A couple years ago I started writing a book on mental illness, my mental illness.
Because I have been somewhat disturbed for as long as I can remember, I started way back.
I’ve taken a few excerpts that reveal states of mind, that I now know as anhedonia. 
It was clearly well developed by the time I was 16 years old.  A number of instances stood out starkly
by virtue of their emptiness in relation to the experiences others were having.  How confusing and unrewarding it must be to be close to me.

       On my 16th birthday Jerry gave me a beautiful diamond engagement ring.  I accepted it.  I liked it but I couldn’t ‘feel’ it, there was no emotion with it.

          He was crying and I could see his pain, but I could only feel a tiny bit of it, just enough to make tears run down my face.  I wanted to give him an explanation.  I looked hard inside myself to find one.  It was almost like staring at a blank wall.  I couldn’t even feel confused, just tired out on the inside-some kind of dull ache.  “Please,” I said, “it’s not about you it’s something wrong with me that I can’t explain.” 

        Other people had feelings, lots of them.  I could see them flash across their faces, they expressed awe, appreciated the beauty around them and talked about their relationships, their connection to other people. Even in the emotionally impoverished environment in which I existed, I could see I was different.  I had anger, fear and pain. 

        I have worked for decades on the anger and fear and pain.  I have overcome much, only to find this nothingness, that this is what I have to look forward to.

1: Psychol Med. 1993 Nov;23(4):957-66.LinksAnhedonia: a neglected symptom of psychopathology.

Snaith P.

Academic Unit of Psychiatry, University of Leeds, St James’ Hospital.

In the last century psychopathologists attached importance to the concept of anhedonia, the loss of ability to experience pleasure. Its role in the diagnosis of melancholia was considered to be crucial. In the present century attention to anhedonia has faded, possibly because of the focus upon depressed mood as the pathognomonic feature of depressive disorders. Research on the symptomatology of endogenous depression did not include the concept; anhedonia was also lacking from the major instruments of psychiatric research, the depression rating scales, Attention was drawn to anhedonia by two authors: by Meehl in the 1960s and by Klein in the 1970s. Meehl considered anhedonia from the point of view of a personality defect predisposing to mental illness; and Klein regarded anhedonia to be a symptom of depressive illness and probably the best clinical marker predicting response to antidepressant drugs. In 1980 the revised DSM presented the concept of ‘loss of interest or pleasure’ as one of the two cardinal symptoms of major depression. Since then there has been a gradual rec

via Anhedonia: a neglected symptom of psychopathology. [Psychol Med. 1993] – PubMed Result.

Why is this important? Because there has been little to no progress on the causes of, importance of or resolution of Anhedonia in the past 16 years!!

I’m on my case again.  This time it’s that swimming Pool I bought.  I really believed I wanted it, I really believed I would use it, I really believed it would help me feel good.  I put it up in the middle of June, now in late August I can count the times I’ve used it on my fingers.  The last time I was in the pool I stood in the middle of it and told myself this feels good, this really feels good, remember how this feels.  I don’t remember how it felt and now every time I look at the pool or think of the pool I just feel guilty for spending so much money on something I’m not using, again. 

Sometimes I walk around downtown or at the mall and look at all the  junk in the world and I say to myself, there is nothing I can buy that’s going to make it any better.  It’s now been over two years since I felt good, since I wanted to use and did use the pool twice a day.  I had enjoyed a two month reprieve from my harsh life.  Then, my primary care provider decided I was stable on Lamictal and no longer needed my antidepressant.  It took me a little over three weeks to dive completely to the bottom, again.  I was so bad I had to restart the antidepressant myself and be on it for a little over a week before I came up enough to call the primary care provider and make an appointment.  Even though I went back up to the top dose of antidepressant, I never got to feel good again.  Since then I tried Seroquel and quickly gained 35 pounds plus. (I have now lost 15)  I continued with the Lamictal until I couldn’t remember why I had walked from one room to another on a regular basis.  That got very scary.  Then I tried the new improved Effexor, Pristique.  I noted no difference whatsoever with that medication, and I know enough to give them the 4-6 weeks trial they really need.  Then I got angry and threw them all away.  Bad move.  For the first time in 15 years I became suicidally depressed.  One side of my brain was thinking of ways to kill me and telling me about it and the other side was saying “Bad, bad idea, we need more meds.”  “We” restarted the handy dandy Wellbutrin, which always pulls me up somewhat, but never enough or long enough.

