|
|
||||||||
From the Behavioral Neurology Unit (Drs. Lim and Alexander), Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA; and the Memory Disorders Research Center (Drs. Lim, Alexander, LaFleche, Schnyer, and Verfaellie), Boston Department of Veterans Affairs and Boston University School of Medicine, MA.
Address correspondence and reprint requests to Dr. Chun Lim, Behavioral Neurology Unit KS-2, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, MA 02215; e-mail: clim{at}bidmc.harvard.edu
Background: Although 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.
Objective: To determine whether CA is a cause of pure amnesia and to assess patterns of cognitive deficits after CA.
Methods: The 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.
Results: The 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.
Conclusions: Diffuse, 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.
Received February 9, 2004. Accepted in final form June 22, 2004.
Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the November 23 issue to find the title link for this article.
This article has been cited by other articles:
![]() |
N. R Grubb, C. Simpson, R. A Sherwood, H. D Abraha, S. M Cobbe, R. E O'Carroll, I. Deary, and K. A A Fox Prediction of cognitive dysfunction after resuscitation from out-of-hospital cardiac arrest using serum neuron-specific enolase and protein S-100 Heart, October 1, 2007; 93(10): 1268 - 1273. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Tiainen, E. Poutiainen, T. Kovala, O. Takkunen, O. Happola, and R. O. Roine Cognitive and Neurophysiological Outcome of Cardiac Arrest Survivors Treated With Therapeutic Hypothermia Stroke, August 1, 2007; 38(8): 2303 - 2308. [Abstract] [Full Text] [PDF] |
||||
![]() |
W. Middelkamp, V. R. Moulaert, J. A Verbunt, C. M van Heugten, W. G. Bakx, and D. T. Wade Life after survival: long-term daily life functioning and quality of life of patients with hypoxic brain injury as a result of a cardiac arrest Clinical Rehabilitation, May 1, 2007; 21(5): 425 - 431. [Abstract] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |