Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lower urinary tract dysfunction is frequent in Parkinson's disease and other Parkinsonian syndromes and can cause urinary incontinence complicating a urgency-frequency syndrome or on the contrary, dysuria. These disorders are a frequent urological presenting complaint due to their impact on the patient's quality of life. Urologists must be aware of the different natural histories of diseases such as Parkinson's disease and Parkinsonian syndromes such as multisystem atrophy, which often have a severe course and are marked by resistance to neuropharmacological treatments. These various diseases can also directly induce urinary symptoms, independently of urological complications. Inversely, the development of urinary disorders, especially obstructive symptoms, in a patient with Parkinsonian syndrome may require review of the neurological diagnosis. Finally, therapeutic management is complex due to the difficulty of using pharmacological treatments, and the risk of deterioration after surgical treatment of obstructive uropathy.
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PMID:[Lower urinary tract dysfunction and parkinsonian syndromes]. 1762 65

Altered sleep and vigilance are among the most frequent symptoms, besides parkinsonism, in movement disorders. As many as 60% of patients with Parkinson's disease (PD) experience insomnia, 15-59% show rapid eye movement (REM) sleep behavior disorders (RBDs), and 30% show excessive daytime sleepiness. Insomnia is a distressing difficulty to maintain sleep, which is exacerbated by motor disability, painful dystonia, restless legs, dysuria, anxiety and depressed mood. Improving night-time motor control by overnight treatment with levodopa, transdermal or long-acting dopamine agonists, or bilateral subthalamus stimulation, can improve sleep continuity. RBDs are violent, enacted dreams that expose the patient or their sleeping partner to night-time injuries. A striking improvement of parkinsonism is observed during these behaviors in PD. RBDs are thought to be caused by lesions in the REM sleep atonia system, and can, in association with other early markers of neurodegenerative diseases, such as olfactory, cognitive and autonomic disturbances, precede parkinsonism by several years. Daytime sleepiness, often with a narcolepsy-like phenotype, is a common occurrence in PD, owing to lesions in the arousal systems of the brain. The use of dopamine agonists increases the risk of sleep attacks, especially when driving, suggesting a drug-disease interaction.
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PMID:Sleep disturbances in patients with parkinsonism. 1839 15

Forty-one Parkinson's disease patients with dementia (21 galantamine group, 20--control group) with onset of dementia at least two years after the manifestation of parkinsonian symptoms participated in this open-label controlled trial of galantamine in maximum dose 16 mg/day. Cognitive, psychiatric and motor symptoms were assessed before and after 4, 12 and 24 weeks of treatment using clinical assessment as well as rating scales, including the Mini-Mental State Examination (MMSE), ADAS-cog, clock drawing test, Frontal Assessment Battery (FAB), and the Neuropsychiatric Inventory (NPI-12) with assessment of caregiver distress. Patients treated with galantamine had better scores on MMSE (p<0,05), ADAS-cog (p<0,05), clock drawing test (p<0,05) and FAB (p<0,01) to the end of the trial comparing to the control group. NPI scores on individual items changed from baseline at week 12 and 24, showing benefits of galantamine treatment as compared to the controls, with significant difference for hallucinations (p=0,0002), anxiety (p=0,04), sleep disorders (p=0,04) and apathy (p=0,006). Galantamine therapy was associated with a significant reduction in caregiver distress (p=0,007), improvement of daily life activity (p=0,003). Gait, freezing and falls were improved in the galantamine group but a mild worsening of tremor was noted in two patients. Adverse events (drooling, postural hypotension, nausea, dysuria) were observed in 7 (30%) of galantamine treated patients.
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PMID:[Efficacy and safety of galantamine (reminyl) in the treatment of dementia in patients with Parkinson's disease (open-label controlled trial)]. 1842 56

An open controlled trial of the use of galantamine at a maximum dose of 16 mg/day included 41 patients with Parkinson's disease with dementia randomized to a galantamine treatment group (21 patients) and a control group (20 patients). Cognitive, neuropsychiatric, and motor symptoms were assessed clinically before the trial and at 4, 12, and 24 weeks, using the Mini Mental State Examination (MMSE), the cognitive Alzheimer's Disease Assessment Scale (ADAS-cog), the clock drawing test, the Frontal Assessment Battery (FAB), and the Neuropsychiatric Inventory (NPI) with assessment of distress in relatives. Patients treated with galantamine had better scores on the MMSE (p < 0.05),ADAS-cog (p < 0.05), the clock drawing test (p < 0.05), and the FAB (p < 0.01) at the end of the study period as compared with the control group. Changes in total point scores on the NPI-12 at the ends of weeks 12 and 24, as compared with the beginning of the trial, were in favor of the group treated with galantamine, with significant changes in the hallucinations (p = 0.0002), anxiety (p = 0.04), sleep disturbance (p = 0.04), and apathy (p = 0.006) sections. Galantamine treatment was accompanied by decreases in the level of distress in patients' relatives (p = 0.007) and improvements in daily activity (p = 0.003). Improvements in gait and decreases in freezing and falls were seen in the galantamine treatment group. However, two patients of this group showed minor increases in tremor. Side effects (drooling, postural hypotension, nausea, dysuria) occurred in seven patients (30%).
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PMID:Efficacy and safety of galantamine (reminyl) for dementia in patients with Parkinson's disease (an open controlled trial). 1897 3

In multiple system atrophy (MSA), parkinsonism and a cerebellar syndrome are associated with autonomic dysfunction. Both bladder neck dysfunction and external sphincter denervation have been implicated in detrusor-sphincter dyssynergia. However, urethral dysfunction may not be adequately reflected by a single global measurement of urethral pressure. Pressure assessment at several levels of the urethra is needed to unravel the mechanisms of bladder-urethra dysfunction. Here, we evaluated the use of multiple sensor pressure transducers to assess bladder-sphincter function in 52 patients with MSA in comparison to patients with Parkinson's disease (PD) who were matched for age and severity in the "off" condition. Urinary dysfunction appeared significantly earlier in MSA (<2 years) than in PD (>5 years). Detrusor under-activity with dysuria was observed in 58% of MSA patients within 4 years and in 76% of patients thereafter. Detrusor-urethral dyssynergia in MSA patients was always better characterized by multiple sensor pressure transducer measurement of bladder and urethral pressure than by a single global measurement. This new approach may prove useful for differential diagnosis of parkinsonian syndromes, and especially MSA.
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PMID:Urodynamic analysis in multiple system atrophy: characterisation of detrusor-sphincter dyssynergia. 2068 7


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