBD), a limbic type, a brain stem type and a cerebral type. Dementia with 2009 The Authors 85
2 H. Oda et al. Table 1 Revised clinical diagnostic criteria for DLB 11 Criteria Central feature Core features (any two = probable DLB; any one = possible DLB) Suggestive features (one or more + a core feature = probable DLB; any one alone = possible DLB) Supportive features (common but lacking diagnostic specificity) Details Dementia defined as progressive cognitive decline Fluctuating cognition Recurrent visual hallucinations Spontaneous features of parkinsonism REM sleep behavior disorder Severe neuroleptic sensitivity Low dopamine transporter uptake in basal ganglia Repeated falls and syncope Transient, unexplained loss of consciousness Systematized delusions Hallucinations in other modalities Relative preservation of medial temporal lobe on CT or MRI scans Decreased tracer uptake on SPECT or PET imaging in occipital regions Prominent slow waves on EEG with temporal lobe transient sharp waves CT, computed tomography; MRI, magnetic resonance imaging; SPECT, single photon emission computed tomography; PET, positron emission tomography; EEG, electroencephalography. Lewy bodies exhibits a clinical overlap between AD and PD. Pathologically, Lewy bodies are present in DLB as well as in PD. In addition, there is a loss of dopamine-producing neurons (in the substantia nigra) similar to that seen in PD and a loss of acetylcholine (ACh)-producing neurons (in the basal nucleus of Meynert and elsewhere) similar to that seen in AD. Cerebral atrophy (or shrinkage) also occurs as the cerebral cortex degenerates. Autopsy series have revealed that the pathology of DLB is often concomitant with the pathology of AD. That is, when Lewy body inclusions are found in the cortex, they often co-occur with AD pathology found primarily in the hippocampus, including neurofibrillary tangles (abnormally phosphorylated tau protein), senile plaques (a-amyloid protein deposits), and granulovacuolar degeneration. Kosaka proposed two distinct pathological subtypes of DLB: (i) the common form, found in approximately 75% of cases, with mixed Lewy body and amyloid pathology; and (ii) the pure form, with only Lewy body pathology. 8 Within DLB, the loss of cholinergic (ACh-producing) neurons is thought to account for the degradation of cognitive and emotional functioning, as in AD, whereas the loss of dopaminergic (dopamineproducing) neurons is thought to account for the degradation of motor control, as in PD. Thus, DLB is similar in to the dementia resulting from both AD and PD. In fact, DLB is often confused in its early stages with AD and/or vascular dementia (multi-infarct dementia). The overlap of neuropathologies and presenting symptoms (cognitive, emotional, and motor) may make an accurate differential diagnosis difficult to make. The need for an early and accurate diagnosis of DLB to enable the proper clinical treatment has been emphasized by reports of severe neuroleptic sensitivity 9 and preferential response to cholinesterase inhibitors in these patients. 10 Careful cognitive assessment may aid in the differential diagnosis between these different types of dementia and can provide theoretical insight into the nature of the underlying impairments. The clinical diagnosis of DLB is supported and facilitated by the recent revision of clinical diagnostic criteria for DLB (Table 1). 11 In most studies examining the clinical criteria for the operational diagnosis of DLB, the specificity of diagnosis has been high, but sensitivity poor. There has been a need for studies examining the neuropsychological profile of DLB and the contribution of neuropsychological evaluation to the diagnostic workup. In the present article, we review the cognitive profile of DLB for future research and clinical issues, such as the problem of differential diagnosis. ATTENTION There have been studies demonstrating a greater attentional impairment in DLB than in AD. Hansen et al. compared nine patients with DLB with nine patients with AD. More severe deficits of attentional function (digit span sub-test from the Wechsler Adult Intelligence Scale-Revised (WAIS-R)) were seen in DLB. 12 Sahgal et al. reported that DLB patients had significantly greater impairment on a computerized delayed matching-to-sample task. 13 Ayre et al. used The Authors
3 Neuropsychology of DLB the Cognitive Drug Research Computerized Assessment System for Dementia Patients (COGDRAS-D) computerized test battery to compare attention in 46 patients with AD and 24 patients with DLB. 14 The DLB group performed significantly worse on simple reaction time (SRT) and choice reaction time (CRT) tasks and digit vigilance (VIG) compared with the AD group. Ballard et al. compared 85 patients with DLB with 80 patients with AD using the COGDRAS-D. 15 They showed that slowed processing speed, attentional impairments, and fluctuations in attentional impairments are significantly more severe in DLB than AD patients. The DLB patients were significantly more impaired than the AD patients on all tests of attention and fluctuating attention. In both DLB and AD, most measures of attentional performance and most indices of fluctuating attention were significantly correlated with the Mini-Mental State Examination (MMSE) score. The severity and fluctuation of attentional impairments are particularly pronounced in DLB patients with MMSE scores of 10 or less. Ballard et al. 15 concluded that their results confirmed that the attentional deficits and fluctuations in attention are substantially more severe in DLB patients than in patients with AD. A number of other factors, such as parkinsonism with slowed motor speed, depression, or general slowing of cognitive processing speed, could theoretically have contributed to these findings. Ballard et al. 15 noticed that deficits of attention became more pronounced with increasing dementia severity and, hence, that these deficits need to be interpreted within the context of overall cognitive deficits. Oda et al. 16 compared 26 patients with DLB with 78 patients with AD and demonstrated that patients with AD had significantly greater scores on the weighted sum score of the Attention of Wechsler Memory Scale-Revised (WMS-R) than did patients with DLB (P = ). The overall pattern is consistent, with DLB patients showing significantly greater impairment on a range of attentional tasks. Both neuropsychological and clinical observations strongly suggest that DLB patients experience great difficulty in sustaining attention. The neural basis of the attentional impairment in DLB requires further investigation, but it is likely that a dysfunction of the basal forebrain cholinergic system is involved. Several lines of evidence support this proposal. Cholinergic neuronal loss and depletion of choline acetyltransferase are seen early in DLB. 17 Administration of anticholinergic drugs can disturb attention and cause hallucinations, whereas cholinesterase inhibitors can improve cognition in DLB. 11 VISUOPERCEPTUAL AND SPATIAL FUNCTIONS Numerous studies have observed greater impairments in DLB compared with AD on visuospatial and constructional tasks. Ala et al. compared 17 patients with autopsy confirmed DLB and 27 patients with autopsy confirmed AD by using copies of the double pentagon from the MMSE. 18 They showed that only two patients with DLB drew the pentagon acceptably, in contrast with 16 AD patients, and that an unacceptable copy of the pentagon was associated with DLB with a sensitivity of 88% and a specificity of 59%. They concluded that their results confirmed the greater visuospatial/constructional impairment of patients with DLB than patients with AD and suggested that the pentagon copying task of the MMSE may be useful in a diagnostic sense. 