Monday, May 31, 2010
Rerun: This Memorial Day
This Memorial Day:
Our men and women are returning from two wars. They have witnessed things and felt things that those of us who stayed home have no clue. Their brains have been overwhelmed, their psychic beings shaken to the core.
This Memorial Day:
Our soldiers may leave the battlefield, but they cannot leave their memories there. Very high percentages are returning home with PTSD, depression, and other mental illnesses. Even those without full-blown symptoms have issues to deal with. Others are ticking time bombs. Suicide will claim more of them than enemy gunfire. Many will attempt to cope by turning to alcohol and drugs.
This Memorial Day:
Many brave men and women have no clue what is about to happen to them. They served as heroes, but, like many who served in Vietnam, may wind up homeless. They may be remembered for their bravery, but we will cross the street to avoid them.
This Memorial Day:
It's not just about flags on graves. It's about serving the people who served our country.
This Memorial Day:
Resolve to do something tangible. Advocate. Donate. Get involved with one of the veteran's organizations. Get involved with a mental health group making an outreach to veterans. Do something. Then keep doing it.
This Memorial Day:
It's our turn now.
Wednesday, May 26, 2010
PTSD - Since When Is An Event Supposed to Justify a Condition?
My good friend Willa Goodfellow (Prozac Monologues) has written an extremely thought-provoking blog piece on PTSD. She summarizes a 2004 article by neuropsychiatrist Nancy Andreasen of the University of Iowa. How we view the condition can be largely attributed to Dr Andreasen.
The phenomenon has been around since the beginning of time, but our understanding remains limited. During World War I, soldiers who experienced "shell shock" were shot as cowards. In World War II, soldiers who suffered "battle fatigue" were given "therapy" to return them to combat in one week. (The therapy, such as exposure to recorded artillery fire sounds, typically exacerbated their distress.) General Patton infamously slapped a bed-ridden soldier.
The postwar DSM-I of 1952 recognized "gross stress disorder," but this was removed from the DSM-II of 1968. The post-Vietnam War era set the scene for its comeback in the DSM-III of 1980. Dr Andreasen was charged with the task of looking into "post-Vietnam syndrome." As Willa describes it:
Given her experience with burn victims, Andreasen pressed for a more inclusive description of the illness. Post Traumatic Stress Disorder entered the new edition, described as a stress reaction to a catastrophic stressor that is outside the range of usual human experience.
Unlike all other mental illnesses, the first criterion for a PTSD diagnosis is an event rather than a symptom. Another way of putting this is that the DSM mandates a valid reason for an individual's response. The DSM-IV of 1994 and this year's draft DSM-5 (due out in 2013) simply play around with the scope of the valid reason. The 1994 version widened the criterion to include events not necessarily outside the range of human experience (such as surviving an auto accident) while the DSM-5 would narrow it again.
Compare this to depression. Psychiatry does not require a valid reason for us to rate a diagnosis. To the contrary, a valid reason - such as bereavement - would rule out a diagnosis (unless the depression were to persist). In this context, depression would be a normal response to an abnormal situation. We are supposed to feel depressed when we lose someone close to us.
We often get clinically depressed for seemingly no reason at all. Since there is no logic to the depression, the thinking goes, we must be thinking and behaving irrationally. And if this significantly interferes with our daily life, we are presumed to have a mental illness. We elicit sympathy or opprobrium, as the case may be.
The same applies across the anxiety spectrum (with the notable exception of PTSD). We don't need a valid reason - such as an intruder entering through the window - to justify a panic attack. Being frightened of your own shadow will do just fine.
So, I'm wondering. What happens to the poor individual who suffers severe trauma for a stupid reason? Not from combat. Not from being exposed to an act of God or an unspeakable outrage. Something stupid, really stupid. Such as perhaps a close encounter with a circus clown. The trauma may be irrational, but then again so is all the rest of mental illness.
Is that person's distress any less?
Suppose two people rupture their ACL. Does the person who ruptured his ACL while playing basketball get treated while the other individual who ruptured hers playing with her dog get sent home? Isn't it the condition - rather than the precipitating event - we're supposed to be treating?
There are no easy answers here. But the questions, the questions ...
The phenomenon has been around since the beginning of time, but our understanding remains limited. During World War I, soldiers who experienced "shell shock" were shot as cowards. In World War II, soldiers who suffered "battle fatigue" were given "therapy" to return them to combat in one week. (The therapy, such as exposure to recorded artillery fire sounds, typically exacerbated their distress.) General Patton infamously slapped a bed-ridden soldier.
The postwar DSM-I of 1952 recognized "gross stress disorder," but this was removed from the DSM-II of 1968. The post-Vietnam War era set the scene for its comeback in the DSM-III of 1980. Dr Andreasen was charged with the task of looking into "post-Vietnam syndrome." As Willa describes it:
Given her experience with burn victims, Andreasen pressed for a more inclusive description of the illness. Post Traumatic Stress Disorder entered the new edition, described as a stress reaction to a catastrophic stressor that is outside the range of usual human experience.
Unlike all other mental illnesses, the first criterion for a PTSD diagnosis is an event rather than a symptom. Another way of putting this is that the DSM mandates a valid reason for an individual's response. The DSM-IV of 1994 and this year's draft DSM-5 (due out in 2013) simply play around with the scope of the valid reason. The 1994 version widened the criterion to include events not necessarily outside the range of human experience (such as surviving an auto accident) while the DSM-5 would narrow it again.
Compare this to depression. Psychiatry does not require a valid reason for us to rate a diagnosis. To the contrary, a valid reason - such as bereavement - would rule out a diagnosis (unless the depression were to persist). In this context, depression would be a normal response to an abnormal situation. We are supposed to feel depressed when we lose someone close to us.
We often get clinically depressed for seemingly no reason at all. Since there is no logic to the depression, the thinking goes, we must be thinking and behaving irrationally. And if this significantly interferes with our daily life, we are presumed to have a mental illness. We elicit sympathy or opprobrium, as the case may be.
The same applies across the anxiety spectrum (with the notable exception of PTSD). We don't need a valid reason - such as an intruder entering through the window - to justify a panic attack. Being frightened of your own shadow will do just fine.
So, I'm wondering. What happens to the poor individual who suffers severe trauma for a stupid reason? Not from combat. Not from being exposed to an act of God or an unspeakable outrage. Something stupid, really stupid. Such as perhaps a close encounter with a circus clown. The trauma may be irrational, but then again so is all the rest of mental illness.
Is that person's distress any less?
Suppose two people rupture their ACL. Does the person who ruptured his ACL while playing basketball get treated while the other individual who ruptured hers playing with her dog get sent home? Isn't it the condition - rather than the precipitating event - we're supposed to be treating?
There are no easy answers here. But the questions, the questions ...
Labels:
John McManamy,
Nancy Andreasen,
PTSD,
Willa Goodfellow
More Thoughts on the Linear and Non-Linear People
In my last blog piece, I asserted there are two types of people, linear and non-linear. This topic came up in two talks I gave last month at the Kansas State DBSA conference. It also ties into a closely-related peanut butter-tofu theme I introduced at the conclusion of my first talk. So let's jump in, conclusion first:
Why don’t I conclude with a short reading from the book I’m working on?
Anyone NOT familiar with Star Trek? The people not familiar, of course, they're not going to raise their hands. That's like asking a room full of psychiatrists, "Anyone here with a mental illness?"
So, I'll read from the draft of the book I'm working on, which, as you will recall, is entitled, "Raccoons Respect My Piss, But Watch Out for Skunks." (Oh, I'm going to fight with the publisher to keep that title.)
So ...
No doubt, you recall the now-classic scene in the movie Star Trek where I attempt to explain the concept of peanut butter to an incredulous Spock.
"Peanut butter is not logical," Spock keeps telling me.
"You of all people would know that peanut butter is logical," I retort. "And if your mother truly loved you, you would feel the same way about peanut butter that I do."
Spock is valiantly trying not to give in to his anger. Although he identifies as a Vulcan his deceased mother was human. Earlier in the movie, his Vulcan father informed him he had a choice between two paths in life, his rational Vulcan self or his emotional human self.
