The purpose of any classification system should be to facilitate understanding and management. A good classification should serve as intellectual shorthand and should convey, in a few key words or phrases, the essence of a clinical situation. An ideal system for all types of voiding dysfunction would include or imply a number of factors:
1. the conclusions reached from urodynamic testing;
2. expected clinical symptoms
3. the approximate site and type of a neurologic lesion, or lack of one.
If the various categories accurately portray pathophysiology, treatment options should then be obvious, and a treatment "menu" should be evident. Most systems of classification for voiding dysfunction were formulated to describe dysfunctions secondary to neurologic disease or injury. The ideal system should be applicable to all types of voiding dysfunction. Based upon the data obtained from the neurourologic evaluation, a given voiding dysfunction can be categorized in a number of descriptive systems. None are perfect.
Sensory neuron lesion Incomplete, balanced Complete, unbalanced Motor neuron lesion Balanced Imbalanced Sensory-motor neuron lesion Upper motor neuron lesion Complete, balanced Complete, unbalanced Incomplete, balanced Incomplete, unbalanced Lower motor neuron lesion Complete, balanced Complete, unbalanced Incomplete, balanced Incomplete, unbalanced Mixed lesion
Upper somatomotor neuron, lower visceromotor neuron Lower somatomotor neuron, upper visceromotor neuron Normal somatomotor neuron, lower visceromotor neuron
Bors-Comarr Classification (see Table 6 and ref. 6)
This classification system was deduced from clinical observation of patients with traumatic spinal cord injury. This system applies only to patients with neurologic dysfunction and considers three factors:
1. The anatomic localization of the lesion;
2. The neurologic completeness of the lesion, and
3. Whether lower urinary tract function is "balanced" or "unbalanced."
The latter terms are based solely on the percentage of residual urine relative to bladder capacity. "Unbalanced" implies greater than 20% residual urine in a patient with an upper motor neuron (UMN) lesion or 10% in a patient with a lower motor neuron (LMN) lesion. This relative residual urine volume was ideally meant to imply coordination (synergy) or dyssynergia of the smooth and striated sphincters during bladder contraction or attempted micturition by abdominal straining or Crede. The determination of the completeness of the lesion is made on the basis of a thorough neurologic examination. The system erroneously assumed that the sacral spinal cord is the primary reflex center for micturition. "LMN" implies collectively the preganglionic and postganglionic parasympathetic autonomic fibers that innervate the bladder and outlet and originate as preganglionic fibers in the sacral spinal cord. The term is used in an analogy to efferent somatic nerve fibers, such as those of the pudendal nerve, which originate in the same sacral cord segment but terminate directly on pelvic floor striated musculature without the interposition of ganglia. "UMN" is used in a similar analogy to the somatic nervous system to describe those descending autonomic pathways above the sacral spinal cord (the origin of the motor efferent supply to the bladder).
In this system, "upper motor neuron bladder" refers to the pattern of micturition that results from an injury to the suprasacral spinal cord after the period of spinal shock has passed, assuming that the sacral spinal cord and the sacral nerve roots are intact and that the pelvic and pudendal nerve reflexes are intact. Lower motor neuron bladder refers to the pattern resulting if the sacral spinal cord or sacral roots are damaged and the reflex pattern through the autonomic and somatic nerves that emanate from these segments is absent. This system implies that if skeletal muscle spasticity exists below the level of the lesion, the lesion is above the sacral spinal cord and is by definition an UMN lesion. This type of lesion is characterized by detrusor hyperreflexia during filling. If flaccidity of the skeletal musculature below the level of a lesion exists, an LMN lesion is assumed to exist, implying detrusor areflexia. Exceptions occur and are classified in a "mixed lesion" group characterized either by detrusor hyperreflexia with a flaccid paralysis below the level of the lesion or by detrusor areflexia with spasticity or normal skeletal muscle tone neurologically below the lesion level.
