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Epilepsy in Prader-Willi syndrome: experience of a national referral centre

Tal Gilboa1, Varda Gross-Tsur

  • 1Child Neurology Unit, Shaare Zedek Medical Center, Jerusalem, Israel. Talgilboa14@gmail.com

Developmental Medicine and Child Neurology
|June 12, 2013
PubMed

Insights

Epilepsy and febrile seizures are less common in Prader-Willi syndrome (PWS) than in Angelman syndrome, often linked to brain abnormalities. Epileptiform activity in PWS is associated with younger age.

Area of Science:

  • Neurology
  • Genetics
  • Pediatrics

Background:

  • Prader-Willi syndrome (PWS) is a complex genetic disorder with variable clinical manifestations.
  • Epilepsy and seizure disorders are known complications in some neurodevelopmental conditions.
  • Characterizing these in PWS is crucial for understanding disease mechanisms and improving patient care.

Purpose of the Study:

  • To investigate the prevalence and characteristics of epilepsy and febrile seizures in a large cohort of individuals with PWS.
  • To identify associated brain abnormalities and electroencephalographic (EEG) features.
  • To compare seizure risks with those in Angelman syndrome.

Main Methods:

  • An observational cohort study reviewing medical records of 126 individuals with genetically confirmed PWS.
  • Data collection included seizure history, medication, neuroimaging, and family history.
  • Electroencephalography (EEG) was performed on 95 participants.

Main Results:

  • Four percent of individuals had epilepsy, and 6.4% experienced febrile seizures.
  • Seizures were associated with specific genetic abnormalities (deletion) and brain imaging findings.
  • Focal epileptiform abnormalities and electrographic seizures were observed in 5% of participants, particularly in younger individuals.

Conclusions:

  • The incidence of epilepsy and febrile seizures in PWS is lower than in Angelman syndrome.
  • Seizure risk in PWS is associated with underlying brain abnormalities.
  • Further research is needed to elucidate the mechanisms of epileptiform activity in PWS and its distinction from Angelman syndrome.
Abstract

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