When pain is the predominant symptom, the condition has been termed narcotic bowel syndrome (NBS). These effects, known as opioid bowel (or gastrointestinal) dysfunction are manifest as constipation, nausea, bloating, ileus and sometimes pain ( 1– 3). It has long been recognized that opiates affect gastrointestinal motility. Treatment involves early recognition of the syndrome, an effective physician patient relationship, graded withdrawal of the narcotic according to a specified withdrawal program and the institution of medications to reduce withdrawal effects. The evidence for the enhanced pain perception is based on: a) activation of excitatory anti-analgesic pathways within a bimodal opioid regulation system, b) descending facilitation of pain at the Rostral Ventral Medulla and pain facilitation via dynorphin and CCK activation, and c) glial cell activation that produces morphine tolerance and enhances opioid induced pain. NBS can occur in patients with no prior gastrointestinal disorder who receive high dosages of narcotics after surgery or acute painful problems, among patients with functional GI disorders or other chronic gastrointestinal diseases who are managed by physicians unaware of the hyperalgesic effects of chronic opioids. This may be due in the United States to increases in using narcotics for chronic non-malignant painful disorders, and the development of maladaptive therapeutic interactions around its use. This syndrome is under recognized and may be becoming more prevalent. Narcotic bowel syndrome (NBS) is a subset of opioid bowel dysfunction that is characterized by chronic or frequently recurring abdominal pain that worsens with continued or escalating dosages of narcotics.
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