The use of this system is illustrated as follows. A complete, unbalanced, UMN lesion, implies a neurologically complete lesion above the level of the sacral spinal cord that results in skeletal muscle spasticity below the level of the injury. Detrusor hyperreflexia exists during filling, but a residual urine volume of greater than 20% of the bladder capacity is left after bladder contraction, implying obstruction in the area of the bladder outlet during the hyperreflexic detrusor contraction. This obstruction is generally due to striated sphincter dyssynergia, typically occurring in patients who are paraplegic and quadriplegic with lesions between the cervical and the sacral spinal cord. Smooth sphincter dyssynergia may be seen as well in patients with spinal cord lesions above the level of T6, usually in association with autonomic hyperreflexia. An LMN lesion, complete, unbalanced, implies a neurologi-
Suprasacral lesion Suprasacral spinal lesion Infrasacral lesion Peripheral autonomic neuropathy Muscular lesion cally complete lesion at the level of the sacral spinal cord or of the sacral roots, resulting in skeletal muscle flaccidity below that level. Detrusor areflexia results, and whatever measures the patient may use to increase intravesical pressure during attempted voiding are not sufficient to decrease residual urine to less than 10% of bladder capacity.
This classification system applies best to spinal cord injury patients with complete neurologic lesions after spinal shock has passed. It is difficult to apply to patients with multicentric neurologic disease and cannot be used at all for patients with non-neurologic disease. The system fails to reconcile the clinical and urodynamic variability exhibited by patients who, by neurological exam alone, seem to have similar lesions. The period of spinal shock that immediately follows severe cord injury is generally associated with bladder areflexia, whatever the status of the sacral somatic reflexes. Temporary or permanent changes in bladder or outlet activity during filling/storage or emptying may occur secondary to a number of factors such as chronic overdistention, infection, and reinnervation or reorganization of neural pathways following injury or disease; such changes make it impossible to always accurately predict lower urinary tract activity solely on the basis of the level of the neurologic lesion. Finally, although the terms "balanced" and "unbalanced" are helpful, in that they describe the presence or absence of a certain relative percentage of residual urine, they do not necessarily imply the true functional significance of a lesion, which depends on the potential for damage to the lower or upper urinary tracts, and also on the social and vocational disability that results.
Hald-Bradley Classification (see Table 7 and ref. 7)
This is described as a simple neurotopographic classification. A supraspinal lesion implies synergy between detrusor contraction and smooth and striated sphincters, but defective inhibition of the voiding reflex. Detrusor hyperreflexia generally occurs and sensation is usually preserved. However, depending on the site of the lesion, detrusor are-flexia and defective sensation may be seen. A suprasacral spinal lesion is roughly equivalent to what is described as a UMN lesion in the Bors-Comarr classification. An infrasacral lesion is roughly equivalent to an LMN lesion. Peripheral autonomic neuropathy is most frequently encountered in the diabetic and is characterized by deficient bladder sensation, gradually increasing residual urine and ultimate decompensation, with loss of detrusor contractility. A muscular lesion can involve the detrusor itself, the smooth sphincter, or any portion, or all, of the striated sphincter. The resultant dysfunction is dependent on which structure is affected. Detrusor dysfunction is the most common and generally results from decompensation, following long-standing bladder outlet obstruction.
Bradley Classification (7)
This is a primarily neurologic system based upon a conceptualization of central nervous system control of the lower urinary tract as including four neurologic "loops." Dysfunctions are classified according to the loop affected.
Loop 1 consists of neuronal connections between the cerebral cortex and the pontine-mesencephalic micturition center; this coordinates voluntary control of the detrusor reflex. Loop 1 lesions are seen in conditions such as brain tumor, cerebrovascular accident or disease, and cerebral trophy with dementia. The final result is characteristically detrusor hyperreflexia.
Loop 2 includes the intraspinal pathway of detrusor muscle afferents to the brain-stem micturition center and the motor impulses from this center to the sacral spinal cord. Loop 2 is thought to coordinate and provide for a detrusor reflex of adequate temporal duration to allow complete voiding. Partial interruption by spinal cord injury results in a detrusor reflex of low threshold and in poor emptying with residual urine. Spinal cord transection of loop 2 acutely produces detrusor areflexia and urinary retention—spinal shock. After this has passed, detrusor hyperreflexia results.
