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July2013 Vol.50 Issue:      3 (Supp.) Table of Contents
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Efficacy of Posterior Tibial Nerve Stimulation on Detrusor Overactivity of Idiopathic Parkinson’s Disease Patients Clinical and Urodynamic Evaluation

Mohamed Y. El-Senousy1, Ehab S. Mohammed1, Hazem A. Fayed1, Ehab A. El-Seidy1, Mohamed K.Khalil1, Mohamed Abo  El-Enen2, Maged M. Ragab2, Mohamed Elnady2, Mohamed R. Taha2

Departments of Neurology1, Urology2, Tanta University; Egypt

 



ABSTRACT

Background: Lower urinary tract dysfunction is often occurs in patients with Parkinson's disease (PD) that is primarily induced by neurogenic detrusor overactivity (NDO). Objective: To evaluate the clinical and urodynamic effects of posterior tibial nerve stimulation (PTNS) on NDO of PD patients. Methods: Thirty-three patients with PD and were subjected to weekly treatment with percutaneous PTNS for 12 weeks. The clinical manifestations such as nocturia, frequency of micturition and incontinence episodes were analyzed before and after PTNS using voiding diary, international prostate symptom (IPSS) and quality of life (QOL) scores.  Filling and voiding cystometry were done for comparison of the urodynamic parameters suggestive of NDO namely volume at first involuntary detrusor contraction (1st IDCV), maximum detrusor pressure (Pdetmax) and maximum cystometric capacity (MCC). Result:  Frequency and leakage episodes have significantly decreased from a mean of 10.5±2.1 and 3.5±1.0 to a mean of 7.8±1.2 and 2.2±0.7 respectively (P<0.01). Meanwhile nocturia decreased from 3.4±0.8 to 2.1±0.8 (P=0.06). IPSS and QOL were significantly better after PTNS. Likewise, urodynamic parameters also significantly improved. Mean 1st IDCV and MCC significantly increased after PTNS from a mean of 150.6±46.6 and 232.9±63.1 to 271.3±67.3 and 329.1±65.7 respectively (P<0.01). No serious adverse events or side effects were observed during or after treatment. Conclusion: The use of PTNS in IPD patients with overactive bladder are encouraging for amelioration of detrusor overactivity and improving bladder storage symptoms. However, long-term follow-up is needed for planning to maintenance protocols. [Egypt J Neurol Psychiat Neurosurg.  2013; 50(3): 265-270]

Key Words: Parkinson's disease, detrusor overactivity, posterior tibial nerve stimulation.

Correspondence to Ehab S. Mohammed, Department of Neurology, Tanta University Egypt.

Tel: +201144656670    E-mail:ehab_metwally70@yahoo.com




INTRODUCTION

 

Patients with Idiopathic Parkinson’s disease (IPD) are usually complaining of lower urinary tract symptoms (LUTS) that significantly affect their quality of life. The incidence of LUTS in those patients ranges from 37% to 70%.1 These are usually storage symptoms in the form of urgency, increased daytime frequency, nocturia, and urge urinary incontinence.2 Neurogenic detrusor overactivity (NDO), is the most commonly recorded urodynamic finding occurring in about 67% of IPD patients. These irritative symptoms deteriorate progressively with the disease severity and significantly affect the quality of life of these patients.3

Oral antimuscarinic agents are usually the preferred treatment option, yet they usually provide only modest clinical improvement and in a significant number of patients they induce unwanted or intolerable

 

side effects such as dry mouth and constipation.4 Another disadvantage is that anticholinergics may further induce or worsen the cognitive impairment especially in these parkinsonian patients.5

The use of percutaneous tibial nerve stimulation (PTNS) was initiated at 1983 by Mc Guire and colleagues6 and subsequently gained popularity after Stoller’s work.7,8 Different experimental and human researches were done on PTNS as neuromodulative treatment in voiding dysfunction with varying degrees of success in different neurologic diseases.9

The aim of this study is to evaluate the efficacy of PTNS as a neuromodulative treatment in management of symptoms of NDO in IPD patients.

