Abrupt deprivation of substrates to neuronal tissue triggers a number of pathological events (the “ischemic
cascade”) that lead to cell death. As this is a process of delayed neuronal cell death and not an instantaneous event, several
pharmacological and non-pharmacological strategies have been developed to attenuate or block this cascade. The most
promising neuroprotectant so far is therapeutic hypothermia and its beneficial effects have inspired researchers to further
improve its protective benefit by combining it with other neuroprotective agents. This review provides an overview of all
neuroprotective strategies that have been combined with therapeutic hypothermia in rodent models of focal cerebral
ischemia. A distinction is made between drugs interrupting only one event of the ischemic cascade from those mitigating
different pathways and having multimodal effects. Also the combination of therapeutic hypothermia with
hemicraniectomy, gene therapy and protein therapy is briefly discussed. Furthermore, those combinations that have been
studied in a clinical setting are also reviewed.
Keywords: Acute ischemic stroke, clinical, combination therapy, experimental, human, hypothermia, neuroprotection, rodent.
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