The Epidemiology and Pathophysiology of Neurogenic Bladder
Published Online: July 30, 2013
David Ginsberg, MD
Neurogenic Bladder: An Introduction
Normal micturition (urination) requires proper function of both the bladder and the urethra, including normal compliance within the bladder detrusor muscle and a physiologically competent urinary sphincter. The process of micturition is controlled by the central nervous system (CNS), which coordinates sympathetic, parasympathetic, and somatic nervous system activity for normal micturition and urinary continence. Dysfunction in voiding can result from mechanical or physiologic abnormalities in the urinary tract that lead to an inability of the sphincter to appropriately increase or decrease its pressure when bladder pressure is increased. Damage to or diseases of the CNS or within the peripheral or autonomic nervous system may lead to neurogenic bladder (NGB) dysfunction. NGB dysfunction may arise as a result of several neurologic conditions. NGB has been found in 40% to 90% of patients in the United States with multiple sclerosis (MS), 37% to 72% of patients with parkinsonism, and 15% of patients with stroke.1,2 It is estimated that 70% to 84% of patients with spinal cord injuries have at least some degree of bladder dysfunction.1,3 Bladder dysfunction is also frequently seen in patients with spina bifida, with vesicoureteral reflux present in up to 40% of children affected by 5 years of age and with up to 60.9% of young adults with spina bifida experiencing urinary incontinence.1,4 Less common scenarios for NGB may include diabetes mellitus with autonomic neuropathy, unintended sequelae following pelvic surgery, and cauda equina syndrome resulting from lumbar spine pathology.1 Many patients with NGB, especially those with multiple sclerosis, cerebrovascular accidents, and spinal cord injury, experience uninhibited bladder contractions.1,5 Bothersome urinary symptoms associated with NGB include urinary incontinence (UI), frequency, and urgency.5 Patients also may have increased risk and incidence of urinary tract infections (UTIs) and bladder outlet obstruction. If not treated optimally, patients with NGB may also be at risk for sepsis and renal failure, and these patients have higher numbers of clinical office and ED visits annually, with up to one-third of these visits leading to a need for hospitalization.1,3 In addition to the physical and clinical burden associated with NGB, the associated urinary incontinence can negatively impact a patient’s quality of life, causing embarrassment, depression, and social isolation.1,6 As diagnostic and treatment options continue to advance for patients with NGB, it is important to reassess its epidemiology and physiology, diagnosis, assessment, and classification, and the impact of the symptoms and complications associated with NGB on the patients affected by this disorder.
Neurologic Disorders and Neurogenic Bladder
Normal urinary tract function is dependent on neural integration between the central and peripheral nervous systems.7 MS, the most common neuroinflammatory disorder of the CNS, may cause lower urinary tract dysfunction and NGB as a result of a disruption of this integration. Urinary symptoms in MS are likely caused by neural demyelization and axonal degradation, and patients with MS lesions in specific CNS regions (encephalic, spinal suprasacral regions) may be more likely to experience major urinary symptoms.7,8 It has also been hypothesized that CNS lesions from MS may exert a local effect on bladder function.8 A variety of patterns may be seen, with detrusor overactivity of the bladder noted in 50% to 90% of patients with MS and detrusor areflexia in 20% to 30% of patients with MS.1,3 Neurogenic lower urinary tract dysfunction is often noted during the first 10 years following MS diagnosis and tends to increase as the patient’s level of disability worsens.7,9 This urinary tract dysfunction can lead to substantial limitations in daily activity for patients with MS.7 More than 80% of patients with MS report genitourinary symptoms, with voiding dysfunction impacting the vast majority of these patients.9,10 In addition, bladder symptoms are frequently mismanaged in patients with MS, often leading to urinary retention and/or subsequent UTI.11 Early and accurate assessment of potential lower urinary tract dysfunction is essential to protect the upper urinary tract, optimize management, and improve quality of life for these patients.7
Idiopathic Parkinson’s Disease