Loop 3 consists of the peripheral detrusor afferent axons and their pathway in the spinal cord; these terminate by synapsing on pudendal motor neurons that ultimately innervate periurethral striated muscle. Loop 3 was thought to provide a neurologic substrate for coordinated reciprocal action of the bladder and striated sphincter. Loop 3 dysfunction could be responsible for detrusor-striated sphincter dyssynergia or involuntary sphincter relaxation.
Loop 4 consists of two components. Loop 4A is the suprasacral afferent and efferent innervation of the pudendal motor neurons to the periurethrla striated musculature which synapse on pudendal motor neurons in Onuf's nucleus—the segmental innervation of the periurethral striated muscle. In contrast to the stimulation of detrusor afferent fibers, which produce inhibitory postsynaptic potentials in pudendal motor neurons through loop 3, pudendal nerve afferents produce excitatory postsynaptic potentials in those motor neurons through loop 4B. These provide for contraction of the periurethral striated muscle during bladder filling and urine storage. The related sensory impulses arise from muscle spindles and tendon organs in the pelvic floor musculature. Loop 4 provides for volitional control of the striated sphincter. Abnormalities of the suprasacral portion result in abnormal responses of the pudendal motor neurons to bladder filling and emptying, manifested as detrasor-striated sphincter dyssynergia, and/or loss of the ability to voluntarily contract the striated sphincter.
This system is sophisticated and reflects the ingenuity and neurophys-iologic expertise of its originator, Dr. William Bradley. For some neurologists, this method may be an excellent way to conceptualize the neurophysiology involved, assuming that they agree on the existence and significance of all four loops. Most urologists find this system difficult to use for many types of neurogenic voiding dysfunction and not at all applicable to non-neurogenic voiding dysfunction. Urodynam-ically, it may be extremely difficult to test the intactness of each loop system, and multicentric and partial lesions are difficult to describe.
The Lapides Classification (see Table 8 and ref. 8)
This is a modification of a system originally proposed by McLellan (a neurologist) in 1939 (9). This remains one of the most familiar systems to urologists and non-urologists because it describes in recognizable shorthand the clinical and cystometric conditions of many types of neurogenic voiding dysfunction.
A sensory neurogenic bladder results from interruption of the sensory fibers between the bladder and spinal cord or the afferent tracts to the brain. Diabetes mellitus, tabes dorsalis, and pernicious anemia are most commonly responsible. The first clinical changes are described as those
Sensory neurogenic bladder Motor paralytic bladder Uninhibited neurogenic bladder Reflex neurogenic bladder Autonomous neurogenic bladder of impaired sensation of bladder distention. Unless voiding is initiated on a timed basis, varying degrees of bladder overdistention can result with resultant hypotonicity. With bladder decompensation, significant amounts of residual urine are found and, at this time, the cystometric curve generally demonstrates a large capacity bladder with a flat high compliance low pressure filling curve.
A motor paralytic bladder results from disease processes that destroy the parasympathetic motor innervation of the bladder. Extensive pelvic surgery or trauma may produce this. Herpes zoster has been listed as a cause as well, but recent evidence suggests that the voiding dysfunction seen with herpes is more related to a problem with afferent input. The early symptoms may vary from painful urinary retention to only a relative inability to initiate and maintain normal micturition. Early cystometric filling is normal but without a voluntary bladder contraction at capacity. Chronic overdistention and decompensation may occur in a large capacity bladder with a flat, low-pressure filling curve; a large residual urine may result.
The uninhibited neurogenic bladder was described originally as resulting from injury or disease to the "corticoregulatory tract." The sacral spinal cord was presumed to be the micturition reflex center, and this "corticoregulatory tract" was believed to exert an inhibitory influence on the sacral micturition reflex center. A destructive lesion in this tract would then result in overfacilitation or lack of inhibition of the micturition reflex. Cerebrovascular accident, brain or spinal cord tumor, Parkinson's disease, and demyelinating disease are the most common causes in this category. The voiding dysfunction is most often characterized symptomatically by frequency, urgency, and urge incontinence. Urodynamically, one sees normal sensation with an involuntary bladder contraction at low filling volumes. Residual urine is characteristically low unless anatomic outlet obstruction or true smooth or striated sphincter dyssynergia occurs. The patient generally can initiate a bladder contraction voluntarily, but is often unable to do so during cystometry because sufficient urine storage cannot occur before detrusor hyperreflexia is stimulated.
