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Year : 2019  |  Volume : 22  |  Issue : 4  |  Page : 432-436

Urinary symptoms in patients with Parkinson's disease and progressive supranuclear palsy: Urodynamic findings and management of bladder dysfunction

1 Department of Neurological Rehabilitation, National Institute of Mental Health and Neuro Sciences, Bengaluru, Karnataka, India
2 Department of Physical Medicine and Rehabilitation, Hosmat Hospital, Bengaluru, Karnataka, India
3 Department of Neurology, National Institute of Mental Health and Neuro Sciences, Bengaluru, Karnataka, India

Date of Submission05-Jan-2018
Date of Acceptance24-Apr-2018
Date of Web Publication25-Oct-2019

Correspondence Address:
Dr. Anupam Gupta
Department of Neurological Rehabilitation, National Institute of Mental Health and Neuro-Sciences, Bengaluru - 560 029
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/aian.AIAN_6_18

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Objective: The objective of this study is to observe urinary symptoms in patients with Parkinson's disease (PD) and progressive supranuclear palsy (PSP) and advice bladder dysfunction management based on urodynamic study (UDS) findings. Patients and Methods: Twenty-two patients (12 males) with PD and PSP (15 and 7, respectively) with urinary symptoms were included in this study. All patients except one were on levodopa and carbidopa medication. UDS was performed, and bladder management determined. Results: Mean age was 60.4 years (range 41–73 years, standard deviation [SD] 8.4). Mean illness duration was 31.9 months (range 9–146 months, SD 31.0) and mean duration of urinary symptoms was 14.8 months (range 1–61 months, SD 15.8). Eighteen patients reported nocturia and 16 patients had urgency with or without urge incontinence. Three patients had retention and straining to void and 3 had mixed urinary complaints. Twelve out of 22 patients had absence of voluntary anal contraction on per-rectal examination. UDS was suggestive of 12 patients with neurogenic detrusor overactivity with or without sphincter dyssynergy. Six patients had normal detrusor pressure, and four patients were found to have contractile detrusor. Ten patients had significant postvoid residual. Bladder management included pharmacotherapy, supportive, and behavioral management as appropriate. Conclusions: Patients with PD/PSP are known to develop urinary symptoms during illness. Clinical complaints and UDS findings do not necessarily match. UDS is required to manage urinary symptoms. Most of the patients respond to oral antimuscarinic medications along with behavioral and supportive therapy.

Keywords: Parkinson's disease, progressive supranuclear palsy, urinary symptoms, urodynamic study

How to cite this article:
Gupta A, Rashmi Krishnan U K, Nageshkumar S, Pal PK, Khanna M, Taly AB. Urinary symptoms in patients with Parkinson's disease and progressive supranuclear palsy: Urodynamic findings and management of bladder dysfunction. Ann Indian Acad Neurol 2019;22:432-6

How to cite this URL:
Gupta A, Rashmi Krishnan U K, Nageshkumar S, Pal PK, Khanna M, Taly AB. Urinary symptoms in patients with Parkinson's disease and progressive supranuclear palsy: Urodynamic findings and management of bladder dysfunction. Ann Indian Acad Neurol [serial online] 2019 [cited 2020 Sep 26];22:432-6. Available from:

   Introduction Top

Parkinson's disease (PD) has typically been considered to be a motor neurodegenerative disorder secondary to basal ganglia dysfunction.[1],[2],[3] It is characteristically diagnosed with the clinical hallmarks of motor parkinsonism, bradykinesia/akinesia, rigidity, tremor, and postural instability, caused by significant synucleinopathy-induced, nigral degeneration-derived dopaminergic striatal denervation. In the past two decades or so, however, it has become more and more accepted that in PD, a variety of intrinsic nonmotor signs and symptoms accompany motor Parkinsonism. These include autonomic (including bladder, bowel, and sexual dysfunction), sleep, sensory, and neuropsychiatric disturbances.[4],[5] These symptoms may arise in early or later stages of the disease in a considerable number of patients and may not be responsive to levodopa. The nonmotor symptoms closely correlate with the progression of extranigral Lewy body and synucleinopathic pathology in PD.[6],[7],[8]

PD patients frequently present with lower urinary tract symptoms, often typical of overactive bladder and associated with the urodynamic finding of neurogenic detrusor overactivity (NDO).[9],[10] As the neurogenic bladder dysfunction can lead to severe damage of the upper and lower urinary tract, this condition needs early diagnosis and treatment. Hence, there is a need to evaluate the patients based on urinary symptoms at the earliest. The prevalence of urinary symptoms is reported to range between 29% and 73% in various studies, which correlate with the severity of the disease and have an adverse impact on quality of life.[9],[11] Patients present with both storage and voiding types of lower urinary tract symptoms-LUTS with former being more common.[12]

