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 carbonyl-carbon 11-WAY-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 homogeneously involved in this condition, further questioning the current classification of primarily generalized epilepsy.
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 carbonyl-carbon11-WAY-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 homogeneously involved in this condition, further questioning the current classification of primarily generalized epilepsy.
Authors: Woo Suk Tae; Seung Bong Hong; Eun Yun Joo; Sun Jung Han; Jae-Wook Cho; Dae Won Seo; Jong-Min Lee; In Young Kim; Hong Sik Byun; Sun I Kim Journal: Korean J Radiol Date: 2006 Jul-Sep Impact factor: 3.500