Sexual abuse perpetrated by adult and juvenile females: an ultimate attempt to resolve a conflict associated with maternal identity.

OBJECTIVE: The purpose of this article is to report the descriptive and phenomenological aspects of adult females (AF) and juvenile females (JF) who sexually abuse children and adolescents. A major focus is to study the relational problems during childhood and adulthood of this specific population and how they echo the relational aspects of their own victimization. METHODOLOGY: Since 1992, clinical and evaluative data were collected from a sample of 13 AF and 15 JF who had committed sexual abuse. The subjects were evaluated in the program for adult and adolescent sex offenders at the outpatient clinic of the Centre de Psychiatrie Légale de Montréal (affiliated with the Institut Philippe Pinel de Montréal). The data were collected by a multidisciplinary team of clinicians: psychiatrists, psychologists, criminologists and sexologists. A team of two or three clinicians who utilized a standardized interview grid evaluated each subject. RESULTS: Mean age at the time of the evaluation was 36.2 years (SD=9.28) for the AF and 14.7 years (SD=1.39) for the JF. A considerable percentage of the sexual abuses occurred in an intra-familial context for both groups (92.3% of the AF; 53.3% of the JF). Half of the AF not only committed sexual but also physical abuse of their victims. In addition, the precocious and repetitive dimension of the sexual abuses perpetrated by 33.3% of the JF was noted. CONCLUSION: This descriptive study reports a set of problematic relationships and a history of victimization among AF and JF. The history of the relationship with their parents frequently revealed that for JF, the father was absent or not very involved and for AF the father was sexually and physically abusive. On the other hand, a disturbed mother-child relationship among both AF and JF sexual abusers highlights an important conflict.

[Treatment progress scale for violent psychosis patients]. / Un instrument de mesure des progrès cliniques pour des patients psychotiques violents.

OBJECTIVES: The dangerousness of psychiatric patients is related to many well-documented factors in literature. To better document the course of dangerousness in most violent psychotic patients with severe and persistent diseases, we have developed a Treatment Progress Scale (TPS). METHOD: The TPS was developed based on the literature research and the expertise of a multidisciplinary team. RESULTS: The instrument has good interrater reliability and has shown to be easy to use, after being implemented for 5 years in a treatment unit at Philippe-Pinel Institute. The instrument provides a systematic assessment of important clinical parameters validating treatment observance and patient evolution over months. It also builds on the daily observations made by different members of the multidisciplinary team, the common language of patients and staff, the transparency of our work with patients, and the clear identification of most treatment targets. It also brings a valued complement to the dangerousness assessment. CONCLUSIONS: The TPS is a relevant instrument for the violent psychotic inpatient specific population. It provides a better identification of treatment progress and helps to specify dangerousness from an evolution perspective. Variations may be developed to assess outpatients and patients in a general setting.

Direct and indirect interactions between cannabinoid CB1 receptor and group II metabotropic glutamate receptor signalling in layer V pyramidal neurons from the rat prefrontal cortex.

At proximal synapses from layer V pyramidal neurons from the rat prefrontal cortex, activation of group II metabotropic glutamate receptors (group II mGlu) by (2S,2'R,3'R)-2-(2',3'-dicarboxycyclopropyl) glycine (DCG IV) induced a long-lasting depression of excitatory postsynaptic currents. Paired-pulse experiments suggested that the depression was expressed presynaptically. Activation of type 1 cannabinoid receptors (CB1) by WIN 55,212-2 occluded the DCG IV-induced depression in a mutually occlusive manner. At the postsynaptic level, WIN 55,212-2 and DCG IV were also occlusive for the activation of extracellular signal-regulated kinase. The postsynaptic localization of active extracellular signal-regulated kinase was confirmed by immunocytochemistry after activation of CB1 receptors. However, phosphorylation of extracellular signal-regulated kinase in layer V pyramidal neurons was dependent on the activation of N-methyl-d-aspartate receptors, consequently to a release of glutamate in the local network. Group II mGlu were also shown to be involved in long-term changes in synaptic plasticity induced by high frequency stimulations. The group II mGlu antagonist (RS)-alpha-methylserine-O-phosphate monophenyl ester (MSOPPE) favoured long-term depression. However, no interaction was found between MSOPPE, WIN 55,212-2 and the CB1 receptor antagonist SR 141716A on the modulation of long-term depression or long-term potentiation and the effects of these drugs were rather additive. We suggest that CB1 receptor and group II mGlu signalling may interact through a presynaptic mechanism in the induction of a DCG IV-induced depression. Postsynaptically, an indirect interaction occurs for activation of extracellular signal-regulated kinase. However, none of these interactions seem to play a role in synaptic plasticities induced with high frequency stimulations.