Background Irritable bowel syndrome and other gastrointestinal (GI) and non-GI disorders such as functional dyspepsia, fibromyalgia, temporomandibular joint disorder, interstitial cystitis/painful bladder syndrome, and chronic fatigue syndrome are known as functional pain syndromes. They commonly coexist within the same individual. The pathophysiologic mechanisms of these disorders are not well understood, but it has been hypothesized that they share a common pathogenesis. Purpose The objective of this review is to discuss the proposed pathophysiologic mechanisms, which have been similarly studied in these conditions. These mechanisms include enhanced pain perception, altered regional brain activation, infectious etiologies, dysregulations in immune and neuroendocrine function, and genetic susceptibility. Studies suggest that these functional disorders are multifactorial, but factors which increase the vulnerability of developing these conditions are shared.

To determine the frequency and aetiology of acute symptomatic seizures in central nervous system (CNS) infections and to assess the clinical factors predicting the occurrence of the seizures, we retrospectively reviewed the medical records of patients diagnosed with CNS infections from 2000 to 2005. One hundred and forty-seven patients were included in the study. The clinical variables between those with and without acute symptomatic seizures were compared. Of the 147 patients, 23% (34/147) had acute symptomatic seizures. A significant relation between clinical variables and the occurrence of acute symptomatic seizures was found: encephalitis as the aetiology of the CNS infection, Glasgow Coma Scale (GCS) < or =12, and neurological deficits. By multiple logistic regression analysis, age of onset >42 years, encephalitis, and GCS < or =12 were found to be independently significant clinical variables for predicting the occurrence of acute symptomatic seizures. Encephalitis and GCS < or =12 are significant clinical variables for predicting the occurrence of acute symptomatic seizures in CNS infection, suggesting that patients with a greater extent of parenchymal damage are more vulnerable to acute symptomatic seizures.