NEUROGENIC BOWEL for all medicalstudent.pptx

NEUROGENIC BOWEL for all medicalstudent

1. Neurogenic bowel 1

2. Neurogenic bowel refers primarily to functional changes in the colon and pelvic floor, although a variety of neurologic conditions affect various other gastrointestinal organs as well SCI is the condition that is most frequently associated with neurogenic bowel dysfunction, although there are many other neurologic conditions contributing to gastrointestinal dysfunction as well.

3. Anatomic and Physiological Considerations Colon serves to desiccate and form fecal matter as it is transported from the ileum to the rectum As a transport and storage organ Functions to absorb water and electrolytes .( 1500ml to 150 ml/d) Colonic propulsion of the fecal contents requires motility (a term frequently misused and often misunderstood).

4. Motility and fecal transport are measured differently For motility, measure colonic wall contractions (by manometrically and/or electronically) The most clinically useful index of overall colonic function is colonic transit time , the amount of time required for contents to pass from the cecum to the outside(uses radio-opaque markers that are swallowed and followed through the intestinal tract with serial abdominal radiographs)

5. Transit and motility are dependent on regular scheduled bowel care.( esp for patient with SCI) Rectal distention can reflexively inhibit peristalsis and affect stomach to prevent gastric emptying.

6. Anorectum The anal canal provides the primary mechanism for fecal continence and is the barrier for evacuation The internal anal sphincter ( IAS ) specialized thickening of the circular smooth muscle layer of the rectum maintains a continuous state of maximal contraction . (responsible for the majority of resting tone in the anal canal) normal resting tone → 50- 100 cmH 2 O

7. The external anal sphincter ( EAS ) is a striated muscle continuous with the pelvic floor and innervated by the pudendal nerves bilaterally Important during events that are an acute threat to continence, such as coughing, acute rectal contraction, or assuming an upright position.

8. The puborectalis tugs the rectum anteriorly and creates an angle between the rectum and the anal canal, the anorectal angle . This kink in the fecal pathway aids in continence The IAS , the EAS , and the puborectalis work together synergistically to maintain continence and are collectively named the anal sphincter mechanism .

9. Neuroanatomy and Physiology of the Gastrointestinal Tract Neural control of the gastrointestinal tract involves Central nervous system(CNS; brain and spinal cord), Autonomic nervous system (sympathetic and parasympathetic), and Enteric nervous system

10. Enteric Nervous System The ENS is a distinct system that has its own set of neurons that coordinate sensory and motor functions. ganglia are interconnected, which allows for integration and processing of data There are three different types of neurons in the ENS based on function: sensory neurons, interneurons, and motor neurons

11. Sensory neurons perceive thermal, chemical, or mechanical stimuli and transform these sensations into action potentials that are conducted to the nervous system. Interneurons serve as conduits between the sensory and motor neurons

12. The numerous synapses between interneurons create a highly organized circuitry that processes sensory input from the gut and other parts of the nervous system, and integrates and generates reflex responses to these stimuli. Motor neurons are the final common pathway.

13. They receive and translate signals to the gut (mucosa, muscle, vasculature) that affect digestive, interdigestive , and emetic functions based on the transmitters released The ENS is the key to proper functioning of the entire gastrointestinal tract It is situated in two primary layers: the submucosal (Meissner’s) plexus and the intramuscular myenteric ( Auerbach’s ) plexu s.