18 Cormack et al. reported that patients with DLB were found to draw significantly worse double pentagons than those with AD or PD. 19 In their report, a correlation between MMSE score and pentagon drawing score was observed in patients with AD; however, DLB patients did not show any significant correlation between MMSE scores and the pentagon drawing score. In order to investigate the hypothesis that DLB patients have a different neuropsychological basis to their drawing impairments to the other dementia groups, the global cognitive performance of subjects was measured using the cognitive section of the Cambridge Mental Disorders in the Elderly Examination (CAMCOG). Cormack et al. 19 found that pentagon copying scores were significantly correlated with all CAMCOG subscales except visual and recent memory in the AD group, whereas DLB patients scores were significantly correlated only with Praxis and Perception. This result suggested that constructional disability was proportionate to global cognitive impairment in the AD group, but there was a dissociation of constructional ability from global cognitive ability in the DLB group. Mori et al. addressed problems in visual perception in patients with DLB and compared them with patients with AD. 20 Mori et al. assessed the visual perception of 24 patients with DLB and 48 patients with DLB by using a subset of the object and spacial vision test battery. The dis The Authors 87
4 H. Oda et al. crimination of object size task was used to examine elementary visual perception, the form discrimination task was used to examine more complex visuoperceptual function that requires analysis of twodimensional visual stimuli, the overlapping figure identification task was used to examine the ability to actively extract concrete shapes and to recognize objects, and the visual counting task was used to examine the ability to explore and identify the spatial relationship of visual stimuli to count targets without duplication or omission. Mori et al. 20 found that DLB subjects performed more poorly than an AD group not only in discriminating size and form and visual counting, but also in identifying overlapping figures. Moreover, DLB subjects with visual hallucinations performed significantly worse on the overlapping figures task. Oda et al. reported that patients with DLB scored significantly worse on the Block Design, Object Assembly, and Digit Symbol subtests of the WAIS-R than did patients with AD. 16 Because the set of the Block Design, Object Assembly, and Digit Symbol is considered to be involved in visual perception/processing meaningful stimuli and visual organization, these results were considered to suggest that patients with DLB have a more severe impairment of both their visual perception of meaningful stimuli and visual organization than do AD patients. Oda et al. 16 also showed that except for Comprehension, Similarities, and Object Assembly, all subtests and IQ of the WAIS-R showed a significant correlation with the MMSE score in the AD group. This suggests that the fall in IQ is proportional to global cognitive impairment in the AD group. However, in the DLB group, there was no correlation between all subtests of the WAIS-R and MMSE score. There seemed to be a dissociation of the IQ from global cognitive abilities in the DLB group. Oda et al. 16 ascribed the lack of correlation between the global cognitive impairment and the fall in intellectual ability in the DLB group to selective impairment of visuoperceptual function in addition to global cognitive impairment. The fact that visual perceptual disturbances in patients with DLB predispose them to visual hallucinations has important clinical implications. First, because visual hallucinations are among the strongest diagnostic predictors of DLB, the neuropsychological assessment of visual perceptual and constructional functions is critical in suspected DLB and its differentiation from AD. Indeed, visuoconstructional tasks, in combination with other tests, can differentiate DLB from normal aging and from AD with high sensitivity and specificity. 21 Furthermore, poor performance on visuoperceptual and constructional tasks may indicate the need for more careful monitoring for the development of hallucinations. It is likely that occipital dysfunction is implicated in visuoperceptual abnormalities of DLB and both the ventral occipitotemporal and dorsal occipitoparietal streams have been implicated. The visuoperceptual dysfunction in DLB can be attributed to accentuated damage in the occipital lobes. Albin et al. demonstrated that regional glucose metabolism was decreased in the occipital association cortex and primary visual area in six patients with autopsy proved DLB. 22 In the study of Ishii et al., using fludeoxyglucose F18 and positron emission tomography (PET), the glucose metabolic rate in the occipital cortices was found to be significantly lower in patients with probable DLB than in controls with probable AD matched for age, sex, disease duration, and MMSE score, despite similar decreases in the parietotemporal lobe in patients with DLB and AD. 23 Similarly, a single photon emission computed tomography (SPECT) study demonstrated that occipital blood flow was significantly lower in patients with DLB than in patients with AD. 24 Therefore, in DLB, not only does the parietotemporal damage provoke visuocognitive dysfunctions, but occipital damage also causes disturbances of visual sensations and intensifies the higher-order visuocognitive dysfunctions. Defective visual perception, resulting in illusions including distortions of form, size, movement, or color, in combination with general defects such as confusion and mental deterioration may cause a sense of strangeness or inexplicable familiarity. The mechanism of occipital involvement and visuoperceptual deficits in DLB is highly speculative. Bashir et al. reported a unique patient with DLB who initially complained of heaviness in the right upper extremity and subsequently developed a dense left homonymous hemianopsia during the course of a rapidly progressing dementia. 25 Their patient fulfilled all the consensus criteria for the clinical diagnosis of probable DLB: their case exhibited progressive cognitive decline, parkinsonism, visual hallucinations, and fluctuating agitation, confusion, and depression. The neuropathologic findings in their patient fulfilled the diagnostic criteria for DLB, proposed by the Consortium on Dementia The Authors
