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You are here: IC Network > Physician's Lounge > Neuroanatomy of the Bladder
The Neuroanatomy of the Bladder The bladder is innervated by both parasympathetic nerve and the
sympathetic nerves. Urination originates with parasympathetic preganglionics at discs S2-S3 & S4.Sympathetic innervation comes from the thoracic and lumbar spinal cord which are located at T10 to L2. The hypogastric nerve carries sympathetic input to the pelvic ganglia and afferent input from the bladder to the thoracolumbar spinal cord (thoracic & lumbar region). Motor input to the bladder is provided by neurons in the pelvic plexus and bladder wall, containing a combination of cholinergic and adrenergic nerve fibers. Voiding relies on activation of mechanoreceptive A fibers in the pelvic nerve. Some afferents in the pelvis and hypogastric nerve can transmit pain input to the spinal nerves - S2-S4. Afferents in the pelvic nerve projecting to the sacral S2 - S4 spinal cord transmit sensation of mucosal irritation and tension, trigger voiding. Afferents in the hypogastric nerve convey sensation of the bladder overdistention, fullness to the thoracolumbar T10 to L2 spinal cord, providing one possible explanation for referred pain. In contrast, mucosal irritation or inflammation are relayed by afferents in the pelvic nerve. This explains referred pain in the vagina, rectum, and perineum. Nerve fibers on each lateral part of the spinal cord that sense touch, pain and temperature is called the spinothalamic tract. The sensations of bladder pain and fullness are transmitted by the lateral spinothalamic tract to the brain. Evidence shows that pain processing in the spinal cord and brain contribute to sensations of bladder discomfort and can not be permanently silenced by targeting the bladder. Capsaicin initially releases afferent neurotransmitters and induces pain, followed by a period of desensitization induced anesthesia. Studies have demonstrated that the human bladder contains capsaicin-sensitive afferents that are involved in pain. If repetitive painful stimuli alters pain processing mechanisms, treatment aimed only at peripheral structures may leave central nerve structurs unaffected. Thus, a collective approach may be suggested.
Intrigued? Read more about it in: Steers W. Tuttle J. Neurogenic Inflammation and Nerve Growth Factor. In G. Sant (Ed.) Interstitial Cystitis. Philadelphia: Lippincott-Raven Publishers, 1997; 67-75. Currently on-sale at AMAZON.COM. |