 

 

SUBJECTS AND METHODS

 

This study was conducted in Urology and Neurology departments, Tanta University Hospital. Thirty-three IPD patients with neurogenic detrusor overactivity were enrolled in this study. Inclusion criteria were IPD patients complaining of overactive bladder symptoms and proved by the presence of involuntary detrusor contractions as a sign of NDO during cystometry. All patients were subjected to history taking, International Prostate Symptom Score (IPSS)10 complete physical and neurological examination and urodynamic evaluation. All men underwent digital rectal examinations and transrectal ultrasound to exclude benign prostatic enlargement (BPE). Screening for UTI was done before the start of the study and on every visit. IPD patients were classified into five stages according to Hoehn and Yahr disability stages.11 Anticholinergic treatment was stopped one month before the initiation of the treatment sessions and written informed consent was obtained from all participants.

The exclusion criteria were patients with sacral or peripheral nerve lesions, active or recurrent urinary tract infection, pregnancy, young age (<18 years), marked prostatic enlargement, diabetes mellitus, urinary stones, stress urinary incontinence, history of previous continence surgery or history of bladder cancer. In addition, patients with associated neurological disease; as multiple sclerosis, cerebrovascular accident, spina bifida or spinal cord lesions were excluded.

The first step of the procedure was a unilateral insertion of disposable needle for PTNS at a point 5 cm above the medial malleolus and posterior to the tibial edge. Electrical stimulation was performed by low voltage electricity with pulse width 200 msec and frequency of 20 Hz (Urgent PC, From Uroplasty, Minnetonka, MN). The stimulation amplitude was individualized and equal to 1.5 times the threshold for evoking toes plantar flexion and/or fanning. All patients received single session weekly (30 minutes) for 12 weeks.

The urodynamic evaluations and definitions were performed according to the most recent International Continence Society (ICS) recommendations.12 Two filling cystometry was needed for comparison; before PTNS (standard) and after PTNS. Cystometry was performed with normal saline at room temperature and filling rate of 20 ml/min. Intravesical, abdominal and detrusor pressures were measured.

The operator recorded the following parameters: volume at the first involuntary detrusor contraction (1st IDCV), maximal detrusor pressure (Pdetmax) at first involuntary detrusor contraction, volume at maximum cystometric capacity (MCCV), detrusor pressure at maximal flow (PdetQmax) and maximal flow rate (Qmax).

Data were presented as mean ±SD. Analysis was performed with SPSS statistical package version12 (SPSS, USA). For statistical purpose, the disease severity stages were divided according to Hoehn and Yahr classification of IPD disability into mild (stages 1 and 2), moderate (stage 3) and severe (stages 4 and 5).

 

RESULTS

 

A total of 33 patients, twenty-five male patients and 8 female patients, their age ranged from 56 to 68 years (mean 62.48±3.72 years) were enrolled in the study. The duration of illness was 4-10.5 years (mean 6.24±1.99 years). According to Hoehn and Yahr classification of IPD disability stage, we have one patient in stage one, seven patients in stage 2, twenty patients in stage 3, four patients in stage 4, one patient in stage 5. Therefore, eight patients had mild, twenty patients had moderate and five patients had severe disability. Baseline IPSS and QOL scores are reported in Table (1).

Following PTNS marked subjective and objective improvement were seen as evidenced by the reduction in all OAB symptoms including voiding frequency, nocturia and urge incontinence episodes (Table 2).

This was also evident when comparing IPSS scores pre and post PTNS. There was a significant improvement in total IPSS score among patients with moderate disability after PTNS, and similarly was the QOL score (Figure 1 and 2 respectively). Patients with mild and severe stages of disability did improve however; this did not reach statistical significance.

