Neurogenic LUT Dysfunction

See 2019 CUA NLUTD Guideline Notes

Classification of Neuromuscular Dysfunction of the Lower Urinary Tract

• Classified based on location of disease: suprapontine, spinal, sacral/infrasacral

Location of lesion	History	PVR	Urodynamics	Sphincter
Suprapontine	Predominantly storage symptoms	Insignificant	Detrusor overactivity	Normal
Spinal (infrapontine-suprasacral)	Storage and voiding symptoms	Usually elevated	Detrusor overactivity Detrusor sphincter dyssynergia (DSD) Lesions between brainstem and T6 may have autonomic dysreflexia and smooth sphincter dyssynergia	Overactive
Sacral/infrasacral (below S2)	Predominantly voiding symptoms	Usually elevated	Underactive (hypocontractile or acontractile) detrusor	Normal or underactive

• Lesions above the brainstem (suprapontine)
  • Typically (with rare exceptions) associated with:
    1. Involuntary bladder contractions (detrusor overactivity) with
    2. Coordinated sphincter function (smooth and striated sphincter synergy)
    • Coordinated voiding is regulated by neurologic centers above the spinal cord
    • Urinary incontinence may occur owing to the detrusor overactivity
  • Sensation and voluntary striated sphincter function are usually preserved, but sensation may be deficient or delayed
  • Detrusor areflexia may, however, occur, either initially or as a permanent dysfunction
• Complete spinal cord lesions
  • After recovering from a period of spinal shock, typically associated with:
    1. Absent sensation
    2. Involuntary bladder contractions (detrusor overactivity)
    3. Smooth sphincter synergy but striated sphincter dyssynergia.
       • A diagnosis of striated/detrusor sphincter dyssynergia (DSD) implies a neurologic lesion that interrupts the neural axis between the pontine-mesencephalic reticular formation and the sacral spinal cord
       • Lesions above spinal cord level T6-T8 (the upper level of the sympathetic outflow) may be associated with smooth sphincter dyssynergia and autonomic hyperreflexia.
  • Incontinence may occur owing to detrusor overactivity; however, the outlet obstruction resulting from striated sphincter dyssynergia can also cause urinary retention and overflow incontinence.
• Disease below S2 (sacral)
  • Typically associated with:
    1. Lack of involuntary bladder contractions
    2. After the period of spinal shock resolves, persistent detrusor areflexia is the rule.
    3. Various forms of decreased compliance during filling (usually resulting from bladder wall fibrosis) may occur and will depend on the type and extent of neurologic insult.
    4. An open smooth sphincter area may result
       • Whether this is caused by sympathetic or parasympathetic decentralization or defunctionalization (or both or neither) has never been determined.
    5. Various types of striated sphincter dysfunction may occur, but commonly an injury in this area is associated with a residual/fixed resting striated sphincter tone (not the same as dyssynergia) and striated sphincter activity is not under voluntary control.
• Interruption of peripheral reflex arc
  • Processes that affect or interrupt the peripheral reflex arc (coordination among spine, bladder, and urethra) may cause storage or emptying dysfunctions that resemble those seen after distal spinal cord or nerve root injury.
    • Detrusor areflexia often develops, and low compliance may result.
    • The smooth sphincter may be relatively incompetent, and the striated sphincter may exhibit fixed residual tone that does not voluntarily relax.
    • True peripheral neuropathy can be motor or sensory, and, at least initially, the usual sequelae can be expected.
• See Table 75-1 for Most Common Patterns of Voiding Dysfunction seen with Various Types of Neurogenic Disease or Injuary

Diseases at or above the brainstem

• Examples: CVA, dementia, TBI, brain tumour, cerebellar ataxia, NPH, cerebral palsy, Parkinson’s, MSA

