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Regional Reductions in Serotonin 1A Receptor Binding in Juvenile Myoclonic Epilepsy
Anna Meschaks, MD;
Per Lindstrom, MD, PhD;
Christer Halldin, PhD;
Lars Farde, MD, PhD;
Ivanka Savic, MD, PhD
Arch Neurol. 2005;62:946-950.
Background Juvenile myoclonic epilepsy (JME) is classified as primarily generalized epilepsy and as such is assumed to lack an anatomic substrate. Although neurochemical abnormalities are probable, few studies have investigated whether they exist in JME. Animal data and the high incidence of myoclonic seizures in serotonin-intoxicated patients suggest that the serotonin system may be disturbed in JME.
Objective To test the hypothesis that JME is associated with a disturbed serotonin system and that this disturbance could be reflected in altered serotonin 1A receptor binding.
Design The serotonin 1A receptor binding potential (BP) was measured with positron emission tomography and serotonin 1A receptor antagonist carbonylcarbon 11WAY-100635. The BP was calculated using a reference tissue model in several limbic and neocortical regions and the raphe nuclei.
Setting Epilepsy clinics of the Karolinska University Hospital, Stockholm, Sweden.
Patients Eleven patients with JME and 11 controls were studied.
Main Outcome Measure Serotonin 1A receptor BP calculated in a set of volumes of interest.
Results The patients with JME showed a reduced BP in the dorsolateral prefrontal cortex, raphe nuclei, and hippocampus.
Conclusions The observed reductions in serotonin 1A receptor BP suggest that the serotonin system is affected in JME. Although the data give no definitive information about underlying mechanisms, they provide a strong argument for the view that not all brain regions are homogenously involved in this condition, further questioning the current classification of primarily generalized epilepsy.
Author Affiliations: Division of Neurology, NEUROTEC (Meschaks and Savic), and Department of Neuroscience (Drs Meschaks and Savic) and Divisions of Neurology (Dr Lindstrom) and Psychiatry (Drs Halldin and Farde), Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.
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