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Re: neuroleptics+depression..(and apathy) linkadge

Posted by Jay on October 20, 2006, at 15:42:44

In reply to Re: neuroleptics+depression, posted by linkadge on October 20, 2006, at 12:58:13

Well, I am *no* chemist, or claim to have ANY advanced knowledge about meds and such. Like many of us, I just like to investigate medications for their possible use....believing hope is eternal.(It is...)

All atypical antipsychotics will not just make "..you sit on the couch and watch TV all day." and "feel less guilty about it." Just adding my personal experience (5+ years of AP use), Zyprexa + AD's can make for good sleep and for a nice day with a "calm" attitude. How? I of course don't know exactly. But I think it has to do with both down AND up regulation, a bit like Abilify, but not to the same degree. Zyprexa is shown to increase concentrations of Dopamine in certain parts of the brain. Risperdal works a bit on the serotonin system which seems to help with sleep. Right now I take a combo of Zyprexa and Risperdal, (plus AD's and MS's), and I function quite well. What I mean by that is that I still get upset over things I should, and I still get a bit angry, or tired, or sad, when I should. But it doesn't mean my whole world is falling apart like it did before medications! Man, THE WAY SOME PEOPLE POST FRIGHTENING STORIES really proves to me that, many people possibly don't, or haven't tried enough or a large enough combination of meds. If you think you have, I will challenge anyone to compare lists with me. :-)The following articles focus more on then just depression, but on the concept of apathy as suggested by Link. Here are a couple of articles I just had a bit of time, to paste.

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http://snipurl.com/zyw7

Efficacy of atypical antipsychotics in depressive syndromes.

Lilly France, 13 rue Pages, 92158 Suresnes cedex, France. quintin_philippe@lilly.com Quintin P,
Thomas P.


Depression is a frequent symptom in psychiatry, either isolated (major depression) or entangled with other psychiatric symptoms (psychotic depression, depression of bipolar disorders). Many antidepressant drugs are available with different pharmacological profiles from different classes: tricyclic antidepressants, monoamine oxydase inhibitors, selective serotonin reuptake inhibitors (SSRI). However, there are some limitations with these drugs because there is a long delay before relief for symptoms, some patients with major depression are resistant to treatment, there is a risk to induce manic symptoms in patients with bipolar disorders and these drugs have no effect on the psychotic symptoms frequently associated to major depression. The leading hypothesis for the search of more efficient new antidepressants has been the amine deficit hypothesis: noradrenaline and/or serotonin deficit and more recently dopamine deficit. Moreover, a dopamine deficit has been also hypothesized as the central mechanism explaining the negative symptoms of schizophrenia. These symptoms are the consequence of a deficit of normal behaviours and include affective flattening, alogia, apathy, avolition and social withdrawal. There is thus a great overlap between symptoms of depression and negative symptoms of schizophrenia. Atypical antipsychotics, in contrast with conventional neuroleptics, have been shown to decrease negative symptoms, most probably through the release of dopamine in prefrontal cortex, thus improving psychomotor activity, motivation, pleasure, appetite, etc. The dopamine deficit in cortical prefrontal areas was thus an unifying hypothesis to explain both some symptoms of depression and negative symptoms of schizophrenia. Studies in animal confirm this view and show that the association of an atypical antipsychotic drug and an SSRI (olanzapine plus fluoxetine) increases synergistically the release of dopamine in prefrontal areas. Moreover, most of the atypical antipsychotics have a large action spectrum, beyond the only dopamine receptors: their effects on the serotonin receptors--particularly the 5-HT2A and 5-HT2C receptors--suggest that their association to SSRI could be a promising treatment for depression. Indeed, SSRI act mainly by increasing the serotonin level in the synapse, thus leading to a non specific activation of all pre- and post-synaptic serotonin receptors. Among them, 5-HT2A/2C receptors have been involved in some of the unwanted effects of SSRI: agitation, anxiety, insomnia, sexual disorders, etc. The inhibition of these receptors could be thus beneficial for patients treated with SSRI. Amisulpride is an unique atypical antipsychotic that selectively blocks dopamine receptors presynaptically in the frontal cortex, possibly enhancing dopaminergic transmission. The antidepressant effect of amisulpride was shown in dysthymia in many clinical studies versus placebo, tricyclic antidepressants, SSRI or others. However, a shorter delay for symptom relief was not demonstrated for amisulpride as compared to comparative antidepressants. Other atypical antipsychotics (clozapine, olanzapine), which act on a large variety of receptors, have shown antidepressant effects--mainly in association with SSRI--in different psychiatric diseases: treatment-resistant major depression, major depression with psychotic symptoms and depression of bipolar disorders, with no increase of manic symptoms in this latter case. Moreover, the delay for symptom relief was greatly shortened. More comparative double-blind studies are required to confirm and to precise the antidepressant effects of atypical antipsychotics. Nevertheless, these studies suggest that atypical anti-psychotics could be of great value in depressive conditions reputed for their resistance to treatment with usual antidepressants. Particularly, new strategies emerge that combine atypical antipsychotics and antidepressants for greater efficacy and more rapid relief of depression symptoms.

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http://snipurl.com/zywb

1: J Neuropsychiatry Clin Neurosci. 2005 Winter;17(1):7-19.

Apathy: why care?
van Reekum R,
Stuss DT,
Ostrander L.
Department of Psychiatry and Kunin-Lunenfeld Applied Reserch Unit, Baycrest Centre for Geriatric Care, University of Toronto, 3560 Bathurst St., Toronto, Ontario, M6A 2E1, Canada. rvanreekum@baycrest.org

This review presents data showing that apathy is common across a number of disorders. Apathy is not only common, but is also associated with significant problems: reduced functional level, decreased response to treatment, poor illness outcome, caregiver distress, and chronicity. Preliminary evidence of treatment efficacy exists for dopaminergic drugs and for amphetamines. *Strong evidence of efficacy exists for acetylcholinesterase inhibitors in Alzheimer's disease, and for atypical antipsychotics in schizophrenia*. Frontal-subcortical system(s) dysfunction is implicated in the causation of apathy; apathy subtypes based on the various frontal-subcortical loops may thus exist. Further research involving diagnosis, pathophysiology, and treatment is suggested.

-----
Jay


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poster:Jay thread:696107
URL: http://www.dr-bob.org/babble/20061020/msgs/696330.html