Neither is right or wrong, father informs son. Both have advantages and disadvantages. Head or heart. Informed decision or gut.
So, here we are - Spock and me - on the bridge of the starship Enterprise. The Romulan renegade Nero has just destroyed Spock's planet and Earth is next. But first, time for a sandwich (priorities are priorities).
Spock keeps trying to explain that Cardassian tofu is logical.
"Yeh," I reply, "but it tastes like shit." I mean, seriously, have you ever seen a happy Cardassian?
"What does happiness have to do with it?" Spock shoots back at me.
***
That's my point. And there we go. We're peanut butter people trying to fit into a tofu world governed by Vulcans.
Now, probably you don't know what any of that means, but I like to leave people confused, I like to irritate, so maybe a pearl of wisdom might pop out.
So in the meantime, as I always tell people, enjoy the peanut butter. (Now you're really going to write on your evaluations I'm crazy.)
After my second talk, the other three speakers and I formed a discussion panel that took questions from the audience. The very first question involved bipolar and creativity. This was my answer:
If I can add something to that, Evelyn. I kind of jokingly referred to the linear people and the non-linear people. It's a idea I got from Nancy Andreasen, who does a lot of work studying creativity at the University of Iowa. She's the first one to do studies into this, and she's doing brain scan studies on creative people right now. Basically, our brains are organized in different ways that encourage us to think outside the box, and sometimes this means we don't test well doing linear tasks.
If there's a multiple choice question, sometimes all four answers look right to me. Because in a non-linear way, I can say, oh yeh, two plus two does equal six. Because if you do it this way and this way - can't you see that?
Or then they ask something stupid. And it's like - wait a second - there's a lot of ambiguity to this question. And that makes me look stupid, because: "Can't you understand the question?" "No, because there's too many possibilities with the answers here."
I've had to learn as part of my own social development - linear people think, "1,2,3,4,5, ..." I go, "1,2,28." And if I come up with a 28 answer in a group of people, they're going to think I'm weird. So I have to dial my 28 answer back to 6. Then it looks like I'm a little bit creative and lively.
Seriously, we're peanut butter people living in a land of tofu. And we have to learn to adapt to tofu, unfortunately. But the world gets its gifts through the peanut butter people.
I think you know where I'm going with that ...
To which my fellow panelist, Kansas WRAP coordinator Karen Cook, added:
"The question is how do you keep from being tofu - and stay peanut butter."
Why don’t I conclude with a short reading from the book I’m working on?
Anyone NOT familiar with Star Trek? The people not familiar, of course, they're not going to raise their hands. That's like asking a room full of psychiatrists, "Anyone here with a mental illness?"
So, I'll read from the draft of the book I'm working on, which, as you will recall, is entitled, "Raccoons Respect My Piss, But Watch Out for Skunks." (Oh, I'm going to fight with the publisher to keep that title.)
So ...
No doubt, you recall the now-classic scene in the movie Star Trek where I attempt to explain the concept of peanut butter to an incredulous Spock.
"Peanut butter is not logical," Spock keeps telling me.
"You of all people would know that peanut butter is logical," I retort. "And if your mother truly loved you, you would feel the same way about peanut butter that I do."
Spock is valiantly trying not to give in to his anger. Although he identifies as a Vulcan his deceased mother was human. Earlier in the movie, his Vulcan father informed him he had a choice between two paths in life, his rational Vulcan self or his emotional human self.
Neither is right or wrong, father informs son. Both have advantages and disadvantages. Head or heart. Informed decision or gut.
So, here we are - Spock and me - on the bridge of the starship Enterprise. The Romulan renegade Nero has just destroyed Spock's planet and Earth is next. But first, time for a sandwich (priorities are priorities).
Spock keeps trying to explain that Cardassian tofu is logical.
"Yeh," I reply, "but it tastes like shit." I mean, seriously, have you ever seen a happy Cardassian?
"What does happiness have to do with it?" Spock shoots back at me.
***
That's my point. And there we go. We're peanut butter people trying to fit into a tofu world governed by Vulcans.
Now, probably you don't know what any of that means, but I like to leave people confused, I like to irritate, so maybe a pearl of wisdom might pop out.
So in the meantime, as I always tell people, enjoy the peanut butter. (Now you're really going to write on your evaluations I'm crazy.)
After my second talk, the other three speakers and I formed a discussion panel that took questions from the audience. The very first question involved bipolar and creativity. This was my answer:
If I can add something to that, Evelyn. I kind of jokingly referred to the linear people and the non-linear people. It's a idea I got from Nancy Andreasen, who does a lot of work studying creativity at the University of Iowa. She's the first one to do studies into this, and she's doing brain scan studies on creative people right now. Basically, our brains are organized in different ways that encourage us to think outside the box, and sometimes this means we don't test well doing linear tasks.
If there's a multiple choice question, sometimes all four answers look right to me. Because in a non-linear way, I can say, oh yeh, two plus two does equal six. Because if you do it this way and this way - can't you see that?
Or then they ask something stupid. And it's like - wait a second - there's a lot of ambiguity to this question. And that makes me look stupid, because: "Can't you understand the question?" "No, because there's too many possibilities with the answers here."
I've had to learn as part of my own social development - linear people think, "1,2,3,4,5, ..." I go, "1,2,28." And if I come up with a 28 answer in a group of people, they're going to think I'm weird. So I have to dial my 28 answer back to 6. Then it looks like I'm a little bit creative and lively.
Seriously, we're peanut butter people living in a land of tofu. And we have to learn to adapt to tofu, unfortunately. But the world gets its gifts through the peanut butter people.
I think you know where I'm going with that ...
To which my fellow panelist, Kansas WRAP coordinator Karen Cook, added:
"The question is how do you keep from being tofu - and stay peanut butter."
Labels:
creativity,
John McManamy,
linear people,
non-linear people
Tuesday, May 25, 2010
Thoughts on the Linear People
The most interesting part of any talk I give is question time. Late last month, I keynoted the Kansas State DBSA conference in Manhattan. A gentleman pointed to a list on the wall of famous people with mental illness. "Where would the world be without these people?" he asked.
"I like to say to people," I replied, "we give you the gift of civilization and how do you treat us? You marginalize us."
I went on to say:
We discovered fire. I don't care if nobody wrote this down. Anyone crazy enough to go out into a burning forest and bring a flaming twig back inside a cave was not normal, was not thinking linearly, okay?
And just everything, from discovering America to painting the Sistine Chapel to writing Beethoven's Ninth to great poetry, great works of literature, to Isaac Newton, great works of science. I mean, literally, every field of human endeavor, we brought the world the gift of civilization and we get marginalized.
We also have to acknowledge the gifts within us. When the bad part of our illness is flaring up, I will trade it in for anything. But I'm not going to trade in my personality. I'll take it bad stuff and all. A lot of people are not there yet with that thought, and I respect that. But once you get your recovery up to a certain level, hey, acknowledge the gifts.
To me, the linear people [my term for so-called "normal" individuals] are dull and boring. I don't like hanging out with them. I much prefer the company of the non-linear people [that's us] which explains why my relationships are just terrible. Because I gravitate to these people.
The next question was seemingly unrelated:
"Before you were ever diagnosed," a lady asked, "did you ever self-medicate with alcohol or drugs?"
"Thank God I didn't," was my immediate response. Then it turned out I found a new angle on the theme I had just explored:
This is kind of a paradox, because growing up in the sixties and seventies - if you didn't do drugs you were really weird. But I didn't see what the big deal was because things are going in my head, I've got racing thoughts, visual things come in - and what people were describing, hey, that's me, normal.
I don't need to take anything. I inhaled and the stuff put me to sleep. If somebody is unfortunate enough to be born linear, maybe they need the drugs to be like us for a little while.
I know with a lot of our population we take drugs to self-medicate, but I think the linear people, they take the drugs to be like us.
Stay tuned for more Q and A ...
"I like to say to people," I replied, "we give you the gift of civilization and how do you treat us? You marginalize us."