Idiopathic Parkinson’s disease (IPD) presents as an extrapyramidal neurologic syndrome, most commonly associated with prominent motor symptoms. However, non-motor symptoms have been recognized in parkinsonism, and urinary symptoms are frequently present in these patients.12 Urinary dysfunction as a manifestation of autonomic failure is common in patients with IPD.13 Studies have shown that urinary storage symptoms (frequency, urgency, urge urinary incontinence) are present in 57% to 83% of patients with IPD, and voiding symptoms (poor force of stream, hesitancy, incomplete emptying) are seen in 17% to 27% of this patient population.12 For most patients, the onset of bladder dysfunction occurs after motor symptoms are evident, and voiding dysfunction tends to increase with neurologic impairment as opposed to disease duration.14 As with NGB associated with other disorders, a patient’s renal function and long-term health may be compromised if urinary dysfunction in IPD is not recognized and addressed promptly. One confounding factor impacting correct diagnosis and management is the potential for clinicians to confuse patients with pure IPD with those who have multiple symptom atrophy, a disorder that manifests with parkinsonian-like motor symptoms but with substantial differences in both neurologic progression and urinary disturbances.12,14 Bladder symptoms may also be the result of coexistant disease processes such as UTI, diabetes, or in men, benign prostatic hypertrophy, which can complicate accurate diagnosis. Appropriate diagnosis is key to management of urinary dysfunction in IPD, and a multidisciplinary approach may be needed for symptom management and optimal patient quality of life.14
The primary urinary complaints in patients with urinary dysfunction due to IPD include urgency, frequency, UI, and nocturia. This is likely due to the urodynamic finding of detrusor overactivity, which may be seen in 45% to 93% of patients with IPD.12 UI in patients with IPD may be of multifactorial origin; not only do the patients have significant bladder dysfunction, but there also are functional problems such as impaired mobility and poor manual dexterity, which can impact the patient’s ability to perform appropriate toileting. Some patients with IPD also experience sleep disturbances and nocturnal polyuria. Management of these patients must take into consideration how IPD influences the lower urinary tract as well the possible pharmacologic effects of anti-parkinsonian agents the patient may be taking.14
Spinal Cord Injury
It is estimated that there are more than 200,000 patients with traumatic spinal cord injury (SCI) in the United States, with an incidence of approximately 12,000 new cases estimated annually.15 Urinary dysfunction is very common in these individuals; approximately 81% of patients with SCI report at least some degree of impaired bladder function within 1 year after injury.16,17 The expected level of bladder dysfunction may potentially be determined by the spinal level at which the SCI occurred. Injury proximal to the sacral spinal cord should lead to an upper motor neuron lesion and detrusor overactivity. Injuries that involve the sacral spinal cord or cauda equina should result in a lower motor neuron lesion and detrusor areflexia. Both of these classifications assume the presence of a complete neurologic lesion; however, the presence of a complete lesion may be variable. In addition, patients with a suprasacral SCI are at risk for detrusor-external sphincter dyssynergia, which can place the patient at risk for incomplete bladder emptying and elevated bladder pressures.1,18 Many patients with SCI do not have well-defined complete lesions, and although the majority of patients demonstrate fairly consistent bladder and sphincter behavior based on neurologic deficit, this is not definitive for all patients with SCI. Thorough urodynamic evaluation to evaluate bladder and sphincter behavior needs to be performed to better assess urinary dysfunction prior to initiation of therapy.18 Management of NGB dysfunction is a critical component of a rehabilitation program for a patient with SCI, as NGB contributes significantly to the overall morbidity of these patients. Losing normal bladder function is disabling and may lead to urinary tract deterioration, urinary incontinence, and reduced quality of life. Principal goals for management are preservation of renal function, improved continence, and reduction of urinary complications such as kidney stones and UTI. Bladder management focuses on therapy to facilitate bladder filling and storage of urine and treatment to facilitate bladder emptying that assists in preserving both renal function and social functioning to allow patients to enjoy a healthier life.16
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