Cannabis for Psychiatric Disorders? ‘Not Today,’ Experts Say

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Tue, 01/09/2024 - 12:18

This transcript has been edited for clarity.

Stephen M. Strakowski, MD: Hello. Thank you all for joining us today. I’m very excited to have some great guests to talk about what I consider an active controversy. I’m Stephen M. Strakowski. I’m a professor and vice chair of psychiatry at Indiana University, and professor and associate vice president at University of Texas in Austin.

Today we’re going to talk about cannabis. As all of you are aware, everyone’s talking about cannabis. We hear constantly on social media and in interviews, particularly with relevance to psychiatric disorders, that everyone should be thinking about using cannabis. That seems to be the common conversation.

Last week, I had a patient who said, “All my friends tell me I need to be on cannabis.” That was their solution to her problems. With that in mind, let me introduce our guests, who are both experts on this, to talk about the role of cannabis in psychiatric disorders today.

First, I want to welcome Dr. Leslie Hulvershorn. Dr. Hulvershorn is an associate professor and chair at Indiana University in Indianapolis. Dr. Christopher Hammond is an assistant professor and the director of the co-occurring disorders program at Johns Hopkins. Welcome!

Leslie A. Hulvershorn, MD, MSc: Thank you.

Christopher J. Hammond, MD, PhD: Thank you.

Dr. Strakowski: Leslie, as I mentioned, many people are talking about how cannabis could be a good treatment for psychiatric disorders. Is that true?

Dr. Hulvershorn: If you look at what defines a good treatment, what you’re looking for is clinical trials, ideally randomized, placebo-controlled clinical trials.

When we look at research related to cannabis, we see very few of those trials, and we see that the cannabis plant is actually quite complicated and there are many different compounds that come from it. So we need to look at all the different compounds.

If you think about THC, delta 9 or delta 8, depending on the version, that’s the active ingredient that we most often think about when we say “cannabis.” If you look at THC studies, there really is no evidence that I could find that it helps psychiatric disorders.

What we do find is an enormous literature, many hunDr.eds of studies, actually, that show that THC actually worsens or even brings on psychiatric disorders. There’s a separate conversation about other compounds within the cannabis plant, like CBD, cannabidiol, where there’s maybe a signal that certain anxiety disorders might be improved by a compound like that.

Certainly, rare forms of epilepsy have been found to be improved with that compound. It really depends on what you’re looking at within the cannabis plant, but if we’re thinking about THC, the answer really is no, this is not a helpful thing. In fact, it’s probably a harmful thing to be ingesting in terms of psychiatric disorders.

Dr. Strakowski: Thank you, Leslie. Chris, what would you add to that? Do we know anything about the use of cannabis in any psychiatric condition?

Dr. Hammond: I definitely would echo what Leslie said. The popular opinion, that the media and the state legislatures have really, in many ways, put the cart before the horse — they speak about cannabis as a medication for the treatment of psychiatric conditions before we have sufficient evidence to say that it’s safe or effective for these conditions. Most of the evidence that we have, particularly in regard to the cannabinoid compound, delta 9, tetrahyDr.ocannabinol, or THC, suggests that that cannabinoid is associated with adverse mental health outcomes across different categories.

Dr. Strakowski: Our group, a long time ago, conducted a study looking at first episode of mania, and found that regular cannabis use increases the risk for subsequent manic episodes. I’m not aware of many other studies like that.

You referred, Chris, to the safety aspect. If you look at social media, the press, and the conversations where cannabis is talked about, there’s no risk, right? This is something anybody can use. There are no negative consequences. Is that true? I mean, is it really risk free?

Dr. Hammond: Research shows that that’s an inaccurate framing of the safety profile of cannabis. Again, as Leslie put it very well, cannabis is many different compounds. Using this catchall phrase of «cannabis» is not very helpful.

In regard to the main bioactive compounds of the cannabis plant, THC and cannabidiol, or CBD, what we know from studies of THC administration and from medications that have been designed to mimic THC and act on receptors that THC acts on is that those medications have clear side effects and adverse events in a percentage of patients who take them, particularly in regard to precipitating panic attacks, dysphoric episodes, and psychosis in some individuals.

Dr. Hulvershorn: I would add that it really depends on the age of the person that you’re talking about and when they’re first exposed to cannabis. If you’re talking about a person, say, under the age of 14 who uses cannabis, there’s a large amount of concern about the worsening of psychosis and mental health symptoms, but also cognitive features like memory.

There’s a very good study that was conducted in New Zealand that followed a large number of kids over time and showed significant decreases in working memory capacity for kids who used quite heavily.

Then you think about pregnant women. That’s very interesting literature, where people are finding that cannabis not only affects brain development but also a host of other systems in the body. For example, I think the risk for asthma is increased. If you look at the genes in the placenta that are affected, it has much to do with the immune system.

Women who are using cannabis during pregnancy are really exposing their fetus to a range of potential risks that we certainly don’t understand well enough, but there’s enough science that suggests this is really concerning.

If you take a step back and look at animal models, even with things like CBD products, which, again, everybody seems to be buying and they’re viewed as very safe — it’s almost hard to find things without CBD these days.

There we find, for example, in developing rats that testicular development seems to be affected with high doses of CBD. There’s just a huge array of effects, even outside of the psychiatric world, that make me very nervous about anyone using, especially a pregnant woman or a young person.

Then there’s a whole separate literature on adults. It’s hard to find studies that suggest this is a great idea. You’re going to find on the mental health side of things, and the cognitive side of things, many effects as well.

I, personally, am agnostic one way or the other. If cannabis turns out to be helpful, great. We love things that are helpful in medicine. We don’t really care where they come from. I’m not biased politically one way or the other. It’s just when you look at the totality of the literature, it’s hard to feel excited about people using cannabis at any age.

Dr. Hammond: It’s difficult to interpret the literature because of some biases there. It speaks to the importance of thoughtful research being done in this space that takes a neutral approach to assessing cannabis and looking for evidence of both potential benefit and potential harm.

The other piece that I think is of value that builds off what Leslie mentioned is the effects of cannabis and THC. The risk for harm appears to be greater in pregnant women and in young people. For adults, I think, we’re also still trying to understand what the effects are.

The other way of parsing out effects and thinking about them is in terms of the acute effects and the acute response in the moment right after one ingests cannabis vs the long-term effects.

After acute ingestion of cannabis, it can precipitate a psychotic episode, dysphoria or severe depressive symptoms, or severe anxiety, and can cause one to be disoriented, have delayed response time, and affect the ability to Dr.ive. In that capacity, it is related to a higher risk for motor vehicle crashes.

Dr. Strakowski: That’s very interesting. In my practice, and maybe it’s atypical, but half to two thirds of my patients, particularly the younger ones, are using cannabis in some form or another. In my experience, if they’re under 21, they’re more likely to use cannabis than alcohol.

What do we tell our patients? Is there a safe level of use? Do we say to never touch it? How do we manage the social pressure and environment that our patients have to live in?

Dr. Hulvershorn: I think about what we call motivational interviewing and the substance use disorder field, which is a style of interacting with someone that’s very neutral to discuss the pros and the cons. In my practice, people are usually coming to us because of problems related to their substance use.

Not everyone is experiencing those, but for those people, it’s a pretty easy discussion. It sounds like you’re getting into trouble. Your athletic performance is suffering. Your scholastic performance is suffering.

You walk them toward understanding that, wait a minute, if I smoked less weed or no weed, I would probably be doing better in this or that domain of my life. That seems to be the most helpful thing, by allowing them to come to that conclusion.

I think it is a more difficult conversation for people who don’t identify any problems related to their use. What is the right answer? Again, I just go back to saying, “Is this good for you? It’s hard to find the literature that suggests that. Is it neutral for you? Maybe, for some people. Is it harmful for some people? Absolutely.”

I think, for me, the most impactful studies have been those that showed for certain people with certain genetic makeup, cannabis is an absolutely terrible idea. Their risk for psychosis development and things like that are so high. For other people, they could smoke weed all day and never have a problem, based on their genetics — maybe. We don’t know. It’s not like we’re doing blood tests to figure out who you are.

The safest advice, I think, is no use. That’s never going to be bad advice.

Dr. Hammond: I mostly agree with Leslie on this point but feel very, very strongly that — in this era, where in the context of popular media, celebrities and other people are stating that cannabis is good and should be put in everything — clinical providers, especially pediatric providers, need to be extremely grounded in the science, and not let popular media sway our approach and strategy for working with these young people.

There’s two decades worth of data from longitudinal studies that have followed individuals from birth or from preadolescence into their thirties and forties, that show us that, for this association between cannabis use and later adverse mental health outcomes, there is a dose effect there.

The earlier an individual starts using, the more frequent they use, and more persistent their use is over time, those individuals have poorer mental health outcomes compared with individuals who choose to abstain or individuals who use just a few times and stop.

There’s also a signal for higher-THC-potency products being associated with poorer mental health outcomes, particularly when used during adolescence.

I apply a motivational interviewing approach as well to disseminate this information to both the young people and their parents about the risks, and to communicate what the data clearly show in regard to using THC-based cannabinoid products, which is that we don’t have evidence that shows that any use is healthy to the developing brain.

There’s a large amount of evidence that suggests it’s harmful to the developing brain, so the recommendation is not to use, to delay the onset of use, if you want to use, until adulthood. Many youth choose to use. For those young people, we meet them where they’re at and try to work with them on cutting down.

Dr. Strakowski: Thank you both. There’s an interesting effort in different states, with lobbying by celebrities and legislators pushing insurance companies to fund cannabis use broadly, including in a number of psychiatric indications, with no FDA approval at this point. Do you support that? Is that a good idea?

Dr. Hammond: Absolutely not.

Dr. Strakowski: Thank you.

Dr. Hammond: I think that’s a very important statement to make. For the medical and healthcare profession to stand strong related to states requiring insurance companies to cover medical cannabis really opens the door to lawsuits that would force insurance companies to cover other undertested bioactive chemicals and health supplements.

There are insufficient safety data for medical cannabis for FDA approval for any condition right now. The FDA has approved cannabinoid-based medications. Those cannabinoid-based medications have really undergone rigorous safety and efficacy testing, and have been approved for very narrow indications, none of which are psychiatric conditions.

They’ve been approved for chemotherapy-associated nausea and vomiting, treatment-resistant seizures related to two rare seizure disorders that emerge during childhood, and related to tuberous sclerosis, and one related to treating multiple sclerosis–associated spasticity and central neuropathic pain.

Dr. Hulvershorn: Steve, I think it’s important for listeners to be aware that there is a process in place for any therapeutic to become tested and reviewed. We see an industry that stands to make an enormous amount of money, and that is really the motivation for this industry.

These are not folks who are, out of the kindness of their heart, just hoping for better treatments for people. There are many ways you could channel that desire that does not include cannabis making money.

It’s really a profit-motivated industry. They’re very effective at lobbying. The public, unfortunately, has been sort of manipulated by this industry to believe that these are healthy, safe, and natural just because they grow in the ground.

Unfortunately, that’s really the issue. I think people just need to keep that in mind. Someone stands to make a large amount of money off of this. This is a very calculated, strategic approach that goes state by state but is nationally organized, and is potentially, like Chris says, for many reasons, really harmful.

I see it as sort of a bullying approach. Like if your Dr.ug works, Medicaid will pay for it. Medicaid in each state will review the studies. The FDA obviously leads the way. To cut the line without the research is really not helpful — circumventing the process that’s been in place for a long time and works well.

Dr. Hammond: Yes, it sets a dangerous precedent.

Dr. Strakowski: I was going to add the same, that it’s potentially dangerous. Thank you both, Dr.s Hulvershorn and Hammond, for a really good, lively discussion. I know we could talk for a very long time about this situation.

I do think it’s clear for listeners, most of whom are practitioners, that at this point in time, there just really does not seem to be strong evidence for the use of cannabis-based products for any psychiatric condition.

I do think we have to approach the people we’re working with around their psychiatric conditions to manage use and abuse wisely, like we would with any other substance. I appreciate everyone who’s tuned in today to watch us. I hope this is useful for your practice. Thank you.

Stephen M. Strakowski, MD, has disclosed the following relevant financial relationships:

  • Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Roche; Procter & Gamble; Novartis; Sunovion
  • Received income in an amount equal to or greater than $250 from: Roche; Procter & Gamble; Novartis; Sunovion; Oxford University Press

Leslie A. Hulvershorn, MD, MSc, has disclosed the following relevant financial relationships:

  • Received income in an amount equal to or greater than $250 from: Greenwich Biosciences, educational grant for Summit

Christopher J. Hammond, MD, PhD, has disclosed the following relevant financial relationships:

  • Received research grant from National Institutes of Health Grants; Bench to Bench Award; Substance Abuse and Mental Health Services Administration; Doris Duke.

A version of this article appeared on Medscape.com.

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This transcript has been edited for clarity.

Stephen M. Strakowski, MD: Hello. Thank you all for joining us today. I’m very excited to have some great guests to talk about what I consider an active controversy. I’m Stephen M. Strakowski. I’m a professor and vice chair of psychiatry at Indiana University, and professor and associate vice president at University of Texas in Austin.

Today we’re going to talk about cannabis. As all of you are aware, everyone’s talking about cannabis. We hear constantly on social media and in interviews, particularly with relevance to psychiatric disorders, that everyone should be thinking about using cannabis. That seems to be the common conversation.

Last week, I had a patient who said, “All my friends tell me I need to be on cannabis.” That was their solution to her problems. With that in mind, let me introduce our guests, who are both experts on this, to talk about the role of cannabis in psychiatric disorders today.

First, I want to welcome Dr. Leslie Hulvershorn. Dr. Hulvershorn is an associate professor and chair at Indiana University in Indianapolis. Dr. Christopher Hammond is an assistant professor and the director of the co-occurring disorders program at Johns Hopkins. Welcome!

Leslie A. Hulvershorn, MD, MSc: Thank you.

Christopher J. Hammond, MD, PhD: Thank you.

Dr. Strakowski: Leslie, as I mentioned, many people are talking about how cannabis could be a good treatment for psychiatric disorders. Is that true?

Dr. Hulvershorn: If you look at what defines a good treatment, what you’re looking for is clinical trials, ideally randomized, placebo-controlled clinical trials.

When we look at research related to cannabis, we see very few of those trials, and we see that the cannabis plant is actually quite complicated and there are many different compounds that come from it. So we need to look at all the different compounds.

If you think about THC, delta 9 or delta 8, depending on the version, that’s the active ingredient that we most often think about when we say “cannabis.” If you look at THC studies, there really is no evidence that I could find that it helps psychiatric disorders.

