This study aimed to test the validity of the 21-item Depression Anxiety Stress Scales (DASS-21) as a routine clinical outcome measure in the private in-patient setting. We hypothesized that it would be a suitable routine outcome instrument in this setting.

All in-patients treated at a private psychiatric hospital over a period of 24 months were included in the study. Data were collected on demographics, service utilization, diagnosis and a set of four routine measures both at admission and discharge. These measures consisted of the Clinical Global Impressions (CGI) scales, Health of the Nation Outcome Scales (HoNOS), the Mental Health Questionnaire (MHQ-14) and DASS-21. The results of these measures were compared.

Of 786 admissions in total, the number of fully completed (ie paired admission and discharge) data sets for the DASS-21 depression, anxiety and stress subscales were 337, 328 and 347, respectively. All subscales showed statistically significant reductions in mean scores from admission to discharge (P < 0.001) and were significantly correlated with all MHQ-14 subscales and significantly related to CGI scale categories. The total DASS-21 and total HoNOS scores were also significantly correlated.

The findings from the present study support the validity of DASS-21 as a routine clinical outcome measure in the private in-patient setting.

The tryptophan metabolite kynurenic acid (KYNA) is an endogenous glutamate/nicotinic receptor antagonist. Previous studies have shown that the concentration of the compound is increased in cerebrospinal fluid (CSF) of patients with schizophrenia. Furthermore, it has been found that the CSF concentration of KYNA is positively correlated to CSF concentrations of the monoamine metabolites homovanillic acid (HVA) and 5-hydroxy indoleacetic acid (5-HIAA) in healthy control subjects.

To study the correlations between KYNA and the monoamine metabolites HVA, 5-HIAA and 4-hydroxy-3-methoxyphenylglycol (HMPG) in CSF of male patients (n= 53, ranging from 20 to 48 years of age) with verified schizophrenia.

CSF was obtained by lumbar puncture, and KYNA analysis was performed with an isocratic reversed-phase high-performance liquid chromatography system connected to a fluorescence detector. HVA, 5-HIAA and HMPG concentrations were measured by mass fragmentography with deuterium-labelled internal standards.

Positive intercorrelations were found between CSF KYNA, HVA and 5-HIAA, while CSF content of HMPG did not correlate to KYNA or any of the monoamine metabolites in CSF.

The results of this study suggest that increased KYNA formation is associated with an increased dopamine and serotonin turnover in male patients with schizophrenia.

Previous studies have suggested that somatoform disorders (SFD) might be associated with changes in the function of the central and autonomic nervous systems. The aim of this study was to examine the possible immunological differences between SFD and healthy controls.

Twenty-four patients with SFD and 13 healthy individuals completed the psychological questionnaires to assess symptom reporting [Symptom Checklist-90 Revised (SCL-90-R)] and to diagnose for SFD [Screening for Somatoform Symptoms scale (SOMS-scale)]. Participants also provided a blood sample taken in the morning, which was analysed with an automated cell counter to determine the number of leucocytes per μl and with flow cytometry to determine lymphocyte subsets.

With the exception of a higher T4/T8 ratio in the patient group, which was mainly because of lower CD8 counts, there were no significant differences in the absolute number of lymphocytes (subsets) between patients with SFD and healthy subjects. A positive correlation between B-lymphocyte subsets (CD19+CD22+, CD19+CD5+, CD19+CD3−) to all scales of the SCL-90-R, except somatisation, were found in SFD. Additionally, a positive correlation was found in SFD between CD14+CD16+ monocytes and somatisation (0.573) on the SCL-90-R scale.

These data indicate that patients with SFD have an enhanced humoral immunity as shown by increased B-cell numbers and furthermore an elevated T4/T8 ratio because of lower CD8 suppressor cells. Further studies will be required to determine whether these alterations in lymphocyte subsets are directly involved in the pathophysiology of SFD.

The present trial was designed to investigate the influence of repetitive transcranial magnetic stimulation (rTMS) on negative schizophrenic symptoms using high-frequency stimulation of the left dorsolateral prefrontal cortex in a simple blind randomized design.

The study was carried out on a 42-year-old patient with schizophrenia (paranoid subtype) with prominent negative symptoms who was first treated with sham rTMS during the first 3 weeks and then with real high frequency during the following 3 weeks. He was rated before and after the sham and after the real rTMS therapy for positive, negative and depressive symptoms.

rTMS was superior to sham treatment in reduction of negative and depressive symptoms.

