全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

Different Apathy Profile in Behavioral Variant of Frontotemporal Dementia and Alzheimer's Disease: A Preliminary Investigation

DOI: 10.1155/2012/719250

Full-Text   Cite this paper   Add to My Lib

Abstract:

Apathy is one of the most common behavioral symptoms of dementia; it is one of the salient features of behavioral variant of frontotemporal dementia (bvFTD) but is also very frequent in Alzheimer's disease. This preliminary investigation was aimed at assessing the type of apathy-related symptoms in a population of bvFTD and AD subjects showing comparable apathy severity. Each patient underwent a comprehensive neuropsychological assessment; behavioral changes were investigated by the neuropsychiatric inventory (NPI), using the NPI-apathy subscale to detect apathetic symptoms. At univariate analysis, bvFTD subjects showed lack of initiation ( , ), reduced emotional output ( , ), and reduced interest toward friends and family members ( , ), more frequently than AD subjects. BvFTD displayed higher scores than AD on NPI total score ( ) and on subscales assessing agitation ( ), disinhibition ( ) and sleep disturbances ( ); conversely, AD subjects were more impaired on memory, constructional abilities, and attention. On multivariate logistic regression, reduced emotional output was highly predictive of bvFTD ( ; ). Our preliminary findings support the hypothesis that apathy is a complex phenomenon, whose clinical expression is conditioned by the site of anatomical damage. Furthermore, apathy profile may help in differentiating bvFTD from AD. 1. Introduction Apathy has been repeatedly reported to be one of the most common noncognitive symptoms of dementia [1–3]. Frequency and severity of apathy vary across different dementia subtypes; it is the most common behavioral symptom of behavioral variant of frontotemporal dementia (bvFTD), with reported prevalence ranging from 62 to 89% of patients [4]; the prevalence of apathy in AD ranges from 25 to 88% [5, 6] with a trend to increase with disease severity [7]. When severity was directly compared, higher levels of apathy have been reported in bvFTD than in AD [8–11]. The functional and neuroanatomical substrates of apathy seem to differ between AD and bvFTD. In bvFTD, apathy severity has been associated with orbitofrontal abnormalities, both in MRI [12] and PET [13] studies, and with volume loss in the dorsal anterior cingulate and dorsolateral prefrontal cortex [14]. On the other hand, in AD apathy severity has been connected to neurofibrillary tangles density in the anterior cingulate gyrus [15] and to grey matter atrophy in the anterior cingulate and in the left medial frontal cortex [16]. These findings were confirmed by a PET study showing the association of apathy with hypometabolism in the bilateral anterior

