Prediction of treatment outcome in cocaine dependent males using quantitative EEG.

This study investigates the existence of outcome related neurophysiological subtypes within a population of abstinent cocaine dependent adults. We have previously reported and replicated the existence of a distinctive quantitative EEG (QEEG) profile in such a population, and demonstrated the persistence of this pattern at one and six month follow-up evaluations. This profile is characterized by significant deficits of absolute and relative delta and theta power, and excess of relative alpha power, as compared with age expected normal values. Abnormalities were greater in anterior than posterior regions, and disturbances in interhemispheric relationships were also observed. In the current study, 35 adult males with DSM-III-R cocaine dependence, were evaluated while residents of a drug-free residential therapeutic community, 5-15 days after last use of crack cocaine. Using multivariate cluster analysis, two neurophysiological subtypes were identified from the baseline QEEGs; Cluster 1 characterized by significant deficits of delta and theta activity, significant excess of alpha activity and more normal amounts of beta activity (alpha CLUS) and Cluster 2 characterized by deficits of delta, more normal amounts of theta and anterior excess of alpha and beta activity beta CLUS). No significant relationships were found between QEEG subtype membership and length of exposure to cocaine, time since last use of cocaine or any demographic characteristics. Further, no significant relationships were found between the commonly reported comorbid clinical features of depression and anxiety and subtype membership. However, a significant relationship was found between QEEG subtype membership and length of stay in treatment, with members of the alpha CLUS retained in treatment significantly longer than members of the beta CLUS.

Neurometric QEEG studies of crack cocaine dependence and treatment outcome.

This paper presents an overview of the quantitative electrophysiological (QEEC) research on cocaine dependence conducted at Brain Research Laboratories of New York University Medical Center. These studies have demonstrated that subjects with DSM-III-R cocaine dependence (without dependence on any other substance) evaluated in the withdrawal state, have replicable abnormalities in brain function when evaluated at baseline (approximately 5 to 10 days after last crack cocaine use), which are still seen at one and six month follow-up evaluations. These abnormalities were characterized by significant excess of relative alpha power and deficit of absolute and relative delta and theta power. Abnormalities were greater in anterior than posterior regions, and disturbances in interhemispheric relationships were also observed. In addition, QEEC subtypes were identified within the population of cocaine dependent subjects at baseline, and these subtypes were found to be significantly related to subsequent length of stay in treatment. The relationship between these QEEG findings and the neuropharmacology of cocaine dependence is discussed.

Quantitative EEG characteristics of children exposed in utero to cocaine.

Quantitative EEGs (QEEGs) were evaluated in a group of 6 school age children with in utero cocaine exposure. Their QEEGs showed significant deviations from age expected normal values. Further, the QEEG profile of brain dysfunction seen in these children was extremely similar to that previously reported in a large population of crack cocaine dependent adults. These abnormalities were characterized by significant excess of relative power in the alpha frequency band, and deficits of absolute and relative power in the delta and theta bands. Characteristic disturbances in interhemispheric relationships were also present. The similarities between the QEEG profiles of those adults with chronic exposure and children with prenatal exposure suggests that the brain dysfunction reflected in the QEEG is not a result of a transient change in neurotransmission, but a more profound alteration which persists in these children at school age. Further study is required to extend these findings to a larger group of children, and to investigate the potential relationship between these neurophysiological abnormalities and the developmental, behavioral and co-morbid features observed in such children.

Diagnostic and assessment issues related to pharmacotherapy for children and adolescents with autism.

Autism involves not only developmental delays but also aberrant behavior, both of which change in nature over time. Rating instruments may be useful to assess maladaptive and adaptive behaviors of autistic children in a standardized way and, perhaps, to measure change due to treatment. With the expansion of basic science, knowledge, and technology, there is increasing evidence that autism is etiologically heterogeneous. Currently, there is no biological marker specific to autism, although hyperserotonemia is a consistent finding in one third of autistic children. An aim of basic science research has been to develop a rational pharmacotherapy based upon the underlying neurochemistry. However, at the present time, this approach has not always been successful. It is expected that the development and use of more restrictive criteria, delineation of subtypes of autism, and interaction of descriptive, behavioral, clinical, and basic research will lead to more effective planning for treatment. The relationship of assessment to treatment response is presented and discussed.