What we do find is an enormous literature, many hunDr.eds of studies, actually, that show that THC actually worsens or even brings on psychiatric disorders. There’s a separate conversation about other compounds within the cannabis plant, like CBD, cannabidiol, where there’s maybe a signal that certain anxiety disorders might be improved by a compound like that.

Certainly, rare forms of epilepsy have been found to be improved with that compound. It really depends on what you’re looking at within the cannabis plant, but if we’re thinking about THC, the answer really is no, this is not a helpful thing. In fact, it’s probably a harmful thing to be ingesting in terms of psychiatric disorders.

Dr. Strakowski: Thank you, Leslie. Chris, what would you add to that? Do we know anything about the use of cannabis in any psychiatric condition?

Dr. Hammond: I definitely would echo what Leslie said. The popular opinion, that the media and the state legislatures have really, in many ways, put the cart before the horse — they speak about cannabis as a medication for the treatment of psychiatric conditions before we have sufficient evidence to say that it’s safe or effective for these conditions. Most of the evidence that we have, particularly in regard to the cannabinoid compound, delta 9, tetrahyDr.ocannabinol, or THC, suggests that that cannabinoid is associated with adverse mental health outcomes across different categories.

Dr. Strakowski: Our group, a long time ago, conducted a study looking at first episode of mania, and found that regular cannabis use increases the risk for subsequent manic episodes. I’m not aware of many other studies like that.

You referred, Chris, to the safety aspect. If you look at social media, the press, and the conversations where cannabis is talked about, there’s no risk, right? This is something anybody can use. There are no negative consequences. Is that true? I mean, is it really risk free?

Dr. Hammond: Research shows that that’s an inaccurate framing of the safety profile of cannabis. Again, as Leslie put it very well, cannabis is many different compounds. Using this catchall phrase of «cannabis» is not very helpful.

In regard to the main bioactive compounds of the cannabis plant, THC and cannabidiol, or CBD, what we know from studies of THC administration and from medications that have been designed to mimic THC and act on receptors that THC acts on is that those medications have clear side effects and adverse events in a percentage of patients who take them, particularly in regard to precipitating panic attacks, dysphoric episodes, and psychosis in some individuals.

Dr. Hulvershorn: I would add that it really depends on the age of the person that you’re talking about and when they’re first exposed to cannabis. If you’re talking about a person, say, under the age of 14 who uses cannabis, there’s a large amount of concern about the worsening of psychosis and mental health symptoms, but also cognitive features like memory.

There’s a very good study that was conducted in New Zealand that followed a large number of kids over time and showed significant decreases in working memory capacity for kids who used quite heavily.

Then you think about pregnant women. That’s very interesting literature, where people are finding that cannabis not only affects brain development but also a host of other systems in the body. For example, I think the risk for asthma is increased. If you look at the genes in the placenta that are affected, it has much to do with the immune system.

Women who are using cannabis during pregnancy are really exposing their fetus to a range of potential risks that we certainly don’t understand well enough, but there’s enough science that suggests this is really concerning.

If you take a step back and look at animal models, even with things like CBD products, which, again, everybody seems to be buying and they’re viewed as very safe — it’s almost hard to find things without CBD these days.

There we find, for example, in developing rats that testicular development seems to be affected with high doses of CBD. There’s just a huge array of effects, even outside of the psychiatric world, that make me very nervous about anyone using, especially a pregnant woman or a young person.

Then there’s a whole separate literature on adults. It’s hard to find studies that suggest this is a great idea. You’re going to find on the mental health side of things, and the cognitive side of things, many effects as well.

I, personally, am agnostic one way or the other. If cannabis turns out to be helpful, great. We love things that are helpful in medicine. We don’t really care where they come from. I’m not biased politically one way or the other. It’s just when you look at the totality of the literature, it’s hard to feel excited about people using cannabis at any age.

Dr. Hammond: It’s difficult to interpret the literature because of some biases there. It speaks to the importance of thoughtful research being done in this space that takes a neutral approach to assessing cannabis and looking for evidence of both potential benefit and potential harm.

The other piece that I think is of value that builds off what Leslie mentioned is the effects of cannabis and THC. The risk for harm appears to be greater in pregnant women and in young people. For adults, I think, we’re also still trying to understand what the effects are.

The other way of parsing out effects and thinking about them is in terms of the acute effects and the acute response in the moment right after one ingests cannabis vs the long-term effects.

After acute ingestion of cannabis, it can precipitate a psychotic episode, dysphoria or severe depressive symptoms, or severe anxiety, and can cause one to be disoriented, have delayed response time, and affect the ability to Dr.ive. In that capacity, it is related to a higher risk for motor vehicle crashes.

Dr. Strakowski: That’s very interesting. In my practice, and maybe it’s atypical, but half to two thirds of my patients, particularly the younger ones, are using cannabis in some form or another. In my experience, if they’re under 21, they’re more likely to use cannabis than alcohol.

What do we tell our patients? Is there a safe level of use? Do we say to never touch it? How do we manage the social pressure and environment that our patients have to live in?

Dr. Hulvershorn: I think about what we call motivational interviewing and the substance use disorder field, which is a style of interacting with someone that’s very neutral to discuss the pros and the cons. In my practice, people are usually coming to us because of problems related to their substance use.

Not everyone is experiencing those, but for those people, it’s a pretty easy discussion. It sounds like you’re getting into trouble. Your athletic performance is suffering. Your scholastic performance is suffering.

You walk them toward understanding that, wait a minute, if I smoked less weed or no weed, I would probably be doing better in this or that domain of my life. That seems to be the most helpful thing, by allowing them to come to that conclusion.

I think it is a more difficult conversation for people who don’t identify any problems related to their use. What is the right answer? Again, I just go back to saying, “Is this good for you? It’s hard to find the literature that suggests that. Is it neutral for you? Maybe, for some people. Is it harmful for some people? Absolutely.”

I think, for me, the most impactful studies have been those that showed for certain people with certain genetic makeup, cannabis is an absolutely terrible idea. Their risk for psychosis development and things like that are so high. For other people, they could smoke weed all day and never have a problem, based on their genetics — maybe. We don’t know. It’s not like we’re doing blood tests to figure out who you are.

The safest advice, I think, is no use. That’s never going to be bad advice.

Dr. Hammond: I mostly agree with Leslie on this point but feel very, very strongly that — in this era, where in the context of popular media, celebrities and other people are stating that cannabis is good and should be put in everything — clinical providers, especially pediatric providers, need to be extremely grounded in the science, and not let popular media sway our approach and strategy for working with these young people.

There’s two decades worth of data from longitudinal studies that have followed individuals from birth or from preadolescence into their thirties and forties, that show us that, for this association between cannabis use and later adverse mental health outcomes, there is a dose effect there.

The earlier an individual starts using, the more frequent they use, and more persistent their use is over time, those individuals have poorer mental health outcomes compared with individuals who choose to abstain or individuals who use just a few times and stop.

There’s also a signal for higher-THC-potency products being associated with poorer mental health outcomes, particularly when used during adolescence.

I apply a motivational interviewing approach as well to disseminate this information to both the young people and their parents about the risks, and to communicate what the data clearly show in regard to using THC-based cannabinoid products, which is that we don’t have evidence that shows that any use is healthy to the developing brain.

There’s a large amount of evidence that suggests it’s harmful to the developing brain, so the recommendation is not to use, to delay the onset of use, if you want to use, until adulthood. Many youth choose to use. For those young people, we meet them where they’re at and try to work with them on cutting down.

Dr. Strakowski: Thank you both. There’s an interesting effort in different states, with lobbying by celebrities and legislators pushing insurance companies to fund cannabis use broadly, including in a number of psychiatric indications, with no FDA approval at this point. Do you support that? Is that a good idea?

Dr. Hammond: Absolutely not.

Dr. Strakowski: Thank you.

Dr. Hammond: I think that’s a very important statement to make. For the medical and healthcare profession to stand strong related to states requiring insurance companies to cover medical cannabis really opens the door to lawsuits that would force insurance companies to cover other undertested bioactive chemicals and health supplements.

There are insufficient safety data for medical cannabis for FDA approval for any condition right now. The FDA has approved cannabinoid-based medications. Those cannabinoid-based medications have really undergone rigorous safety and efficacy testing, and have been approved for very narrow indications, none of which are psychiatric conditions.

They’ve been approved for chemotherapy-associated nausea and vomiting, treatment-resistant seizures related to two rare seizure disorders that emerge during childhood, and related to tuberous sclerosis, and one related to treating multiple sclerosis–associated spasticity and central neuropathic pain.

Dr. Hulvershorn: Steve, I think it’s important for listeners to be aware that there is a process in place for any therapeutic to become tested and reviewed. We see an industry that stands to make an enormous amount of money, and that is really the motivation for this industry.

These are not folks who are, out of the kindness of their heart, just hoping for better treatments for people. There are many ways you could channel that desire that does not include cannabis making money.

It’s really a profit-motivated industry. They’re very effective at lobbying. The public, unfortunately, has been sort of manipulated by this industry to believe that these are healthy, safe, and natural just because they grow in the ground.

Unfortunately, that’s really the issue. I think people just need to keep that in mind. Someone stands to make a large amount of money off of this. This is a very calculated, strategic approach that goes state by state but is nationally organized, and is potentially, like Chris says, for many reasons, really harmful.

I see it as sort of a bullying approach. Like if your Dr.ug works, Medicaid will pay for it. Medicaid in each state will review the studies. The FDA obviously leads the way. To cut the line without the research is really not helpful — circumventing the process that’s been in place for a long time and works well.

Dr. Hammond: Yes, it sets a dangerous precedent.

Dr. Strakowski: I was going to add the same, that it’s potentially dangerous. Thank you both, Dr.s Hulvershorn and Hammond, for a really good, lively discussion. I know we could talk for a very long time about this situation.

I do think it’s clear for listeners, most of whom are practitioners, that at this point in time, there just really does not seem to be strong evidence for the use of cannabis-based products for any psychiatric condition.

I do think we have to approach the people we’re working with around their psychiatric conditions to manage use and abuse wisely, like we would with any other substance. I appreciate everyone who’s tuned in today to watch us. I hope this is useful for your practice. Thank you.

Stephen M. Strakowski, MD, has disclosed the following relevant financial relationships:

  • Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Roche; Procter & Gamble; Novartis; Sunovion
  • Received income in an amount equal to or greater than $250 from: Roche; Procter & Gamble; Novartis; Sunovion; Oxford University Press

Leslie A. Hulvershorn, MD, MSc, has disclosed the following relevant financial relationships:

  • Received income in an amount equal to or greater than $250 from: Greenwich Biosciences, educational grant for Summit

Christopher J. Hammond, MD, PhD, has disclosed the following relevant financial relationships:

  • Received research grant from National Institutes of Health Grants; Bench to Bench Award; Substance Abuse and Mental Health Services Administration; Doris Duke.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Stephen M. Strakowski, MD: Hello. Thank you all for joining us today. I’m very excited to have some great guests to talk about what I consider an active controversy. I’m Stephen M. Strakowski. I’m a professor and vice chair of psychiatry at Indiana University, and professor and associate vice president at University of Texas in Austin.

Today we’re going to talk about cannabis. As all of you are aware, everyone’s talking about cannabis. We hear constantly on social media and in interviews, particularly with relevance to psychiatric disorders, that everyone should be thinking about using cannabis. That seems to be the common conversation.

Last week, I had a patient who said, “All my friends tell me I need to be on cannabis.” That was their solution to her problems. With that in mind, let me introduce our guests, who are both experts on this, to talk about the role of cannabis in psychiatric disorders today.

First, I want to welcome Dr. Leslie Hulvershorn. Dr. Hulvershorn is an associate professor and chair at Indiana University in Indianapolis. Dr. Christopher Hammond is an assistant professor and the director of the co-occurring disorders program at Johns Hopkins. Welcome!

Leslie A. Hulvershorn, MD, MSc: Thank you.

Christopher J. Hammond, MD, PhD: Thank you.

Dr. Strakowski: Leslie, as I mentioned, many people are talking about how cannabis could be a good treatment for psychiatric disorders. Is that true?

Dr. Hulvershorn: If you look at what defines a good treatment, what you’re looking for is clinical trials, ideally randomized, placebo-controlled clinical trials.

When we look at research related to cannabis, we see very few of those trials, and we see that the cannabis plant is actually quite complicated and there are many different compounds that come from it. So we need to look at all the different compounds.

If you think about THC, delta 9 or delta 8, depending on the version, that’s the active ingredient that we most often think about when we say “cannabis.” If you look at THC studies, there really is no evidence that I could find that it helps psychiatric disorders.

What we do find is an enormous literature, many hunDr.eds of studies, actually, that show that THC actually worsens or even brings on psychiatric disorders. There’s a separate conversation about other compounds within the cannabis plant, like CBD, cannabidiol, where there’s maybe a signal that certain anxiety disorders might be improved by a compound like that.

Certainly, rare forms of epilepsy have been found to be improved with that compound. It really depends on what you’re looking at within the cannabis plant, but if we’re thinking about THC, the answer really is no, this is not a helpful thing. In fact, it’s probably a harmful thing to be ingesting in terms of psychiatric disorders.

Dr. Strakowski: Thank you, Leslie. Chris, what would you add to that? Do we know anything about the use of cannabis in any psychiatric condition?

Dr. Hammond: I definitely would echo what Leslie said. The popular opinion, that the media and the state legislatures have really, in many ways, put the cart before the horse — they speak about cannabis as a medication for the treatment of psychiatric conditions before we have sufficient evidence to say that it’s safe or effective for these conditions. Most of the evidence that we have, particularly in regard to the cannabinoid compound, delta 9, tetrahyDr.ocannabinol, or THC, suggests that that cannabinoid is associated with adverse mental health outcomes across different categories.

Dr. Strakowski: Our group, a long time ago, conducted a study looking at first episode of mania, and found that regular cannabis use increases the risk for subsequent manic episodes. I’m not aware of many other studies like that.

You referred, Chris, to the safety aspect. If you look at social media, the press, and the conversations where cannabis is talked about, there’s no risk, right? This is something anybody can use. There are no negative consequences. Is that true? I mean, is it really risk free?

Dr. Hammond: Research shows that that’s an inaccurate framing of the safety profile of cannabis. Again, as Leslie put it very well, cannabis is many different compounds. Using this catchall phrase of «cannabis» is not very helpful.

In regard to the main bioactive compounds of the cannabis plant, THC and cannabidiol, or CBD, what we know from studies of THC administration and from medications that have been designed to mimic THC and act on receptors that THC acts on is that those medications have clear side effects and adverse events in a percentage of patients who take them, particularly in regard to precipitating panic attacks, dysphoric episodes, and psychosis in some individuals.

