College of Psychology: Faculty Proceedings, Presentations, Speeches and Lectures

Title

Recovery from Hypoxic Encephalopathy Due to Wolff Parkinson White Syndrome

Event Location / Date(s)

Vancouver, British Columbia, Canada / October 13-16, 2010

Document Type

Conference Proceeding

Presentation Date

10-13-2010

Conference Name / Publication Title

30th Annual Meeting of the National Academy of Neuropsychology

Description

Abstract

Objectives: Wolff Parkinson White Syndrome (WPW) is a rare congenital disorder that causes arrhythmia and sudden cardiac arrest (CA). This case demonstrates hypoxic encephalopathy due to CA with good subsequent cognitive recovery. The patient was a 30-year-old woman with a Bachelor's degree that had CA due to WPW with 6–12 min of hypoxia, tonic-clonic seizures, and 3 days of coma. MRI was unremarkable but EEG showed diffuse slowing consistent with metabolic encephalopathy and spiking indicative of right hemisphere seizure activity

Method: Neuropsychological examinations of intellectual, memory, executive, language, and personality functioning were conducted at 1 month and at 8 years after CA. Results: Intelligence (Wechsler Adult Intelligence Scale-Third Edition [WAIS-III] IQ = 89, Wechsler Adult Intelligence Scale-Fourth Edition [WAIS-IV] IQ = 96) and Working Memory (99, 100) were relatively intact over time and consistent with premorbid estimates (Wide Range Achievement Test-Third Edition [WRAT-3] Reading = 105, Wide Range Achievement Test-Fourth Edition [WRAT-4] = 103, WAIS Vocabulary = 9, 10). Memory (Wechsler Memory Scale-Third Edition; WMS-III General Memory = 69, Immediate = 72), Processing Speed (76), executive (Trails B < 55, Wisconsin Card Sorting Test; [WCST] perseverations = 90), and language functioning (FAS = 60) were impaired 1 month after CA. Memory (Wechsler Memory Scale-Fourth Edition [WMS-IV] Delayed Memory = 82, Immediate = 83), Processing Speed (84), executive (Trails = 85, WCST perseverations = 97), and language (FAS = 85) functioning improved significantly at follow-up.

Conclusion: Anoxic encephalopathy after CA produces characteristic marked impairment of memory, executive function, and processing speed that can be seen at the post-acute stage of recovery and typically has a poor prognosis. However, good recovery of cognitive functions appears to occur in some cases. Prognosis may be mediated by age, gender, and cerebral reserve. Working memory and intelligence are relatively resistant to hypoxic encephalopathy, and reading vocabulary appears to provide a reasonable estimate of premorbid ability that remains stable during recovery.

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