Irritable bowel syndrome or IBS is a functional pain disorder afflicting nearly
12% of the population. It is characterized by chronic abdominal pain associated with
altered bowel habits with no specific evidence of identifiable organic disease. Sufferers often
experience elevated anxiety and may not respond to traditional pain medications or treatments.
Recent research using brain imaging technology has begun to shed light on this troubling pain
disorder transforming our current understanding of IBS. Normal GI function depends on integration of
intestinal motor, sensory, autonomic and central nervous system activity interacting with the
brain via bi-directional circuits collectively termed the brain gut axis. Via these pathways,
the brain processes visceral information to create sensations including emotional and cognitive
perceptions and triggers analgesic pathways capable of modulating ascending nociceptor input.
Upon gut distension, spinal afferents originating in all layers of the gut
wall carry sensory input to the central nervous system. Nociceptive
input that evokes pain sensation travels along multiple pathways to the brain.
Upon arrival at the thalamus, signals are routed to the somatosensory and
cingulate cortices as well as the insula prefrontal cortex and hypothalamus.
In the somatosensory cortex pain sensation is localized. Meanwhile the cingulate prefrontal and
insular cortices contribute to pain perception, intensity, emotional experience and coping.
The hypothalamus, an area responsible for stress
responses and the initiator of the HPA axis is also activated during
pain sensation via its connections with the cingulate and prefrontal cortices.
The signal cascade eventually triggers a fundamental pain control system.
Descending influences from the periaqueductal gray in the midbrain to the dorsolateral ponds
and rostral ventral medial medulla modulate nociceptive transmission at the spinal level.
Functional MRI of IBS sufferers shows decreased cortical activation in both the cingulate cortex
and the insula during painful gut stimulation. Subsequent structural MRI shows significant
cortical thinning in the cingulate cortex insula and prefrontal cortex of IBS patients.
It is clear that in IBS the brain gut axis is altered. But thinned under activated cortex is not
the only abnormality seen. Further analysis shows that the hypothalamus in IBS patients is enlarged.
When considered together, these findings may help
explain the experience of sustained abdominal pain and anxiety in IBS.
Inadequate stimulation of upstream cortical centers
may result in inadequate stimulation of the brain stems pain control system.
And hyperactivity in the hypothalamus may contribute to IBS associated stress and anxiety.
But in light of these discoveries, researchers face new questions. This cortical thinning;
a result of glia, astrocytes, neurons or even dendritic spines disappearing or shrinking
or perhaps there is a reduced synaptic density.
Is the opposite true in areas that show increased gray matter like the hypothalamus.
Do abnormalities in the brain predispose individuals to chronic pain or are
functional and structural deficits a product of chronic pain conditions.
Further exploration of the brain gut axis will illuminate these issues potentially
providing insights into developing effective pain management programs for sufferers of IBS.