A kinematic study of progressive apraxia with and without dementia
1999; Wiley; Volume: 14; Issue: 2 Linguagem: Inglês
10.1002/1531-8257(199903)14
ISSN1531-8257
AutoresRichard J. Caselli, George E. Stelmach, John N. Caviness, Dagmar Timmann, Todd Royer, Bradley F. Boeve, Joseph E. Parisi,
Tópico(s)Neurobiology of Language and Bilingualism
ResumoMovement DisordersVolume 14, Issue 2 p. 276-287 Article A kinematic study of progressive apraxia with and without dementia Richard J. Caselli MD, Corresponding Author Richard J. Caselli MD Department of Neurology, Mayo Clinic, Scottsdale, Arizona, U.S.A.Department of Neurology, Mayo Clinic, 13400 E. Shea Blvd., Scottsdale, AZ 85259, U.S.A.Search for more papers by this authorGeorge E. Stelmach PhD, George E. Stelmach PhD Motor Control Laboratory, Arizona State University, Tempe, Arizona, U.S.A.Search for more papers by this authorJohn N. Caviness MD, John N. Caviness MD Department of Neurology, Mayo Clinic, Scottsdale, Arizona, U.S.A.Search for more papers by this authorDagmar Timmann MD, Dagmar Timmann MD Department of Neurology, University of Essen, GermanySearch for more papers by this authorTodd Royer BS, Todd Royer BS Motor Control Laboratory, Arizona State University, Tempe, Arizona, U.S.A.Search for more papers by this authorBradley F. Boeve MD, Bradley F. Boeve MD Department of Neurology, Mayo Clinic, Scottsdale, Arizona, U.S.A.Search for more papers by this authorJoseph E. Parisi MD, Joseph E. Parisi MD Department of Pathology, Mayo Clinic, Rochester, Minnesota, U.S.A.Search for more papers by this author Richard J. Caselli MD, Corresponding Author Richard J. Caselli MD Department of Neurology, Mayo Clinic, Scottsdale, Arizona, U.S.A.Department of Neurology, Mayo Clinic, 13400 E. Shea Blvd., Scottsdale, AZ 85259, U.S.A.Search for more papers by this authorGeorge E. Stelmach PhD, George E. Stelmach PhD Motor Control Laboratory, Arizona State University, Tempe, Arizona, U.S.A.Search for more papers by this authorJohn N. Caviness MD, John N. Caviness MD Department of Neurology, Mayo Clinic, Scottsdale, Arizona, U.S.A.Search for more papers by this authorDagmar Timmann MD, Dagmar Timmann MD Department of Neurology, University of Essen, GermanySearch for more papers by this authorTodd Royer BS, Todd Royer BS Motor Control Laboratory, Arizona State University, Tempe, Arizona, U.S.A.Search for more papers by this authorBradley F. Boeve MD, Bradley F. Boeve MD Department of Neurology, Mayo Clinic, Scottsdale, Arizona, U.S.A.Search for more papers by this authorJoseph E. Parisi MD, Joseph E. Parisi MD Department of Pathology, Mayo Clinic, Rochester, Minnesota, U.S.A.Search for more papers by this author First published: 17 January 2001 https://doi.org/10.1002/1531-8257(199903)14:2 3.0.CO;2-UCitations: 11AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Abstract BACKGROUND Prehension is an ideationally simple, cued Movement requiring proximal (transport) and distal (manipulation) limb control. Patients with this syndrome of progressive apraxia are unable to perform many activities of daily living that require prehension. There is little known about how this syndrome kinematically disrupts such movements or whether concurrent dementia might play a critical role. OBJECTIVES Using prehension as a paradigm for an ideationally simple, cued functional movement, we sought to (1) characterize the kinematic features of progressive apraxia in general, and (2) contrast the kinematic differences between apraxic patients with and without dementia. METHODS Eight patients with the syndrome of progressive apraxia (including five without dementia, one of whom had autopsy-confirmed corticobasal ganglionic degeneration, and three with dementia, one of whom had autopsy-confirmed Alzheimer's disease) were compared with eight age-matched normal control subjects on a prehension task using an Optotrak camera system. RESULTS Compared with control subjects, apraxic subjects had slowed reaction time, slowed transport and manipulation kinematics, greater lateral deviation from the linear prehension trajectory, greater intermanual asymmetry, motor programming disturbances, and mild transport-manipulation uncoupling. There were minor differences between the apraxia subgroups such as greater intermanual differences and impaired grip aperture velocity in the nondemented group, and overall slower movement in the demented group. CONCLUSIONS There are major kinematic differences between apraxic and control subjects on a prehension task. The differences between clinical-pathologic subgroups are more subtle, and the movement disorder itself rather than concurrent dementia is the greatest determinant of motor disability. REFERENCES 1Caselli RJ, Jack CR Jr, Petersen RC, Wahner HW, Yanagihara T. Asymmetric cortical degenerative syndromes: clinical and radiologic correlations. Neurology 1992; 42: 1462– 1468. 