Use of Electrical Stimulation of the Posterior Tibial Nerve in Patients

with Bladder Hyperactivity as a Substitute for Pharmacological Therapy

based on Solifenacin Succinate and Oxybutynin Hyloridrate

Fabiana Bianchi Perez

, Jos

e Natal de Souza

, Nathalia Cristina Rosa

Cristiano Jacques Miosso

and Adson Ferreira da Rocha

Department of Medicine, University of Brasilia, Brasilia, DF, Brazil

Department of Pharmacology, University Alfredo Nasser, Aparecida de Goi

ania, GO, Brazil

Department of Physiology, University Alfredo Nasser, Aparecida de Goi

ania, GO, Brazil

University of Bras

ılia at Gama, Gama, DF, Brazil

Keywords:

Electrical Stimulation, Neurogenic Bladder Incontinence, Posterior Tibial Nerve, Parasympathetic System

Inhibitor, Anticholinergic Syndrome.

Abstract:

In a previous paper, we proposed a technique for the therapeutic use of Transcutaneous Electrical Nerve Stim-

ulation (TENS) of the posterior tibial nerve. The goal was to treat patients with signs of urinary incontinence

(UI) due to detrusor overactivity (DO). We now conduct a comparison between our proposed TENS technique

and the most commonly used treatment against DO, namely the pharmacological therapy based on solifenacin

succinate and oxybutynin hydrochloride. Our goal is to show that the TENS of the posterior tibial nerve treats

UI associated with DO, as well or better than the pharmacological treatment, but without the adverse side ef-

fects of the drugs (the so-called cholinergic syndrome). Method: we applied the proposed posterior tibial nerve

TENS in 21 patients, including the TENS Burst anaesthetic current. We treated each patient in 10 sessions, 2

times per week, for 20 minutes each session. Each patient could control the current intensity, in order to keep

it at comfortable levels, and in order to still be able to move the halux, thus simulating the Babinski reﬂex.

Results: we observed that with the proposed TENS approach and with the removal of the pharmacological

treatment, the cholinergic syndrome symptoms disappeared after 3 days without drugs, whereas we attained

the modulation of the non-inhibited detrusor contractions. Conclusion: this research provides evidence of the

proposed TENS technique’s efﬁciency in eliminating the effects of the hyperactive bladder, while avoiding the

symptoms of cholinergic syndrome associated to the more common pharmacological treatment. The statistical

tests showed that the reductions of DO symptoms and of the cholinergic syndrome were signiﬁcantly improved

over the pharmacological treatment (p < 0.01). This improves patients’ life quality by reducing or eliminating

the social discomfort and hygiene problems associated to UI while avoiding the cholinergic syndrome.

1 INTRODUCTION

Detrusor hyperactivity is a type of urinary inconti-

nence, associated to severe social discomfort and hy-

giene problems. It also leads to important changes in

urinary frequency (including an increased number of

enuresis cases) and to the need for using urinary-loss

protection devices (Coyne et al., 2003; O’Conor et al.,

1998).

Among the possible treatment modalities, phar-

macological therapy is a common approach (Diokno

and Ingber, 2006), based for example on solifenacin

succinate and oxybutinin hydrochloride. However,

this approach usually leads to strong side effects, such

as dry mouth, blurred vision, and intestinal consti-

pation, which are jointly called the cholinergic syn-

drome.

In this context, we propose and evaluate a differ-

ent type of treatment based on electrical stimulation

of the posterior tibial nerve, with the purpose of re-

ducing the detrusor hyperactivity while avoiding the

cholinergic syndrome. We applied the proposed pro-

tocol in 10 sessions and with 21 patients, and our re-

sults suggest that the treatment reduces the effects of

detrusor hyperactivity without the side effects of the

pharmacological treatment.

Perez, F., Souza, J., Rosa, N., Miosso, C. and Rocha, A.

Use of Electrical Stimulation of the Posterior Tibial Nerve in Patients with Bladder Hyperactivity as a Substitute for Pharmacological Therapy based on Solifenacin Succinate and Oxybutynin

Hyloridrate.

