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| 번호 | 제목 | 등록일 | 조회수 |
|---|---|---|---|
| 58 | Rectal Wall Properties in Patients With Acute and Chronic Spinal Cord Lesions [2002년 5월 DCR] | 2011-11-17 | 3521 |
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K. Krogh, Ph.D., C. Mosdal, M.D., H. Gregersen, D.M.Sc., S. Laurberg, D.M.Sc.
From the Surgical Research Unit, Department of Surgery L, Section AAS and †Department of Neurosurgery, University Hospital of Aarhus, and Department of Surgery A, Aalborg Hospital and Centre for Sensorymotor Interaction, Institute of Electronic Systems, Aalborg University, Aalborg, Denmark
PURPOSE: Most patients with spinal cord injuries suffer from constipation or fecal incontinence. This study was designed to observe rectal wall properties and the rectoanal inhibitory reflex in patients with acute and chronic spinal cord injury.
METHODS: Rectal wall properties were studied by rectal impedance planimetry, a method for simultaneous registration of pressure and rectal cross-sectional area during distention. Twenty-five patients with spinal cord injury (14 with supraconal lesions and 11 with conal/cauda equina
lesions) were studied one to four weeks after injury, and 17 were available for follow-up after 6 to 14 months. Results were compared with 15 healthy volunteers. RESULTS: Rectal tone was significantly higher (P < 0.05) than normal in patients with acute and chronic supraconal lesions but significantly lower (P <0.05) in patients with acute and chronic conal/cauda equina lesions. The proportion of subjects with single giant rectal contractions was significantly higher than normal (33 percent) after acute supraconal spinal cord injury (77 percent; P = 0.02) but not after acute conal/cauda equina lesions (45 percent; P = 0.69). Phasic giant contractions only occurred in patients with spinal cord injury (once or more in 8 of 25 patients), but they were not
correlated with the level of the lesion. Rectal tone and the number of giant rectal contractions did not change significantly from the acute to the chronic phase of spinal cord injury. The amplitude of the rectoanal inhibitory reflex at distention pressures of 5 and 10 cm H2O was significantly lower than normal in patients with acute and chronic conal/cauda equina lesions (acute, 5 and 44 percent vs. 37 and 82 percent (P <0.05); chronic, 6 percent (P < 0.05) and 66 percent (P = NS)) but not in patients with supraconal spinal cord injury (acute, 32 and 83 percent; chronic, 61 and 85 percent (all P = NS)). CONCLUSION: Rectal tone is stimulated by the sacral spinal cord but inhibited by supraspinal centers
within the central nervous system. Likewise, rectal contractility is inhibited by supraspinal centers, and the rectoanal inhibitory reflex is stimulated by the sacral spinal cord. Alterations caused by either type of spinal cord lesion are present after one to four weeks and do not change significantly within the first year. Colorectal and anal sphincter dysfunction resulting in severe constipation and fecal incontinence
are common complications of spinal cord injury (SCI). Although the number of SCI patients is large, and approximately 30 percent of these patients consider colorectal dysfunction a greater problem than either bladder or sexual dysfunction, colorectal and anal sphincter dysfunction after SCI are only incompletely understood. In most previous studies that used balloons for pressure-volume measurement or directly infused
water into the rectum, colorectal or rectal compliance was reduced in patients with chronic supraconal SCI (lesions above the conus medullaris, which left the sacral outflow from the spinal cord intact) but was normal in patients with lesions of the conus medullaris or cauda equina.6,9 Furthermore, rectal hyperreactivity resulting in giant rectal contractions during balloon distention was found in some patients. However, the usefulness of pressure-volume measurements has been questioned. Rectal impedance
planimetry with measurement of rectal crosssectional area (CSA) is theoretically a better method for description of rectal wall properties because it avoids the errors of volume-based methods. Immediately after sustaining acute SCI, patients are in spinal shock, which significantly reduces reflex
activity below the level of the spinal cord lesion. However, the duration of the spinal shock phase affecting the colorectum is unknown, and longitudinal studies are needed to describe possible changes in anorectal function from the acute to the chronic phase of SCI. Furthermore, because approximately 40 percent of patients have incomplete spinal cord lesions, it is clinically very important to study rectal wall properties after complete as well as incomplete SCI. The rectoanal inhibitory reflex, which mediates relaxation of the internal anal sphincter during rectal
distention, is conducted through intramural nerve fibers but may be influenced by the central nervous system (CNS). However, results from studies of the ectoanal inhibitory reflex in supraconal and conal/ cauda equina lesions are conflicting. The aim of the present study was to compare rectal wall properties in acute and chronic supraconal and conal/cauda equina lesions with those of healthy volunteers by means of rectal impedance planimetry. Furthermore, the aim was to obtain additional information about the rectoanal inhibitory reflex by studying it in acute and chronic SCI. DISCUSSION
Most SCI patients in the present study had constipation and fecal incontinence. Colorectal function was most severely affected in the acute phase, and at follow-up, it had improved in most patients. Chronic SCI is known to affect colorectal motility, resulting in prolonged colonic transit times, but colorectal function in patients with acute SCI has not been studied in detail before.
