To provide a comprehensive review and evaluation of the literature pertaining to the psychiatric sequelae of deep brain stimulation (DBS) of the subthalamic nucleus (STN) in patients with Parkinson’s disease (PD).

A structured search of the EMBASE, PsychINFO and MEDLINE databases was performed on articles published since the first use of STN DBS in 1993 for PD until March 2007. Non-human studies were excluded, along with studies reporting on unilateral DBS and studies reporting on the use of STN DBS for indications other than idiopathic PD. Ninety-seven articles were selected for inclusion in the review.

Patients with advanced PD have a high rate of psychiatric morbidity. STN DBS has been shown to be an effective treatment for the control of motor symptoms in advanced PD. Neurobehavioural side-effects are, however, relatively common following STN DBS. Side-effects include impaired executive function and verbal fluency, depression, hypomania, apathy, postoperative delirium, anxiety disorders and psychotic symptoms, especially hallucinations. The alteration in dopaminergic medication following surgery as well as the direct effect of STN stimulation both appear to contribute to the short-term and long-term postoperative psychiatric complications. Methodological issues that limit the applicability of the current literature in this field are highlighted.

STN DBS is an effective treatment for the motor symptoms of advanced PD. However, further research is needed to assess the extent to which STN DBS contributes to or exacerbates psychiatric morbidity over and above that associated with advanced PD. Careful neuropsychiatric evaluation and monitoring are required in this patient group.

To evaluate the absence and size of massa intermedia (MI), a midline thalamic structure, and its gender-specific alteration in patients with schizophrenia and bipolar disorder.

Thirty-five patients with schizophrenia (17 females and 18 males), 21 patients with bipolar disorder (15 females and 6 males) and 89 healthy controls (50 females and 39 males) were evaluated by magnetic resonance imaging. Thin-slice magnetic resonance images of the brain were evaluated. MI was determined in coronal and sagittal images, and area of the MI was measured on the sagittal plane.

Females had a significantly lower incidence of absent MI compared with males in the healthy control group. The absence of MI in schizophrenia and bipolar patients was not higher than the incidence in healthy controls. The size of MI showed a gender difference. The mean MI area size was smaller in female schizophrenia patients than in female controls, while no significant difference was observed between male schizophrenia patients and their controls.

The size of MI, a gender difference midline structure, is smaller in females with schizophrenia, and the results of this study support other studies of structural aberration of the thalamus and other midline structures in the brains of patients with schizophrenia.

Previous studies have suggested that antidepressant treatment of depression may potentiate dopamine transmission through increased sensitivity of postsynaptic D2 receptors.

D2 receptor function was assessed in 24 patients with major depression before and 16 patients after 16 weeks of treatment with cognitive behavioural therapy (CBT) using a challenge with a selective D2 antagonist, sulpiride. Four hundred milligrams of sulpiride was administered orally on two test days and response was measured by the change in prolactin levels and changes in self-rating scale measures of mood, anxiety and pleasure.

The prolactin response to sulpiride (as measured by the maximum prolactin level) was significantly increased after CBT (z = −2.792, p = 0.005). Sulpiride resulted in an improvement on mood ratings on both test days, but after CBT, this effect was significantly diminished as measured by the Profile of Mood States score (t = −2.27, p = 0.038).

After 16 weeks of CBT, we detected an enhanced prolactin response to sulpiride, suggesting an increased sensitivity of D2 receptor functioning.

Psychopathological, neuropsychological and genetic findings indicate an association between ASD Spectrum Disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD). The goal of this study was to compare the neuropsychological profiles of attention functions in children with ADHD and with ASD and without comorbid ADHD. The hypothesis was that either ADHD and autistic children with comorbid ADHD symptoms were more impaired in inhibition and sustained attention performance and that all individuals with ASD show more deficits in divided attention.

Children aged 6 to 18 years old with ADHD (n = 30) or ASD with (n = 21) and without comorbid ADHD (n = 20) and 30 healthy children were included consecutively. Psychopathology was evaluated using the KIDDIE-SADS and symptom checklists for ADHD and ASD according to DSM-IV. Assessed neuropsychological functioning included inhibition, sustained as well as divided attention and alertness tasks.

Age and IQ-corrected z-scores were used. Statistically significant group effects were found for the variables sustained attention median (F = 3.2, = .02), hits (F = 3.3, p = .02) and false alarms (F = 3.9, p = .01), divided attention hits (F = 3.3, p = .02), errors (F = 3.1, p = .03) and false alarms (F = 3.3, p = .03) and alertness false alarms (F = 2.9, p = .04). Pearson Correlations revealed associations between ADHD symptoms and sustained attention in the ADHD group and between ADHD symptoms and inhibition in the ASD+ group.

Our hypothesis was partly confirmed as ADHD children showed more deficits in sustained attention and ASD children in divided attention tasks. However there was no evidence that children with ASD and comorbid ADHD symptoms have a specific profile in comparison to pure ASD children.