420 replies to this topic

[anon2042]

Thanks for responding. It appears that most of folks in this thread have only anticipatory anhedonia, but some may also have consummatory. I think that psychologically lack of motivation is a very natural result of consummatory anhedonia, so that could explain the co-morbid anticipatory & consummatory anhedonias. Think about it, amnesiagirl: do you lack motivation/anticipatory pleasure because of the fact that doing things doesn't make you feel anything, or is the lack of motivation/anticipatory pleasure an issue of its own? Do you see a relation between the two, not physiologically, but psychologically?

As for Zyprexa, it was medievil who suggested that it balances monoamine phasic-tonic relation. I don't know if it's true. Not going to try it myself anyway.

I'd like to say that the lack of motivation/anticipatory pleasure is an issue of its own. It's a complex issue because I am pretty sure I have not felt "happy" since my amnesia. It's like my mood scale has been shifted in the negative direction, and now where most people have "happy" I have "neutral". When I am doing something, it's more an issue of, "Do I feel relaxed and comfortable" to determine whether I "like" it or it's "fun" - I generally classify "good" events and feelings as the lack of extreme negative emotions, instead of the presence of good ones, which if it's there, is extremely limited. Does that make sense? Often I'll do things because I think I should do them for routine, and I may even be bored by them, but I will do them if they don't overstimulate me and make me upset.

medivil, if you could mention other meds that balance monoamine phasic-tonic relations I'd be very interested.

Dissolvedisolve, thanks for the report on racetams and anhedonia. I wasn't thinking specially it would help with anhedonia, but I have depression/anxiety which is why I was trying the aniracetam. I haven't had an increase in anxiety but an increase in irritability, which I'm trying to figure out.

[Vieno]

It's very difficult for me to determine whether you have consummatory anhedonia or not. The fact that you feel music suggests that you can feel pleasure, but sometimes feeling music can mean multiple things. For example, thoughts associated with lyrics or on the other hand memories can make one experience emotions which in turn can be mistakenly interpreted as consummatory pleasure. Also, saying that music doesn't induce any feelings at all for someone with consummatory anhedonia is incorrect: rather than being completely unable to experience any pleasure, it's just extremely diminished. So diminished, that I personally see no reason to listen to music, it's useless in terms of getting a pleasurable experience.

I do relate to how you describe determining whether you like something or not. When positive feelings are not possible, it's all about lack of negative ones. However, because I have no problem with anticipation, the anticipation of future events' pleasantness makes me like things in advance: in other words, want them. I suppose you don't get this wanting feeling.

What do you amnesiagirl think about the lists of consummatory and anticipatory aspects posted by Dissolvedissolve on the page six? Basically, even one clear 'yes' for a consummatory aspect rules consummatory anhedonia out.

E: Amnesiagirl, I believe that in addition to possible physiological issues, you also have significant psychological problems. Fear of rejection is very much of an psychological issue: physiological things can only excarbate or diminish it whilst excarbating or diminishing everything else at the same time. Qualitatively, no chemistry will help you with fear of rejection, for example. Anxiety is similar: drugs can diminish it, but they can't change it qualitatively, meaning, removing the negative thoughts. Anxiety is excited negative thinking: if you remove the psychological aspect, which is negative thinking, you have a fast-witted brain free of anxiety.

Edited by Vieno, 11 December 2012 - 07:12 PM.

[anon2042]

Hi, yes I mentioned the lists in my previous post, that I didn't relate strongly to any of them, but could relate to being in a situation that decreased overstimulation and increased physical factors for relaxation.

Wanting is difficult. Family members have held things over my head as a "motivation", but they don't understand it just doesn't work. Do you want to go on a vacation? Do you want a new (fill in the blank)? I don't really care one way or the other, and in fact, things that involve one-time experiences (concerts, trips, etc.) I do not want to experience at this time, as my capacity for enjoying things is so blunted. I do sometimes want things that will make day to day tasks easier, or to try a new supplement, etc. I also will sometimes set up a plan in my head for the day's schedule. I feel satisfied when I can organize things, so if I figure out a route in my head that makes it easy to get my errands done and also pass by a restaurant that I haven't been to, that gets closer to "wanting" something for me. If a place is closed on the route, my routine gets thrown off and I can get upset. But it's not necessarily very strongly like, "I am so looking forward to getting to that restaurant when my chores are done!" but, "I planned this out, and I have to go from point A to B to C for it to be complete".

