Hippocampal volume loss following childhood convulsive status epilepticus is not limited to prolonged febrile seizures

Authors

  • Michael Yoong,

    Corresponding author
    1. Neurosciences Unit, UCL Institute of Child Health, London, United Kingdom
    2. Imaging and Biophysics Unit, UCL Institute of Child Health, London, United Kingdom
    3. Young Epilepsy, Lingfield, Surrey, United Kingdom
    • Address correspondence to Michael Yoong, Child Life and Health, 20 Sylvain Place, Edinburgh EH9 1UW, U.K. E-mail: michael.yoong@ed.ac.uk

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  • Marina M. Martinos,

    1. Developmental Cognitive Neurosciences Unit, UCL Institute of Child Health, London, United Kingdom
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  • Richard F. Chin,

    1. Neurosciences Unit, UCL Institute of Child Health, London, United Kingdom
    2. Edinburgh Neurosciences, Muir Maxwell Epilepsy Centre, The University of Edinburgh, Edinburgh, United Kingdom
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  • Christopher A. Clark,

    1. Imaging and Biophysics Unit, UCL Institute of Child Health, London, United Kingdom
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    • Both authors are joint last authors.
  • Rodney C. Scott

    1. Neurosciences Unit, UCL Institute of Child Health, London, United Kingdom
    2. Imaging and Biophysics Unit, UCL Institute of Child Health, London, United Kingdom
    3. Department of Neurology, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire, U.S.A
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    • Both authors are joint last authors.

Summary

Purpose

Childhood convulsive status epilepticus (CSE), in particular prolonged febrile seizures (PFS), has been linked with mesial temporal sclerosis (MTS). Previous studies have shown that hippocampal injury occurs in the acute phase immediately following CSE, but little is known about the longer term evolution of such injury. This study aimed to investigate the longer term outcome of childhood CSE with sequential magnetic resonance imaging (MRI) looking for progressive hippocampal injury during the first year post-CSE.

Methods

Eighty children (0.18–15.5 years) underwent brain MRI 1 month post-CSE, 50 with a repeat MRI at 6 months and 46 with repeat MRI at 12 months post-CSE. Thirty-one control subjects without neurologic problems had a single brain MRI for comparison. Hippocampal volumes were measured from each MRI scan by two independent observers, and hippocampal growth rates were estimated in each patient with suitable imaging.

Key Findings

Hippocampal volume loss was found in 20–30% of patients and was not associated with the etiology or clinical features of CSE, including seizure duration or focality. A borderline association was found between a history of previous seizures (p = 0.063) and the number of previous febrile seizures (p = 0.051), suggesting that multiple insults may be important in the pathogenesis of progressive hippocampal injury.

Significance

It is apparent that progressive hippocampal damage can occur after CSE of any etiology and is not limited to PFS. Repeated seizures may play an important role, but further follow-up is needed to determine any other risk factors and proportion of children showing initial volume loss progress to clinical MTS and temporal lobe epilepsy.

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