ABSTRACT
We tested the relation between a single short tonic-clonic seizure elicited by flurothyl vapors and changes of learning in Morris water maze (MWM) in Wistar rats. Oxidative stress usually accompanies seizures. Large melatonin doses were applied immediately before and after seizures to test consequences on learning impairment. One hour of hypobaric hypoxia (8000 m) three days prior to the seizure served as an activator of intrinsic antioxidant systems. Learning in MWM (7 days) started 24 h after seizures. Following seizures, latencies in MWM were longer than in controls and were shortened by hypoxia and preventive melatonin application. Melatonin was also applied before hypoxia to influence free radical (FR) production and intrinsic antioxidant activation. Some behavioral characteristics were changed and preconditioning effect of hypoxia was reduced. Melatonin after seizure (150 s and 6 h) had negligible effect. Results allow us to hypothesize about the role of FR and the beneficial effect of melatonin on the behavioral consequences of seizures.
Subject(s)
Antioxidants/therapeutic use , Learning Disabilities/etiology , Learning Disabilities/prevention & control , Melatonin/therapeutic use , Seizures/complications , Analysis of Variance , Animals , Automatism/etiology , Automatism/prevention & control , Blood-Brain Barrier/drug effects , Blood-Brain Barrier/physiopathology , Convulsants/toxicity , Disease Models, Animal , Flurothyl/toxicity , Hypoxia/complications , Male , Maze Learning/drug effects , Rats , Reaction Time/drug effects , Seizures/chemically induced , Seizures/pathology , Time FactorsABSTRACT
A functional analysis indicated that chronic eye poking exhibited by a woman with profound mental retardation persisted in the absence of social contingencies. We initiated a procedure in which a therapist delivered a punisher (mild reprimand) contingent on eye poking in the presence, but not the absence, of a neutral stimulus (wristbands). Subsequently, eye poking was suppressed when the participant wore the wristbands in novel environments without the reprimand contingency.
Subject(s)
Association Learning , Automatism/prevention & control , Behavior Therapy/methods , Eye Injuries/prevention & control , Self-Injurious Behavior/prevention & control , Automatism/psychology , Eye Injuries/psychology , Female , Generalization, Psychological , Humans , Intellectual Disability/psychology , Intellectual Disability/therapy , Middle Aged , Reinforcement, Verbal , Self-Injurious Behavior/psychology , Social Environment , Transfer, PsychologyABSTRACT
This article deals with surprising delinquent behaviour of a limited kind--in time and nature. This delinquent behaviour manifests itself during actual life stress conditions where in the person's past there is evidence of psychotraumatization. The author offers an etiological theory concerning the medicine of behaviour and psychosomatics. The application of this theory to consider delinquency an important branch of behavioural sciences and medicine is concretized, updated and the evolution of the concept towards a sectorial approach becomes the main topic of the present work. A sector of faulty interaction between the individual with a psychotraumatic history and the environment is activated during life stress conditions, and may lead to behavioural or psychosomatic disturbances. Case histories are presented, concretizing the sectorial faulty behaviour following an impaired reality testing and impulse control in a vulnerable field of interaction with the environment. The legal implications are discussed, in the light of an inconsistent mens rea, offering at the same time a judicial psychiatric rehabilitation model. The advantages of this approach, which has been developed during the past seven years, are mentioned. A continuous interprofessional dialogue between judges and psychiatrists has made possible this rather enlightened attitude towards this special kind of delinquent behaviour promoting rehabilitation instead of unnecessary social ostracism or 'social death'.
Subject(s)
Automatism , Criminal Psychology , Life Change Events , Psychophysiologic Disorders , Adolescent , Adult , Automatism/etiology , Automatism/prevention & control , Automatism/psychology , Community Psychiatry , Female , Forensic Psychiatry , Humans , Male , Models, Psychological , Prohibitins , Psychophysiologic Disorders/etiology , Psychophysiologic Disorders/prevention & control , Psychophysiologic Disorders/psychology , Risk FactorsABSTRACT
Kainic acid (KA 4-14 mg/kg) administered intraperitoneally (i.p.) produces automatisms (scratching until third postnatal week, "wet dog" shakes thereafter), and clonic and tonic-clonic seizures in rats aged 7, 12, 18, 25, and 90 days. Administration of carbamazepine (CBZ) i.p. (25 or 50 mg/kg), phenobarbital (PB 20-80 mg/kg), clonazepam (CZP 0.2 or 1 mg/kg), or valproate (VPA 200 mg/kg) influenced neither incidence nor latency of automatisms. Clonic seizures that are regularly observed after the third postnatal week in controls were either abolished or substantially suppressed by any of the aforementioned antiepileptic drugs (AEDs). Tonic-clonic seizures observed in the first 3 postnatal weeks were suppressed only by solvent [including propyleneglycol (PEG), ethanol, and water]; the effect of AEDs on tonic-clonic seizures was proconvulsant instead. The automatisms were most resistant to AED therapy. These results induce some doubts about the adequacy of the KA model for identifying AEDs effective against complex partial seizures, but forthcoming AEDs that suppress automatisms in the KA rat model might also be active against human complex partial seizures.