Dr. Hulvershorn: I would add that it really depends on the age of the person that you’re talking about and when they’re first exposed to cannabis. If you’re talking about a person, say, under the age of 14 who uses cannabis, there’s a large amount of concern about the worsening of psychosis and mental health symptoms, but also cognitive features like memory.

There’s a very good study that was conducted in New Zealand that followed a large number of kids over time and showed significant decreases in working memory capacity for kids who used quite heavily.

Then you think about pregnant women. That’s very interesting literature, where people are finding that cannabis not only affects brain development but also a host of other systems in the body. For example, I think the risk for asthma is increased. If you look at the genes in the placenta that are affected, it has much to do with the immune system.

Women who are using cannabis during pregnancy are really exposing their fetus to a range of potential risks that we certainly don’t understand well enough, but there’s enough science that suggests this is really concerning.

If you take a step back and look at animal models, even with things like CBD products, which, again, everybody seems to be buying and they’re viewed as very safe — it’s almost hard to find things without CBD these days.

There we find, for example, in developing rats that testicular development seems to be affected with high doses of CBD. There’s just a huge array of effects, even outside of the psychiatric world, that make me very nervous about anyone using, especially a pregnant woman or a young person.

Then there’s a whole separate literature on adults. It’s hard to find studies that suggest this is a great idea. You’re going to find on the mental health side of things, and the cognitive side of things, many effects as well.

I, personally, am agnostic one way or the other. If cannabis turns out to be helpful, great. We love things that are helpful in medicine. We don’t really care where they come from. I’m not biased politically one way or the other. It’s just when you look at the totality of the literature, it’s hard to feel excited about people using cannabis at any age.

Dr. Hammond: It’s difficult to interpret the literature because of some biases there. It speaks to the importance of thoughtful research being done in this space that takes a neutral approach to assessing cannabis and looking for evidence of both potential benefit and potential harm.

The other piece that I think is of value that builds off what Leslie mentioned is the effects of cannabis and THC. The risk for harm appears to be greater in pregnant women and in young people. For adults, I think, we’re also still trying to understand what the effects are.

The other way of parsing out effects and thinking about them is in terms of the acute effects and the acute response in the moment right after one ingests cannabis vs the long-term effects.

After acute ingestion of cannabis, it can precipitate a psychotic episode, dysphoria or severe depressive symptoms, or severe anxiety, and can cause one to be disoriented, have delayed response time, and affect the ability to Dr.ive. In that capacity, it is related to a higher risk for motor vehicle crashes.

Dr. Strakowski: That’s very interesting. In my practice, and maybe it’s atypical, but half to two thirds of my patients, particularly the younger ones, are using cannabis in some form or another. In my experience, if they’re under 21, they’re more likely to use cannabis than alcohol.

What do we tell our patients? Is there a safe level of use? Do we say to never touch it? How do we manage the social pressure and environment that our patients have to live in?

Dr. Hulvershorn: I think about what we call motivational interviewing and the substance use disorder field, which is a style of interacting with someone that’s very neutral to discuss the pros and the cons. In my practice, people are usually coming to us because of problems related to their substance use.

Not everyone is experiencing those, but for those people, it’s a pretty easy discussion. It sounds like you’re getting into trouble. Your athletic performance is suffering. Your scholastic performance is suffering.

You walk them toward understanding that, wait a minute, if I smoked less weed or no weed, I would probably be doing better in this or that domain of my life. That seems to be the most helpful thing, by allowing them to come to that conclusion.

I think it is a more difficult conversation for people who don’t identify any problems related to their use. What is the right answer? Again, I just go back to saying, “Is this good for you? It’s hard to find the literature that suggests that. Is it neutral for you? Maybe, for some people. Is it harmful for some people? Absolutely.”

I think, for me, the most impactful studies have been those that showed for certain people with certain genetic makeup, cannabis is an absolutely terrible idea. Their risk for psychosis development and things like that are so high. For other people, they could smoke weed all day and never have a problem, based on their genetics — maybe. We don’t know. It’s not like we’re doing blood tests to figure out who you are.

The safest advice, I think, is no use. That’s never going to be bad advice.

Dr. Hammond: I mostly agree with Leslie on this point but feel very, very strongly that — in this era, where in the context of popular media, celebrities and other people are stating that cannabis is good and should be put in everything — clinical providers, especially pediatric providers, need to be extremely grounded in the science, and not let popular media sway our approach and strategy for working with these young people.

There’s two decades worth of data from longitudinal studies that have followed individuals from birth or from preadolescence into their thirties and forties, that show us that, for this association between cannabis use and later adverse mental health outcomes, there is a dose effect there.

The earlier an individual starts using, the more frequent they use, and more persistent their use is over time, those individuals have poorer mental health outcomes compared with individuals who choose to abstain or individuals who use just a few times and stop.

There’s also a signal for higher-THC-potency products being associated with poorer mental health outcomes, particularly when used during adolescence.

I apply a motivational interviewing approach as well to disseminate this information to both the young people and their parents about the risks, and to communicate what the data clearly show in regard to using THC-based cannabinoid products, which is that we don’t have evidence that shows that any use is healthy to the developing brain.

There’s a large amount of evidence that suggests it’s harmful to the developing brain, so the recommendation is not to use, to delay the onset of use, if you want to use, until adulthood. Many youth choose to use. For those young people, we meet them where they’re at and try to work with them on cutting down.

Dr. Strakowski: Thank you both. There’s an interesting effort in different states, with lobbying by celebrities and legislators pushing insurance companies to fund cannabis use broadly, including in a number of psychiatric indications, with no FDA approval at this point. Do you support that? Is that a good idea?

Dr. Hammond: Absolutely not.

Dr. Strakowski: Thank you.

Dr. Hammond: I think that’s a very important statement to make. For the medical and healthcare profession to stand strong related to states requiring insurance companies to cover medical cannabis really opens the door to lawsuits that would force insurance companies to cover other undertested bioactive chemicals and health supplements.

There are insufficient safety data for medical cannabis for FDA approval for any condition right now. The FDA has approved cannabinoid-based medications. Those cannabinoid-based medications have really undergone rigorous safety and efficacy testing, and have been approved for very narrow indications, none of which are psychiatric conditions.

They’ve been approved for chemotherapy-associated nausea and vomiting, treatment-resistant seizures related to two rare seizure disorders that emerge during childhood, and related to tuberous sclerosis, and one related to treating multiple sclerosis–associated spasticity and central neuropathic pain.

Dr. Hulvershorn: Steve, I think it’s important for listeners to be aware that there is a process in place for any therapeutic to become tested and reviewed. We see an industry that stands to make an enormous amount of money, and that is really the motivation for this industry.

These are not folks who are, out of the kindness of their heart, just hoping for better treatments for people. There are many ways you could channel that desire that does not include cannabis making money.

It’s really a profit-motivated industry. They’re very effective at lobbying. The public, unfortunately, has been sort of manipulated by this industry to believe that these are healthy, safe, and natural just because they grow in the ground.

Unfortunately, that’s really the issue. I think people just need to keep that in mind. Someone stands to make a large amount of money off of this. This is a very calculated, strategic approach that goes state by state but is nationally organized, and is potentially, like Chris says, for many reasons, really harmful.

I see it as sort of a bullying approach. Like if your Dr.ug works, Medicaid will pay for it. Medicaid in each state will review the studies. The FDA obviously leads the way. To cut the line without the research is really not helpful — circumventing the process that’s been in place for a long time and works well.

Dr. Hammond: Yes, it sets a dangerous precedent.

Dr. Strakowski: I was going to add the same, that it’s potentially dangerous. Thank you both, Dr.s Hulvershorn and Hammond, for a really good, lively discussion. I know we could talk for a very long time about this situation.

I do think it’s clear for listeners, most of whom are practitioners, that at this point in time, there just really does not seem to be strong evidence for the use of cannabis-based products for any psychiatric condition.

I do think we have to approach the people we’re working with around their psychiatric conditions to manage use and abuse wisely, like we would with any other substance. I appreciate everyone who’s tuned in today to watch us. I hope this is useful for your practice. Thank you.

Stephen M. Strakowski, MD, has disclosed the following relevant financial relationships:

  • Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Roche; Procter & Gamble; Novartis; Sunovion
  • Received income in an amount equal to or greater than $250 from: Roche; Procter & Gamble; Novartis; Sunovion; Oxford University Press

Leslie A. Hulvershorn, MD, MSc, has disclosed the following relevant financial relationships:

  • Received income in an amount equal to or greater than $250 from: Greenwich Biosciences, educational grant for Summit

Christopher J. Hammond, MD, PhD, has disclosed the following relevant financial relationships:

  • Received research grant from National Institutes of Health Grants; Bench to Bench Award; Substance Abuse and Mental Health Services Administration; Doris Duke.

A version of this article appeared on Medscape.com.

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How to avoid ethnic bias when diagnosing schizophrenia

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How to avoid ethnic bias when diagnosing schizophrenia

In patients with psychotic symptoms, why are African-Americans more likely than whites to be diagnosed with schizophrenia? After more than 30 years of debate, some answers—and remedies for the problem—are becoming clear.

In psychiatry, where interpersonal interactions are key to eliciting diagnostic symptoms and signs, there is an intrinsic risk of misinterpretation when clinician and patient are of different cultural, ethnic, or socioeconomic backgrounds. This article analyzes four factors that contribute to misinterpretation and to ethnic misdiagnosis of schizophrenia. Culturally sensitive strategies are offered to avoid diagnostic bias in clinical practice.

SCHIZOPHRENIA MISDIAGNOSIS

Large epidemiologic studies report similar rates of schizophrenia and bipolar disorder in African-American and white populations.1 Although patients of both races have been wrongly diagnosed with schizophrenia, the pattern is stronger and more persistent in African-Americans.

Box 1

Diagnostic criteria for schizophrenia: Characteristic symptoms (Criterion A)

Two (or more) of the following, each present for a significant portion of time during a 1-month period (or less if successfully treated):

  • Delusions
  • Hallucinations
  • Disorganized speech (eg, frequent derailment or incoherence)
  • Grossly disorganized or catatonic behavior
  • Negative symptoms (ie, affective flattening, alogia, or avolition)

Note: Only one Criterion A symptom is required if delusions are bizarre or hallucinations consist of a voice keeping up a running commentary on the person’s behavior or thoughts, or two or more voices conversing with each other.

295.30 Paranoid type

A type of schizophrenia in which the following criteria are met:

  1. Preoccupation with one or more delusions or frequent auditory hallucinations
  2. None of the following is prominent: disorganized speech, disorganized or catatonic behavior, or flat or inappropriate affect.

Source: DSM-IV-TR

In the 1970s, Simon et al2 studied 192 hospitalized patients, of whom all African-Americans and 85% of whites had been identified clinically as having schizophrenia. Using a structured interview, the researchers found that only 40% of the African Americans and 50% of the whites met diagnostic criteria for schizophrenia. African-Americans with mood disorders were found to be at particular risk of schizophrenia misdiagnosis.

In the 1980s, among 76 patients with a clinical diagnosis of schizophrenia, Mukherjee et al3 diagnosed one-half (52%) with bipolar disorder using a structured clinical interview. Schizophrenia misdiagnoses were more common in African-Americans (86%) and Hispanics (83%) than in whites (51%). In particular, African-Americans were most likely to be misdiagnosed with paranoid schizophrenia. African-Americans complained more commonly than whites of auditory hallucinations, which may represent an ethnic difference in symptomatic presentation of psychotic mood disorders.

In the 1990s, colleagues and I conducted two studies—one of 173 patients in a Tennessee psychiatric hospital4 and the other of 490 patients in an Ohio psychiatric emergency service5—and found yet again that African-Americans were more likely than whites to be diagnosed with schizophrenia. In the hospital study, higher rates of schizophrenia diagnosis were associated with lower rates of mood disorder diagnosis. This inverse relationship implied that African-Americans with mood disorders were being misdiagnosed with schizophrenia.

Men were more likely than women to be diagnosed with schizophrenia, suggesting that African-American men were most likely to be misdiagnosed. When adjustments were made for gender, black women were found to be at higher risk for misdiagnosis than white women.

Lawson et al6 extended this research in a population-based study of African-Americans living in Tennessee. They found that African-Americans constituted 16% of the state’s population but 48% of psychiatric inpatients diagnosed with schizophrenia and 37% of psychiatric outpatients.

CONSEQUENCES OF INACCURATE DIAGNOSIS

Differentiating between schizophrenia (Box 1) and a psychotic mood disorder (Box 2) is more than a semantic exercise. Schizophrenia implies a chronic, unremitting, debilitating illness that worsens over time. Though this perception of schizophrenia is not entirely accurate, in clinical practice its diagnosis imparts a bleak prognosis that may lower the clinician’s expectations for the patient.7

Schizophrenia misdiagnosis also may lead the psychiatrist to rely excessively on antipsychotics, rather than attempting thymoleptic and psychotherapy trials. Studies suggest that African-American patients are more likely than similar white patients to receive antipsychotics4,8,9 and less likely to receive psychotherapy.5,10

Reasons why African-Americans are often misdiagnosed with schizophrenia remain unclear but probably include four contributing factors:

  • differences in symptom presentation compared with whites
  • failure by clinicians to identify affective symptoms in African-Americans
  • minority patients’ wariness when dealing with health services
  • and racial stereotyping.

DIFFERENCES IN SYMPTOM EXPRESSION

African-American patients with mood disorders or schizophrenia are more likely than are similar white patients to complain of auditory hallucinations.11-13 For example, Strakowski et al14 examined 330 patients with nonaffective and psychotic diagnoses in a study that was used to develop DSM-IV criteria for schizophrenia. Auditory hallucinations were rated as more severe in African-American than in similar white patients.

 

 

Box 2

Major depressive episode with psychotic features: Characteristic symptoms

MAJOR DEPRESSIVE EPISODE

Five or more of the following symptoms present during the same 2-week period and representing a change from previous functioning; must include either depressed mood or loss of interest or pleasure.

  • Depressed mood
  • Markedly diminished interest or pleasure
  • Significant weight loss
  • Insomnia or hypersomnia
  • Psychomotor agitation or retardation
  • Fatigue
  • Feelings of worthlessness or excessive guilt
  • Diminished ability to concentrate

SEVERE MAJOR DEPRESSION WITH PSYCHOTIC FEATURES

Mood-congruent

Delusions or hallucinations whose content is entirely consistent with the typical depressive themes of personal inadequacy, guilt, disease, death, nihilism, or deserved punishment

Mood-incongruent

Delusions or hallucinations whose content does not involve typical depressive themes. Includes symptoms such as persecutory delusions, thought insertion, thought broadcasting, and delusions of control

Source: DSM-IV-TR

African-American patients also are more likely than whites to exhibit so-called Schneiderian first-rank symptoms of schizophrenia,15 including:

  • delusions of thought broadcasting or insertion
  • auditory hallucinations of voices conversing about the patient in the third person.