Cerebrovascular accident

• After an initial acute CVA, urinary retention from detrusor areflexia often occurs
• The most common long-term expression of LUT dysfunction after CVA is phasic detrusor overactivity
  • Urinary incontinence within 7 days of a stroke is a more powerful prognostic indicator for poor survival and functional dependence than a depressed level of consciousness
• Sensation is variable but most typically intact, and thus the patient has urinary urgency and frequency with detrusor overactivity.
  • The appropriate response to detrusor overactivity is to try to inhibit the involuntary bladder contraction by voluntarily and forcefully contracting the striated sphincter. If this can be accomplished, only urgency and frequency result; if not, the result is urgency urinary incontinence
    • Patients with lesions in only the basal ganglia or thalamus have normal sphincter function.
    • The majority of patients with involvement of the cerebral cortex and/or internal capsule are unable to forcefully contract the striated sphincter under these circumstances, and may therefore have incontinence
• Possible mechanisms for the incontinence associated with involuntary bladder contractions in patients who have sustained a CVA (2):
  1. Impaired striated sphincter control
  2. Lack of appreciation of bladder filling and impending bladder contraction
• In general, the smooth sphincter is unaffected after CVA and remains synergic; true detrusor striated sphincter dyssynergia does not occur in this situation, although pseudodyssynergia (electromyographic sphincter “flare” during filling cystometry that is secondary to attempted inhibition of an involuntary bladder contraction by voluntary contraction of the striated sphincter) has been found to occur
• The guarding reflex in these patients usually remains intact
• Detrusor hypocontractility or areflexia may rarely persist after CVA; poor flow rates and high residual urine volumes in a man with LUTS before CVA usually indicate prostatic obstruction. However, a full urodynamic evaluation to exclude detrusor overactivity with impaired contractility as a cause of symptoms is advisable before committing such a patient to surgical reduction of bladder outlet obstruction.
• In the functional system of classification (see Pathophysiology and Classification of LUT Dysfunction Chapter Notes), the most common type of LUT dysfunction after CVA would be characterized as a failure to store secondary to detrusor overactivity, specifically involuntary bladder contractions. In the International Continence Society classification system, the dysfunction would most likely be classified as overactive neurogenic detrusor function, normal sensation, low capacity, normal compliance, and normal urethral closure function during storage; regarding voiding, the description would be normal detrusor activity and normal urethral function, assuming that no anatomic obstruction existed.
• Management
  • In the absence of coexisting significant bladder obstruction or significantly impaired contractility, is directed at decreasing bladder contractility and increasing bladder capacity

Dementia

• Urinary dysfunction does not consistently accompany dementia; when voiding dysfunction occurs the result is typically incontinence. It is difficult to ascertain whether the pathophysiology and considerations are similar to those in the stroke patient or whether the incontinence reflects a situation in which the individual has simply lost the awareness of the desirability of voluntary urinary control.
• Therapy that inhibits muscarinic brain receptors may be contraindicated in Alzheimer disease if current theories about its cause are valid (cortical cholinergic loss).

Traumatic brain injury

• There may be an initial period of detrusor areflexia when LUT dysfunction occurs.
• With lesions above the PMC, detrusor overactivity and coordinated sphincter function are the most frequent manifestations of chronic LUT dysfunction.
• In patients who have more isolated brainstem injuries with involvement below the PMC, additional findings may include detrusor striated sphincter dyssynergia.

Brain tumour

• When LUT dysfunction occurs, it usually consists of detrusor overactivity and urinary incontinence
  • Urinary retention has also been described in patients with space-occupying lesions of the frontal cortex, in the absence of other associated remarkable neurologic deficits.
  • Posterior fossa tumors is usually associated with retention or difficulty voiding is the rule; incontinence rarely reported.
• In general, smooth and striated sphincters are synergic

Cerebellar ataxia

• LUT dysfunction typically manifests with incontinence, usually detrusor overactivity and sphincter synergy.
• Retention or high postvoid residual urine volume may occur as well. When present, impaired emptying is most commonly caused by detrusor areflexia, but it may also be associated with detrusor striated sphincter dyssynergia, presumably a result of spinal cord involvement

Normal-pressure hydrocephalus

• A condition of progressive dementia and ataxia occurring in patients with normal cerebrospinal fluid pressure and distended cerebral ventricles, but with no passage of air over the cerebral convexities on pneumoencephalography.
• When voiding dysfunction occurs, it is usually incontinence secondary to detrusor overactivity with synergic sphincters

Cerebral palsy

• A nonprogressive injury of the brain that typically occurs during the first year of life (but potentially up to 3 years of age) and produces neuromuscular disability and/or specific symptom complexes of cerebral dysfunction. In general, the cause is infection or a period of hypoxia. Affected children exhibit delayed gross motor development, abnormal motor performance, altered muscle tone, abnormal posture, and exaggerated reflexes.
• Most children and adults with only CP have urinary control and what seems to be normal storage and emptying.
• Some individuals with CP exhibit significant phasic detrusor overactivity and coordinated sphincters dysfunction

