Chronic abdominal pain accompanying intestinal inflammation emerges from the hyperresponsiveness of neuronal,immune and endocrine signaling pathways within the intestines,the peripheral and the central nervous system....Chronic abdominal pain accompanying intestinal inflammation emerges from the hyperresponsiveness of neuronal,immune and endocrine signaling pathways within the intestines,the peripheral and the central nervous system.In this article we review how the sensory nerve information from the healthy and the hypersensitive bowel is encoded and conveyed to the brain.The gut milieu is continuously monitored by intrinsic enteric afferents,and an extrinsic nervous network comprising vagal,pelvic and splanchnic afferents.The extrinsic afferents convey gut stimuli to second order neurons within the superficial spinal cord layers.These neurons cross the white commissure and ascend in the anterolateral quadrant and in the ipsilateral dorsal column of the dorsal horn to higher brain centers,mostly subserving regulatory functions.Within the supraspinal regions and the brainstem,pathways descend to modulate the sensory input.Because of this multiple level control,only a small proportion of gut signals actually reaches the level of consciousness to induce sensation or pain.In inflammatory bowel disease(IBD)and irritable bowel syndrome(IBS)patients,however,long-term neuroplastic changes have occurred in the brain-gut axis which results in chronic abdominal pain.This sensitization may be driven on the one hand by peripheral mechanisms within the intestinal wall which encompasses an interplay between immunocytes,enterochromaffin cells,resident macrophages,neurons and smooth muscles.On the other hand,neuronal synaptic changes along with increased neurotransmitter release in the spinal cord and brain leads to a state of central wind-up.Also life factors such as but not limited to inflammation and stress contribute to hypersensitivity.All together,the degree to which each of these mechanisms contribute to hypersensitivity in IBD and IBS might be diseaseand even patient-dependent.Mapping of sensitization throughout animal and human studies may significantly improve our understanding of sensitization in IBD and IBS.On the long run,this knowledge can be put forward in potential therapeutic targets for abdominal pain in these conditions.展开更多
Background:The 11th revision of the International Classification of Diseases and Related Health Problems(ICD-11)was released on June 18,2018,by the World Health Organization and will come into effect on January 1,2022...Background:The 11th revision of the International Classification of Diseases and Related Health Problems(ICD-11)was released on June 18,2018,by the World Health Organization and will come into effect on January 1,2022.Apart from the chapters on the classification of diseases in the conventional medicine(CM),a new chapter,traditional medicine(TM)conditions–Module 1,was added.Low back pain(LBP)is one of the common reasons for the physician visits.The classification codes for LBP in the ICD-11 are vital to documenting accurate clinical diagnoses.Methods:The qualitative case study method was adopted.The secondary use data for 100 patients were randomly selected using the ICD-11 online interface to find the classification codes for both the CM section and the TM Conditions–Module 1(TM1)section for LBP diagnosis.Results:Of the 27 codes obtained from the CM section,six codes were not relevant to LBP,whereas the other 21 codes represented diagnoses of LBP and its related diseases or syndromes.In the TM1 section,six codes for different patterns and disorders represented the diagnoses for LBP from the TM perspective.Conclusion:This study indicates that specific diagnoses of LBP can be represented by the combination of CM classification codes and TM1 classification codes in the ICD-11;the CM codes represent specific and accurate clinical diagnoses for LBP,whereas the TM1 codes add more accuracy to the diagnoses of different patterns from the TM perspective.展开更多
文摘Chronic abdominal pain accompanying intestinal inflammation emerges from the hyperresponsiveness of neuronal,immune and endocrine signaling pathways within the intestines,the peripheral and the central nervous system.In this article we review how the sensory nerve information from the healthy and the hypersensitive bowel is encoded and conveyed to the brain.The gut milieu is continuously monitored by intrinsic enteric afferents,and an extrinsic nervous network comprising vagal,pelvic and splanchnic afferents.The extrinsic afferents convey gut stimuli to second order neurons within the superficial spinal cord layers.These neurons cross the white commissure and ascend in the anterolateral quadrant and in the ipsilateral dorsal column of the dorsal horn to higher brain centers,mostly subserving regulatory functions.Within the supraspinal regions and the brainstem,pathways descend to modulate the sensory input.Because of this multiple level control,only a small proportion of gut signals actually reaches the level of consciousness to induce sensation or pain.In inflammatory bowel disease(IBD)and irritable bowel syndrome(IBS)patients,however,long-term neuroplastic changes have occurred in the brain-gut axis which results in chronic abdominal pain.This sensitization may be driven on the one hand by peripheral mechanisms within the intestinal wall which encompasses an interplay between immunocytes,enterochromaffin cells,resident macrophages,neurons and smooth muscles.On the other hand,neuronal synaptic changes along with increased neurotransmitter release in the spinal cord and brain leads to a state of central wind-up.Also life factors such as but not limited to inflammation and stress contribute to hypersensitivity.All together,the degree to which each of these mechanisms contribute to hypersensitivity in IBD and IBS might be diseaseand even patient-dependent.Mapping of sensitization throughout animal and human studies may significantly improve our understanding of sensitization in IBD and IBS.On the long run,this knowledge can be put forward in potential therapeutic targets for abdominal pain in these conditions.
文摘Background:The 11th revision of the International Classification of Diseases and Related Health Problems(ICD-11)was released on June 18,2018,by the World Health Organization and will come into effect on January 1,2022.Apart from the chapters on the classification of diseases in the conventional medicine(CM),a new chapter,traditional medicine(TM)conditions–Module 1,was added.Low back pain(LBP)is one of the common reasons for the physician visits.The classification codes for LBP in the ICD-11 are vital to documenting accurate clinical diagnoses.Methods:The qualitative case study method was adopted.The secondary use data for 100 patients were randomly selected using the ICD-11 online interface to find the classification codes for both the CM section and the TM Conditions–Module 1(TM1)section for LBP diagnosis.Results:Of the 27 codes obtained from the CM section,six codes were not relevant to LBP,whereas the other 21 codes represented diagnoses of LBP and its related diseases or syndromes.In the TM1 section,six codes for different patterns and disorders represented the diagnoses for LBP from the TM perspective.Conclusion:This study indicates that specific diagnoses of LBP can be represented by the combination of CM classification codes and TM1 classification codes in the ICD-11;the CM codes represent specific and accurate clinical diagnoses for LBP,whereas the TM1 codes add more accuracy to the diagnoses of different patterns from the TM perspective.
