The defecation reflex is a complex, coordinated process involving intrinsic and extrinsic neural pathways, along with voluntary control, to eliminate fecal material from the large intestine.
I. Essential Features and Mechanism of the Defecation Reflex
The rectum is typically empty or nearly empty. When fecal material enters and distends the rectum, it triggers the rectosphincteric reflex, which is central to the defecation process.
• Rectal Distention and Internal Sphincter Relaxation: As the rectum fills, it contracts, and the internal anal sphincter relaxes. This is an involuntary reflex.
• Urge to Defecate: Distention of the rectum by fecal material elicits a sensation that signals the urge for defecation. This urge typically occurs when the rectum is filled to about 25% of its capacity.
• External Anal Sphincter Contraction: Defecation is normally prevented because the external anal sphincter is maintained in a state of tonic contraction. This tonic contraction is maintained by reflex activation through dorsal roots in the sacral segments.
• Accommodation of the Rectum: The internal sphincter's relaxation is transient because receptors within the rectal wall can accommodate the stimulus of distention. This means the internal anal sphincter regains its tone, and the sensation of urgency subsides until more contents pass into the rectum. This allows the rectum to act as a storage organ, accommodating large quantities of material.
• Voluntary Defecation: When environmental conditions are conducive for defecation, voluntary acts accompany the process.
◦ The external anal sphincter is voluntarily relaxed.
◦ The smooth muscle of the rectum contracts, forcing the feces out of the body.
◦ Intra-abdominal pressure is increased by voluntary contractions of the diaphragm and musculature of the abdominal wall. This can be achieved by expiring against a closed glottis, a maneuver known as the Valsalva maneuver. This increased pressure forces the pelvic floor downward.
II. Regulation of the Defecation Reflex
The control of defecation involves a sophisticated interplay of the enteric, autonomic, and somatic nervous systems.
• Intrinsic (Enteric) Nervous System (ENS): The aperistaltic reflex, which can be initiated in the colon and contributes to material movement, is mediated by nerves within the myenteric plexus, which appear to be predominantly inhibitory. While the ENS coordinates activities and local reflexes, the sources do not explicitly detail its independent role in the defecation reflex pathway itself beyond coordinating colonic contractions.
• Extrinsic (Autonomic) Nervous System (ANS):
◦ Parasympathetic System: The smooth muscle of the rectum contracts during defecation, which is influenced by parasympathetic activity.
◦ Sympathetic System: The sympathetic system generally depresses contractions. However, in the context of bladder emptying (which shares similar control principles with defecation), cooperation with the sympathetic division (which has antagonistic effects on the internal urethral sphincter) is required. For defecation, the internal anal sphincter relaxation is part of the reflex, and its tone is regulated by neural and humoral influences.
• Somatic Nervous System and Central Control:
◦ Voluntary Control: The ability to prevent defecation by tonic contraction of the external anal sphincter is a voluntary act. The control of the external anal sphincter is mediated by pathways within the spinal cord that lead to the cerebral cortex.
◦ Higher Centers: Emotional state can significantly influence colonic motility, indicating a strong influence of higher centers of the central nervous system on motility. For example, nervousness before an examination can lead to diarrhea.
III. Applied Clinical Aspects
Disruptions in the normal mechanisms and regulation of the defecation reflex can lead to several clinical conditions:
• Loss of Voluntary Control (Spinal Cord Injuries): Damage to the spinal cord pathways leading to the cerebral cortex can result in a loss of voluntary control of defecation. In paraplegic patients lacking the tonic contraction of the external anal sphincter, the rectosphincteric reflex may lead to spontaneous defecation. This can also be seen in autonomic dysreflexia where noxious stimuli from the colon (or bladder) can trigger an exaggerated sympathetic response, leading to dangerous hypertension in individuals with spinal cord injuries above T6, as the inhibitory signals from the brain cannot descend below the injury.
• Hirschsprung's Disease (Congenital Megacolon): This severe condition is characterized by the absence of neuronal ganglion cells of the enteric nervous system in the distal colon. The involved segment, which always includes the internal anal sphincter and often extends proximally into the rectum, exhibits increased tone, has a very narrow lumen, and is devoid of propulsive activity. As a result, the colon proximal to the diseased segment becomes dilated (megacolon), leading to intestinal obstruction and absence of defecation early in infancy. Surgical removal of the diseased segment is the treatment.
• Constipation: This often results from abnormally delayed transit of material through the colon. While often dietary in origin (e.g., lack of fiber), alterations in motility and transit are also frequently caused by emotional factors.
• Irritable Bowel Syndrome (IBS): This common gastrointestinal disorder often presents with altered bowel habits (constipation and/or diarrhea) and abdominal pain. In IBS, alterations in colonic motility are frequently caused by emotional factors, indicating the strong influence of higher CNS centers. During stress, patients with IBS and constipation may exhibit increased segmentation in the sigmoid colon, while those with diarrhea may show decreased segmentation.