Selenium and Epilepsy (Research)

Peer-Reviewed Professional Journals

·    Brauer, A. U., et al.  Molecular actions of selenium in the brain:  neuroprotective mechanisms of an essential trace element.  Rev Neurosci.  15(1):19-32, 2004.

Institute of Cell Biology and Neurobiology, Center for Anatomy, Charite University Medical School, Berlin, Germany.

In addition to acting as an essential nutrient for the immune system and overall body function, it is apparent that selenium also plays a critical role in the operation of the nervous system.  Selenium itself is a constituent of selenoproteins, which are primarily involved in antioxidant function and redox status.  However, apart from its covalent incorporation into these proteins, selenium also performs neuroprotective actions independent of translational processes.  Furthermore, low selenium intake has detrimental effects on proper brain function, such as epileptic episodes and neuronal cell death, which have, in turn, been shown to be mitigated by higher selenium levels.  Understanding the mechanisms of selenium action will be crucial to determining its potential as a preventive and therapeutic agent against excitatory brain damage.

·    Ramaekers, V., et al.  Selenium deficiency triggering intractible seizures.  Neuropediatrics.  25(4):217-223, 1994.

Department of Paediatric Neurology, University of Aachen, Germany.

Two children with severe neurodevelopmental retardation and elevated liver function tests developed intractable seizures during the first year of life.  Detectable neurometabolic conditions have been ruled out.  At the time of seizures evidence for systemic selenium deficiency could be documented.  The youngest patient, who manifested intractable fits from the fourth day of life, died at the age of ten months.  Neuropathologic examination was consistent with Progressive Neuronal Degeneration of Childhood (PNDC) with liver disease or formerly known as Alpers disease.  In the oldest child, whose diet was normally balanced, fits started from the age of 11 months and features of long-standing selenium deficiency became apparent from the age of 1 1/2 years and consisted of liver function disturbances, depigmented hair and osteoarthropathy.  Oral substitution with selenium supplements in both children (3-5 micrograms/kg body weight) resulted in reduction of seizures and improvement of the EEG recordings after two weeks while liver function became normal.  Two of the seleno-dependent enzymes Glutathione Peroxidase (GPX) and Phospholipid Hydroperoxide Glutathione Peroxidase (PHGPX) are speculated to play a key-role in the defence of neuronal cells against oxygen radical formation and peroxidative processes.  These findings support the hypothesis that the presence of selenium depletion in the brain amongst patients with epilepsy constitutes an important triggering factor for the origin of intractable seizures and subsequent neuronal damage.

·    Rayman, M. P.  The importance of selenium to human health.  Lancet.  356(9225):233-241, 2000.

Selenium supplementation reduces intractable epileptic seizures in children.

·    Weber, G. F., et al.  Glutathione peroxidase deficiency and childhood seizures.  Lancet.  337(8755):1443-1444, 1991.

[no abstract available].