Progressive supranuclear palsy (PSP) is a common atypical neurodegenerative parkinsonian disorder, which is a sporadic disease with onset in fifth to seventh decade of life more commonly and first described as a distinct clinicopathological entity by Steele, Richardson, and Olszewski in the early 1960s.[13],[14],[15],[16] A proportion of patients with PSP is known to develop urinary complaints, which might be mild or late onset and adversely affect the quality of life, health economics, and require early institutionalization.[17] Urgency, urge incontinence, high volumes of residual urine are the micturitional disturbances found in PSP. Yamamoto et al. observed that urinary storage dysfunction in patients with PSP is not different from PD or multiple system atrophy (MSA), but voiding dysfunction is milder than in patients with MSA and more severe than in patients with PD.[18]

The objective of this study was to report the urodynamic profile of patients with PD and PSP with neurogenic bladder dysfunction based on urodynamic study (UDS) findings. We also wanted to observe the correlation between clinical symptoms and neurogenic bladder pattern in patients with urinary symptoms in PD and PSP. The bladder management strategy was based also on the UDS findings.

   Patients and Methods Top

This prospective, cross-sectional study was conducted in the Department of neurological rehabilitation of a quaternary hospital-based research institute. It was part of a nonfunded project for a period of 2 years (October 2015–September 2017). The local ethics committee approval was obtained for the project, and informed consent was taken from all the patients before enrolling them for the study. Patients diagnosed with PD and PSP with urinary complaints were included in this study. Patients of all ages and both sex included irrespective of the duration of illness and type of urinary complaints. Patients with MSA, patients with parkinsonian disorders such as traumatic, drug-induced, and vascular PD were excluded from the study.

Patient selection

Patients with PD (diagnosed according to 'the UK PD society brain bank clinical diagnostic criteria' by the neurologist) and PSP (diagnosed according to “The National Institute for Neurological Disorders and Stroke-Society for PSP criteria” for the diagnosis of clinically probable PSP by the neurologist) with urinary symptoms were recruited in the study. During the study, a total of 483 patients with PD and PSP were referred from the Department of Neurology to our department for rehabilitation (predominantly balance, gait, and activity of daily living training-related issues). During the same period, 48 patients with PD and PSP, who were having urinary complaints, were referred for UDS and bladder dysfunction management. Sixteen patients seen in outpatient services in both the departments expressed desire to get further investigated (including UDS) from their native places. The remaining 32 patients were assessed in detail including further investigations. After initial clinical assessment, they were advised to report back with 3 days bladder (voiding) diary and abdominal (kidneys, ureters, and bladder [KUB]) ultrasound report (to observe prostate status in male patients and to observe postvoid residual (PVR) urine in bladder and backpressure changes in the ureter and kidney). In 10 patients, UDS could not be done on the scheduled appointment and date because of some reasons (most common being the inadequate bowel preparation) and eventually patients were lost. Hence, the study included 22 patients of PD and PSP with urinary symptoms, who did undergo UDS.

Patients' sociodemographic profile was noted. Their illness duration and severity of impairment and disability were assessed using appropriate scales. Urinary complaints and duration were noted. Medical comorbidities and the medications they were put on for these illnesses as well as for PD and PSP were also noted.


Filling and voiding cystometry was carried out using multichannel pressure recording technology with Life-Tech Urolab Primus (USA) system. Patients were given a bowel program on previous day and enema on the morning of procedure for bowel evacuation. All the bladder sensations were defined according to the International Continence Society-guidelines and terminology and comprehensibly explained before the study.[19] Filling cystometry was performed with the patients in the supine position on the urodynamic table. Bladder filling was done with normal saline at rate of 10 ml/min with two-lumen 6 Fr catheter in urethra. Patients were made to sit during voiding phase to void urine. Recordings were made during the filling and voiding phase. Sphincter electromyography was performed to observe sphincter activity and possible synergic/detrusor sphincter dyssynergia (DSD) pattern. It was done using anal patch surface electrodes. The complete data were captured, and analysis of graph and values of relevant pressures was done.[20],[21] The final urodynamic diagnosis was made, and management determined and instituted consisting of pharmacotherapy, supportive and behavioral measures.

