B. Hesselmann

Effects of tryptophan depletion in fully remitted patients with seasonal affective disorder during summer.

BACKGROUND Deficiencies in brain serotonin function are believed to play an important role in the pathophysiology of seasonal affective disorder/winter type (SAD). However, no direct evidence has been reported so far that lowered brain serotonin activity causes the symptoms of SAD. METHODS We studied 11 SAD patients who had suffered recurrent winter depressive episodes of SAD and were fully recovered and off treatment during the summer. In a randomized, balanced, double-blind crossover design patients received two amino acid beverages, one containing tryptophan and the other containing no tryptophan but otherwise identical. Behavioural ratings and plasma total and free tryptophan concentrations were assessed at baseline before administration of the amino acid beverages and at several time points afterwards. RESULTS The tryptophan-free amino acid beverage induced significant decreases of plasma total and free tryptophan levels and both levels increased during sham depletion (condition x time interaction: P < 0.001). Tryptophan depletion, but not sham depletion caused a transient return of depressive symptoms (condition x time interaction: P < 0.001). CONCLUSIONS The present study demonstrates that SAD patients in remission during the summer are vulnerable to a return of depression when depleted of tryptophan. This finding supports the importance of serotonergic mechanisms in the pathophysiology of SAD.

Mirtazapine in seasonal affective disorder (SAD): a preliminary report

Beside light therapy, selective serotonin reuptake inhibitors (SSRI) are the recommended treatment for patients suffering from Seasonal Affective Disorder (SAD). They seem to particularly resolve the atypical symptoms of SAD, while tricyclic antidepressants tend to worsen them. The latter has been linked to the broader spectrum of neurotransmitter modulation tricyclics enfold. Mirtazapine is a novel antidepressant providing a broad spectrum of neurotransmitter modulation on a basis of high selectivity. In order to evaluate the antidepressant efficacy of mirtazapine in the treatment of SAD, eight depressed and drug‐naive SAD patients entered a 4 week drug surveillance and received 30 mg of mirtazapine per day. Clinical response was assessed using the Structured Interview Guide for the Hamilton Depression Rating Scale, Seasonal Affective Disorder Version (SIGH‐SAD). Our preliminary results show that mirtazapine was not only well tolerated by the patients but also efficacious in the treatment of SAD. Copyright

IBZM-SPECT imaging of dopamine D2 receptors with typical and atypical antipsychotics

Considerable progress has been achieved over the past 15 years in uncovering the biological basis of major psychiatric disorders. Since psychopharmacological treatment is thought tc act on the underlying biological basis of the disease, brain imaging techniques enable us to understand the mechanism of action of such compounds. One important tool used to determine patterns of brain dysfunction and how psychopharmacological agents such as antipsychotic compounds work is single-photon emission computerised tomography (SPECT). This technique allows determination of striatal D(2) receptor occupancy rates, which are associated with the extrapyramidal side effects (EPS) of antipsychotic drugs. Studies have confirmed that atypical antipsychotic agents have lower occupancy rates than typical agents. No association has been found between D(2) receptor occupancy rates n the striatum and antipsychotic efficacy, and it therefore appears that striatal D(2) receptor occupancy rates are not necessary for the antipsychotic effect of such agents in schizophrenia. The availability of more refined radioligands will help us not only to understand the action of antipsychotics but also the pathophysiology of schizophrenia.