Micturition Disturbance in Parkinson's Disease

Fitzmaurice, Helen; Fowler, Clare J.; Rickards, D.; Kirby, Roger; Quinn, Niall; Marsden, C. D.; Milroy, E. J. G.; Turner-Warwick, Richard

doi:10.1111/j.1464-410x.1985.tb07025.x

Cited by 104 publications

(59 citation statements)

References 7 publications

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“…In some patients with Parkinson's disease, levodopa has been reported to aggravate the detrusor hyperreflex (14). Study of the hyper active bladder response induced by a dopa mine agonist in rats would help to elucidate the mechanism of the hyperreflex in such…”

Section: Discussionmentioning

confidence: 99%

Effects of apomorphine on urinary bladder motility in anesthetized rats.

1990

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Abstract-We studied the effects of apomorphine (AM) on bladder motility in anesthetized rats in which Tyrode's solution was continuously infused into the bladder at a constant rate, inducing an almost constant rate of bladder contraction accompanying micturition. AM at a dose of 1 mg/kg, i.v., caused a hyperactive bladder response, during which micturition disappeared. AM (12.5 /cg for intra cerebroventricular (i.c.v.) injection or 50 ag for intrathecal (i.t.) injection also caused a hyperactive response in about half of the rats. Supersensitization to AM appeared in reserpine-treated rats (2.5 mg/kg, i.p., 48 and 24 hr before the experiment). Haloperidol (1 mg/kg; i.v.) or SCH 23390 (5 mg/kg, i.v.) completely suppressed the hyperactive bladder response induced by AM (5 mg/kg, i.v.), and then the bladder contraction accompanying micturition reappeared after administration of these drugs. Pretreatment with sulpiride (100 mg/kg, i.p.) for 60 min, which hardly affected the bladder contraction induced by infusion of Tyrode's solution, suppressed the hyperactive bladder response induced by AM. These results suggest that the hyperactive bladder response induced by i.v.-injected AM results from synchronous stimulation of the micturition reflex centers in the brain stem and sacral cord and that the hyperactive bladder response is elicited via both D, and D2 receptors.With regard to the dopaminergic neurons in rats that affect urinary bladder motility, Sillen et al. (1-3) have shown that dopamine re ceptors exist in the micturition reflex center of the mesencephalic-pontine region and that a hyperactive urinary bladder response is in duced upon stimulation of these receptors with dopaminergic agonists. Although urinary bladder motility is also controlled by the mic turition reflex center in the sacral cord, very little is known about the effects of dopamine agonists on this center. Recently, we studied the effects of diazepam, baclofen and mor phine on the micturition reflex centers in both the brain stem and sacral cord and found that the inhibitory effects of these drugs on blad der motility were related to both of these mic turition reflex centers (4-6). In the present experiments, the effects of apomorphine (AM), which stimulates dopaminergic re ceptors, on urinary bladder motility were ex amined in an attempt to provide additional evidence for dopaminergic innervation in the micturition reflex centers of the brain stem and sacral cord. Materials and MethodsThe methods used for recording bladder contraction were described in our previous papers (4-6). Male Wistar rats (weighing 250-350 g) were anesthetized with urethane (1.0 g/kg, s.c.) and a-chloralose (25 mg/kg, s.c.). The bladder was exposed through a midline incision in the abdomen, and a needle (1 /4) attached to a silicone tube (O.D., 1.0 mm and I.D., 0.5 mm, 30-40 cm in length) was inserted into the bladder through the left ureter. After ligation of the left ureter around the needle, the bladder was put back into the abdominal cavity, and the incision was sutu...

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Section: Discussionmentioning

confidence: 99%

Effects of apomorphine on urinary bladder motility in anesthetized rats.

1990

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“…In addition to the known e¡ect of PD in causing DO, the e¡ects of medication need to be considered also. Studies that have looked at bladder behaviour in patients with PD who go ''o¡'' have shown variable results [Fitzmaurice et al, 1985;Uchiyama et al, 2003]. The only aspect of bladder function which consistently is improved in the ''on condition'' is voiding and patients are more likely to empty their bladders easily and e¡ectively when ''on'' [Uchiyama et al, 2003].…”

Section: Treatment Of Bladder Symptoms In Pdmentioning

confidence: 99%

Update on the neurology of Parkinson's disease

Fowler

2006

Neurourology and Urodynamics

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The di¡erential diagnosis of a patient with apparent Parkinson's Disease (PD) and bladder symptoms is considered and the bladder dysfunction of Multiple System Atrophy (MSA) is reviewed. Recent insights into the progression of the neuropathology of PD have enabled thinking about the stage of the disease at which bladder dysfunction is likely to occur and the expected clinical context of the problem. Bladder symptoms of neurological origin are likely in a patient who has had treated motor symptoms for some years and in whom the ongoing neuropathology has progressed beyond involvement of the basal ganglia, so that symptoms due to cortical dysfunction as well as the adverse e¡ects of dopaminergic medication are also confounding factors. Bladder symptoms in a man with lesser neurological disability should be investigated to exclude underlying out£ow obstruction. Possible management options are considered. Neurourol. Urodynam. 26: 103^109, 2007.

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“…In patients with PD, the prevalence of lower urinary tract symptoms (LUTS) identified by validated questionnaires is around 30% 3,4 . Previous urodynamic studies of PD patients with LUTS have revealed that the most frequent abnormality is detrusor overactivity, resulting in nocturia, urinary urgency and frequency and urge incontinence , 5,6 .…”

Section: Introductionmentioning

confidence: 99%