The transient increase in sICAM-1 and TNF-alpha found in the internal jugular blood of MWoA patients assessed ictally can be induced by sensory neuropeptides released from activated trigeminal endings. The progressive decrease in sICAM-1 levels during attacks and the down-regulation of LFA-1 expression by lymphocytes could antagonize their transvascular migration, supporting the hypothesis of sterile inflammation in the dura mater during migraine attacks.

This article discusses different aspects concerning classification/nomenclature, biochemical properties and pathophysiological roles of reactive oxygen species (ROS) which are pivotal to interpret the concept of oxidative stress. In vitro studies in both the prokaryotes and eukaryotes clearly demonstrate that exogenous or constitutive and inducible endogenous sources of ROS together with cofactors such as transition metals can damage virtually all the biomolecules. This adverse chemistry is at the origin of structural and metabolic defects that ultimately may lead to cell dysfunction and death as underlying mechanisms in tissue degeneration processes. The same biomolecular interpretation of aging has been proposed to embodies an oxidative stress-based process and oxidative stress may virtually accompany all the inflammatory events. As a consequence, ROS have proposed to play several roles in the pathogenesis of chronic-degenerative conditions, such as athero-thrombotic events, neurodegeneration, cancer, some forms of anemia, auto-immune diseases, and the entire comorbidity of uremia and diabetes. Nowadays, the chance to investigate biochemical and toxicological aspects of ROS with advanced biomolecular tools has, if needed, still more emphasized the interest on this area of biomedicine. These technological advancements and the huge information available in literature represent in our time a challenge to further understand the clinical meaning of oxidative stress and to develop specific therapeutic strategies.

Summary The levels of some pro‐ and anti‐inflammatory cytokines [interleukin (IL)‐1β, tumor necrosis factor (TNF)‐α, IL‐6, IL‐10, and transforming growth factor (TGF)‐β], were measured by enzyme‐linked immunosorbent assay (ELISA) method in the plasma of patients affected by obstructive sleep apnea syndrome (OSAS) at 22:00 hours before polysomnographic recording and immediately after the first obstructive apnea causing an SaO2 below 85%. Significantly higher levels of TNF‐α were found in OSAS patients assessed before polysomnography compared with the control group (P < 0.01). A slight but significant increase in the plasma levels of IL‐6 was also present (P < 0.05). Conversely, a significant decrease in the plasma levels of IL‐10 was evident at baseline in OSAS patients (P < 0.04). No significant difference emerged between the mean values of IL‐1α and TGF‐β between OSAS patients and controls. The present data support a prevailing activation of the Th1‐type cytokine pattern in OSAS patients, which is not associated with the severity and duration of OSAS. This can have important consequences for the outcome of OSAS patients, especially with regard to the increased risk for developing atherosclerosis and cardiovascular and cerebrovascular diseases. Immediately after the first obstructive apnea causing an SaO2 <85%, a significant variation was observed in the plasma levels of TNF‐α in OSAS patients compared with those measured before the beginning of polysomnographic recording (P < 0.001). The role played by this further increase in TNF‐α levels after the obstructive apnea in OSAS patients remains to be established in the light of the pathogenic mechanisms of this sleep disorder.

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Neurotoxic events occur in MS patients, and they can be responsible for oligodendrocyte and neuronal cell death in patients with this demyelinating disease. The manipulation of glutamate-altered homeostasis or antagonizing glutamate receptor-mediated excitotoxicity may have therapeutic implications in MS patients.