Effects of levodopa on cognitive functioning in moderate-to-severe Parkinson’s disease (MSPD)

Comprehensive Epilepsy, New York University Medical Center, New York, NY 10016, USA.
Journal of Neural Transmission (Impact Factor: 2.4). 11/2004; 111(10-11):1333-41. DOI: 10.1007/s00702-004-0145-8
Source: PubMed


Although improved cognition has been reported in patients with mild Parkinson's disease (PD) following the administration of levodopa, mixed results have been found in moderately-to-severely affected PD patients (MSPD), particularly in studies conducted since 1980. In the present study, 16 MSPD patients were tested on separate days, once following overnight levodopa withdrawal and once while optimally treated. A battery of neuropsychological tests that assess a range of cognitive functions (i.e., attention, language, visuospatial, memory, and executive), as well as a measure of depression, were used. Although patients performed better on a measure of confrontation naming in the untreated than in the treated condition, there were no significant differences for any of the other cognitive variables or for the depression scale variable. Thus, these data suggest that there are generally no adverse or beneficial effects of levodopa therapy on cognition in MSPD patients.

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    • "Although PD also involves degeneration of many other brainstem projection nuclei (Scatton et al., 1983; Del Tredici et al., 2002; Jellinger, 2011) such as serotonin and norepinephrine (McCormick et al., 1985), the role of these systems in executive dysfunction and perceptual timing deficits is unclear. However, because levodopa does not reliably treat PD-related cognitive symptoms (Cools et al., 2001, 2002; Morrison et al., 2004; Pascual- Sedano et al., 2008 "
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    ABSTRACT: Patients with Parkinson's disease (PD) have deficits in perceptual timing, or the perception and estimation of time. PD patients can also have cognitive symptoms, including deficits in executive functions such as working memory, planning, and visuospatial attention. Here, we discuss how PD-related cognitive symptoms contribute to timing deficits. Timing is influenced by signaling of the neurotransmitter dopamine in the striatum. Timing also involves the frontal cortex, which is dysfunctional in PD. Frontal cortex impairments in PD may influence memory subsystems as well as decision processes during timing tasks. These data suggest that timing may be a type of executive function. As such, timing can be used to study the neural circuitry of cognitive symptoms of PD as they can be studied in animal models. Performance of timing tasks also maybe a useful clinical biomarker of frontal as well as striatal dysfunction in PD.
    Frontiers in Integrative Neuroscience 10/2013; 7:75. DOI:10.3389/fnint.2013.00075
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    • "The studies that lend support to this model are indicated by identification codes (see below) and their results (i.e., differences, lack of differences, and correlations) are represented by gray lines with their extreme points corresponding to compared samples. Identification codes: Caviness et al. (2007) (1), Cools et al. (1984) (2a, 2b), Cooper et al. (1991) (3a, 3b, 3c, 3d), Delaveau et al. (2005) (4), de Vries et al. (2010) (5), Fama and Sullivan (2002) (6a, 6b, 6c), Floel et al. (2005) (7), Floel et al. (2008) (8), Girotti et al. (1986) (9a, 9b, 9c, 9d), Growdon et al. (1998) (10a, 10b), Hasbroucq et al. (2003) (11), Morrison et al. (2004) (12), Mortimer et al. (1982) (13), Muslimovic et al. (2007) (14a, 14b, 14c, 14d, 14e, 14f, 14g, 14h), Pavão et al. (unpublished) (15a, 15b, 15c), Sabbe et al. (2004) (16), Seo et al. (2010) (17a, 17b, 17c), Stocchi et al. (2005) (18), Vandenbossche et al. (2009) (19a, 19b, 19c), Verbaan et al. (2007) (20a, 20b), Wilkinson and Jahanshahi (2007) (21a, 21b; see Table S1 in Supplementary Material for a summary of the original data). "
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    ABSTRACT: Parkinson's disease (PD) symptoms have been collectively ascribed to malfunctioning of dopamine-related nigro-striatal and cortico-striatal loops. However, some doubts about this proposition are raised by controversies about the temporal progression of the impairments, and whether they are concomitant or not. The present study consists of a systematic revision of literature data on both functional PD impairments and dopaminergic medication effects in order to draw a coherent picture about the disease progression. It was done in terms of an explanatory model for the disruption of implicit knowledge acquisition, motor and cognitive impairments, and the effects of dopaminergic medication on these functions. Cognitive impairments arise at early stages of PD and stabilizes while disruption of implicit knowledge acquisition and motor impairments, are still in progression; additionally, dopaminergic medication reduces motor impairments and increases disruption of implicit knowledge acquisition. Since this model revealed consistency and plausibility when confronted with data of others studies not included in model's formulation, it may turn out to be a useful tool for understanding the multifaceted characteristics of PD.
    Frontiers in Integrative Neuroscience 08/2012; 6:56. DOI:10.3389/fnint.2012.00056
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    • "Reports in the literature on the eVects of levodopa on cognitive function are inconsistent, perhaps in part because individual variability in performance is seen across drug conditions (e.g., Mattay et al. 2002). A study employing standardized neuropsychological tests failed to Wnd any eVect of levodopa on cognitive performance in moderately-to-severely aVected PD patients (Morrison et al. 2004). Other studies have found improved performance in the on condition for demanding experimental working memory tasks (e.g., Fournet et al. 2000; Moustafa et al. 2008), and Lewis et al. (2005) found beneWts of treatment speciWc to the manipulation component of working memory tasks. "
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    ABSTRACT: The role of attention in grasping movements directed at common objects has not been examined in Parkinson's disease (PD), though these movements are critical to activities of daily living. Our primary objective was to determine whether patients with PD demonstrate automaticity in grasping movements directed toward common objects. Automaticity is assumed when tasks can be performed with little or no interference from concurrent tasks. Grasping performance in three patient groups (newly diagnosed, moderate, and advanced/surgically treated PD) on and off of their medication or deep brain stimulation was compared to performance in an age-matched control group. Automaticity was demonstrated by the absence of a decrement in grasping performance when attention was consumed by a concurrent spatial-visualization task. Only the control group and newly diagnosed PD group demonstrated automaticity in their grasping movements. The moderate and advanced PD groups did not demonstrate automaticity. Furthermore, the well-known effects of pharmacotherapy and surgical intervention on movement speed and muscle activation patterns did not appear to reduce the impact of attention-demanding tasks on grasping movements in those with moderate to advanced PD. By the moderate stage of PD, grasping is an attention-demanding process; this change is not ameliorated by dopaminergic or surgical treatments. These findings have important implications for activities of daily living, as devoting attention to the simplest of daily tasks would interfere with complex activities and potentially exacerbate fatigue.
    Experimental Brain Research 08/2010; 205(1):69-80. DOI:10.1007/s00221-010-2341-0 · 2.04 Impact Factor
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