Parkinson disease

• A neurodegenerative disorder of unknown cause that affects primarily the dopaminergic neurons of the substantia nigra
  • Classic symptoms include tremor, skeletal rigidity, and bradykinesia
  • The gold standard for the diagnosis of PD is the neuropathologic examination
• LUT dysfunction occurs in 35-70% of patients with PD
  • It has been hypothesized that dopamine modulates the normal micturition reflex, and therefore neurogenic degeneration in the nigrostriatal pathway leads to the significant LUT dysfunction associated with PD
  • When LUT dysfunction does occur:
    • Symptoms usually consist of urgency, frequency, nocturia, and urgency incontinence.
    • The most common urodynamic finding is detrusor overactivity
    • The smooth sphincter is synergic
    • Pseudodyssynergia may occur, as well as a delay in striated sphincter relaxation (bradykinesia) at the onset of voluntary micturition, both of which can be urodynamically misinterpreted as true dyssynergia
    • Impaired detrusor contractility may also occur, either in the form of low amplitude or poorly sustained contractions or a combination. Detrusor areflexia is relatively uncommon in PD.
  • PET scanning shows brain responses with bladder filling.
  • The time from onset of PD to initiation of LUTS is ≈5 years
• TURP should not be contraindicated in patients with PD, because external sphincter acontractility is extremely rare in such patients. However, one must be cautious with such patients, and a complete urodynamic or video-urodynamic evaluation is advisable. Poorly sustained bladder contractions, sometimes with slow sphincter relaxation, should make one less optimistic regarding the results of outlet reduction in the male.

Multiple system atrophy

• A progressive neurodegenerative disease of unknown cause; results from glial α-synucleinopathy
• Symptoms encompass parkinsonism and cerebellar, autonomic (including urinary and erectile problems), and pyramidal cortical dysfunction in a multitude of combinations
• The neurologic lesions of MSA consist of cell loss and gliosis in widespread areas and occur to a significantly greater degree than with PD. This more diffuse nature of cell loss probably explains why bladder symptoms may occur earlier and be more severe than in PD, and why erectile function may be affected as well
• The initial urinary symptoms of MSA are urgency, frequency, and urgency incontinence, occurring up to 4 years before the diagnosis is made.
  • As would be expected from the central nervous system (CNS) areas affected, detrusor overactivity is frequently found
  • Decreased compliance may also occur, reflecting distal spinal involvement of the locations of the cell bodies of autonomic neurons innervating the LUT.
  • As the disease progresses, difficulty in initiating and maintaining voiding may occur, probably from pontine and sacral cord lesions, and this usually is associated with a poor prognosis.
  • Cystourethrography or video-urodynamic studies may reveal an open bladder neck (different than PD), and many patients exhibit evidence of striated sphincter denervation on motor unit electromyography.
• Management
  • The treatment of LUTS caused by MSA is difficult
  • Treatment of detrusor overactivity during filling may worsen problems initiating voluntary micturition or worsen impaired contractility during emptying.
  • Patients usually have smooth and striated sphincter insufficiency predisposing females to sphincteric incontinence and making outlet-reducing procedures (prostatectomy) hazardous in males (different than PD)
  • Conversely, drug treatment for sphincteric incontinence may further worsen emptying problems.
  • In general, the goal in these patients is to facilitate storage, and CIC would often be desirable. Unfortunately, patients with advanced disease often are not candidates for CIC.
  • Some patients do respond well to desmopressin administration for predominant nocturia; however, the majority of the patients do not respond well to antimuscarinic or other types of therapy

Diseases primarily involving the spinal cord

• Examples: MS, SCI, transverse myelitis, tabes dorsalis, pernicious anemia, spinal dysraphism, poliomyelitis