Sorry if this is still unclear and doesn't make a ton of sense. It's confusing for me too, because I don't know what things used to be like. I'm fairly certain there is something wrong though. I may have a few instances where the traditional definition of anhedonia may lift a bit, but it's usually motivated by something else than "pleasure" (sense of organization, duty, impulse). It's all very difficult.

One thing I was thinking about that I'd like to discuss is anhedonia and addiction. I have had friends who have had addictive personalities across the board. If it wasn't strict substance abuse, they'd turn to something else that was just as damaging. Mental Illness and addiction often go hand in hand, and I know this, because I am harassed by doctors/etc. continually about dispensing medications. At this point some of the only things I haven't tried are the "dangerous" things, like opiates and stimulants. But my whole life, pretty much across the board, I have never ever had issues with addiction of any kind. I don't drink (never had), had no interest in substances, and even things like caffeine and benzos never phased me. Part of this could be that I'm crappy at responding to any sort of substance, but I never had addictive tendencies in any area of my life, other than perhaps video gaming, but it wasn't to the point where one would call it an "addiction". Interestingly enough, I lost the ability to play any kind of video game, even small ones on my phone, post amnesia. I'm not sure why. Having this change would be a huge indication that something was lifting in my anhedonia. I don't know if I could say that it gave me pleasure right before the memory loss (I apparently was still playing them right up until my ECT) but in the past it had, and I was able to start up the game and continue in it. I've lost that ability.

Anyway, I always get comments on how unusual this is with my diagnosis (you're sure you never drank? you're sure you never were a drug addict?), so I wonder if this could be related to anhedonia/dopamine? Not at all saying that I *want* to have addiction, but the fact that I'm basically unable and have always been unable to have it I guess is somewhat unusual. Alternatively, I wonder if people with anhedonia have gotten into cycles with addiction more out of habit than out of pleasure, and then they find it difficult to stop. But since those with anhedonia have trouble starting and engaging in events, the likelihood may be less?

Just something I was thinking about - if anyone feels that they have a similar story to share or thoughts, please do.

[Dissolvedissolve]

As far as addiction, I would add that I have absolutely no tendency toward dependence on substances. I drink sometimes, but I have no attraction to drink frequently or outside of social settings. Literally the only thing I've been dependent on was caffeine for around a month at one point simply because of a lack of access to sleep.

A lack of a tendency for addiction fits with the dopamine angle, since dopamine is implicated in obsessions and addictions. For instance, here's a discussion of a dopamine agonist, pramipexole, and its tendency to increase addiction:

Several unusual adverse effects of pramipexole (and related D3-preferring dopamine agonist medications such as ropinirole) may include compulsive gambling, hypersexuality, and overeating,[15] even in patients without any prior history of these behaviours.[16] These behaviors have been reported to manifest in almost 14% of patients on DA agonist therapies. Other compulsive behaviors such as excessive shopping have been reported.[17] L-DOPA is an indirect acting DA agonist with no specificity for any receptor subtypes. As it is the precursor for dopamine it is rarely associated with these disorders. These side effects are thought to be linked to the D3 activity of pramipexole, as D3 receptors are heavily expressed in brain regions involved in mood, behavior, and reward.[18]

→ source (external link)

I just quoted Wikipedia, but you can obviously check out the references if you want.

[Vieno]

Amnesiagirl, I recommend you to seek for therapeutic help. You may not need long-term psychotherapy, but I think that you need to figure out yourself. Searching for drugs here is useless unless you figure out your psychological function. Perhaps talk to some quick-witted friend who is a good listener or something?

[anon2042]

I don't understand why it's relevant or helpful to call me out on how I'm apparently doing the wrong thing repeatedly in this thread - it only serves to throw the thread off topic and to further alienate me from this forum. I don't presume to know the cause of anyone's problems, nor call them out on what treatment is going to "fix" them, especially based on about a two paragraph window into that person's life. If you have personal advice for me that you would like to share, please PM me. Thank you.

