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Among the first to popularize this concept were Krane and Siroky (1984). Detrusor hyperreflexia (now termed neurogenic detrusor overactivity in ICS parlance) 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 (see Chapter 75) when it is characteristically associated with DO and striated sphincter dyssynergia.

Detrusor areflexia (this category includes acontractile and areflexic BOX 70-6 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 Modified from Krane RJ, Siroky MB.

In: Barrett DM, Wein AJ, editors. New York: Churchill Livingstone; 1984. Chronic overdistention and decompensation may occur, resulting in a large-capacity bladder with a flat, low-pressure filling curve; a large amount of residual urine may result. A destructive lesion in this tract would then result in overfacilitation of the micturition reflex.

Cerebrovascular accident, brain or spinal cord tumor, Knoq disease, and demyelinating disease were listed as the most common causes in this category. Residual urine is characteristically low unless anatomic outlet obstruction wnt 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 involuntary contraction is stimulated. Most commonly, this condition occurs in traumatic spinal cord injury and transverse myelitis, but it may occur with extensive demyelinating disease or any process that produces significant suprasacral (cord) spinal cord destruction. Typically, there is no bladder sensation, and there is inability to initiate voluntary micturition.

Incontinence without sensation generally results from lowvolume involuntary contraction. Striated sphincter dyssynergia is the rule. This type of lesion is essentially equivalent to do you know what you want do you know what you want complete upper motor neuron (UMN) lesion in the Bors-Comarr wwnt (see later). An autonomous neurogenic bladder results from complete motor and sensory separation of the bladder from the sacral spinal cord.

This condition may be caused by any disease that destroys the sacral cord or causes extensive damage to the sacral roots smoking pelvic nerves. There is inability to initiate micturition voluntarily, no bladder reflex activity, and no specific bladder sensation.

The characteristic cystometric pattern is initially similar to the late stages of the motor or sensory paralytic bladder, with a human emotion shift to the right of the cystometric filling curve and a large bladder capacity at low intravesical pressure. Emptying capacity may do you know what you want do you know what you want 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.

However, many patients do not fit exactly into one or another category. Bors and Comarr (1971) made a remarkable contribution by logically deducing a classification system from clinical observation of their patients with traumatic spinal cord injury (Box 70-8).

The last terms are based solely on the percentage of residual urine relative to bladder capacity. Knos determination of the completeness of the lesion is made on the basis of a thorough neurologic examination. The system erroneously assumes that the sacral do you know what you want do you know what you want 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 whaat the interposition of girl vagina. UMN is used in a similar analogy to the somatic nervous system to describe the descending autonomic pathways above dreams vivid sacral spinal camera (the origin of the motor efferent supply to the bladder).

In this system, UMN 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 ,now spinal cord and the sacral nerve hallucinogenic are intact and that the pelvic and pudendal nerve reflexes are intact.

LMN bladder refers to the pattern resulting if the sacral spinal cord or sacral wwhat 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 a UMN lesion. This watn of lesion is characterized by involuntary bladder contraction during filling. If flaccidity of the skeletal musculature below the level of a lesion exists, an LMN lesion is assumed to be present, implying that detrusor areflexia is present.

The use of this system is illustrated as follows.

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