Cognitive dysfunction and dementia in Parkinson?s disease

Bosboom, J.L.; Stoffers, Diederick; Wolters, E.Ch.

doi:10.1007/s00702-004-0168-1

Cited by 236 publications

(176 citation statements)

References 122 publications

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“…Concomitant neurodegenerative pathology (in particular Alzheimer’s disease or cortical Lewy body pathology) and other PD-related pathology (in particular degeneration of the dopaminergic, or other associated noradrenergic, serotonergic, and especially cholinergic systems) have been described [6, 7]. Cognitive improvement without aggravating motor symptoms in PDD patients treated with cholinesterase inhibitors seems to support a profound cholinergic deficiency [1, 6,8,9,10]. …”

Section: Introductionmentioning

confidence: 99%

“…In the early stages of PD, cognitive dysfunctions, apart from those related to fine motor control, are most frequently reported in executive functions, working memory, and spatial behavior [1, 2]. These cognitive functions are sensitive to frontal lobe dysfunction, which coincides with the nigrostriatal dopaminergic degeneration in PD [3,4,5].…”

Section: Introductionmentioning

confidence: 99%

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Heterogeneity of Cognitive Dysfunction in Parkinson’s Disease: A Cohort Study

Verleden¹,

Vingerhoets²,

Santens

2007

Eur Neurol

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Aims: The aim of this study was to examine the heterogeneity of cognitive dysfunction in Parkinson’s disease (PD) and to evaluate the contribution of cognitive criteria to the diagnosis of dementia in PD. Methods: In a sample of 100 consecutive PD patients with motor fluctuations, an extensive neuropsychological test battery was administered. Each PD patient’s cognitive profile was then compared with current cognitive criteria for dementia in PD. Results: Principal component analysis of the major test variables resulted in three components: one concerned with memory/attention, one with visuospatial, and one with executive/motor functions. Eighteen percent of our cohort showed no significant impairment on either domain. Fifty-one percent showed impairment in one cognitive domain, most frequently in the executive/motor component (88%). Twenty-four percent performed below normal on two cognitive components, most often executive/motor and memory/attention deficits (96%), and only 7% of our cohort had significant impairment on each derived cognitive component. Depending on the used criteria, 10–30% percent of our cohort could be categorized as PD patients with dementia. Conclusions: Future guidelines for a uniform diagnosis of dementia in PD are needed for clinical use and therapeutic management.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Heterogeneity of Cognitive Dysfunction in Parkinson’s Disease: A Cohort Study

Verleden¹,

Vingerhoets²,

Santens

2007

Eur Neurol

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“…Compared with other AChEIs, including Galantamine and Rivastigmine, the cholinergic agonist Donepezil has performed favorably for treating cognitive impairment in patients with PD and NCDLB, improving cognition, but with fewer side effects [73,74]. Donepezil has been shown to produce significant improvements in cognition and behavior which disappeared when Donepezil was withdrawn, but treatment gains were restored on recommencement of Donepezil [75].…”

Section: Symptom Treatment Of Cholinergic Lewy Pathologymentioning

confidence: 99%

“…Based on researchdemonstrating Donepezil's efficacy in treating cholinergic impairment in patients with PD and NCDLB, and its effectiveness in reducing constipation and increasing bowel motility in non geriatric patients [73][74][75][76][77][78][79][88][89][90]93,94]. Donepezil has been used specifically to treatconstipation in PD and NCDLB patients, with consequent significant reduction of the symptom of constipation, without exacerbation or instigation of other symptoms [39].…”

Section: Symptom Treatment Of Cholinergic Lewy Pathology In the Ensmentioning

confidence: 99%

Mechanisms of α‐Synuclein Pathology and Treatment in the Enteric Nervous System

Lepkowsky¹

2017

IJGS

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Abstractα-synuclein (Lewy Body) pathology is commonly found in the enteric nervous system (ENS) of patients diagnosed with Neurocognitive Disorder with Lewy Bodies (NCDLB) and Parkinson's Disease (PD). Lewy pathology in the ENS can produce symptoms of bowel immotility, including constipation, obstipation, and bowel impaction. These symptoms significantly reduce the quality of life for the patient, producing hardship for the patient and care providers. In Lewy body patients, medical intervention using acetylcholinesterase inhibitors (AChEIs) can significantly reduce or alleviate bowel immotility. The specific mechanism through which the cholinergic agonist Donepezil mitigates Lewy Body bowel immotility is explained. Practice, 1143 Deer Trail Lane, Solvang, California 93463, USA, Tel: 805-688-1229 Fax: 805-686-9382; E-mail: clepkowsky@gmail.com of α-synuclein aggregates in the MP predates cognitive and motor functional manifestations of Lewy body diseases so consistently that it has been nominated as a potential biomarker for Lewy pathology [10,17,30]. Symptomatic Manifestations of Cholinergic Lewy Pathology in the ENSLewy body cholinergic impairment in the ENS manifests symptomatically as gastric immotility and constipation [13,[31][32][33][34][35][36][37][38][39][40][41]. Increased colonic transit time and impaired gastric emptying are frequently found in PD patients [35,42]. The prevalence of constipation in PD is at least three times that of the general population, leading some researchersto suggest that constipation might be a universal feature of PD [47,48]. Bowel immotility can occur 20 years before diagnosis of PD or NCDLB, suggesting that it might be a prodromal symptom for both disorders [5,19,36,44,[49][50][51][52].As α-synuclein pathology advances in the ENS, symptoms of gastric immotility advance from constipation to obstipation and impaction. Escalating gastric immotility in PD and NCDLB can interfere with mobility, sleep, cognition, and mood, increasing the cost of care, and potentially debilitating and/or dramatically reducing the quality of life for patients. [4,34,36,[53][54][55][56] Potential Exacerbation of ENS Symptoms by AntiParkinson MedicationLPD and NCDLB patients with significant Parkinsonian motoric/gait features are often prescribed L-dopa agents like Carbidopa-Levodopa (known also by the brand names Sinemet and Stalevo) in order to preserve gait, balance, and other basic motor functions [40,57,58]. Carbidopa-Levodopa's potential side effects include constipation [59]. which can complicate or exacerbate gastric immotility due to ENS Lewy pathology. Medications frequently used for the treatment of resting tremor in PD and NCDLB includeTrihexyphenidyl (marketed as Artane or Trihex) and Benztropinemesylate (marketed as Cogentin), identified as definite anticholinergics that can also exacerbate gastric immotility through suppression of the cholinergic neurotransmitter pathways innervating the ENS [58,[60][61][62].

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“…The hallmarks of PD are the formation of protein aggregates (Lewy bodies) containing α-synuclein and ubiquitin in the cytoplasm and axon, ultimately motor symptoms resulting from loss of dopaminergic neurons and these hallmarks [4,5]. PD includes various motor symptoms, such as tremor, bradykinesia, rigidity, postural instability, and altered gait pattern, as well as non-motor symptoms, such as cognitive impairment and bladder dysfunction [6][7][8][9]. The administration of L-dihydroxyphenylalanine (L-DOPA), a precursor of dopamine, is an effective treatment of PD; however, long-term use of L-DOPA produces negative side effects [10].…”

Section: Introductionmentioning

confidence: 99%