Here’s part of a letter I had written to the primary care provider to help her understand the situation;

“Reducing the Wellbutrin has not worked well.  When I reduced from 450 mg to 300 mg I started getting nervous and bit all my fingernails off again.  Soon after reducing to 150 mg I started shaking my leg/ foot and getting unfocused, irritable and losing the will or energy to exercise.  I had no idea how irritable I get until I started monitoring this symptom and looking at some historical incidents.  When I reduced further I quickly became very depressed, tired, anxious, irritable, asocial and sensitive to sound.  I was too depressed and upset to call so I increase to 150 mg for a week, and called a soon as I was able to talk without crying, to get another appointment.  A week later I returned to 300 mg.  I started getting some energy back and I was much less depressed,  however, I was still shaking my foot and crying when I wake up in the morning because I’m upset with my meds or, I think of something sad.  I was also still pretty irritable, easily annoyed (bitchy) and socially disconnected.  Last week I went back to 450 mg of Wellbutrin.  I feel pretty good today and I’m not afraid to go on this week’s business trip.”

I went on to say;  “My experience and research indicated I have a dopamine imbalance, which dwarfs any other neurotransmitter problems I may have.  As you know, Wellbutrin is one of the few antidepressants that primarily target dopamine.” 

So why am I not getting medications that target dopamine, why, why ,why!  I’m going to find out when I see the doctor on September 21.

Do NOT go to this link if you are easily offended. It is not my fault if you resemble the the subjects studied.  I warned you…http://knowledgeisnecessity.blogspot.com/2009/05/new-imaging-studies-reveal-brains-of.html Diane

Lonely is the catalyst for social interaction and avoidance of lonely is the glue that holds people together. I see the lonely people, they are everywhere. Lonely, a word to describe the pain of wanting to be close to other people, of yearning for connection, it is a very positive emotion. That is one double edge, good thing, about having anhedonia. I don’t get lonely, that is I can only recall feeling lonely once in my life, over 30 years ago for a short period of time. That is the only way I know the pain of lonely, that some people live with on a daily basis. I have nearly no craving for social interaction. I don’t understand “chat”. I do not enjoy people -in general. There are only a few people I care to see at all. They are the people who, for some reason I don’t understand, reach out to me, so I imitate them and reach back. For the first time I have a couple precious relationships. For the first time in over 50 years, I know if I went away, as I have dozens of times, I would miss a couple people. Perhaps that’s a step in learning to be lonely.

Donations are very welcome!

50% of donations go to NAMI ( The National Alliance on Mental Illness). 50% of donations go toward my Brain Transplant…It shouldn’t be too hard to find one; there are a lot of people running around who obviously are NOT using theirs…thank you!

Anhedonia
Written by Colin Brennan, medical journalist

Anhedonia is the inability to gain pleasure from enjoyable experiences.

It was first identified in the 19th century, but was largely ignored until the late 1980s in favour of more obvious depressive symptoms such as low mood, poor concentration, tiredness, disturbed appetite and sleep, and suicidal thoughts.

Anhedonia is now recognised as a core symptom of depression and research by the Institute of Psychiatry in London is throwing new light on the links between the brain and depressive illness.

Symptoms of anhedonia
People with anhedonia have an incredibly flat mood. They can’t react properly or feel anything. There is no variation of mood, making it difficult to take things forward.

It is best described by examples. An anhedonic mother gains no joy from playing with her baby, a footballer isn’t excited when he scores the winning goal, a teenager is left unmoved by passing her driving test.

Anhedonia places a great strain on relationships and is usually accompanied by a loss of sex drive.

Anhedonia and depression
Depression affects one in every five people at some time in their lives and is a potentially fatal illness through suicide.

Depression can be triggered by a sad event like a bereavement, by a physical illness or by imbalances in brain chemistry.

Not everybody who has depression has anhedonia. While rare in mild depression, it can be a serious problem for people who are severely depressed.

Anhedonia can continue after depression, but usually it goes away at the same time.

Antidepressant medicines only partially deal with anhedonia symptoms.

Watching the brain in action
There have been various studies to try to identify the specific areas of the brain involved with anhedonia and depression.

An imaging technique called functional magnetic resonance imaging (fMRI) is used to scan the brain at work.

For example, as you talk, you use the brain cells in the front part of your brain. The increase in neural activity means there is an increased need for oxygen in this area.

Oxygen is delivered by the haemoglobin, which carries oxygen in the blood to all the cells of the body.

The fMRI scan picks up the difference in the magnetic properties of oxygenated and deoxygenated haemoglobin as the oxygen is delivered to the active area of the brain.

This means scientists can see changes in the brain as they happen. Not only can the activity of the brain be recorded when the person moves or signals the answer to a question by pressing a button, it can also be observed when the brain is active during thinking or planning.

Studies on depression and anhedonia
Some differences in the brains of depressives have already been observed. For example, in comparison with healthy volunteers, depressives have:

smaller hippocampi (the area that deals with emotion)
larger white matter lesions
differences in brain metabolism.
One study found that when depressed people were shown film clips designed to cause passing sadness, they activated areas of the brain that were not involved in the reaction of a group of healthy controls. The investigators suggested that this activation might disconnect the limbic system, which is linked to both rage and pleasure, from the normal prioritisation of emotional importance.