Data analysis

Data were analyzed using Statistical package for social science SPSS version 17.0 (IBM, IL, Chicago, USA). Descriptive statistics included frequency, mean, and standard deviation for quantitative variables such as age, duration of illness, duration of urinary complaints, and illness severity scores. It also included detrusor characteristics and management advised.

   Results Top

Patient profile

Fifteen patients had PD and 7 were diagnosed to have PSP. Gender distribution was almost equal with 12 males and 10 females in the study. Their age ranged from 41 to 73 years (mean 60.4 years, standard deviation [SD] 8.4). Unified PD Rating Scale-UPDRS was used to assess the severity of illness in patients with PD.[22] Scores ranged from 15 to 48 with a mean score of 19.9 (SD 17.9) suggesting that the patients were either early PD patients or “good responders” to dopaminergic medications. Similarly, PSP rating scale was used for patients with PSP (0–100). The score ranged from 9 to 56 with a mean score of 18.6 and SD 11.9. The duration of illness varied from 9 to 146 months with a mean of 31.9 months and SD 31.0. The duration of urinary symptoms varied from 1 to 61 months with a mean of 14.8 months and SD15.8. Twenty-one patients were taking dopaminergic medication (combination of levodopa and carbidopa) at the time of assessment and procedure in rehabilitation. About the medical comorbidities; five patients had hypertension, three had type-2 diabetes mellitus, one patient was on antidepressants, and nine patients were diagnosed with dementia. All were taking medications as per the advice of physician/neurophysician.

Urinary complaints and Abdominal (kidneys, ureters, bladder) Ultrasound

Eighteen patients had a complaint of nocturia, (increased night time frequency), which was found to be the most common urinary complaint. This was followed by the complaints of urgency with or without urge incontinence, which was noted in 16 patients. Three patients had obstructive urinary complaints in the form of hesitancy and straining to void and retention. Three patients had mixed urinary complaints.

Ultrasound (KUB) was suggestive of significant PVR in three patients. No patient was reported to be showing back pressure changes in the form of hydroureter or hydronephrosis. Out of 12 males, 1 patient was observed to be having prostate enlargement.

Urodynamic findings

Per rectal/anal examination is routinely performed in all patients before commencing saline cystometrography. The examination suggested that 20 patients had anal reflex present whereas it was absent in the other two. Voluntary anal contraction (VAC) was present in only 10 patients and absent in the remaining 12.

During filling cystometrography, 14 patients were found to have normal cystometric capacity. Their urodynamic findings are mentioned in [Table 1].
Table 1: Bladder characteristics in patients with Parkinson's disease and progressive supranuclear palsy based on urodynamic findings

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During voiding10 patients were found to have significant PVR. This was remarkably different to what was observed with ultrasound, which suggested only three patients to be having significant PVR. Twelve patients had nil/insignificant PVR.

Based on UDS findings (especially detrusor characteristics), eight patients were advised antimuscarinic medications (tolterodine-6, and oxybutynin-2), ten patients were advised timed voiding, and eight patients were put on clean intermittent self-catheterization, with or without anti-muscarinic. Four patients were advised voluntary micturition without supportive therapy.

   Discussion Top

PD patients are known to develop LUTS following motor disorder. There are reports suggesting direct correlation between dopaminergic denervation and LUTS, which effectively means onset or worsening of urinary complaints with worsening of motor disorder.[5],[23]

Storage symptoms have been known to be more common with nocturia or night time frequency reported to be the most common complaint in patients with PD.[18] Hesitancy with straining to void is reported to be the most common voiding complaint in some studies.[5],[24],[25] In the present study, we also observed nocturia, urgency, and urge incontinence to be the most common complaints (72.7%), but only three patients had complaints of straining to void, and the remaining three patients had mixed urinary symptoms. Hence, voiding complaints were less commonly observed in our pool of patients, which is difficult to explain with the small sample size.

Constipation has been reported to be present in more than half of the patients with PD with one-fifth reporting fecal incontinence.[5],[26] Although we did neither record bowel-related complaints in patients nor was the objective of the study to advise bowel management; however, it is interesting to note that 12 out of 22 patients had absent “voluntary anal contraction-VAC” with the majority (20/22) had anal reflex and tone present. The absence of VAC is of significance as it may lead to the episodes of bowel incontinence in these patients and while giving “bowel program”, one has to be mindful of it.

