Seasonal depressive disorder: a controlled study in Tunisian psychiatric sample

Seasonal affective disorder is considered as a clinical subtype of major depression. The criteria for seasonal pattern has been recently described in the international classification of mental disorders. The aim of this study was to compare the clinical characteristics of patients with major depression and with a seasonal and a non seasonal pattern. The study was conducted at the psychiatric ward at Monastir university hospital. 16 inpatients with major depression and seasonal pattern, diagnosed with DSM-IV criteria, were matched in age, sex and diagnostic sub-type to 32 inpatients with non seasonal mood disorders. Clinical symptoms and short term course during the most recent depressive episode were obtained. The onset of the depression with seasonal pattern was frequently in winter. It was marked by significantly higher rates of anxiety. The patients with seasonal depression had significantly higher rates of dysphoria, atypical vegetative symptomatology and lower rates of psychotic characteristics and suicidal thoughts. No differences were found as to the psychiatric family histories or the age at the first depressive episode. This study could focus of the novel psychiatric entity and may lead to the development of the genetic and neurobiologic research related to seasonal affective disorder.     

Pharmacological modulation of the effects induced by ketamine at subanesthetic doses]

The similarity between ketamine effects and endogenous psychoses has created interest in the capacity of antipsychotic medications to block ketamine effects. In healthy subjects, a sub-anaesthetic single dose of lorazepam, typical neuroleptics, such as haloperidol, and atypical neuroleptics, such as clozapine and olanzapine, failed to block ketamine-induced positive and negative symptoms resembling schizophrenia. However, haloperidol is able to decrease ketamine-induced impairment in executive cognitive functions. Recently, lamotrigine reduced ketamine-induced psychotic symptoms, perceptual alterations, and cognitive impairments. In schizophrenic subjects, single doses of olanzapine do not decrease the effects of ketamine. However, long term treatment with clozapine has been reported to decrease ketamine-induced positive symptoms. Pharmacological modulation of the effects of NMDA receptor antagonists, such as ketamine, may lead to development of novel therapeutic agents for psychiatric illnesses such as schizophrenia.     

Theory of Mind and social reserve: Alternative hypothesis of progressive Theory of Mind decay during different stages of Alzheimer’s disease

Although Theory of Mind (ToM) is thought to be impaired in Alzheimer’s disease (AD), it remains unclear whether this impairment is linked to the level of task complexity, the heterogeneity of the studied patients, or the implication of executive dysfunctions. To elucidate this point, 42 AD patients, divided into two subgroups [moderate AD (mAD) patients (n = 19) and early AD (eAD) patients (n = 23)], and 23 matched healthy older subjects (HO) were enrolled. All participants were given (1) a false-belief task (cognitive ToM), (2) a revised version of the “Reading the Mind in the Eyes” test (affective ToM), and (3) a composite task designed to assess ToM abilities with minimal cognitive demands. Participants were also given executive tasks assessing inhibition, shifting, and updating processes. We observed a significant impairment of cognitive and composite ToM abilities in eAD patients compared with mAD patients. There was no impairment of affective ToM. Stepwise regression revealed that measures of global efficiency and executive functions (EFs) were the best predictors of progressive decay of ToM scores. These results indicate that cognitive aspects of ToM are more sensitive to AD progression than affective tasks. They also show that ToM abilities are more affected by dementia severity than by task complexity. One explanation of our results is the presence of compensatory mechanisms (social reserve) in AD.     

Effects of sub-chronic exposure to cadmium on some parameters of calcium and iodine metabolisms in the Shaw's jird Meriones shawi

In the present work we determined effects of a sub-chronic exposure to cadmium on some parameters of calcium and iodine metabolisms in Meriones shawi, a desert rodent species occupying the arid steppes of Tunisia and other countries. Fourteen jirds of both sex were equally divided into a control group receiving diet without cadmium and a treated group receiving cadmium in the diet during 30, 45, 60 and 90 days. At the end of each period, 5 jirds from each group were sacrificed. In cadmium-treated group, cadmium accumulation and total metallothioneins synthesis in the liver and kidneys were high and dependant on the duration of treatment. Cadmium caused significant modifications in the body weight and in the relative weights of the liver, femur and thyroids, in parallel to a decrease in calcium content in serum and in femur. Cadmium also decreased iodine content in serum and in the thyroids. Several impairments were dependant on the duration of exposure and were more pronounced at the end of the experiment. In conclusion, a sub-chronic exposure to cadmium induces perturbations in calcium and iodine metabolisms in Meriones shawi. However, effects on calcium seem to be more evident. We can conclude also that Meriones shawi is an indicator of cadmium presence in arid environments.     