In 2005 the Institute of Psychiatry in London used fMRI to compare 12 people with anhedonia and depression to 12 healthy individuals. They identified three areas of the brain that worked differently:

ventromedial prefrontal cortex – the front part of the brain associated with empathy and regulation of negative emotions
ventral striatum – the area of the brain that signals reward
amygdala – almond shaped area of the brain associated with mood and ‘forgetting’ fears (memory of recent events).
All three are involved in the brain’s reaction to sad and happy stimuli.

In those people with anhedonia, the prefrontal cortex had to work harder to register happiness, and there was less activity in the amygdala and striatum.

The study’s authors believe this lack of activity may be what causes the prefrontal cortex not to process happy (rewarding) experiences. In effect, the reward system of the brain breaks down, resulting in anhedonia.

It’s hoped the findings of these studies will eventually lead to new treatments that could target specific regions of brain – either with existing drugs that can be shown to work, or with new medicines or psychological treatments.

Living with anhedonia
Lizzie Gardiner, a writer and single mother from South London, spoke to NetDoctor about how depression and anhedonia affected her life.

After several short bouts of the illness in her teenage years, Lizzie was hit by a major depression at the age of 31. It was brought on by a series of events: the break-up of her marriage, a move from one end of the country to another, bad health, financial problems and the threat of eviction.

Driven by the need to keep the lives of her two children as normal as possible, antidepressants and psychological treatment helped Lizzie through. She didn’t know about anhedonia then, but has since taken part in the Institute of Psychiatry’s research.

Lizzie’s anhedonia took many forms and partly remains with her. She still can’t gain pleasure from her own achievements or see that her children are a credit to her as well as to themselves.

One of her darkest moments was when she sat down to listen to Elgar’s Enigma variations. To her horror, she felt unmoved by the music she had always loved.

Lizzie has learned to live with her symptoms, and says being given information and reassurance helped when she was depressed. ‘Up to now it has been an invisible illness,’ she said.

‘If the research can show physical evidence that depression is caused by changes in the brain, it will be immensely helpful in removing the stigma that is attached to it.’
http://organizedwisdom.com/Anhedonia&url=www.netdoctor.co.uk/special_reports/
depression/anhedonia.htm

Donations are very welcome!

50% of donations go to NAMI (The National Alliance on Mental Illness). 50% of donations go toward my Brain Transplant…
It shouldn’t be too hard to find one;
there are a lot of people running around who obviously are NOT using theirs…thank you!

Please head on over to the HOME page and talk to me! Diane

Deep Brain Stimulation to Reward Circuitry Alleviates Anhedonia in Refractory Major Depression
Thomas E Schlaepfer1,2, Michael X Cohen3,4, Caroline Frick1, Markus Kosel1, Daniela Brodesser1, Nikolai Axmacher3, Alexius Young Joe5, Martina Kreft1, Doris Lenartz6 and Volker Sturm

“Deep brain stimulation (DBS) to different sites allows interfering with dysfunctional network function implicated in major depression. Because a prominent clinical feature of depression is anhedonia—the inability to experience pleasure from previously pleasurable activities—and because there is clear evidence of dysfunctions of the reward system in depression, DBS to the nucleus accumbens might offer a new possibility to target depressive symptomatology in otherwise treatment-resistant depression. Three patients suffering from extremely resistant forms of depression, who did not respond to pharmacotherapy, psychotherapy, and electroconvulsive therapy, were implanted with bilateral DBS electrodes in the nucleus accumbens. Stimulation parameters were modified in a double-blind manner, and clinical ratings were assessed at each modification. Additionally, brain metabolism was assessed 1 week before and 1 week after stimulation onset. Clinical ratings improved in all three patients when the stimulator was on, and worsened in all three patients when the stimulator was turned off. Effects were observable immediately, and no side effects occurred in any of the patients. Using FDG-PET, significant changes in brain metabolism as a function of the stimulation in fronto–striatal networks were observed. No unwanted effects of DBS other than those directly related to the surgical procedure (eg pain at sites of implantation) were observed. Dysfunctions of the reward system—in which the nucleus accumbens is a key structure—are implicated in the neurobiology of major depression and might be responsible for impaired reward processing, as evidenced by the symptom of anhedonia. These preliminary findings suggest that DBS to the nucleus accumbens might be a hypothesis-guided approach for refractory major depression.”
Perhaps I don’t need a brain transplant-a little deep brain stimulation may do the trick!   Diane

