No abstract

The sudden onset, short duration and stereotyped features of panic attacks, and the fear aura of seizures starting at the mesial aspects of the temporal lobe, suggest common mechanisms underlying panic disorder (PD) and mesiotemporal epilepsy (MTLE). However, current consensus emphasizes the importance of differentiating the two entities based on 1) intact consciousness in panic attacks, 2) poor response to antiepileptics, and 3) unsuccessful electrophysiological attempts to demonstrate a relationship. We report two cases with a diagnosis of PD that had been partially responsive to first line treatments. During the EEG session, both patients developed panic symptoms with minimal EEG changes in response to paper bag-hyperventilation (PB-HV), and several minutes later presented a clear ictal EEG pattern associated with very different clinical symptoms, but both with strong fear content. Z-scored LORETA analysis showed increased current source densities (CSD) at the right amygdala in both subjects during the induced panic symptoms. Several areas were involved during the seizure, different in each subject. Yet, a very significant increase at the amygdala was found in both cases. The LORETA Z-scored source correlation (LSC) analysis also showed similar abnormal patterns during the panic symptoms in both patients, and marked differences during the seizure. These findings show a major role of amygdalar hyperactivity in both fear-related conditions for the two patients, and are discussed in relation to existing models of PD in general. Abnormal overactivation at mesiotemporal regions is poorly represented at the surface recordings but can be detected by the appropriate analytical techniques.

BackgroundDespite the devastating impact of anxiety disorders (ADs) worldwide, long-lasting debates on causes and remedies have not solved the clinician’s puzzle: who should be treated and how? Psychiatric classifications conceptualize ADs as distinct entities, with strong support from neuroscience fields. Yet, comorbidity and pharmacological response suggest a single “serotonin dysfunction” dimension. Whether AD is one or several disorders goes beyond academic quarrels, and the distinction has therapeutic relevance. Addressing the underlying dysfunctions should improve treatment response. By its own nature, neurophysiology can be the best tool to address dysfunctional processes.PurposeTo search for neurophysiological dysfunctions and differences among panic disorder (PD), agoraphobia-social-specific phobia, obsessive–compulsive disorder (OCD) and generalized anxiety disorder.MethodsA sample population of 192 unmedicated patients and 30 aged-matched controls partook in this study. Hypothesis-related neurophysiological variables were combined into ten independent factors: 1) dysrhythmic patterns, 2) delta, 3) theta, 4) alpha, 5) beta (whole-head absolute power z-scores), 6) event-related potential (ERP) combined latency, 7) ERP combined amplitude (z-scores), 8) magnitude, 9) site, and 10) site of hyperactive networks. Combining single variables into representative factors was necessary because, as in all real-life phenomena, the complexity of interactive processes cannot be addressed through single variables and the multiplicity of potentially implicated variables would demand an extremely large sample size for statistical analysis.ResultsThe nonparametric analysis correctly classified 81% of the sample. Dysrhythmic patterns, decreased delta, and increased beta differentiated AD from controls. Shorter ERP latencies were found in several individual patients, mostly from the OCD group. Hyperactivities were found at the right frontorbital-striatal network in OCD and at the panic circuit in PD.ConclusionsOur findings support diffuse cortical instability in AD in general, with individual differences in information processing deficits and regional hyperactivities in OCD and PD. Study limitations and the rationale behind the variable selection and combination strategy will be discussed before addressing the therapeutic implications of our findings.

The relationship between psychiatric symptoms that respond to anticonvulsants and epileptic activity is still debated. Evidence linking electroencephalographic changes to treatment response is scarce and controversial, partly because of the poor scalp representation of limbic electrical activity. We studied the clinical relevance of focal topographic changes in the resting EEG, the visual evoked potential and the P300 response in 90 psychiatric patients, by evaluating response to anticonvulsants and development of neurological complications. The group with focal changes was compared to a group with epileptiform activity but no focal changes and a group with normal or diffusely altered EEG. Focal EEG and EP changes predicted good response to anticonvulsants, while the presence of epileptiform activity did not. Clinical seizures developed only in patients with focal changes and no anticonvulsants medication. Structural abnormalities and selective neuropsychological deficits were seen only in the focal group. There was an association of symptom type and the site of focus. We concluded that focal EEG and EP changes in psychiatric patients have important theoretical as well as practical implications.

If behavior results from brain function, some evidence of dysfunction could be expected in children with major behavioral problems. Yet, neurophysiologic studies in these children are frequently normal. We hypothesized a relationship between maturational asymmetry and behavior, given the role of hemispheric imbalance in adult psychopathology. The purpose of this study was to investigate whether age-sensitive neurophysiologic measures could identify behaviorally relevant maturational asymmetries in otherwise healthy children. Ninety-five children were studied; reasons for testing were behavioral (19), academic (12), medical nonneurologic (16), and mixed (28), along with 20 control subjects. Academic, behavioral (Child Behavioral Checklist), and psychometric (Wechsler Intelligence Scale for Children-Revised; WISC-R) measures were analyzed in relation to four neurophysiologic parameters: P300 Latency, P300 Latency Asymmetry, Maturational Z-score, and Maturational Z-score Asymmetry, within a canonical design. The highest correlation was behavior with Maturational Z-score Asymmetry. Academic scores were predicted by the three-variable interaction of P300 Latency,Maturational Z-score, and Maturational Z-score Asymmetry. We concluded that behavior was strongly influenced by maturational asymmetry, while academic performance depended on both global maturation and maturational asymmetry. Our results suggest that behavioral disturbances can have a neural substrate despite apparently normal electroencephalograms (EEGs) and event-related potentials (ERPs). They open the possibility for specific therapeutic interventions to improve behavior and performance, and, perhaps, prevent major psychopathology in later life.