Bladder Function
The normal control of bladder function and the urinary system involves a lot of areas of the central nervous system from the frontal lobes down through the palms and the spinal cord. So it is not surprising that in MS bladder function frequently is affected and in a great variety of ways. We have identified two main patterns: hyperreflexivity and hyporeflexivity. The first is the more common because upper motor neuron lesions in those pathways often result in reflex incontinence. If it also affects the sphincter, there may be detrusor-sphincter-dyssynergia that may impair complete voiding in the setting of incontinence. Hyporeflexive patients often cannot void well because of poor detrusor muscle contractions, although they may have overflow incontinence. Patients with neurogenic bladder often require catheterization, either intermittent or indwelling.
Medication to improve bladder contraction has been used as an option, but not with a lot of evidence of success. Hyperreflexive patients, some with dyssynergia, often attempt to reduce their excessive detrusor contractions with medication. If the bladder can be relaxed sufficiently, they can catheterize themselves or use an indwelling catheter. Some patients have surgical augmentation of the bladder to increase storage capacity, and then depend on catheterization. Others have had to have urinary diversion into a bag worn on the abdomen or have undergone surgical rhizotomy to abolish the bladder reflexes and produce continence. Suffice it to say that all of these solutions are imperfect, and the complications of neurogenic bladder: incontinence, urinary retention, infection, stones, hydronephrosis remain common and often disabling complications for patients with MS.
FES
There are basically two ways by which we might apply electrical stimulation. The first, neuromodulation, is by stimulating afferent nerves to try modulating what's going on in the central nervous system. The other basic application is to stimulate efferent nerves to directly produce activities in the organs they supply. The most obvious example would be making the bladder contract in order to produce micturation.
Afferent stimulation has been tried in a variety of ways for many years. In the 1980s, there was great interest in dorsal column stimulation. A variety of publications reported modest improvements, but the results were not very consistent when measured objectively. One paper expressed doubt that dorsal column stimulation would have any place in the routine management of MS. Sacral nerve stimulation, also afferent, is being used in non-MS patients with some success. One can stimulate the sacral dermatomes and peripheral nerves in a variety of ways. Again, some reports show symptomatic improvement and sometimes urodynamic improvement, although typically the numbers are small and the studies not well controlled.
Efferent stimulation is a bit more controllable in an engineering sense. You are not just modulating the black box of the central nervous system, but applying signals directly to the peripheral nerves. The best-known example of that is a root stimulation device developed for SCI patients and now being used in a large number of patients in other countries. The follow-up extends to 20 years.
The main part of this procedure is to put electrodes on the sacral roots to stimulate the parasympathetic efferent fibers and thereby produce bladder contraction. More recently, this has been enhanced by posterior rhizotomy to remove reflex bladder contractions and improve continence. Once this procedure was added it became possible to produce not only micturition, but also continence. The results in SCI patients have been reported in some 60 or 70 publications. The first 500 SCI patients, reported on 5 years ago, showed about a 90 percent rate of successful micturation on demand. This reduced the urinary infection because of the lower residuals. The rhizotomy increased their bladder capacity and compliance and decreased their reflex continence.
The ability to eliminate bladder contractions resulted in low storage pressure, which was beneficial to the upper urinary tract. Removing the sacral sensory also reduced the dangerous rise in blood pressure these patients sometimes get.
There is very little published on applying this technique to MS. I am familiar with the work of one researcher who has had experience with just nine MS patients. All had incomplete cord lesions and were treated with electrodes on their sacral anterior roots, usually along with rhizotomy. Six had full rhizotomy, L-2 through 4. Two of them had a partial sensory rhizotomy, and one had none. All have been followed for up to 13 years. Five of the nine had been able to produce micturition, three for the periods of 13, 7, and 4 years. Two were able to produce for a shorter time. One patient developed a late infection of the implant and another developed damage to his roots, possibly from progression of disease after 7 months, and those patients then ceased using the device. But a majority of the patients were made continent by their rhizotomy.
There are significant differences in MS patients, particularly because many of them will have incomplete cord lesions, although that is more and more the pattern we also see in spinal cord injury. We need to address this issue and, in particular, what incomplete lesions mean in terms of rhizotomy. A patient with an incomplete cord lesion may not wish to have rhizotomy if that involves losing sacral sensation or losing some desirable reflex function. Obviously, the variety of lesions in MS is quite different from those we see in SCI. Applications of FES in the MS population will have to be adjusted to handle variation in lesions.
When dealing with patients with incomplete cord lesions, we wish to preserve what useful sensation they might have in sacral segments. At the same time, we wish to eliminate the reflexes that hinder micturition and continence. So, it would be desirable if we could find alternatives to the destructive procedure. Having said that, of course, the impairment produced by rhizotomy may greatly reduce disability, but nevertheless, we would prefer do it without rhizotomy.
Neuromodulation is an historical technique that has not been fully evaluated in this population. Sensory stimulation has had mixed results, but it has not been studied very thoroughly or in large numbers in MS. The ability to produce unidirectional stimulation gives us the possibility of blocking by collision some of the natural afferent traffic and this may be one way of reducing reflexes without permanent rhizotomy. It also would avoid transmission of impulses toward the cord and the causing of pain by stimulation of a mixed nerve. We have used size selective stimulation in animals to avoid contraction of the anal sphincter to produce reliable defecation. We might also use this for blocking small fibers to reduce dyssynergia.
We need further technical development of the techniques that are already in use in SCI and adapt them to MS. In particular, we need to find ways of reducing hyperreflexivity. As many have said, we need adequate numbers for that, with good selection criteria and outcome measures. This is an unsolved problem and a significant one in MS and electrical stimulation. While FES has been successful in some other diagnoses, it has not been fully examined in this group. It may have potential in other neurological diseases if we cannot only initiate, but also stop, the transmission of impulses in nerves.
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