• Multiple sclerosis
  • Primarily a disease of adults ages 20-50 years with a 2x predilection for women
  • The disease is believed to be immune mediated and is characterized by neural demyelination in the brain and spinal cord; it is characterized, in general, by axonal sparing. The demyelinating process most commonly involves the lateral corticospinal (pyramidal) and reticulospinal columns of the cervical spinal cord
  • Common symptoms include optic nerve dysfunction, pyramidal tract abnormalities (hyper-reflexia), ataxia, bowel dysfunction, neurogenic bladder, and bowel and sexual dysfunction
  • 50-90% report voiding symptoms at some time; the prevalence of incontinence is cited as 37-72%
  • Urodynamic findings
    • Detrusor overactivity is the most common abnormality detected
    • In general, the smooth sphincter is synergic
    • Striated sphincter dyssynergia coexists with overactivity in 30-65% of patients
    • The prevalence of coexistent impaired detrusor contractility or areflexia ranges from 12-38%, a phenomenon that can considerably complicate treatment efforts
    • One must be careful to distinguish urodynamic pseudodyssynergia from true striated sphincter dyssynergia
    • Sensation is frequently intact in these patients
  • The most common functional classification applicable to patients with LUT dysfunction secondary to MS would be storage failure secondary to detrusor overactivity. This is commonly complicated by striated sphincter dyssynergia, with varying sequelae based on the patient’s ability to empty completely at acceptable voiding pressures. Other abnormalities, and especially combined deficits, are obviously possible
  • Progressive neurologic disease in patients with MS rarely causes upper urinary tract damage, even when severe spasticity and disability exist
  • Management
    • At present there is no consensus on optimal bladder management for patients with MS, and management is most commonly predicated on symptomatic and urodynamic findings.
    • Caution should be exercised in recommending irreversible therapeutic options, because a significant proportion of patients with MS, both with and without new symptoms, will develop changes in their detrusor compliance and urodynamic pattern.
      • Surgical intervention for MS appears to be diminishing with improved pharmacologic management and the realization of the alternating neurologic picture of lower urinary dysfunction associated with MS
• Spinal cord injury
  • The majority of SCIs occur at or above the T12 spinal column (vertebral) level, with injury to one of the 8 cervical segments accounting for the patients with tetraplegia and with patients with paraplegia having injury in the thoracic, lumbar, or sacral regions of the spinal cord.
  • Urologic complications of SCI (8):
    1. UTI
    2. Sepsis
    3. Upper urinary tract and LUT deterioration
    4. Urolithiasis
    5. Sexual and reproductive dysfunction
    6. Autonomic hyperreflexia (dysreflexia)
    7. Skin complications
    8. Depression (which can complicate urologic management)
  • Despite the strong correlation between neurologic and urodynamic findings, it is not perfect, and a neurologic examination is no substitute for a urodynamic evaluation in these patients when one is determining risk factors and treatment
  • Spinal shock
    • A temporary physiologic disorganization of spinal cord that may be expected after a significant SCI
    • Defined as the loss of motor, sensory, reflex, and autonomic neurologic function below the level of SCI
    • Classically starts within one hour after the neurologic injury.
    • Bladder is acontractile and areflexic. The bladder neck is usually closed and competent
    • The smooth sphincter mechanism appears to be functional. Some electromyographic activity may be recorded from the striated sphincter
    • The normal guarding reflex (striated sphincter response during filling) is absent and there is no voluntary control
    • Urinary retention is the rule, and catheterization is necessary to circumvent this problem
      • Once the patient is medically stable and can regulate fluid intake, the indwelling catheter can be removed and clean intermittent catheterization should be started.
    • Spinal shock usually lasts 6-12 weeks in complete suprasacral spinal cord lesions but may last up to 1 or 2 years.
      • May last a shorter period of time in incomplete suprasacral lesions and only a few days in some.
        • The exception is sacral SCI which has persistent detrusor areflexia
      • Resolution of spinal cord shock classically begins with the initial return of the bulbocavernosus reflex followed by the eventual restoration of the deep tendon reflexes (DTR) below the level of spinal cord injury.
    • Initial urodynamics should be performed within 3 months of SCI onset regardless of spinal shock resolution and then repeated after spinal shock has resolved.
      • The ideal time to perform initial urodynamics is after spinal shock has resolved, which can take up to 3 months in most cases.
        • Nearly two-thirds of patients had unfavorable urodynamic parameters (detrusor overactivity, vesicoureteral reflux and high detrusor filling pressures) within 40 days after SCI.