Edited by amnesiagirl, 14 December 2012 - 05:26 AM.

[nupi]

Amnesiagirl, I recommend you to seek for therapeutic help. You may not need long-term psychotherapy, but I think that you need to figure out yourself. Searching for drugs here is useless unless you figure out your psychological function. Perhaps talk to some quick-witted friend who is a good listener or something?

While I agree that she should probably talk to a professional (I'd assume someone coming from ECT would do so anyhow), I quite frankly disagree that searching for drugs is useless (you harping about it is, however).

As for yourself, did you ever try Kava? I had an interesting experience with that last night - very peaceful, mildly euphoric, almost dream-like state (one of these days I am going to megadose Kava to see what happens). Kava is thought to be gabaergic but there has to be another component to it - would be interesting to see how you react to it.

[Vieno]

Okay. I stop telling you what to do. But I want to keep this as a thread for consummatory anhedonia, so based on that, I hope that you won't ask "what drugs to take" for a cluster of symptoms that only slightly possibly include some consummatory anhedonia because that is off-topic. At least as much as the rules of life I'm promoting here...

Nupi: I'm not seeing any particular reason to try Kava. Many drugs induce euphoria and that's not what I'm looking for. Kava does operate on dopamine too but it appears to be a MAO-B inhibitor and MAOIs don't appear to be of any use for consummatory anhedonia.

Instead, I've done khat, which contains cathinone which is very similar to amphetamine. I will need to try it more to see if it really abolishes consummatory anhedonia, but so far the results are somewhat promising. I'll let you know later how all is going.

[Anewlife]

I might have consummatory anhedonia, atleast to a small degree.

I am told it is due to not seeing a benefit in something perhaps subconsciously.

The way it is treated is to treat other conditions, stress, anxiety, phobias, there is usually something holding the person back in life.

[medievil]

Intra-accumbens infusion of a muscarinic antagonist reduces food intake without altering the incentive properties of food-associated cues


Michelle L Perry,^1,2 Matthew E. Andrzejewski,³ Susan M. Bushek,² and Brian A. Baldo²

[url=""%20rid="id308886_ai"]Author information ►[/url] [url=""%20rid="id308886_cpl"]Copyright and License information ►[/url]


The publisher's final edited version of this article is available at Behav Neurosci

Go to:

Abstract

Previous work has implicated the cholinergic system in modulating feeding behavior; however its specific function remains unclear. The present work aimed to characterize potential dissociations between the central cholinergic modulation of the incentive properties of food and food-associated cues, versus consummatory behaviors. Three separate experiments demonstrated that intra-accumbens infusion of muscarinic antagonist scopolamine, 3 hours prior to the testing session, significantly decreased food intake. General motor activity in anticipation of food was not diminished. Experiments also showed that scopolamine did not impair operant responding for a food-associated conditioned reinforcer (CR) nor was d-amphetamine potentiation of CR responding altered by scopolamine pretreatment. This study contributes to the growing evidence that goal-seeking behaviors are mediated by a distinct set of neural processes than those governing food ‘reward.’

Ive noticed myself buscopan in megadoses or that asthma anticholinergic dimish actual reward without me wanting to do those activity's less.
Those are non selective antimuscarinics, id like to identify the receptors.

[medievil]

Manipulation of catechol-O-methyl-transferase (COMT) activity to influence the attenuation of substance seeking behavior, a subtype of Reward Deficiency Syndrome (RDS), is dependent upon gene polymorphisms: a hypothesis.

Blum K, Chen TJ, Meshkin B, Waite RL, Downs BW, Blum SH, Mengucci JF, Arcuri V, Braverman ER, Palomo T.