In all patients, baseline urodynamics showed neurogenic detrusor overactivity, characterized by low 1st IDCV, high pressure at 1st IDC and decreased maximum cystometric capacity. Following PTNS urodynamics showed statistically significant increase in 1st IDCV and maximum CCV and a significant decrease in Pdetmax. On the other hand, the change in PdetQmax and Qmax was not statistically significant (Table 3).

One month after the end of last session, 23 patients reported a subjective worsening of symptoms returning to the pretreatment level. Meanwhile all patients reported recurrence of all symptoms at three months of follow up.


 

Table 1. Relation between IPSS, QOL and IPD disability stages.

 

Stages of disability

IPSS

(Mean ±SD)

QOL

(Mean ±SD)

Mild (8)

6.3±1.3

2.5±1.1

Moderate (20)

10.55±2.6

4.3±1.1

Severe (5)

16.20±4.2

5.2±0.8

One way ANOVA P=0.001, IPSS International Prostate Symptom Score, QOL Quality Of Life Score

 

Table 2. Voiding diary pre and post PTNS.

 

 

Pre PTNS

Post PTNS

P-value

Nocturia

3.4±0.8

2.1± 0.8

0.06

Frequency

10.58±2.1

7.88±1.2

0.001

Urge Incontinence

3.52±1.09

2.24±0.7

0.04

PTNS Posterior Tibial Nerve Stimulation

 

 

 

Figure 1. Relation between IPSS at different stages of Parkinsonism before and after PTNS

 

 

 

Figure 2. Relation between QOL at different stages of Parkinsonism before and after PTNS.

Table 3. Urodynamic parameters of IPD patients before and after PTNS.

 

Parameters

Before PTNS

After PTNS

P-value

1st IDCV

150.6±46.6

271.3±67.3

0.001

Pdetmax

32.03±8.6

28.15±5.5

0.03

MCCV

232.9±63.1

329.1±65.7

0.001

PdetQmax

40.58±7.9

37.39±5.3

0.06

Qmax

12.09±2.6

13.21±2.12

0.06

1st IDCV First Involuntary Detrusor Contraction, Pdetmax Maximal Detrusor Pressure At First Involuntary Detrusor Contraction, MCCV Volume At Maximum Cystometric Capacity, PdetQmax Detrusor Pressure At Maximal Flow, Qmax Maximal Flow Rate

 

 


DISCUSSION

 

Most of the lower urinary tract symptoms associated with IPD is due to urinary storage problems.3 The commonest reported finding is neurogenic detrusor overactivity that is commonly treated with anticholinergic drugs.13 However, estimates of the persistence of patients on drug therapy may be as low as 20% at 6 months.14 Dry mouth and constipation are the most commonly reported adverse events. This is further aggravated in the elderly patients of Parkinsonism by the added cognitive impairment well known of anti-muscarinics.15

Sacral nerve stimulation is effective in these refractory patients however, it is expensive and requires implantation and therefore may not always be suitable in such elderly frail adults who have several co-morbidities.9

PTNS is a minimally invasive office based treatment that proved effective in treatment of overactive bladder due to different reasons but would it be suitable for the older adults of Parkinsonism.8

In the current study, a statistically significant decrease in leakage episodes and voiding frequency (p<0.05) and a trend towards significance (p=0.06) in nocturia were observed following PTNS. This successful outcome of PTNS for overactive bladder symptoms in patients with IPD is in line with published results in patients with detrusor overactivity due to different neurogenic conditions.15-17

The Overactive Bladder Innovative therapy trial (OrBIT) is a nonblinded, randomized, multicenter, controlled study of 100 patients that compared the effectiveness of PTNS with that of extended release tolterodine. The reduction in episodes of nocturia and urge incontinence was similar between both groups. At 12 weeks follow-up, 79.5% of PTNS patients considered themselves cured or improved compared with 54.8% of tolterodine patients.14

In a similar study, Krivobordov and colleagues in 2006 examined the effect of PTNS in 29 patients with NDO due to Parkinson’s disease. An over 50% symptomatic improvement was achieved in 26 of 29 patients including 6 patients who were refractory to anticholinergic agents.16

Similarly, there was also a significant change in IPSS and QOL after PTNS in patients with moderate disability but not in patients with mild and severe disability. This might be attributed to the small sample size in both groups with mild (eight patients) and severe (five patients) stages of the disease.