It has been reported that in levodopa naïve mild PD patients, initially the dose causes deterioration of urinary dysfunction; however, with chronic use, the urinary symptoms tend to improve.[27] In the present study, all patients except 1 was taking levodopa plus carbidopa at the time of reporting to us as well as during the time UDS was performed and the dosage was not altered. Hence, the effect of this particular medication on urinary complaints and UDS observation is impossible to comment on in the present study.

In PD, degeneration of basal ganglia results in partial or total disconnection of the micturition reflex from the voluntary control resulting in uninhibited detrusor contractions at low bladder volumes. This is mediated through D1 receptors. Cell depletion in the substantia nigra results in loss of this inhibition resulting in detrusor overactivity.[28],[29] Similarly, frontal lobe dysfunction with tau protein accumulation and neuropathological changes in the substantia nigra, striatum, medial globus pallidus, subthalamic nucleus, and several brainstem nuclei are responsible for urinary dysfunction in patients with PSP.[30],[31]

Studies in the past have suggested that the majority of the patients with PD were found to have overactive detrusor with detrusor-sphincter synergy based on UDS.[32],[33] Our study showed that mixed results with almost equal number of patients with overactive detrusor had synergic and dyssynergic sphincter. However, with a small sample size in our study, it will not be appropriate to draw conclusions or corroborate or refute the findings of earlier studies. The important observation was that more than half of the patients were found to have overactive detrusor in the present study. Six out of 22 patients (27.3%) were found to have normal detrusor pressure, meaning thereby that they showed no/minimal detrusor activity during filling phase and were able to generate normal pressure during voiding phase. Two-third of these patients had PSP as diagnosis whereas the remaining two were cases of PD. Four of these patients were advised voluntary micturition without medication, supportive, or behavioral measures. The remaining two had nonrelaxing sphincter and were advised timed voiding with clean intermittent self-catheterization (CISC) for bladder emptying. Intact sensations make it painful for them to perform timed voiding with CISC as compared to patients with myelopathy with sensory loss or impairment. Most of the patients, who reported in the follow-up showed good compliance with the management advised. Eight patients, found to have NDO, were advised with antimuscarinic medications in the form of either tolterodine or oxybutynin. Most of the patients responded well with a combination of oral anticholinergic (antimuscarinic) medication along with behavioral and supportive management.

Although anticholinergic medications are the first-choice drugs for the management of NDO, one must balance the therapeutic benefits with potential adverse effects. These medications are known to cross blood–brain barrier and adversely affect cognition/patients with dementia.[34],[35] One important observation in the study was as many as nine patients were already diagnosed as having dementia (6 patients with PSP and 3 with PD). The role of anticholinergic medications has to be carefully observed in these patients. A newer medication Mirabegron, which is a beta-3 adrenergic agonist and causes suppression of the detrusor contractility, has to be tried especially in patients already having dementia associated with PD/PSP. We have no experience with this medication due to nonavailability locally.

Patients with nonrelaxing sphincters or DSD were advised medications such as Duloxetine (Selective serotonin-norepinephrine reuptake inhibitor-SNRI) or imipramine (Tricyclic Antidepressant) with varying doses and results. We have limited experience with these medications in patients with PD and PSP but have used them extensively in myelopathy patients with mixed results.

Other than oral antimuscarinic medications, there are some other management options such as local botulinum toxin A injections or deep brain stimulation (DBS) especially in patients with advanced PD.[36],[37] DBS has been reported to influence NDO also and in turn helps in management of urinary symptoms.

   Conclusions Top

Patients with PD and PSP are known to develop urinary symptoms during illness. Clinical complaints and UDS findings do not necessarily match in patients. UDS is recommended to manage these symptoms. Most of the patients respond to oral antimuscarinic medications along with behavioral and supportive therapy. As these patients, especially those with PSP, are known to develop cognitive decline/dementia during illness, the patients need to be followed up regularly to observe deterioration. Some patients may require other methods of bladder management such as botulinum toxin injections and DBS, etc.

