Successful methylphenidate treatment of apathy after subcortical infarcts

Watanabe, Kenji; Em, Martin; León, Ovidio A. De; Gaviria, Moisés; Dg, Pavel; Dw, Trepashko

doi:10.1176/jnp.7.4.502

Cited by 44 publications

(4 citation statements)

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“…In addition, several case series as well as at least one randomized control trial have suggested that drugs with dopamine-stimulating properties, such as methyphenidate (Hermann et al, 2008; Watanabe et al, 1995), amantadine (Andersson et al, 1992), bupropion (Corcoran, Wong & O'Keane, 2004), and bromocriptine (Powell, al-Adawai, Morgan & Greenword, 1996), improve apathy and related disorders of motivation.…”

Section: Discussionmentioning

confidence: 99%

Mood and motor trajectories in Parkinson's disease: Multivariate latent growth curve modeling.

Zahodne¹,

Marsiske²,

Okun³

et al. 2012

Neuropsychology

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Objective Apathy is a common feature of Parkinson's disease (PD) that can manifest independently of depression, but little is known about its natural progression in medically-managed patients. The present study sought to characterize and compare trajectories of apathy, depression, and motor symptoms in PD over 18 months. Method Data from a sample of 186 PD patients (mean disease duration of 8.2 years) followed by the University of Florida Movement Disorders Center were obtained from a clinical research database. Scores on the Unified Parkinson's Disease Rating Scale (motor portion), Apathy Scale, and Beck Depression Inventory at three time-points (baseline, 6 months, 18 months) were analyzed in a structural equation modeling framework. Results A multivariate growth model controlling for age, sex, education, and disease duration identified linear worsening of both apathy (slope estimate = 0.73; p <.001) and motor symptoms (slope estimate = 1.51; p <.001), and quadratic changes in depression (slope estimate = 1.18; p = .07). All symptoms were positively correlated. Higher education was associated with lower apathy, depression, and motor severity. Advanced age was associated with greater motor and apathy severity. Female sex and longer disease duration were associated with attenuated motor worsening. Antidepressant use was associated only with depression scores. Conclusions These longitudinal results support the differentiation of apathy and depression in PD. Like motor progression, apathy progression may be linked at least partially to dopaminergic neurodegeneration. Empirically-supported treatments for apathy in PD are needed.

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Section: Discussionmentioning

confidence: 99%

Mood and motor trajectories in Parkinson's disease: Multivariate latent growth curve modeling.

Zahodne¹,

Marsiske²,

Okun³

et al. 2012

Neuropsychology

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“…What do we know form animal models (Watanabe et al, 1995) is that apathy should be subserved by four different circuits, which mediates the motivational working memory, the cognitive coloring of motivation, the integration of arousal into motivation, and the reward memory into motivational response.…”

Section: Conclusive Statementmentioning

confidence: 99%

“…As with akinetic mutism, even for apathy, it was observed a substantial response to treatment with dopamine-agonists, suggesting a common role of dopaminergic pathways in both conditions (Marin et al, 1995; Watanabe et al, 1995; Lichter and Cummings, 2001). Apathy that appears in experimental models of Alzheimer's disease can be also interpreted as an alteration of cholinergic disconnections of structures of the ACC, e.g., basal nucleus of the amygdala (Mega and Cohenour, 1997; Mega et al, 1997), and the paramedian thalamic portions, probably for their intrinsic role of connecting basal forebrain to the ARAS system, deriving from the cholinergic pedunculo-pontine projections.…”

Section: Introductionmentioning

confidence: 99%

Neural Correlates for Apathy: Frontal-Prefrontal and Parietal Cortical- Subcortical Circuits

Moretti

Signori

2016

Front. Aging Neurosci.

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Apathy is an uncertain nosographical entity, which includes reduced motivation, abulia, decreased empathy, and lack of emotional involvement; it is an important and heavy-burden clinical condition which strongly impacts in everyday life events, affects the common daily living abilities, reduced the inner goal directed behavior, and gives the heaviest burden on caregivers. Is a quite common comorbidity of many neurological disease, However, there is no definite consensus on the role of apathy in clinical practice, no definite data on anatomical circuits involved in its development, and no definite instrument to detect it at bedside. As a general observation, the occurrence of apathy is connected to damage of prefrontal cortex (PFC) and basal ganglia; “emotional affective” apathy may be related to the orbitomedial PFC and ventral striatum; “cognitive apathy” may be associated with dysfunction of lateral PFC and dorsal caudate nuclei; deficit of “autoactivation” may be due to bilateral lesions of the internal portion of globus pallidus, bilateral paramedian thalamic lesions, or the dorsomedial portion of PFC. On the other hand, apathy severity has been connected to neurofibrillary tangles density in the anterior cingulate gyrus and to gray matter atrophy in the anterior cingulate (ACC) and in the left medial frontal cortex, confirmed by functional imaging studies. These neural networks are linked to projects, judjing and planning, execution and selection common actions, and through the basolateral amygdala and nucleus accumbens projects to the frontostriatal and to the dorsolateral prefrontal cortex. Therefore, an alteration of these circuitry caused a lack of insight, a reduction of decision-making strategies, and a reduced speedness in action decision, major responsible for apathy. Emergent role concerns also the parietal cortex, with its direct action motivation control. We will discuss the importance of these circuits in different pathologies, degenerative or vascular, acute or chronic.

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“…The efficacy of such agents in ADHD remains undisputed. Side effect profiles and undesired biologic activities limit their use in subjects with late-life dementia [89, 90], and definitive evidence for their utility in treating the cognitive dysfunction seen in these disorders is limited [89, 91–98]. …”

Section: Shared Treatment Strategiesmentioning

confidence: 99%

Attention-Deficit/Hyperactivity Disorder in Older Adults: Prevalence and Possible Connections to Mild Cognitive Impairment

Ivanchak

Fletcher

Jicha

2012

Curr Psychiatry Rep

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Attentional deficits are frequently seen in isolation as the presenting sign and symptom of neurodegenerative disease, manifest as mild cognitive impairment (MCI). Persistent ADHD in the geriatric population could well be misconstrued as MCI, leading to the incorrect assumption that such persons are succumbing to a neurodegenerative disease process. Alternatively, the molecular, neuroanatomic, or neurochemical abnormalities seen in ADHD may contribute to the development of de novo late life neurodegenerative disease. The present review examines the issue of causality vs confound regarding the association of ADHD with MCI, suggesting that both are tenable hypotheses.

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Successful methylphenidate treatment of apathy after subcortical infarcts

Abstract: A patient with prominent apathy secondary to multiple subcortical infarcts was treated successfully with methylphenidate. SPECT and reaction time testing showed selective improvement of frontal system function, consistent with a recent model of frontal-subcortical circuits and behavior.

Cited by 44 publications

References 0 publications

Mood and motor trajectories in Parkinson's disease: Multivariate latent growth curve modeling.

Mood and motor trajectories in Parkinson's disease: Multivariate latent growth curve modeling.

Neural Correlates for Apathy: Frontal-Prefrontal and Parietal Cortical- Subcortical Circuits

Attention-Deficit/Hyperactivity Disorder in Older Adults: Prevalence and Possible Connections to Mild Cognitive Impairment

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