These symptoms were once used to diagnose schizophrenia, but their lack of specificity has been well documented.2,16 First-rank symptoms of schizophrenia depend on the specific form of the hallucination or delusion, are likely to be influenced by a patient’s culture, and may be misleading in multicultural populations. Though first-rank symptoms now occupy a minor role in U.S. diagnostic systems, they might continue to sway clinicians—even when using structured diagnostic interviews—to inappropriately diagnose schizophrenia in lieu of affective disorders in minority patients.15

To extend this finding, our group16 studied rates and severity of affective and psychotic symptoms—particularly first-rank symptoms—in 100 patients with psychotic mania who met DSM-III-R criteria for bipolar disorder (80%) or schizoaffective disorder, bipolar type (20%) as determined by structured diagnostic interview. No differences in affective symptoms between African-American and white patients were seen. African-Americans were more likely to endorse auditory hallucinations and to report severe auditory hallucinations of voices commenting on their behavior—the only first-rank symptom on which they differed from whites.

Though their affective symptoms were similar, African-Americans were significantly more likely than whites to have been diagnosed with a schizophrenia-spectrum disorder. Because misdiagnosis of African-Americans could not be explained by psychotic symptoms—which were as severe as those of white patients—these findings suggest other mechanisms were at work.

UNIDENTIFIED AFFECTIVE SYMPTOMS

Underidentification of mood disorders in African-American patients may also lead to over-diagnosis of schizophrenia. In a sample of 99 patients, colleagues and I17 compared clinical diagnoses made in a psychiatric emergency service with those by research investigators using a structured clinical interview. Reasons for diagnostic differences were identified and divided into two categories:

  • the same symptoms were recorded but applied differently to diagnostic criteria (criterion variance)
  • different information was recorded, which led to diagnostic discrepancies (information variance).

Differences occurred significantly more often in African-American than in white patients, but only information variance was associated with ethnicity. This suggests that clinicians are less likely to elicit appropriate information from African-American than from white psychiatric patients. The fact that researchers obtained this information during diagnostic interviews suggests that the patients could provide it when given appropriate prompts. Specifically, affective symptoms were less likely to be elicited by clinicians than by researchers.

PATIENT WARINESS

Minority patients, when interacting with clinicians of the majority population, may project “protective wariness.”18 Specific behaviors include hesitancy or reluctance to fully engage with the care provider as a precaution against being exploited or harmed. Cultural misunderstandings19 and patient concerns about past reports of minorities receiving substandard or unethical health care20 may contribute to this behavior.

Whaley21 compared nonpathologic distrust and paranoia in 404 community-living African-Americans and whites. Some were healthy, and some had diagnoses of schizophrenia or depression. African-Americans—particularly those with psychiatric disorders—showed higher levels of distrust than whites. Distrust was also associated with depression in African-Americans but not in whites. Whaley concluded that:

  • depressed African-Americans may exhibit more distrust toward clinicians than do whites
  • this distrust puts African-Americans at risk of being perceived as paranoid and being misdiagnosed with paranoid schizophrenia.

Table

Remedial actions to avoid ethnic bias in diagnosing schizophrenia

ProblemRemedies
Failure to recognize differences in symptom expressionBecome familiar with ethnic differences in how patients describe symptoms
Incorporate structured interviews or rating scales into the clinical assessment
Failure to elicit affective symptomsIncorporate structured interviews or rating scales into the clinical assessment
Maintain a high index of suspicion for affective symptoms (see Box 2)
Misinterpreted protective warinessClarify the patient’s degree of suspicion; consider this in the historical context of abuses toward minorities by majority populations
Become familiar with ethnic differences in how symptoms are described
Covert and overt stereotyping and cultural insensitivityReview practice patterns
Consult with culturally sensitive clinicians as necessary
 

 

Though Whaley did not report differences in distrust between African-American men and women, others have noted that distrust of health providers may be more common in minority men.18

RACIAL STEREOTYPING

Compared with similar white men, African-American men with mental disorders are more likely to be:

  • referred for mental health care through social and legal—rather than medical—systems and to be involuntarily committed
  • perceived as violent—even though controlled research suggests they are not. This misperception can lead to excessive medication and restraints.22

Differential treatment of African-American men may create a cycle of distrust, hostility, and additional inappropriate treatment. Together, these factors may increase the risk that African-American men will be misdiagnosed with schizophrenia.

Past racism in biomedical and psychiatric practice and research has been documented23,24 and more recently reviewed by Lawson.19 Historically, African-Americans were perceived to have a “primitive psychic” nature that was thought to be more susceptible to schizophrenia than depression.19 Whether these or similar racist stereotypes continue to inject ethnic bias into clinical assessment requires further study.

WHERE DO WE GO FROM HERE?

Although research into methods to eliminate ethnicity bias is sparse, the work reviewed in this article suggests ways that psychiatrists can minimize this problem (Table).

Obtain comprehensive information. Use structured interviews, such as the Structured Clinical Interview for DSM-IV (SCID), and rating scales, such as the Hamilton Depression Scale, which require clinicians to ask about all types of symptoms, particularly affective symptoms.

Review treatment records. Review your practice patterns for evidence of schizophrenia over-diagnosis in African-Americans or other ethnic groups. Examine ethnic differences in legal referrals or use of restraints or seclusion, which may indicate an ethnic bias in how threats are perceived. Only by being aware of bias can one correct it.

Become familiar with cultural and ethnic differences in idioms of distress. Specifically, review research in cultural psychiatry to identify potential differences among cultural groups in how they describe psychiatric symptoms. Talk with colleagues or friends from other cultural groups, and read literature from different ethnic perspectives to increase your cultural sensitivity.

Consult with psychiatrists with expertise in cultural variability of clinical presentation when the diagnosis or threat assessment seems unclear. Consultation is recommended if a patient’s diagnosis is uncertain or if you detect bias in your practice.

These interventions require clinicians to become familiar with psychosocial differences in how patients of various cultural and ethnic groups express psychiatric symptoms. With this understanding, we can better engage wary patients, obtain valid information, and improve clinical practice and patient outcomes.

Finally, psychiatry’s diagnostic systems need to continually address how patient assessment is influenced by ethnicity, culture, gender, and other socio-demographic factors. Studies are needed to examine the contributions of multiple factors—such as symptom differences and stereotyping—that contribute to ethnic-related diagnostic disparities.

Related resources

  • Paul AM. Painting insanity black: Why are there more black schizophrenics? Salon.com Dec. 1, 1999. http://www.salon.com/books/it/1999/12/01/schizo/index.html
  • Alarcon RD, Westermeyer J, Foulks EF, Ruiz P. Clinical relevance of contemporary cultural psychiatry. J Nerv Ment Dis 1999;187: 465-71.
  • Williams DR, Neighbors HW, Jackson JS. Racial/ethnic discrimination and health: findings from community studies. Am J Public Health 2003;93:200-8.
  • Lin KM, Smith MW, Ortiz V. Culture and psychopharmacology. Psychiatr Clin North Am 2001; 24:523-38.

Acknowledgement

Preparation of this manuscript was supported in part by National Institutes of Health grant MH56352.

References

1. Robins LN, Regier DA (eds). Psychiatric disorders in America: the Epidemiologic Catchment Area study. New York: The Free Press. 1991.

2. Simon RJ, Fleiss JL, Gurland BJ, et al. Depression and schizophrenia in hospitalized black and white mental patients. Arch Gen Psychiatry 1973;28:509-12.

3. Mukherjee S, Shukla S, Woodle J, et al. Misdiagnosis of schizophrenia in bipolar patients: a multiethnic comparison. Am J Psychiatry 1983;140:1571-4.

4. Strakowski SM, Shelton RC, Kolbrener ML. The effects of race and comorbidity on clinical diagnosis in patients with psychosis. J Clin Psychiatry 1993;54:96-102.

5. Strakowski SM, Lonczak HS, Sax KW, et al. The effects of race on diagnosis and disposition from a psychiatric emergency service. J Clin Psychiatry 1995;56:101-7.

6. Lawson WB, Hepler N, Holladay J, Cuffel B. Race as a factor in inpatient and outpatient admissions and diagnosis. Hosp Comm Psychiatry 1994;45:72-4.

7. Hoffman H, Kupper Z, Kunz B. Hopelessness and its impact on rehabilitation outcome in schizophrenia—an exploratory study. Schizophr Res 2000;43:147-58.

8. Walkup JT, McAlpine DD, Olfson M, et al. Patients with schizophrenia at risk for excessive antipsychotic dosing. J Clin Psychiatry 2000;61:344-8.

9. Segal SP, Bola JR, Watson MA. Race, quality of care, and antipsychotic prescribing practices in psychiatric emergency services. Psychiatr Serv 1996;47:282-6.

10. Flaskerud JH, Hu L. Racial/ethnic identity and amount and type of psychiatric treatment. Am J Psychiatry 1992;149:379-84.

11. Adebimpe VR, Klein HE, Fried J. Hallucinations and delusions in black psychiatric patients. J Natl Med Assoc 1981;73:517-20.

12. Adebimpe VR, Chu CC, Klein HE, Lange MH. Racial and geographic differences in the psychopathology of schizophrenia. Am J Psychiatry 1982;139:888-91.

13. Fabrega H, Jr, Mezzich J, Ulrich RF. Black-white differences in psychopathology in an urban psychiatric population. Compr Psychiatry 1988;29:285-97.

14. Strakowski SM, Flaum M, Amador X, et al. Racial differences in the diagnosis of psychosis. Schizophr Res 1996;21:117-24.

15. Schneider K. Clinical psychopathology (translated by Hamilton MW). New York: Grune and Stratton, 1959.

16. Strakowski SM, McElroy SL, Keck PE, Jr, West SA. Racial influence on diagnosis in psychotic mania. J Aff Disord. 1996;39:157-62.

17. Strakowski SM, Hawkins JM, Keck PE, Jr, et al. The effects of race and information variance on disagreement between psychiatric emergency service and research diagnoses in first-episode psychosis. J Clin Psychiatry 1997;58:457-63.

18. Jones BE, Gray BA. Problems in diagnosing schizophrenia and affective disorders among blacks. Hosp Comm Psychiatry 1986;37:61-5.

19. Neighbors HW, Jackson JS, Campbell L, Williams D. The influence of racial factors on psychiatric diagnosis: A review and suggestions for research. Comm Ment Health J 1989;25:301-11.

20. Lawson WB. Racial and ethnic factors in psychiatric research. Hosp Comm Psychiatry 1986;37:50-4.

21. Whaley AL. Ethnicity/race, paranoia, and psychiatric diagnoses: Clinician bias versus sociocultural differences. J Psychopathol Behav Assess 1997;19:1-20.

22. Lawson WB, Yesavage JA, Werner RD. Race, violence, and psychopathology. J Clin Psychiatry 1984;45:294-7.

23. Spurlock J. Psychiatric states. In: Williams RA (ed). Textbook of black-related diseases. New York: McGraw-Hill, 1975.

24. Thomas A, Sillen S. Racism and psychiatry. New York: Brunner/Mazel, 1972.

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In patients with psychotic symptoms, why are African-Americans more likely than whites to be diagnosed with schizophrenia? After more than 30 years of debate, some answers—and remedies for the problem—are becoming clear.

In psychiatry, where interpersonal interactions are key to eliciting diagnostic symptoms and signs, there is an intrinsic risk of misinterpretation when clinician and patient are of different cultural, ethnic, or socioeconomic backgrounds. This article analyzes four factors that contribute to misinterpretation and to ethnic misdiagnosis of schizophrenia. Culturally sensitive strategies are offered to avoid diagnostic bias in clinical practice.

SCHIZOPHRENIA MISDIAGNOSIS

Large epidemiologic studies report similar rates of schizophrenia and bipolar disorder in African-American and white populations.1 Although patients of both races have been wrongly diagnosed with schizophrenia, the pattern is stronger and more persistent in African-Americans.

Box 1

Diagnostic criteria for schizophrenia: Characteristic symptoms (Criterion A)

Two (or more) of the following, each present for a significant portion of time during a 1-month period (or less if successfully treated):

  • Delusions
  • Hallucinations
  • Disorganized speech (eg, frequent derailment or incoherence)
  • Grossly disorganized or catatonic behavior
  • Negative symptoms (ie, affective flattening, alogia, or avolition)

Note: Only one Criterion A symptom is required if delusions are bizarre or hallucinations consist of a voice keeping up a running commentary on the person’s behavior or thoughts, or two or more voices conversing with each other.

295.30 Paranoid type

A type of schizophrenia in which the following criteria are met:

  1. Preoccupation with one or more delusions or frequent auditory hallucinations
  2. None of the following is prominent: disorganized speech, disorganized or catatonic behavior, or flat or inappropriate affect.

Source: DSM-IV-TR

In the 1970s, Simon et al2 studied 192 hospitalized patients, of whom all African-Americans and 85% of whites had been identified clinically as having schizophrenia. Using a structured interview, the researchers found that only 40% of the African Americans and 50% of the whites met diagnostic criteria for schizophrenia. African-Americans with mood disorders were found to be at particular risk of schizophrenia misdiagnosis.

In the 1980s, among 76 patients with a clinical diagnosis of schizophrenia, Mukherjee et al3 diagnosed one-half (52%) with bipolar disorder using a structured clinical interview. Schizophrenia misdiagnoses were more common in African-Americans (86%) and Hispanics (83%) than in whites (51%). In particular, African-Americans were most likely to be misdiagnosed with paranoid schizophrenia. African-Americans complained more commonly than whites of auditory hallucinations, which may represent an ethnic difference in symptomatic presentation of psychotic mood disorders.

In the 1990s, colleagues and I conducted two studies—one of 173 patients in a Tennessee psychiatric hospital4 and the other of 490 patients in an Ohio psychiatric emergency service5—and found yet again that African-Americans were more likely than whites to be diagnosed with schizophrenia. In the hospital study, higher rates of schizophrenia diagnosis were associated with lower rates of mood disorder diagnosis. This inverse relationship implied that African-Americans with mood disorders were being misdiagnosed with schizophrenia.