Hyperhomocysteinemia and schizophrenia: case control study

Objectives

Homocysteine (Hcys) is a sulphur-containing amino acid that has been widely investigated for its putative role in neuropsychiatric disorders. Elevated plasma homocysteine levels have been associated with schizophrenia. Among other factors, low folate and vitamin B12 levels have been implicated in the increase in homocysteine. The aim of the study was to determine plasma Hcys, folate and vitamin B12, and the frequency and severity of hyperhomocysteinemia in patients with schizophrenia, and to investigate the association between Hcys and clinical features and its relationship with folate and vitamin B12 levels.

Methods

This was a case-control study carried out on 61 (54 males and seven females, mean age = 33.3 ± 9.2) inpatients with chronic schizophrenia according to DSM-IV criteria and 46 (25 males and 21 females, mean age = 45.9 ± 14.2) healthy controls. Most of patients (90.2%) were treated by first generation antipsychotics with a mean daily dosage of 401.6 mg chlorpromazine equivalents. Total homocysteine serum levels were determined quantitatively by fluorescence-polarization immunoassay (FPIA) with an AxSYM analyzer™ (Abbott). Quantitative vitamin B12 and folate serum levels were measured with an Elecsys 2010 analyzer™ (Roche Diagnostics). Differences between patients and controls were examined using a two-way Ancova with gender and diagnosis as independent variables, adjusting for age.

Results

Patients with schizophrenia showed higher plasma Hycs and lower plasma folate than controls (mean = 16.1 μmol/L in patients versus 10.9 μmol/L in controls; P = 0.028 for Hycs and 4.2 μg/L in patients versus 8.2 μg/L in controls; P < 0.001 for folate). Patients and controls did not differ in vitamin B12 levels. Both male and female patients had increased plasma Hcys compared to controls. Hyperhomocysteinemia (Hcys levels > 15 μmol/L) was present in 34.4% of the patients versus 15.2% in controls. The prevalence of moderate hyperhomocysteinemia (Hcys levels: 15–29 μmo/L) was 26.2% and that of intermediate hyperhomocysteinemia (Hcys levels: 30–100 μmol/L) was 8.2%. In patients with schizophrenia, plasma Hcys was not correlated with age (r = 0.07; P = 0.56), duration of illness (r = –0.04; P = 0.78) and did not differ with gender and clinical sub-types. Moreover, plasma Hcys was higher in patients without family history of psychiatric disorders (19.2 μmol/L) versus 12.7 μmol/L in patients with family history of psychiatric disorders (P = 0.032). Concerning therapeutic features, plasma Hcys did not differ with type of antipsychotic and was not related to daily dosage of antipsychotics. A negative correlation was found between plasma Hcys and vitamin B12 levels (r = –0.26; P = 0.04).

Conclusion

These results confirm an increase of Hcys levels in schizophrenic patients and suggest that it is associated with absence of family history of psychiatric disorders and with low vitamin B12 levels. Hyperhomocyteinemia could be related to the pathophysiology of aspects of this illness. Homocysteine should be considered as a factor to consider in monitoring and management of patients with schizophrenia.     

Altered antioxidant defense system in clinically stable patients with schizophrenia and their unaffected siblings

Objective

To determine Red Blood Cell (RBC) antioxidant enzyme activities and plasma Thiobarbituric Acid Reactive Substances (TBARS) in clinically stable patients with schizophrenia and their unaffected siblings.

Methods

A case-control study carried out on three groups: 60 schizophrenic patients treated with neuroleptics, 33 of their unaffected siblings and 30 healthy controls with no family psychiatric history. Biological markers were measured on fasting patients after a period of tobacco abstinence: RBC antioxidant enzyme activities – superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) – by spectrophotometry and plasma levels of TBARS by spectrofluorimetry.

Results

RBC SOD and CAT activities were significantly lower in schizophrenic patients and their unaffected siblings compared to the control group (P < 0.001). Schizophrenic patients also had significantly lower RBC GSH-Px activity than controls (P = 0.03), whereas their unaffected siblings had significantly higher RBC GSH-Px activity than controls (P = 0.04). Plasma TBARS were higher in schizophrenic patients than their unaffected siblings: 2.1 ± 0.8 μmol/l vs. 1.7 ± 0.6 μmol/l (P = 0.06).

Conclusions

Our results showed a decrease in antioxidant enzyme activities and an increase in lipid peroxidation confirming the existence of oxidative stress in schizophrenic patients treated with neuroleptics. Additionally, this suggests that the increase in GSH-Px activity in unaffected siblings would be a protective mechanism against oxidative stress and damage. Other studies are necessary to confirm these findings.