Although human evoked potentials (EPs) have been recorded for 40 years, and EP recovery cycles for more than 30 years, the proposed research represents virtually a new area in the study of abstinence from cocaine abuse. Very little is known about the basic neurophysiological effects, in humans, of the chronic abuse of cocaine or the effects of abstinence from abuse. This study is designed to add to that knowledge base and is based on several related levels of observation: (1) chronic cocaine exposure and withdrawal appears to mimic clinical features of psychiatric disorders, for example, affective disorder or schizophrenia; (2) Somatosensory evoked potential (SEP) characteristics, including recovery cycles, have been shown to be deviant in many psychiatric disorders; 3) SEP characteristics are deviant in early abstinent substance abusers and SEP recovery cycles are deviant in early abstinent cocaine abusers; 4) SEP characteristics tend to normalize with psychiatric treatments, such as antidepressant medications which influence biogenic amine function; and 5) chronic cocaine exposure is said to alter biogenic amine levels. This proposal plans to study somatosensory evoked potential (SEP) recovery cycles at three time points during early abstinence in chronic cocaine users. The dynamic neurophysiological properties of SEP events arising in known neural generators will be measured and related to duration of abstinence.
The aims are (1) to measure recovery functions of 7 early SEP components, up to and including negativity at 60 msec poststimulus (N60), (2) to identify which components deviate from normal at initial testing in early abstinent cocaine users, and (3) to determine the extent to which these deviant components change systematically during the first 4 weeks of cocaine abstinence. Eight interstimulus intervals, from 0 to 90 msec, will be used. This project is relevant to both the clinical neuroscience of drug usage and to drug effects on sensory processes. The objective of this project is to contribute toward definition and understanding of basic human neurophysiological mechanisms associated with abstinence from substance abuse, in particular from cocaine.

Agency
National Institute of Health (NIH)
Institute
National Institute on Drug Abuse (NIDA)
Type
Research Project (R01)
Project #
5R01DA006728-02
Application #
2118905
Study Section
Drug Abuse Clinical and Behavioral Research Review Committee (DACB)
Project Start
1991-09-30
Project End
1994-08-31
Budget Start
1992-09-01
Budget End
1993-08-31
Support Year
2
Fiscal Year
1992
Total Cost
Indirect Cost
Name
Temple University
Department
Psychiatry
Type
Schools of Medicine
DUNS #
City
Philadelphia
State
PA
Country
United States
Zip Code
19122
Raimo, E B; Roemer, R A; Moster, M et al. (1999) Alcohol-induced depersonalization. Biol Psychiatry 45:1523-6
Eluri, R; Paul, C; Roemer, R et al. (1998) Single-voxel proton magnetic resonance spectroscopy of the pons and cerebellum in patients with schizophrenia: a preliminary study. Psychiatry Res 84:17-26
Shan, Y; Moster, M L; Roemer, R A (1996) The peak latency of orbital presaccadic spike potential with horizontal eye movements. Chin Med Sci J 11:69-72
Roemer, R A; Richelson, E; Shagass, C et al. (1996) A method to estimate in vivo D2 receptor occupancy by antipsychotic drugs. J Psychiatry Neurosci 21:325-33
Shan, Y; Moster, M L; Roemer, R A (1995) The effects of time point alignment on the amplitude of averaged orbital presaccadic spike potential (SP). Electroencephalogr Clin Neurophysiol 95:475-7
Roemer, R A; Cornwell, A; Dewart, D et al. (1995) Quantitative electroencephalographic analyses in cocaine-preferring polysubstance abusers during abstinence. Psychiatry Res 58:247-57
Shagass, C; Roemer, R A (1992) Evoked potential topography in major depression. I. Comparisons with nonpatients and schizophrenics. Int J Psychophysiol 13:241-54
Shagass, C; Roemer, R A (1992) Evoked potential topography in major depression. II. Comparisons between subgroups. Int J Psychophysiol 13:255-61
Roemer, R A; Shagass, C; Dubin, W et al. (1992) Quantitative EEG in elderly depressives. Brain Topogr 4:285-90