Men were more likely than women to be diagnosed with schizophrenia, suggesting that African-American men were most likely to be misdiagnosed. When adjustments were made for gender, black women were found to be at higher risk for misdiagnosis than white women.

Lawson et al6 extended this research in a population-based study of African-Americans living in Tennessee. They found that African-Americans constituted 16% of the state’s population but 48% of psychiatric inpatients diagnosed with schizophrenia and 37% of psychiatric outpatients.

CONSEQUENCES OF INACCURATE DIAGNOSIS

Differentiating between schizophrenia (Box 1) and a psychotic mood disorder (Box 2) is more than a semantic exercise. Schizophrenia implies a chronic, unremitting, debilitating illness that worsens over time. Though this perception of schizophrenia is not entirely accurate, in clinical practice its diagnosis imparts a bleak prognosis that may lower the clinician’s expectations for the patient.7

Schizophrenia misdiagnosis also may lead the psychiatrist to rely excessively on antipsychotics, rather than attempting thymoleptic and psychotherapy trials. Studies suggest that African-American patients are more likely than similar white patients to receive antipsychotics4,8,9 and less likely to receive psychotherapy.5,10

Reasons why African-Americans are often misdiagnosed with schizophrenia remain unclear but probably include four contributing factors:

  • differences in symptom presentation compared with whites
  • failure by clinicians to identify affective symptoms in African-Americans
  • minority patients’ wariness when dealing with health services
  • and racial stereotyping.

DIFFERENCES IN SYMPTOM EXPRESSION

African-American patients with mood disorders or schizophrenia are more likely than are similar white patients to complain of auditory hallucinations.11-13 For example, Strakowski et al14 examined 330 patients with nonaffective and psychotic diagnoses in a study that was used to develop DSM-IV criteria for schizophrenia. Auditory hallucinations were rated as more severe in African-American than in similar white patients.

 

 

Box 2

Major depressive episode with psychotic features: Characteristic symptoms

MAJOR DEPRESSIVE EPISODE

Five or more of the following symptoms present during the same 2-week period and representing a change from previous functioning; must include either depressed mood or loss of interest or pleasure.

  • Depressed mood
  • Markedly diminished interest or pleasure
  • Significant weight loss
  • Insomnia or hypersomnia
  • Psychomotor agitation or retardation
  • Fatigue
  • Feelings of worthlessness or excessive guilt
  • Diminished ability to concentrate

SEVERE MAJOR DEPRESSION WITH PSYCHOTIC FEATURES

Mood-congruent

Delusions or hallucinations whose content is entirely consistent with the typical depressive themes of personal inadequacy, guilt, disease, death, nihilism, or deserved punishment

Mood-incongruent

Delusions or hallucinations whose content does not involve typical depressive themes. Includes symptoms such as persecutory delusions, thought insertion, thought broadcasting, and delusions of control

Source: DSM-IV-TR

African-American patients also are more likely than whites to exhibit so-called Schneiderian first-rank symptoms of schizophrenia,15 including:

  • delusions of thought broadcasting or insertion
  • auditory hallucinations of voices conversing about the patient in the third person.

These symptoms were once used to diagnose schizophrenia, but their lack of specificity has been well documented.2,16 First-rank symptoms of schizophrenia depend on the specific form of the hallucination or delusion, are likely to be influenced by a patient’s culture, and may be misleading in multicultural populations. Though first-rank symptoms now occupy a minor role in U.S. diagnostic systems, they might continue to sway clinicians—even when using structured diagnostic interviews—to inappropriately diagnose schizophrenia in lieu of affective disorders in minority patients.15

To extend this finding, our group16 studied rates and severity of affective and psychotic symptoms—particularly first-rank symptoms—in 100 patients with psychotic mania who met DSM-III-R criteria for bipolar disorder (80%) or schizoaffective disorder, bipolar type (20%) as determined by structured diagnostic interview. No differences in affective symptoms between African-American and white patients were seen. African-Americans were more likely to endorse auditory hallucinations and to report severe auditory hallucinations of voices commenting on their behavior—the only first-rank symptom on which they differed from whites.

Though their affective symptoms were similar, African-Americans were significantly more likely than whites to have been diagnosed with a schizophrenia-spectrum disorder. Because misdiagnosis of African-Americans could not be explained by psychotic symptoms—which were as severe as those of white patients—these findings suggest other mechanisms were at work.

UNIDENTIFIED AFFECTIVE SYMPTOMS

Underidentification of mood disorders in African-American patients may also lead to over-diagnosis of schizophrenia. In a sample of 99 patients, colleagues and I17 compared clinical diagnoses made in a psychiatric emergency service with those by research investigators using a structured clinical interview. Reasons for diagnostic differences were identified and divided into two categories:

  • the same symptoms were recorded but applied differently to diagnostic criteria (criterion variance)
  • different information was recorded, which led to diagnostic discrepancies (information variance).

Differences occurred significantly more often in African-American than in white patients, but only information variance was associated with ethnicity. This suggests that clinicians are less likely to elicit appropriate information from African-American than from white psychiatric patients. The fact that researchers obtained this information during diagnostic interviews suggests that the patients could provide it when given appropriate prompts. Specifically, affective symptoms were less likely to be elicited by clinicians than by researchers.

PATIENT WARINESS

Minority patients, when interacting with clinicians of the majority population, may project “protective wariness.”18 Specific behaviors include hesitancy or reluctance to fully engage with the care provider as a precaution against being exploited or harmed. Cultural misunderstandings19 and patient concerns about past reports of minorities receiving substandard or unethical health care20 may contribute to this behavior.

Whaley21 compared nonpathologic distrust and paranoia in 404 community-living African-Americans and whites. Some were healthy, and some had diagnoses of schizophrenia or depression. African-Americans—particularly those with psychiatric disorders—showed higher levels of distrust than whites. Distrust was also associated with depression in African-Americans but not in whites. Whaley concluded that:

  • depressed African-Americans may exhibit more distrust toward clinicians than do whites
  • this distrust puts African-Americans at risk of being perceived as paranoid and being misdiagnosed with paranoid schizophrenia.

Table

Remedial actions to avoid ethnic bias in diagnosing schizophrenia

ProblemRemedies
Failure to recognize differences in symptom expressionBecome familiar with ethnic differences in how patients describe symptoms
Incorporate structured interviews or rating scales into the clinical assessment
Failure to elicit affective symptomsIncorporate structured interviews or rating scales into the clinical assessment
Maintain a high index of suspicion for affective symptoms (see Box 2)
Misinterpreted protective warinessClarify the patient’s degree of suspicion; consider this in the historical context of abuses toward minorities by majority populations
Become familiar with ethnic differences in how symptoms are described
Covert and overt stereotyping and cultural insensitivityReview practice patterns
Consult with culturally sensitive clinicians as necessary
 

 

Though Whaley did not report differences in distrust between African-American men and women, others have noted that distrust of health providers may be more common in minority men.18

RACIAL STEREOTYPING

Compared with similar white men, African-American men with mental disorders are more likely to be:

  • referred for mental health care through social and legal—rather than medical—systems and to be involuntarily committed
  • perceived as violent—even though controlled research suggests they are not. This misperception can lead to excessive medication and restraints.22

Differential treatment of African-American men may create a cycle of distrust, hostility, and additional inappropriate treatment. Together, these factors may increase the risk that African-American men will be misdiagnosed with schizophrenia.

Past racism in biomedical and psychiatric practice and research has been documented23,24 and more recently reviewed by Lawson.19 Historically, African-Americans were perceived to have a “primitive psychic” nature that was thought to be more susceptible to schizophrenia than depression.19 Whether these or similar racist stereotypes continue to inject ethnic bias into clinical assessment requires further study.

WHERE DO WE GO FROM HERE?

Although research into methods to eliminate ethnicity bias is sparse, the work reviewed in this article suggests ways that psychiatrists can minimize this problem (Table).

Obtain comprehensive information. Use structured interviews, such as the Structured Clinical Interview for DSM-IV (SCID), and rating scales, such as the Hamilton Depression Scale, which require clinicians to ask about all types of symptoms, particularly affective symptoms.

Review treatment records. Review your practice patterns for evidence of schizophrenia over-diagnosis in African-Americans or other ethnic groups. Examine ethnic differences in legal referrals or use of restraints or seclusion, which may indicate an ethnic bias in how threats are perceived. Only by being aware of bias can one correct it.

Become familiar with cultural and ethnic differences in idioms of distress. Specifically, review research in cultural psychiatry to identify potential differences among cultural groups in how they describe psychiatric symptoms. Talk with colleagues or friends from other cultural groups, and read literature from different ethnic perspectives to increase your cultural sensitivity.

Consult with psychiatrists with expertise in cultural variability of clinical presentation when the diagnosis or threat assessment seems unclear. Consultation is recommended if a patient’s diagnosis is uncertain or if you detect bias in your practice.

These interventions require clinicians to become familiar with psychosocial differences in how patients of various cultural and ethnic groups express psychiatric symptoms. With this understanding, we can better engage wary patients, obtain valid information, and improve clinical practice and patient outcomes.

Finally, psychiatry’s diagnostic systems need to continually address how patient assessment is influenced by ethnicity, culture, gender, and other socio-demographic factors. Studies are needed to examine the contributions of multiple factors—such as symptom differences and stereotyping—that contribute to ethnic-related diagnostic disparities.

Related resources

  • Paul AM. Painting insanity black: Why are there more black schizophrenics? Salon.com Dec. 1, 1999. http://www.salon.com/books/it/1999/12/01/schizo/index.html
  • Alarcon RD, Westermeyer J, Foulks EF, Ruiz P. Clinical relevance of contemporary cultural psychiatry. J Nerv Ment Dis 1999;187: 465-71.
  • Williams DR, Neighbors HW, Jackson JS. Racial/ethnic discrimination and health: findings from community studies. Am J Public Health 2003;93:200-8.
  • Lin KM, Smith MW, Ortiz V. Culture and psychopharmacology. Psychiatr Clin North Am 2001; 24:523-38.

Acknowledgement

Preparation of this manuscript was supported in part by National Institutes of Health grant MH56352.

In patients with psychotic symptoms, why are African-Americans more likely than whites to be diagnosed with schizophrenia? After more than 30 years of debate, some answers—and remedies for the problem—are becoming clear.

In psychiatry, where interpersonal interactions are key to eliciting diagnostic symptoms and signs, there is an intrinsic risk of misinterpretation when clinician and patient are of different cultural, ethnic, or socioeconomic backgrounds. This article analyzes four factors that contribute to misinterpretation and to ethnic misdiagnosis of schizophrenia. Culturally sensitive strategies are offered to avoid diagnostic bias in clinical practice.

SCHIZOPHRENIA MISDIAGNOSIS

Large epidemiologic studies report similar rates of schizophrenia and bipolar disorder in African-American and white populations.1 Although patients of both races have been wrongly diagnosed with schizophrenia, the pattern is stronger and more persistent in African-Americans.

Box 1

Diagnostic criteria for schizophrenia: Characteristic symptoms (Criterion A)

Two (or more) of the following, each present for a significant portion of time during a 1-month period (or less if successfully treated):

  • Delusions
  • Hallucinations
  • Disorganized speech (eg, frequent derailment or incoherence)
  • Grossly disorganized or catatonic behavior
  • Negative symptoms (ie, affective flattening, alogia, or avolition)

Note: Only one Criterion A symptom is required if delusions are bizarre or hallucinations consist of a voice keeping up a running commentary on the person’s behavior or thoughts, or two or more voices conversing with each other.

295.30 Paranoid type

A type of schizophrenia in which the following criteria are met:

  1. Preoccupation with one or more delusions or frequent auditory hallucinations
  2. None of the following is prominent: disorganized speech, disorganized or catatonic behavior, or flat or inappropriate affect.

Source: DSM-IV-TR

In the 1970s, Simon et al2 studied 192 hospitalized patients, of whom all African-Americans and 85% of whites had been identified clinically as having schizophrenia. Using a structured interview, the researchers found that only 40% of the African Americans and 50% of the whites met diagnostic criteria for schizophrenia. African-Americans with mood disorders were found to be at particular risk of schizophrenia misdiagnosis.

In the 1980s, among 76 patients with a clinical diagnosis of schizophrenia, Mukherjee et al3 diagnosed one-half (52%) with bipolar disorder using a structured clinical interview. Schizophrenia misdiagnoses were more common in African-Americans (86%) and Hispanics (83%) than in whites (51%). In particular, African-Americans were most likely to be misdiagnosed with paranoid schizophrenia. African-Americans complained more commonly than whites of auditory hallucinations, which may represent an ethnic difference in symptomatic presentation of psychotic mood disorders.

In the 1990s, colleagues and I conducted two studies—one of 173 patients in a Tennessee psychiatric hospital4 and the other of 490 patients in an Ohio psychiatric emergency service5—and found yet again that African-Americans were more likely than whites to be diagnosed with schizophrenia. In the hospital study, higher rates of schizophrenia diagnosis were associated with lower rates of mood disorder diagnosis. This inverse relationship implied that African-Americans with mood disorders were being misdiagnosed with schizophrenia.

Men were more likely than women to be diagnosed with schizophrenia, suggesting that African-American men were most likely to be misdiagnosed. When adjustments were made for gender, black women were found to be at higher risk for misdiagnosis than white women.

Lawson et al6 extended this research in a population-based study of African-Americans living in Tennessee. They found that African-Americans constituted 16% of the state’s population but 48% of psychiatric inpatients diagnosed with schizophrenia and 37% of psychiatric outpatients.

CONSEQUENCES OF INACCURATE DIAGNOSIS

Differentiating between schizophrenia (Box 1) and a psychotic mood disorder (Box 2) is more than a semantic exercise. Schizophrenia implies a chronic, unremitting, debilitating illness that worsens over time. Though this perception of schizophrenia is not entirely accurate, in clinical practice its diagnosis imparts a bleak prognosis that may lower the clinician’s expectations for the patient.7

Schizophrenia misdiagnosis also may lead the psychiatrist to rely excessively on antipsychotics, rather than attempting thymoleptic and psychotherapy trials. Studies suggest that African-American patients are more likely than similar white patients to receive antipsychotics4,8,9 and less likely to receive psychotherapy.5,10

Reasons why African-Americans are often misdiagnosed with schizophrenia remain unclear but probably include four contributing factors:

  • differences in symptom presentation compared with whites
  • failure by clinicians to identify affective symptoms in African-Americans
  • minority patients’ wariness when dealing with health services
  • and racial stereotyping.

