The bladder temporarily stores urine and then expels it in a controlled manner. This process relies on a complex communication network between the bladder muscle and the central nervous system. The coordination of storage and release is managed by the micturition reflex, a specialized spinal reflex that integrates motor and sensory signals to maintain continence until urination is consciously initiated.
The Spinal Nerves Controlling the Bladder
Bladder function is governed by three distinct sets of peripheral nerves originating from different spinal cord segments: the sympathetic and parasympathetic nerves (autonomic nervous system), and the somatic nervous system. Sympathetic input originates from the thoracolumbar region (T11 through L2) and travels via the hypogastric nerve.
The parasympathetic nerves (pelvic nerves) arise from sacral segments S2 through S4. Both autonomic systems innervate the detrusor muscle (the muscular wall of the bladder) and the internal urethral sphincter. The somatic nervous system uses the pudendal nerve, also arising from S2 to S4, to control the external urethral sphincter.
These three nerve pathways coordinate the storage and emptying phases. They carry efferent (motor) signals from the spinal cord to the bladder and afferent (sensory) signals from stretch receptors in the bladder wall back toward the brain and spinal cord. This sensory feedback loop allows the brain to perceive bladder fullness.
How the Nerves Manage Urine Storage
The default state of the bladder is storage, characterized by low internal pressure and a high-resistance outlet. During filling, the sympathetic nervous system (T11-L2) is dominant. Sympathetic signals cause the detrusor muscle to relax, allowing the bladder to expand without increasing internal pressure.
Simultaneously, sympathetic nerves signal the internal urethral sphincter to contract, keeping the outlet closed and preventing leakage. This involuntary mechanism is reinforced by the somatic nervous system, which provides voluntary control over continence. The pudendal nerve maintains continuous contraction of the external urethral sphincter.
Sensory information from mechanoreceptors in the bladder wall travels to the spinal cord. Low-level input triggers a spinal “guarding reflex” that reinforces sympathetic and somatic activity. This combination of detrusor relaxation and sphincter contraction ensures urine is retained until voiding.
How the Nerves Initiate Voiding
When sensory input indicates critical fullness, a series of events overrides the storage mechanism, signaling the central nervous system to switch to emptying. The primary coordinating center for this switch is the Pontine Micturition Center (PMC), a cluster of neurons in the brainstem.
When activated, the PMC inhibits sympathetic neurons (storage) and activates parasympathetic neurons (voiding). Parasympathetic activation (S2-S4) signals the detrusor muscle to contract, generating the pressure needed to expel urine. Simultaneously, parasympathetic activity causes the involuntary internal sphincter to relax.
Finally, the PMC coordinates the inhibition of somatic input to the external sphincter via the pudendal nerve. This voluntary relaxation of the external sphincter, coupled with detrusor contraction and internal sphincter relaxation, allows for coordinated urine flow.
Causes and Effects of Nerve Damage to the Bladder
Disruption to this intricate nerve network can result in a neurogenic bladder, a condition covering dysfunctions where brain and bladder signals are impaired due to neurological damage. Common causes include traumatic events like Spinal Cord Injury, or progressive diseases such as Multiple Sclerosis, long-term diabetes, or stroke.
The effect depends on the location of the nerve injury, typically resulting in two main outcomes. Damage leading to an overactive bladder causes the detrusor muscle to contract too frequently or without warning, resulting in urinary urgency and incontinence. Conversely, damage that paralyzes the detrusor muscle or prevents sphincter opening leads to an underactive bladder, causing urinary retention.