Материал: Oxford American Handbook of Urology ( PDFDrive )

502 CHAPTER 13 Neuropathic bladder

Box 13.1 Clinical consequences of damage to the nerves innervating the LUT

Clinical focal neurological examination for nerve pathways

•Motor function

•Tibialis anterior (L4–S1): controls dorsiflexion of foot

•Gastrocnemius (L5–S2): controls plantarflexion of foot

•Toe extensors (L5–S2): controls toe extension

•Sensory function: perianal/perineal sensation S2/S3

Reflexes

•Anal reflex (S2–5)

•Gently stroke mucocutaneous junction of circumanal skin

•If visible contraction (anal “wink”) absent, suggests peripheral nerve or sacral (conus medullaris) abnormality

•Bulbocavernosus reflex (BCR) (S2–4)

•Elicited by squeezing glans to cause reflex contraction of anal sphincter

•Absence of BCR suggests sacral nerve damage

Bladder neck function in the female

Approximately 75% of continent young women and 50% of perimenopausal continent women have a closed bladder neck during the bladderfilling phase. 25% of continent young women and 50% of perimenopausal continent women have an open bladder neck and yet they remain continent (because of their functioning distal sphincter mechanism, the external sphincter).1,2

Presacral neurectomy (to destroy afferent pain pathways) does not lead to incontinence because of maintenance of the somatic innervation of the external sphincter.

Sympathetic motor innervation of the bladder

Division of the hypogastric plexus of nerves during procedures such as a retroperitoneal lymph node dissection for metastatic testis tumors results in paralysis of the bladder neck. This is of significance during ejaculation, where normally sympathetic activity results in seminal emission and closure of the bladder neck so that the ejaculate is directed distally into the posterior and then anterior urethra.

If there is failure of emission or the bladder neck is incompetent, the patient develops retrograde ejaculation. They remain continent of urine because the distal urethral sphincter remains functional, being innervated by somatic neurons from S2–4.

During pelvic fracture, the external sphincter and/or its somatic motor innervation may be damaged, such that it is incompetent and unable to maintain urinary continence. Preservation of bladder neck function (the sympathetic innervation of the bladder neck usually remains intact) can preserve continence. However, if in later life the patient undergoes a TURP or bladder neck incision for symptomatic prostatic obstruction, they may well be rendered incontinent because their one remaining sphincter mechanism (the bladder neck) will be divided during these operations.

504 CHAPTER 13 Neuropathic bladder

Physiology of urine storage and micturition

Urine storage

During bladder filling, bladder pressure remains low despite a substantial increase in volume. The bladder is thus highly compliant. Its high compliance is partly due to elastic properties (viscoelasticity) of the connective tissues of the bladder and partly due to the ability of detrusor smooth muscle cells to increase their length without any change in tension.

The detrusor is able to do this as a consequence of prevention of transmission of activity from preganglionic parasympathetic neurons to postganglionic efferent neurons—a so-called gating mechanism within the parasympathetic ganglia. In addition, inhibitory interneuron activity in the spinal cord prevents transmission of afferent activity from sensors of bladder filling.

Micturition

A spinobulbar-spinal reflex, coordinated in the pontine micturition center in the brainstem (also known as Barrington’s nucleus or the M region), results in simultaneous detrusor contraction, urethral relaxation, and subsequent micturition. Receptors located in the bladder wall sense increasing tension as the bladder fills (rather than stretch). This information is relayed, by afferent neurons, to the dorsal horn of the sacral cord. Neurons project from here to the periaqueductal gray matter (PAG) in the pons.

The PAG is thus informed about the state of bladder filling. The PAG and other areas of the brain (limbic system, orbitofrontal cortex) input into the pontine micturition center (PMC) and determine whether it is appropriate to start micturition.

At times when it is appropriate to void, micturition is initiated by relaxation of the external urethral sphincter and pelvic floor. Urine enters the posterior urethra and this, combined with pelvic floor relaxation, activates afferent neurons, which results in stimulation of the PMC, located in the brainstem.

Activation of the PMC switches on a detrusor contraction via a direct communication between neurons of the PMC and the cell bodies of parasympathetic, preganglionic motoneurons located in the sacral intermediolateral cell column of S2–4. At the same time that the detrusor contracts, the urethra (the external sphincter) relaxes.

