Article

The brain-gut Axis in abdominal pain syndromes

Center for Neurobiology of Stress, Division of Digestive Diseases, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California, USA.
Annual review of medicine (Impact Factor: 15.48). 02/2011; 62:381-96. DOI: 10.1146/annurev-med-012309-103958
Source: PubMed

ABSTRACT The importance of bidirectional brain-gut interactions in gastrointestinal (GI) illness is increasingly recognized, most prominently in the area of functional GI syndromes such as irritable bowel syndrome (IBS), functional dyspepsia, and functional chest pain. The brain receives a constant stream of interoceptive input from the GI tract, integrates this information with other interoceptive information from the body and with contextual information from the environment, and sends an integrated response back to various target cells within the GI tract. This system is optimized to assure homeostasis of the GI tract during physiological perturbations and to adapt GI function to the overall state of the organism. In health, the great majority of interoceptive information reaching the brain is not consciously perceived but serves primarily as input to autonomic reflex pathways. In patients with functional abdominal pain syndromes, conscious perception of interoceptive information from the GI tract, or recall of interoceptive memories of such input, can occur in the form of constant or recurrent discomfort or pain. This is often associated with alterations in autonomic nervous system output and with emotional changes. A model is proposed that incorporates reported peripheral and central abnormalities in patients with IBS, extrapolates similar alterations in brain-gut interactions to patients with other chronic abdominal pain syndromes, and provides novel treatment targets.

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    • "Known mechanisms of visceral pain pathogenesis include the following: (1) peripheral sensitization: inflammation, injury, or noxious stimuli in peripheral tissues cause sensitization of afferent nerve fibers; (2) central sensitization: sustained, amplified incoming noxious signals from the peripheral are transmitted through the visceral afferent fibers to activate neurons in the spinal dorsal horn; (3) noxious stimulation is transmitted to the spinal cord, leading to activation of endogenous descending facilitation, enhancing transmission of nociceptive information in the spinal dorsal horn. Signals arising from the gastrointestinal tract are transmitted into the brain through the visceral afferent pathways, which can be divided into the parasympathetic and sympathetic afferent pathways [7] [9]. The parasympathetic afferent pathways transmit incoming signals along the vagus nerve to the solitary nucleus, which then transmits the signals to various cortical limbic structures [8]. "
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    • "Known mechanisms of visceral pain pathogenesis include the following: (1) peripheral sensitization: inflammation, injury, or noxious stimuli in peripheral tissues cause sensitization of afferent nerve fibers; (2) central sensitization: sustained, amplified incoming noxious signals from the peripheral are transmitted through the visceral afferent fibers to activate neurons in the spinal dorsal horn; (3) noxious stimulation is transmitted to the spinal cord, leading to activation of endogenous descending facilitation, enhancing transmission of nociceptive information in the spinal dorsal horn. Signals arising from the gastrointestinal tract are transmitted into the brain through the visceral afferent pathways, which can be divided into the parasympathetic and sympathetic afferent pathways [7] [9]. The parasympathetic afferent pathways transmit incoming signals along the vagus nerve to the solitary nucleus, which then transmits the signals to various cortical limbic structures [8]. "
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    ABSTRACT: Irritable bowel syndrome (IBS) is a functional bowel disorder that causes recurrent abdominal (visceral) pain. Epidemiological data show that the incidence rate of IBS is as high as 25%. Most of the medications may lead to tolerance, addiction and toxic side effects. Moxibustion is an important component of traditional Chinese medicine and has been used to treat IBS-like abdominal pain for several thousand years in China. As a mild treatment, moxibustion has been widely applied in clinical treatment of visceral pain in IBS. In recent years, it has played an irreplaceable role in alternative medicine. Extensive clinical studies have demonstrated that moxibustion for treatment of visceral pain is simple, convenient, and inexpensive, and it is being accepted by an increasing number of patients. There have not been many studies investigating the analgesic mechanisms of moxibustion. Studies exploring the analgesic mechanisms have mainly focused on visceral hypersensitivity, brain-gut axis neuroendocrine system, and immune system. This paper reviews the latest developments in moxibustion use for treatment of visceral pain in IBS from these perspectives. It also evaluates potential problems in relevant studies on the mechanisms of moxibustion therapy to promote the application of moxibustion in the treatment of IBS.
    Evidence-based Complementary and Alternative Medicine 07/2014; 2014(2014). DOI:10.1155/2014/895914 · 1.88 Impact Factor
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    • "Helicobacter pylori infection, visceral hypersensitivity, gastric motility or accommodation abnormalities, acid and psychosocial factors have all been suggested to play a role in the pathogenesis of the symptoms of FD [10] [11]. Recently, dysfunction of the bidirectional brain–gut interactions has been widely accepted as a key mechanism [12] [13] [14] [15]. More specifically, brain imaging studies have found different brain activation during gastric distension in patients with FD compared with healthy controls suggesting abnormal processing of visceral stimuli at the level of the central nervous system (CNS) [16] [17] [18]. "
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    ABSTRACT: Recently, there is an increasing interest in the study of the role of brain dysfunction in the pathogenesis of symptoms of functional dyspepsia (FD). More specifically, abnormal brain activities in patients with FD during the resting state have been proven by several positron emission tomography (PET) studies. Resting-state functional magnetic resonance imaging (fMRI) is also a valuable tool in investigating spontaneous brain activity abnormalities in pathological conditions. In the present study, we examined the amplitude of low-frequency fluctuations (ALFF) and fractional (f)ALFF changes in patients with FD by using fMRI. Twenty-nine patients with FD and sixteen healthy controls participated in this study. Between-group differences in ALFF/fALFF were examined using a permutation-based nonparametric test after accounting for the gender and age effects. The results revealed a significant between-group difference in fALFF but not in ALFF in multiple brain regions including the right insula, brainstem and cerebellum. Seed-based resting-state functional connectivity analysis revealed that FD patients have increased correlations between the right cerebellum and multiple brain regions including the bilateral brainstem, bilateral cerebellum, bilateral thalamus, left para-/hippocampus, left pallidum and left putamen. Furthermore, fLAFF values in the right insula were positively correlated with the severity of the disease. These findings have provided further evidence of spontaneous brain activity abnormalities in FD patients which might contribute to our understanding of the pathophysiology of the disease.
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