14. These plexi have an estimated 10 to 100 million neurons, plus two to three glial cells per neuron. The ENS glial cells resemble CNS astrocytes and are much less abundant than the 20 to 50 glial cells per neuron in the CNS. The coordination of segment-to-segment function is largely regulated by the ENS. The ENS also has its own blood-nerve barrier , similar to the blood-brain barrier of the CNS

15. Gastrointestinal Neurosensory System Enteric Nervous System Sensory Neurons The ENS relays chemical, mechanical, and thermal sensory information to the CNS through vagal afferents and spinal afferents . Vagal and spinal sensory neuron endings supply the muscle, mucosa, and ganglia of the ENS . Spinal sensory neurons also supply the serosa and mesentery and their blood vessels Vagal afferent nerve endings act as chemical, thermal, and mechanical receptors

16. These directly monitor various changes in the gastrointestinal tract such as chemical, temperature, muscle tension, and mucosal brushing. Chemical receptors are located in the mucosal epithelium of the stomach and intestinal lumen in close proximity with the lamina propria , constantly determining acidity, osmolarity , and the concentration of glucose, fatty acids, and amino acids

17. The existence of nociceptors (C or A δ fibers ) in the gastrointestinal tract has not been established Temperature change in the lumen is detected by thermoreceptors that play a role in the brain’s perception and regulation of core temperature Mechanical receptors provide data on distention or contraction, and connect with myenteric ganglia. They are also found in rectal muscles and contribute to pelvic innervation

18. Spinal afferent nerve endings are distributed extensively throughout the bowel, relaying chemical, thermal and mechanical information. In the mucosa , they detect chemical changes related to injury, ischemia, infection, or inflammation that contribute to pain and discomfort In the serosa and mesentery , they recognize visceral distention and contraction

19. Mechanoreceptors (whether derived from vagal or spinal afferents) are either low or high in threshold. Low threshold receptors detect normal nonconscious and conscious sensations such as satiety, hunger, gaseousness, and nausea.

20. High-threshold receptors detect distention or contraction beyond a set threshold and perceive painful stimuli, eliciting acute, sharp visceral pain. Activation of both low- and high-threshold receptors contributes to the range of symptoms that are felt along the gastrointestinal tract Vagal afferents are primarily implicated in the emetic response, and spinal afferents are primarily implicated in the sensation of nausea

21. Gastrointestinal Neuromotor System The muscles of the gastrointestinal tract carry out essential functions throughout the gut, including propulsion, grinding, mixing, absorption, storage, and disposal. These muscles are composed of “self-excitable” smooth muscles .

22. The interstitial cells of Cajal act like a pacemaker and allow propagation of electrical slow waves into the circular muscle layer, which generates spreading muscle contraction. These smooth muscles act like an electrical syncytium (interconnected)where action potentials are conducted in three dimensions from one smooth muscle fiber to another through gap junctions

23. The gastrointestinal tract muscles respond to influences of the vagal efferents and the ENS microcircuitry based on excitatory or inhibitory innervation of motor neurons Contraction is mediated by the release of excitatory neurotransmitters by vagal afferents at the neuromuscular junctions( acetylcholine and substance P) Conversely, the release of nitric oxide, ATP, and vasoactive intestinal peptide from the inhibitory motor neurons impedes contractile activity and facilitates relaxation.

24. The sympathetic and parasympathetic nervous systems seem to modulate the ENS , rather than directly controlling the smooth muscles of the bowel Sympathetic nervous system stimulation tends to promote the storage function by enhancing anal tone and inhibiting colonic contractions, although little clinical deficit occurs from bilateral sympathectomy .

25. Parasympathetic activity enhances colonic motility , and its loss is often associated with difficulty with evacuation DWE, including impactions and functional obstructions, such as Ogilvie’s pseudoobstructive syndrome

26. Intestinal Motility The ENS is designed to control the various patterns of motility in the intestinal tract The interdigestive migrating motor complex pattern occurs during fasting in the stomach and the small intestine It is responsible for removal of waste from the intestinal lumen throughout the fasting period

27. The brainstem sends signals that are transmitted to vagal efferents , which convert migrating motor complex motility to segmentation motility with the increase in bulk and nutrients, especially lipids This subsequently becomes peristaltic motility, which is propagated through brief segments of intestine at a time.

