Neurogenic Bowel, Disordered Glycemic Control and Chronic Spinal Cord Injury: A Preliminary Investigation

Special Article – Spinal Cord Injury Rehabilitation

Phys Med Rehabil Int. 2017; 4(2): 1113.

Neurogenic Bowel, Disordered Glycemic Control and Chronic Spinal Cord Injury: A Preliminary Investigation

Stillman M¹*, Graves D¹, Lenneman C² and Williams S¹

¹Department of Rehabilitation Medicine, Sidney Kimmel Medical College of Thomas Jefferson University, USA

²Department of Internal Medicine, University of Louisville School of Medicine, USA

*Corresponding author: Stillman M, Departments of Internal Medicine and Rehabilitation Medicine, Sidney Kimmel Medical College of Thomas Jefferson University, 1100 Walnut Street, Suite 601, Philadelphia, PA 19107, USA

Received: March 20, 2017; Accepted: April 13, 2017; Published: April 20, 2017


Objective/Background: To evaluate potential links between neurogenic bowel and disordered glycemic control in individuals with chronic spinal cord injury (SCI).

Design: Administration of a validated neurogenic bowel questionnaire to participants with SCI, followed by oral glucose tolerance testing (OGTT) and Hemoglobin A1c (HbA1c) assessment in injured subjects and non-injured controls.

Methods: Assessment of severity of neurogenic bowel, HbA1c, and performance on OGTT in individuals with SCI (n=19) and non-injured controls (n=10).

Outcome Measures: Correlation between classification of severity of neurogenic bowel, HbA1c levels, and serum glucose and insulin values during a 4-part OGTT.

Results or Findings: Subjects with SCI had significantly higher insulin levels at 30 minutes and insulin and glucose levels at 60 and 120 minutes than non-injured controls. Average HbA1c levels were no different between the groups (5.52 vs 5.56).Individuals with severe neurogenic bowel had nonsignificant elevations in insulin levels at 30, 60, and 120 minutes and in glucose levels at 120 minutes when compared with those with moderate, mild, or very mild neurogenic bowel.

Conclusion: While not reaching statistical significance, these results may indicate a link between the altered bowel function and post-prandial hyperglycemia of chronic SCI and indicate a need for further study.

Keywords: Spinal Cord Injury; Hyperglycemia; Neurogenic Bowel


SCI: Spinal Cord Injury; DM: Diabetes Mellitus; IGT: Impaired Glucose Tolerance; OGTT: Oral Glucose Tolerance Test; HbA1c: Hemoglobin A1c


Several authors have investigated the prevalence of disordered glycemic control in chronic spinal cord injury (SCI). Duckworth et al found diabetes mellitus (DM) in over half of veterans with SCI undergoing oral glucose tolerance tests (OGTT) [1], Bauman and Spungen described either frank DM or impaired glucose tolerance (IGT) in 56 percent of subjects with SCI [2], and Elder et al conducted OGTT on 12 individuals with injuries, reporting an average 2 hour glucose level of 142, within the range of IGT [3].

Various etiologies of hyperglycemia in SCI have been posited, but have all assumed a causative link to altered skeletal muscle. Duckworth and Elder offered a potential connection between DM and replacement of skeletal muscle with adipose tissue, while Bauman theorized that the post-prandial hyperglycemia of SCI could be related to structural changes in denervated muscle. While these ideas are partly supported by experimental findings, none has been proven, and other potential explanations remain unexplored.

Several authors have demonstrated complicated relationships between upper gastrointestinal motility and glucose regulation. Specifically, rapid gastric emptying seems to be associated with elevated post-prandial serum glucose levels, and suppression of duodenal flow events attenuates small bowel glucose absorption and post-prandial hyperglycemia [4,5]. While no authors to our knowledge have evaluated objective physiologic measures of gut motility and function in SCI, we hypothesized that the “hyper-reflexic” high-tone bowel that often accompanies upper motor neuron injuries [6] may also alter glucose uptake from the bowel.

In this article, we report preliminary data evaluating the effects of severity of neurogenic bowel on disordered glucose metabolism in individuals with chronic SCI. We sought to demonstrate that severity of neurogenic bowel would positively correlate with serum glucose and insulin levels on OGTT, hoping to then explore potential explanatory mechanisms.

Materials and Methods

Data were collected from 19 adults with SCI and 10 without, all of whom responded to informational brochures distributed through an outpatient rehabilitation facility in Louisville, KY. As this work represents a subset analysis of a study investigating fecal bacterial patterns and systemic inflammatory markers in individuals with SCI, inclusion criteria were relatively broad but exclusion criteria were quite specific. Those eligible had to have sustained an injury over 1 year prior to enrollment (for those with SCI) and were between the ages of 18 and 75. Exclusion criteria included: i) being pregnant or lactating; ii) taking probiotics, prebiotics, or non-topical steroid medications; iii) smoking; iv) having been diagnosed with or treated for DM; v) having taken systemic antibiotics or investigational drugs within one month of enrollment; vi) having a significant acute or chronic infection; vii) active psychosis or substance abuse; viii) having had a myocardial infarction or coronary artery bypass grafting within the previous 6 months; and ix) having known severe cardiopulmonary, hepatic, renal, or cerebrovascular disease.

Once screened and consented, participants were administered Krough et al’s validated neurogenic bowel questionnaire [7] by which individuals may be assigned designations of “very minor” (score 0-6), “minor” (score 7-9), “moderate” (score of 10-13), or “severe” (score of 14 or higher) bowel dysfunction. They were then assigned scores and severity classifications and underwent 2 hour OGTTs (fasting samples followed by collections at 30, 60, and 120 minutes) and testing for hemoglobin A1c (HbA1c). All study procedures were approved by the University of Louisville Institutional Review Board.

Data for the glucose and insulin levels were analyzed using repeated measures general linear models (GLM) using an alpha level of .05 for all analyses. Demographic and classification data were analyzed using independent groups t-test and Pearson correlation coefficient.


Among 19 participants with SCI, 37% (n=7) were female, average age was 50.9 years (range 25-70), average duration of injury was 11.37 years (range 1-45), and average bowel score was 11.84 (range 2-19). Ten of the 19 (52.6%) had tetraplegia, and 14 (73.7%) had motor complete (AIS A or B) injuries. Among the 10 non-injured controls, half were female and average age was 43.3 years.

During OGTT, mean glucose and insulin levels were significantly higher among subjects with SCI than those without (Table 1), though HbA1clevels in the two groups were nearly identical (5.52 for those with SCI vs 5.56 for controls). There were no significant differences in HbA1c, glucose, or insulin levels between subjects with complete or incomplete injuries or between those with paraplegia or tetraplegia (Table 2). Additionally, there were no significant differences between the bowel scores of those with motor complete and motor incomplete injuries (X2=16.42, df=12, p=.173) or tetraplegia versus paraplegia (X2=14.22, df=12, p=.281). Four participants with SCI had 120 minute glucose levels between 140 and 200 (criteria for IGT), while 1 had a level over 200 (criteria for DM).