A neurologic basis for the overactive bladder

The functions of the lower urinary tract (LUT) to store and periodically release urine are dependent on neural circuits in the brain and spinal cord. This paper reviews the central neural control of micturition and how disruption of this control can lead to bladder overactivity and incontinence.

Neuroanatomic, electrophysiologic, and pharmacologic techniques have provided information about the neural circuitry and the neurotransmitters involved in the central nervous control of voiding. Experimental models of neural injury, including spinal cord transection, cerebral infarction, and localized brain lesions, have been studied to identify the mechanisms contributing to the neurogenic overactive bladder.

Normal storage of urine is dependent on 1) spinal reflex mechanisms that activate sympathetic and somatic pathways to the urethral outlet and 2) tonic inhibitory systems in the brain that suppress the parasympathetic excitatory outflow to the urinary bladder. Voiding is mediated by inhibition of sympathetic-somatic pathways and activation of a spinobulbospinal parasympathetic reflex pathway passing through a micturition center in the rostral pons. Damage to the brain can induce bladder overactivity by reducing suprapontine inhibition. Damage to axonal pathways in the spinal cord leads to the emergence of primitive spinal bladder reflexes triggered by C-fiber bladder afferent neurons. The C-fiber afferent neurotoxin capsaicin, administered intravesically, has been useful in treating certain types of neurogenic bladder overactivity.

The central nervous mechanisms controlling the LUT are organized in the brain and spinal cord as simple on-off switching circuits that are under voluntary control. Damage to central inhibitory pathways or sensitization of peripheral afferent terminals in the bladder can unmask primitive voiding reflexes that trigger bladder overactivity.