28. Peristaltic activity gradually evolves into powerful contractions sustained through long portions of circular muscle along the small and large bowel. These “giant migratory contractions” (GMCs) propel waste through the lumen, particularly in the large intestine

29. Motility of the Anus, Rectum, and Pelvic Floor Normal defecation and maintenance of fecal continence entail a highly coordinated mechanism that involves the levator ani , puborectalis , and the external (EAS) and internal anal sphincter (IAS) muscles . The pelvic floor is composed of the levator ani , the underlying sheets of which form a sling.

30. The levator ani , puborectalis , and EAS are skeletal muscles that constantly maintain tone and sustain pelvic organs in place against the forces of gravity. Simultaneous contraction of these muscles prevents the involuntary loss of stool and helps maintain the regular pattern of defecation

31. Physiology of Normal Defecation The rectum is usually empty until just before defecation. Perception of rectal contents and pressures is essential for signaling voluntary contraction of the anal sphincter. Normal defecation begins with reflexes triggered by rectosigmoid distention produced by approximately 200 mL of feces

32. A rectorectal reflex occurs in which the bowel proximal to the distending bolus contracts and the bowel wall distally relaxes, serving to propel the bolus further caudal Reflex relaxation of the IAS also occurs, which is enhanced by, but does not require, an extrinsic nerve supply This relaxation, called the rectoanal inhibitory reflex , correlates with the urge labeled “the call to stool

33. One can then volitionally contract the levator ani to open the proximal anal canal and relax the EAS and puborectalis muscles. This allows a straighter, shorter, and more open anorectal passage which permits the bolus to pass. Increasing the intraabdominal pressure by squatting and by Valsalva’s maneuver assists bolus elimination.

34. For 90% of normal individuals, only the contents of the rectum are expulsed, whereas 10% will clear the entire contents of the left side of the colon from the splenic flexure distally Defer defecation by volitionally contracting the puborectalis muscle and EAS.

35. The EAS generally tenses in response to small rectal distentions via a spinal reflex , although reflexive relaxation of the EAS occurs in the presence of greater distentions . These spinal cord reflexes are centered in the conus medullaris and are augmented and modulated by higher cortical influences. When cortical control is disrupted, as by SCI, the EAS reflexes usually persist and allow spontaneous defection. .

36. During sleep the colonic activity, anal tone, and protective responses to abdominal pressure elevations are all decreased , while rectal tone increases The gastrocolonic response or gastrocolic reflex refers to the increased colonic activity in the first 30 to 60 minutes after a meal

37. This increased colonic activity appears to be modulated both by hormonal effects , from release of peptides from the upper gastrointestinal tract (gastrin, motilin , cholecystokinin) that increase the contractility of the colonic smooth musculature, and by a reduction in the threshold for spinal cord–mediated vesicovesical reflexes.

38. Upper gastrointestinal receptor stimulation also results in increased activity in the colon, possibly because of reflexively increased parasympathetic efferent activity to the colon

39. In persons with SCI the measured increase in colonic activity after a meal is blunted as compared with that in normal subjects. The gastrocolonic response is often used therapeutically, even in patients with SCI, to enhance bowel evacuation during this 30- to 60-minute postprandial time frame.

40. The EAS is physically larger than the IAS, and its contraction is under both reflex and volitional control. The volitional control is learned during the course of normal maturation. Normal baseline reflex action of the anorectal mechanism allows spontaneous stool elimination . The EAS is innervated by the S2 through S4 nerve roots via the pudendal nerve , and the puborectalis muscle is from the S1 to S5 roots

41. Pathophysiology of Gastrointestinal Dysfunction Nausea, Vomiting, and Bloating Neurologic dysfunction that affects the inhibitory motor neurons in the ENS at any level of the neural axis from the brain, spinal cord, afferent nerves, or efferent nerves can lead to spasticity of the gastric or intestinal and colonic musculature The digestive muscles perform as an electrical syncytium

42. Inhibitory motor neurons allow propagation of contractile activity in an organized, segmental, and aboral pattern When inhibitory motor neurons are inactivated or destroyed by disease, the circular muscles contract continuously and non-systematically. These contractions are incapable of forward propulsion, causing functional obstruction