References

[1]  S. Srikanth, A. V. Nagaraja, and E. Ratnavalli, “Neuropsychiatric symptoms in dementia-frequency, relationship to dementia severity and comparison in Alzheimer's disease, vascular dementia and frontotemporal dementia,” Journal of the Neurological Sciences, vol. 236, no. 1-2, pp. 43–48, 2005.
[2]  J. C. Chen, S. Borson, and J. M. Scanlan, “Stage-specific prevalence of behavioral symptoms in Alzheimer's disease in a multi-ethnic community sample,” American Journal of Geriatric Psychiatry, vol. 8, no. 2, pp. 123–133, 2000.
[3]  M. S. Mega, J. L. Cummings, T. Fiorello, and J. Gornbein, “The spectrum of behavioral changes in Alzheimer's disease,” Neurology, vol. 46, no. 1, pp. 130–135, 1996.
[4]  M. F. Mendez, E. C. Lauterbach, and S. M. Sampson, “An evidence-based review of the psychopathology of frontotemporal dementia: a report of the ANPA Committee on Research,” Journal of Neuropsychiatry and Clinical Neurosciences, vol. 20, no. 2, pp. 130–149, 2008.
[5]  T. N. Chase, “Apathy in neuropsychiatric disease: diagnosis, pathophysiology, and treatment,” Neurotoxicity Research, vol. 19, no. 2, pp. 266–278, 2011.
[6]  A. M. Landes, S. D. Sperry, and M. E. Strauss, “Prevalence of apathy, dysphoria, and depression in relation to dementia severity in Alzheimer's disease,” Journal of Neuropsychiatry and Clinical Neurosciences, vol. 17, no. 3, pp. 342–349, 2005.
[7]  S. E. Starkstein, R. Jorge, R. Mizrahi, and R. G. Robinson, “A prospective longitudinal study of apathy in Alzheimer’s disease,” Journal of Neurology, Neurosurgery & Psychiatry, vol. 77, no. 1, pp. 8–11, 2006.
[8]  T. W. Chow, M. A. Binns, J. L. Cummings et al., “Apathy symptom profile and behavioral associations in frontotemporal dementia vs dementia of Alzheimer type,” Archives of Neurology, vol. 66, no. 7, pp. 888–893, 2009.
[9]  M. L. Levy, B. L. Miller, J. L. Cummings, L. A. Fairbanks, and A. Craig, “Alzheimer disease and frontotemporal dementias: behavioral distinctions,” Archives of Neurology, vol. 53, no. 7, pp. 687–690, 1996.
[10]  C. Marra, D. Quaranta, M. Zinno et al., “Clusters of cognitive and behavioral disorders clearly distinguish primary progressive aphasia from frontal lobe dementia, and Alzheimer's disease,” Dementia and Geriatric Cognitive Disorders, vol. 24, no. 5, pp. 317–326, 2007.
[11]  L. Rozzini, G. Lussignoli, A. Padovani, A. Bianchetti, and M. Trabucchi, “Alzheimer disease and frontotemporal dementia,” Archives of Neurology, vol. 54, no. 4, p. 350, 1997.
[12]  G. Zamboni, E. D. Huey, F. Krueger, P. F. Nichelli, and J. Grafman, “Apathy and disinhibition in frontotemporal dementia: insights into their neural correlates,” Neurology, vol. 71, no. 10, pp. 736–742, 2008.
[13]  F. Peters, D. Perani, K. Herholz et al., “Orbitofrontal dysfunction related to both apathy and disinhibition in frontotemporal dementia,” Dementia and Geriatric Cognitive Disorders, vol. 21, no. 5-6, pp. 373–379, 2006.
[14]  L. Massimo, C. Powers, P. Moore et al., “Neuroanatomy of apathy and disinhibition in frontotemporal lobar degeneration,” Dementia and Geriatric Cognitive Disorders, vol. 27, no. 1, pp. 96–104, 2009.
[15]  G. A. Marshall, L. A. Fairbanks, S. Tekin, H. V. Vinters, and J. L. Cummings, “Neuropathologic correlates of apathy in Alzheimer's disease,” Dementia and Geriatric Cognitive Disorders, vol. 21, no. 3, pp. 144–147, 2006.
[16]  L. G. Apostolova, G. G. Akopyan, N. Partiali et al., “Structural correlates of apathy in Alzheimer's disease,” Dementia and Geriatric Cognitive Disorders, vol. 24, no. 2, pp. 91–97, 2007.
[17]  G. A. Marshall, L. Monserratt, D. Harwood, M. Mandelkern, J. L. Cummings, and D. L. Sultzer, “Positron emission tomography metabolic correlates of apathy in Alzheimer disease,” Archives of Neurology, vol. 64, no. 7, pp. 1015–1020, 2007.
[18]  R. S. Marin, “Apathy: a neuropsychiatric syndrome,” Journal of Neuropsychiatry and Clinical Neurosciences, vol. 3, no. 3, pp. 243–254, 1991.
[19]  R. S. Marin, “Differential diagnosis and classification of apathy,” American Journal of Psychiatry, vol. 147, no. 1, pp. 22–30, 1990.
[20]  R. S. Marin, “Apathy: Concept, Syndrome, Neural Mechanisms, and Treatment,” Seminars in Clinical Neuropsychiatry, vol. 1, no. 4, pp. 304–314, 1996.