5 Neuropsychology of DLB with Lewy Bodies. 1 In addition; their patient exhibited a striking predominance of neurofibrillary tangles in the right inferotemporal and occipital cortices. However, in general, the pathologic features of DLB (including Lewy bodies) hardly affect the occipital lobes. 8 In a PET study with (+)-[ 11 C]- dihydrotetrabenazine, a greater reduction of blood-tobrain ligand transport occurred in occipital cortex in DLB than in AD. 26 Bodis-Wollner speculated that in patients affected by PD, as well as in the monkey model of this disease, the visual defects may be caused by systemic dopaminergic deficiency. 27 Conversely, involvement of the occipital cholinergic system also has been assumed. The activity of a cholinergic enzyme, namely choline acetyltransferase, is reportedly lower in the temporoparietal and occipital neocortex in patients with DLB compared with those with AD. 28 MEMORY With regard to memory, in general DLB subjects perform better on tests of episodic (declarative) memory than do AD patients, and this appears particularly true on tests of verbal rather than visual memory. Shimomura et al. demonstrated that patients with DLB scored significantly better (P < 0.05 on the verbal memory subtest of the Alzheimer Disease Assessment Scale (ADAS) than did AD patients who were comparable in the global severity of dementia and the global assessment of cognitive impairment. 29 To determine what the degree to which elementary visual perceptual dysfunction may contribute to visual memory impairment in DLB, Oda et al. compared patients with DLB with AD patients using the WMS- R. 16 In that study, the DLB group showed significantly better scores than did the AD group on Verbal Memory (P < ) and Delayed Recall (P < ) of the WMS-R. However, the DLB and AD groups demonstrated comparable scores on Visual Memory ( vs , respectively; P = ). The authors speculated that the selective visuoperceptual impairment in DLB may explain this similarity: the relatively preserved short- and mediumterm recall would compensate for severe visuoperceptual impairment in the DLB group on the visual memory tasks. Lambon Ralph et al. reported that both DLB and AD groups exhibited impaired performance across a range of tasks designed to assess semantic memory. 30 Whereas patients with AD showed equivalent comprehension of written words and picture stimuli, patients with DLB demonstrated more severe semantic deficits for pictures than words. The major pathological substrate of more severe amnestic deficits in AD relative to DLB likely reflects the burden of neurofibrillary tangles in the entorhinal cortex and surrounding medial temporal lobe regions in AD. NEUROPSYCHOLOGICAL DIFFERENTIATION OF DLB FROM AD The third report of the DLB Consortium mentioned that a double discrimination can help differentiate DLB from AD, with relative preservation of confrontation naming and short- and medium-term recall as well as recognition, and greater impairment on verbal fluency, visual perception, and performance tasks. 1 Ala et al. reported a retrospective study in which pathologically confirmed cases of AD and DLB could be differentiated on the basis of a subscore derived from the MMSE. 31 Based on the greater impairment of attentional and visuospatial function, and the relative preservation of memory function in DLB compared with AD, Ala et al. 31 derived a weighted score, calculated as follows: Ala score = Attention 53Memory + Construction An Ala score <5 was associated with a pathological diagnosis of DLB with a sensitivity of 82% and a specificity of 81%. By using the Ala score and the z-score in the medial occipital lobe from a brain SPECT study, Hanyu et al. derived a combined index of SPECT/MMSE that achieved a high discrimination between DLB and AD with a sensitivity of 81% and a specificity of 85%. 32 Oda et al. derived a weighted score consisting of the Object Assembly subtest of the WAIS-R and the Logical Memory II subtest of the WMS-R to differentiate DLB from AD 16 that had a sensitivity of 81% and a specificity of 76%. SUMMARY AND CONCLUSIONS Given that DLB is a relatively new disease concept, most of the work so far has been concerned with the first step of characterization and description of DLB as a separate disease. Most of the studies suggest that in the early stages of the disease, DLB patients tend to exhibit pronounced visual perceptual, attentional, and frontal executive impairments, whereas 2009 The Authors 89
6 H. Oda et al. memory functions are generally less impaired than in AD patients. However, given the overlap and variability of symptoms, the neuropsychological profile of DLB has not yet been clearly distinguished from that of AD. In the future, the challenge of DLB research will lie in developing a theoretical model that can link evidence from pathophysiological and imaging studies with clinical and neuropsychological data. This will facilitate treatment of the disease. REFERENCES 1 McKeith IG, Galasko D, Kosaka K et al. Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): Report of the consortium on DLB international workshop. Neurology 1996; 47: Holdorff B. Friedrich Heinrich Lewy ( ) and his work. J Hist Neurosci 2002; 11: Okazaki H, Lipkin LE, Aronson SM. Diffuse intracytoplasmic ganglionic inclusions (Lewy type) associated with progressive dementia and quadriparesis in flexion. J Neuropathol Exp Neurol 1961; 20: Kosaka K, Oyanagi S, Matsushita M, Hori A. Presenile dementia with Alzheimer-, Pick- and Lewy-body changes. Acta Neuropathol 1976; 36: Kosaka K. Lewy bodies in cerebral cortex, report of three cases. Acta Neuropathol 1978; 42: Kosaka K, Yoshimura M, Ikeda K, Budka H. Diffuse type of Lewy body disease: Progressive dementia with abundant cortical Lewy bodies and senile changes of varying degree. A new disease? Clin Neuropathol 1984; 3: Troster AI. Neuropsychological characteristics of dementia with Lewy bodies and Parkinson s disease with dementia: Differentiation, early detection, and implications for mild cognitive impairment and biomarkers. Neuropsychol Rev 2008; 18: Kosaka K. Diffuse Lewy body disease in Japan. J Neurol 1990; 237: McKeith IG, Perry RH, Fairbairn AF, Jabeen S, Perry EK. Operational criteria for senile dementia of Lewy body type (SDLT). Psychol Med 1992; 22: Samuel W, Caligiuri M, Galasko D et al. Better cognitive and psychopathologic response to donepezil in patients prospectively diagnosed as dementia with Lewy bodies: A preliminary study. Int J Geriatr Psychiatry 2000; 15: McKeith IG, Dickson DW, Lowe J et al. Diagnosis and management of dementia with Lewy bodies: Third report of the DLB Consortium. Neurology 2005; 65: Hansen L, Salmon D, Galasko D et al. The Lewy body variant of Alzheimer s disease: A clinical and pathological entity. Neurology 1990; 40: Sahgal A, Galloway PH, McKeith IG, Edwardson JA, Lloyd S. A comparative study of attentional deficits in senile dementias of Alzheimer and Lewy body types. Dementia 1992; 3: Ayre G, Ballard C, Pincock C, McKeith I, Sahgal A, Wesnes K. Double dissociation between dementia with Lewy bodies and Alzheimer s disease on tests of attentional and mnemonic function: The role