ABSTRACT
Twenty-three PTSD subjects were exposed to either: (1) standard eye movement desensitization (EMD), (2) a variant of EMD in which eye movements were engendered through a light tracking task, or (3) a variant of EMD in which fixed visual attention replaced eye movements. All three interventions produced significant positive changes in all dependent measures and these changes were maintained at follow-up. No significant differences between groups were observed. It was concluded that the eye movements peculiar to EMD are not essential to treatment outcome. The implications of the present findings and previous reports are discussed and recommendations for future research provided.
Subject(s)
Attention , Desensitization, Psychologic/methods , Eye Movements , Fixation, Ocular , Stress Disorders, Post-Traumatic/therapy , Adolescent , Adult , Arousal , Female , Follow-Up Studies , Humans , Imagination , Male , Middle Aged , Stress Disorders, Post-Traumatic/psychology , Treatment OutcomeABSTRACT
The purpose of the present study was to examine whether doses of phenytoin and phenobarbital that blocked kindled seizures in rats also disrupted operant behavior. Subjects initially were exposed to a kindling procedure in which repeated electrical stimulation of the amygdala evoked generalized seizures. After kindling, they were trained under a multiple fixed-ratio 30 interresponse-time-greater than 10-sec schedule of food delivery. Once each day, 6 days per week, 30-min exposures to this schedule were followed immediately by amygdaloid stimulation which occurred at no other time. Response rate, reinforcement rate and duration of forelimb clonus were recorded. When response rates were stable, 5 rats were tested with phenytoin (25, 50, 75 and 100 mg/kg) and 5 others were tested with phenobarbital (10, 25 and 40 mg/kg). Results indicated that doses of phenytoin that controlled kindled seizures also affected operant behavior. For this drug, the ED50 for forelimb clonus was 62 mg/kg. For response rate under the fixed-ratio and interresponse-time components, it was 48 and 58.2 mg/kg, respectively. Dose-response curves for the behavioral and antiseizure effects of phenobarbital were similar. However, for this drug the ED50 for forelimb clonus (18.9 mg/kg) was significantly lower than for response rate under the fixed ratio component (37.4 mg/kg).
Subject(s)
Amygdala/physiology , Conditioning, Operant/drug effects , Kindling, Neurologic/drug effects , Phenobarbital/pharmacology , Phenytoin/pharmacology , Seizures/prevention & control , Animals , Male , Rats , Reinforcement, PsychologyABSTRACT
Ethanol (1.5 g/kg) administered intraperitoneally to kindled rats blocked the seizures normally elicited in these subjects by electrical stimulation of the amygdala. Tolerance to this anticonvulsant effect developed following a series of ethanol intubations delivered at 48-hr intervals only when an amygdaloid stimulation was administered during each period of ethanol intoxication. Subjects stimulated 1 hr following each intubation were tolerant to the intraperitoneal test dose after only five intubations (2 g/kg), whereas those stimulated 1 hr prior to each intubation displayed no tolerance during the course of 20 such trials. Even at high intubation doses (5 g/kg), significant levels of tolerance to the anticonvulsant effect of the intraperitoneal test dose were not observed in subjects unstimulated during each period of post-intubation intoxication. These findings emphasize the important role of response contingency in ethanol tolerance; tolerance develops readily for only those effects of alcohol that repeatedly manifest themselves during the periods of ethanol exposure.
Subject(s)
Ethanol/pharmacology , Seizures/prevention & control , Amygdala , Animals , Behavior, Animal/drug effects , Dose-Response Relationship, Drug , Drug Tolerance , Electric Stimulation , Ethanol/administration & dosage , Injections, Intraperitoneal , Kindling, Neurologic/drug effects , Rats , Time FactorsABSTRACT
Ethanol (1.5 g/kg, IP) administered to kindled rats blocked the seizures normally elicited in these subjects by electrical stimulation of the amygdala. Tolerance to this anticonvulsant effect developed following a series of ethanol injections only when the amygdaloid stimulation was administered during the periods of ethanol intoxication. Control subjects stimulated each day prior to ethanol administration displayed no tolerance to ethanol's anticonvulsant effects. Such findings emphasize the important role of learning in the development of alcohol tolerance and support the view that tolerance develops more rapidly for responses that are affected by the alcohol exposure.
