Juvenile myoclonic epilepsy (JME) appears in adolescence with myoclonic, absence, and generalized tonic clonic (GTC) seizures with paroxysmal activity of polyspike and slow wave (PSW), or spike and wave (SW) complexes in EEG. Our aim was to analyze the clinical characteristics, background EEG activity, and paroxysmal events in 41 patients with JME. Background EEG activity was analyzed with visual, quantitative (QEEG), and neurometric parameters. Our JME patients started with absence seizures at 11.4 1.5 years old, myoclonic seizures at 13.6 2.5 years, and GTC seizures at 15.1 0.8 years. The seizures presented in awakening at 7:39 h with sleep deprivation, alcoholic beverage intake, and stress as the most frequent precipitant factors. Paroxysmal activity was of PSW and fast SW complexes with 40.5 62.6 events/hour and a duration of 1.7 s. Right asymmetric paroxysmal activity was present in 68.3% of patients. Background EEG activity was abnormal in 31.7% of patients with visual analysis. With QEEG beta AP (absolute power) increase and AP delta decrease were the most frequent abnormalities found. Spectral analysis showed that 48.7% of patients had normal results, and 26.8 3% and 24.4% had higher and lower frequencies than 10.156 Hz, respectively. We concluded that, with visual analysis, background EEG activity was abnormal in a few patients and the abnormalities increased when QEEG was used.
Juvenile myoclonic epilepsy (JME) is a genetically-determined disease that appears in adolescence with myoclonic seizures, absence, and generalized tonic clonic (GTC) seizures that are characteristically present for two hours after awakening. Electroencephalogram (EEG) shows paroxysmal activity of polyspike and slow wave (PSW) or fast spike and wave complexes in frontocentral leads with a frequency of three- to five-hertz and a variable duration of events [1–3]. JME presents during childhood or adolescence with an absence of seizures in 40% of patients, and myoclonic and GTC seizures at some point in adolescence at approximately 17 years of age . Some patients with JME have a family history of disease in variable ranges, depending on the population that is studied. Currently, some genes were postulated to partially explain the origin of the disease . From a physiological point of view, it has been postulated that an imbalance exists between the excitatory and inhibitory neural networks that are located in the medial frontal regions, with a strong interrelation with the thalamocortical networks that regulate the sleep–wake cycle [6,7]. This alteration has been corroborated through EEG current source analysis studies, voxel-based morphometry, magnetic resonance spectroscopy, and functional magnetic resonance [8–10].
total of 41 patients were selected, 16 men and 25 women, with a mean age of 21.1 11.5 years (range of 12- to 68-years). A family history of epilepsy was present in 12 (29.2%) patients. The epilepsy age onset was of 13.6 2.5 years. All the patients had myoclonic seizures with age onset at 13.6 1.71 years. A total of 33 (80.4%) patients had GTC seizures with a mean onset age of 15.1 0.8 years. Only nine (21.9%) patients had absence seizures with a mean age onset of 11.4 1.5 years. Seizures are characteristically present in the first hours of the morning after awakening; our patients had seizures at 7:39 3.2 a.m. Patients with JME have many factors that increase the risk of seizures. In our group, the factors leading to seizures were sleep deprivation in 18 (43.9%) patients, alcoholic beverage intake in 8 (19.5%), stress in 7 (17.0%), photic stimulus in 1 (2.4%), menstruation in 1 (2.4%), and videogame playing in 1 (2.4%) patient. Only 4 patients (9.7%) had a diagnosis of JME at the time of entry into the study, and 23 (56.1%) patients had treatment with antiepileptic drugs. However, only 11 (26.8%) had treatment with valproate and 4 (9.7%) had treatment with levetiracetam, an antiepileptic drug that has demonstrated antiepileptic utility in JME. The mean daily dose of valproate was 661.7 194.8 mg/day.