DIFFERENCES IN SYMPTOM EXPRESSION

African-American patients with mood disorders or schizophrenia are more likely than are similar white patients to complain of auditory hallucinations.11-13 For example, Strakowski et al14 examined 330 patients with nonaffective and psychotic diagnoses in a study that was used to develop DSM-IV criteria for schizophrenia. Auditory hallucinations were rated as more severe in African-American than in similar white patients.

 

 

Box 2

Major depressive episode with psychotic features: Characteristic symptoms

MAJOR DEPRESSIVE EPISODE

Five or more of the following symptoms present during the same 2-week period and representing a change from previous functioning; must include either depressed mood or loss of interest or pleasure.

  • Depressed mood
  • Markedly diminished interest or pleasure
  • Significant weight loss
  • Insomnia or hypersomnia
  • Psychomotor agitation or retardation
  • Fatigue
  • Feelings of worthlessness or excessive guilt
  • Diminished ability to concentrate

SEVERE MAJOR DEPRESSION WITH PSYCHOTIC FEATURES

Mood-congruent

Delusions or hallucinations whose content is entirely consistent with the typical depressive themes of personal inadequacy, guilt, disease, death, nihilism, or deserved punishment

Mood-incongruent

Delusions or hallucinations whose content does not involve typical depressive themes. Includes symptoms such as persecutory delusions, thought insertion, thought broadcasting, and delusions of control

Source: DSM-IV-TR

African-American patients also are more likely than whites to exhibit so-called Schneiderian first-rank symptoms of schizophrenia,15 including:

  • delusions of thought broadcasting or insertion
  • auditory hallucinations of voices conversing about the patient in the third person.

These symptoms were once used to diagnose schizophrenia, but their lack of specificity has been well documented.2,16 First-rank symptoms of schizophrenia depend on the specific form of the hallucination or delusion, are likely to be influenced by a patient’s culture, and may be misleading in multicultural populations. Though first-rank symptoms now occupy a minor role in U.S. diagnostic systems, they might continue to sway clinicians—even when using structured diagnostic interviews—to inappropriately diagnose schizophrenia in lieu of affective disorders in minority patients.15

To extend this finding, our group16 studied rates and severity of affective and psychotic symptoms—particularly first-rank symptoms—in 100 patients with psychotic mania who met DSM-III-R criteria for bipolar disorder (80%) or schizoaffective disorder, bipolar type (20%) as determined by structured diagnostic interview. No differences in affective symptoms between African-American and white patients were seen. African-Americans were more likely to endorse auditory hallucinations and to report severe auditory hallucinations of voices commenting on their behavior—the only first-rank symptom on which they differed from whites.

Though their affective symptoms were similar, African-Americans were significantly more likely than whites to have been diagnosed with a schizophrenia-spectrum disorder. Because misdiagnosis of African-Americans could not be explained by psychotic symptoms—which were as severe as those of white patients—these findings suggest other mechanisms were at work.

UNIDENTIFIED AFFECTIVE SYMPTOMS

Underidentification of mood disorders in African-American patients may also lead to over-diagnosis of schizophrenia. In a sample of 99 patients, colleagues and I17 compared clinical diagnoses made in a psychiatric emergency service with those by research investigators using a structured clinical interview. Reasons for diagnostic differences were identified and divided into two categories:

  • the same symptoms were recorded but applied differently to diagnostic criteria (criterion variance)
  • different information was recorded, which led to diagnostic discrepancies (information variance).

Differences occurred significantly more often in African-American than in white patients, but only information variance was associated with ethnicity. This suggests that clinicians are less likely to elicit appropriate information from African-American than from white psychiatric patients. The fact that researchers obtained this information during diagnostic interviews suggests that the patients could provide it when given appropriate prompts. Specifically, affective symptoms were less likely to be elicited by clinicians than by researchers.

PATIENT WARINESS

Minority patients, when interacting with clinicians of the majority population, may project “protective wariness.”18 Specific behaviors include hesitancy or reluctance to fully engage with the care provider as a precaution against being exploited or harmed. Cultural misunderstandings19 and patient concerns about past reports of minorities receiving substandard or unethical health care20 may contribute to this behavior.

Whaley21 compared nonpathologic distrust and paranoia in 404 community-living African-Americans and whites. Some were healthy, and some had diagnoses of schizophrenia or depression. African-Americans—particularly those with psychiatric disorders—showed higher levels of distrust than whites. Distrust was also associated with depression in African-Americans but not in whites. Whaley concluded that:

  • depressed African-Americans may exhibit more distrust toward clinicians than do whites
  • this distrust puts African-Americans at risk of being perceived as paranoid and being misdiagnosed with paranoid schizophrenia.

Table

Remedial actions to avoid ethnic bias in diagnosing schizophrenia

ProblemRemedies
Failure to recognize differences in symptom expressionBecome familiar with ethnic differences in how patients describe symptoms
Incorporate structured interviews or rating scales into the clinical assessment
Failure to elicit affective symptomsIncorporate structured interviews or rating scales into the clinical assessment
Maintain a high index of suspicion for affective symptoms (see Box 2)
Misinterpreted protective warinessClarify the patient’s degree of suspicion; consider this in the historical context of abuses toward minorities by majority populations
Become familiar with ethnic differences in how symptoms are described
Covert and overt stereotyping and cultural insensitivityReview practice patterns
Consult with culturally sensitive clinicians as necessary
 

 

Though Whaley did not report differences in distrust between African-American men and women, others have noted that distrust of health providers may be more common in minority men.18

RACIAL STEREOTYPING

Compared with similar white men, African-American men with mental disorders are more likely to be:

  • referred for mental health care through social and legal—rather than medical—systems and to be involuntarily committed
  • perceived as violent—even though controlled research suggests they are not. This misperception can lead to excessive medication and restraints.22

Differential treatment of African-American men may create a cycle of distrust, hostility, and additional inappropriate treatment. Together, these factors may increase the risk that African-American men will be misdiagnosed with schizophrenia.

Past racism in biomedical and psychiatric practice and research has been documented23,24 and more recently reviewed by Lawson.19 Historically, African-Americans were perceived to have a “primitive psychic” nature that was thought to be more susceptible to schizophrenia than depression.19 Whether these or similar racist stereotypes continue to inject ethnic bias into clinical assessment requires further study.

WHERE DO WE GO FROM HERE?

Although research into methods to eliminate ethnicity bias is sparse, the work reviewed in this article suggests ways that psychiatrists can minimize this problem (Table).

Obtain comprehensive information. Use structured interviews, such as the Structured Clinical Interview for DSM-IV (SCID), and rating scales, such as the Hamilton Depression Scale, which require clinicians to ask about all types of symptoms, particularly affective symptoms.

Review treatment records. Review your practice patterns for evidence of schizophrenia over-diagnosis in African-Americans or other ethnic groups. Examine ethnic differences in legal referrals or use of restraints or seclusion, which may indicate an ethnic bias in how threats are perceived. Only by being aware of bias can one correct it.

Become familiar with cultural and ethnic differences in idioms of distress. Specifically, review research in cultural psychiatry to identify potential differences among cultural groups in how they describe psychiatric symptoms. Talk with colleagues or friends from other cultural groups, and read literature from different ethnic perspectives to increase your cultural sensitivity.

Consult with psychiatrists with expertise in cultural variability of clinical presentation when the diagnosis or threat assessment seems unclear. Consultation is recommended if a patient’s diagnosis is uncertain or if you detect bias in your practice.

These interventions require clinicians to become familiar with psychosocial differences in how patients of various cultural and ethnic groups express psychiatric symptoms. With this understanding, we can better engage wary patients, obtain valid information, and improve clinical practice and patient outcomes.

Finally, psychiatry’s diagnostic systems need to continually address how patient assessment is influenced by ethnicity, culture, gender, and other socio-demographic factors. Studies are needed to examine the contributions of multiple factors—such as symptom differences and stereotyping—that contribute to ethnic-related diagnostic disparities.

Related resources

  • Paul AM. Painting insanity black: Why are there more black schizophrenics? Salon.com Dec. 1, 1999. http://www.salon.com/books/it/1999/12/01/schizo/index.html
  • Alarcon RD, Westermeyer J, Foulks EF, Ruiz P. Clinical relevance of contemporary cultural psychiatry. J Nerv Ment Dis 1999;187: 465-71.
  • Williams DR, Neighbors HW, Jackson JS. Racial/ethnic discrimination and health: findings from community studies. Am J Public Health 2003;93:200-8.
  • Lin KM, Smith MW, Ortiz V. Culture and psychopharmacology. Psychiatr Clin North Am 2001; 24:523-38.

Acknowledgement

Preparation of this manuscript was supported in part by National Institutes of Health grant MH56352.

References

1. Robins LN, Regier DA (eds). Psychiatric disorders in America: the Epidemiologic Catchment Area study. New York: The Free Press. 1991.

2. Simon RJ, Fleiss JL, Gurland BJ, et al. Depression and schizophrenia in hospitalized black and white mental patients. Arch Gen Psychiatry 1973;28:509-12.

3. Mukherjee S, Shukla S, Woodle J, et al. Misdiagnosis of schizophrenia in bipolar patients: a multiethnic comparison. Am J Psychiatry 1983;140:1571-4.

4. Strakowski SM, Shelton RC, Kolbrener ML. The effects of race and comorbidity on clinical diagnosis in patients with psychosis. J Clin Psychiatry 1993;54:96-102.

5. Strakowski SM, Lonczak HS, Sax KW, et al. The effects of race on diagnosis and disposition from a psychiatric emergency service. J Clin Psychiatry 1995;56:101-7.

6. Lawson WB, Hepler N, Holladay J, Cuffel B. Race as a factor in inpatient and outpatient admissions and diagnosis. Hosp Comm Psychiatry 1994;45:72-4.

7. Hoffman H, Kupper Z, Kunz B. Hopelessness and its impact on rehabilitation outcome in schizophrenia—an exploratory study. Schizophr Res 2000;43:147-58.

8. Walkup JT, McAlpine DD, Olfson M, et al. Patients with schizophrenia at risk for excessive antipsychotic dosing. J Clin Psychiatry 2000;61:344-8.

9. Segal SP, Bola JR, Watson MA. Race, quality of care, and antipsychotic prescribing practices in psychiatric emergency services. Psychiatr Serv 1996;47:282-6.

10. Flaskerud JH, Hu L. Racial/ethnic identity and amount and type of psychiatric treatment. Am J Psychiatry 1992;149:379-84.

11. Adebimpe VR, Klein HE, Fried J. Hallucinations and delusions in black psychiatric patients. J Natl Med Assoc 1981;73:517-20.

12. Adebimpe VR, Chu CC, Klein HE, Lange MH. Racial and geographic differences in the psychopathology of schizophrenia. Am J Psychiatry 1982;139:888-91.

13. Fabrega H, Jr, Mezzich J, Ulrich RF. Black-white differences in psychopathology in an urban psychiatric population. Compr Psychiatry 1988;29:285-97.

14. Strakowski SM, Flaum M, Amador X, et al. Racial differences in the diagnosis of psychosis. Schizophr Res 1996;21:117-24.

15. Schneider K. Clinical psychopathology (translated by Hamilton MW). New York: Grune and Stratton, 1959.

16. Strakowski SM, McElroy SL, Keck PE, Jr, West SA. Racial influence on diagnosis in psychotic mania. J Aff Disord. 1996;39:157-62.

17. Strakowski SM, Hawkins JM, Keck PE, Jr, et al. The effects of race and information variance on disagreement between psychiatric emergency service and research diagnoses in first-episode psychosis. J Clin Psychiatry 1997;58:457-63.

18. Jones BE, Gray BA. Problems in diagnosing schizophrenia and affective disorders among blacks. Hosp Comm Psychiatry 1986;37:61-5.

19. Neighbors HW, Jackson JS, Campbell L, Williams D. The influence of racial factors on psychiatric diagnosis: A review and suggestions for research. Comm Ment Health J 1989;25:301-11.

20. Lawson WB. Racial and ethnic factors in psychiatric research. Hosp Comm Psychiatry 1986;37:50-4.

21. Whaley AL. Ethnicity/race, paranoia, and psychiatric diagnoses: Clinician bias versus sociocultural differences. J Psychopathol Behav Assess 1997;19:1-20.

22. Lawson WB, Yesavage JA, Werner RD. Race, violence, and psychopathology. J Clin Psychiatry 1984;45:294-7.

23. Spurlock J. Psychiatric states. In: Williams RA (ed). Textbook of black-related diseases. New York: McGraw-Hill, 1975.

24. Thomas A, Sillen S. Racism and psychiatry. New York: Brunner/Mazel, 1972.

References

1. Robins LN, Regier DA (eds). Psychiatric disorders in America: the Epidemiologic Catchment Area study. New York: The Free Press. 1991.

2. Simon RJ, Fleiss JL, Gurland BJ, et al. Depression and schizophrenia in hospitalized black and white mental patients. Arch Gen Psychiatry 1973;28:509-12.

3. Mukherjee S, Shukla S, Woodle J, et al. Misdiagnosis of schizophrenia in bipolar patients: a multiethnic comparison. Am J Psychiatry 1983;140:1571-4.

4. Strakowski SM, Shelton RC, Kolbrener ML. The effects of race and comorbidity on clinical diagnosis in patients with psychosis. J Clin Psychiatry 1993;54:96-102.

5. Strakowski SM, Lonczak HS, Sax KW, et al. The effects of race on diagnosis and disposition from a psychiatric emergency service. J Clin Psychiatry 1995;56:101-7.

6. Lawson WB, Hepler N, Holladay J, Cuffel B. Race as a factor in inpatient and outpatient admissions and diagnosis. Hosp Comm Psychiatry 1994;45:72-4.

7. Hoffman H, Kupper Z, Kunz B. Hopelessness and its impact on rehabilitation outcome in schizophrenia—an exploratory study. Schizophr Res 2000;43:147-58.

8. Walkup JT, McAlpine DD, Olfson M, et al. Patients with schizophrenia at risk for excessive antipsychotic dosing. J Clin Psychiatry 2000;61:344-8.

9. Segal SP, Bola JR, Watson MA. Race, quality of care, and antipsychotic prescribing practices in psychiatric emergency services. Psychiatr Serv 1996;47:282-6.

10. Flaskerud JH, Hu L. Racial/ethnic identity and amount and type of psychiatric treatment. Am J Psychiatry 1992;149:379-84.

11. Adebimpe VR, Klein HE, Fried J. Hallucinations and delusions in black psychiatric patients. J Natl Med Assoc 1981;73:517-20.

12. Adebimpe VR, Chu CC, Klein HE, Lange MH. Racial and geographic differences in the psychopathology of schizophrenia. Am J Psychiatry 1982;139:888-91.

