• C Lim, M P Alexander, G LaFleche, D M Schnyer, and M Verfaellie.
• Behavioral Neurology Unit KS-2, Department of Neurology, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, MA 02215, USA. clim@bidmc.harvard.edu
• Neurology. 2004 Nov 23;63(10):1774-8.

BackgroundAlthough cardiac arrest (CA) is commonly cited as a cause of amnesia, patients referred to the authors' center with a diagnosis of "amnesia" after CA rarely have isolated memory deficits.ObjectiveTo determine whether CA is a cause of pure amnesia and to assess patterns of cognitive deficits after CA.MethodsThe authors used cognitive assessment of 11 consecutive patients referred for memory deficits after CA, targeted at deficit domains identified in the literature reviews, and analysis of specific case reports and prospective studies of cognition after CA.ResultsThe most common pattern of impairment in their patients was a combination of memory and motor deficits with variable executive impairment. No patient had isolated memory impairment. The case reports do not support the claim that isolated amnesia is a residual of CA; most cases of isolated amnesia are caused by subacute episodes of anoxia or excitotoxic injury. The prospective reports identify highly variable patterns of impairment, but isolated amnesia remains rare.ConclusionsDiffuse, sudden ischemic-hypoxic injury caused by cardiac arrest (CA) does not preferentially damage memory systems. Subacute or stepwise hypoxic or excitotoxic injury may cause isolated hippocampal injury and amnesia. The common pattern of impairment in the postacute phase after CA is a combination of memory, subtle motor, and variable executive deficits.

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