of the basal forebrain. J Psychopharmacol 1998; A12 (Suppl.): A62 A Ballard C, O Brien J, Gray A et al. Attention and fluctuating attention in patients with dementia with Lewy bodies and Alzheimer disease. Arch Neurol 2001; 58: Oda H, Yamamoto Y, Maeda K. The neuropsychological profile in dementia with Lewy bodies and Alzheimer s disease. Int J Geriatr Psychiatry 2009; 24: Tiraboschi P, Hansen LA, Alford M et al. Early and widespread cholinergic losses differentiate dementia with Lewy bodies from Alzheimer disease. Arch Gen Psychiatry 2002; 59: Ala TA, Hughes LF, Kyrouac GA, Ghobrial MW, Elble RJ. Pentagon copying is more impaired in dementia with Lewy bodies than in Alzheimer s disease. J Neurol Neurosurg Psychiatry 2001; 70: Cormack F, Aarsland D, Ballard C, Tovee MJ. Pentagon drawing and neuropsychological performance in dementia with Lewy Bodies, Alzheimer s disease, Parkinson s disease and Parkinson s disease with dementia. Int J Geriatr Psychiatry 2004; 19: Mori E, Shimomura T, Fujimori M et al. Visuoperceptual impairment in dementia with Lewy bodies. Arch Neurol 2000; 57: Ferman TJ, Smith GE, Boeve BF et al. Neuropsychological differentiation of dementia with Lewy bodies from normal aging and Alzheimer s disease. Clin Neuropsychol 2006; 20: Albin RL, Minoshima S, D Amato CJ, Frey KA, Kuhl DA, Sima AAF. Fluorodeoxyglucose positron emission tomography in diffuse Lewy body disease. Neurology 1996; 47: Ishii K, Imamura T, Sasaki M et al. Regional cerebral glucose metabolism in dementia with Lewy bodies and Alzheimer s disease. Neurology 1998; 51: Ishii K, Yamaji S, Kitagaki H, Imamura T, Hirono N, Mori E. Regional cerebral blood flow difference between dementia with Lewy bodies and AD. Neurology 1999; 53: Bashir K, Elble RJ, Ghobrial M, Struble RG. Hemianopsia in dementia with Lewy bodies. Arch Neurol 1998; 55: Koeppe RA, Gilman S, Junck L, Wernette K, Frey KA. Differentiating Alzheimer s disease from dementia with Lewy bodies and Parkinson s disease with (+)-[ 11 C]dihydrotetrabenazine positron emission tomography. Alzheimers Dement 2008; 4: S67 S Bodis-Wollner I. Visual deficits related to dopamine deficiency in experimental animals and Parkinson s disease patients. Trends Neurosci 1990; 13: Perry EK, Haroutunian V, Davis KL et al. Neocortical cholinergic activities differentiate Lewy body dementia from classical Alzheimer s disease. Neuroreport 1997; 8: Shimomura T, Mori E, Yamashita H et al. Cognitive loss in dementia with Lewy bodies and Alzheimer disease. Arch Neurol 1998; 55: Lambon Ralph MA, Powell J, Howard D, Whitworth AB, Garrard P, Hodges JR. Semantic memory is impaired in both dementia with Lewy bodies and dementia of Alzheimer s type: A comparative neuropsychological study and literature review. J Neurol Neurosurg Psychiatry 2001; 70: Ala TA, Hughes LF, Kyrouac GA, Ghobrial MW, Elble RJ. The Mini-Mental State exam may help in the differentiation of dementia with Lewy bodies and Alzheimer s disease. Int J Geriatr Psychiatry 2002; 17: Hanyu H, Shimizu S, Hirao K et al. Differentiation of dementia with Lewy bodies from Alzheimer s disease using Mini-Mental State Examination and brain perfusion SPECT. J Neurol Sci 2006; 250: The Authors
ORIGINAL CONTRIBUTION. Visuoperceptual Impairment in Dementia With Lewy Bodies
ORIGINAL CONTRIBUTION Visuoperceptual Impairment in Dementia With Lewy Bodies Etsuro Mori, MD, PhD; Tatsuo Shimomura, MD; Misato Fujimori, PhD; Nobutsugu Hirono, MD, PhD; Toru Imamura, MD, PhD; Mamoru
More informationPentagon copying is more impaired in dementia with Lewy bodies than in Alzheimer s disease
J Neurol Neurosurg Psychiatry 2001;70:483 488 483 Center for Alzheimer Disease and Related Disorders, Department of Neurology, Southern Illinois University School of Medicine, Springfield, Illinois, USA
More informationRevised criteria for the clinical diagnosis of dementia with Lewy. Dementia with Lewy bodies. (Dementia with Lewy Bodies)
Dementia with Lewy bodies First described: Okazaki H, 1961, Diffuse intracytoplasmic ganglionic inclusions (Lewy type) associated with progressive dementia and quadriparesis in flexion. J Neuropathol Exp
More informationMOVEMENT DISORDERS AND DEMENTIA
MOVEMENT DISORDERS AND DEMENTIA FOCUS ON DEMENTIA WITH LEWY BODIES MADHAVI THOMAS MD NORTH TEXAS MOVEMENT DISORDERS INSTITUTE, INC DEMENTIA de men tia dəˈmen(t)sh(ē)ə/ nounmedicine noun: dementia a chronic
More informationIntroduction, use of imaging and current guidelines. John O Brien Professor of Old Age Psychiatry University of Cambridge
Introduction, use of imaging and current guidelines John O Brien Professor of Old Age Psychiatry University of Cambridge Why do we undertake brain imaging in AD and other dementias? Exclude other causes
More informationPathogenesis of Degenerative Diseases and Dementias. D r. Ali Eltayb ( U. of Omdurman. I ). M. Path (U. of Alexandria)
Pathogenesis of Degenerative Diseases and Dementias D r. Ali Eltayb ( U. of Omdurman. I ). M. Path (U. of Alexandria) Dementias Defined: as the development of memory impairment and other cognitive deficits
More informationORIGINAL CONTRIBUTION. Attention and Fluctuating Attention in Patients With Dementia With Lewy Bodies and Alzheimer Disease
ORIGINAL CONTRIBUTION Attention and Fluctuating Attention in Patients With Dementia With Lewy Bodies and Alzheimer Disease Clive Ballard, MRCPsych, MD; John O Brien, MRCPsych, DM; Alistair Gray, BSc; Franchesca
More informationDementia Update. October 1, 2013 Dylan Wint, M.D. Cleveland Clinic Lou Ruvo Center for Brain Health Las Vegas, Nevada
Dementia Update October 1, 2013 Dylan Wint, M.D. Cleveland Clinic Lou Ruvo Center for Brain Health Las Vegas, Nevada Outline New concepts in Alzheimer disease Biomarkers and in vivo diagnosis Future trends
More informationWHAT IS DEMENTIA? An acquired syndrome of decline in memory and other cognitive functions sufficient to affect daily life in an alert patient
DEMENTIA WHAT IS DEMENTIA? An acquired syndrome of decline in memory and other cognitive functions sufficient to affect daily life in an alert patient Progressive and disabling Not an inherent aspect of
More informationDementia Update. Daniel Drubach, M.D. Division of Behavioral Neurology Department of Neurology Mayo Clinic Rochester, Minnesota
Dementia Update Daniel Drubach, M.D. Division of Behavioral Neurology Department of Neurology Mayo Clinic Rochester, Minnesota Nothing to disclose Dementia Progressive deterioration in mental function
More informationLewy body disease (LBD) is the second most common
REGULAR ARTICLES Lewy Body Disease: Can We Diagnose It? Michelle Papka, Ph.D. Ana Rubio, M.D., Ph.D. Randolph B. Schiffer, M.D. Christopher Cox, Ph.D. The authors assessed the accuracy of published clinical
More informationNeuropsychological Evaluation of
Neuropsychological Evaluation of Alzheimer s Disease Joanne M. Hamilton, Ph.D. Shiley-Marcos Alzheimer s Disease Research Center Department of Neurosciences University of California, San Diego Establish
More informationSatoh M. 1, Ishikawa H. 1, Meguro K. 1,2, Kasuya M. 1, Ishii H. 3, and Yamaguchi S. 2