The study has some limitations such as small sample size, which is mainly because of patients' reluctance to get short-term admission in neurological rehabilitation department for detailed work-up and UDS.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

   References Top

Mhyre TR, Boyd JT, Hamill RW, Maguire-Zeiss KA. Parkinson's disease. Subcell Biochem 2012;65:389-455.  Back to cited text no. 1
Alves G, Wentzel-Larsen T, Aarsland D, Larsen JP. Progression of motor impairment and disability in Parkinson disease: A population-based study. Neurology 2005;65:1436-41.  Back to cited text no. 2
Hornykiewicz O. Basic research on dopamine in Parkinson's disease and the discovery of the nigrostriatal dopamine pathway: The view of an eyewitness. Neurodegener Dis 2008;5:114-7.  Back to cited text no. 3
Wolters ECh. Non-motor extranigral signs and symptoms in Parkinson's disease. Parkinsonism Relat Disord 2009;15 Suppl 3:S6-12.  Back to cited text no. 4
Sakakibara R, Kishi M, Ogawa E, Tateno F, Uchiyama T, Yamamoto T, et al. Bladder, bowel, and sexual dysfunction in Parkinson's disease. Parkinsons Dis 2011;2011:924605.  Back to cited text no. 5
Chaudhuri KR, Schapira AH. Non-motor symptoms of Parkinson's disease: Dopaminergic pathophysiology and treatment. Lancet Neurol 2009;8:464-74.  Back to cited text no. 6
Honig H, Antonini A, Martinez-Martin P, Forgacs I, Faye GC, Fox T, et al. Intrajejunal levodopa infusion in Parkinson's disease: A pilot multicenter study of effects on nonmotor symptoms and quality of life. Mov Disord 2009;24:1468-74.  Back to cited text no. 7
Wolters EC, Braak H. Parkinson's disease: Premotor clinico-pathological correlations. J Neural Transm 2006;113:303-12.  Back to cited text no. 8
Defreitas GA, Lemack GE, Zimmern PE, Dewey RB, Roehrborn CG, O'Suilleabhain PE, et al. Distinguishing neurogenic from non-neurogenic detrusor overactivity: A urodynamic assessment of lower urinary tract symptoms in patients with and without parkinson's disease. Urology 2003;62:651-5.  Back to cited text no. 9
Sakakibara R, Tateno F, Kishi M, Tsuyuzaki Y, Uchiyama T, Yamamoto T, et al. Pathophysiology of bladder dysfunction in Parkinson's disease. Neurobiol Dis 2012;46:565-71.  Back to cited text no. 10
Sakakibara R, Uchiyama T, Yoshiyama M, Hattori T. Disturbance of micturition in Parkinson's disease. No To Shinkei 2001;53:1009-14.  Back to cited text no. 11
Uchiyama T, Sakakibara R, Yamamoto T, Ito T, Yamaguchi C, Awa Y, et al. Urinary dysfunction in early and untreated Parkinson's disease. J Neurol Neurosurg Psychiatry 2011;82:1382-6.  Back to cited text no. 12
Bower JH, Maraganore DM, McDonnell SK, Rocca WA. Incidence of progressive supranuclear palsy and multiple system atrophy in Olmsted county, Minnesota, 1976 to 1990. Neurology 1997;49:1284-8.  Back to cited text no. 13
Schrag A, Ben-Shlomo Y, Quinn NP. Prevalence of progressive supranuclear palsy and multiple system atrophy: A cross-sectional study. Lancet 1999;354:1771-5.  Back to cited text no. 14
Nath U, Ben-Shlomo Y, Thomson RG, Morris HR, Wood NW, Lees AJ, et al. The prevalence of progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome) in the UK. Brain 2001;124:1438-49.  Back to cited text no. 15
Steele JC, Richardson JC, Olszewski J. Progressive supranuclear palsy. A heterogeneous degeneration involving the brain stem, basal ganglia and cerebellum with vertical gaze and pseudobulbar palsy, nuchal dystonia and dementia. Arch Neurol 1964;10:333-59.  Back to cited text no. 16
Xie T, Kang UJ, Kuo SH, Poulopoulos M, Greene P, Fahn S, et al. Comparison of clinical features in pathologically confirmed PSP and MSA patients followed at a tertiary center. NPJ Parkinsons Dis 2015;1:15007.  Back to cited text no. 17
Yamamoto T, Tateno F, Sakakibara R, Furukawa S, Asahina M, Uchiyama T, et al. Urinary dysfunction in progressive supranuclear palsy compared with other parkinsonian disorders. PLoS One 2016;11:e0149278.  Back to cited text no. 18