Reflex neurogenic bladder describes the postspinal shock condition that exists after complete interruption of the sensory and motor pathways between the sacral spinal cord and the brain stem. Most commonly, this occurs in traumatic spinal cord injury and transverse myelitis, but may occur with extensive demyelinating disease or any process that produces significant spinal cord destruction as well. Typically, there is no bladder sensation and there is inability to initiate voluntary micturition. Incontinence without sensation generally occurs because of low volume involuntary bladder contraction. Striated sphincter dyssynergia is the rule. This type of lesion is essentially equivalent to a complete UMN lesion in the Bors-Comarr system.
An autonomous neurogenic bladder results from complete motor and sensory separation of the bladder from the sacral spinal cord. This may be caused by any disease that destroys the sacral cord or causes extensive damage to the sacral roots or pelvic nerves. There is inability to voluntarily initiate micturition, no bladder reflex activity, and no specific bladder sensation. This type of bladder is equivalent to a complete LMN lesion in the Bors-Comarr system and is also the type of dysfunction seen in patients with spinal shock. This characteristic cystometric pattern is initially similar to the late stages of the motor or sensory paralytic bladder, with a marked shift to the right of the cystometric filling curve and a large bladder capacity at low intravesical pressure. However, decreased compliance may develop, secondary either to chronic inflammatory change or to the effects of denervation/centralization with secondary neu-romorphologic and neuropharmacologic reorganizational changes. Emptying capacity may vary widely, depending on the ability of the patient to increase intravesical pressure and on the resistance offered during this increase by the smooth and striated sphincters.
These classic categories in their usual settings are usually easily understood and remembered, and this is why this system provides an excellent framework for teaching some fundamentals of neurogenic voiding dysfunction to students and non-urologists. Unfortunately, many patients do not exactly "fit" into one or another category. Gradations of sensory, motor, and mixed lesions occur, and the patterns produced after different types of peripheral denervation/defunctionali-zation may vary widely from those which are classically described. The system is applicable only to neuropathic dysfunction.
Table 9 A Urodynamic Classification"
Detrusor hyperreflexia (or normoreflexia) Coordinated sphincters Striated sphincter dyssynergia Smooth sphincter dyssynergia Nonrelaxing smooth sphincter Detrusor areflexia
Coordinated sphincters Nonrelaxing striated sphincter Denervated striated sphincter Nonrelaxing smooth sphincter
"Adapted with permission from ref. 10.
Urodynamic Classification (see Table 9 and ref. 10)
Systems of classification have evolved based solely on objective urodynamic data. When exact urodynamic classification is possible, this sort of system can provide an exact description of the voiding dysfunction that occurs. If a normal or hyperreflexic detrusor exists with coordinated smooth and striated sphincter function and without anatomic obstruction, normal bladder emptying should occur.
Detrusor hyperreflexia is most commonly associated with neurologic lesions above the sacral spinal cord. Striated sphincter dyssynergia is most commonly seen after complete suprasacral spinal cord injury, following the period of spinal shock. Smooth sphincter dyssynergia is seen most classically in autonomic hyperreflexia when it is characteristically associated with detrusor hyperreflexia and striated sphincter dyssynergia. Detrusor areflexia may be secondary to bladder muscle decompensation or to various other conditions that produce inhibition at the level of the brain-stem micturition center, the sacral spinal cord, bladder ganglia, or bladder smooth muscle.
