[Relationship between functional constipation and brain-gut-microbiota axis]. Chen Qiyi,Jiang Jun Zhonghua wei chang wai ke za zhi = Chinese journal of gastrointestinal surgery Although with the higher prevalence, the overall treatment result of functional constipation is still not satisfied at home and abroad. The diagnosis and treatment of functional constipation are still to focus on colon itself. Functional constipation has complex interactions among intestinal flora, intestinal autonomic nerve and central nervous system. Patients with functional constipation have different degrees of mental and psychological dysfunction, and abnormal brain function can result in disorders of colon dynamics, secretion and immune function. At the same time, there is a significant imbalance of intestinal flora in patients with functional constipation. Intestinal flora plays an important role in the release of neurotransmitter and the activity of hypothalamic-pituitary-adrenal axis (HPA axis). Intestinal flora is an important regulator of development, maturity and activity of central nervous system. Therefore, the interaction in the brain-gut-microbiota axis may provide a broader strategy for the diagnosis and treatment of functional constipation and neuropsychiatric disorder.

Mechanisms controlling normal defecation and the potential effects of spinal cord injury. Brading A F,Ramalingam T Progress in brain research Spinal cord injury frequently leads to bowel dysfunction with the result that emptying the bowel can occupy a significant part of the day and reduce the quality of life. This chapter contains an overview of the function and morphology of the normal distal gut in the human, and of gut behaviour in normal defecation. In humans, this can be monitored and is described, but knowledge of the mechanisms controlling it is limited. Work on animals has shown that the intrinsic activity of the smooth muscles and their interactions with the enteric nervous system can program the activity that is necessary to expel waste material, but the external anal sphincter is controlled through somatic nerves. The gut however also receives input from the central nervous system through autonomic nerves, and a spinal reflex centre exists. Voluntary effort to induce defecation can influence all the control mechanisms, but the precise importance of each is not understood. The behaviour and properties of the individual muscles in the normal human rectum and anal canal are described, including their responses to intrinsic nerve stimulation and adrenergic and cholinergic agonists. The effects of established spinal cord injury are then considered. For convenience, supraconal and conal/cauda equina lesions are considered as two categories. Prolongation of transit times and disordered defecation are common problems. Supraconal lesions result in reduced resting anal pressures and increased risk of fecal incontinence. The acute effects of spinal cord injury are described, with injury causing ileus (prolonged total gastrointestinal transit times), constipation (prolonged colonic transit times) and fecal incontinence (passive leakage). 10.1016/S0079-6123(05)52023-5

Neurophysiology of the brain stem in Parkinson's disease. Bove Cecilia,Travagli R Alberto Journal of neurophysiology Parkinson's disease (PD) is predominantly idiopathic in origin, and a large body of evidence indicates that gastrointestinal (GI) dysfunctions are a significant comorbid clinical feature; these dysfunctions include dysphagia, nausea, delayed gastric emptying, and severe constipation, all of which occur commonly before the onset of the well-known motor symptoms of PD. Based on a distinct distribution pattern of Lewy bodies (LB) in the enteric nervous system (ENS) and in the preganglionic neurons of the dorsal motor nucleus of the vagus (DMV), and together with the early onset of GI symptoms, it was suggested that idiopathic PD begins in the ENS and spreads to the central nervous system (CNS), reaching the DMV and the substantia nigra pars compacta (SNpc). These two areas are connected by a recently discovered monosynaptic nigro-vagal pathway, which is dysfunctional in rodent models of PD. An alternative hypothesis downplays the role of LB transport through the vagus nerve and proposes that PD pathology is governed by regional or cell-restricted factors as the leading cause of nigral neuronal degeneration. The purpose of this brief review is to summarize the neuronal electrophysiological findings in the SNpc and DMV in PD. 10.1152/jn.00056.2019