Grieving is about loss; usually most painfully about the loss of love or a loved one. Even small losses may result in the emotional pain known as grieving. Sadness and grieving respond well to therapy and are most likely to dissipate on their own overtime. These states are often diagnosed inaccurately as depression, they are not. Nor will they respond to antidepressants, because there is no significant chemical imbalance, for the antidepressant to address.

Depression is a whole different thing. Depression may eventually result from multiple underdressed grief and sadness issues that have rotted for so long they have become the homeostatic condition of the biochemistry of individual. In this case antidepressants and therapy are both appropriate. But that’s not the only kind of depression there is. Many people, usually the descendents of biochemically depressed individuals are born biochemically depressed individuals. All the therapy in the world will not do any good. If the person is fortunate they may find antidepressants or a combination of antidepressants that effectively lift their mood and allow them to operate on a whole different, non-depressed, level. These people could also benefit from significant therapy after the depression has lifted, but not until then. Why therapy after the depression has lifted? Because a person who is primarily depressed and has always been primarily depressed will be confronted with whole new ways of being in the world that would benefit from and be supported by a therapeutic relationship. This is the best way to prevent relapse. Rarely is a person who has been depressed for a significant amount of time, that is years or decades, in a financial position to maintain the medication and therapy necessary to stay well.

25 years ago, when I was being treated for depression, I had excellent insurance. I worked for the County of Santa Barbara psychiatric inpatient unit and had access to the best psychiatrist, the best resources. I had the privilege of being a patient of Dr. Joseph Johnson, who would on a weekly basis, spend an hour with me. At that time, that was the standard. I had the best medications and excellent therapy. Consequently, it was one of my most “well” periods. Then came managed care. Dr. Johnson was permitted 15 minutes per patient. He could no longer do psychotherapy; he could no longer even do a decent medication assessment. He went from being a very happy appearing person to being a very frustrated, border on angry appearing, person. Just before resigning from the clinic, he briefly expressed to me that he could no longer work under those conditions, that wasn’t fair to his patients. Nothing has been the same since managed care and as far as I can see none of it is good.

Recently in the New York Times there have been several articles on the inability of antidepressants to address mild and moderate depression. Some of that information is provided in the post just prior to this one. I will be commenting on that for the next couple days. I will say, at this time, the issue of depression has become much too simplistic. Saying “depression” is like saying “cancer”. There are hundreds if not thousands of types, severities and causes. In general, every successful treatment starts with an accurate diagnosis. Spare no cost in getting an accurate diagnosis, it is your life you are wasting if you don’t.

Now here’s the challenge, if I’m treated for a disorder someone needs to get paid. If there is going to be a payment through some type of insurance, there must be an ICD code, specifically a selection from ICD-9 codes 290-319: mental disorders, in the case of a mental illness. This code does not contain sadness or grieving, consequently, anyone who is sad or grieving will be given a depression or anxiety code. We are now comparing apples to oranges in any study and getting poor inaccurate results.
Let’s take a look at this on a very basic level. I’m running antidepressant trial. Included are 6 individuals who are really sad, 10 individuals who are grieving, and 15 individuals who are truly clinically depressed. Just to complicate matters, five of the 15 depressed individuals actually had a bipolar disorder, which is usually first diagnosed as depression. In short form, the result of my trial will be useless. The result of a meta-analysis based on a number of such trials will be just as useless. You begin to see why we have made such poor progress with the treatment of depression in the past 50 years.

I am not dreaming

Of a hope-victory-life.

I am just dreaming

Of a hope-survival-life.

~

Yesterday my need was world-conquest.

I failed.

Today my need is my own survival.

I am failing.

Tomorrow my need will be a surrendered life.

I shall fail.

By: Sri Chinmoy

via Survival Poem — Sri Chinmoy Poetry.

Almost every day feels like a fight against that “surrendered life”. As I fight I try not to think about it, how that “surrended life” would look, dependency, poverty, SSI disability. Trapped face-to-face with the term second-class citizen, no transportation no escape. Perhaps sharing a room with someone I don’t know and have no interest in getting know-and then a succession of someones. The glance is so bleak only suicide comes to mind to comfort me. They do that-they do that all the time. That is how it has been.
Then on Monday-I started crying-because I knew everything was OK. More precisely because I felt everything was okay. For decades I lived in some state of anxiety all the time and even when inside my head, I knew everything was okay, my body and my emotions could never be convinced. We are tight, we are afraid, we are ready, it will never really be okay. Monday my brain said everything is okay and my body said yes, everything is okay and my emotional body took a deep breath and whispered yes, everything is okay. I cried tears of overwhelming relief. I think my new medication is working.
Diane

Lifting the Curtain on Depression         By BENEDICT CAREY

via Depression – Reporter’s File – Lifting the Curtain on Depression – NY Times Health.

In Brief:

Each patient experiences depression differently, and the symptoms can vary significantly from case to case.

Available treatments do not work for as many as half of chronically depressed patients.

Researchers have long focused on the role of serotonin, but new therapeutic paradigms are needed.

Recent brain imaging studies may have uncovered surprising targets for intervention.

Depression is no monochromatic black veil, no shared melancholy, as is often claimed. Instead, the disorder is more like a virus that amplifies each sufferer’s particular vulnerabilities, whether anxiety, helplessness, self-doubt, anger or some combination of these. The subjective experience varies from person to person, yet treatment is far from personalized.

Progress has slowed as researchers grapple with one of the most difficult aspects of the disorder: it is impossible to predict who will respond to what therapy, and many sufferers find no relief from anything now available, including medication. While depression appears in many forms, therapeutic options remain worryingly limited.

“We’re at a point where we need to find new treatments, because it’s very clear that the old ones simply don’t work well for many people,” said Dr. Thomas Insel, director of the National Institute of Mental Health. “Our thinking about depression has to change, and it is changing.”

Some people are genetically predisposed to react more strongly than others to life’s inevitable blows. Scientists have traced this susceptibility in part to how the body processes a neural messenger called serotonin, which is linked to mood, and helps cells learn and communicate. For the past 20 years, depression researchers have focused heavily on this connection, both to understand the disorder and find better treatments. A serotonin “deficit” or “imbalance” has become synonymous with depression itself in the public consciousness, an easy catch-all explanation reinforced in drug ads and awareness campaigns.

But it is increasingly clear that serotonin is only one piece of the puzzle. Even when used aggressively by psychiatrists, selective serotonin reuptake inhibitors like Prozac and Zoloft, which prolong the action of the neurotransmitter in the brain, speed recovery in only about half of seriously afflicted patients. In a small number of young people, these drugs seem to backfire, making patients more likely to harm themselves or to think about it.

Indeed, many sufferers of moderate depression may be more likely to recover with talk therapy, particularly cognitive behavior therapy, in which patients learn techniques for defusing their own reflexive, self-defeating thoughts.

Despite the clear need, better therapies for depression have been slow coming. Newer alternatives, like Effexor and Cymbalta, are not S.S.R.I.’s but so-called S.N.R.I.’s; they prolong the activity of a brain messenger called norepinephrine, as well as serotonin. But this extra effect does not seem to make much difference for most patients, and experts consider these drugs to be essentially an extension of S.S.R.I. therapy, not a real departure.

“We really need to find better, more precise targets” for depression drugs, Dr. Insel said.

Assaults on depression based primarily on serotonin have hit a wall, in effect, forcing psychiatrists and researchers to explore entirely new notions about the causes of the disorder and possible options for treatment.

Recently investigators have explored the role of the hippocampus, an area deep in the brain critical to memory formation, in severe depression. They have looked more closely at the activity of the glutamate system, a brain messenger that jump-starts activity along neural networks. And they have used brain imaging to try to pinpoint areas in the brain that flare up or go quiet when people are suffering from spasms of despair.

Brain imaging has already paid off in an unexpected way. In a series of brain-imaging experiments performed at the University of Toronto and at Emory University in Atlanta, Dr. Helen Mayberg, a neurologist, has found that activity in a part of the brain known as Brodman area 25 is strongly associated with the experience of despair.

Brodman area 25 is uncharted territory; before these studies appeared, no one suspected it was linked to depression. But the researchers went one step further, implanting electrodes into the brains of severely and chronically depressed patients in an effort to quiet this area. The results were encouraging. Depression this severe can seem unbreakable, but most of the patients treated — more than a dozen have had the surgery — have improved enough that they have been able to return to work and to reconnect with family, friends and children. Most continue on drug therapy, as well.

It is a radical experiment, but it has made the darkness of depression visible, a first for psychiatry. If there are many different permutations of depression, then imaging techniques like these should soon help doctors differentiate them. Dr. Mayberg’s work already suggests that depression looks different in the brains of people who respond to talk therapy, compared with those who do well on antidepressants.

Scientists also are rethinking the pharmaceutical approach to depression, and in striking ways. Ketamine, a narcotic better known in nightclubs as “Special K,” has shown antidepressant effects in animal studies, but because of its reputation as a street drug it was never taken seriously as a potential therapy.

But last year scientists at the National Institutes of Health reported in a small study that some severely depressed patients recovered within hours after taking the drug intravenously. Most of them remained in improved condition for more than a week. Now the N.I.H. is running a large-scale study to determine how long the therapeutic effect lasts, and in whom.

The sudden scientific interest in ketamine has been criticized as a desperate stab at what has been an unsolvable medical puzzle, the treatment of chronic depression. But there is hope in the paradigm shift that has led to ketamine’s re-evaluation, and a welcome sign of change. The research already has scientists scrambling to find related compounds that don’t have the side effects of ketamine, as well as drugs that could sustain its effects once the initial treatment was stopped.

After reporting results from the 2006 ketamine study, the lead author, Dr. Carlos Zarate, chief of the mood and anxiety disorders research unit of the National Institute of Mental Health, summed up the findings this way: “What the study tells us is that we can break the sound barrier.”

He wasn’t just talking about breaking the hold of a devastating chronic disorder. He was talking about the science of depression itself, which was badly in need of a shake-up.

Although it is the particular enemy of teachers and sports coaches, apathy often gets a good philosophical press, especially in ethical systems that regard desire and worldly interest as low and unworthy. Plato recognizes the need for passion or eros even in the advanced contemplative state of the philosopher, but Hindu, Buddhist, Stoical and some Christian traditions have all looked askance at desire, equating the summum bonum with a kind of torpid vacuity. Hobbes shrewdly points out that while we live we have desires and Alexander Pope sides with the energetic: ‘In lazy Apathy let Stoics boast, Their Virtue fix’d; ‘tis fix’d as in a frost’ (An Essay on Man, ii). However, like Stoics and Buddhists, Kant found apathy to be particularly excellent: bliss is a state of ‘complete independence from inclinations and desires’ and this freedom is both itself a virtue and presupposed by other virtues. Aquinas, however, recognizes the desolation involved in turning away from what is good, and classifies it as a leading or capital sin. See accidie, ataraxia, autonomy/heteronomy, love.”

How then do they differ, apathy and anhedonia? I say, there is no choice in anhedonia. Only passionate souls-who know they are missing something important to THEM- experience anhedonia. Diane

via apathy: Definition, Synonyms from Answers.com.

Op-Ed ContributorA Case of Chronic Denial Sign in to Recommend

by HILLARY JOHNSON

Published: October 20, 2009

EARLIER this month, a study published in the journal Science answered a question that medical scientists had been asking since 2006, when they learned of a novel virus found in prostate tumors called xenotropic murine leukemia virus-related virus, or XMRV: Was it a human infection?

Health Guide: Chronic Fatigue XMRV is a gammaretrovirus, one of a family of viruses long-studied in animals but not known to infect people. In animals, these retroviruses can cause horrendous neurological problems, immune deficiency, lymphoma and leukemia. The new study provided overwhelming evidence that XMRV is a human gammaretrovirus — the third human retrovirus (after H.I.V. and human lymphotropic viruses, which cause leukemia and lymphoma). Infection is permanent and, yes, it can spread from person to person (though it is not yet known how the virus is transmitted).

That would have been news enough, but there was more. XMRV had been discovered in people suffering from chronic fatigue syndrome, a malady whose very existence has been a subject of debate for 25 years. For sufferers of this disease, the news has offered enormous hope. Being seriously ill for years, even decades, is nightmarish enough, but patients are also the targets of ridicule and hostility that stem from the perception that it is all in their heads. In the study, 67 percent of the 101 patients with the disease were found to have XMRV in their cells. If further study finds that XMRV actually causes their condition, it may open the door to useful treatments. At least, it will be time to jettison the stigmatizing name chronic fatigue syndrome.

The illness became famous after an outbreak in 1984 around Lake Tahoe, in Nevada. Several hundred patients developed flu-like symptoms like fever, sore throat and headaches that led to neurological problems, including severe memory loss and inability to understand conversation. Most of them were infected with several viruses at once, including cytomegalovirus, Epstein-Barr and human herpesvirus 6. Their doctors were stumped. The Centers for Disease Control and Prevention, the nation’s presumed bulwark against emerging infectious diseases, dismissed the epidemic and said the Tahoe doctors “had worked themselves into a frenzy.” The sufferers, a C.D.C. investigator told me at the time, were “not normal Americans.”

When, by 1987, the supposed hysteria failed to evaporate and indeed continued erupting in other parts the country, the health agency orchestrated a jocular referendum by mail among a handful of academics to come up with a name for it. The group settled on “chronic fatigue syndrome” — the use of “syndrome” rather than “disease” suggested a psychiatric rather than physical origin and would thus discourage public panic and prevent insurers from having to make “chronic disbursements,” as one of the academics joked.

An 11th-hour plea by a nascent patient organization to call the disease by the scientific name used in Britain, myalgic encephalomyelitis, was rejected by the C.D.C. as “overly complicated and too confusing for many nonmedical persons.”

Had the agency done nothing in response to this epidemic, patients would now be better off. The name functioned as a kind of social punishment. Patients were branded malingerers by families, friends, journalists and insurance companies, and were denied medical care. (It’s no coincidence that suicide is among the three leading causes of death among sufferers.) Soon the malady came to be widely considered a personality disorder or something that sufferers brought upon themselves. A recent study financed by the C.D.C. suggested that childhood trauma or sexual abuse, combined with a genetic inability to handle stress, is a key risk factor for chronic fatigue syndrome.

Many people don’t realize how severe this illness can be. It is marked by memory and cognition problems, and physical collapse after any mental or physical exertion. The various co-infections that occur only make matters worse. Many patients are bedridden. And recovery is rare. A significant number of patients have been ill for more than two decades.

Dr. Nancy Klimas, an immunologist at the University of Miami School of Medicine who treats AIDS and chronic fatigue syndrome, remarked in The Times last week that if given the choice she would prefer to have AIDS: “My H.I.V. patients for the most part are hale and hearty,” she said, noting that billions of dollars have been spent on AIDS research. “Many of my C.F.S. patients, on the other hand, are terribly ill and unable to work or participate in the care of their families.”

Congress has appropriated money for research on chronic fatigue syndrome, too, though in far smaller amounts, but the C.D.C. has seemed unwilling to spend it productively. A decade ago, investigations by the inspector general for the Department of Health and Human Services and what was then called the General Accounting Office revealed that for years government scientists had been funneling millions meant for research on this disease into other pet projects.

As public health officials focused on psychiatric explanations, the virus apparently spread widely. In the new study, active XMRV infections were found in 3.7 percent of the healthy controls tested. Roughly the same degree of infection in healthy people has been found in the prostate research. If this is representative of the United States as a whole, then as many as 10 million Americans may carry the retrovirus.

It is estimated that more than a million Americans are seriously ill with the disease. (Not everyone infected with XMRV will necessarily get chronic fatigue syndrome — in the same way that not all of the 1.1 million Americans infected with H.I.V. will get AIDS.)

Hints that a retroviral infection might play a role in chronic fatigue syndrome have been present from the beginning. In 1991, Dr. Elaine DeFreitas, a virologist at the Wistar Institute in Philadelphia, found retroviral DNA in 80 percent of 30 chronic fatigue patients. The C.D.C. went so far as to try to replicate her effort, but refused to follow her exacting methods for finding the virus. In addition, the centers’ blood samples became contaminated, and some people at the agency said that administrators ended the research prematurely. Rather than admit any such failure, the C.D.C. publicly criticized Dr. DeFreitas’s findings.

That episode had a chilling effect on other researchers in the field, and the search for the cause was largely abandoned for 20 years.

Now, Judy Mikovits, the retrovirus expert at the Whittemore Peterson Institute, in Reno, Nev., who led the recent study, has revisited the cold case. Not surprisingly, the institute is private, created by the parents of a woman who suffers from chronic fatigue syndrome. But Dr. Mikovits collaborated with scientists at the National Cancer Institute and the Cleveland Clinic.

When she began her work on this disease in 2006, Dr. Mikovits, a 22-year veteran of the National Cancer Institute, knew little about chronic fatigue syndrome. But she was intrigued that an unusually high number of patients being followed by a Nevada doctor were suffering rare lymphomas and leukemias; at least one had died. And she was also impressed that the doctor, Dan Peterson, had built an extraordinary repository of more than 8,000 chronic fatigue syndrome tissue samples going back as far as 1984.

“My hypothesis was, ‘This is a retrovirus,’ and I was going to use that repository to find it,” Dr. Mikovits told me.

What she found was live, or replicating, XMRV in both frozen and fresh blood and plasma, as well as saliva. She has found the virus in samples going back to 1984 and in nearly all the patients who developed cancer. She expects the positivity rate will be close to 100 percent in the disease.

“It’s amazing to me that anyone could look at these patients and not see that this is an infectious disease that has ruined lives,” Dr. Mikovits said. She has also given the disease a properly scientific new name: X-associated neuroimmune disease.

For patients who have been abandoned to quackish theories and harsh ideologies about their illness for 25 years, the dismantling of “chronic fatigue syndrome” can’t come soon enough.

The ground under me, it’s nicer, but I am still crawling through the world.  When I feel bad I feel terrible.  When I feel good, I only feel bad.  I don’t see any end to this.  I only go for help, I only let someone know how I feel, when I don’t think I can take it for another day, but I have become so good at looking good, that when I will admit how bad I feel, how desperate I am, no one believes me.  They seem to think something must have just happened that I won’t talk about, some tragedy or overblown disappointment that I can identify and define.  Nothing bad has happened, not this week, not this month, probably not even this year.  It may have happened 30 or 40 years ago, but I’ve been over that stuff over and over and going over it again is not going to help.  I think if I have to talk to one more damn useless archaeological therapist I’ll scream.  I’m stuck in emotional overdrive without a definable catalyst.  I can’t see how I got here, I can’t see what keeps me here, and I can’t see how to get out-it’s hopeless.

MY problem-or one of MY problems as I see it…

“ Depression, stress and the adrenal axis

Carmine M. Pariante

Institute of Psychiatry, King’s College London

Download the briefing as a PDF file

Depression is characterised by an over activity of the hypothalamic-pituitary-adrenal (HPA) axis that resembles the neuro-endocrine response to stress. These abnormalities participate in the development of depressive symptoms. Moreover, antidepressants directly regulate HPA axis function. These novel findings are reshaping our understanding of the causes and treatment of this disabling disorder.

Major depression – major importance

Costing more than 30 billion pounds every year in the UK and the US alone, major depression is a significant cause of disability and the most important cause of suicide worldwide. Why should neuro-endocrinologists bother with depression? Depression is characterised by an over activity of the hypothalamic-pituitary-adrenal (HPA) axis that resembles the neuro-endocrine response to stress. In this Briefing I will claim that HPA axis hyperactivity is not a mere epiphenomenon of depression, but rather a crucial biological mechanism in the pathogenesis of this disorder and a fundamental target for its successful treatment.

HPA axis activity is governed by the secretion of corticotropin-releasing hormone (CRH) from the hypothalamus. CRH activates the secretion of adrenocorticotropic hormone (ACTH) from the pituitary. ACTH, in turn, stimulates the secretion of glucocorticoids (cortisol in humans) from the adrenal glands. Glucocorticoids interact with their receptors – the corticosteroid receptors – in almost every tissue in the body, and the best known effect is the regulation of energy metabolism. By binding to corticosteroid receptors in the brain, glucocorticoids also inhibit the further secretion of CRH from the hypothalamus and ACTH from the pituitary (negative feedback).

Three lines of evidence demonstrate the link between stress, depression and the HPA axis. First, depression, in its core symptoms of dysphoric or low mood, inability to take pleasure and low energy, is a universal cross-cultural response to stressful events, particularly when the stress is chronic or the individual has no control over the situation. Second, stress activates the HPA axis, leading to a powerful release of glucocorticoids into the bloodstream; depression, especially when severe, is also characterised by over activity of the HPA axis. Third, treatments that modify the stress response, like “talking therapies” improving the ability to cope with stress, have an antidepressant effect; moreover, known antidepressants directly decrease HPA axis activity.

Facts and questions

The HPA axis abnormalities in patients with major depression are remarkably similar to those present in animals experiencing chronic stress. Depressed patients have an increased drive to the HPA axis, as shown by the larger production of CRH in the brain. They also have an impaired negative feedback by glucocorticoids. Finally, they have an increased volume of the adrenal and pituitary glands. One accepted explanation for the HPA axis over activity in depression is that, because of the reduced function of the corticosteroid receptors, circulating cortisol is unable to successfully inhibit HPA axis activity (“glucocorticoid resistance”). Consistent with this, antidepressants directly increase the expression and function of corticosteroid receptors in the brain, thus enhancing the negative feedback and reducing HPA axis activity.

“One way to conceptualise depression is a pathological stress response gone awry”…Charles B. Nemeroff, 1996

There is, however, a big unanswered question (see Figure). Does the fact that depressed patients have a hyperactive HPA axis actually mean that a lot of cortisol is flooding their brain, and that the depressive symptoms are consequence of this putative “toxic” effect of cortisol (Pathway A)? Or is the opposite true: that patients have a hyperactive HPA axis as a compensatory mechanism, because their brain is resistant to the effects of circulating cortisol (Pathway B)? The question is not trivial, especially in our quest for a more effective treatment. In the first scenario, our recommendation should be the lowering of cortisol levels. In the second scenario, our recommendation should be the administering of more cortisol. The situation is complicated by the fact that increased cortisol levels in the bloodstream do not necessarily translate into increased effects of glucocorticoids on the brain, because the brain sensitivity to cortisol is also regulated by the function of the corticosteroid receptors as well as by efflux systems at the blood-brain barrier. In what seems to be a clear effort of nature to tease us all, depression has been described in endocrine disorders characterised by elevated cortisol levels, like Cushing’s disease, but also in disorders characterised by low cortisol levels, like Addison’s disease. Moreover, high and low levels of cortisol give similar functional and morphological changes in the brain. Even more strikingly, both the lowering of cortisol levels and the administering of cortisol have antidepressant effects in depressed patients.

LIKE CANCER, DEPRESSION HAS BEEN ESTABLISHED TO BE NOT JUST ONE, BUT MANY DISORDERS-NO DOUBT THERE ARE MANY FACTORS AND COMBINATIONS OF FACTORS INVOLVED.  UNDER TREATMENT IS A KILLER !  MY HPA AXIS HAS CRASHED!  IT MAY NEED MULTIPLE SUPPORTS AND REHABILITATIVE TREATMENTS, IF IN FACT IT EVER CAN BECOME HEALTHY.  I WILL SETTLE FOR A LOT OF SYMPTOM RELIEF!  ANY IDEAS??

read more here>>>via British Society for Neuroendocrinology – 19. Depression, stress and the adrenal axis.

Main Entry: in·do·lent Pronunciation: \-lənt\Function: adjective Etymology: Late Latin indolent-, indolens insensitive to pain, from Latin in- + dolent-, dolens, present participle of dolēre to feel painDate: 16631 a : causing little or no pain b : slow to develop or heal 2 a : averse to activity, effort, or movement : habitually lazy b : conducive to or encouraging laziness c : exhibiting indolence synonyms see lazy— in·do·lent·ly adverb

via indolent – Definition from the Merriam-Webster Online Dictionary.

via The Core of Depression-27.

I want my Dopamine-and I want it NOW!
If you can read and understand this:
“The nucleus accumbens receives projections from midbrain regions (such as the ventral tegmental area), from regions involved in emo- tion (such as the amygdala, orbitofrontal cortex, and medial prefrontal cortex), from motor regions (such as the dorsal caudate and globus pallidus), and from regions involved in memory (such as the hippocampus).” Just click the link and enjoy the rest of this lengthy, educational and facinatimng article. Diane

Difficulties Experiencing Simple Pleasures May Be Caused By Smaller Brains

An area of the brain is smaller in those with anhedonia, or an inability to enjoy simple pleasures as much as the average person.

Yet another biological link between mental illnesses like depression and schizophrenia and brain physiology has been discovered by scientists at the Douglas Mental Health University Institute in Montreal.

Anhedonia, or the inability to experience simple pleasures as strongly as the average person, is a symptom of illnesses such as depression. It also may be because of a smaller area of the brain in which pleasures are processed. Douglas researchers have discovered that patients who suffer from anhedonia also have smaller area of the brain called the anterior caudate. This area of the brain, located in the center regions, is responsible for pleasure and reward.

According to MRI scans of patients with varying degrees of anhedonia, those who suffered the most from this ailment processed pleasurable images, such as a beautiful waterfall, in the part of the brain responsible for cognition rather than in the anterior caudate. The twenty-nine patients chosen for the study had no previously diagnosed mental illness. Their degrees of anhedonia were measured by a questionnaire that contained questions such as “I genegenerally agree that making love is an intense pleasure” that were rated on a scale from “strongly disagree” to “strongly agree”, with those choosing “strongly disagree” on such questions to be considered highly anhedonic.

“The hypothesis is that because they don’t feel pleasure as high as other people, when they analyze positive information, they have to process it at a more cognitive level,” explained lead author Philippe-Olivier Harvey to the Montreal Gazette. “So there is a genuine lack of pleasure and they have to compensate for this by an overactivation of this (cognitive) region of the brain.”

In those who enjoyed pleasure normally, this cognitive area of the brain, located just behind the forehead, was not active.

These findings are significant for advocates of the biological connections of various mental illnesses. It also will make treatment of some forms of depression and schizophrenia easier as a simple MRI scan can tell physicians why the patient is having a difficult time feeling pleasure and adjust treatment accordingly.

“It has been well established that anhedonia is a key symptom of major depression and schizophrenia,” said Douglas researcher Martin Lepage. “We chose to study this core symptom in hopes of finding a vulnerability marker to better diagnose these mental illnesses.”

via Anhedonia – Difficulties Experiencing Simple Pleasures May Be Caused By Smaller Brains.;

John Martz | March 12th, 2007

Anhedonia is a blog full of cartoons by Bart Vliegen. This piece that invites the reader to construct a rock song out of its list of cliche words, and which looks like it comes straight of a Moleskine sketchbok, stood out as a personal favourite.

via Anhedonia « Drawn! The Illustration and Cartooning Blog.