High-frequency rTMS applied over the left dorsolateral prefrontal cortex led to a reduction of severity of negative symptoms in a patient with chronic schizophrenia and may be beneficial as an augmentation option to antipsychotics in the treatment of negative symptoms of schizophrenia.

There has been a long interest in the relationship between folate and depression.

In this paper, we report baseline measures of red cell folate that were collected during a randomized trial of 107 patients with major depression. Red cell folate levels were examined for association with percentage improvement in depressive symptoms during treatment with fluoxetine or nortriptyline. The influences of possible confounding factors were assessed.

The low red cell folate group (defined in relation to the median) had a significantly poorer response to nortriptyline. This effect of red cell folate levels was not present in those treated with fluoxetine. No relationships were found between red cell folate levels and possible confounding factors of age, nutritional status, alcohol history, depression subtype, depression severity and chronicity of depression.

Response to nortriptyline was affected by red cell folate status. It may, therefore, be beneficial to consider folate augmentation in patients with major depression, particularly if treated with nortriptyline.

Déjà vu occurs both in normal experience and as a neuropsychiatric symptom. Its pathogenesis is partially understood. We describe an iatrogenic case with implications for the neuropharmacological basis of déjà vu.

A 42-year-old woman received 5-hydroxytryptophan, in combination with carbidopa, as treatment for palatal tremor, on two occasions, separated by 1 week. On each occasion, she experienced intense, protracted déjà vu, lasting for several hours. We discuss her case in relation to the neuroanatomical and neuropharmacological basis of déjà vu.

The serotonergic system is involved in the genesis of déjà vu.

Hallervorden-Spatz syndrome is characterized by pyramidal and extrapyramidal signs, and dysarthria and dementia. Psychiatric symptomatology can emerge in the course of the disorder. Mutations in the pantothenate kinase 2 gene have been found in many cases. We report a case with psychosis as sole presenting symptom.

A 41-year-old man presented with change in behavior and paranoid delusional ideation. Six months later, spasticity, extrapyramidal rigidity and dysarthria were added to the picture. Eventually, the patient became mute and wheel-chair bound. The brain magnetic resonance imaging (MRI) was consistent with iron depositions in the globus pallidus and substantia nigra.

In this case, the combination of clinical and MRI findings was consistent with Hallervorden-Spatz syndrome. The combination of psychiatric and MRI findings should lead to further neurological investigation.

Deep brain stimulation (DBS) of the subthalamic nuclei (STN) can result in depression despite the obvious motor improvement.

Two patients with serious life-threatening depressive episodes are described. In the first case, the trigger for depression was a slight adjustment of the left stimulating electrode’s contact. In the second case, reducing both the dopaminergic therapy and the voltage of DBS resulted in the manifestation of depressive symptoms.

DBS-induced depression possibly has pathogenetic differences from ordinary Parkinson’s disease depression. The STN region seems to be a sensitive zone that influences emotions.

We describe the presentation of a young woman with long-standing complex partial seizures with occasional secondary generalization, who presented with complex visual hallucinations (CVHs) and delusions.

Routine biological workup including magnetic resonance imaging revealed an area of significant left-sided occipital gliosis. Video telemetry monitoring revealed a left occipital focus for the origin of the electrographic seizure discharge.

CVHs occur in a range of organic states, including epilepsy, and can be understood in terms of the underpinning neuroanatomy and neurotransmitter systems of the visual system.

To observe spike activity in electroencephalograms (EEGs), patients with symptomatic partial epilepsy are rarely monitored during the hyperventilation stages.

A 38-year-old woman suffered from a ruptured arteriovenous malformation in the left temporal lobe. One and a half years later, the patient experienced her first generalized convulsion. EEG showed small spikes in the posterior of the left temporal lobe, which was observed during the hyperventilation and posthyperventilation stages. Because the location of the spikes correlated with the site of the lesion as observed from radiographic findings, she was diagnosed with lateral temporal lobe epilepsy. Drug treatment resulted in no further convulsive episodes and the patient has since returned to work.

EEG recordings during hyperventilation should be regarded as an effective technique in analyzing epilepsy because of its ease and cost-effectiveness compared with other methods such as single-photon emission computed tomography.