Risk factors for psychogenic nonepileptic seizures in children and adolescents with epilepsy.

There is evidence that psychogenic nonepileptic seizures (PNES) remain underdiagnosed, especially in children and adolescents. Diagnosis of such events is even more difficult in patients that do have epilepsy, leading to delayed diagnosis and treatment and, consequently, iatrogenic complications. This study aimed to evaluate possible risk factors in children with epilepsy who had PNES. Seizures and epileptic syndromes were classified according to International League Against Epilepsy guidelines. Patients were evaluated with a structured psychiatric anamnesis and classified according to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition; Classification of Mental and Behavioral Disorders: Diagnostic Criteria for Research; and Schedule for Affective Disorders and Schizophrenia for School-Age Children--Epidemiological Version. Risk factors such as head trauma, physical, sexual and psychological abuse, and psychiatric diagnoses, among others, were investigated. Family history of epilepsy and psychiatric illness were detected by review of medical records and/or follow-up interviews. Gender was not a predictive factor, and although older children had a higher risk for PNES, younger children also presented truly psychogenic events mimicking epileptic seizures. The most common associated psychiatric diagnosis was depression. Family histories for epilepsy and psychiatric illness were a frequent finding. An inadequate family environment was more common than sexual or physical abuse. Current knowledge obtained from adults with PNES has been used to understand children with PNES. However, this study of children with epilepsy revealed some similarities and many differences. These features may help to identify predictive factors in a population in need of adequate diagnosis of and therapy for this long-lasting pathology.

Psychophysics of electrical stimulation of striate cortex in macaques.

Macaques indicated their detection of onset or alteration of 0.2-ms pulses applied in various configurations through electrodes implanted in striate cortex. When microelectrodes were introduced and left in place, the threshold for detection of 100-Hz pulses nearly doubled within 24 h. However, for chronically implanted platinum-alloy macroelectrodes detection thresholds usually remained stable for many months, independently of location within striate cortex or its immediately subjacent white matter. Thresholds were unaffected by the visual conditions, such as light versus darkness, or movement of the eyes; but in one animal blind after acute glaucoma thresholds for loci in striate cortex were permanently decreased by about 50%. Learning to respond to electrical stimulation of the optic tract produced no tendency to respond to such stimulation of striate cortex. Onset of stimulation at a given locus could be detected even in the face of continuous supraliminal stimulation at four surrounding loci on a 3-mm radius. The surround stimulation did alter the threshold of the central locus, but such stimuli could not summate if they were subliminal by some 10%. Cessation of stimulation that had been continuing for 1 min to 1 h could be detected if it were being applied at a level 20-75% above that needed for detection of stimulus onset. Continuous stimulation had a pronounced "priming" effect, in that modulation of frequency or intensity of such stimulation by as little as 5% could be detected (e.g., 20 microA in a background of 500 microA, or <2-ms interpulse interval with pulses at 50 Hz). Using pulses inserted in various phase relations to ongoing pulses at 2-5 Hz, it could be determined that stimulus pulses were surrounded by a strong facilitatory period for about 30 ms, which was then replaced by refractoriness. Given the congruence of macaque and human visual anatomy and psychophysics, these results further encourage efforts to develop a cortical prosthesis for the blind.

Depressão em crianças e adolescentes com epilepsia / Depression in epileptic children and adolescents

A epilepsia, uma condição neurológica, apresenta uma freqüência elevada de transtornos psiquiátricos, em especial a depressão, que é a comorbidade psiquiátrica mais comum nesta população. Sabe-se que o transtorno depressivo pode comprometer muito mais a qualidade de vida de um paciente com epilepsia do que a gravidade da doença em si, daí a importância do seu diagnóstico. Entretanto, há poucos estudos sobre a prevalência e apresentação clínica da depressão nas crianças e adolescentes com epilepsia e nenhum sobre o seu tratamento. Este artigo tem como objetivo estudar as razões para o subdiagnóstico deste transtorno psiquiátrico e revisar as evidências para a ocorrência de possíveis mecanismos fisiopatológicos comuns. Para tal, revisamos estudos em modelos animais de epilepsia que demonstram uma diminuição de neurotransmissores implicados nos mecanismos patogênicos e tratamento da depressão Adicionalmente, estudamos as evidências oferecidas pelos estudos de neuroimagem e neuropsicológicos que corroboram a existência de uma disfunção das estruturas límbicas - frontais e temporais - nos pacientes com transtorno depressivo, que aparentemente também existe em pacientes com epilepsia. Portanto, este artigo de revisão dá evidência de que o conceito de relação causa-efeito para a ocorrência de depressão em pacientes com epilepsia precisa ser revisto.

The diagnostic role of short duration outpatient V-EEG monitoring in children.

Video-electroencephalographic monitoring enables correlation between behavioral and EEG data, however, because it requires prolonged hospitalization, it may be stressful and expensive. This study aimed to assess the benefits and limitations of this procedure in children. We analyzed 39 children classified according to clinical complaints: doubts about epilepsy classification in 23 (Group I); differential diagnosis with nonepileptic events in eight (Group II); and differential diagnosis between cognitive decline and subtle seizures in eight (Group III). Clinical episodes were recorded in 37 patients (94.9%). In Group I, seizure type was reclassified in 11 patients and epileptic syndrome in nine. In two patients a previously unnoticed seizure type was recorded. In Group II, four patients presented epileptic seizures. In Group III, nonconvulsive status was detected in five. Video-electroencephalographic monitoring enabled major modification of therapeutic approach in 21 patients and guided new neuroimaging studies in 10 patients. In conclusion, in patients with frequent seizures, short video-electroencephalographic monitoring allows proper classification of epileptic syndromes, and diagnosis of nonepileptic seizures, promoting introduction of appropriate treatment with a relatively low cost.