The transition from acute to chronic pain appears to occur in discrete pathophysiological and histopathological steps. Stimuli initiating a nociceptive response vary, but receptors and endogenous defence mechanisms in the periphery interact in a similar manner regardless of the insult. Chemical, mechanical, and thermal receptors, along with leucocytes and macrophages, determine the intensity, location, and duration of noxious events. Noxious stimuli are transduced to the dorsal horn of the spinal cord, where amino acid and peptide transmitters activate second-order neurones. Spinal neurones then transmit signals to the brain. The resultant actions by the individual involve sensory-discriminative, motivational-affective, and modulatory processes in an attempt to limit or stop the painful process. Under normal conditions, noxious stimuli diminish as healing progresses and pain sensation lessens until minimal or no pain is detected. Persistent, intense pain, however, activates secondary mechanisms both at the periphery and within the central nervous system that cause allodynia, hyperalgesia, and hyperpathia that can diminish normal functioning. These changes begin in the periphery with upregulation of cyclo-oxygenase-2 and interleukin-1β-sensitizing first-order neurones, which eventually sensitize second-order spinal neurones by activating N-methyl-d-aspartic acid channels and signalling microglia to alter neuronal cytoarchitecture. Throughout these processes, prostaglandins, endocannabinoids, ion-specific channels, and scavenger cells all play a key role in the transformation of acute to chronic pain. A better understanding of the interplay among these substances will assist in the development of agents designed to ameliorate or reverse chronic pain.

We evaluated the mortality and morbidity of acute cerebral infarction as related to modifiable factors: glucose level, temperature, hematocrit, hemoglobin and platelet count. We studied 177 patients with acute cerebral infarction in the territory of the middle cerebral artery, admitted within 24 h of stroke onset. Blood was drawn on admission and temperature was recorded every 2 h, selecting the highest during the 1st day. Patient follow-up lasted 6 months. Barthel Index and Neurological Score of patients were evaluated at admission and on days 1, 4, 7, 14, 21 and at 3 and 6 months. A Glasgow Scale was administered at 6 months. Forty-five of 177 patients died within this period. These patients reached a temperature of 38.3 ± 0.76 °C, while temperature in those surviving was 36.9 ± 0.46°C ( p < 0.001). Glucose level in surviving patients was 112.7 ± 37 and 193.3 ± 104.8 mg/dl in those who died (p < 0.001). The other parameters were similar in both groups. Using multiple linear regression, temperature was the only variable having a statistically significant influence on morbidity (p < 0.001).

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