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atypical antipsychotic & depression

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I was wondering if atypical antipsychotics are commonly used in the treatment of depression?

My pdoc just recently put me on 200mg of amisulpride (Solian), next to Effexor XR 225mg and Remeron 30mg.

If have severe depression and anxiety and these last few weeks I've been sort of hypersensitive. Meaning, I can't stand anything, especially noise. It's like my brain refuses to filter any of the stimuli it gets leading to some sort of overload. At the end of the day I'm exhausted and my head feels like it's going to burst.

My pdoc defined it as being "hyper esthetic emotional syndrome". Did any of you hear of it before?

Anywayz, it's just a name ofcourse. By putting me on a neuroleptic, the hypersensitivity and exhaustion should go away. Apart from that, it should have an antidepressive action as well.

Does anyone have experiences with antipsychotics for depression?


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I have never heard of the name/diagnosis he gave you; never heard of the med you've added either! ;) But...it makes sense. I know that my psychiatrist started me on lamictal almost a year ago. It isn't an antipsychotic, but it was designed to be used for bipolar treatment. I am not bipolar, but we've found (as have many) that it works very well to help stabilize my depression, along with my regular AD. I believe that Swede was or is taking an antipsychotic (zyprexa, I think) along with ADs; that may have been prescribed for another condition. It seems like he found that they worked well together.

Hopefully you will get some replies from more experienced members!


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I cannot give you any first hand knowledge, Autumn.

I have fibromyalgia and am sensitive to light, touch and sounds.

HYPERESTHETIC: Marked by abnormal acuteness of sensitivity.
I did find this info that may put some light on the subject. :hearts:

Glad to hear your taking good care.


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Karen & Lindsay,

thanks for your replies. I did some more "research" myself and I found on article on augmentation with an antipsychotic for depression.

Augmentation With Atypical Antipsychotics

by Gordon Parker, M.D., Ph.D.

Psychiatric Times October 2002 Vol. XIX Issue 10


My experience of 15 years in a tertiary referral mood disorders unit has validated many recent studies suggesting that resistance to antidepressant treatment is more common than previously judged or conceded. About four years ago, I commenced testing augmentation of antidepressant drugs with atypical antipsychotics in treatment-resistant subjects and observed dramatically rapid improvement in a percentage of my patients. I have since learned that other psychiatrists have come to a similar conclusion by a similar testing process. This should not be viewed as necessarily challenging the zeitgeist of evidence-based treatment guidelines and consensus statements as the gold standard, but should encourage discussion as to how formalized efficacy data and clinically observed effectiveness data may best complement each other.

I observed two distinct improvement patterns in those patients who responded to the augmenting strategy. The first group of patients described a rapid improvement in mood, often in response to a low-dose atypical (e.g., olanzapine [Zyprexa] 2.5 mg to 5 mg) and generally in close association with restoration of sleep and a reduction in any anxiety symptoms. Improvement in these patients was usually evident in one to three days. Once improvement had occurred and patients were euthymic, the atypical could generally be ceased after another day or two, allowing the antidepressant and/or mood-stabilizing medication as the only necessary maintenance strategy -- at least, until any future episode.

In a second group of subjects, there was a slow and generally incomplete remission. There was a specific augmenting effect, since the patient would usually report a worsening of mood if the atypical was ceased. When the atypical was recommenced, the patient would again generally report partial benefit. In such patients, a higher dose of the atypical was generally required.

I was unable to find any treatment or practice guidelines advocating the use of antipsychotic or neuroleptic drugs for the management of depression, although one review suggested that the older antipsychotic drugs had antidepressant properties. Robertson and Trimble (1982) had evaluated more than 30 double-blind trials of typical antipsychotics, which were generally compared with a tricyclic or irreversible monoamine oxidase inhibitor antidepressant drug. Thus, their review did not consider typical neuroleptics as augmenting agents only as singleton antidepressants in head-to-head comparisons with antidepressant drugs. Their review data indicated that the antipsychotics were just as effective as the antidepressants, appeared comparatively free of side effects and tended to have an earlier onset of action. It is of interest that this antidepressant potential of antipsychotic drugs has been ignored in formal treatment guidelines, perhaps reflecting concerns about side effects of the older antipsychotic drugs, particularly tardive dyskinesia.