DOI: 10.5220/0005826602750281

In Proceedings of the 9th International Joint Conference on Biomedical Engineering Systems and Technologies (BIOSTEC 2016) - Volume 1: BIODEVICES, pages 275-281

ISBN: 978-989-758-170-0

275

2 BACKGROUND

In pharmacological therapy applied to disorders of the

detrusor and external urhetral sphincter, it is impor-

tant to analyze the neurophysiology of urination, and

its physio-pathological disorders. The injury or ill-

ness of the nervous system is an important compli-

cation of the urinary tract (UT). Specially, the neu-

rogenic bladder has several possible causes such as

spinal cord injury, stroke, brain stem injury, lesions in

the cerebral cortex, peripheral nervous system injury,

multiple sclerosis, quadriplegia and paraplegia.

2.1 Urination Control

The urination control is a neural-physiological pro-

cess which is controlled by the sympathetic and the

parasympathetic systems. The continence phase is

controlled by the sympathetic system with the alpha

1 and beta 2 adrenergics receptors. These are re-

sponsible for the contraction of the external sphincter

ureter and the perineum and detrusor muscles. The

parasympathetic system, on the other hand, controls

the urination itself based on a different mechanism,

using the perineum muscle and urethral sphincter to

relax and the detrusor muscle contract. Figure 1 illus-

trates this process.

2.2 Bladder Hyperactivity

Involuntary loss of urine is a problem of social order

and hygiene, causing embarrassment and changes in

behavior such as social isolation, low self-esteem and

psychosocial disorders (Oliveira et al., 2007). The

most common etiology of urinary incontinence is neu-

rogenic (Monteiro et al., 2009; van der Pal et al.,

2006; Coyne et al., 2003; Fischer-Sgrott et al., 2009).

The four handles or neurological pathways in the

control of urination, and which are related to each

other, are: the core trunk detrusor cerebral cortex

(loop I), the core detrusor muscle spinal / sacral brain-

stem (loop II)-sacral urethral sphincter of the bladder

(loop III), and the sacral-brain (loop IV). Pathways I

and IV are responsible for voluntary control of urina-

tion. Pathways II and III, on the other hand, regulate

the contractions of the detrusor bladder emptying to

promote and coordinate efforts between the detrusor

and urethra (Stephenson and O’Conor, 2004).

The neurogenic bladder dysfunction is deﬁned as

a neurological disease produced by nerve damage

that interferes with the mechanisms of voluntary and

involuntary urination, thus causing changes in nor-

mal bladder function. The neurogenic bladder cor-

responds to the overactive and/or underactivity of the

Figure 1: Neurophysiology of urination: 1) Motor cortex;

2) afferent nerve; 3) Parasympathetic ganglion; 4) Pontine

“continence” center (L-region) – 4a: Nerve impulses stimu-

late contraction of muscle-hypogastric nerve and 4b: Nerve

impulses stimulate relaxation of internal urethral sphincter

muscle-pudendal nerve.

detrusor (Azevedo et al., 1990).

The underactive bladder retention or overﬂow is

characterized by urinary loss that occurs when intra-

vesical pressure exceeds urethral pressure. This is as-

sociated with bladder distention, but in the absence

of detrusor activity. This overﬂow happens when one

reaches the limits of distensibility or compliance of

the bladder (Miltrano, 2009).

According to the International Continence Soci-

ety, the overactive bladder is deﬁned as a neurogenic

injury due to the presence of involuntary detrusor con-

tractions during the ﬁlling phase (Coelho, 2009). This

is characterized by urinary incontinence, urinary fre-

quency, nocturia and urgency (Fischer-Sgrott et al.,

2009; Jones III et al., 1988; O’Conor et al., 1998;

Guidi et al., 2005).

3 PHARMACHOLOGICAL

TREATMENT

Several drugs have been developed for treating the

overactive bladder. However, in our clinical practice

we observed that most become innocuous at the end,

leading to a symptom reduction that only lasts during

BIODEVICES 2016 - 9th International Conference on Biomedical Electronics and Devices

276

drug usage. Other drugs with proven clinical effects,

on the other hand, must be used for long periods and

show severe adverse effects, resulting in high dropout

rates.

