GUT MOTILITY- In spinal cord injury
Updated: Jan 10
Bowel disturbances are commonly experienced as a secondary complication in spinal cord injury (SCI). Common complications include constipation, abdominal discomfort, abdominal distension, nausea, bowel accidents and as a result altered community engagement. These bowel disturbances create discomfort and interrupt social and family activities.
SCI has been acknowledged to impair communication via the gut-brain-axis. There have been many speculations to the causation of this (directly through neural interruptions at the gut wall and indirectly through altered gastrointestinal tract (GIT) hormone release), though a common agreement is the result. Altered motility of the GIT and therefore delayed emptying time occurs as a result of an interruption to integral messages from the brain to the gut. In cases this has been observed to lead to autonomic dysreflexia.
Lets wind it back a little and look at the importance of GIT motility. GIT motility is essential in moving the contents of our intestines. This movement is dependent on neuromuscular (nerve to muscle) communication. Communication between the GIT and the brain (gut-brain-axis) is important in maintaining neuromuscular activities.
We have already discussed the potential impairment of this path due to SCI though there are several other influences that can cause a disruption. Medications are a well-known influencer of GIT health, and in particular antibioticS. Post SCI several medications are a part of everyday life and these can impact gut function. Furthermore, recurrent infections lead to an increase in antibiotic use. Antibiotic medications have a well established impact on our ‘good’ gut bacteria though recent observations have acknowledged an impact on digestive motility. Through interaction with the enteric nervous system (ENS), the neuronal dependant motility reflexes are effected. Simply this means that AB’s interrupt the nerves present in out guts that relay messages to the brain the initiate the reflexes in guts that create movement.
Now this does not have to be the end of this discussion! There are several interventions and dietary changes that can support your gut health and healing and promote regular bowel movements.
- Pre and pro biotics: Pre and probiotics support the life living in out gut. Probiotic foods, examples: yogurt, miso, kombucha, sauerkraut, enhance the life (live bacteria) within out guts. Whilst prebiotic foods, examples: leeks, ginger, asparagus, artichokes, feed and fuel the bacteria within the gut.
- PHGG: Is a prebiotic fibre, acting as a fuel source for good bacteria in the GIT. Its ingestion has been associated with a reduction in symptoms such as abdominal pain, constipation diarrhoea, IBS and small intestinal bacterial overgrowth (SIBO).
- Fibre: Ensuring you are consuming adequate (minimum of 3 cups/day) vegetables and fruits (2 cups/day) will ensure you are not only receiving a good amount of fibre but will also increase your micro nutrient status (vitamin C, E, A, zinc, magnesium…to name a few). Fibre is essential for clearance of toxins and waste along with maintaining a heathy gut.
- Hydration: The benefits of adequate hydration, shoot for 2L/ day, goes further then being hydrated. This supports your GIT’s ability to move waste through and make easy to pass stools.
- Vagus nerve stimulation: Humming, singing and breath work all assist in toning the vagus nerve. This nerve is the key player in the connection from gut-to-brain. Its stimulation is associated with improved GIT motility.
Additionally, personalised formulations and dietary adjustments from your nutritionist can help to fast track GIT healing and bowel health.
Gondim FA, de Oliveira GR, Thomas FP. (2010). Upper gastrointestinal motility changes following spinal cord injury. Neurogastroenterol Motil. 2010 Jan;22(1):2-6. doi: 10.1111/j.1365-2982.2009.01410.x.
Delungahawatta T, Amin JY, Stanisz AM, Bienenstock J, Forsythe P, Kunze WA. (2017). Antibiotic driven changes in gut motility suggest direct modulation of enteric nervous system. Front Neurosci. doi:10.3389/fnins.2017.00588.