Perioperative cerebral damage can result in various clinical sequela ranging from minor neurocognitive deficits to catastrophic
neurological morbidity with permanent impairment and death. The goal of neuroprotective treatments is to reduce the clinical effects of
cerebral damage through two major mechanisms: increased tolerance of neurological tissue to ischemia and changes in intra-cellular responses
to energy supply deprivation. In this review, we present the clinical evidence of intravenous anesthetics on perioperative neuroprotection,
and we also provide a critical perspective for future studies. The neuroprotective efficacy of the intravenous anesthetics thiopental,
propofol and etomidate is unproven. Lidocaine may be neuroprotective in non-diabetic patients who have undergoing cardiac surgery
with cardiopulmonary bypass (CBP) or with a 48-hour infusion, but conclusive data are lacking. There are several limitations of
clinical studies that evaluate postoperative cognitive dysfunction (POCD), including difficulties in identifying patients at high-risk and a
lack of consensus for defining the “gold-standard” neuropsychological testing. Although a battery of neurocognitive tests remains the
primary method for diagnosing POCD, recent evidence suggests a role for novel biomarkers and neuroimaging to preemptively identify
patients more susceptible to cognitive decline in the perioperative period. Current evidence, while inconclusive, suggest that intravenous
anesthetics may be both neuroprotective and neurotoxic in the perioperative period. A critical analysis on data recorded from randomized
control trials (RCTs) is essential in identifying patients who may benefit or be harmed by a particular anesthetic. RCTs will also contribute
to defining methodologies for future studies on the neuroprotective effects of intravenous anesthetics.
Keywords: Neuroprotection, intravenous anesthetic, neurotoxicity, neuropsychological testing.
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