Confusion, dementia and anticholinergics in Parkinson's disease.

Smet, Yves De; Ruberg, Merle; Serdaru, M; Dubois, Bruno; Lhermitte, F; Agid, Yves

doi:10.1136/jnnp.45.12.1161

Cited by 125 publications

(55 citation statements)

References 27 publications

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“…The cholinergic deficit, possibly superposed on a normal age-related deterioration of the cholinergic system (Perry, 1992), is strongly correlated with cognitive impairment in both conditions (Mattila, 2001;Kuhl, 1996;Perry, 1985) and therefore, is likely to constitute an important mechanism in the development of dementia. This is further supported by the propensity of anticholinergic agents to elicit cognitive dysfunction in PD-patients (Bedard, 1999;de Smet, 1982) and the clinical beneficial results of cholinesterase inhibitors in disorders with associated dementia (see later).…”

Section: Pathophysiology Of Cognitive Deficits and Dementia In Pdmentioning

confidence: 72%

Cognitive dysfunction and dementia in Parkinson?s disease

2004

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Summary. Parkinson's disease (PD) is a slowly progressive neurodegenerative disorder mainly characterized by degeneration of dopaminergic neurons in the substantia nigra and the ventral tegmental area, in combination with a varying loss of central noradrenergic (locus coeruleus), cholinergic (nucleus basalis of Meynert) and serotonergic (dorsal raphe nuclei) integrity, leading to a multitude of motor and non-motor behavioral disturbances.Apart from the clinical motor hallmarks, in the early stages of disease, subtle cognitive dysfunction might be seen comprising mainly executive dysfunction, with secondary visuospatial and mnemonic disturbances. In about 20-40% of patients, these problems may eventually proceed to dementia, which constitutes an important risk factor for caregiver distress, decreased quality of life and nursing home placement. Dementia in PD is typically characterized by a progressive dysexecutive syndrome with attentional deficits and fluctuating cognition, often accompanied by psychotic symptoms. It is thought to be the result of a combination of both subcortical and cortical changes. PD-related dopaminergic deficiency in the nucleus caudatus and mesocortical areas (due to degeneration of projections from the substantia nigra and ventral tegmental area) and cholinergic deficiency in the cortex (due to degeneration of ascending projections from the nucleus basalis of Meynert), combined with additional Alzheimer-pathology and cortical Lewy bodies, may greatly contribute to dementia.Current treatment of dementia in PD is based on compensation of the profound cholinergic deficiency. Recent studies with the cholinesterase inhibitors galantamine, donepezil and rivastigmine show promising results in improving cognition and ameliorating psychotic symptoms, which must further be confirmed in randomized controlled trials.

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Section: Pathophysiology Of Cognitive Deficits and Dementia In Pdmentioning

confidence: 72%

Cognitive dysfunction and dementia in Parkinson?s disease

2004

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“…It may occur with systemic disease, in the context of fever, infection, or renal failure, and with medications including anticholinergic treatment or amantadine [ 58 ]. In the perioperative state, especially when PD patients receive pain medications, there is also a signifi cantly increased risk of a confusional state with hallucinations [ 59 ].…”

Section: Deliriummentioning

confidence: 99%

Psychosis in Parkinson’s Disease

Bountouni

Zis

Schrag

2014

Neuropsychiatric Symptoms of Movement Disorders

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“…Virtually all classes of anti-parkinsonian medications may produce psychosis. Some studies suggest that dopamine agonists are more likely culprits than levodopa [ 42,[44][45][46] , and anticholinergics are a frequent trigger especially in elderly PD patients [ 47 ] . While dopaminergic medications contribute to PD psychosis, several intrinsic factors also play a role [42][43][44][45][46][47][48][49] .…”

Section: Pathophysiologymentioning

confidence: 99%

Psychosis and Parkinson’s Disease

Vaughan

Goldman

2012

Movement Disorder Emergencies

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The clinical spectrum of Parkinson's disease (PD) psychosis ranges from mild illusions to formed hallucinations or even frank delusions. Hallucinations occur in about one-third of PD patients treated with chronic dopaminergic therapy and are most often visual. Delusions are less common but typically consist of wellsystematized, thematic ideas such as paranoia or in fi delity. PD psychosis may be due to extrinsic (i.e., pharmacological treatment) and/or intrinsic (i.e., diseaserelated) factors. Risk factors for the development of psychosis include older age; advanced disease; akinetic-rigid motor phenotype; concomitant cognitive impairment, depression, or sleep disturbances; and multiple medical problems. When psychosis in PD develops acutely, becomes troublesome or frightening, or poses a safety risk, medical attention is necessary. Medical management of acute psychosis typically includes the following: identifying and addressing speci fi c causes (e.g., infection, medications), reducing or discontinuing medications for PD and other conditions that may aggravate psychosis, and introducing antipsychotic medications. Since antipsychotics with dopamine-blocking properties may worsen parkinsonism, medications with greater serotonergic properties such as clozapine and quetiapine are favored. Effective and well-studied treatments that improve PD psychosis without worsening motor function are still needed. Patient Vignettes Patient 1A 67-year-old man with a 7-year history of Parkinson's disease (PD) presented to the emergency department with agitation. For the past 2 weeks he had accused his wife of having an affair with the neighbor, believed that strangers were living in his house, and insisted that the dog gates were installed to prevent him from leaving the house. He had threatened family members, and fi nally his wife called the paramedics to bring him to the hospital. His medications included the following: carbidopa/levodopa 25/100 mg-2 tablets every 4 h (total eight tablets daily) along with entacapone 200 mg with each dose, carbidopa/levodopa CR 50/200 mg nightly, amitriptyline 25 mg nightly, and aspirin. His medical history revealed frequent urinary tract infections. On examination, he was confused and exhibited motor features of PD including bradykinesia, rigidity, and rest tremor. He was afebrile, and laboratory tests revealed normal blood counts and electrolytes. Urinalysis was suspicious for infection with positive leukocyte esterase and increased white cells. Neuroimaging did not reveal intracranial hemorrhage or evidence of acute stroke. He was admitted to the psychiatric ward for further management of his psychosis. Patient 2A 70-year-old man with a 15-year history of akinetic-rigid PD presented to the emergency department after lighting his bedspread on fi re to kill the insects which he thought were infesting his bed. En route, he called the police claiming that the ambulance driver had kidnapped him against his will. Over the past year, he was reported to spend most of the day in his bedroom...

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Confusion, dementia and anticholinergics in Parkinson's disease.

Cited by 125 publications

References 27 publications

Cognitive dysfunction and dementia in Parkinson?s disease

Cognitive dysfunction and dementia in Parkinson?s disease

Psychosis in Parkinson’s Disease

Psychosis and Parkinson’s Disease

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