43. This can be manifested as dysphagia, gastroparesis , or chronic intestinal or colonic pseudoobstruction , which might be associated with anorexia, abdominal pain, and diarrhea and constipation Inhibitory motor neurons can be affected by autonomic neuropathy, dysfunction of neurons in the myenteric plexus, or degeneration of smooth muscle

44. Abdominal Pain and Discomfort Arise from gastrointestinal tract distention and powerful contractions. High-threshold and silent mechanoreceptors sense severe distention and intense contractions when there is ischemia, injury, or inflammation. Mechanical and chemical irritants stimulate mechanoreceptors in the ENS and translate signals to the brain and spinal cord from muscle stretching and contractions

45. Diarrhea Diarrhea occurs when there is overstimulation of secretomotor neurons by histamine from inflammatory and immune-mediated cells in the mucosa and submucosa , or overstimulation by vasoactive intestinal peptide and serotonin from mucosal enterochromaffin cells, or overstimulation by all three substances.

46. Moreover, these substances influence presynaptic inhibitory receptors to block the release of norepinephrine from the postganglionic sympathetic fibers that inhibit secretomotor neurons. Bacterial overgrowth in the gut can be a factor in chronic inflammatory states presenting with diarrhea .

47. Defecation Dysfunction Constipation Constipation can be a huge enigma in neurologic states. Infrequent, incomplete emptying of hard stools is due to decreased water and electrolyte secretion into the lumen, resulting from reduced excitation of the secretomotor neurons in the ENS .

48. Norepinephrine released by sympathetic stimulation inhibits the firing of secretomotor neurons by hyperpolarization. Release of excitatory neurotransmitters is reduced in the secretory epithelium , decreasing the secretion of water and electrolytes.

49. A lack of rectal sensation and a decreased urge to defecate can be strongly associated with constipation in various conditions that present with lesions in the brain, spinal cord, sacral nerves, and hypogastric and pudendal nerves . Outlet obstruction can ensue because of delayed colonic transit times and lack of perineal and rectoanal sensation .

50. Fecal Incontinence Occurs in neurologic conditions with lesions affecting the lumbar spinal cord, cauda equina, S2–S4 nerves, pudendal nerve, and pelvic floor nerves . Denervation leads to impaired perineal and rectoanal sensation, aberrant contraction, loss of tone, and weakening of the pelvic floor muscles and the EAS. These contribute to unexpected loss of stool and abnormal defecation, and diminished support for pelvic structures.

51. Parasympathetic augmentation can occur and might further complicate matters, since it contributes to weakness in the IAS and increases the risk for incontinence. It is always important to rule out overflow incontinence resulting from constipation

52. Upper Motor Neurogenic Bowel Any destructive CNS process above conus (from SCI to dementia) Most commonly seen in SCI patients Presents with difficult bowel evacuation (DWE) due to rectal sphincter dyssynergia Normal or increased anal sphincter tone

53. Intact anocutaneous & bulbocavernosus reflexes Palpable puborectalis muscle sling Normal anal verge appearance Protective vesicorectal reflex intact (EAS pressure increase in response to increased intraabdominal pressure)

54. Lower motor neurogenic bowel Polyneuropathy Conus medullaris or cauda equina lesions Pelvic surgery Vaginal delivery or Even chronic straining during defecation can impair the somatic innervation of the anal sphincter mechanism can also produce sympathetic & parasympathetic innervation deficits

55. Commonly presents with fecal incontinence Loss of protective vesicorectal reflex ( stool soilage from increased intra abdominal pressure asso : with everyday activities) Reduced anal tone Reduced or absent anocutaneous & bulbocavernosus reflexes

56. Anal canal is shortened Puborectalis muscle ridge may not be palpable Anal-to-buttock contour appear flattened & scalloped Excessive perineal descent & even rectal prolapse may occur with valsalva’s maneuver

57. THANK YOU