[21]  R. Levy and B. Dubois, “Apathy and the functional anatomy of the prefrontal cortex-basal ganglia circuits,” Cerebral Cortex, vol. 16, no. 7, pp. 916–928, 2006.
[22]  R. G. Brown and G. Pluck, “Negative symptoms: The 'pathology' of motivation and goal-directed behaviour,” Trends in Neurosciences, vol. 23, no. 9, pp. 412–417, 2000.
[23]  G. E. Alexander, M. R. DeLong, and P. L. Strick, “Parallel organization of functionally segregated circuits linking basal ganglia and cortex,” Annual Review of Neuroscience, vol. 9, pp. 357–381, 1986.
[24]  F. A. Middleton and P. L. Strick, “Basal-ganglia 'projections' to the prefrontal cortex of the primate,” Cerebral Cortex, vol. 12, no. 9, pp. 926–935, 2002.
[25]  D. Neary, J. S. Snowden, L. Gustafson et al., “Frontotemporal lobar degeneration: a consensus on clinical diagnostic criteria,” Neurology, vol. 51, no. 6, pp. 1546–1554, 1998.
[26]  G. McKhann, D. Drachman, M. Folstein, R. Katzman, D. Price, and E. M. Stadlan, “Clinical diagnosis of Alzheimer's disease: Report of the NINCDS‐ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease,” Neurology, vol. 34, no. 7, pp. 939–944, 1984.
[27]  M. F. Folstein, S. E. Folstein, and P. R. McHugh, “Mini-mental state. A practical method for grading the cognitive state of patients for the clinician,” Journal of Psychiatric Research, vol. 12, no. 3, pp. 189–198, 1975.
[28]  J. C. Morris, “Clinical dementia rating: a reliable and valid diagnostic and staging measure for dementia of the Alzheimer type,” International Psychogeriatrics, vol. 9, supplement 1, pp. 173–178, 1997.
[29]  G. A. Carlesimo, C. Caltagirone, and G. Gainotti, “The Mental Deterioration Battery: normative data, diagnostic reliability and qualitative analyses of cognitive impairment. The Group for the Standardization of the Mental Deterioration Battery,” European Neurology, vol. 36, no. 6, pp. 378–384, 1996.
[30]  P. Caffarra, G. Vezzadini, F. Dieci, F. Zonato, and A. Venneri, “Rey-Osterrieth complex figure: normative values in an Italian population sample,” Neurological Sciences, vol. 22, no. 6, pp. 443–447, 2002.
[31]  P. Caffarra, G. Vezzadini, F. Dieci, and A. Venneri, “Una versione abbreviata del test di Stroop: dati normativi nella popolazione italiana,” Nuova Rivista di Neurologia, vol. 12, pp. 111–115, 2002.
[32]  I. Appollonio, M. Leone, V. Isella et al., “The frontal assessment battery (FAB): normative values in an Italian population sample,” Neurological Sciences, vol. 26, no. 2, pp. 108–116, 2005.
[33]  C. Marra, G. Gainotti, E. Scaricamazza, C. Piccininni, M. Ferraccioli, and D. Quaranta, “The Multiple Features Target Cancellation (MFTC): an attentional visual conjunction search test. Normative values for the Italian population,” Neurological Sciences. In press.
[34]  G. Gainotti, G. Miceli, and C. Caltagirone, “Constructional apraxia in left brain damaged patients: a planning disorder?” Cortex, vol. 13, no. 2, pp. 109–118, 1977.
[35]  J. L. Cummings, “The Neuropsychiatric Inventory: assessing psychopathology in dementia patients,” Neurology, vol. 48, no. 5, pp. S10–S16, 1997.
[36]  D. E. Clarke, J. Y. Ko, E. A. Kuhl, R. van Reekum, R. Salvador, and R. S. Marin, “Are the available apathy measures reliable and valid? A review of the psychometric evidence,” Journal of Psychosomatic Research, vol. 70, no. 1, pp. 73–97, 2011.
[37]  D. W. Hosmer and S. Lemeshow, Applied Logistic Regression, John Wiley and Sons, New York, NY, USA, 2000.
[38]  M. Sollberger, C. M. Stanley, S. M. Wilson et al., “Neural basis of interpersonal traits in neurodegenerative diseases,” Neuropsychologia, vol. 47, no. 13, pp. 2812–2827, 2009.
[39]  J. Moll, R. Zahn, R. de Oliveira-Souza et al., “Impairment of prosocial sentiments is associated with frontopolar and septal damage in frontotemporal dementia,” NeuroImage, vol. 54, no. 2, pp. 1735–1742, 2011.
[40]  L. G. Apostolova and J. L. Cummings, “Neuropsychiatric manifestations in mild cognitive impairment: a systematic review of the literature,” Dementia and Geriatric Cognitive Disorders, vol. 25, no. 2, pp. 115–126, 2008.
[41]  K. Rascovsky, D. P. Salmon, G. J. Ho et al., “Cognitive profiles differ in autopsy-confirmed frontotemporal dementia and AD,” Neurology, vol. 58, no. 12, pp. 1801–1808, 2002.

Full-Text

comments powered by Disqus

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133

WeChat 1538708413