My colleague and I elected to write up a case series of two dozen non-psychotically depressed patients treated with an atypical antipsychotic (Parker and Malhi, 2001). However, journal assessors were critical of case series data and judged that only a randomized, controlled treatment study was acceptable. Our paper, in which we described clinical features and considered the possible psychopharmacological rationale for atypicals, was eventually published.

In a case series report, Ostroff and Nelson (1999) described eight non-psychotic responders to a selective serotonin reuptake inhibitor remitting within one week of risperidone (Risperdal) augmentation. In 2001, Shelton et al. reported a controlled study whereby a small number of subjects with recurrent, non-psychotic, treatment-resistant depression were randomly assigned to receive olanzapine alone, fluoxetine (Prozac) alone, or the two drugs in combination. The combination produced significantly greater improvement than either monotherapy strategy over the next eight weeks, with the combination therapy being associated with a very rapid improvement in mood state. This report is the only published randomised, controlled trial examining the impact of augmenting with an atypical antipsychotic and hopefully will encourage studies of other atypical drugs as augmenting agents.

Atypical augmentation is now being built into treatment recommendations and guidelines. While Trivedi and Kleiber (2001) included the theoretical combined use of an antidepressant and an antipsychotic, Fava (2001) noted the positive reports of the combination of an antidepressant and an atypical in reviewing strategies for managing treatment-resistant depression.

Can we add to the story? Perhaps by offering more clinical impressions. Our observations suggest that patients with narrowly defined melancholic depression (particularly when their depression is marked by psychomotor disturbance) are more likely to receive augmenting benefit. Patients with bipolar disorder also appear highly likely to respond. Thus, not only did some of our patients with established bipolar disorder describe "riding a high" out of their depression -- but several patients who had never previously responded did so following atypical initiation. Our patients did not always report this improvement, so clinicians may need to probe for this information. When a severely depressed patient improves rapidly, both the patient and the physician may judge it as a rapid return to an euthymic state and miss features indicative of a "high." In such patients, these "highs" are generally slight and transient, but can be dissected from abrupt euthymia. This might suggest that atypicals act on the putative "switch" mechanism.

In a refined observational study, I treated 10 consecutive patients with treatment-resistant melancholic depression with olanzapine augmentation and monitored improvement over the next week (Parker, 2002). Six patients showed rapid and substantive improvement over that brief interval. This study is informative in that daily ratings of mood, anxiety, insomnia and depression identified differential effects across those parameters. Thus, these six patients showed dramatic improvements in insomnia and anxiety, while their depression improved somewhat more slowly.

Such results raise the possibility that atypicals might be of benefit merely because they restore sleep, but most patients contemplating that possibility with me have generally rejected it on the basis that mood improvement occurs somewhat more slowly than sleep and anxiety benefits.

I began seeking views of other clinicians, expecting few to have tried such an augmentation strategy. The majority of clinicians I consulted also reported positive results using atypicalsas augmenting agents. It has now become quite rare for us to see a treatment-resistant patient at our tertiary referral service who has not been tried on an atypical antipsychotic prior to our assessment.

In the last decade there have been major advances in newer antidepressants. Each advance has emerged after careful evaluation involving controlled studies of large samples and up to a decade in investigation time. Following introduction of each drug, clinicians seek to understand their clinical effectiveness (as against their tested efficacy) and generally develop some gradual understanding about each drug's profile and, more important, the comparative benefits and situations where the drug might be recommended. This is obviously a slow process, respecting the scientific paradigm.

By contrast, the augmentation story overviewed here is extraordinary. We now have atypical antipsychotic drugs -- that lack an indication as either antidepressants or as antidepressant-augmenting drugs -- being widely used by psychiatrists when the published literature comprises only one controlled study and two case series.

Quo vadis? We need to be very cautious in using atypical antipsychotics as either antidepressant drugs (unsupported at the moment) or as augmenting antidepressant agents (the presumptive strategy) until clarification studies accrue. We need to establish that true augmentation occurs and is not merely a reflection of an anxiolytic phenomenon, or there is a risk that these antipsychotics may be used for patients who have a primary anxiety disorder, as occurred with the typical antipsychotic drugs in the past. Even if atypicals are beneficial, we must be aware of both immediate and long-term side effects, which must be respected in cost-benefit decisions. Since we do not know the long-term side effects of these drugs, great caution needs to be exerted, particularly when used on an ongoing basis. We need to establish whether there is an intra-class differential or whether there is a non-specific class augmentation benefit and if there is depression subtype specificity when we hypothesize that melancholic and bipolar depression is preferentially responsive.