The rectal tone was increased in patients with supraconal spinal cord lesions but reduced in patients with conal or cauda equina lesions.
Single giant rectal contractions occurred significantly more frequently than normal in patients with acute supraconal SCI but not in patients with acute conal/cauda equina lesions. Neither rectal tone or the
number of single giant rectal contractions changed significantly from the acute to the chronic phase of either type of lesion. Thus, rectal wall properties caused by either type of SCI were already present one to four weeks after SCI and remained essentially constant afterward. During the spinal shock phase, reflex activity is lost below the level of the lesion. The duration and extent to which the spinal shock phase affects the rectum is unknown. Denny-Brown and Graeme Robertson found that the rectal wall was completely inactive, lacking any contractile activity, in a patient who had sustained a supraconal SCI four days earlier, and Kuhn reported that clinically, the spinal shock phase affected the colorectum for two months until reflex defecation occurred. However, the present study indicates that in most patients, spinal shock affects the rectum for less than four weeks.
Most giant rectal contractions were single contractions that initially occurred during distention. This
appears to be an exaggeration of the normal small contractions initially seen on distention. The increased frequency in patients with supraconal SCI must be caused by loss of inhibitory input from supraconal centers in the CNS. This is clinically important, because most patients with supraconal SCI induce defecation by digital stimulation of the rectum, thereby probably inducing a giant rectal contraction and the rectoanal inhibitory reflex. Eight patients showed runs of giant rectal contractions, with a frequency of approximately three per
minute. Phasic giant rectal contractions were readily recognizable, but they had no correlation to the level of SCI. They began within seconds after a distention was started and lasted for the duration of the two minute distention but stopped between distensions. Therefore, they must have been induced by rectal distention and not a regularly occurring pattern superimposed on the distention curve. Clusters of giant rectal contractions and increased rectal contractility were seen in studies that used rectal manometry in patients with chronic supraconal lesions, and interestingly, they disappeared after sacral posterior rhizotomy or alcohol block of the sacral outflow for the rectosigmoid. Some evidence exists that morphine may induce spike activity in the rectal wall in healthy subjects and SCI patients. However, because only three patients in the present study took morphine, and none of these were among those who had phasic giant contractions, this cannot explain our findings. Phasic contractions with a frequency of three per minute have also been found during rectal distention
in healthy subjects, but in the present study, none of the phasic contractions in the control group were strong enough to reduce the lumen by 25 percent or more. Thus, it appears that phasic giant contractions are another sign of rectal hyperreactivity caused by loss of central inhibitory modulation. Spontaneous phasic contractions with the same frequency of three per minute have been found in healthy subjects and have been termed the rectal motor complex. Sympathetic innervation is believed to increase tone of the external anal sphincter. Accordingly, we
found that anal resting pressure was significantly lower than normal in patients with chronic supraconal lesions but not in those with conal/cauda equina lesions. The rectoanal inhibitory reflex, which mediates relaxation of the internal anal sphincter during rectal distention, is conducted through intramural nerve fibers but may be influenced by the CNS. The reflex is reduced or absent during spinal shock, but it is disputed whether it is exaggerated or not in the chronic phase of supraconal SCI. It was increased or normal in adult patients with conal or cauda equina lesions but reduced in children with spina bifida lesions of the same area. The rectoanal inhibitory reflex was present in all patients and healthy subjects in the present study (including the patients with complete conal/cauda equina lesions). This confirms that the reflex is generated within the enteric nervous system. In the chronic phase, the amplitude was significantly reduced in patients with conal or cauda equina lesions, but there was a strong trend toward a hyperreactive reflex in patients with supraconal lesions. This may indicate that the rectoanal inhibitory reflex receives excitatory input from the sacral spinal cord but inhibitory input from supraspinal centers in the CNS. |
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