CYRIC Annual Report 2009 VIII 15. Occipital Glucose Metabolic Decrease by Donepezil Treatment Correlated with the Improvement of Visual Hallucinations in Dementia with Lewy Bodies: the Osaki-Tajiri Project
More informationConfusional state. Digit Span. Mini Mental State Examination MMSE. confusional state MRI
10 304 29 3 confusional state MRI 29 3 304 311 2009 Key Words memory test attention brain region causative disease subcortical dementia 1 Confusional state Digit Span 1 1 5 4 Mini Mental State Examination
More informationThe ABCs of Dementia Diagnosis
The ABCs of Dementia Diagnosis Dr. Robin Heinrichs, Ph.D., ABPP Board Certified Clinical Neuropsychologist Associate Professor, Psychiatry & Behavioral Sciences Director of Neuropsychology Training What
More informationDementia. Stephen S. Flitman, MD Medical Director 21st Century Neurology
Dementia Stephen S. Flitman, MD Medical Director 21st Century Neurology www.neurozone.org Dementia is a syndrome Progressive memory loss, plus Progressive loss of one or more cognitive functions: Language
More informationBrain imaging for the diagnosis of people with suspected dementia
Why do we undertake brain imaging in dementia? Brain imaging for the diagnosis of people with suspected dementia Not just because guidelines tell us to! Exclude other causes for dementia Help confirm diagnosis
More informationClinicopathologic and genetic aspects of hippocampal sclerosis. Dennis W. Dickson, MD Mayo Clinic, Jacksonville, Florida USA
Clinicopathologic and genetic aspects of hippocampal sclerosis Dennis W. Dickson, MD Mayo Clinic, Jacksonville, Florida USA The hippocampus in health & disease A major structure of the medial temporal
More informationDementia. Assessing Brain Damage. Mental Status Examination
Dementia Assessing Brain Damage Mental status examination Information about current behavior and thought including orientation to reality, memory, and ability to follow instructions Neuropsychological
More informationDiagnosis before NIA AA The impact of FDG PET in. Diagnosis after NIA AA Neuropathology and PET image 2015/10/16
The impact of FDG PET in degenerative dementia diagnosis Jung Lung, Hsu MD, Ph.D (Utrecht) Section of dementia and cognitive impairment Department of Neurology Chang Gung Memorial Hospital, Linkou, Taipei
More informationErin Cullnan Research Assistant, University of Illinois at Chicago
Dr. Moises Gaviria Distinguished Professor of Psychiatry, University of Illinois at Chicago Director of Consultation Liaison Service, Advocate Christ Medical Center Director of the Older Adult Program,
More informationHow to Diagnose Early (Prodromal) Lewy Body Dementia. Ian McKeith MD, FRCPsych, F Med Sci.
How to Diagnose Early (Prodromal) Lewy Body Dementia Ian McKeith MD, FRCPsych, F Med Sci. Parkinson s Disease Lewy Body Disease Time PD Dementia Lewy Body Dementias Dementia with Lewy Bodies (DLB) Diagnostic
More informationThe Spectrum of Lewy Body Disease: Dementia with Lewy Bodies and Parkinson's Disease Dementia
Disclosures Research support, Parkinson Society Canada, Canadian Institutes of Health Research, Ministry of Economic Development and Innovation, Teva Novartis clinical trial, Principal Investigator CME
More informationT he prevalence of Parkinson s disease (PD) is nearly 1% in
708 PAPER Donepezil for cognitive impairment in Parkinson s disease: a randomised controlled study D Aarsland, K Laake, J P Larsen, C Janvin... See end of article for authors affiliations... Correspondence
More informationNon Alzheimer Dementias
Non Alzheimer Dementias Randolph B Schiffer Department of Neuropsychiatry and Behavioral Science Texas Tech University Health Sciences Center 9/11/2007 Statement of Financial Disclosure Randolph B Schiffer,,
More information7/3/2013 ABNORMAL PSYCHOLOGY SEVENTH EDITION CHAPTER FOURTEEN CHAPTER OUTLINE. Dementia, Delirium, and Amnestic Disorders. Oltmanns and Emery
ABNORMAL PSYCHOLOGY SEVENTH EDITION Oltmanns and Emery PowerPoint Presentations Prepared by: Ashlea R. Smith, Ph.D. This multimedia and its contents are protected under copyright law. The following are
More informationNeuro degenerative PET image from FDG, amyloid to Tau
Neuro degenerative PET image from FDG, amyloid to Tau Kun Ju Lin ( ) MD, Ph.D Department of Nuclear Medicine and Molecular Imaging Center, Chang Gung Memorial Hospital ( ) Department of Medical Imaging
More informationDISCLOSURES. Objectives. THE EPIDEMIC of 21 st Century. Clinical Assessment of Cognition: New & Emerging Tools for Diagnosing Dementia NONE TO REPORT
Clinical Assessment of Cognition: New & Emerging Tools for Diagnosing Dementia DISCLOSURES NONE TO REPORT Freddi Segal Gidan, PA, PhD USC Keck School of Medicine Rancho/USC California Alzheimers Disease
More informationRound table: Moderator; Fereshteh Sedaghat, MD, PhD Brain Mapping in Dementias and Non-invasive Neurostimulation
Round table: Moderator; Fereshteh Sedaghat, MD, PhD Brain Mapping in Dementias and Non-invasive Neurostimulation 1. Reflection of Mild Cognitive Impairment (MCI) and Dementias by Molecular Imaging, PET
More informationYin-Hui Siow MD, FRCPC Director of Nuclear Medicine Southlake Regional Health Centre
Yin-Hui Siow MD, FRCPC Director of Nuclear Medicine Southlake Regional Health Centre Today Introduction to CT Introduction to MRI Introduction to nuclear medicine Imaging the dementias The Brain ~ 1.5
More informationClinical features of dementia with lewy bodies in 35 Chinese patients
Han et al. Translational Neurodegeneration 2014, 3:1 Translational Neurodegeneration RESEARCH Open Access Clinical features of dementia with lewy bodies in 35 Chinese patients Ding Han, Qiong Wang, Zhongbao
More informationHallucinations and signs of parkinsonism help distinguish patients with dementia and cortical
161Journal of Neurology, Neurosurgery, and Psychiatry 1997;62:16-21 Alzheimer's Treatment and Research Center, Department of Neurology, Ramsey Clinic/Health- Partners, University of Minnesota, St Paul,
More informationMild Cognitive Impairment
Mild Cognitive Impairment Victor W. Henderson, MD, MS Departments of Health Research & Policy (Epidemiology) and of Neurology & Neurological Sciences Stanford University Director, Stanford Alzheimer s
More informationORIGINAL CONTRIBUTION. Diagnostic Accuracy of Dementia With Lewy Bodies. to be the second
ORIGINAL CONTRIBUTION Diagnostic Accuracy of Dementia With Lewy Bodies Ursula Hohl, MD; Pietro Tiraboschi, MD; Lawrence A. Hansen, MD; Leon J. Thal, MD; Jody Corey-Bloom, MD, PhD Background: Diagnostic
More informationALZHEIMER S DISEASE. Mary-Letitia Timiras M.D. Overlook Hospital Summit, New Jersey
ALZHEIMER S DISEASE Mary-Letitia Timiras M.D. Overlook Hospital Summit, New Jersey Topics Covered Demography Clinical manifestations Pathophysiology Diagnosis Treatment Future trends Prevalence and Impact
More informationA prospective study of dementia with Lewy bodies
Age and Ageing 998; 27: 6-66 998, British Geriatrics Society A prospective study of dementia with Lewy bodies CLIVE G. BALLARD, JOHN O'BRIEN, KATH LOWERX GARETH A. AYRE, RICHARD HARRISON, ROBERT PERRY,
More informationOLD AGE PSYCHIATRY. Dementia definition TYPES OF DEMENTIA. Other causes. Psychiatric disorders of the elderly. Dementia.
