Hypothermia and Ischemic Stroke

The use of tissue plasminogen activator (tPA) is the major treatment method for acute ischemic stroke, but it reaches only a very limited number of stroke patients. Although neuroprotectants may be useful in stroke patients in principle, promising animal data have not yet been successfully transferred to stroke patients. However, many arguments favor the successful translation of therapeutic hypothermia (TH) to stroke patients: it is a multimodal method, there is a strong correlation between fever and outcome in stroke patients, and TH has been shown to be beneficial in other kinds of acute brain injury (resuscitation, perinatal asphyxia). In addition, it is useful in controlling intracranial pressure caused by brain edema. So far, available data from clinical studies are not sufficient to recommend TH for the routine treatment of acute ischemic stroke. The quality of trials and the number of stroke patients treated by TH are far too low to prove efficacy or futility, but multicenter randomized controlled clinical trials are on their way. Studies in awake stroke patients will use TH very early in the clinical setting, which implies certain problems. The use of TH in awake individuals requires methods to suppress cold-induced vegetative responses such as shivering and sympathic activation, clinically relevant side effects that need to be monitored and treated carefully. In mass-occupying ischemic stroke, randomized trials will evaluate the neuroprotective effects of controlling edema and intracranial pressure. Because the optimal depth, duration, and methods of cooling are not clear, only large randomized controlled trials will set the baseline from which TH as a neuroprotective therapy can be optimized and brought successfully to stroke patients.