Deafferentation of the Urinary Bladder and Implantation of a Sacral Anterior Root Stimulator (SARS) for Treatment of the Neurogenic Bladder in Paraplegic Patients / Deafferentation der Harnblase und Implantation von sakralen Vorderwurzelstimulatoren (SARS) zur Behandlung der neurogenen Blase bei querschnittgelähmten Patienten

Abstract

Since 25 years electrical stimulation has become an established and widely acknowledged therapy option. Today, FES is widely employed, e.g. for cardiostimulation, diaphragm stimulation, kinetotherapy, for treatment of tremor in Parkinson patients, and finally for bladder stimulation in patients with bladder voiding dysfunctions. Brindley was the first researcher who succeeded in stimulating the spinal nerves via implanted electrodes in an animal model. In the years 1978/79 Brindley implanted five paraplegic patients with so-called sacral anterior root stimulators; all of them were able to void under stimulation. This method of sacral anterior root stimulation (SARS) proved an alternative to frequent one-way catheterisation for patients with severe voiding dysfunctions, without achieving complete continence, however. The following study is to provide an overview over the latest insights in the context of implanting sacral anterior root stimulators; it discusses the preconditions required for such interventions and presents criteria to decide in which cases there is a contraindication for sacral deafferentation of the posterior roots. Moreover, it contrasts advantages and disadvantages of the intradural and extradural implantation methods and presents the currently available long-term follow-up results with SDAF and SARS for treatment of bladder voiding dysfunctions.

Effect of spinal anterior root stimulation and sacral deafferentation on bladder and sexual dysfunction in spinal cord injury

“…Our study is one of the largest cohorts on SARS-SDAF to date, and the findings on significant decrement of neurogenic bladder dysfunction underline the effect of the procedure and implant as an effective treatment modality in SCI patients. These findings are in line with other studies [11,13,17]. The high VAS satisfaction scores and lesser nuisance of bladder dysfunction affirm the positive effect of the combined SARS-SDAF on bladder function of SCI subjects.…”

“…This is probably especially true considering that the majority of patients have an ISNSCI score of A or B. However, reflex erection can be compensated in 30% of the cases through electrostimulation [17].…”

“…The stimulation results in simultaneous contraction in the detrusor's soft muscles innervated by the pelvic plexus and the striated muscles of the pelvic floor innervated by the pudendal nerve. The short pulsatile stimulations and the long intervals help to keep continuity of micturition, since the striated pelvic muscle instantly relaxes by the stimulation cessation, while the smooth detrusor muscle slowly reacts, leading to poststimulus voiding [17]. The implant used was primarily intrathecal 2 or 3 channel implants (before 2001: Finetech Ltd., UK, and after 2001: RBM, Hamburg, Reinhard Becker company).…”

Tetranectin Knockout Mice Develop Features of Parkinson Disease

“…Clinical treatments are mainly limited to the DA precursor L-DOPA and inhibitors of DA metabolism, which supplement reduced striatal DA [18], and deep-brain stimulation of the basal ganglia, which can alleviate tremor [19]. The development of treatments that actually arrest PD progression requires a more detailed understanding of the molecular mechanisms responsible for LB formation and other early pathogenic events that precede the loss of dopaminergic neurons.…”

“…Ideally, a robust animal model of PD will exhibit progressive LB formation, loss of striatal dopamine terminals, loss of dopaminergic neurons in the SNc, and behavioral endophenotypes of PD, including motor and other behavioral symptoms [18,19]. We suggest that many of the pathogenic processes leading to PD are present in TN -/- mice, such as inclusion formation and increased striatal DA and DAT, which are signs of a compensatory response and model the preclinical disease.…”