13. Fabrega H, Jr, Mezzich J, Ulrich RF. Black-white differences in psychopathology in an urban psychiatric population. Compr Psychiatry 1988;29:285-97.

14. Strakowski SM, Flaum M, Amador X, et al. Racial differences in the diagnosis of psychosis. Schizophr Res 1996;21:117-24.

15. Schneider K. Clinical psychopathology (translated by Hamilton MW). New York: Grune and Stratton, 1959.

16. Strakowski SM, McElroy SL, Keck PE, Jr, West SA. Racial influence on diagnosis in psychotic mania. J Aff Disord. 1996;39:157-62.

17. Strakowski SM, Hawkins JM, Keck PE, Jr, et al. The effects of race and information variance on disagreement between psychiatric emergency service and research diagnoses in first-episode psychosis. J Clin Psychiatry 1997;58:457-63.

18. Jones BE, Gray BA. Problems in diagnosing schizophrenia and affective disorders among blacks. Hosp Comm Psychiatry 1986;37:61-5.

19. Neighbors HW, Jackson JS, Campbell L, Williams D. The influence of racial factors on psychiatric diagnosis: A review and suggestions for research. Comm Ment Health J 1989;25:301-11.

20. Lawson WB. Racial and ethnic factors in psychiatric research. Hosp Comm Psychiatry 1986;37:50-4.

21. Whaley AL. Ethnicity/race, paranoia, and psychiatric diagnoses: Clinician bias versus sociocultural differences. J Psychopathol Behav Assess 1997;19:1-20.

22. Lawson WB, Yesavage JA, Werner RD. Race, violence, and psychopathology. J Clin Psychiatry 1984;45:294-7.

23. Spurlock J. Psychiatric states. In: Williams RA (ed). Textbook of black-related diseases. New York: McGraw-Hill, 1975.

24. Thomas A, Sillen S. Racism and psychiatry. New York: Brunner/Mazel, 1972.

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Schizoaffective disorder: Which symptoms should be treated first?

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Schizoaffective disorder: Which symptoms should be treated first?

Psychiatry has used the term “schizoaffective disorder” for more than 60 years, but its specific meaning remains uncertain. Patients who meet its diagnostic criteria typically present with a confusing blend of mood and psychotic symptoms, and we often classify them as being schizoaffective because we don’t know where else to put them.

Much of our difficulty in trying to determine what schizoaffective disorder is can be blamed on insufficient data. We do not know the specific cause of either schizophrenic or mood disorders, and today’s concepts of these broad diagnoses probably encompass multiple etiologies.

Based on the evidence and clinical experience, this article presents:

  • the evolution of schizoaffective disorder as a psychiatric diagnosis
  • the four main concepts that attempt to explain the disorder’s cause
  • and a practical approach for managing these patients’ complicated symptoms.

Origins of schizoaffective disorder

When Jacob Kasanin1 riginated the term schizoaffective disorder in 1933, psychiatry was struggling to integrate Emil Kraepelin’s and Eugene Bleuler’s two competing and complementary schemes for understanding psychotic disorders.

Kraepelin had proposed that the major psychoses could be divided between dementia praecox and manic-depressive insanity (and to a lesser extent, paraphrenia), based on the presenting symptoms and—importantly—course of illness:2

  • Manic-depressive insanity typically included periods of full recovery of mental functions between episodes.
  • Dementia praecox was defined by a steady deterioration of mental function and personality from which patients rarely recovered.

Box

DSM-IV CRITERIA FOR SCHIZOAFFECTIVE DISORDER

  1. An uninterrupted period of illness during which, at some time, there is either a major depressive episode, a manic episode, or a mixed episode concurrent with symptoms that meet Criterion A for schizophrenia:
  2. During the same period of illness, there have been delusions or hallucinations for at least 2 weeks in the absence of prominent mood symptoms.
  3. Symptoms that meet criteria for a mood episode are present for a substantial portion of the total duration of the active and residual periods of the illness.
  4. The disturbance is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition.

Specific type:

Bipolar type: If the disturbance includes a manic or a mixed episode (or a manic or a mixed episode and major depressive episodes)

Depressive type: If the disturbance only includes major depressive episodes.

Source: Diagnostic and statistical manual of mental disorders (4th ed., TR). Washington, DC: American Psychiatric Association, 2000.

This distinction was a landmark in psychiatry but did not offer a specific understanding of the mental or brain dysfunctions underlying these conditions nor a cross-sectional means to diagnose a patient’s condition.

Bleuler was less concerned with predicting course and outcome. Instead, he wished to understand his observations that patients commonly exhibited a disjunction among psychological processes that were integrated in healthy individuals.3 He described the cause of this loss of psychological integration as the “schizophrenias” or, literally, “split mind.” In the schizophrenias, he identified symptoms that seemed to reflect this psychological disjunction, such as flat affect, ambivalence, and splitting of cognition from emotion and behavior.

Because Kraepelin described many of these same symptoms in dementia praecox, clinicians tended to equate the schizophrenias with dementia praecox. However, many more patients with Bleuler’s schizophrenia recovered than did those with Kraepelin’s dementia praecox (essentially by definition). Therefore, some “schizophrenic” patients appeared to meet Kraepelin’s diagnosis of manic-depressive insanity. At this point, Kasanin stepped into the fray with his concept of schizoaffective disorder.

Kasanin’s conceptualization

Kasanin recognized that many patients exhibited a blending of Bleuler’s schizophrenia symptoms with those of Kraepelin’s manic-depressive (affective) illness.1 Moreover, unlike patients with dementia praecox, these blended patients exhibited:

  • good premorbid adjustment
  • typically a sudden illness onset with marked emotional turmoil
  • few symptoms of withdrawal or passivity
  • and a relatively short course with complete recovery.

In reporting these patients and subsequently originating the term “schizoaffective psychosis,” Kasanin tried to identify a homogeneous patient population that could be distinguished from the more broadly conceptualized Bleulerian schizophrenias and the more narrowly defined Kraepelinian categories.

The term “schizoaffective disorder” has evolved from this beginning. Interestingly, most—if not all—of the nine cases reported by Kasanin would be diagnosed with an affective disorder with psychotic features under today’s diagnostic criteria.4 Nonetheless, the term “schizoaffective disorder” was adopted by psychiatry (particularly in the United States) and has been used to classify patients who present with features of both schizophrenia and affective illness but cannot be clearly described as having either.

Evolutions from DSM-I to DSM-III

In American nosology, schizoaffective disorder was included as a subtype of schizophrenia in DSM-I (1952)5 and DSM-II (1968)6 and then reclassified in DSM-III (1980)7 as a “psychotic disorder not elsewhere classified.” Remarkably, none of these classifications provided criteria for diagnosing schizoaffective disorder.

 

 

Shortly before publication of DSM-III, Robert Spitzer, MD, and colleagues at the New York Neuropsychiatric Institute developed diagnostic criteria for schizoaffective disorder as part of their research diagnostic criteria (RDC).8 The RDC separated patients with affective and certain types of psychotic symptoms, suggestive of schizophrenia at that time, into two types—schizoaffective mania and schizoaffective depression—based on the polarity of the mood symptoms.

The psychotic symptoms identified as “schizophrenic” by the RDC were certain first-rank symptoms designated by Kurt Schneider, such as delusions of being controlled or mood-incongruent hallucinations. [Note: In recent studies, neither first-rank symptoms nor other subtypes of psychotic symptoms (moodincongruent delusions or hallucinations) have been shown to specifically identify patients with schizophrenia.9,10 In fact, no psychotic symptoms are considered pathognomonic for any specific disorder at this time.]

The RDC also introduced the idea that schizoaffective disorder was distinct from psychotic mood disorder in that:

  • psychotic symptoms persisted for a specific period (1 week), during which mood symptoms were absent
  • and mood and psychotic symptoms overlapped at some time during the course of illness.

These criteria were then adopted with modifications in DSM-III-R,11 which provided the first widely-accepted, well-defined criteria for schizoaffective disorder.

DSM-III-R and DSM-IV

DSM-III-R defined schizoaffective disorder based on relationships between affective syndromes and the criteria for schizophrenia. Specifically, the diagnosis required the presence of a full depressive or manic syndrome while the patient also met criteria for schizophrenia. To distinguish schizoaffective disorder from psychotic mood disorders, DSM-III-R required that psychotic symptoms persist for 2 weeks in the absence of “prominent” mood symptoms.

Unfortunately, “prominent” was not defined, leaving a fair amount of discretion to clinicians and making it difficult to standardize research studies. In addition, the predictive utility of 2 weeks of psychosis has not been strongly validated. In fact, the time span at which psychosis without a mood disorder identifies a new syndrome is not known.

To rule out schizophrenia, the mood syndrome could not have been “brief” relative to the psychosis; again, what “brief” meant was difficult to put into practice. Notably, there was no specific requirement to rule out mood disorders (i.e., that the psychosis was not brief relative to the duration of mood symptoms).

DSM-IV slightly modified these criteria,12 but their basic flavor from DSM-III-R was retained. Despite their limitations, the diagnostic criteria in DSM-III-R and DSM-IV at least provided clinicians and scientists the means to consistently identify schizoaffective disorder. The diagnostic criteria (Box) are still considered reliable today.13

Four concepts of schizoaffective disorder

Relatively few studies of schizoaffective disorder exist, so the diagnosis remains poorly validated. At least four concepts have been developed (Figure).4

Concept 1: Schizoaffective disorder is a variant of schizophrenia. Many of the characteristics of schizoaffective disorder that Kasanin first described, such as rapid onset and confusion, were identified as good prognostic indicators in later concepts of schizophrenia. Some family history studies also suggest a link between schizophrenic and schizoaffective disorders.15

Concept 2: Schizoaffective disorder is a variant of mood disorder. 9 Schizoaffective disorder represents a pernicious type of mood disorder in which psychotic symptoms persist and the course of illness is worse than in other variants (although better than in schizophrenia).16 Family studies are unclear about links between mood and schizoaffective disorders.17

Figure FOUR CONCEPTS THAT SEEK TO EXPLAIN SCHIZOAFFECTIVE DISORDER


Figure. Four conceptualizations explain schizoaffective disorder as (1) a type of schizophrenia; (2) a type of mood disorder; (3) a heterogeneous combination of patients with schizophrenia, mood disorder, and “real” schizoaffective disorder; and (4) as part of a continuum of psychotic disorders from worst prognosis (schizophrenia) to best prognosis (major depression).Concept 3: Schizoaffective disorder represents a heterogeneous combination of schizophrenia and mood disorder. Specifically, schizoaffective disorder may comprise a group of patients with severe psychotic mood disorders and either good-prognosis schizophrenia or schizophrenia with numerous affective symptoms.

A subgroup of patients with “true” schizoaffective disorder (distinct from schizophrenic or mood disorders) might also exist.18 As a twist on this idea, others have suggested that schizoaffective disorder, bipolar type is simply a variant of bipolar disorder, whereas schizoaffective disorder, depressed type is more closely akin to schizophrenia. The fact that depression occurs at some time in most patients with schizophrenia supports this view.

Concept 4: Psychotic disorders share a genetic vulnerability and exist on a continuum (from worst to best prognosis) from schizophrenia, to schizoaffective disorder, to psychotic then nonpsychotic bipolar and major depressive disorders.19

A lack of definitive evidence prevents us from choosing among these concepts; good studies support and discount each possibility.

 

 

Patient management

When faced with a patient who meets criteria for schizoaffective disorder, I believe practical considerations can guide treatment. The label “schizoaffective disorder” reminds us to consider treatment of these patients broadly (in contrast, for example, to the label “schizophreniform disorder,” which implies a stronger link to schizophrenia than outcome studies support21).

Treat the mood component first. In most patients with schizoaffective disorder, it is difficult to distinguish between diagnoses of schizophrenia or mood disorder. It is prudent to begin by aggressively treating the mood component, because psychotic mood disorders generally respond more favorably to treatment than does schizophrenia. Use mood stabilizers for patients with a history of mania and antidepressants in depressed patients with no history of mania.

As is true for psychotic mood disorders, concurrent administration of an antipsychotic is often warranted. Recent studies strongly suggest that atypical antipsychotics are preferred over traditional neuroleptics to treat psychotic patients in general, and this preference extends to patients with schizoaffective disorder.4,14,20

Some—if not most—atypical antipsychotics may have mood-stabilizing or antidepressant properties and may permit monotherapy of patients with schizoaffective disorder. Controlled clinical trials have not examined these agents as long-term maintenance therapy for the mood component of schizoaffective disorder, however. Until such studies are completed, many patients may require long-term mood-stabilizer or antidepressant therapy, with or without ongoing antipsychotic treatment.4,14

The next step. Alternate treatments should be considered for patients in whom trials of atypical antipsychotics have failed, both in combination with thymoleptics and in monotherapy. Conventional antipsychotics, particularly depot formulations, are a reasonable intervention, particularly in schizoaffective patients with minimal mood symptoms.

Clozapine remains a first-line choice for patients with treatment-resistant psychotic disorders and should be considered in patients with treatment-resistant schizoaffective disorder as well.

Conclusion

Patients meeting criteria for schizoaffective disorder typically present with a complex and confusing combination of affective and psychotic symptoms. The diagnosis continues to be applied predominantly to patients who are otherwise difficult to classify, and the diagnostic criteria supporting the presence of a distinct condition remain poorly validated.

Schizoaffective disorder probably defines a heterogeneous group of patients, but—practically speaking—they can often be managed by following algorithms for psychotic mood disorders.4,13 The most prudent long-term approach seems to be to keep treatment options flexible, with careful attention to managing symptoms as they wax and wane, rather than rigidly fixing on a single medication or type of medication.

Related resources

  • National Mental Health Association factsheet on schizoaffective disorder www.nmha.org/infoctr/factsheets/52.cfm
  • Reichenberg A, Weiser M, Rabinowitz, J, et al. A population-based cohort study of premorbid intellectual, language, and behavioral functioning in patients with schizophrenia, schizoaffective disorder, and nonpsychotic bipolar disorder. Am J Psychiatry 2002;159(12):2027-35.
  • Robinson DG, Woerner, MG, Alvir JM, et al. Predictors of medication discontinuation by patients with first-episode schizophrenia and schizoaffective disorder. Schizophr Res 2002;57(2-3):209-19.
References

1. Kasanin J. The acute schizoaffective psychoses. Am J Psychiatry 1933;113:97-126.

2. Kraepelin E. Dementia praecox and paraphrenia, together with manic depressive insanity. Translated from original texts by The Classics of Psychiatry and Behavioral Sciences Library. Delran, NJ; Gryphon Editions, 1993.