2Caselli RJ, Jack CR Jr. Asymmetrical cortical degeneration syndromes: a proposed clinical classification. Arch Neurol 1992; 49: 770– 780. 3Caselli RJ. Focal and asymmetric cortical degeneration syndromes. Neurologist 1995; 1: 1– 19. 4Caselli RJ, Reiman EM, Timmann D, et al. Progressive apraxia in clinically discordant monozygotic twins. Arch Neurol 1995; 52: 1004– 1010. 5Leiguarda R, Lees AJ, Merello M, Starkstein S, Marsden CD. The nature of apraxia in corticobasal degeneration. J Neurol Neurosurg Psychiatry 1994; 57: 455– 459. 6Gibb WRG, Luthert PJ, Marsden CD. Corticobasal degeneration. Brain 1989; 112: 1171– 1192. 7Riley DE, Lang AE, Lewis A, et al. Cortical-basal ganglionic degeneration. Neurology 1990; 40: 1203– 1212. 8Lippa CF, Smith TW, Fontneau N. Corticonigral degeneration with neuronal achromasia: a clinicopathologic study of two cases. J Neurol Sci 1990; 98: 301– 310. 9Sawle GV, Brooks DJ, Marsden CD, Frackowiak RSJ. Corticobasal degeneration. Brain 1991; 114: 541– 556. 10Jagust WJ, Davies P, Tiller-Borcich JK, Reed BR. Focal Alzheimer's disease. Neurology 1990; 40: 14– 19. 11Eberhard D, Lopes M, Trugman J, Brashear H. Alzheimer's disease in a case of corticobasal ganglionic degeneration with severe dementia. J Neurol Neurosurg Psychiatry 1996; 60: 109– 110. 12Boeve BF, Maraganore DM, Parisi JE, et al. Disorders mimicking the 'classical' clinical syndrome of cortico-basal ganglionic degeneration: report of nine cases [Abstract]. Mov Disord 1996; 11: 351. 13Pillon B, Blin J, Vidailhet M, et al. The neuropsychological pattern of corticobasal degeneration: comparison with progressive supranuclear palsy and Alzheimer's disease. Neurology 1995; 45: 1477– 1483. 14Massman P, Kreiter K, Jankovic J, Doody R. Neuropsychological functioning in cortico-basal ganglionic degeneration: differentiation from Alzheimer's disease. Neurology 1996; 46: 720– 726. 15Jeannerod M. The Neural and Behavioural Organization of Goal Directed Movements. Oxford: Clarendon Press, 1988. 16Marteniuk RG, Leavitt JL, MacKenzie CL, Athenes S. Functional relationships between grasp and transport components in a prehension task. Human Movement Science 1990; 9: 149– 176. 17Jeannerod M. Mechanism of visuomotor coordination: a study in normal and brain damaged subjects. Neuropsychologia 1986; 24: 41– 78. 18Damasio AR, Benton AL. Impairment of hand movements under visual guidance. Neurology 1979; 29: 170– 178. 19Jeannerod M, Michel F, Prablanc C. The control of hand movements in a case of hemianesthesia following a parietal lesion. Brain 1984; 107: 899– 920. 20Kokmen E, Naessens JM, Offord KP. A short test of mental status: description and preliminary results. Mayo Clin Proc 1987; 62: 281– 288. 21Lezak MD. Neuropsychological Assessment, 2nd ed. New York, NY: Oxford University Press, 1983. 22McKhann G, Drachman D, Folstein M, Katzman R, Price D, Stadlan E. 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 1984; 34: 939– 944. 23Kertesz A. Western Aphasia Battery. New York, NY: Grune and Stratton, 1982. 24Jeannerod M. The formation of finger grip during prehension, a cortically mediated visuomotor pattern. Behav Brain Res 1986; 19: 99– 116. 25Clark MA, Merians AS, Kothari A, et al. Spatial planning deficits in limb apraxia. Brain 1994; 117: 1093– 1106. 26Rapscak SZ, Ochipa C, Anderson KC, Poizner H. Progressive ideomotor apraxia: evidence for a selective impairment of the action production system. Brain Cogn 1995; 27: 213– 236. 27Denes G, Mantovan MC, Gallana A, Cappelletti JY. Limb-kinetic apraxia. Mov Disord 1998; 13: 468– 476. 28Poizner H, Mack L, Verfaellie M, Rothi LJG, Heilman KM. Three dimensional computer graphic analysis of apraxia: neural representations of learned movement. Brain 1990; 113: 85– 101. 29Alberts JL, Tresilian JR, Stelmach GE. The coordination and phasing of a bilateral prehension task: the influence of Parkinson's disease. Brain 1998; 121: 725– 742. 30Tresilian JR, Stelmach GE, Adler CH. Stability of reach-to-grasp movement patterns in Parkinson's disease. Brain 1997; 120: 2093– 2111. 31Binkofski F, Dohle C, Posse S, et al. Human anterior intraparietal area subserve prehension: a combined lesion and functional MRI activation study. Neurology 1998; 50: 1253– 1259. 32Cambier J, Masson M, Dairou R, Henin D. Etude anatomo-clinique d'une forme parietale de maladie de Pick. Rev Neurol 1981; 137: 33– 38. 33Lang A, Bergeron C, Pollanen M, Ashby P. Parietal Pick's disease mimicking cortical-basal ganglionic degeneration. Neurology 1994; 44: 1436– 1440. 34Gibb W, Luthert P, Marsden CD. Clinical and pathological features of corticobasal degeneration. Adv Neurol 1990; 53: 51– 54. Citing Literature Volume14, Issue2March 1999Pages 276-287 ReferencesRelatedInformation
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