3.1 Anticolinergics: The Most Used

Drugs

Stimulation of muscarinic receivers M2 and M3 cause

bladder contractions. Anticholinergic drugs inhibit

these receivers, causing the decrease of contractions’

amplitude and the increase of the ﬁrst contraction vol-

ume, thus resulting in a higher bladder functional ca-

pacity.

These drugs’ parasympatholytic action occurs se-

lectively on these receptors. Yet, they have uncom-

fortable system effects, since the inhibition of mus-

carinic receivers do not occur only in the bladder,

where M2 and M3 receivers predominate. In the blad-

der, the M2 muscarinic are predominant, but the M3

receivers are more functionally important, mediating

direct contraction of detrusor muscle (Chapple et al.,

2002).

This prevents the interaction of acetylcholine with

receptors and inhibits the release of this neurotrans-

mitter in the synaptic cleft post-ganglionic.

There are two types of anticholinegic: (i) I-Mixed

(antispasmodics) — combine action antimuscarinic

with relax direct muscule (receiver independent) and

local anesthetic. The main representative of these

groups and cloridrat oxibutina. (ii) II-Pure — repre-

sented by tolterodine, propantelina, darifenacin, and

vamicamide. They are classiﬁed also with aminoter-

ciarios or aminoquaternarios. The difference between

the two groups refers to the ability of the blood brain

barrier crossing aminioterciarios.

The use of anthicholinergic is not free of side ef-

fects. Its major side effects are: dry mouth, consti-

pation and blurred vision, headache, dyspepsia and

even diarrhea, which corroborates with a dropout rate

of treatment during the ﬁrst three months around

25,5% (Diokno and Ingber, 2006).

A survey showed that only 18% patients remained

taking anticholinergic by one period exceeding six

months. The activation of M3 receivers is due to the

detrusor contraction, but also to the contraction of the

smooth muscles of the gut and salivary glands (Dio-

kno and Ingber, 2006; Chapple et al., 2002).

The ability of the blood brain barrier to cross

the antimuscarinic agents can lead to cognitive alter-

ations, especially in the elderly. These side effects

occur by the relative loss of selectivity for the bladder

over other organs (Appell, 2003).

Other central effects include dizziness, memory

loss and drowsiness, the presence of receptors M1 in

the neocortex, hippocampus and neostratum (Appell,

2003).

Muscarinic receptor antagonists are formally not

recommended for patients with closed angle glau-

come and should be used with care in case of in-

fravesical obstruction, dur to the possibility of pre-

cipitating urinary retention.

4 TREATMENTS BASED ON

ELECTRICAL STIMULATION

The existing electrical stimulation techniques for UI

treatment are based on applying electrical current di-

rectly over the perineum muscle. This approach uses,

in the case of male patients, internal anal electrodes

and, in the case of female patients, internal or surface

vaginal electrodes. These techniques are embarrass-

ing, invasive (in the case of internal electrodes), and

may cause discomfort and burns in patients with ab-

normal sensibility (Marques, 2008).

Treatments with transcutaneous electrical stimu-

lation in the posterior tibial nerve aim at reducing UI

and assume that bladder neural projections exist in

that nerve’s path (Fischer-Sgrott et al., 2009).

The TENS current is used for the treatment of

urinary incontinence by bladder hyperactivity (BH).

The electrodes are placed bilaterally in the medial re-

gion of the legs, causing motor and sensory stimu-

lation as the current is applied (Fischer-Sgrott et al.,

2009). During each session, the patient’s neurologi-

cal physiotherapist or urological physiotherapist ob-

serves the stimulation caused by the motor current,

and the sensory way is not changed to modulate the

current ﬂow. This technique promotes the reduction

of involuntary detrusor contractions (Marques, 2008).

