Disorders of the nervous system can produce a variety of gastrointestinal (GI) dysfunctions. Among these, lesions in various brain structures can cause appetite loss (hypothalamus), decreased peristalsis (presumably the basal ganglia, pontine defecation center/Barrington’s nucleus), decreased abdominal strain (presumably parabrachial nucleus/Kolliker-Fuse nucleus) and hiccupping and vomiting (area postrema/dorsal vagal complex). In addition, decreased peristalsis with/without loss of bowel sensation can be caused by lesions of the spinal long tracts and the intermediolateral nucleus or of the peripheral nerves and myenteric plexus. Recently, neural diseases of inflammatory etiology, particularly those affecting the PNS, are being recognized to contribute to GI dysfunction. Here, we review neuroinflammatory diseases that potentially cause GI dysfunction. Among such CNS diseases are multiple sclerosis, neuromyelitis optica spectrum disorder, myelin oligodendrocyte glycoprotein associated disorder, and autoimmune encephalitis. Peripheral nervous system diseases impacting the gut include Guillain-Barre syndrome, chronic inflammatory demyelinating polyneuropathy, acute sensory-autonomic neuropathy/acute motor-sensory-autonomic neuropathy, acute autonomic ganglionopathy, myasthenia gravis and acute autonomic neuropathy with paraneoplastic syndrome. Finally, collagen diseases, such as Sjogren syndrome and systemic sclerosis, and celiac disease affect both CNS and PNS. These neuro-associated GI dysfunctions may predate or present concurrently with brain, spinal cord or peripheral nerve dysfunction. Such patients may visit gastroenterologists or physicians first, before the neurological diagnosis is made. Therefore, awareness of these phenomena among general practitioners and collaboration between gastroenterologists and neurologists are highly recommended in order for their early diagnosis and optimal management, as well as for systematic documentation of their presentations and treatment.
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