What causes bladder dysfunction?

Updated: Jan 04, 2019
  • Author: Gregory T Carter, MD, MS; Chief Editor: Elizabeth A Moberg-Wolff, MD  more...
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Classification of a neurogenic bladder depends on the location of the lesion along the central nerve pathway and includes sacral, suprasacral, and suprapontine lesions. [2]

Lesions of the peripheral nerves or the sacral micturition center cause detrusor areflexia. These lesions may affect the conus medullaris, the cauda equina, and S2-S4 peripheral nerves. Common causes of sacral lesions are trauma, stenosis, tumors, peripheral neuropathy, and infection. In general, these lead to variable loss of parasympathetic and somatic nerve function. Detrusor areflexia, bladder neck incompetence, or loss of external sphincter function may occur and present as bladder distention with overflow incontinence.

Lesions of the spinal cord or brainstem below the pontine micturition center, but above the sacral micturition center, lead to uninhibited bladder contractions with uncoordinated sphincter activity. Suprasacral lesions are associated with the group of neurogenic bladder problems caused by spinal cord lesions from trauma, tumors, or spina bifida, as well as multiple sclerosis or transverse myelitis. These lesions cause interruption of the spinobulbospinal reflex. Two pathological mechanisms are in play here. The first is an acute areflexia and then detrusor hyperreflexia. The second is detrusor-sphincter dyssynergia, where the external sphincter contracts at the same time the detrusor contracts. Individuals with lesions below the pontine micturition center have both detrusor hyperreflexia and detrusor-sphincter dyssynergia.

Suprapontine lesions lead to uninhibited bladder contractions, which may be secondary to loss of cerebral cortex inhibition at the sacral micturition center. These lesions are often due to cardiovascular events, multiple sclerosis, dementia, brain tumors, or trauma. Suprapontine lesions are located at or between the pontine micturition center and the cerebral cortex and involve the spinobulbospinal reflex. They may or may not coincide with sacral lesions. These lesions present as uninhibited bladder contractions with retained voluntary urethral sphincter relaxation during micturition.

In the context of neuropathic lesions, abnormalities along the micturition centers and peripheral nerves present with varying manifestations; however, most eventually develop into fibromuscular bladder dysfunction.

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