Regarding the TENS current for the treatment of BH,

some researchers propose a sequence of pulses with

a frequency of around 20 Hz and with a duration of

around 200 milliseconds per pulse (Amarenco et al.,

2003). The therapies based on electrical currents can

be used in neurological patients with abnormal sensi-

tivity, because applying electrical stimulation results

in rhythmic ﬂexing of the hallux, thus indicating the

correct placement of electrodes and conﬁrming this

to be intact innervation (Maciel and Souto, 2009;

Fischer-Sgrott et al., 2009). However, in individu-

als with Babinski’s reﬂex, it is difﬁcult to apply the

current therapeutic modulation due to incorrect motor

response from these individuals, so it becomes impos-

sible to control the current intensity and the electro-

motor response (Perez, 2011).

In the case of hyposensitivity, the dose should be

Use of Electrical Stimulation of the Posterior Tibial Nerve in Patients with Bladder Hyperactivity as a Substitute for Pharmacological

Therapy based on Solifenacin Succinate and Oxybutynin Hyloridrate

277

(a)

(b)

(c)

Figure 2: (a) Positioning of the 4 electrodes, two for

each channel, used to apply the electrical currents during

the TENS sessions. (b) Detail of the electrode position-

ing. Source: (Marques, 2008). (c) The connection be-

tween the posterior tibial nerve and the detrusor muscle;

source: http://www.bladderclinic.com.au/images/bladder-

conditions/neurogenic-bladder.png.

applied until it causes rhythmic inﬂections of the big

toe, and it should then be reduced until the motor ac-

tion disappears. The provided dose agrees with sev-

eral studies arguing that the ideal intensity must be

maintained according to the threshold of each patient

and below the motor threshold (Fischer-Sgrott et al.,

2009; Maciel and Souto, 2009; Amarenco et al., 2003;

C.Kabay et al., 2009).

The use of TENS in the current technique of pos-

terior tibial nerve can reduce the uninhibited detrusor

contractions and improve the quality of life of patients

with DO due to a reduction of urinary incontinence

and of the number of times that the patient urinates.

This can result in a better quality of sleep, humor, and

personal relationships, as well as in less embarrass-

ment and in reduction of stress. It can also potentially

reduce the use of medication while reducing or elim-

inating the sings of anticholinergic syndrome.

5 METHODS

In order to collect preliminary data, we started with

an assessment of patient’s urological history, using

validated questionnaires applied at Unifesp. The pa-

tients’ selection and inclusion criteria included over-

active bladder and concomitant use of anticholiner-

gics.

We then performed the Babinski test in the case of

patients with hyposensitivity and hyperreﬂexia (a pre-

requisite for patients to remain in the study was the

presence of a neurological dysfunction such as multi-

ple sclerosis). We only started the Electrotherapy in

the case of patients with absence of the Babinski re-

ﬂex in at least one lower limb.

The patients who were selected to participate in

the study were then submitted to a physio-therapeutic

protocol. The main procedure consisted in applying

in an electrical current to the posterior tibial nerve,

according to the following steps.

On the ﬁrst evaluation day, we applied the phys-

iotherapy assessment protocol forms, which the pa-

tient completed in the Urogynecology laboratory at

Unifesp. We instructed the patient to complete a void-

ing diary for three days after treatment.

During the neurological assessment, a physical

examination showed no sensory deﬁcit and bilateral

Babinski’s reﬂex. Given that no pathological reﬂex

existed, we positioned the electrodes in the path of

the posterior tibial nerve, to detect whether innerva-

tion was intact, by using electrical stimulation (we

used the TENS NEURODYN/FES portable device, by

Ibramed Ltda). This stimulation was based on a se-

quence of 200-millisecond pulses, with a frequency of

20 Hz, following the recommendation in (Amarenco

et al., 2003).