Schäfer W, Abrams P, Liao L, Mattiasson A, Pesce F, Spangberg A, et al. Good urodynamic practices: Uroflowmetry, filling cystometry, and pressure-flow studies. Neurourol Urodyn 2002;21:261-74.  Back to cited text no. 19
Gupta A, Kumar SN, Taly AB. Urodynamic profile in acute transverse myelitis patients: Its correlation with neurological outcome. J Neurosci Rural Pract 2017;8:44-8.  Back to cited text no. 20
[PUBMED]  [Full text]  
Gupta A, Taly AB. Urodynamic profile of patients with neurogenic bladder following non-traumatic myelopathies. Ann Indian Acad Neurol 2013;16:42-6.  Back to cited text no. 21
[PUBMED]  [Full text]  
Fahn S, Elton RL. Members of the UPDRS development committee. The Unified Parkinson's disease rating scale. In: Fahn S, Marsden CD, Caine DB, Goldstein M, editors. Recent Developments in Parkinson's Disease. Vol. 2. Florham Park, NJ: Macmillan Healthcare Information; 1987. p. 153-63, 293-304.  Back to cited text no. 22
Sakakibara R, Shinotoh H, Uchiyama T, Sakuma M, Kashiwado M, Yoshiyama M, et al. Questionnaire-based assessment of pelvic organ dysfunction in Parkinson's disease. Auton Neurosci 2001;92:76-85.  Back to cited text no. 23
Lemack GE, Dewey RB Jr., Roehrborn CG, O'Suilleabhain PE, Zimmern PE. Questionnaire-based assessment of bladder dysfunction in patients with mild to moderate Parkinson's disease. Urology 2000;56:250-4.  Back to cited text no. 24
Campos-Sousa RN, Quagliato E, da Silva BB, de Carvalho RM Jr., Ribeiro SC, de Carvalho DF, et al. Urinary symptoms in Parkinson's disease: Prevalence and associated factors. Arq Neuropsiquiatr 2003;61:359-63.  Back to cited text no. 25
Edwards LL, Pfeiffer RF, Quigley EM, Hofman R, Balluff M. Gastrointestinal symptoms in Parkinson's disease. Mov Disord 1991;6:151-6.  Back to cited text no. 26
Brusa L, Petta F, Pisani A, Moschella V, Iani C, Stanzione P, et al. Acute vs. chronic effects of l-dopa on bladder function in patients with mild Parkinson disease. Neurology 2007;68:1455-9.  Back to cited text no. 27
Yeo L, Singh R, Gundeti M, Barua JM, Masood J. Urinary tract dysfunction in Parkinson's disease: A review. Int Urol Nephrol 2012;44:415-24.  Back to cited text no. 28
Blackett H, Walker R, Wood B. Urinary dysfunction in Parkinson's disease: A review. Parkinsonism Relat Disord 2009;15:81-7.  Back to cited text no. 29
Williams DR, Lees AJ. Progressive supranuclear palsy: Clinicopathological concepts and diagnostic challenges. Lancet Neurol 2009;8:270-9.  Back to cited text no. 30
Donker Kaat L, Boon AJ, Kamphorst W, Ravid R, Duivenvoorden HJ, van Swieten JC, et al. Frontal presentation in progressive supranuclear palsy. Neurology 2007;69:723-9.  Back to cited text no. 31
Araki I, Kuno S. Assessment of voiding dysfunction in Parkinson's disease by the international prostate symptom score. J Neurol Neurosurg Psychiatry 2000;68:429-33.  Back to cited text no. 32
Ventimiglia B, Patti F, Reggio E, Failla G, Morana C, Lopes M, et al. Disorders of micturition in neurological patients. A clinical study of 786 patients. J Neurol 1998;245:173-7.  Back to cited text no. 33
Todorova A, Vonderheid-Guth B, Dimpfel W. Effects of tolterodine, trospium chloride, and oxybutynin on the central nervous system. J Clin Pharmacol 2001;41:636-44.  Back to cited text no. 34
Kay GG, Abou-Donia MB, Messer WS Jr., Murphy DG, Tsao JW, Ouslander JG, et al. Antimuscarinic drugs for overactive bladder and their potential effects on cognitive function in older patients. J Am Geriatr Soc 2005;53:2195-201.  Back to cited text no. 35
Knüpfer SC, Schneider SA, Averhoff MM, Naumann CM, Deuschl G, Jünemann KP, et al. Preserved micturition after intradetrusor onabotulinumtoxinA injection for treatment of neurogenic bladder dysfunction in Parkinson's disease. BMC Urol 2016;16:55.  Back to cited text no. 36
Winge K, Nielsen KK, Stimpel H, Lokkegaard A, Jensen SR, Werdelin L, et al. Lower urinary tract symptoms and bladder control in advanced Parkinson's disease: Effects of deep brain stimulation in the subthalamic nucleus. Mov Disord 2007;22:220-5.  Back to cited text no. 37


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