Neurogenic bladder dysfunction

Uninhibited bladder is usually due to damage to the brain from a stroke or brain tumor. This can cause reduced sensation of bladder fullness, low capacity bladder and urinary incontinence. Unlike other forms of neurogenic bladder, it does not lead to high bladder pressures that can cause kidney damage.[1]

In spastic neurogenic bladder (also known as upper motor neuron or hyper-reflexive bladder), the muscle of the bladder (detrusor) and urethral sphincter do not work together and are usually tightly contracted at the same time. This phenomenon is also called detrusor external sphincter dyssynergia (DESD). This leads to urinary retention with high pressures in the bladder that can damage the kidneys. The bladder volume is usually smaller than normal due to increased muscle tone in the bladder. Spastic neurogenic bladder is usually caused by damage to the spinal cord above the level of the 10th thoracic vertebrae (T10).[1][2]

In flaccid bladder (also known as lower motor neuron or hypotonic bladder), the muscles of the bladder lose ability to contract normally. This can cause the inability to void urine even if the bladder is full and cause a large bladder capacity. The internal urinary sphincter can contract normally, however urinary incontinence is common. This type of neurogenic bladder is caused by damage to the peripheral nerves that travel from the spinal cord to the bladder.[1]

Mixed type of neurogenic bladder can cause a combination of the above presentations. In mixed type A, the bladder muscle is flaccid but the sphincter is overactive. This creates a large, low pressure bladder and inability to void, but does not carry as much risk for kidney damage as a spastic bladder. Mixed type B is characterized by a flaccid external sphincter and a spastic bladder causing problems with incontinence.[1]

Damage to the brain or spinal cord is the most common cause of neurogenic bladder. Damage to the brain can be caused by stroke, brain tumors, multiple sclerosis, Parkinson's disease or other neurodegenerative conditions.[3] Bladder involvement is more likely if the damage is in the area of the pons. Damage to the spinal cord can be caused by traumatic injury, demyelinating disease, syringomyelia, cauda equina syndrome, or spina bifida. Spinal cord compression from herniated disks, tumor, or spinal stenosis can also result in neurogenic bladder.[1][3]

Damage to the nerves that travel from the spinal cord to the bladder (peripheral nerves) can cause neurogenic bladder, usually the flaccid type. Nerve damage can be caused by diabetes, alcoholism, and vitamin B12 deficiency. Peripheral nerves can also be damaged as a complication of major surgery of the pelvis, such as for removal of tumors.[1]

Emptying the bladder with the use of a catheter is the most common strategy for managing urinary retention from neurogenic bladder. For most patients, this can be accomplished with intermittent catherization which involves no surgery or permanently attached appliances. Intermittent catheterization involves using straight catheters (which are usually disposable or single-use products) several times a day to empty the bladder.[3] This can be done independently or with assistance. For people who are unable to use disposable straight catheters, a Foley catheter allows continuous drainage of urine into a sterile drainage bag that is worn by the patient but are associated with higher rates of complications.[6]

Oxybutynin is a common anti-cholinergic medication used to reduce bladder contractions by blocking M3 muscarinic receptors in the detrusor.[6] Its use is limited by side effects such as dry mouth, constipation and decreased sweating. Tolterodine is a longer acting anticholinergic that may have fewer side effects.[4]

For urinary retention, cholinergics (muscarinic agonists) like bethanechol can improve the squeezing ability of the bladder. Alpha blockers can also reduce outlet resistance and allow complete emptying if there is adequate bladder muscle function.[4]

Botulinum toxin (Botox) can be used through two different approaches. For spastic neurogenic bladder, the bladder muscle (detrusor) can be injected which will cause it to be flaccid for 6-9 months. This prevents high bladder pressures and intermittent catherization must be used during this time.[4]

Botox can also be injected into the external sphincter to paralyze a spastic sphincter in patients with detrusor sphincter dyssynergia.[5]

There are various strategies to alter the interaction between the nerves and muscles of the bladder, including nonsurgical therapies (transurethral electrical bladder stimulation), minimally invasive procedures (sacral neuromodulation pacemaker), and operative (reconfiguration of sacral nerve root anatomy).[4]

Surgical interventions may be pursued if medical approaches have been maximized. Surgical options include creation of a stoma that bypasses the urethra to empty the bladder directly. This conduit may be created from the appendix (Mitrofanoff stoma) or a portion of the ileum (‘Yang-Monti’ conduit).[4] The ileum and [[ascending colon can also be used to create a pouch accessible for catherization (Indiana pouch). Urethral stents or urethral sphincterotomy are other surgical approaches that can reduce bladder pressures but require use of an external urinary collection device.[5]