Source

Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC, USA. drd2gene@aol.com

Abstract

There are common genetic mechanisms responsible for both drug effects and subsequent seeking behavior. In 1996, we coined the term Reward Deficiency Syndrome (RDS). Past and current treatment of substance seeking behavior, a subtype of Reward Deficiency Syndrome (RDS), is considered by most to be inadequate. Recently, we evaluated a complex named Synaptamine [Haveos (SG8839R)]. The main difference with an older studied variant and the latest variant is the inclusion of a proprietary form of Rhodiola rosea, a known catechol-O-methyl-transferase inhibitor (COMT) to potentially enhance the activity of presynaptic released dopamine. In this regard, based on the current literature we hypothesize that manipulation of catechol-O-methyl-transferase (COMT) activity to influence the attenuation of substance seeking behavior, is dependent upon gene polymorphisms. In this regard we hypothesize that carrying the LL genotype with low COMT activity should as theorized, increase the reward induced by substance-induced dopamine release and may indeed increase the propensity to type 1 alcoholism and possibly other drugs that activate the dopaminergic system. Thus when alcohol is present in low COMT LL genotype, increasing COMT activity, not inhibiting it should assist in the reduction of social consumption or abuse. Alternatively, under physiological conditions (no psychoactive substances present (e.g. alcohol) carrying the DRD2 A1 allele with associated low D2 receptors should, as theorized, increase craving behavior because of a low or hypodopaminergic state causing the individual to seek out substances that increase the release of dopamine for subsequent activation of unbound D2 sites in the nucleus accumbens. Thus, in the absence of alcohol or other psychoactive drugs (dopamine releasers), especially during recovery or rehabilitation, decreasing, not increasing COMT activity, should result in enhanced synaptic dopamine as physiologically released, thereby proliferating D2 receptors while reducing stress, increasing well-being, reducing craving behavior and preventing relapse. Based on this hypothesis, we believe that adding the COMT inhibitor R. rosea (as Rhodimin) to our amino-acid and chromium combination in DUI offenders and other illegal drug-related crimes, increases the potential for more targeted neurochemical rebalancing and enhanced relapse prevention. Finally, we hypothesize that these data coupled together provide evidence that the combination of enkephalinase inhibition, neurotransmitter precursor loading, brain tryptophan enhancing and COMT inhibition as well as DNA analysis of the individual's genome, may be useful as an adjunct to therapy when used in outpatient recovery, specifically to assist in reducing craving behavior and preventing relapse.

Since da is mostly related to antipacatory maybe more relevant ot the other thread, but parkinson comt inhibitors may be of therapeutic use.

Neuroimage. 2005 Oct 15;28(1):175-84. Epub 2005 Jul 14.
The rewards of music listening: response and physiological connectivity of the mesolimbic system.

Menon V, Levitin DJ.

Source

Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, CA 94305, USA. menon@stanford.edu

Abstract

Although the neural underpinnings of music cognition have been widely studied in the last 5 years, relatively little is known about the neuroscience underlying emotional reactions that music induces in listeners. Many people spend a significant amount of time listening to music, and its emotional power is assumed but not well understood. Here, we use functional and effective connectivity analyses to show for the first time that listening to music strongly modulates activity in a network of mesolimbic structures involved in reward processing including the nucleus accumbens (NAc) and the ventral tegmental area (VTA), as well as the hypothalamus and insula, which are thought to be involved in regulating autonomic and physiological responses to rewarding and emotional stimuli. Responses in the NAc and the VTA were strongly correlated pointing to an association between dopamine release and NAc response to music. Responses in the NAc and the hypothalamus were also strongly correlated across subjects, suggesting a mechanism by which listening to pleasant music evokes physiological reactions. Effective connectivity confirmed these findings, and showed significant VTA-mediated interaction of the NAc with the hypothalamus, insula, and orbitofrontal cortex. The enhanced functional and effective connectivity between brain regions mediating reward, autonomic, and cognitive processing provides insight into understanding why listening to music is one of the most rewarding and pleasurable human experiences.

Guys the what we propose is the reward receptor mu doesnt cause music reward, opiates dont enhance this, also when im anhedonic i get the full food reward, especially good in mcdonalds wich is orgasm haha.

[Vieno]

I guess the relevant question is: do stimulants and/or psychedelics restore your ability to feel music?

Also, music does many things. Some maybe opioid related, some not.

[medievil]

Yes definatly, at high doses make it sound extremely pleasuring inducing, especially my old GBL 2CD combo, that was insane.

Yeah for sure, it induces emotions wich i find pleasant.

[Vieno]

Excellent. All I need to know

[medievil]

Neuropsychopharmacology. 2013 Feb;38(3):423-36. doi: 10.1038/npp.2012.197. Epub 2012 Sep 26.
Disrupted-in-schizophrenia-1 Gln31Leu polymorphism results in social anhedonia associated with monoaminergic imbalance and reduction of CREB and β-arrestin-1,2 in the nucleus accumbens in a mouse model of depression.