      • Videourodynamics with fluoroscopy is the gold standard for urodynamic investigation in patients with neurogenic bladder.
      • The Society of Urodynamics, Female Pelvic Medicine and Urogenital Reconstruction best practice policy on antibiotic prophylaxis during urodynamics recommends that patients with SCI receive a single antibiotic dose to avoid symptomatic UTI and bacteremia.
  • Suprasacral spinal cord injury
    • The characteristic pattern in a patient with a complete lesion above the sacral spinal cord is detrusor overactivity, smooth sphincter synergia (with lesions below the sympathetic outflow), striated sphincter dyssynergia, and absent sensation below the level of the lesion
      • Lesions at or above the spinal cord level of T7 or T8 (the spinal column level of T6) may result in smooth sphincter dyssynergia as well
      • The striated sphincter dyssynergia causes a functional obstruction with poor emptying and high detrusor pressure.
      • Occasionally, incomplete bladder emptying may result from what seems to be a poorly sustained or absent detrusor contraction.
    • Neurologic examination shows spasticity of skeletal muscle distal to the lesion, hyperreflexic DTRs, and abnormal plantar responses. There is impairment of superficial and deep sensation
    • The guarding reflex is absent or weak in most patients with a complete suprasacral SCI. In incomplete lesions the reflex is often preserved but quite variable
    • From a functional standpoint, the voiding dysfunction most commonly seen in suprasacral SCI represents both a filling or storage and an emptying or voiding failure. Although the urodynamics are “safe” enough in some individuals to allow only periodic stimulation of bladder reflex activity, many will require some form of additional treatment.
  • Sacral spinal cord injury
    • Typically, a depression of DTRs below the level of a complete lesion with varying degrees of flaccid paralysis. Sensation is usually absent below the lesion level. Detrusor areflexia with high or normal compliance is the common initial result. However, decreased compliance may also develop
    • The classic outlet findings are described as a competent but nonrelaxing smooth sphincter and a striated sphincter that retains some fixed tone but is not under voluntary control. Closure pressures are decreased in both areas
  • Management
    • Although generally correct, the correlation between somatic neurologic findings and urodynamic findings in suprasacral and sacral SCI patients is not exact, especially in patients with paraplegia resulting from spinal cord lesions at column level T10 to L2.
    • If bladder pressures are suitably low or if they can be sufficiently and safely lowered with nonsurgical or surgical management, the problem can be treated primarily as an emptying failure. CIC can then be continued as a safe and effective way of satisfying many of the goals of treatment. The role of additive antimuscarinic administration is supported in this patient population.
      • 2019 AUA Update on SCI: For indwelling catheters a suprapubic catheter is preferred over a urethral catheter as there is less risk of urethral erosion and epididymo-orchitis in men. However, there is no difference between the 2 catheters regarding risk of UTI, bladder stones or urinary incontinence from NDO.
      • In the absence of bladder outlet obstruction there is currently no role for medication in treating urinary retention in these patients.
    • Alternatively, sphincterotomy, urethral stenting, or intrasphincteric injection of onabotulinumtoxinA can be used in males to lower the detrusor leak point to an acceptable level and render the patient incontinent, thus converting the dysfunction primarily to a storage failure (incontinence), which can be obviated either by timed stimulation or with an external collecting device. In the dexterous SCI patient, the former approach using CIC is becoming predominant.
    • Electrical stimulation of the anterior sacral roots with some form of deafferentation is also now a distinct reality. Although used sparingly, as with all patients with neurologic impairment, a careful initial evaluation and periodic, routine follow-up evaluation must be performed to identify and correct the following risk factors and potential complications: bladder overdistention, high-pressure storage, high detrusor leak point pressure, vesicoureteral reflux (VUR), stone formation (lower and upper tracts), and complicating infection, especially in association with reflux.
    • Potential risk factors and complications are those previously described, with particular emphasis on storage pressure, which can result in silent upper tract decompensation and deterioration in the absence of VUR. The treatment of such a patient is usually directed toward producing or maintaining low-pressure storage while circumventing emptying failure with CIC when possible.
    • Bowel management
      • Approximately 60% of patients will have fecal incontinence and 40% will have constipation.
      • The goal of a neurogenic bowel regimen is to accomplish complete evacuation of the rectum on a regular basis, thereby reducing the risk of fecal impaction. This goal is achieved with adequate fluid intake, balanced diet, appropriate physical activity and a regular bowel routine.