I went on to say:
We discovered fire. I don't care if nobody wrote this down. Anyone crazy enough to go out into a burning forest and bring a flaming twig back inside a cave was not normal, was not thinking linearly, okay?
And just everything, from discovering America to painting the Sistine Chapel to writing Beethoven's Ninth to great poetry, great works of literature, to Isaac Newton, great works of science. I mean, literally, every field of human endeavor, we brought the world the gift of civilization and we get marginalized.
We also have to acknowledge the gifts within us. When the bad part of our illness is flaring up, I will trade it in for anything. But I'm not going to trade in my personality. I'll take it bad stuff and all. A lot of people are not there yet with that thought, and I respect that. But once you get your recovery up to a certain level, hey, acknowledge the gifts.
To me, the linear people [my term for so-called "normal" individuals] are dull and boring. I don't like hanging out with them. I much prefer the company of the non-linear people [that's us] which explains why my relationships are just terrible. Because I gravitate to these people.
The next question was seemingly unrelated:
"Before you were ever diagnosed," a lady asked, "did you ever self-medicate with alcohol or drugs?"
"Thank God I didn't," was my immediate response. Then it turned out I found a new angle on the theme I had just explored:
This is kind of a paradox, because growing up in the sixties and seventies - if you didn't do drugs you were really weird. But I didn't see what the big deal was because things are going in my head, I've got racing thoughts, visual things come in - and what people were describing, hey, that's me, normal.
I don't need to take anything. I inhaled and the stuff put me to sleep. If somebody is unfortunate enough to be born linear, maybe they need the drugs to be like us for a little while.
I know with a lot of our population we take drugs to self-medicate, but I think the linear people, they take the drugs to be like us.
Stay tuned for more Q and A ...
Monday, May 24, 2010
Schizophrenia: In Their Own Voices
Last week I was at a one-day conference put on by NAMI San Diego and the Senior Mental Health Partnership. My good friend Sally Shepherd (pictured here) was one of the speakers. Just days before, she had been informed that a study she had played a major role in designing and implementing had been accepted by The Schizophrenia Bulletin. The study sheds important light on how those with schizophrenia see themselves.
Sally and her fellow investigators interviewed 38 individuals with schizophrenia aged 50 and over, living in board and cares and unemployed. They asked six very basic questions, and essentially listened, just listened.
Significantly, only a quarter of the interviewees included relationships with family members in their criteria for "quality of life." Nearly half had never married. The remaining participants reported experiencing significant marital discord, including emotional abuse. Only two remained in long-term marriages.
In their own voices ...
Early Experience with Schizophrenia
But when you are labeled a schizophrenic or have psychosis and you don't understand it because you didn't learn about it prior to and you're like, all of a sudden you're in this nightmare, and with nobody to help you because nobody understands, nobody's in it with you. The whole world is dead; you're the only one alive in this big graveyard, which is the world. You have to survive with no money and no place to sleep and all these dead people trying to kill you or whatever, rob you of your sanity is more like it, same thing.
Personal Loss
It's not what I thought I'd have when I was younger. I thought I'd be doing something else. I didn't think I was going to be on Social Security when I was younger. I thought I was going to be a scientist.
Loss of Independence
In '98, I was sitting in the courtyard in the unit I was on. I was smoking my cigarette and went to find my [counselor]. I told her, "I don't want to die here, V. I don't want to die at [State Hospital]. V, what can I do?"
Self-Doubt
I asked her once, "Where did we go wrong? Why are we in these board and care homes?" I feel like we're here because people have given up on us or we've given up on ourselves.
Hopes and Dreams
I'm going to feel regretful because I never lived lived; I never had a chance to live. I never had a life. If I was just 21 and had accomplished my dream of a good job and my wife, my kids ...
Resignation
I have a roof over my head, I have food and clothing and my computer and my stereo, and if I compare my life with some of those starving in other countries, it's like I'm living in heaven compared to them.
Wednesday, May 19, 2010
Rerun: My Life as an International Awardee
From Oct 2009 ...
In the first piece to this series, I recalled my shock and dismay over being informed that I was to receive the Mogens Schou Award for Public Service, a major international award. In the second installment, I related how hearing Nobel Laureate John Nash at the 2007 APA in San Diego helped me understand the importance of what a little bit of recognition can do for one's recovery. To pick up where I left off ...
Three weeks following the APA, I was off to Pittsburgh for the Seventh International Conference on Bipolar Disorder to collect my Award. I knew I would be overexcited - hypomanic in a bipolar context - and as a precaution I arranged to have a platonic conference date to act as my frontal lobes.
The conference organizers comped me with a hotel suite (a suite!) that had real towels, plus a view out the windows. To contrast with the first conference I attended in 2001, back then I had a Priceline deal at a hotel a good long walk away from the venue.
I recall back in 2001 registering and helping myself to coffee and Danish, plus a yogurt and a juice, while trying to juggle my conference materials as I sat myself in a cramped space and attempted to make small talk with a very attractive European pharmacy expert. The Joe Cool act didn't fly. My coffee was slopping over the rim of my saucer, and the only way I would be able to negotiate my Danish was if my elbow were to suddenly sprout fingers.
Nevertheless, I managed to get through the day without totally embarrassing myself.
On the evening of Day Two of that conference I made my first minor faux pas (that is to say, the first one that I noticed). I hadn't bothered to take my sport jacket to the second day of the meeting. But now we were being shuttled off to a more formal setting at the Carnegie Museum, and I couldn’t exactly go up the elevator to retrieve my jacket.
I was definitely out of place as I gamely introduced myself to Michael Thase MD, one of the Conference organizers. A roving photographer asked a group of us to pose. Me, Dr Thase, and a darkly-tanned blond Dutch pediatric psychiatrist in open-toed stilettos. I so totally did not belong in this picture.
The occasion was the first-ever presentation of the Mogens Schou Awards and dinner, where I managed not to further embarrass myself. Later, the shuttle dropped us off at the conference venue, and I set off on my own into the night, back to my hotel.
Fast Forward, June 2007: The second evening of the conference was once again reserved for the Mogens Schou Awards and dinner, once more held at the Carnegie Museum. This time, I showed up dressed to kill, in a black business suit and a Thomas Pink shirt that probably threw me back for far more than my suit.
The cocktail hour portion of the evening was coming to a close. It was time for me to move forward toward a small stage platform and hover. On a small table were four Plexiglas Awards, resplendently bathed in discreet overhead lighting.
David Kupfer MD, head of the psych department at UPitt, issued some opening remarks and handed over the first Award of the night - Education and Advocacy - to Adriano Camargo, president of the Brazilian Association for Affective Disorders. Ellen Frank PhD of UPitt and a pioneer in a certain type of talking therapy for bipolar - then presented two Awards to the University of Barcelona powerhouse research team of Francesc Colom PsyD, PhD and Eduard Vieta MD, PhD. There was one Award remaining on the table.
Michael Thase approached the podium, with the Public Service Award in his hand. "I'm pleased tonight," he began, "to show our gratitude for the man who is my favorite person in medical journalism ..."
SuddenIy I was on the podium, shaking hands with Dr Thase. Then I had the Award crooked in my arm. The applause died down. It was my turn to speak.
I could have told these people what it was like for me back in 2001. But no one had to know that. This was my moment, my time. I belonged in this picture.
But life has a way of intervening. The next day, a certain psychic undertow began to kick in. I woke up much later than usual and spent the last day of the conference in a sort of anti-climatic semi-coma. By the time I flew out the next day, I felt a cold coming on. Back on my mountain, my mood dropped like a manhole cover. My batteries were dead. No energy. I needed to hibernate.
None of this Award going to my head business for me. My brain and my immune system have a way of keeping me in my place. Before enlightenment - draw water, chop wood. After enlightenment - draw water, chop wood.
I found it gratifying that I was not exactly the same person drawing water and chopping wood, but the positive strides I was making in moving my life forward had blinded me to the fact that I was pushing myself way too hard. That plus the fact the last two or three years of my life were catching up with me. Too many life-changing events compressed into way too short a period of time with nothing but factory-reject vulnerability genes to handle the load.