Psychiatric disorders of the elderly OLD AGE PSYCHIATRY Dementia Depression Delusional disorder/late onset schizophrenia Delirium Dementia definition LOCALISATION OF CEREBRAL FUNCTION Impairment of multiple
More informationUpdate on functional brain imaging in Movement Disorders
Update on functional brain imaging in Movement Disorders Mario Masellis, MSc, MD, FRCPC, PhD Assistant Professor & Clinician-Scientist Sunnybrook Health Sciences Centre University of Toronto 53 rd CNSF
More informationDementia and Healthy Ageing : is the pathology any different?
Dementia and Healthy Ageing : is the pathology any different? Professor David Mann, Professor of Neuropathology, University of Manchester, Hope Hospital, Salford DEMENTIA Loss of connectivity within association
More informationDementia Past, Present and Future
Dementia Past, Present and Future Morris Freedman MD, FRCPC Division of Neurology Baycrest and University of Toronto Rotman Research Institute, Baycrest CNSF 2015 Objectives By the end of this presentation,
More informationDelirium & Dementia. Nicholas J. Silvestri, MD
Delirium & Dementia Nicholas J. Silvestri, MD Outline Delirium vs. Dementia Neural pathways relating to consciousness Encephalopathy Stupor Coma Dementia Delirium vs. Dementia Delirium Abrupt onset Lasts
More informationDementia With Lewy Bodies: A Review Of Clinical Diagnosis, Neuropathology And Management Options Tanis J. Ferman, Ph.D.
Dementia With Lewy Bodies: A Review Of Clinical Diagnosis, Neuropathology And Management Options Tanis J. Ferman, Ph.D. Table 1. Core And Supportive Features For The Clinical Diagnosis Of DLB. 13 1. The
More informationNeuropathology of Neurodegenerative Disorders Prof. Jillian Kril
Neurodegenerative disorders to be discussed Alzheimer s disease Lewy body diseases Frontotemporal dementia and other tauopathies Huntington s disease Motor Neuron Disease 2 Neuropathology of neurodegeneration
More informationNeuroimaging for dementia diagnosis. Guidance from the London Dementia Clinical Network
Neuroimaging for dementia diagnosis Guidance from the London Dementia Clinical Network Authors Dr Stephen Orleans-Foli Consultant Psychiatrist, West London Mental Health NHS Trust Dr Jeremy Isaacs Consultant
More informationNature, prevalence and clinical significance. Barcelona, Spain
Nature, prevalence and clinical significance Jaime Kulisevsky Barcelona, Spain 1 Non motor (neuropsychiatric) symptoms are an integral part of Parkinson s s disease (PD) Affective disorders And are associated
More informationNew life Collage of nursing Karachi
New life Collage of nursing Karachi Presenter: Zafar ali shah Faculty: Raja khatri Subject: Pathophysiology Topic :Alzheimer s Disease Post RN BScN semester 2 nd Objective Define Alzheimer s Describe pathophysiology
More informationDifferential Diagnosis of Alzheimer s Disease and Other Types of Dementia with Development of Neuroimaging Techniques (PET, SPECT, and MRI)
www.jmscr.igmpublication.org Impact Factor 1.1147 ISSN (e)-2347-176x Differential Diagnosis of Alzheimer s Disease and Other Types of Dementia with Development of Neuroimaging Techniques (PET, SPECT, and
More information212 Index C-SB-13,
Index A Acetylcholinesterase inhibitor, treatment, 15 Age-associated memory impairment (AAMI), 5 Alzheimer s disease (AD), 40, 95 96 apolipoprotein E genotype and risk for, 58 cellular neurodegeneration
More informationMild Cognitive Impairment (MCI)
October 19, 2018 Mild Cognitive Impairment (MCI) Yonas E. Geda, MD, MSc Professor of Neurology and Psychiatry Consultant, Departments of Psychiatry & Psychology, and Neurology Mayo Clinic College of Medicine
More informationClinical Differences Among Four Common Dementia Syndromes. a program of Morningside Ministries
Clinical Differences Among Four Common Dementia Syndromes a program of Morningside Ministries Introduction Four clinical dementia syndromes account for 90% of all cases after excluding reversible causes
More informationCaring Sheet #11: Alzheimer s Disease:
CARING SHEETS: Caring Sheet #11: Alzheimer s Disease: A Summary of Information and Intervention Suggestions with an Emphasis on Cognition By Shelly E. Weaverdyck, PhD Introduction This caring sheet focuses
More informationCHAPTER 5 NEUROPSYCHOLOGICAL PROFILE OF ALZHEIMER S DISEASE
CHAPTER 5 NEUROPSYCHOLOGICAL PROFILE OF ALZHEIMER S DISEASE 5.1 GENERAL BACKGROUND Neuropsychological assessment plays a crucial role in the assessment of cognitive decline in older age. In India, there
More informationThe Person: Dementia Basics
The Person: Dementia Basics Objectives 1. Discuss how expected age related changes in the brain might affect an individual's cognition and functioning 2. Discuss how changes in the brain due to Alzheimer
More informationImproving diagnosis of Alzheimer s disease and lewy body dementia. Brain TLC October 2018
Improving diagnosis of Alzheimer s disease and lewy body dementia Brain TLC October 2018 Plan for this discussion: Introduction to AD and LBD Why do we need to improve diagnosis? What progress has been
More informationDEMENTIA 101: WHAT IS HAPPENING IN THE BRAIN? Philip L. Rambo, PhD
DEMENTIA 101: WHAT IS HAPPENING IN THE BRAIN? Philip L. Rambo, PhD OBJECTIVES Terminology/Dementia Basics Most Common Types Defining features Neuro-anatomical/pathological underpinnings Neuro-cognitive
More informationIan McKeith MD, F Med Sci, Professor of Old Age Psychiatry, Newcastle University
