The Australian and New Zealand journal of psychiatry
-
Aust N Z J Psychiatry · Dec 2008
Randomized Controlled Trial Comparative StudyShyness 3: randomized controlled trial of guided versus unguided Internet-based CBT for social phobia.
In two previous randomized controlled trials Titov et al. demonstrated significant benefit from an Internet- and email-based treatment programme for social phobia. The present study (Shyness 3) explores whether participants are able to complete this programme independently. ⋯ The reliability of this Internet-based treatment programme for social phobia has been confirmed. The therapist-guided condition was superior to the self-guided condition, but a subgroup of participants still benefited considerably from the latter. These data confirm that self-guided education or treatment programmes for common anxiety disorders can result in significant improvements.
-
Aust N Z J Psychiatry · Dec 2008
ReviewStress and anxiety in schizophrenia and depression: glucocorticoids, corticotropin-releasing hormone and synapse regression.
Stress during childhood and adolescence has implications for the extent of depression and psychotic disorders in maturity. Stressful events lead to the regression of synapses with the loss of synaptic spines and in some cases whole dendrites of pyramidal neurons in the prefrontal cortex, a process that leads to the malfunctioning of neural networks in the neocortex. Such stress often shows concomitant increases in the activity of the hypothalamic-pituitary-adrenal system, with a consequent elevated release of glucocorticoids such as cortisol as well as of corticotropin-releasing hormone (CRH) from neurons. ⋯ Both GR and CRH receptors in the spines can modulate NMDA receptors, reducing their activation by glutamate and hence spine stability. In contrast, glucocorticoids, probably acting on nerve terminal and astrocyte GRs, can release glutamate, so promoting NMDA receptor activation. It is suggested that spine stability is under dual control by glucocorticoids and CRH, released during stress to change the stability of synaptic spines, leading to the malfunctioning of cortical neural networks that are involved in depression and psychoses.