This classification system is easiest to use when detrusor hyperreflexia or normoreflexia exists. Thus, a typical T10 level paraplegic exhibits detrusor hyperreflexia, smooth-sphincter synergia, and striated-sphincter dyssynergia. When a voluntary or hyperreflexic contraction cannot be elicited, the system is more difficult to use, because it is not appropriate to speak of true sphincter dyssynergia in the absence of an opposing bladder contraction. There are obviously many variations and extensions of such a system. Such systems work only when total urodynamic agreement exists among classifiers. Unfortunately, there
The International Continence Society Classification'2
Bladder Function Detrusor activity Normal or stable
Bladder Function Detrusor activity
Bladder sensation Normal
Increased or hypersensitive Reduced or hyposensitive Absent
Urethral Function Normal Obstructive Overactive Mechanical
Bladder capacity Normal High Low
Compliance Normal High Low
Urethral Function Normal Incompetent
"Adapted with permission from ref. 11.
are many voiding dysfunctions that do not fit neatly into a urodynamic classification system that is agreed upon by all "experts." As sophisticated urodynamic technology and understanding improve, this type of classification system may supplant some others in general use.
International Continence Society Classification Table 10 and r7f.yX) *
This is in many ways an extension of a urodynamic classification system. The storage and voiding phases of micturition are described separately, and, within each, various designations are applied to describe bladder and urethral function (11).
Normal bladder function during filling/storage implies no significant rises in detrusor pressure (stability). Overactive detrusor function indicates the presence of involuntary contractions. If owing to neurologic disease, the term detrusor hyperreflexia is used; if not, the phenomenon is known as detrusor instability. Bladder sensation can be categorized only in qualitative terms as indicated. Bladder capacity and compliance (A) volume/A pressure) are cystometric measurements. Normal urethral function during filling/storage indicates a positive urethral closure pressure (urethral pressure minus bladder pressure) even with increases in intra-abdominal pressure. Incompetent urethral function during filling/ storage implies urine leakage in the absence of a detrusor contraction. This may be secondary to genuine stress incontinence, intrinsic sphincter dysfunction, or an involuntary fall in urethral pressure in the absence of a detrusor contraction.
During the voiding/emptying phase of micturition, normal detrusor activity implies voiding by a voluntarily initiated, sustained contraction that also can be suppressed voluntarily. An underactive detrusor defines a contraction of inadequate magnitude or/and duration to empty the bladder with a normal time span. An acontractile detrusor is one that cannot be demonstrated to contract during urodynamic testing. Areflexia is defined as acontractility owing to an abnormality of neural control, implying the complete absence of centrally coordinated contraction. Normal urethral function during voiding indicates opening prior to micturition to allow bladder emptying. An obstructed urethra is one which contracts against a detrusor contraction or fails to open (nonrelaxation) with attempted micturition. Contraction may be owing to smooth or striated sphincter dyssynergia. Striated sphincter dyssynergia is a term that should be applied only when neurologic disease is present. A similar syndrome but without neurologic disease is called dysfunctional voiding. Mechanical obstruction is generally anatomical and caused by BPH, urethral or bladder neck stricture, scarring or compression, or, rarely, kinking of a portion of the urethra during straining.
Voiding dysfunction in a classic T10 level paraplegic after spinal shock has passed would be classified as follows:
1. Storage phase: overactive hyperreflexic detrusor, absent sensation, low capacity, normal compliance, normal urethral closure function.
2. Voiding phase: overactive obstructive urethral function, ? normal detrusor activity (actually, hyperreflexic).
The voiding dysfunction of a stroke patient with urgency incontinence would most likely be classified during storage as overactive hyperreflexic detrusor, normal sensation, low capacity, normal compliance, and normal urethral closure function. During voiding, the dysfunction would be classified as normal detrusor activity and normal urethral function, assuming that no anatomic obstruction existed.
The Functional System (see Tables 1 and 2)
Classification of voiding dysfunction can also be formulated on a simple functional basis, describing the dysfunction in terms of whether the deficit produced is primarily one of the filling/storage or emptying phase of micturition (see Table 1) (1,12). This type of system was proposed initially by Quesada et al. (13), and is an excellent alternative when a particular dysfunction does not readily lend itself to a generally agreed upon classification elsewhere. This simple-minded scheme assumes only that, whatever their differences, all "experts" would agree on the two-phase concept of micturition and upon the simple overall mechanisms underlying the normality of each phase (see section on normal lower urinary tract function).
Storage failure results either because of bladder or outlet abnormalities or a combination. Bladder abnormalities include involuntary bladder contractions, low compliance, and hypersensitivity. The outlet abnormalities include only an intermittent or continuous decrease in outlet resistance.