I believe most definitions of depression don’t do it justice.  For me it is a pervasive psychic pain, so inhumane that at its worse, I curl up into a tight ball to escape it, but there is no contraction powerful enough to crush it.  Fortunately, I spend only about 3% of my time there, although at some points in my life it has been much more.  Approximately, another 15% of the time the pain mixes so intimately with anxiety, I can’t stop moving, but I can’t accomplish anything either. I can’t sit down I can’t focus, it’s as though my psyche has jumped up and is trying to escape the pain by running and hiding from it inside myself.  As you can see it’s totally an inside job.  At some point I will reach the shuffling stage, where I drag myself around trying to fix everything, on the exterior, I believe is deteriorating or out of control, another 15% of the possibility of enjoying life -vanished.  After a cycle of this or some combination anhedonia is a relief, although it holds no joy or comfort.  It is a step up out of the morass, where I can turn back into the robotic producer of results, provider of services, caretaker, organizer, teacher, all those things that make me look “normal” most of the time.  Normal, take a shower, put on my makeup, dressed up and smile-as normal as I get, but not very rewarding.  Who lives to look good?  At this point, I guess I do, about 65% of the time.  So, if you’re adding we’ve covered 98% of the terrain of my life.  Of course, if that’s all there was, I would only have a depressive type diagnosis, however, my behavior the other 2% of the time, has earned me a bipolar diagnosis. That’s when I’m energized, alarmingly social and behaving in a manner that would shock my mother, to say the least.  In fact, I’ve been known to shock myself.  Although I put myself in some extremely dangerous situations, during these forays into the other world, it’s the anhedonia that’s killing me. Overdosing on nothingness with no hope of escape. More meds please.  Diane

I love technical info:

Acute stress reduces reward
responsiveness: implications for depression
by
Bogdan R, Pizzagalli DA.
Department of Psychology,
Harvard University,
33 Kirkland Street, Cambridge,
MA 02138, USA.
Biol Psychiatry. 2006 Nov 15;60(10):1147-54. ABSTRACT

“BACKGROUND: Stress, one of the strongest risk factors for depression, has been linked to “anhedonic” behavior and dysfunctional reward-related neural circuitry in preclinical models. METHODS: To test if acute stress reduces reward responsiveness (i.e., the ability to modulate behavior as a function of past reward), a signal-detection task coupled with a differential reinforcement schedule was utilized. Eighty female participants completed the task under both a stress condition, either threat-of-shock (n = 38) or negative performance feedback (n = 42), and a no-stress condition. RESULTS: Stress increased negative affect and anxiety. As hypothesized based on preclinical findings, stress, particularly the threat-of-shock condition, impaired reward responsiveness. Regression analyses indicate that self-report measures of anhedonia predicted stress-induced hedonic deficits even after controlling for anxiety symptoms. CONCLUSIONS: These findings indicate that acute stress reduces reward responsiveness, particularly in individuals with anhedonic symptoms. Stress-induced hedonic deficit is a promising candidate mechanism linking stressful experiences to depression.  http://www.biopsychiatry.com/anhedonia.htm  “If you would just beat the crap out of the ___ who is threatening to shock you, depression would be unnecessary!   Diane

I said to my sister Mary “do you think it’s possible for someone to have been depressed for so long they don’t know the difference, they can’t recall ever having experienced anything else, if in fact they ever have?”  Mary has been depressed for so long as I can remember, and I’m older than she is.  She has a dysthymic disorder, with frequent drops into major depressive episodes.  She has basically been wandering around the country lost, for the past 30 years, and continues to wander.  I don’t think I’ve ever seen her happy, but that may reflect my filtering of experience.  Some families have the most likely to succeed person.  We have the most likely to commit suicide person.  I am surprised she is still with us.  She rejects all concrete offers of help. I feel pain in my heart when I think about her.

Dysthymic Disorder: eMedicine Psychiatry.

Major depressive disorder, dysthymia, double depression, and some apparently transient dysphorias may all be manifestations of the same disease process. These varieties of depressive mood states, while distinct diagnostic entities, share similar symptoms and respond to similar pharmacologic and psychotherapeutic approaches.^2,3

Although dysthymia was traditionally considered less severe than major depression, the consequences of dysthymia are increasingly recognized as grave and include severe functional impairment, increased morbidity from physical disease, and increased risk of suicide.

Of note, an estimated 75% of people with dysthymia meet criteria for at least 1 major depressive episode, referred to as double depression.⁴ Those with dysthymia who have depressive episodes tend to have longer periods of depression and spend less time fully recovered.⁵  In a 10-year follow-up study of people with dysthymia, 75% experienced some (at least 2 m) period of recovery from major depression; the mean time to recovery was 52 months from study entry. In this study, most (70%) of those who recovered experienced a relapse into another episode of depression, most commonly in the 3 years following recovery.⁶

Age

Most often, patients with dysthymia recall unexplained unhappiness in preadolescent childhood. Whether DSM-IV-TR adequately addresses dysthymia in children and adolescents is a matter of some controversy.¹⁰