Neurogenic bladder

Ravindra Kumar Garg MD (Dr. Garg of King George's Medical University in Lucknow, India, has no relevant financial relationships to disclose.)
Peter J Koehler MD PhD, editor. (

Dr. Koehler of Maastricht University has no relevant financial relationships to disclose.

Originally released October 19, 2014; last updated April 16, 2020; expires April 16, 2023

This article includes discussion of neurogenic bladder, neurogenic lower urinary tract dysfunction, neurogenic urinary bladder, neurogenic detrusor overactivity, and neurogenic bladder dysfunction. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.


Bladder dysfunction is often a disabling manifestation of a variety of brain disorders, such as normal pressure hydrocephalus, dementia with Lewy bodies, vascular dementia, and frontotemporal dementia. Bladder dysfunction in brain disorders manifests with detrusor overactivity (urinary frequency, urgency, and urge incontinence). The spinal disorders, like trauma, infection, ischemia, hemorrhage, tumor, inflammation, and degeneration, produce capacity, hyperreflexic, and overactive bladder. Bladder dysfunction will also result from lesions of the conus medullaris, cauda equina, or peripheral nerves. Congenital Zika syndrome has been implicated in lower urinary tract dysfunction. A lower motor neuron type of urinary bladder manifests with an areflexic detrusor, a large hypotonic bladder, a tight and competent internal sphincter, and failure to empty. The acute cauda equina syndrome is often an emergency requiring urgent imaging and surgery. Clinical details, like history of illness, physical examination and pad count along with urodynamic studies are helpful in determining the optimum bladder treatment. Early treatment is essential to prevent renal damage and secondary bladder-wall changes, thus, improving long-term outcomes. Intradetrusor injections of onabotulinum toxin A have been found effective in improving the bladder function and quality of life. A review indicated that mirabegron, a β3-adrenoceptor agonist, is effective in neurogenic bladder unresponsive to antimuscarinic drugs. Surgical treatment is indicated if all other forms of treatment, oral pharmacologic or intradetrusor injection, and intermittent catheterization fails. Bladder augmentation is the gold standard surgical procedure. The author discusses various aspects of neurogenic bladder.

Key points


• Neurogenic bladder is a dysfunction of the lower urinary tract due to disease of the CNS or PNS involved in the control of micturition.


• A significant number of spinal cord injury patients have neurogenic bladder.


• Clinical manifestations of neurogenic bladder vary, depending on the level of neurologic involvement.


• Clinical details along with urodynamic studies are helpful in determining the possible causes of neurogenic bladder.


• Treatment is targeted to preserve renal function, to keep patients continent, to improve quality of life, and to prevent urinary tract infection.


• Clean, intermittent self-catheterization is the best treatment for neurogenic bladder dysfunction.


• In addition, anticholinergics, antimuscarinic drugs, and botulinum toxin plays an important role in the management.


• Surgical options are reserved for refractory neurogenic bladder.

Historical note and terminology

Neurogenic bladder is a dysfunction of the lower urinary tract due to diseases of the central nervous system or peripheral nervous system involved in the control of micturition. Hippocrates (c.460-370 BC) is credited with some of the first clinical descriptions of paralysis, bladder incontinence, and constipation related to spinal cord injury. In 1895, William Gowers (1845-1915) recognized 3 possible mechanisms of bladder dysfunction in acute myelopathy. First, he suggested that bladder dysfunction might result from spinal pathology. He observed the phenomenon of “retention of urine and subsequent overflow incontinence." Second, he noted that if the lumbar enlargement was involved, the bladder was paralyzed and urine flowed from the bladder as it entered in it. And finally, he explained that if the spinal cord is disconnected from higher centers, there is intermittent involuntary reflex bladder emptying (Lees et al 2012).

During World War I, almost half of the patients with spinal cord injury died from urinary tract infection or renal failure. In 1925, based on his experiments with cats, Frederick James Fitzmaurice Barrington (1884-1956) described Barrington nucleus or the pontine micturition center. This nucleus was thought to contain neurons that have an essential role in the control of bladder contraction (Barrington 1925). Bors and Comarr published a landmark textbook, Neurologic Urology, on the neurogenic bladder in 1971, which was then considered an authoritative work in the field (Bors and Comarr 1971).

Clean intermittent catheterization was first described in 1880 by William Frederick Teevan 1880 (1834-1887) (Teevan 1880). In 1954, Ludwig Guttmann (1899-1980), in England, described a sterile non-touch technique of intermittent catheterization for the initial management of neurogenic bladder in spinal cord injury. Subsequently, Dr. Jack Lapides (1914-1995), at Michigan University, contributed extensively to the development of clean, intermittent catheterization. In 1927, DK Rose first introduced the cystometrograph. The term "urodynamics" was introduced by Dr. David M. Davis of Philadelphia, Pennsylvania in 1954.

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