The treatment protocol consisted of 10 sessions,

twice a week and lasting 20 minutes each. We applied

the TENS current through two channels, using four

electrodes positioned transcutaneously and bilaterally

in the lower limb (2 electrodes per channel). For each

BIODEVICES 2016 - 9th International Conference on Biomedical Electronics and Devices

278

channel, one electrode was ﬁxed to the posterior me-

dial malleolus and the other 10 cm above. The inten-

sity parameter due to hyposensitivity was measured

through the signal engine rhythmic inﬂections of the

hallux. A maximum intensity of 30 mA was applied,

for safety reasons. In the case of patients with nor-

mal sensibility, the current intensity was adjusted for

comfort.

6 RESULTS AND DISCUSSION

This paper presents the results of 21 case studies mon-

itored by descriptive assessments from the Unifesp

Physiotherapeutic Protocol in Urogynecology and the

voiding diary for three days. The patients were sub-

mitted to physiotherapeutic treatment with transcuta-

neous electrical stimulation in order to attenuate uro-

logical clinical complaints. This justiﬁes the choice

of a treatment by elective electrostimulation separated

from other techniques such as kinesiotherapy. We ap-

plied both evaluation procedures before treatment and

after 10 TENS sessions.

According to (C.Kabay et al., 2009), when ap-

plied to people suffering from multiple sclerosis, the

technique noticeably decreased nocturia in 75% of pa-

tients. Marques reports decrease in nocturia with 38%

of symptoms relief (Marques, 2008). Another study

found improvement in nighttime urination in 21% of

cases (F. E. Govier et al., 2001). Tables 1 and 2 show

that before and after 10 sessions of electrical stimula-

tion of the posterior tibial nerve, there was a decrease

in the signs of enureses, as well as a reduction in the

need for urine-loss protection, and of symptoms asso-

ciated to the cholinergic syndrome.

We can explain the improvement of urinary ur-

gency conditions based on a study in which urody-

namic evaluation with electrical stimulation of the

posterior tibial nerve revealed that the maximum blad-

der capacity can increase together with a decrease of

involuntary detrusor contractions during standard cys-

tometry (Amarenco et al., 2003).

This research aimed at verifying the efﬁcacy of the

electrical stimulation as applied to the posterior tib-

ial nerve in order to control the detrusor hyperactiv-

ity (while reducing the symptoms related to the non-

inhibitted detrusor contractions and the anticholiner-

gic syndrome).

We analyzed ﬁve conditions and symptoms before

and after applying the proposed electrical stimulation

protocol: i) number of enuresis cases per night; ii)

number of needed urine-protection devices (UPD) per

day; iii) dry mouth; iv) intestinal constipation; and

v) blurred vision. Tables 1 and 2 describe the obtained

results.

We then conducted a statistical analysis of the

measured conditions and symptoms. The null hy-

potheses refer to each condition or symptom being the

same or even worse after the stimulation sessions, as

compared to the values measured before them. The

preliminary normality tests we performed indicated

that the measured values do not follow a normal dis-

tribution, and therefore we used the non-parametric

Wilcoxon test in order to evaluate the main null hy-

potheses.

Table 3 shows the p-values obtained for the null-

hypothesis associated to each of the considered con-

dition or symptom. Note that the low values (p < 0.1)

indicate that the null hypothesis can be rejected. This

suggests that the applied electrical stimulation proto-

col signiﬁcantly reduces the corresponding condition

or symptom.

Hence, the applied electrical stimulation can in-

hibit or reduce the adverse effects of the anticholin-

ergic drugs. This conservative and non-invasive tech-

nique was hence beneﬁcial to the evaluated patients

suffering from detrusor hyperactivity.

These results are the beginning of an intense

planned study of the use of electrical stimulation of

the posterior tibial nerve in patients with bladder hy-

peractivity as a substitute for pharmacological ther-

apy based on solifenacin succinate and oxybutinin hy-

drochloride. By increasing the sample size and by

evaluating the patients for longer periods, we want to

further evaluate other impacts of the proposed proto-

col, including long-term effects.

7 CONCLUSION

Patients with hyperactive bladder that use anticholin-

ergic drugs may present the cholinergic syndrome,

characterized by dry mouth, intestinal constipation,

and blurred vision. These symptoms add to the prob-

lems caused by the non-inhibited detrusor contrac-

tions, including loss of urine and enuresis. By replac-

ing the pharmacological approach by the electrical

stimulation of the posterior tibial nerve, we observed

an improvement of the hyperactive bladder condition

(p < 0.01), without the inconvenience associated to

the cholinergic syndrome.

