During abstinence from alcohol, craving is elicited by the cues and contexts previously associated with alcohol, which contribute to relapse. To prevent the craving and relapse experienced by alcoholics, cue-exposure therapy (CET) has been used to extinguish the association between alcohol and alcohol-related cues and contexts. This study applied CET, using a virtual reality (VR) system, to eight members of an Alcoholics Anonymous group for eight sessions. Cues and contexts most likely to elicit an urge to drink were selected through a preliminary survey in order to compose VR-CET scenarios: a glass, a bottle, food, and a bar were judged to be the most tempting for people in alcohol dependence and abstinence. Using these cues and contexts, a Japanese-style pub and a western bar were created. Each session was administered for 30 minutes by a psychiatrist and included an introduction, immersion, VR navigation, interviews about feelings, and self-report questionnaires about cravings. The eight sessions consisted of initial and closing sessions and person-, object-, and situation-focused sessions. As a result, a reduction in cue-elicited craving after VR-CET was reported. A mean score of 15.75 (SD = 10.91) on the Alcohol Urge Questionnaire in the first session decreased to 11.50 (SD = 5.76) in the final session. This study suggests that using virtual reality can enhance the effectiveness of CET.

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The purpose of the present paper was to determine whether the brief exposure of neurons to antipsychotic drugs is associated with the activation of extracellular signal-regulated kinases (ERK) and cyclic adenosine 3 ¢ ,5 ¢ -monophosphate (cAMP) response element (CRE) binding protein (CREB).The activation of ERK-1/2 and CREB can be monitored by immunoblotting with antibodies that specifically recognize p-ERK-1/2 (phosphorylated on Thr-202 and Tyr-204) and p-CREB (phosphorylated on Ser-133). In hippocampal neuron cultures at 25 days in vitro (DIV), the levels of ERK and CREB phosphorylation significantly increased after treatment with haloperidol (50 nmol/L) and risperidone (50 nmol/L), except when risperidone was administered at the p-CREB level. However, risperidone also increased the p-CREB level at an insignificant rate in the same direction. At 10 DIV, none of the antipsychotic drugs significantly increased the level of ERK and CREB phosphorylation. The difference between levels of ERK and CREB phosphorylation in response to haloperidol and risperidone at 25 DIV was also observed. Risperidone significantly increased the level of ERK-1/2 phosphorylation, but not the level of CREB phosphorylation. Haloperidol, in contrast, had a different effect. These data indicate that neuronal maturation affects the phosphorylation of ERK and CREB in response to antipsychotic drugs. Furthermore, these results demonstrate that different antipsychotic drugs could lead to different profiles of ERK and CREB phosphorylation in neurons.

Eye movement desensitization and reprocessing (EMDR) has emerged as a promising new treatment for trauma and other anxiety-based disorders. However, the neurobiological mechanism of EMDR has not been well understood. This study reports changes in the resting regional cerebral blood flow after successful EMDR treatment in two patients with posttraumatic stress disorder (PTSD). Brain 99mTc-ECD-SPECT (Technetium 99m–ethyl cysteinate dimmer–single photon emission computerized tomography) was performed before and after EMDR, and, in addition, a pre- and posttreatment comparison was made with 10 non-PTSD participants as a control group. After EMDR, cerebral perfusion increased in bilateral dorsolateral prefrontal cortex and decreased in the temporal association cortex. The differences between participants and normal controls also decreased. Changes appeared mainly in the limbic area and the prefrontal cortex. These results are in line with current understanding of neurobiology of PTSD. EMDR treatment appears to reverse the functional imbalance between the limbic area and the prefrontal cortex.