Ian McKeith MD, F Med Sci, Professor of Old Age Psychiatry, Newcastle University Design of trials in DLB and PDD What has been learnt from previous trials in these indications and other dementias? Overview
More informationFDG-PET e parkinsonismi
Parkinsonismi FDG-PET e parkinsonismi Valentina Berti Dipartimento di Scienze Biomediche, Sperimentali e Cliniche Sez. Medicina Nucleare Università degli Studi di Firenze History 140 PubMed: FDG AND parkinsonism
More informationWhat if it s not Alzheimer s? Update on Lewy body dementia and frontotemporal dementia
What if it s not Alzheimer s? Update on Lewy body dementia and frontotemporal dementia Dementia: broad term for any acquired brain condition impairing mental function such that ADLs are impaired. Includes:
More informationPatterns of Cognitive Impairment in Dementia
Patterns of Cognitive Impairment in Dementia Lindsay R. Clark, PhD Assistant professor (CHS) Department of Medicine - Division of Geriatrics & Gerontology UW-Madison School of Medicine & Public Health
More informationDEMENTIA? 45 Million. What is. WHAT IS DEMENTIA Dementia is a disturbance in a group of mental processes including: 70% Dementia is not a disease
What is PRESENTS DEMENTIA? WHAT IS DEMENTIA Dementia is a disturbance in a group of mental processes including: Memory Reasoning Planning Learning Attention Language Perception Behavior AS OF 2013 There
More informationORIGINAL CONTRIBUTION. The Progression of Cognition, Psychiatric Symptoms, and Functional Abilities in Dementia With Lewy Bodies and Alzheimer Disease
ORIGINAL CONTRIBUTION The Progression of Cognition, Psychiatric Symptoms, and Functional Abilities in Dementia With Lewy Bodies and Alzheimer Disease Karina Stavitsky, BS; Adam M. Brickman, PhD; Nikolaos
More informationAmyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative
ORIGINAL RESEARCH E. Matsusue S. Sugihara S. Fujii T. Kinoshita T. Nakano E. Ohama T. Ogawa Cerebral Cortical and White Matter Lesions in Amyotrophic Lateral Sclerosis with Dementia: Correlation with MR
More informationORIGINAL ARTICLE. Early and Widespread Cholinergic Losses Differentiate Dementia With Lewy Bodies From Alzheimer Disease
ORIGINAL ARTICLE Early and Widespread Cholinergic Losses Differentiate Dementia With Lewy Bodies From Alzheimer Disease Pietro Tiraboschi, MD; Larry A. Hansen, MD; Michael Alford, BA; Annette Merdes, MD;
More informationWhat APS Workers Need to Know about Frontotemporal, Lewy Body and Vascular Dementias
What APS Workers Need to Know about Frontotemporal, Lewy Body and Vascular Dementias Presenter: Kim Bailey, MS Gerontology, Program & Education Specialist, Alzheimer s Orange County 1 1 Facts About Our
More informationPatterns of Cognitive Impairment in Dementia
Patterns of Cognitive Impairment in Dementia Lindsay R. Clark, PhD Assistant professor (CHS) Department of Medicine - Division of Geriatrics & Gerontology UW-Madison School of Medicine & Public Health
More informationRole of TDP-43 in Non-Alzheimer s and Alzheimer s Neurodegenerative Diseases
Role of TDP-43 in Non-Alzheimer s and Alzheimer s Neurodegenerative Diseases Keith A. Josephs, MD, MST, MSc Professor of Neurology 13th Annual Mild Cognitive Impairment (MCI) Symposium: Alzheimer and Non-Alzheimer
More informationCASE 49. What type of memory is available for conscious retrieval? Which part of the brain stores semantic (factual) memories?
CASE 49 A 43-year-old woman is brought to her primary care physician by her family because of concerns about her forgetfulness. The patient has a history of Down syndrome but no other medical problems.
More informationCOGNITIVE IMPAIRMENT IN PARKINSON S DISEASE
1 GENERAL INTRODUCTION GENERAL INTRODUCTION PARKINSON S DISEASE Parkinson s disease (PD) is a neurodegenerative movement disorder, named after James Parkinson who described some of its characteristic
More informationDementia. Aetiology, pathophysiology and the role of neuropsychological testing. Dr Sheng Ling Low Geriatrician
Dementia Aetiology, pathophysiology and the role of neuropsychological testing Dr Sheng Ling Low Geriatrician Topics to cover Why is dementia important What is dementia Differentiate between dementia,
More informationDLB is recognized as the second major form of dementia
ORIGINAL RESEARCH R. Takahashi K. Ishii N. Miyamoto T. Yoshikawa K. Shimada S. Ohkawa T. Kakigi K. Yokoyama Measurement of Gray and White Matter Atrophy in Dementia with Lewy Bodies Using Diffeomorphic
More informationParkinson e decadimento cognitivo. Stelvio Sestini
Parkinson e decadimento cognitivo Stelvio Sestini Patients with PD can develop a spectrum of cognitive symptoms Heterogeneity of cognitive deficits The cognitive symptoms can evolve to dementia (Mov Disorder
More informationFTD basics! Etienne de Villers-Sidani, MD!
FTD basics! Etienne de Villers-Sidani, MD! Frontotemporal lobar degeneration (FTLD) comprises 3 clinical syndromes! Frontotemporal dementia (behavioral variant FTD)! Semantic dementia (temporal variant
More informationFact Sheet Alzheimer s disease
What is Alzheimer s disease Fact Sheet Alzheimer s disease Alzheimer s disease, AD, is a progressive brain disorder that gradually destroys a person s memory and ability to learn, reason, make judgements,
More informationAlzheimer's disease (AD), also known as Senile Dementia of the Alzheimer Type (SDAT) or simply Alzheimer s is the most common form of dementia.