We also emphasize that the proposed approach is

noninvasive, does not cause pain, and is cheaper than

the continuous use of solifenacin succinate and oxy-

butynin hydrochloride. It therefore has an important

effect on the patients’ quality of life, in terms of social

and economical aspects.

Use of Electrical Stimulation of the Posterior Tibial Nerve in Patients with Bladder Hyperactivity as a Substitute for Pharmacological

Therapy based on Solifenacin Succinate and Oxybutynin Hyloridrate

279

Table 1: Cases of enuresis per night and number of used urine-loss protection per day for all male and female participants, as

measured before and after the electrical stimulation (ES) sessions. We interrupted the pharmacological treatment (medication

A or B) in all cases, after the ES started.

Patient ID Genre Age NIC

Medication Before Electrical Stimulation After Electrical Stimulation

type Enuresis/night ULP/day Enuresis/night ULP/day

1 Female 46 NO A 3 1 0 0

2 Female 55 YES A 4 3 3 0

3 Male 22 YES A 6 0 0 0

4 Female 67 YES A 3 4 0 1

5 Male 25 YES A 3 3 0 1

6 Female 76 CE A 3 6 1 1

7 Female 56 YES B 2 5 0 0

8 Male 64 CE B 2 6 0 1

9 Male 79 YES B 3 3 0 0

10 Female 50 CE A 1 0 0 0

11 Female 67 YES A 4 0 0 0

12 Male 72 YES – 3 8 1 3

13 Male 67 YES A 0 3 0 0

14 Male 63 YES A 1 4 0 1

15 Female 43 YES B 2 2 0 0

16 Male 70 CE B 7 1 2 0

17 Female 41 YES B 0 0 0 0

18 Female 57 YES – 3 2 0 0

19 Female 52 YES B 1 0 0 0

20 Female 41 YES A 0 0 0 0

21 Male 89 YES A 4 3 1 0

Table 2: Symptoms of the cholinergic syndrome.

Patient ID

Before Electrical stimulation After Electrical Stimulation

Dry mouth Intestinal constipation Blurred Vision Dry mouth Intestinal constipation Blurred Vision

1 NO YES NO NO NO NO

2 NO YES NO NO NO NO

3 YES YES NO NO YES NO

4 YES NO NO NO NO NO

5 YES YES NO NO NO NO

6 YES NO YES NO NO NO

7 NO YES NO NO NO NO

8 YES NO NO NO NO NO

9 YES NO NO NO NO NO

10 YES NO NO NO NO NO

11 YES YES NO NO YES NO

12 NO NO NO NO NO NO

13 YES YES NO NO NO NO

14 YES YES YES NO YES NO

15 NO YES NO NO NO NO

16 YES NO NO NO NO NO

17 YES YES YES NO NO NO

18 NO YES NO NO NO NO

19 YES NO NO NO NO NO

20 YES NO NO NO NO NO

21 YES YES YES NO NO NO

ACKNOWLEDGEMENTS

The authors thank Doctor Denise Sistorelli Diniz, a

neurologist at the Hospital das Cl

ınicas, at the Fed-

eral University of Goi

as, for her assistance and use-

ful comments and suggestions. We also thank the Al-

fredo Nasser School (Unifan).

BIODEVICES 2016 - 9th International Conference on Biomedical Electronics and Devices

280

Table 3: Results, in terms of p-values, of the statistical tests

regarding the null hypothesis that each symptom or condi-

tion after the electrical stimulation (EE) is equal or worse

than before the EE.

Condition or symptom p-value

Enuresis 7.9 · 10

−6

Need for urine-loss protection 2.9 · 10

−4

Dry mouth

∗

9.8 · 10

−7

Intestinal constipation

∗

0.002

Blurred vision

∗

0.021

∗

Symptoms associated to the cholinergic syndrome.

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