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Bladder function of patients with P arkinson's disease
Author(s) -
Sakakibara Ryuji,
Tateno Fuyuki,
Nagao Takeki,
Yamamoto Tatsuya,
Uchiyama Tomoyuki,
Yamanishi Tomonori,
Yano Masashi,
Kishi Masahiko,
Tsuyusaki Yohei,
Aiba Yosuke
Publication year - 2014
Publication title -
international journal of urology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.172
H-Index - 67
eISSN - 1442-2042
pISSN - 0919-8172
DOI - 10.1111/iju.12421
Subject(s) - medicine , anticholinergic , disease , overactive bladder , dopaminergic , anticholinergic agents , deep brain stimulation , levodopa , dopamine , parkinson's disease , urology , pathology , alternative medicine
Bladder function of patients with P arkinson's disease alters significantly: the majority of patients have overactive bladder (urinary urgency/frequency) with little or no post‐void residuals. This seems to be the result of an altered brain–bladder relationship, as in P arkinson's disease, the frontal‐basal ganglia D1 dopaminergic circuit that normally suppresses the micturition reflex is altered. The pathophysiology of the bladder dysfunction in P arkinson's disease differs from that in multiple system atrophy; therefore, it might also aid in differential diagnosis. The effects of levodopa, the major drug to treat motor dysfunction, on the bladder in P arkinson's disease vary significantly; therefore, add‐on therapy is often required. Anticholinergic drugs are the first‐line treatment, with particular care for cognitive function in elderly patients. The second‐line treatment includes serotonergics drug, desmopressin and others. Newer modalities include deep brain stimulation that improves the bladder in P arkinson's disease; and botulinum toxin is promising, particularly in difficult cases. These treatments might be beneficial in maximizing the patients' quality of life.