The PMC inhibits the somatic motoneurons located in Onuf nucleus (the activation of which causes external sphincter contraction) by exciting GABA and glycine-containing, inhibitory neurons in the intermediolateral cell column of the sacral cord, which in turn project to the motoneurons in Onuf nucleus. In this way, the PMC relaxes the external sphincter.

Micturition is an example of a positive feedback loop, the aim being to maintain bladder contraction until the bladder is empty. As the detrusor contracts, tension in the bladder wall rises. The bladder wall tension receptors are stimulated and the detrusor contraction is driven harder.

PHYSIOLOGY OF URINE STORAGE AND MICTURITION 505

One of the problems of positive feedback loops is their instability. Several inhibitory pathways exist to stabilize the storage–micturition loop.

•Tension receptors activate bladder afferents, which, via the pudendal and hypogastric nerves, inhibit S2–4 parasympathetic motor nerve output. An ongoing detrusor contraction cannot be overridden.

•Afferents in the anal and genital regions and in the distribution of the posterior tibial nerve stimulate inhibitory neurons in the sacral cord, and these neurons inhibit S2–4 parasympathetic motor nerve output. This pathway can override an ongoing detrusor contraction. It is hypothesized that this system prevents involuntary detrusor contraction during sexual activity, defecation, and while walking, running, and jumping.

Excitatory neurotransmission in the normal detrusor is exclusively cholinergic, and reciprocal relaxation of the urethral sphincter and bladder neck is mediated by nitrous oxide (NO), released from postganglionic parasympathetic neurons.

506 CHAPTER 13 Neuropathic bladder

Bladder and sphincter behavior in the patient with neurological disease

A variety of neurological conditions are associated with abnormal bladder and sphincter function (e.g., spinal cord injury [SCI], spina bifida (myelomeningocele), MS). The bladder and sphincters of such patients are described as neuropathic. A discussion of bladder and sphincter problems and urinary incontinence in the patient without neurological disease can be found in Chapter 4.

Patients with neurological disease may have abnormal bladder function or abnormal sphincter function or, more commonly, both. The bladder may be overactive or underactive, as may the sphincter, and any combination of bladder and sphincter over or underactivity may coexist. “Activity” here means bladder and sphincter pressure.

In the normal lower urinary tract during bladder filling, the detrusor muscle is inactive and the sphincter pressure is high. Bladder pressure is therefore low and the high sphincter pressure maintains continence.

During voiding, the sphincter relaxes and the detrusor contracts. This leads to a short-lived increase in bladder pressure, sustained until the bladder is completely empty. The detrusor and sphincter thus function in synergy—when the sphincter is active, the detrusor is relaxed (storage phase), and when the detrusor contracts, the sphincter relaxes (voiding phase).

An overactive bladder (OAB) is a recently defined clinical disorder during which patients experience urgency with or without urge incontinence, usually accompanied by frequency and/or nocturia in the absence of causative infection or identified pathological conditions.

The bladder intermittently contracts during bladder filling, thus developing high pressures when normally bladder pressure should be low. In between these waves of contraction, bladder pressure returns to normal or near normal levels.

In a patient with an underlying neurological problem, bladder overactivity is commonly called detrusor hyperreflexia (DH) or neurogenic detrusor overactivity (NDO). Detrusor overactivity (DO) is a urodynamic observation characterized by involuntary detrusor (bladder muscle) contractions during bladder filling.

In other patients the bladder wall is stiffer than normal, a condition known as poor compliance. Bladder pressure rises progressively during filling; such bladders are unable to store urine at low pressures.

Some patients have a combination of DH and poor compliance. The opposite end of the spectrum of bladder behavior is the underactive bladder, which is low pressure during filling and voiding. This is called detrusor areflexia.

An overactive sphincter generates high pressure during bladder filling, but it also does so during voiding, when normally it should relax. This pathologic condition is known as detrusor-external sphincter dyssynergia (DESD, or detrusor sphincter dyssynergia [DSD]). DSD is always associated with detrusor overactivity, although NDO may occur with synergic sphincter function (i.e., without DSD).