Similiarly, emptying failure can occur because of bladder or outlet abnormalities or a combination of the two. The bladder side includes inadequate or unsustained bladder contractility, and the outlet side includes anatomic obstruction and sphincter(s) dyssynergia.
Failure in either category generally is not absolute, but more frequently relative. Such a functional system can easily be "expanded" and made more complicated to include etiologic or specific urodynamic connotations (see Table 2). However, the simplified system is perfectly workable and avoids argument in those complex situations in which the exact etiology or urodynamic mechanism for a voiding dysfunction cannot be agreed upon.
Proper use of this system for a given voiding dysfunction obviously requires a reasonably accurate notion of what the urodynamic data show. However, an exact diagnosis is not required for treatment. It should be recognized that some patients do not have only a discrete storage or emptying failure, and the existence of combination deficits must be recognized to properly utilize this system of classification. The classic T10 paraplegic after spinal shock generally exhibits a relative failure to store because of detrusor hyperreflexia and a relative failure to empty because of striated sphincter dyssynergia. With such a combination deficit, to utilize this classification system as a guide to treatment one must assume that one of the deficits is primary and that significant improvement will result from its treatment alone, or, that the voiding dysfunction can be converted primarily to a disorder either of storage or emptying by means of nonsurgical or surgical therapy. The resultant deficit can then be treated or circumvented. Using the same example, the combined deficit in a T10 paraplegic can be converted primarily to a storage failure by procedures directed at the dyssynergic striated sphincter; the resultant incontinence (secondary to detrusor hyperreflexia) can be circumvented (in a male) with an external collecting device. Alternatively, the deficit can be converted primarily to an emptying failure by pharmacologic or surgical measures designed to abolish or reduce the detrusor hyperreflexia, and the resultant emptying failure can then be circumvented with clean intermittent catheterization. Other examples of combination deficits include impaired bladder contractility with sphincter dysfunction, bladder outlet obstruction with detrusor hyperactivity, bladder outlet obstruction with sphincter malfunction, and detrusor hyperactivity with impaired contractility.
One of the advantages of this functional classification is that it allows the individual the liberty of "playing" with the system to suit his or her preferences without an alteration in the basic concept of "keep it simple but accurate and informative." For instance, one could easily substitute "overactive or oversensitive bladder" and "outlet insufficiency" for "because of the bladder" and "because of the outlet" under "failure to store" in Table 1. One could choose to subcategorize the bladder reasons for overactivity (see Table 2) in terms of neurogenic, myogenic, or anatomic etiologies and further subcategorize neurogenic in terms of increased afferent activity, decreased inhibitory control, increased sensitivity to efferent activity, and so forth. The system is flexible.
An additional advantage to the functional system is that the underlying concepts can be used repeatedly to simplify many areas in neurourol-ogy. One logical extension makes urodynamics become more readily understandable (see Table 3), whereas a different type of adaptation functions especially well as a "menu" for the categorization of all the types of treatment for voiding dysfunction (see Tables 4 and 5).
The major problem with the functional system is that not every voiding dysfunction can be reduced or converted primarily to a failure of storage or emptying. Additionally, although the functional classification of therapy that is a correlate of this scheme is entirely logical and complete, there is a danger of accepting an easy therapeutic solution and of thereby overlooking an etiology for a voiding dysfunction that is reversible at the primary level of causation. Non-neurogenic voiding dysfunctions, however, can be classified within this system, including those involving only the sensory aspect of micturition.
It is obvious that no type of system is perfect. Each offers something to every clinician; although his or her level and type of training, interests, experience, and prejudices regarding the accuracy and interpretation of urodynamic data will determine a system's usefulness. The ideal approach to a patient with voiding dysfunction continues to be a thorough neurourologic evaluation. If the clinician can classify a given patient's voiding dysfunction in each system or can understand why this cannot be done, there is enough working knowledge to proceed with treatment. However, if the clinician is familiar with only one or two of these systems and a given patient does not fit these, and the reason is uncertain, the patient should certainly be studied further and the voiding dysfunction better characterized, at least before irreversible therapy is undertaken.
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