Neurogenic Bowel Dysfunction in subjects with Brain Injury: Prevalence, Risk Factors, Clinical Characterization and Physiopathology.
Bowel dysfunction (BD) or neurogenic bowel as is used generally in the neurology field refers to clinical manifestations that include fecal incontinence, impaired spontaneous rectal evacuation, and slow colonic transit or colonic inertia . Data from studies in patients with sacral cord injury show that BD is a highly prevalent problem and rated by patients as one of their worst sequels. However, there are scarce data on BD after brain injury (BI). Only the occurrence of fecal incontinence (FI) right or shortly after BI has received some attention and it has been deemed mainly due to the impact of brain damage on patient mobility and cognitive functions. However, data on this issue are scarce and other precipitating factors of FI, such as the presence of diarrhea or liquid stools have not been taken into account before. Moreover, predictive factors of post-BI development of other BD such as constipation or abdominal pain or distensiom have not been previously evaluated. The incidence figures and impact on quality of life of these gut dysfunctions in BI patients are also unknown.
There are no data on the potential mechanisms underlying altered bowel functions in patients with BI.
In this thesis we present 2 studies: In study 1 we aimed to evaluate the prevalence, clinical characteristics, impact on QOL and risk factors of long-term clinically significant BD in patients that have experienced acute brain injury and are stabilized.
Our data show that around 50% of patients report some form of clinically significant BD more than two years after their acute neural injury. The most frequent bowel complaints are those related to bowel emptying. Abdominal pain and distention were also reported by a significant number of patients as well as FI.
Our estimation of long-term FI after BI is significantly greater than previously reported in these patients one year after injury Relating to clinical traits of neurogenic bowel dysfunction, our data show that BI patients who develop constipation after injury mostly show clinical features of dissynergic defecation.
Regarding FI development after the initial phase of injury taking into account the presence of diarrhea, site of BI seem to have a significant influence on the likelihood of presenting FI on the long-term.
Interestingly, we observed patients with basal ganglia and posterior brain territory affected (vs. anterior territory affected) were more likely to report FI.
We have also observed that patients with posterior brain areas affected, excluding basal ganglia are more likely to present FI compared to those with anterior circulation involved, who are more likely to report constipation.
In the study 2 we report on clinical manifestations and GI motor physiology parameters of patients that developed bowel dysfunction after BI and maintained it at the moment of the study, after at least 2 years from the brain event. We compared them to a sample of patients, who had not suffered any brain injury and were free of any other relevant neurological disease or impairment. Thus, we aimed to compare clinical features and physiological measurements of BD in BI and control patients. One of the main study findings is that patients who develop constipation after BI have few differentiated clinical characteristics compared to constipated controls. As our data suggest, BI patients show increased odds for presenting fewer bowel movements per week, and decreased odds for reporting abdominal pain associated to their constipation and feeling of incomplete evacuation.
The HR anorectal manometry performed in these patients showed that BI patients with constipation needed higher rectal volumes to trigger the RAI reflex compared to constipated controls.
The WMC studies revealed that BI patients with constipation had higher odds of presenting delayed motor activity affecting the stomach, the small bowel compared to constipated controls.
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