Curse you, 5HHT polymorphism!
Monday, May 17, 2010
Sunday, May 16, 2010
Rerun: The Borderline Personality Disorder Matzoh Ball
From last year ...
My final (for right now) Borderline Personality Disorder Awareness Month installment:
Until just a very short time ago, psychiatry treated borderline personality disorder as one big matzoh ball on the table. Freud and his followers, of course, were to blame for the embarrassment. If only these idiots were to go away, the thinking went, they might take their matzoh ball with them.
Then, psychiatry conceded that yes, the matzoh ball was here to stay, but where to put it? In the schizophrenia casserole? In the bipolar stew?
The borderline matzoh ball didn't deserve it's own dish. A soup, maybe, but certainly not a soup of the day, and definitely not where customers could find it on the menu.
Real mental illness involved scientists talking about tangible stuff such as heritable traits and brain biology, not Freudian cultists babbling nonsense about emotional attachments and integrating aspects of one's self.
Get over it, psychiatry. The borderline matzoh ball is not only here to stay, it rates a featured place on the specials board. In 2008, the NIMH reported on a series of brain imaging studies led by Michael Minzenberg MD of the University of California, Davis.
Previous brain scan research pointed the way by linking a wide range of behaviors to heightened activity in the primitive limbic regions of the brain, most notably the amygdala which mediates arousal and fear. Thus, a hypersensitive limbic system, in response to stress or even just perceived stress, may override the thinking cortical areas of the brain.
In short, people go crazy. Depression, anxiety, mania, aggression, and psychosis are just some of the possible responses. Individuals vulnerable to stress also tend to behave destructively, such as reaching for the bottle or over-eating or sexual promiscuity or self-harm.
There is an added complication: While the limbic region of the brain appears to be overdeveloped, certain cortical regions - most prominently the anterior cingulate cortex (ACC) - appear to be underdeveloped. The ACC, it turns out, is wired into the limbic fear hub.
Perhaps you see where this is going: The ACC acts as a key modulator to limbic over-excitement, and when this part of the brain is not booting up right, the thinking parts of the brain are not only taken off-line, they remain out of commission long enough for people to notice.
In the first study, Minzenberg and colleagues compared the brain scans of borderline patients with healthy controls. While in an MRI machine, the subjects viewed images of "scary faces" (a very common experiment in functional or fMRI). Predictably, the borderline patients displayed overactivity in the amygdala and underactivity in the ACC. In the words of the NIMH:
"Since ACC activity would normally increase to dampen an overactive amygdala, this suggested weak regulation of emotion in the circuit."
Next, the researchers employed structural or anatomical MRI to compare grey matter in the same subjects. The studies found that relative to the controls, the borderline subjects showed increased grey matter density in parts of the amygdala (image below top, red areas) and decreased grey matter in parts of the ACC (image below bottom, yellow area at right). As the NIMH describes it:
"This suggested an abnormality in the number or architecture of neurons in these key components of the emotion-regulating circuit, which other evidence links to impaired functioning of the serotonin chemical messenger system."
Some quick disclaimers here. The amygdala and the ACC and its connecting circuitry have been implicated with regard to depression and other behaviors. Thus, these studies cannot be cited as irrefutable proof of the borderline diagnosis. For that to happen, we would have to find out what is wrong in the brain that is unique to borderline (or for that matter any other mental illness) and then connect the dots.
What the brain scans do show is that borderline undeniably shares a similar pattern of underlying brain dysregulation as other illnesses regarded as biological, on the same order of magnitude as bipolar and schizophrenia and the rest.
We can even take it a step further. Think of borderline as a condition where its victims constantly view the world as threatening and unpredictable. So, when we're discussing fear factor miscues in the brain, which illness does it best apply to? So ...
Get ready, which illness then becomes the featured dish of biological psychiatry?
Holy cow! The humble Freudian matzoh ball.
Further reading from mcmanweb:
Psychiatry's Big Bang
In addition, an NIMH study under review shows the ventromedial prefrontal cortex modulating amygdala activity through the cingulate. Ah, a part of the brain associated with "thinking," your protection against lashing out like a caged beast. Thus, if you happen to be in the middle of a heated marital dispute, this is probably the time to draw in a slow breath and very calmly say, "I hear you. I think we can work something out."
If your amygdala is doing the talking, however, it may come out something like this: "And besides, you’re lousy in bed!"
At this stage, storming out the door in a huff may be your best option. The amygdala is getting through to the cortex, but the cortex is clearly having difficulty getting through to the amygdala. You probably will be sleeping on the couch tonight, but thankfully you can count on your cortex not to let your behavior escalate from regrettable to extreme. But suppose your top-down circuitry is faulty?
As Dr Meyer-Lindenberg explained, we need a breakdown in the brain’s control mechanisms to become violent. ...
My final (for right now) Borderline Personality Disorder Awareness Month installment:
Until just a very short time ago, psychiatry treated borderline personality disorder as one big matzoh ball on the table. Freud and his followers, of course, were to blame for the embarrassment. If only these idiots were to go away, the thinking went, they might take their matzoh ball with them.
Then, psychiatry conceded that yes, the matzoh ball was here to stay, but where to put it? In the schizophrenia casserole? In the bipolar stew?
The borderline matzoh ball didn't deserve it's own dish. A soup, maybe, but certainly not a soup of the day, and definitely not where customers could find it on the menu.
Real mental illness involved scientists talking about tangible stuff such as heritable traits and brain biology, not Freudian cultists babbling nonsense about emotional attachments and integrating aspects of one's self.
Get over it, psychiatry. The borderline matzoh ball is not only here to stay, it rates a featured place on the specials board. In 2008, the NIMH reported on a series of brain imaging studies led by Michael Minzenberg MD of the University of California, Davis.
Previous brain scan research pointed the way by linking a wide range of behaviors to heightened activity in the primitive limbic regions of the brain, most notably the amygdala which mediates arousal and fear. Thus, a hypersensitive limbic system, in response to stress or even just perceived stress, may override the thinking cortical areas of the brain.
In short, people go crazy. Depression, anxiety, mania, aggression, and psychosis are just some of the possible responses. Individuals vulnerable to stress also tend to behave destructively, such as reaching for the bottle or over-eating or sexual promiscuity or self-harm.
There is an added complication: While the limbic region of the brain appears to be overdeveloped, certain cortical regions - most prominently the anterior cingulate cortex (ACC) - appear to be underdeveloped. The ACC, it turns out, is wired into the limbic fear hub.
Perhaps you see where this is going: The ACC acts as a key modulator to limbic over-excitement, and when this part of the brain is not booting up right, the thinking parts of the brain are not only taken off-line, they remain out of commission long enough for people to notice.
In the first study, Minzenberg and colleagues compared the brain scans of borderline patients with healthy controls. While in an MRI machine, the subjects viewed images of "scary faces" (a very common experiment in functional or fMRI). Predictably, the borderline patients displayed overactivity in the amygdala and underactivity in the ACC. In the words of the NIMH:
"Since ACC activity would normally increase to dampen an overactive amygdala, this suggested weak regulation of emotion in the circuit."
Next, the researchers employed structural or anatomical MRI to compare grey matter in the same subjects. The studies found that relative to the controls, the borderline subjects showed increased grey matter density in parts of the amygdala (image below top, red areas) and decreased grey matter in parts of the ACC (image below bottom, yellow area at right). As the NIMH describes it:
"This suggested an abnormality in the number or architecture of neurons in these key components of the emotion-regulating circuit, which other evidence links to impaired functioning of the serotonin chemical messenger system."
Some quick disclaimers here. The amygdala and the ACC and its connecting circuitry have been implicated with regard to depression and other behaviors. Thus, these studies cannot be cited as irrefutable proof of the borderline diagnosis. For that to happen, we would have to find out what is wrong in the brain that is unique to borderline (or for that matter any other mental illness) and then connect the dots.
What the brain scans do show is that borderline undeniably shares a similar pattern of underlying brain dysregulation as other illnesses regarded as biological, on the same order of magnitude as bipolar and schizophrenia and the rest.
We can even take it a step further. Think of borderline as a condition where its victims constantly view the world as threatening and unpredictable. So, when we're discussing fear factor miscues in the brain, which illness does it best apply to? So ...
Get ready, which illness then becomes the featured dish of biological psychiatry?
Holy cow! The humble Freudian matzoh ball.
Further reading from mcmanweb:
Psychiatry's Big Bang
In addition, an NIMH study under review shows the ventromedial prefrontal cortex modulating amygdala activity through the cingulate. Ah, a part of the brain associated with "thinking," your protection against lashing out like a caged beast. Thus, if you happen to be in the middle of a heated marital dispute, this is probably the time to draw in a slow breath and very calmly say, "I hear you. I think we can work something out."
If your amygdala is doing the talking, however, it may come out something like this: "And besides, you’re lousy in bed!"
At this stage, storming out the door in a huff may be your best option. The amygdala is getting through to the cortex, but the cortex is clearly having difficulty getting through to the amygdala. You probably will be sleeping on the couch tonight, but thankfully you can count on your cortex not to let your behavior escalate from regrettable to extreme. But suppose your top-down circuitry is faulty?
As Dr Meyer-Lindenberg explained, we need a breakdown in the brain’s control mechanisms to become violent. ...
Friday, May 14, 2010
Rerun: Piecing Together the Borderline Puzzle
More on borderline personality disorder, from last year ...
May is Borderline Personality Disorder Awareness Month. Our story so far:
In 1980, borderline personality disorder received formal recognition as a diagnosis with its inclusion into the DSM-III. The catch was that the illness was consigned to "Axis II," widely regarded as psychiatry's wrong side of the tracks. As an editorial by John Oldham MD of the Menniger Clinic in this month's American Journal of Psychiatry explains:
The decision derived from the belief that borderline and other personality disorders were "caused during early development by parental neglect, abuse, or inconstancy." The prototypical image of a patient was that of an angry volatile individual prone to reject help, blame others, and behave self-destructively. "Too often, this behavior was seen as willfully oppositional, and borderline personality disorder patients were spoken of as dreaded pariahs."
Our current clinical and scientific knowledge, Dr Oldham advises, is changing those perceptions. Core "heritable endophenotypes" of affective dysregulation and impulsive aggression have been identified. Brain scans reveal specific abnormalities, namely a hyperactive limbic system, in particular the amygdala (which mediates arousal and fear). Thus, certain individuals are primed to overanticipate and overreact when their personal dealings hit a snag.
This state of emotional overdrive is difficult to extinguish, owing to impairment in the cortical areas to inhibit this limbic-driven emotionality or impulsivity.
As if this isn't bad enough, this phenomenon of "brain gone wild" interferes with forming emotional attachments during child development, which may be magnified by lack of adequate parental support. As Dr Oldham describes it:
"These combined etiological factors produce arrested, distorted, or incomplete integration of aspects of self and others, resulting in early onset and persistence of profound interpersonal difficulties. Normal early development becomes derailed, and the crucial developmental milestone of basic trust is not achieved."
No wonder no one has come up with a med to treat borderline patients. As a second editorial - by Otto Kernberg MD and Robert Michels MD of Cornell - explains, only 30 percent of patients with borderline respond satisfactorily to meds over the long term.
(Editorial sidebar: Psychiatry has unofficially used response to meds as an indicator of whether the illness is biological or merely a construct of the mind. Thus, borderline gets nowhere near the same respect as schizophrenia, which - ironically - evidences similarly low and perhaps even worse response rates.)
Dialectical behavioral therapy and other talking therapies produce beneficial results in the short term, but Drs Kernberg and Michels caution that "basic underlying chronic personality dispositions may remain unchanged."
Thus, years and decades after completion of therapy, individuals with borderline may still face major challenges in personal satisfaction with how their lives are going. On one hand, borderline has been dubbed the "good prognosis diagnosis," based on research showing an 80 percent remission rate over ten years. But the authors caution that these findings are focused more on DSM symptoms, "and much less on the subtle and permanent features of their difficulties in work, love, social life, and creativity."
The bad news is that despite the significant gains in our body of knowledge, "the relationships between clinical symptoms, deeper psychological structures, and underlying neurobiological systems are, as yet, to be explored."
The good news is we are learning as we go. As the authors conclude:
"Borderline patients have long been to psychiatry what psychiatry has been to medicine - a subject of public health significance that is underrecognized, undertreated, underfunded and stigmatized by the larger discipline. As with psychiatry and medicine, this is changing. New knowledge, new attitudes, and new resources promise new hope for persons with borderline personality."
Further reading from mcmanweb:
Borderline Personality Disorder
Those who live with individuals with borderline describe the experience as akin to walking on eggs. By contrast, Anne compared her dealings with people to "walking on shifting boards." The world is far from a safe place, and the ground beneath her could collapse any second.
"It’s like demons possess me," she related. Something inside of yourself so overwhelms you that you want to change it instantly. Such as slitting your wrists, impulsive sex, alcohol, and acting out. She described individuals with borderline as spontaneous and lively and loving until they get hurt. Then they screw up and fall apart. The irony, she said, is people with this disorder want to help so much, but the problem is they have trouble relating to people.
She emphasized that people with borderline can change (another speaker referred to the illness as "the good prognosis diagnosis"). Anne concluded with reference to her favorite bumper sticker, "Don’t believe everything you think."
Labels:
borderline personality disorder,
DSM,
John McManamy,
puzzle
Tuesday, May 11, 2010
Rerun: Borderline Personality Disorder - Searching for Respect
This from last year ...
In recognition of Borderline Personality Disorder Awareness Month, the second in a series:
Psychiatry has had one hell of a time trying to figure out borderline personality disorder, but we all know it when we see it. Case in point (from an article in this month's American Journal of Psychiatry):
"Ms A" told her therapist of an embarrassing episode in which she had shouted at a store clerk she perceived as rude. What set off the incident was the clerk would not accept her credit card.
Her therapist asked whether it was store policy not to accept credit cards or whether the clerk had singled out her credit card in particular.
"What difference does it make?" the patient responded in a fury. "Even if it was the policy of the store and not directed at me, he still should have been courteous!"
The patient then exploded into a screaming rage: "You’re not interested in empathizing with my feeling of being humiliated - only in figuring out how I caused the whole incident! It’s clear that you don’t care about me ... "
Yep, know it when we see it. Um - but what the hell is it?
As another article in the AJP (by leading expert John Gunderson MD of Harvard) makes clear, the very name borderline indicates various attempts at figuring out what the illness is NOT. In the words of outspoken critic Hagop Akiskal MD of UCSD, borderline over the decades has resembled "an adjective in search of a noun."
Back in the 1930s and into the 50s, it was thought that the noun had to be schizophrenia. According to the theory, it was believed that, in certain situations, some patients regressed into "borderline schizophrenia."
In the late 60s, those nouns became neurosis and psychosis. In a psychoanalytic framework, "borderline personality organization" occupied that nebulous middle ground between neurotic patients (who were considered treatable) and those who were written off as psychotics. "Neurotics who drive their shrinks crazy" would be another way to describe what clinicians observed in their offices.
Give psychoanalysis credit for bringing coherence to the phenomenon, including recognition of: emotional instability, need to attach to others, distorted sense of self and others, reliance on "splitting," and fears of abandonment.
From there, borderline progressed to a "syndrome," still within the purview of psychoanalysis. In 1980 - with the publication of the first modern DSM (DSM III), psychiatry formally recognized the diagnosis as "borderline personality disorder," but in the context of an endangered species consigned to a doomed habitat (Axis II).
Soon after, with the near-total collapse of psychoanalysis, borderline lost its chief group of champions, thereby leaving the diagnosis open to attack. Psychiatry's new generation of whizz kids reached for their chainsaws, along with the mandatory new noun. This time, the noun was depression, as in borderline being some kind of atypical depression.
But the diagnosis found support in new research that convincingly validated the illness, with a course that differed from schizophrenia and depression. Those with borderline showed clear signs of vulnerability to stress, but this - ironically - suggested yet another noun, PTSD (where there exists a substantial overlap).
The diagnosis entered the DSM-IV of 1994 virtually unchanged, though the question was raised about whether a patient could be considered borderline if he or she responded to meds. Against this backdrop emerged the hypothesis that borderline had to do with breakdowns in two key neurotransmitter systems, which translated to either: 1) difficulty in controlling impulses, or 2) emotional (affective) dysregulation.
Meanwhile (and predictably) bipolar became borderline's new candidate noun. Bipolar (with the new "bipolar II" diagnosis) was taking over territory formerly occupied by depression, and borderline was the next logical direction for expansion. But new studies pointed to critical distinctions between the two illnesses, including a failure in borderline patients to "mentalize," that is the capacity to relate to one's own mental states and the states of others.
Coincident with these findings was the success of the first therapy designed specifically for borderline patients, dialectical behavioral therapy. This brought on board a new generation of champions, which may have turned the tide in borderline's favor once and for all.
Still, as Dr Gunderson points out, for a highly prevalent, disabling, and deadly illness that virtually everyone these days acknowledges, borderline still has a long way to go before achieving respect. Psychiatrists receive virtually no training in the illness, few new investigators are entering the field, and proven treatments are often unavailable.
An upgrade to Axis I (in the company of bipolar, schizophrenia, etc) would be a step in the right direction. Says Dr Gunderson:
"It belongs on Axis I to signify its severity, its morbidity, and its unstable course. But it belongs there too to prioritize its usage and to underscore the need for its treatment to be reimbursed."
How about changing the name? Dr Gunderson kinda likes borderline, arguing that the term signifies the illness' "unclear boundaries while reminding us of an unwanted truth, namely, that psychiatric disorders, like other medical conditions, are heterogeneous and have flexible boundaries."
Me? I would go with "No-Noun Disease."
Further reading from mcmanweb:
Borderline Personality Disorder
Unexpectedly, the first borderline discussion there occurred during question time at a packed luncheon symposium on bipolar II. One of the presenters, Terence Ketter MD of Stanford, happened to say that as opposed to bipolar disorder, which is about MOOD lability (volatility), borderline personality disorder is about EMOTIONAL lability. As soon as they develop an emotion stabilizer (analogous to a mood stabilizer), he said, borderline personality disorder will become an Axis I disorder rather than Axis II.
Axis I disorders, as categorized by the DSM-IV, include bipolar disorder, depression, anxiety, schizophrenia, and other illnesses regarded as biologically-based and treatable with medications. Axis II disorders tend to get a lot less respect. As well as borderline personality disorder, these include antisocial personality disorder, narcissistic personality disorder, and a host of behaviors that impede personal and social function.
During the same round of questions, S Nassir Ghaemi MD of Emory University said that he thought borderline personality disorder was a "clinical condition" rather than a disease. As such, the condition is more appropriate for psychotherapy rather than medications treatment. Hagop Akiskal MD of the University of California, San Diego, was decidedly less accommodating: "I don’t have any use for the borderline diagnosis," he asserted.
Dr Akiskal, the leading proponent of the mood spectrum, has been badmouthing borderline for decades. A 1985 article he co-authored had this title: "Borderline: An Adjective in Search of a Noun." Dr Akiskal has made a study of personality, but in the context of temperaments distributed along a continuum ranging from benign to affective illness. ...
Update May 10
A lot has happened since I wrote this a year ago. Stay tuned ...
Friday, May 7, 2010
Rerun: May is Borderline Personality Disorder Awareness Month
This from last year ...
Yes, the heading is real, and it's about time. In April, 2008, in response to public advocacy efforts, the US House of Representatives unanimously passed House Resolution 1005 supporting the month of May as "Borderline Personality Disorder Awareness Month."
The resolution stated that "despite its prevalence, enormous public health costs, and the devastating toll it takes on individuals, families, and communities, [borderline personality disorder] only recently has begun to command the attention it requires."
I came across this nugget of information late last night while quickly scanning this month's American Journal of Psychiatry, where I was flabbergasted (a good sign) to find two editorials and three articles devoted to borderline.
Minutes before, I had been clicking through a PDF of the program book of the American Psychiatric Association's upcoming annual meeting which I will be attending in San Francisco in two weeks. The topic index to the program book lists 20 sessions devoted to mood disorders and 18 sessions devoted to personality disorders.
Knock me over with a feather. In the seven years I have been attending APA meetings, you would hardly know borderline and related illnesses fell under the purview of psychiatry. Three years earlier, with the intention of bringing myself up to speed on borderline, I found but three or four sessions on the program devoted to the illness. In fact - at a session on bipolar II at that particular meeting - two of the panelists and some of the audience questioned the validity of the borderline diagnosis in the first place.
A lot as changed since then. For starters, we know that the illness cannot be written off as mere bad behavior or as a variant of a mood disorder. Rather, it is abundantly clear that we are dealing with a serious medical illness that condemns four percent of the population to tortured lives, with suicide rates on a par with depression and bipolar.
Individuals with borderline face extreme difficulty responding to their environment, a process that science is showing to be mediated by the biology of the brain.
We also know that individuals with borderline respond well to certain types of talking therapy, and that their long term outcomes are exceptionally favorable. The only reason that meds work less well for those with borderline is because it is patently obvious we haven't come up with the right meds.
A very strong case can now be made - indeed, an undeniably airtight one - that the highest priority for the next DSM is to shift borderline personality disorder from Axis II - psychiatry's version of Siberia - to Axis I, in the same company as depression, bipolar, schizophrenia, and other illnesses the profession takes seriously.
NAMI has been successful in promoting public awareness for borderline while the NIMH has invested greater resources in research. In January this year, Time magazine devoted a feature article to the illness, and over the past two or three years we have witnessed a number of popular new books on the topic.
So, back to last night: In the space of ten minutes, from two different sources, I came up with undeniable evidence that psychiatry is finally starting to give borderline the respect it deserves. This is the result of incremental changes over a long period of time rather than an overnight sensation.
But - overnight - it suddenly occurred to me that this new professional respect, combined with public awareness, has to be one of the three most significant mental health events I've encountered since I began writing about my illness ten years ago, equal to the recognition of bipolar in young kids and to the mind-boggling advances in brain science.
The effect is bound to significantly improve the lives of countless individuals, long neglected and even held in contempt by professionals who should have known better. It is also likely to generate a backlash, particularly if people start perceiving borderline as a fad diagnosis.
So ...
I will pay a return visit to this months AJP for a long deep perusal, plus check out other sources, and will be reporting back in a series of blog posts this week. Stay tuned ...
Update May 7, 2010
In Feb this year, the DSM-5 Task Force released a proposed revision that would eliminate the artificial distinction between Axis I and Axis II disorders. In addition, as well as the curent "categorical" approach that separates out borderline from antisocial and other personality disorders, there would also be a "dimensional" element that acknowledges the overlap. More on this in upcoming blogs ...
Further reading from mcmanweb:
Borderline Personality Disorder
In true Axis I depression, Dr Paris explained, when patients come out of a depression, they are nice people again. Individuals with personality disorders, by contrast, can come out of a depression and still have problems with life. Unfortunately, clinicians prefer not to want to hear about personality. It means trouble. They would rather throw more meds at the problem.
The world is complicated, Dr Paris noted, but we want it simple, and therein lies the challenge: In the bipolar II symposium, the presenters were discussing difficult-to-treat depressions. The depressions they were talking about were those that acted suspiciously like bipolar, which strongly implies using mood stabilizers instead of antidepressants.
Dr Paris was also talking about difficult-to-treat depressions, but the ones he described pointed to personality issues and a long course in talking therapy. These patients are not going to get better fast, he warned. Clinicians have to plan for chronicity. Moreover, in a true personality disorder, the course of the illness is different. These individuals are not going to become bipolar over time. ...
Wednesday, May 5, 2010
The Miracle
Shit happens. Two tons of it unexpectedly crashed down on my head on Sunday. In two seconds, my living situation turned upside down. Totally. The rest of the day was spent absorbing the alternating body blows of raging anger and despairing depression. I managed to reach out to some friends, who validated my feelings and who offered practical advice.
I didn’t ask them to take sides. The kind of friends I have wouldn’t do that, anyway. Shit happens. My feelings were a natural - and normal - byproduct of shit happening. My friends understand that.
“I know how you feel.” Five magic words. I wasn’t alone in the world.
As fate would have it, a short while earlier, another good friend had also experienced two tons of shit. Very different set of circumstances. Almost the exact same feelings. We both needed to get out of the house. With her six-year-old son, we did pizza and bowling. We finished up outdoors, slurping ice cream, in a state of conditional armistice with the raging host inside our heads.
I woke up the next day with my brain settling down, but this morning I felt myself going under. Seriously going under. I couldn’t go back to sleep, I couldn’t get myself out of bed. The terrible thought hit me: What if this time, all my coping skills fail me? What if this time, there is no coming back out of it? What if this time, my opportunistic depression, the nemesis that has relentlessly stalked me just about my entire life, stops toying with me? What if this time, the depression finishes the job?
I needed to get out of bed. I couldn’t. The depression had the upper hand. Ten months before, intense sciatic pain pinned me to the mattress. The mental pain I experienced this morning was just as strong, stronger. Each moment I remained horizontal only increased its strength.
What if this time ...
My mind flashed to the individual who had initiated the chain of circumstances that found me in this wretched condition. Suddenly, I visualized myself taking a heavy glass and throwing it at his head. Hard, really hard. Nolan Ryan hard. With the thought, a power surge of unadulterated cosmic anger coursed through every micro-circuit of my being.
I looked around. I was out of bed, halfway across the room. Me here, the bed there. How did that happen? No idea, not a clue.
I gathered myself, took a few breaths. I’m up, I decided. May as well shower. I pulled myself together, got in the car, and headed out to do the things I needed to do. I did them. The lady handed me over a legal agreement. I signed on the dotted line. It was done. Infinite relief.
Who knows? Tomorrow I may feel like shit again. Yet another whole new load of shit may come crashing down on my head. Today, my depression served notice on me. It let me know who was the true master of my brain. It let me know in its own way that it will be back. But on this day, today, I was - miraculously - granted a reprieve.
If you happen to encounter me face-to-face, you have a good chance of catching me laughing, really laughing. Depression is my constant companion. Any moment it makes itself scarce is a gift. It always returns, and one day I fear it will return for good. Which is why when I laugh, I don’t just laugh. I laugh my ass off.
It's been that kind of day.
I didn’t ask them to take sides. The kind of friends I have wouldn’t do that, anyway. Shit happens. My feelings were a natural - and normal - byproduct of shit happening. My friends understand that.
“I know how you feel.” Five magic words. I wasn’t alone in the world.
As fate would have it, a short while earlier, another good friend had also experienced two tons of shit. Very different set of circumstances. Almost the exact same feelings. We both needed to get out of the house. With her six-year-old son, we did pizza and bowling. We finished up outdoors, slurping ice cream, in a state of conditional armistice with the raging host inside our heads.
I woke up the next day with my brain settling down, but this morning I felt myself going under. Seriously going under. I couldn’t go back to sleep, I couldn’t get myself out of bed. The terrible thought hit me: What if this time, all my coping skills fail me? What if this time, there is no coming back out of it? What if this time, my opportunistic depression, the nemesis that has relentlessly stalked me just about my entire life, stops toying with me? What if this time, the depression finishes the job?
I needed to get out of bed. I couldn’t. The depression had the upper hand. Ten months before, intense sciatic pain pinned me to the mattress. The mental pain I experienced this morning was just as strong, stronger. Each moment I remained horizontal only increased its strength.
What if this time ...
My mind flashed to the individual who had initiated the chain of circumstances that found me in this wretched condition. Suddenly, I visualized myself taking a heavy glass and throwing it at his head. Hard, really hard. Nolan Ryan hard. With the thought, a power surge of unadulterated cosmic anger coursed through every micro-circuit of my being.
I looked around. I was out of bed, halfway across the room. Me here, the bed there. How did that happen? No idea, not a clue.
I gathered myself, took a few breaths. I’m up, I decided. May as well shower. I pulled myself together, got in the car, and headed out to do the things I needed to do. I did them. The lady handed me over a legal agreement. I signed on the dotted line. It was done. Infinite relief.
Who knows? Tomorrow I may feel like shit again. Yet another whole new load of shit may come crashing down on my head. Today, my depression served notice on me. It let me know who was the true master of my brain. It let me know in its own way that it will be back. But on this day, today, I was - miraculously - granted a reprieve.
If you happen to encounter me face-to-face, you have a good chance of catching me laughing, really laughing. Depression is my constant companion. Any moment it makes itself scarce is a gift. It always returns, and one day I fear it will return for good. Which is why when I laugh, I don’t just laugh. I laugh my ass off.
It's been that kind of day.
Tuesday, May 4, 2010
A Smart Dopamine Med May Do Wonders For You (the problem is one doesn't exist)
Another extract from a much lengthier mcmanweb article published three years ago:
The April 2007 American Journal of Psychiatry features an editorial by Bruce Cohen MD, PhD and William Carlezon PhD, both of Harvard, entitled "Can’t Get Enough of That Dopamine." As the authors point out, "through their many connections, dopamine neurons participate in the modulation of expectation, reward, memory, activity, attention, drives, and mood - the very substrates of psychiatric illness."
Not surprisingly, dopamine dysregulation is implicated in schizophrenia, bipolar, depression, ADD, and substance use. Stimulants and various recreational drugs enhance dopamine signaling while antipsychotics set up a dopamine blockade.
Now here’s the catch. The editorial cites a University of Toronto study appearing in the same issue that shows what dopamine blockade does throughout the brain. Yes, antipsychotics work well in clearing up mania and psychosis, but often at the expense of making patients feel worse.
The study involved 12 patients diagnosed with schizophrenia who had been placed on either Zyprexa or Risperdal. They were given PET scans and queried about their subjective feelings. Those who reported lower states of well-being and higher dysphoria tended to turn up scans that showed greater dopamine blockade.
The striatum region of the brain, above the brainstem, is "dopamine central." From there, dopamine-active neurons project into other brain regions. The study found that blockade of dopamine receptors in the striatum strongly corresponded to a sense of impaired mental function. The study also found that blockade in "extrastriatal" regions such as the temporal lobe correlated to altered emotional regulation.
The effect is about as subtle as the IRS freezing all your bank accounts. True, your mania or psychosis may be gone, but now you may not be able to adequately think or feel. Who wants to live like that? Naturally, the patient gets blamed for noncompliance. According to the editorial:
Without adequate dopamine signaling, our patients do not feel "well." When dopamine systems are dysfunctional, patients seek a change. This may involve stopping a medication, such as antipsychotic drugs that block dopamine. Alternatively, it may be manifest as taking a drug, such as cocaine, that enhances dopamine activity. Either way patients are probably seeking to restore dopamine function.
Obviously, for a lot of us, antipsychotics and stimulants are a godsend. But we also know that our dopamine meds are too dumb to figure out in which regions of the brain they are not wanted. Our current inventory works directly on the dopamine system, but the editorial suggests that a smarter strategy may lie in developing meds with an indirect effect. One possibility is targeting the endorphin, dynorphin, whose neurons are engaged in a feedback loop with dopamine. Another is by learning more about the intracellular signaling connected with dopamine transmission and reception.
In the meantime, we are stuck with the low-tech solutions of considering easing off on antipsychotics doses and just saying no to (street) drugs. Maybe your psychiatrist can come up with some creative work-arounds, but first he or she needs to listen your concerns, really listen.
Full article
The April 2007 American Journal of Psychiatry features an editorial by Bruce Cohen MD, PhD and William Carlezon PhD, both of Harvard, entitled "Can’t Get Enough of That Dopamine." As the authors point out, "through their many connections, dopamine neurons participate in the modulation of expectation, reward, memory, activity, attention, drives, and mood - the very substrates of psychiatric illness."