Lipina TV, Fletcher PJ, Lee FH, Wong AH, Roder JC.

Source

Centre of Neurodevelopment and Cognitive Functions, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.

Abstract


Disrupted-in-schizophrenia-1 (DISC1) is associated with mental disorders, including major depression. We previously showed that DISC1-Q31L mutant mice have depression-like behaviors and can therefore be used to study neurobiological mechanisms of depression and antidepressant (AD) medication action. First, we found reduced levels of dopamine, serotonin and norepinephrine in the nucleus accumbens (NAC) of DISC1-Q31L mutants. Next, we assessed social-conditioned place preference as a reward-dependent task and the capacity of distinct ADs to correct impaired social behavior in DISC1-Q31L mice. Bupropion, but not fluoxetine or desipramine, was able to correct deficient social facilitation, social reward, and social novelty in DISC1-Q31L mutants, whereas all three ADs were able to improve social motivation and behavioral despair in DISC1-Q31L mutants. Furthermore, we sought to correlate social anhedonia with molecular and cellular features including dendritic spine density, β-arrestin-1,2, and cAMP-response-element-binding protein (CREB) in the NAC as biomarkers related to depression and the DISC1 pathway. DISC1-Q31L mutants showed reduced levels of β-arrestin-1,2, CREB, and spine density in the NAC, further supporting the construct validity of the genetic model. Bupropion induced the greatest effect on CREB in DISC1-Q31L mutants, whereas all studied ADs corrected the reduced levels of β-arrestin-1,2 and modestly ameliorated deficient spine density in this brain region. Overall, we find neurobiological changes accompanying social anhedonia in the NAC of DISC1-Q31L mutant mice, consistent with a role for DISC1 in regulating social reward as an endophenotype of depression.

[airplanepeanuts]

Did Dhea do anything for you medievil?

[medievil]

Im not sure i allways take several sups at once, dont have patience to test things one by one and think several sups togheter are more beneficial anyway, i do think it helped, as the houseowner threw away most of my sups because i stained he's carpet and other stuff by accident offcourse and had a whole stash for years as someone solled me all the one's he used, so he also tought i took everything at once, either way afterwards i got psychosis of mdpv while i never even got close to something shizophrenic like for a year, the thing is right before i took sertraline wich is a sigma antagonist and dhea is a sigma agonist, also i started getting massively better the same time i started using preg another sigma agonist. Ever since i feel a bit closer to shizophrenia so want to try sigma agonist therapy for a while to get away again, it massively got better over the weeks again tough, still when i start to withdrawal of a gabergic or something i get a bit psychotic toughts wich wasnt the case at all the year i pretty much a full recovery.

Oh right as for anhedonia not really.

[airplanepeanuts]

You're so talkative at the moment...

... as the houseowner threw away most of my sups because i stained he's carpet and other stuff by accident offcourse and had a whole stash for years as someone solled me all the one's he used, so he also tought i took everything at once

That's a funny story.

.
Oh right as for anhedonia not really.

That's too bad. So for anhedonia only stimulants really work, right?

[medievil]

In my case stimulants completely cure most of my symptions, GBL and treshold psychedelics cure just anhedonia.

[Vieno]

Whitetealeaves, for medievil anhedonia does not mean what anhedonia means for most. Be aware of that.

[medievil]

Anhedonia in Japanese patients with Parkinson's disease: analysis using the Snaith-Hamilton Pleasure Scale.

Miura S, Kida H, Nakajima J, Noda K, Nagasato K, Ayabe M, Aizawa H, Hauser M, Taniwaki T.

