Cellular and Molecular Mechanisms of Ischemic Tolerance
It has been estimated that 20-40% of the patient population diagnosed with stroke have experienced a brief episode of antecedent transient ischemic attack (TIA). This brain malady has been described clinically as an ischemia-related event which produces a neurologic deficit without obvious structural damage.1,2 At present, very limited information is available concerning the etiology of TIA and its subsequent correlation as a risk factor for stroke. Some studies indicate that prior exposure to TIA increases the likelihood of sustaining a full-blown ischemic attack by 7-13-
fold. The controversial nature of existing reports has contributed significantly to the lack of consensus regarding the potential outcome for patients who sustain TIA before stroke onset, and those who do not.3-6 In terms of postepisode neurological status, TIA prior to stroke has been documented to be beneficial, while in other instances it has been reported to result in no demonstrable difference, or a worsened condition. Apparently, the number, severity, and time-course between TIAs each play a role in influencing the overall degree of impairment. However, the wide range of effects observed in epidemiological studies may also be attributed to other unknown variables.