Not surprisingly, dopamine dysregulation is implicated in schizophrenia, bipolar, depression, ADD, and substance use. Stimulants and various recreational drugs enhance dopamine signaling while antipsychotics set up a dopamine blockade.
Now here’s the catch. The editorial cites a University of Toronto study appearing in the same issue that shows what dopamine blockade does throughout the brain. Yes, antipsychotics work well in clearing up mania and psychosis, but often at the expense of making patients feel worse.
The study involved 12 patients diagnosed with schizophrenia who had been placed on either Zyprexa or Risperdal. They were given PET scans and queried about their subjective feelings. Those who reported lower states of well-being and higher dysphoria tended to turn up scans that showed greater dopamine blockade.
The striatum region of the brain, above the brainstem, is "dopamine central." From there, dopamine-active neurons project into other brain regions. The study found that blockade of dopamine receptors in the striatum strongly corresponded to a sense of impaired mental function. The study also found that blockade in "extrastriatal" regions such as the temporal lobe correlated to altered emotional regulation.
The effect is about as subtle as the IRS freezing all your bank accounts. True, your mania or psychosis may be gone, but now you may not be able to adequately think or feel. Who wants to live like that? Naturally, the patient gets blamed for noncompliance. According to the editorial:
Without adequate dopamine signaling, our patients do not feel "well." When dopamine systems are dysfunctional, patients seek a change. This may involve stopping a medication, such as antipsychotic drugs that block dopamine. Alternatively, it may be manifest as taking a drug, such as cocaine, that enhances dopamine activity. Either way patients are probably seeking to restore dopamine function.
Obviously, for a lot of us, antipsychotics and stimulants are a godsend. But we also know that our dopamine meds are too dumb to figure out in which regions of the brain they are not wanted. Our current inventory works directly on the dopamine system, but the editorial suggests that a smarter strategy may lie in developing meds with an indirect effect. One possibility is targeting the endorphin, dynorphin, whose neurons are engaged in a feedback loop with dopamine. Another is by learning more about the intracellular signaling connected with dopamine transmission and reception.
In the meantime, we are stuck with the low-tech solutions of considering easing off on antipsychotics doses and just saying no to (street) drugs. Maybe your psychiatrist can come up with some creative work-arounds, but first he or she needs to listen your concerns, really listen.
Full article
Monday, May 3, 2010
Dopamine - Serotonin's Secret Weapon
Following is a slightly edited extract from a lengthy article I published on mcmanweb three years ago ...
For two years running, dopamine has received my Newsletter’s coveted "Neurotransmitter of the Year" award. A review article in the March 2007 Archives of General Psychiatry by Boadie Dunlop MD and Charles Nemeroff MD, PhD, both of Emory University, makes a strong case for a three-peat:
Yes, serotonin is the neurotransmitter we tend to think of when it comes to depression, but, as the authors point out, a large number of animal studies, plus gene research and neuroimaging on humans and other findings "support the hypothesis that major depression is associated with a state of reduced dopamine transmission."
The research that led to the "monoamine hypothesis of depression" of the 1960s clearly fingered dopamine, along with serotonin and norepinephrine. But tricyclic antidepressants were hitting the scene at about the same time, all but assuring that dopamine would be overlooked. The later emergence of SSRIs meant that serotonin would grab all the attention. This despite the fact, as the authors point out:
"Most antidepressant treatments do not directly enhance dopamine neurotransmission, which may contribute to residual symptoms, including impaired motivation, concentration, and pleasure."
The authors go on to say that "anhedonia, the absolute or relative inability to experience pleasure, is one of two symptoms required for the diagnosis of major depression." Anhedonia is universally regarded as a "core" symptom of depression. It is well-established that dopamine plays a central role in the brain’s reward system, which includes inducing feelings of pleasure and positive mood states.
The authors cite a 2005 University of Toronto study of the brain scans of 24 subjects who were administered amphetamine. The subjects who were severely depressed had a hypersensitive response to the rewarding effects of the drug, and their scans revealed activation in the ventrolateral prefrontal and orbitofrontal cortices, and in two subcortical regions of the brain (the caudate and putamen).
As Dunlop and Nemeroff explain: "These findings further implicate dopamine circuit dysfunction in major depression."
In this context, the first generation of antidepressants may be the most modern. MAOIs prevent degradation of dopamine, as well as norepinephrine and serotonin. For individuals with atypical depression (leaden, fatigued, and lethargic describe some of the characteristics), MAOIs may represent an early treatment option rather than a late one.
The tricyclics that came out around the same time as MAOIs may also indirectly boost dopamine in the prefrontal cortex via their norepinephrine action.
Enter the new generation antidepressants such as SSRIs. Ironically, as the authors point out, when SSRIs work well it may be due to interactions between the serotonin system and the dopamine system. The authors cite a 1996 German study that found that those who responded to SSRIs - but not those who failed to respond - "exhibited increased dopamine binding to D2 receptors in the striatum and that the degree of increase in D2 binding correlated with improvement in Hamilton Depression Scale score."
In other words, dopamine may be serotonin’s secret weapon. It’s still way too soon to draw this conclusion, but we definitely have the basis for a strong hypothesis, not to mention "Neurotransmitter of the Year" distinctions for years to come.
Much more on dopamine on mcmanweb
For two years running, dopamine has received my Newsletter’s coveted "Neurotransmitter of the Year" award. A review article in the March 2007 Archives of General Psychiatry by Boadie Dunlop MD and Charles Nemeroff MD, PhD, both of Emory University, makes a strong case for a three-peat:
Yes, serotonin is the neurotransmitter we tend to think of when it comes to depression, but, as the authors point out, a large number of animal studies, plus gene research and neuroimaging on humans and other findings "support the hypothesis that major depression is associated with a state of reduced dopamine transmission."
The research that led to the "monoamine hypothesis of depression" of the 1960s clearly fingered dopamine, along with serotonin and norepinephrine. But tricyclic antidepressants were hitting the scene at about the same time, all but assuring that dopamine would be overlooked. The later emergence of SSRIs meant that serotonin would grab all the attention. This despite the fact, as the authors point out:
"Most antidepressant treatments do not directly enhance dopamine neurotransmission, which may contribute to residual symptoms, including impaired motivation, concentration, and pleasure."
The authors go on to say that "anhedonia, the absolute or relative inability to experience pleasure, is one of two symptoms required for the diagnosis of major depression." Anhedonia is universally regarded as a "core" symptom of depression. It is well-established that dopamine plays a central role in the brain’s reward system, which includes inducing feelings of pleasure and positive mood states.
The authors cite a 2005 University of Toronto study of the brain scans of 24 subjects who were administered amphetamine. The subjects who were severely depressed had a hypersensitive response to the rewarding effects of the drug, and their scans revealed activation in the ventrolateral prefrontal and orbitofrontal cortices, and in two subcortical regions of the brain (the caudate and putamen).
As Dunlop and Nemeroff explain: "These findings further implicate dopamine circuit dysfunction in major depression."
In this context, the first generation of antidepressants may be the most modern. MAOIs prevent degradation of dopamine, as well as norepinephrine and serotonin. For individuals with atypical depression (leaden, fatigued, and lethargic describe some of the characteristics), MAOIs may represent an early treatment option rather than a late one.
The tricyclics that came out around the same time as MAOIs may also indirectly boost dopamine in the prefrontal cortex via their norepinephrine action.
Enter the new generation antidepressants such as SSRIs. Ironically, as the authors point out, when SSRIs work well it may be due to interactions between the serotonin system and the dopamine system. The authors cite a 1996 German study that found that those who responded to SSRIs - but not those who failed to respond - "exhibited increased dopamine binding to D2 receptors in the striatum and that the degree of increase in D2 binding correlated with improvement in Hamilton Depression Scale score."
In other words, dopamine may be serotonin’s secret weapon. It’s still way too soon to draw this conclusion, but we definitely have the basis for a strong hypothesis, not to mention "Neurotransmitter of the Year" distinctions for years to come.
Much more on dopamine on mcmanweb
Labels:
depression,
dopamine,
John McManamy,
serotonin
Sunday, May 2, 2010
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