Source

Division of Respirology, Neurology, and Rheumatology, Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume, Fukuoka 830-0011, Japan. shiroh46@med.kurume-u.ac.jp

Abstract


BACKGROUND:

Anhedonia, a lowered ability to experience physical or social pleasure, has recently been recognized as a non-motor symptom of Parkinson's disease.
OBJECTIVE:

To identify the frequency of anhedonia and the factors influencing hedonic tone in Japanese patients with Parkinson's disease.
PATIENTS AND METHODS:

We recruited 86 consecutive outpatients with a clinical diagnosis of PD attending two Japanese hospitals (one university hospital and one community hospital) in February 2010. We used the self-rating Snaith-Hamilton Pleasure Scale (SHAPS) translated into Japanese language from the original English version to assess and quantify hedonic tone as a subjectively experienced phenomenon. We studied the association of anhedonia with the variables age, age at onset, gender, disease duration, disease severity and antiparkinsonian drugs.
RESULTS:

Thirty-nine patients (45%) were male and 47 (55%) were female. Mean age was 72.01±9.07 (49-89) years, with mean age at onset of 64.93±11.42 (31-88) years. Mean disease duration was 7.20±5.54 (1-23) years. The mean Hoehn and Yahr scale was 2.76±0.78. The mean SHAPS score of the total sample was 1.19±1.86. The SHAPS score of 14 patients (16.3%) was 3 or more, indicating anhedonia. The mean SHAPS score was lower in patients taking pramipexole (0.58±0.97) than in patients not taking pramipexole (1.57±2.16). Multiple linear regression analysis identifiedpramipexole as a significant negative influencing factor on the SHAPS score, while disease severity and entacapone treatment were identified as positive influencing factors. The age, onset age, gender, disease duration, and use of pergolide, amantadine, zonisamide, selegiline, anticholinergic agents and droxidopa did not significantly affect the SHAPS score.
CONCLUSION:

Anhedonia is not rare non-motor symptom in Japanese patients with Parkinson's disease. This study suggests an anti-anhedonic property of pramipexole.

[Vieno]

Oh for god's sake, yeah right "inability to feel pleasure". Bullshit, that's flattened emotions, apathy and lack of excitement and anticipation that they experience with Parkinson's. Let's remember the awfulness of the terminology in this context... when do you learn medievil? :D

[medievil]

I didnt even read the abstract, likewise bad at replying to emails, med is ADHD:D

[Vieno]

Lol anyway check this out, scroll down: http://www.cnschroni...oad/BJPsych.pdf

Seriously, WTF? Can there be a scale more ridiculous? What the hell is that supposed to measure? Psychiatry is a mess.

Edited by Vieno, 11 May 2013 - 05:31 PM.

[medievil]

HAHAHAHAHA wtf are those questions, funny as fuck.

I enjoy looking at the blue sky, eating bread and chatting to my mum, i love the pleasure of her giving me a nightkiss and the praise for making my bed up.

[medievil]

On dr bob some guys said prami worked for anhedonia tough.

And roti added to dex yesterday added some sort of pleasure, but can be placebo.

[medievil]

Diphynhydramine has rewarding aspects, and antimuscarinics despite being horrible are abused, i beleive they also can work for anhedonia since cholinergics can also cause anhedonia.

[Vieno]

I think it would be everyone's benefit if you would separate consummatory anhedonia (CA) from anticipatory anhedonia (AA). I'm not a big fan of this division but it's the best we've got at the moment. I don't have the latter at all yet my first is the strongest kind, just did some opium and had zero effects.

So what do you think, do those substances you just mentioned work for CA or AA? They look interesting since most of the potential anti-CA agents are recreational drugs.

E: Indeed, do cholinergics cause CA or AA? In litearature, anhedonia refers to AA virtually always, or perhaps sometimes to a combination of CA and AA. I doubt it ever refers to CA alone, never seen that happen.

Edited by Vieno, 12 May 2013 - 09:39 AM.

[Hip]

(Duplicate post removed)

Edited by Hip, 14 May 2013 - 07:24 PM.

[Hip]

If anticipatory anhedonia is the loss of enjoyment in advance of an activity, and consummatory anhedonia is the loss of enjoyment from doing an activity, then what is the name of the anhedonia that describes the loss of enjoyment on completion of an activity?

The last type of anhedonia is what I get most: when I finish something, instead of feeling a sense of achievement, and a sense of pleasure and reward for completing a task, I feel nothing.

So for example, normally even simple tasks, such as tiding up your desk, tend to give a healthy person a feeling of reward and satisfaction afterwards, on completion of the task. But for me that good feeling of satisfaction does not arrive when I finish a task.