The role of the antihypertensive therapy in preventing vascular cognitive disorders in elderly persons without a history of stroke is a matter of debate. This review focuses on cognitive disorders in elderly hypertensive patients.

Relevant papers were identified by searches in PubMed from 1946 until February 2007 using the keywords ‘cerebral blood flow autoregulation’, ‘vascular cognitive disorders’, ‘neuroimaging in hypertension’, ‘antihypertensive treatment’ and ‘neuroprotection in cerebral ischemia’.

Excessive blood pressure lowering in patients with long-standing hypertension may increase the risk of cerebral hypoperfusion, white matter lesions and consequent cognitive decline. White matter lesions have been found in the majority of patients with long-standing hypertension. They correlate with vascular cognitive disorders, particularly impairments of attention and executive function, while memory is relatively preserved. Cerebral small vessel disease in elderly patients should be taken into account when antihypertensive treatment is considered. Renin–angiotensin blockade, some calcium channel blockers and statins are thought to possess neuroprotective action.

For prevention of cerebral hypoperfusion in elderly hypertensives blood pressure lowering should be cautiously controlled. The increased risk of white matter lesions is an indication for early neuroprotection. The combination of renin–angiotensin blockade or calcium channel blockers with statins may become a promising preventive strategy against cognitive decline in elderly hypertensives. Cerebral white matter protection is a future challenge.

Emotion perception may be impaired after stroke. No study on emotion perception after stroke has taken the influence of post-stroke depressive symptoms into account, although depressive symptoms themselves may hamper emotion perception.

To compare the perception of emotional facial expressions in stroke patients with and without depressive symptoms.

Twenty-two stroke patients participated whose depressive symptoms were classified using the Montgomery-Åsberg Depression Rating Scale (cutoff = 10) and who were compared with healthy controls. Emotion recognition was measured using morphed images of facial expressions.

Patients with depressive symptoms performed worse than controls on all emotions; patients without depressive symptoms performed at control level. Patients with depressive symptoms were less sensitive to the emotions anger, happiness and sadness compared with patients without depressive symptoms.

Post-stroke depressive symptoms impair emotion perception. This extends findings in bipolar disorder indicating that emotion perception deficits are strongly related to the level of depression.

Pain perception is reported to be altered in patients with depression and schizophrenia. However, few studies have investigated the pain perception in patients with bipolar disorders. We therefore aimed to compare pain sensitivity between patients with bipolar disorder, schizophrenia and controls.

Study groups consisted of 30 patients with bipolar disorder, and control groups consisted of 27 patients with schizophrenia and 59 healthy subjects. Pain perception was assessed with cold pressor test (CPT) by exposure to ice-water.

Patients with schizophrenia had significantly higher pain thresholds (PTh) than patients with bipolar disorder. There were no differences between the PTh of patients with schizophrenia and healthy control subjects. However, patients with bipolar disorder had significantly lower pain tolerance (PT) in the CPT than patients with schizophrenia and corresponding healthy control subjects.

The higher PTh in the schizophrenia group compared with the bipolar group found in this study supports further investigation of a potential difference in the pain perception between patients with schizophrenia and bipolar disorder. Theoretical implications of these findings and possible relevant behavioural and neurochemical mechanisms are discussed.

The purpose of present study was to evaluate the efficacy of the addition of reboxetine in patients that had not previously responded, or had done so only partially, over 6 weeks of conventional pharmacological treatment with venlafaxine.

This open-label, prospective and multicentric study included 40 outpatients diagnosed with major depressive disorder according to the DSM-IV criteria. Efficacy was assessed using the 21-item Hamilton Depression Rating Scale (HAMD) and the Clinical Global Impression-Improvement (CGI-I). Safety was evaluated by recording spontaneously reported adverse events. Data were analysed on an intent-to-treat basis, using the last-observation-carried-forward method.

Mean HAMD reduction was 34.9% (P < 0.0001). The percentages of responders (≥50% reduction in HAMD) and patients considered as benefiting from complete remission (HAMD ≤ 10 points) at week 6 were 27.5 and 12.5%, respectively. By the end of the treatment, the score of CGI-I decreased 24.8% (P < 0.0001). Percentage of patient improving (CGI < 4 points) was 47.5%. The most common non-serious adverse events were constipation, nervousness, anxiety and insomnia.

These findings suggest that the combined treatment of reboxetine and venlafaxine, in venlafaxine-resistant patients, may be an effective and well-tolerated strategy.

Heroin dependence is a serious illness associated with an increased risk of suicidal behaviour. There are many risk factors associated with heroin dependence. The current study examined the sociodemographic and clinical characteristics of a number of young adult heroin-dependent patients who had attempted suicide.

We studied a group of 108 young adult heroin-dependent patients in our in-patient clinics. All diagnoses were made according to DSM-IV diagnostic criteria using the Structured Clinical Interview for DSM-IV Axis I-II Disorders (SCID-I, II). The age range of patients was 18–24 years. Their substance abuse histories were assessed by semistructured interview. The Addiction Severity Index (ASI) was administered to all the patients. Serum total cholesterol and high-density lipoprotein cholesterol (HDL-C) levels were routinely measured. In the statistical analyses, Student’s t test, and chi-squared tests were applied.

Of the 108 heroin-dependent patients, 40 (37.0%) had histories of attempted suicide. There was a statistically significant difference in the age at which heroin use had commenced between female attempters [mean = 16.82, standard deviation (SD) = 3.06] and nonattempters (mean = 18.32, SD = 2.68, t= 2.25, P < 0.05). Both the male (mean = 33.35, SD = 4.05) and the female (mean = 28.00, SD = 5.36) attempters had significantly higher ASI scores than did the male (mean = 20.16, SD = 3.80) and the female (mean = 18.88, SD = 4.14) nonattempters (t= 14.34, P < 0.001; t= 5.25, P < 0.001, respectively). A significant difference in total cholesterol (mean = 131.8, SD = 19.3; mean = 172.2, SD = 21.3, t= 3.9, P < 0.05) and HDL-C (mean = 30.9, SD = 1.0 and mean = 54.8, SD = 13.7; t= 5.1, P < 0.05) levels between the group of violent and nonviolent suicide attempters was revealed.

These results suggest that suicide attempts in young adult heroin-dependent patients are associated with more profound biopsychosocial pathology and decreased serum cholesterol levels. In particular, low levels of total cholesterol and HDL-C might indeed be associated with violent suicide attempts in young heroin-dependent patients.

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.

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.