My observations suggest that augmentation by an atypical requires a potentially effective antidepressant to be augmented, a situation generally not readily judged in advance. Thus, I have seen patients who failed to benefit from augmentation while receiving an SSRI or a selective norepinephrine reuptake inhibitor but, when the antidepressant drug has been substituted with a TCA or an irreversible MAOI, have shown an almost immediate response. We need to establish if augmentation can be rapidly tapered or ceased in those patients who have returned to a euthymic state and, conversely, those situations that might determine a true need for an ongoing augmenting strategy. Finally and most important, we need to understand the biological rationale for such an augmentation phenomenon, as it may provide us with a greater understanding of the perturbations underpinning bipolar disorder and melancholic depression in particular.

(Dr. Parker is professor of psychiatry at University of New South Wales, Euroa Centre, The Prince of Wales Hospital.)

I guess it makes a little more sense to me now. I hope it'll work. I'm feeling pretty drowsy at the moment. It think it's because of the meds (not sure). The tiredness is annoying at this point really. I've read neuroleptics can cause this somnolence in the beginning. I hope it'll go away soon though.

Amisulpride (Solain) isn't available in the US (it's only marketed in Europe and Australia). That's probably why you've never heard of it before...

Thanks for your help!


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  • 1 year later...

Hi again,

I haven't taken Solian but had two tries with quetiapine. Both times were in combination of other ADs, both times had to stop it because of short term memory loss, ED and agitation. I also felt detached and disoriented at times. I know this log hasn't been active for a while but the topic is great. It would be nice to have a combinent drug therapy topic line. Maybe after I have been around for a while. I have noticed that a lot of us are one more than one psycho-active drug. Newly and currently on three psych meds and am schedule to bump up to a fourth in a month. There are some awesome papers posted here! :hearts: to all the contributors on this page!

Enjoy peace and be safe..... w :mad1::bump::shocked: :shocked: :blush21::tear2::nod::cry:

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Indeed, risperidone did work with me; however, I was stuck on depakote and clonazepam during this time and I was really a zombie. I didn't know for sure what one was making me this way; but, it was way too much for me. I couldn't get anything done and I was passed out cold by 7-8 at night. Not good. I hated it.

During this time I experimented without my doc knowing and gradually went off the clonazepam and then depakote. I just took the risperidone for about 3 days prn. It worked great in just centering everything and I was able to focus more. It was okay; but, I think I would have to use it in conjunction with an AD, maybe the one I am on now, Wellbutrin (great stuff). I was at a place where I couldn't get the risperidone and she tried me on geodone, the lowest dose. It was a little too sedating; but, maybe I would have to get use to it. The thing with risperidone is that I could break the tablet in half and not take the full dose if I didn't need it. Cons about risperidone, it makes you fat. Pros about geodone, it doesn't.

Yeah, weigh the odds, whats more important, treating the disease or dealing with the side effects.



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I have been on the emsam patch for a year and a half it works very well for atypical depression there is a study about 2 years ago from Harvard in there Journal about MAOI's and atypical depression. I tried the MAOI Nardil by mouth it worked very well but I had serious blood pressure problems and had to come off. I was so glad when EMSAM was finally approved, which is a MAOI but in a patch form therby bypassing a lot of the side effects of MAOI's.

You have to follow a lot of dietary restrictions but for great relief it is far worth the price of doing without some food.

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  • 1 year later...

I know this is an old thread but i have to comment ( ihave just started another post myself because i was aunable to find any imfo , as oon as i did imfo on related sites like this came flooding in,thanks to everyone.)

As an update to atypical i have been treated as ,major dep for 12 years with very heavy meds which kept bombing out, as a last resort thaey put me into a clinic dropped all my meds not nice 600effexor 1000 lithium gone in to 2 days YUK!!

and started me on cipramal as an AD and Lamotrigine as an antiphyscotic with diazapam as a back up when the anxiety got out of hand.Then they put me on a intense 2 week course of CBT and hear we are 6 weeks later struggling but seeing some slight improvement even on a lower dose of AD and reclassified me as Atypical unreal.... after researching it over the last 6 weeks i can see the connection with my issues with have been treated as major depression alone...

Have a nice day.....

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