Surgery: light – thermal – and electrical application – Light – thermal – and electrical application – Electrical therapeutic systems
Reexamination Certificate
2000-01-31
2002-05-21
Bockelman, Mark (Department: 3762)
Surgery: light, thermal, and electrical application
Light, thermal, and electrical application
Electrical therapeutic systems
Reexamination Certificate
active
06393323
ABSTRACT:
FIELD OF THE INVENTION
The present invention relates to lower urinary dysfunctions and to methods for improving same, and more particularly to an implantable electronic stimulator to prevent detrusor-sphincter dyssynergia and reduce detrusor hyperreflexia, in order to reduce the urgency and frequency of urination.
BACKGROUND OF THE INVENTION
Normal urinary control and voiding are the result of complex interactions of smooth muscle, voluntary muscle, cerebral inhibition and the autonomic nervous system (ANS). These interactions are explained hereinafter with reference to FIG.
1
.
The bladder B is a stretchable chamber defined by the pelvic floor muscle group, which includes a wall of smooth detrusor muscle M containing stretch receptors innervated with parasympathetic neurons P of autonomic nerve fibers A. The base of the bladder B, called the internal urethral sphincter
1
, is part of the detrusor muscle M and opens automatically when the bladder B contracts. A skeletal external urethral sphincter muscle E surrounds the urethra U at the bladder outlet and is innervated by somatic motor neurons S. As may be seen, the nerves that control the detrusor muscle also control the external urethral sphincter E. The somatic nerve fibers S and the autonomic nerve fibers A originate from sacral segments S
2
, S
3
and S
4
in a dorsal root D and a ventral root V. The dorsal root D transmits sensations from the bladder B to the spinal cord whereas the ventral root V transmits impulses from the spinal cord to the bladder B. The ventral root V is composed of somatic A-alpha fibers which innervate the external urethral sphincter E and of parasympathetic A-delta fibers which innervate the detrusor muscle M. The sympathetic system plays a role particularly in the area of the bladder neck and the proximal urethra during continence, increasing the bladder outlet resistance.
Urination or bladder voiding is a spinal reflex involving neurological control in the bladder wall or external urethral sphincter, in the autonomic center of the spinal cord and in the central nervous system (CNS) at the level of the Pontine Micturition Center (PMC) in the mid-brain, which is under the control of the cerebral cortex.
When the bladder is empty, the detrusor muscle is relaxed, the stretch receptors are quiescent and the external urethral sphincter is contracted and closed. The bladder becomes distended as it fills with urine from the kidneys and the stretch receptors are stimulated up to a threshold. The stretch receptors stimulate neurons to the sacral cord in a spinal reflex arc. The stretch receptors also stimulate the parasympathetic neurons through an ascending pathway to the PMC. The cerebral cortex through the PMC generates impulses through a descending pathway to suppress the spinal reflex arc.
Bladder voiding is voluntarily induced by interrupting the descending pathway from the cerebral cortex which inhibits the contraction of the external urethral sphincter, thereby acting together with the afferent pathway from the bladder stretch receptors to the cerebral cortex, resulting in external urethral sphincter relaxation, detrusor muscle contraction and initiating bladder voiding. Bladder voiding is delayed by activating the descending pathway from the cerebral cortex which inhibits contraction of the detrusor muscle and stimulates contraction of the external urethral sphincter, thereby overriding the ascending pathway from the bladder stretch receptors to the cerebral cortex.
A lower urinary dysfunction such as neurogenic bladder dysfunction manifests itself as partial or complete urinary retention, incontinence or frequent urination. Common problems associated therewith include urinary infections, urinary calculi, renal damage and “detrusor-sphincter dyssynergia”, or simultaneous contraction of the detrusor muscle and the external urethral sphincter, which leads to increased bladder pressure, incontinence and ultimately kidney failure. Neurogenic bladder dysfunction may result (1) from congenital abnormalities such as myelomeningocele, filum terminale syndrome and other lesions of the spinal cord and cauda equina, (2) from diseases such as syphilis, diabetes mellitus, brain or spinal cord tumors, cerebrovascular accidents, ruptured intervertebral disk, and demyelinating or degenerative diseases such as multiple sclerosis and amyotrophic lateral sclerosis, or (3) from injuries of the brain, spinal cord or local nerve supply to the urinary bladder and its outlet, such as with transverse myelitis and transsection of the cord.
The most common acquired cause of severe neurogenic bladder dysfunction is spinal cord injury (SCI) or transsection resulting in paraplegia or quadriplegia. Paraplegic and quadriplegic patients exhibit involuntary control over their bladder and sphincter functions. In SCI patients, the brain cannot send messages below the level of injury, and messages from organs innervated by regions below the level of injury cannot reach the brain. Immediately after the SCI, the bladder becomes atonic, distended and, if neglected, exhibits continuous overflow dribbling during the “spinal shock” phase. Lesions to the lower spinal cord (sacral and lumbar segments) produce a flaccid paralysis of the bladder with overfilling thereof, while upper cord lesions (thoracic and cervical lesions) produce an automatic or spastic reflex bladder that empties spontaneously or as the result of somatic stimuli, with detrusor muscle hyperreflexia and detrusor-sphincter dyssynergia. Hyperreflexia consists of an hyperactivity of the ANS. It occurs when the overfull bladder sends impulses to the spinal cord, where they travel upward until they are blocked by the lesion at the level of injury. Since the impulses cannot reach the brain, the reflex arc stays activated, which increases activity of the sympathetic portion of the ANS and causes spasms.
Several treatment modalities are available to manage patients with neurogenic bladder dysfunction, such as indwelling (continuous) urethral catheter drainage or intermittent catheterization, to prevent overdistention of the detrusor muscle. However, the presence of the catheter in the male patient predisposes to urethritis, periurethritis, abscess formation and urethral fistula. Consequently, incision of the external urethral sphincter or sphincterotomy is often required to minimize outlet resistance and to maximize emptying of the bladder using condom drainage when the patient becomes incontinent.
Pharmacological management with medications producing an antispasmodic or anticholinergic effect on the bladder may alternatively be used to reduce spastic reflexes and involuntary contractions of the detrusor muscle, with some undesirable side effects.
Surgical procedures such as permanent urinary diversion may further be used to lower the risk of kidney damage. Upper tract diversion is accomplished by ileal or colon conduit. Permanent suprapubic cystostomy affords control in some patients only, and cutaneous vesicostomy with an external appliance may be used only in patients with no upper tract damage. Other surgical procedures such as ureterosigmoidostomy, cutaneous intubated ureterostomies and nephrostomies are not recommended, since most patients also lose rectal sphincter control, and indwelling catheters increase risks of stone formation and infection.
Devices such as artificial sphincters implanted around the urethra have also been used to control urinary continence in some patients.
Total functional recovery in any form of neurogenic bladder with the above-mentioned techniques remained uncommon.
Electrical stimulation of organs such as with pacemakers and cochlear implants was developed to restore organ functions impaired by a neurological disorder or an organ failure. Electrical stimulation may be used for pain relief, for maintaining or increasing a range of movement, for strengthening a muscle or for facilitating voluntary motor function. Functional Electrical Stimulation (FES) or Functional Neuromuscular Stimulation (FNS) attempts to restore neuromuscular function by a
Elhilali Mostafa
Sawan Mohamad
(Ogilvy Renault)
Anglehart James
Bockelman Mark
McGill University
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