Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0677481 (urinary frequency)
 1,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seven patients complaining of nocturnal urinary frequency were treated following a sleep-micturition chart. By clinical analysis of the data, the causes of nocturnal urinary frequency were divided into three diagnostic categories: a small bladder capacity group, a sleep disorder group and a large nocturnal urinary volume group. The three groups were treated by anticholinergic agents, sleeping pills and restriction of water intake at night respectively. With the administration of anti-cholinergic agents or sleeping pills nocturnal bladder capacity increased. By restriction of water intake at night nocturnal urinary volume decreased. In all patients nocturnal urinary frequency decreased and sleep efficiency was improved.
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PMID:Systematic treatment for nocturnal urinary frequency following a sleep-micturition chart. 1045 11

Non-motor symptoms are increasingly recognized to adversely impact on the quality of life of patients with in Parkinson's disease (PD), particularly as the disease progresses. Autonomic symptom severity in patients with PD seems to correlate with older age, greater disease severity, psychiatric complications, sleep disorders, and higher doses of dopaminergic medication. The following therapeutic strategies are frequently used in the treatment of PD-related dysautonomia: 1. Orthostatic hypotension: fludrocortisone, midodrine, and droxidopa; 2. Sialorrhea: glycopyrrolate and botulinun toxin injections; 3. Constipation: symbiotic yogurt and bulking agents, macrogol, lubiprostone, mosapride citrate and tegaserod, pyridostigmine bromide, botulinum toxin injections and sacral nerve stimulation; 4. Urinary frequency: oxybutynin, tolterodine, solifenacin, darifenacin, botulinum toxin injections; 5. Erectile dysfunction: sildenafil and other phosphodiesterase type 5 inhibitors. More effective symptomatic and pathogenesis-targeted therapies are needed to ameliorate the non-motor symptoms of PD that usually do not respond well to dopaminergic medications.
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PMID:Treatment of dysautonomia associated with Parkinson's disease. 2008 97

Nocturia, awaking from sleep to void, has a negative impact on health and well-being. Nocturia affects men and women and is more prevalent among the elderly. More than two nocturnal voids is considered to be a clinically meaningful threshold associated with significant negative outcomes for health and well-being, and the timing of awakening has a significant bearing on the negative consequences of nocturia. Several serious underlying pathophysiologic conditions may be associated with nocturia. A thorough history and assessment of number and times of voids, void volume, and fluid intake is essential for determining the etiology of a patient's nocturia. With data obtained from the frequency-volume chart (FVC), which is used to collect quantitative voiding data, a patient's nocturia may be classified as global polyuria, nocturnal polyuria, reduced bladder capacity, or a combination of these categories. Global polyuria is defined as 24-hr urinary output that exceeds 40 ml/kg body weight and results in increased 24-hr urinary frequency. Nocturnal polyuria is defined as more than 20% of daily urine output at night in young patients and more than 33% in elderly patients. Reduced bladder capacity may be a result of idiopathic or neurogenic detrusor overactivity, bladder outlet obstruction, or reduced nocturnal bladder capacity. The pathophysiology underlying the findings of the FVC falls into five main categories: global polyuria, nocturnal polyuria, reduced bladder capacity, sleep disorders, and circadian clock disorders. This review discusses the epidemiology, etiology, and pathophysiology of nocturia.
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PMID:Terminology, epidemiology, etiology, and pathophysiology of nocturia. 2472 50

The prodromal phase of spinocerebellar ataxias (SCAs) has not been systematically studied. Main findings come from a homogeneous SCA type 2 (SCA2) population living in Cuba. The aim of this study was to characterize extensively the prodromal phase of SCA2 by several approaches. Thirty-seven non-ataxic SCA2 mutation carriers and its age- and sex-matched controls underwent clinical assessments, including standardized neurological exam, structured interviews and clinical scales, and looking for somatic and autonomic features, as well as a neuropsychological battery, antisaccadic recordings, and MRI scans. Main clinical somatic features of non-ataxic mutation carriers were cramps, sensory symptoms, sleep disorders, and hyperreflexia, whereas predominating autonomic symptoms were pollakiuria/nocturia, constipation, and frequent throat clearing. Cognitive impairments included early deficits of executive functions and visual memory, suggesting the involvement of cerebro-cerebellar-cerebral loops and/or reduced cholinergic basal forebrain input to the cortex. Antisaccadic task revealed impaired oculomotor inhibitory control but preserved ability for error correction. Cognitive and antisaccadic deficits were higher as carriers were closer to the estimated onset of ataxia, whereas higher Scale for the Assessment and Rating of Ataxia (SARA) scores were associated most notably to vermis atrophy. The recognition of early features of SCA2 offers novel insights into the prodromal phase and physiopathological base of the disease, allowing the assessment of its progression and the efficacy of treatments, in particular at early phases when therapeutical options should be most effective.
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PMID:Comprehensive study of early features in spinocerebellar ataxia 2: delineating the prodromal stage of the disease. 2490 24