As regards the changes in urodynamic parameters suggestive of NDO, the difference in mean 1st IDCV volume and mean MCC at baseline and after PTNS in this study was statistically significant. Mean Pdetmax at first involuntary detrusor contraction was also statistically significant meanwhile the change in PdetQmax and Qmax did not reach statistical significance.

Kabay and colleagues in 2009 reported nearly the same results with statistically significant change in 1st IDCV, MCC, Pdetmax, PdetQmax and Qmax. The significant change in PdetQmax and Qmax in his study might be attributed to the inclusion of multiple system atrophy (MSA) patients since there were 7 patients out of the 32 patients had pseudodyssynergia.17

Unfortunately, 70% of our patients reported worsening of the symptoms one month after stoppage of treatment. In addition all patients reported such worsening of symptoms three months post treatment. This is in agreement with the study of van der Pal and colleagues18 in which 64% of patients reported greater than 50% worsening in frequency and incontinence episodes after a 6-week pause in treatment. These results might be explained according to the urodynamic findings where PTNS delays the occurrence of involuntary detrusor contractions rather than eliminating it. Such results highlight the necessity of maintenance PTNS therapy for the treatment of detrusor overactivity.

These few reports on the use of PTNS in the management of symptoms of neurogenic detrusor overactivity in Parkinsonian patients is very encouraging in terms of amelioration of the irritative urinary symptoms and consequently improving the quality of life of such patients.

However, all these reports are not placebo-controlled trials or randomized trials comparing the use of PTNS to anticholinergics and none evaluated the long-term effect or maintenance scheme of this neuromodulative treatment. We believe a multi center placebo controlled trial would be very informative but would also be very difficult to accomplish with such techniques. However, giving the above results, we do think that PTNS could be offered safely to those patients who fail anticholinergics or who cannot take the medication.

 

Conclusion

The use of PTNS in IPD patients with overactive bladder are encouraging for amelioration of neurogenic detrusor overactivity and improving bladder storage symptoms. However, more long term follow up studies are needed to plan the best maintenance protocol.

 

[Disclosure: Authors report no conflict of interest]

 

REFERENCES

 

1.        Araki I, Kitahara M, Oida T, Kuno S. Voiding dysfunction and Parkinson's disease: urodynamic abnormalities and urinary symptoms. J Urol. 2000; 164: 1640-3.

2.        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.

3.        Mohamed ES, Ragab MM. Idiopathic Parkinson's disease: Lower urinary tract dysfunction and urodynamic abnormalities. Egypt J Neurol Psychiat Neurosurg. 2010; 47: 381-6.

4.        Winge K, Fowler CJ. Bladder dysfunction in Parkinsonism: mechanisms, prevalence, symptoms, and management. Mov Disord. 2006; 21: 737-45.

5.        Di Stasi SM, Giannantoni A, Vespasiani G, Navarra P, Capelli G, Massoud R, et al. Intravesical electromotive administration of oxybutynin in patients with detrusor hyperreflexia unresponsive to standard anticholinergic regimens. J Urol. 2001; 165: 491-8.

6.        McGuire EJ, Zhang SC, Horwinski ER, Lytton B. Treatment of motor and sensory detrusor instability by electrical stimulation. J Urol 1983; 129: 78-9.

7.        Cooperberg MR, Stoller ML. Percutaneous neuromodulation. Urol Clin North Am. 2005; 32: 71-8.

8.        Stoller ML. Nerve stimulation for pelvic floor dysfunction. Eur Urol. 1999; 35:16.

9.        MacDiarmid SA, Staskin DR. Percutaneous tibial nerve stimulation (PTNS): A literature-based assessment. Curr Bladder Dysfunct Rep. 2009; 4: 29-33.