      • In a systematic review of non-pharmacological therapies for chronic constipation, a transanal irrigation system appeared promising in decreasing constipation and fecal incontinence.
      • If further therapy is needed, patients with SCI should be started on medications such as cisapride, prucalopride or neostigmine.
  • Autonomic hyperreflexia (dysreflexia) (See 2019 CUA NLUTD Guideline Notes)
    • Potentially fatal emergency unique to the SCI patient
    • Onset after injury is variable—usually soon after spinal shock, but it may occur up to years after injury, and distal spinal cord viability is a prerequisite.
    • Represents an acute massive disordered autonomic (primarily sympathetic) response in patients with SCI above the cord level of T6-T8 (the sympathetic outflow) to specific stimuli below the level of the lesion
    • Symptoms (5):
      1. Pounding headache
      2. Hypertension
      3. Flushing and sweating above the level of the lesion
      4. Bradycardia
         • Tachycardia or arrhythmia may be present
      5. Hypertension
         • May vary in severity from causing a mild headache before voiding to life-threatening cerebral hemorrhage or seizure
    • The pathophysiology is that of nociceptive stimulation via afferent impulses that ascend through the cord and elicit reflex motor outflow, causing arteriolar, pilomotor, and pelvic visceral spasm and sweating. Normally, the reflexes would be inhibited by secondary output from the medulla, but because of the SCI this does not occur below the lesion level.
    • The stimuli for this exaggerated response commonly arise from the bladder or rectum and typically involve distention. Precipitation may be the result of simple LUT instrumentation, tube change, catheter obstruction, or clot retention, and in such cases the symptoms resolve quickly if the stimulus is withdrawn.
    • Ideally, any endoscopic procedure in susceptible patients should be done using spinal anesthesia or carefully monitored general anesthesia.
    • Acutely, the hemodynamic effects of this syndrome may be managed with β- and/or α-adrenergic blocking agents.
      • Sublingual nifedipine is capable of alleviating this syndrome when given during cystoscopy (10 to 20 mg) and of preventing it when given orally 30 minutes before cystoscopy (10 mg)
      • No consensus on the acute pharmacologic management of autonomic dysreflexia when necessary;
  • Vesicoureteral reflux
    • Incidence between 17-25% in SCI patients, more common in those with suprasacral SCI.
      • Persistent reflux can lead to chronic renal damage and may be an important factor in the long-term survival of SCI patients.
    • Contributing factors include:
      1. Elevated intravesical pressure during filling and emptying
      2. Infection
    • Management
      • The best initial treatment for VUR in a patient with voiding dysfunction secondary to neurologic disease or injury is to normalize LUT urodynamics (i.e., decrease storage pressures and decrease outlet resistance) as much and as quickly as possible.
        • Depending on the clinical circumstances, this may be achieved by pharmacotherapy, urethral dilatation (in the myelomeningocele patient), neuromodulation, deafferentation, augmentation cystoplasty, or sphincterotomy
  • Urinary tract infection
    • Relatively common in patients with SCI.
    • Bacteriuria should be treated only when the patient has signs or symptoms of a UTI
    • Risk factors for symptomatic UTIs in patients with SCI:
      • Bladder overdistention
      • Increased bladder filling pressures
      • Vesicoureteral reflux
      • Bladder stones
  • Sexual dysfunction in males
    • After SCI most men have erectile and ejaculatory dysfunction.
      • Rates of successful intercourse after SCI in men range from 5% to 75%, and only 10% with SCI can ejaculate.
    • Erectile dysfunction in men can be managed using the same options available to the general population.
    • Only 10% of men with SCI are able to achieve natural conception. Infertile men with SCI can achieve fertility with medical intervention that restores ejaculatory function and normal semen quality.
  • Spinal cord injury in women
    • Management complicated by lack of an appropriate external collecting device
    • Surgical intervention for SUI in this population may be beneficial in well-selected patients
    • Fertility is not impaired in most women with SCI
  • Spinal cord injury and bladder cancer
    • Strong association between the development of bladder cancer (squamous cell carcinoma) and long-term indwelling catheterization
      • Some patients have no obvious tumors visible at endoscopy, and the diagnosis is made by bladder biopsy
  • Follow-up
    • See 2019 CUA NLUTD Guideline Notes
• Transverse Myelitis
  • Acute transverse myelitis is a rapidly developing condition with motor, sensory, and sphincter abnormalities, usually with a well-defined upper sensory limit and no signs of spinal cord compression or other neurologic disease
  • May result from a variety of mechanisms: parainfectious, autoimmune, vascular, or demyelinating
  • Presentation
    • Bladder dysfunction may occur simultaneously with the motor dysfunction or more commonly follows it