CHAPTER 3 Alzheimer's disease (AD), also known as Senile Dementia of the Alzheimer Type (SDAT) or simply Alzheimer s is the most common form of dementia. This incurable, degenerative, terminal disease
More informationAssessment at the bedside or in the clinic using the history, examination and laboratory tests to distinguish between different types of dementia
Assessment at the bedside or in the clinic using the history, examination and laboratory tests to distinguish between different types of dementia AP Passmore Content Common dementia syndromes (older people)
More informationUse a diagnostic neuropsychology HOW TO DO IT PRACTICAL NEUROLOGY
170 PRACTICAL NEUROLOGY HOW TO DO IT Pract Neurol: first published as 10.1046/j.1474-7766.2003.08148.x on 1 June 2003. Downloaded from http://pn.bmj.com/ Use a diagnostic neuropsychology on 16 October
More informationORIGINAL CONTRIBUTION. An Investigation of Clinical Correlates of Lewy Bodies in Autopsy-Proven Alzheimer Disease
ORIGINAL CONTRIBUTION An Investigation of Clinical Correlates of Lewy Bodies in Autopsy-Proven Alzheimer Disease Yaakov Stern, PhD; Diane Jacobs, PhD; James Goldman, MD; Estrella Gomez-Tortosa, PhD; Bradley
More informationDiagnosis and Treatment of Alzhiemer s Disease
Diagnosis and Treatment of Alzhiemer s Disease Roy Yaari, MD, MAS Director, Memory Disorders Clinic, Banner Alzheimer s Institute 602-839-6900 Outline Introduction Alzheimer s disease (AD)Guidelines -revised
More informationClinical Diagnosis. Step 1: Dementia or not? Diagnostic criteria for dementia (DSM-IV)
Step 1: Dementia or not? Diagnostic criteria for dementia (DSM-IV) A. The development of multiple cognitive deficits manifested by both 1 and 2 1 1. Memory impairment 2. One (or more) of the following
More informationMentis Cura November
Mentis Cura November 29 2012 www.mentiscura.com New Facts on Alzheimer s Death rank nr. 2-5 in western countries Fastest growing disease in: Cost Incedence Death rate People with Alzheimer s 2012 36 million
More informationUniversity of Groningen. Visual hallucinations in Parkinson's disease Meppelink, Anne Marthe
University of Groningen Visual hallucinations in Parkinson's disease Meppelink, Anne Marthe IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite from
More informationQuantitative analysis for a cube copying test
86 99 103 2010 Original Paper Quantitative analysis for a cube copying test Ichiro Shimoyama 1), Yumi Asano 2), Atsushi Murata 2) Naokatsu Saeki 3) and Ryohei Shimizu 4) Received September 29, 2009, Accepted
More informationImaging of Alzheimer s Disease: State of the Art
July 2015 Imaging of Alzheimer s Disease: State of the Art Neir Eshel, Harvard Medical School Year IV Outline Our patient Definition of dementia Alzheimer s disease Epidemiology Diagnosis Stages of progression
More informationDementia with Lewy Bodies. A Distinct Non-Alzheimer Dementia Syndrome?
Brain Pathology 8: 299-324(1998) Dementia with Lewy Bodies. A Distinct Non-Alzheimer Dementia Syndrome? Paul G. Ince 1, 2, Elaine K. Perry 1, Chris. M. Morris 1 MRC Neurochemical Pathology Unit 1, University
More informationThe Frontal Lobes. Anatomy of the Frontal Lobes. Anatomy of the Frontal Lobes 3/2/2011. Portrait: Losing Frontal-Lobe Functions. Readings: KW Ch.
The Frontal Lobes Readings: KW Ch. 16 Portrait: Losing Frontal-Lobe Functions E.L. Highly organized college professor Became disorganized, showed little emotion, and began to miss deadlines Scores on intelligence
More informationAn old man with hallucination
An old man with hallucination Inter-hospital Geriatric Meeting 30 March 2012 Speaker: Dr Siu Chun Yue Chairman: Dr Leung Chi Shing Caritas Medical Center History Admission 4/2011 75/M Premorbid: ADLI,
More informationEARLY ONSET FRONTOTERMPORAL DEMENTIA AND ALZHEIMERS DISEASE: DIAGNOSIS, TREATMENT AND CARE
EARLY ONSET FRONTOTERMPORAL DEMENTIA AND ALZHEIMERS DISEASE: DIAGNOSIS, TREATMENT AND CARE John Rudge, BA Hons This thesis is presented as partial requirement for the degree of Doctor of Psychology at
More informationDementia and Delirium: A Neurologist s Approach to Altered Mental Status. Case 1 4/7/11. Which of the following evaluations is your next step?
Dementia and Delirium: A Neurologist s Approach to Altered Mental Status S. Andrew Josephson, MD Director, Neurohospitalist Program Medical Director, Inpatient Neurology University of California San Francisco
More informationAlzheimer s disease dementia: a neuropsychological approach
Alzheimer s disease dementia: a neuropsychological approach Dr. Roberta Biundo, PhD Neuropsychology Coordinator at Parkinson s disease and movement disorders unit of San Camillo rehabilitation hospital
More informationOverview of neurological changes in Alzheimer s disease. Eric Karran
Overview of neurological changes in Alzheimer s disease Eric Karran Alzheimer s disease Alois Alzheimer 1864-1915 Auguste D. 1850-1906 Case presented November 26 th 1906 Guildford Talk.ppt 20 th March,
More informationClinical Features and Treatment of Parkinson s Disease
Clinical Features and Treatment of Parkinson s Disease Richard Camicioli, MD, FRCPC Cognitive and Movement Disorders Department of Medicine University of Alberta 1 Objectives To review the diagnosis and
More informationDelirium, Dementia, and Amnestic Disorders. Dr.Al-Azzam 1
Delirium, Dementia, and Amnestic Disorders Dr.Al-Azzam 1 Introduction Disorders in which a clinically significant deficit in cognition or memory exists The number of people with these disorders is growing
More informationThe current state of healthcare for Normal Aging, Mild Cognitive Impairment, & Alzheimer s Disease
The current state of healthcare for Normal Aging, g, Mild Cognitive Impairment, & Alzheimer s Disease William Rodman Shankle, MS MD FACP Director, Alzheimer s Program, Hoag Neurosciences Institute Neurologist,
More informationThe Spectrum of Age-Associated Astroglial Tauopathies. Dennis W. Dickson MD Department of Neuroscience Mayo Clinic, Jacksonville, FL
The Spectrum of Age-Associated Astroglial Tauopathies Dennis W. Dickson MD Mayo Clinic, Jacksonville, FL Thorn-shaped astrocytes TSA were first reported by Ikeda (1995), as tau-positive astrocytes in various
More informationPiano playing skills in a patient with frontotemporal dementia: A longitudinal case study
International Symposium on Performance Science ISBN 978-94-90306-01-4 The Author 2009, Published by the AEC All rights reserved Piano playing skills in a patient with frontotemporal dementia: A longitudinal
More informationPerception, attention, and working memory are disproportionately impaired in dementia with Lewy bodies compared with Alzheimer s disease
J Neurol Neurosurg Psychiatry 21;7:157 164 157 University Department of Psychiatry, Addenbrooke s Hospital, Cambridge CB2 2QQ, UK J Calderon G E Berrios University Department of Neurology RJPerry J R Hodges
More informationCognitive-Motor Interference in Persons with Parkinson Disease
Cognitive-Motor Interference in Persons with Parkinson Disease Tara L. McIsaac, PhD, PT Associate Professor of Physical Therapy A.T. Still University Arizona School of Health Sciences October 11, 2014
More informationDementia. Amber Eker, MD. Assistant Professor Near East University Department of Neurology
Dementia Amber Eker, MD Assistant Professor Near East University Department of Neurology Dementia An acquired syndrome consisting of a decline in memory and other cognitive functions Impairment in social
More information