10.     Wasserman NF. Benign prostatic htperplasia: a review and ultrasound classification. Radiol Clin North Am. 2006; 44(5): 689-710.

11.     Hoehn MM, Yahr MD. Parkinsonism: onset, progression and mortality. Neurology. 1967; 17: 427-42.

12.     Haylen BT, de Ridder D, Freeman RM, Swift SE, Berghmans B, Lee J, et al. An International Urogynecological Association (IUGA)/International Continence Society (ICS) joint report on the terminology for female pelvic floor dysfunction. Neurourol Urodyn. 2010; 29: 4-20.

13.     Defreitas GA, Lemack GE, Zimmern PE, Dewey RB, Roehrborn CG, O'Suilleabhain PE. 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.

14.     Alhasso AA, McKinlay J, Patrick K, Stewart L. Anticholinergic drugs versus non-drug active therapies for overactive bladder syndrome in adults. Cochrane Database Syst Rev. 2006; (4): CD003193.

15.     Peters KM, Macdiarmid SA, Wooldridge LS, Leong FC, Shobeiri SA, Rovner ES, et al. Randomized trial of percutaneous tibial nerve stimulation versus extended-release tolterodine: results from the overactive bladder innovative therapy trial. J Urol. 2009; 182: 1055-61.

16.     Krivoborodov GG, Gekht AB, Korshunova ES. [Tibial neuromodulation in the treatment of neurogenic detrusor hyperactivity in patients with Parkinson's disease]. Urologia. 2006; 4:3-6. [Article in Russian]

17.     Kabay SC, Kabay S, Yucel M, Ozden H. Acute urodynamic effects of percutaneous posterior tibial nerve stimulation on neurogenic detrusor overactivity in patients with Parkinson's disease. Neurourol Urodyn. 2009; 28: 62-7.

18.     van der Pal F, van Balken MR, Heesakkers JP, Debruyne FM, Bemelmans BL. Percutaneous tibial nerve stimulation in the treatment of refractory overactive bladder syndrome: is maintenance treatment necessary? BJU Int. 2006; 97: 547-50.

 

 

 

 

 


 

              

الملخص العربي

 

فاعلية تنبية العصب الظنبوبي الخلفي في علاج زيادة نشاط العضلة النافصة البولية في مرضي مرض باركنسون

دراسة سريرية وديناميكية بولية

 

غالبا ما يعاني مرضي باركنسون من اختلال في وظائف مجري القناة البولية السفلية الذي ينتج في معظم الأحيان من زيادة نشاط العضلة النافصة وهو ما يعود بالسلب علي الحياة اليومية للمريض.

وقد هدفت هذه الدراسة الي تقييم الأعراض السريرية ودراسة ديناميكية المثانة البولية في مرضي مرض باركنسون قبل وبعد علاج زيادة نشاط العضلة البولية النافصة عن طريق تنبية العصب الظنبوبي الخلفي.

وقد شملت هذه الدراسة ثلاثة وثلاثون مريضا بمرض باركنسون مصحوبا بزيادة نشاط العضلة النافصة البولية.

وقد تم إخضاع هؤلاء المرضي الي دورات علاج اسبوعي لمدة اثني عشر أسبوعا بواسطة تنبيه العصب الظنبوبي الخلفي عن طريق الجلد. وقد تم تسجيل وتحليل شكوي المرضي خاصة التبول الليلي اللارادي وعدم القدرة علي التحكم في التبول قبل وبعد العلاج.

وقد وجدت هذه الدراسة تحسنا ملحوظا بعد العلاج في إنقاص شكوي المرضي بما قد يشجع علي استخدام هذه الطريقة في دراسات بعيدة المدي تسهم في مساعدة مرضي مرض باركنسون في تحسين اعتلال القناة البولية السفلية مما يحسن أداءهم في الحياة اليومية.

 

 



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