3. Bleuler E. Text-book of psychiatry. Translated from original texts by The Classics of Psychiatry and Behavioral Sciences Library. Delran, NJ: Gryphon Editions, 1994.

4. Keck PE, Jr, McElroy SL, Strakowski SM/, West SA. Pharmacologic treatment of schizoaffective disorder. Psychopharmacology 1994;114:529-38.

5. Diagnostic and statistical manual of mental disorders. Washington, DC: American Psychiatric Association, 1952.

6. Diagnostic and statistical manual of mental disorders (2nd ed). Washington, DC: American Psychiatric Association, 1968.

7. Diagnostic and statistical manual of mental disorders (3rd ed). Washington, DC: American Psychiatric Association, 1980.

8. Spitzer RL, Endicott J, Robins E. Research diagnostic criteria. Rationale and reliability. Arch Gen Psychiatry 1978;35:773-82.

9. Pope HG, Jr, Lipinski JF. Diagnosis of schizophrenia and manic-depressive illness: a reassessment of the specificity of ‘schizophrenic’ symptoms in the light of current research. Arch Gen Psychiatry 1978;35:811-28.

10. Strakowski SM, McElroy SL, Keck PE, Jr, West SA. Racial influence on diagnosis in psychotic mania. J Affect Disord 1996;39:157-62.

11. Diagnostic and statistical manual of mental disorders (3rd ed, rev). Washington, DC: American Psychiatric Press, 1987.

12. Diagnostic and statistical manual of mental disorders (4th ed). Washington, DC: American Psychiatric Press, 1994.

13. Keck PE, Jr., McElroy SL, Strakowski SM. New developments in the pharmacologic treatment of schizoaffective disorder. J Clin Psychiatry 1996;57S:41-8.

14. Clayton PJ. Schizoaffective disorders. J Nerv Ment Dis 1982;170:646-50.

15. Kendler KS, Spitzer RL, Williams JBW. Psychotic disorders in DSM-III-R. Am J Psychiatry 1989;146:953-62.

16. Strakowski SM, Keck PE, Jr, Sax KW, McElroy SL, Hawkins JM. Twelve-month outcome of patients with DSM-III-R schizoaffective disorder: comparisons to matched patients with bipolar disorder. Schizophrenia Res 1999;35:167-74.

17. Maier W, Lichtermann D, Minges J, Heun R, Hallmayer J, Benkert O. Schizoaffective disorder and affective disorders with mood-incongruent psychotic feathers: keep separate or combine? Evidence from a family study. Am J Psychiatry 1992;149:1666-73.

18. Kendler KS, McGuire M, Gruenberg AM, Walsh D. Examining the validity of DSM-III-R schizoaffective disorder and its putative subtypes in the Roscommon Family Study. Am J Psychiatry 1995;152:755-64.

19. Crow TJ. A continuum of psychosis, one human gene and not much else—the case for homogeneity. Schizophrenia Res 1995;17:135-45.

20. Strakowski SM, DelBello MP, Adler CM. Comparative tolerability of drug treatments for bipolar disorder. CNS Drugs 2001;15:701-18.

21. Strakowski SM. Diagnostic validity of schizophreniform disorder. Am J Psychiatry 1994;151:815-24.

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Psychiatry has used the term “schizoaffective disorder” for more than 60 years, but its specific meaning remains uncertain. Patients who meet its diagnostic criteria typically present with a confusing blend of mood and psychotic symptoms, and we often classify them as being schizoaffective because we don’t know where else to put them.

Much of our difficulty in trying to determine what schizoaffective disorder is can be blamed on insufficient data. We do not know the specific cause of either schizophrenic or mood disorders, and today’s concepts of these broad diagnoses probably encompass multiple etiologies.

Based on the evidence and clinical experience, this article presents:

  • the evolution of schizoaffective disorder as a psychiatric diagnosis
  • the four main concepts that attempt to explain the disorder’s cause
  • and a practical approach for managing these patients’ complicated symptoms.

Origins of schizoaffective disorder

When Jacob Kasanin1 riginated the term schizoaffective disorder in 1933, psychiatry was struggling to integrate Emil Kraepelin’s and Eugene Bleuler’s two competing and complementary schemes for understanding psychotic disorders.

Kraepelin had proposed that the major psychoses could be divided between dementia praecox and manic-depressive insanity (and to a lesser extent, paraphrenia), based on the presenting symptoms and—importantly—course of illness:2

  • Manic-depressive insanity typically included periods of full recovery of mental functions between episodes.
  • Dementia praecox was defined by a steady deterioration of mental function and personality from which patients rarely recovered.

Box

DSM-IV CRITERIA FOR SCHIZOAFFECTIVE DISORDER

  1. An uninterrupted period of illness during which, at some time, there is either a major depressive episode, a manic episode, or a mixed episode concurrent with symptoms that meet Criterion A for schizophrenia:
  2. During the same period of illness, there have been delusions or hallucinations for at least 2 weeks in the absence of prominent mood symptoms.
  3. Symptoms that meet criteria for a mood episode are present for a substantial portion of the total duration of the active and residual periods of the illness.
  4. The disturbance is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition.

Specific type:

Bipolar type: If the disturbance includes a manic or a mixed episode (or a manic or a mixed episode and major depressive episodes)

Depressive type: If the disturbance only includes major depressive episodes.

Source: Diagnostic and statistical manual of mental disorders (4th ed., TR). Washington, DC: American Psychiatric Association, 2000.

This distinction was a landmark in psychiatry but did not offer a specific understanding of the mental or brain dysfunctions underlying these conditions nor a cross-sectional means to diagnose a patient’s condition.

Bleuler was less concerned with predicting course and outcome. Instead, he wished to understand his observations that patients commonly exhibited a disjunction among psychological processes that were integrated in healthy individuals.3 He described the cause of this loss of psychological integration as the “schizophrenias” or, literally, “split mind.” In the schizophrenias, he identified symptoms that seemed to reflect this psychological disjunction, such as flat affect, ambivalence, and splitting of cognition from emotion and behavior.

Because Kraepelin described many of these same symptoms in dementia praecox, clinicians tended to equate the schizophrenias with dementia praecox. However, many more patients with Bleuler’s schizophrenia recovered than did those with Kraepelin’s dementia praecox (essentially by definition). Therefore, some “schizophrenic” patients appeared to meet Kraepelin’s diagnosis of manic-depressive insanity. At this point, Kasanin stepped into the fray with his concept of schizoaffective disorder.

Kasanin’s conceptualization

Kasanin recognized that many patients exhibited a blending of Bleuler’s schizophrenia symptoms with those of Kraepelin’s manic-depressive (affective) illness.1 Moreover, unlike patients with dementia praecox, these blended patients exhibited:

  • good premorbid adjustment
  • typically a sudden illness onset with marked emotional turmoil
  • few symptoms of withdrawal or passivity
  • and a relatively short course with complete recovery.

In reporting these patients and subsequently originating the term “schizoaffective psychosis,” Kasanin tried to identify a homogeneous patient population that could be distinguished from the more broadly conceptualized Bleulerian schizophrenias and the more narrowly defined Kraepelinian categories.

The term “schizoaffective disorder” has evolved from this beginning. Interestingly, most—if not all—of the nine cases reported by Kasanin would be diagnosed with an affective disorder with psychotic features under today’s diagnostic criteria.4 Nonetheless, the term “schizoaffective disorder” was adopted by psychiatry (particularly in the United States) and has been used to classify patients who present with features of both schizophrenia and affective illness but cannot be clearly described as having either.

Evolutions from DSM-I to DSM-III

In American nosology, schizoaffective disorder was included as a subtype of schizophrenia in DSM-I (1952)5 and DSM-II (1968)6 and then reclassified in DSM-III (1980)7 as a “psychotic disorder not elsewhere classified.” Remarkably, none of these classifications provided criteria for diagnosing schizoaffective disorder.

 

 

Shortly before publication of DSM-III, Robert Spitzer, MD, and colleagues at the New York Neuropsychiatric Institute developed diagnostic criteria for schizoaffective disorder as part of their research diagnostic criteria (RDC).8 The RDC separated patients with affective and certain types of psychotic symptoms, suggestive of schizophrenia at that time, into two types—schizoaffective mania and schizoaffective depression—based on the polarity of the mood symptoms.

The psychotic symptoms identified as “schizophrenic” by the RDC were certain first-rank symptoms designated by Kurt Schneider, such as delusions of being controlled or mood-incongruent hallucinations. [Note: In recent studies, neither first-rank symptoms nor other subtypes of psychotic symptoms (moodincongruent delusions or hallucinations) have been shown to specifically identify patients with schizophrenia.9,10 In fact, no psychotic symptoms are considered pathognomonic for any specific disorder at this time.]

The RDC also introduced the idea that schizoaffective disorder was distinct from psychotic mood disorder in that:

  • psychotic symptoms persisted for a specific period (1 week), during which mood symptoms were absent
  • and mood and psychotic symptoms overlapped at some time during the course of illness.

These criteria were then adopted with modifications in DSM-III-R,11 which provided the first widely-accepted, well-defined criteria for schizoaffective disorder.

DSM-III-R and DSM-IV

DSM-III-R defined schizoaffective disorder based on relationships between affective syndromes and the criteria for schizophrenia. Specifically, the diagnosis required the presence of a full depressive or manic syndrome while the patient also met criteria for schizophrenia. To distinguish schizoaffective disorder from psychotic mood disorders, DSM-III-R required that psychotic symptoms persist for 2 weeks in the absence of “prominent” mood symptoms.

Unfortunately, “prominent” was not defined, leaving a fair amount of discretion to clinicians and making it difficult to standardize research studies. In addition, the predictive utility of 2 weeks of psychosis has not been strongly validated. In fact, the time span at which psychosis without a mood disorder identifies a new syndrome is not known.

To rule out schizophrenia, the mood syndrome could not have been “brief” relative to the psychosis; again, what “brief” meant was difficult to put into practice. Notably, there was no specific requirement to rule out mood disorders (i.e., that the psychosis was not brief relative to the duration of mood symptoms).

DSM-IV slightly modified these criteria,12 but their basic flavor from DSM-III-R was retained. Despite their limitations, the diagnostic criteria in DSM-III-R and DSM-IV at least provided clinicians and scientists the means to consistently identify schizoaffective disorder. The diagnostic criteria (Box) are still considered reliable today.13

Four concepts of schizoaffective disorder

Relatively few studies of schizoaffective disorder exist, so the diagnosis remains poorly validated. At least four concepts have been developed (Figure).4

Concept 1: Schizoaffective disorder is a variant of schizophrenia. Many of the characteristics of schizoaffective disorder that Kasanin first described, such as rapid onset and confusion, were identified as good prognostic indicators in later concepts of schizophrenia. Some family history studies also suggest a link between schizophrenic and schizoaffective disorders.15

Concept 2: Schizoaffective disorder is a variant of mood disorder. 9 Schizoaffective disorder represents a pernicious type of mood disorder in which psychotic symptoms persist and the course of illness is worse than in other variants (although better than in schizophrenia).16 Family studies are unclear about links between mood and schizoaffective disorders.17

Figure FOUR CONCEPTS THAT SEEK TO EXPLAIN SCHIZOAFFECTIVE DISORDER


Figure. Four conceptualizations explain schizoaffective disorder as (1) a type of schizophrenia; (2) a type of mood disorder; (3) a heterogeneous combination of patients with schizophrenia, mood disorder, and “real” schizoaffective disorder; and (4) as part of a continuum of psychotic disorders from worst prognosis (schizophrenia) to best prognosis (major depression).Concept 3: Schizoaffective disorder represents a heterogeneous combination of schizophrenia and mood disorder. Specifically, schizoaffective disorder may comprise a group of patients with severe psychotic mood disorders and either good-prognosis schizophrenia or schizophrenia with numerous affective symptoms.

A subgroup of patients with “true” schizoaffective disorder (distinct from schizophrenic or mood disorders) might also exist.18 As a twist on this idea, others have suggested that schizoaffective disorder, bipolar type is simply a variant of bipolar disorder, whereas schizoaffective disorder, depressed type is more closely akin to schizophrenia. The fact that depression occurs at some time in most patients with schizophrenia supports this view.

Concept 4: Psychotic disorders share a genetic vulnerability and exist on a continuum (from worst to best prognosis) from schizophrenia, to schizoaffective disorder, to psychotic then nonpsychotic bipolar and major depressive disorders.19

A lack of definitive evidence prevents us from choosing among these concepts; good studies support and discount each possibility.

 

 

Patient management

When faced with a patient who meets criteria for schizoaffective disorder, I believe practical considerations can guide treatment. The label “schizoaffective disorder” reminds us to consider treatment of these patients broadly (in contrast, for example, to the label “schizophreniform disorder,” which implies a stronger link to schizophrenia than outcome studies support21).

Treat the mood component first. In most patients with schizoaffective disorder, it is difficult to distinguish between diagnoses of schizophrenia or mood disorder. It is prudent to begin by aggressively treating the mood component, because psychotic mood disorders generally respond more favorably to treatment than does schizophrenia. Use mood stabilizers for patients with a history of mania and antidepressants in depressed patients with no history of mania.

As is true for psychotic mood disorders, concurrent administration of an antipsychotic is often warranted. Recent studies strongly suggest that atypical antipsychotics are preferred over traditional neuroleptics to treat psychotic patients in general, and this preference extends to patients with schizoaffective disorder.4,14,20

Some—if not most—atypical antipsychotics may have mood-stabilizing or antidepressant properties and may permit monotherapy of patients with schizoaffective disorder. Controlled clinical trials have not examined these agents as long-term maintenance therapy for the mood component of schizoaffective disorder, however. Until such studies are completed, many patients may require long-term mood-stabilizer or antidepressant therapy, with or without ongoing antipsychotic treatment.4,14

The next step. Alternate treatments should be considered for patients in whom trials of atypical antipsychotics have failed, both in combination with thymoleptics and in monotherapy. Conventional antipsychotics, particularly depot formulations, are a reasonable intervention, particularly in schizoaffective patients with minimal mood symptoms.

Clozapine remains a first-line choice for patients with treatment-resistant psychotic disorders and should be considered in patients with treatment-resistant schizoaffective disorder as well.

Conclusion

Patients meeting criteria for schizoaffective disorder typically present with a complex and confusing combination of affective and psychotic symptoms. The diagnosis continues to be applied predominantly to patients who are otherwise difficult to classify, and the diagnostic criteria supporting the presence of a distinct condition remain poorly validated.

Schizoaffective disorder probably defines a heterogeneous group of patients, but—practically speaking—they can often be managed by following algorithms for psychotic mood disorders.4,13 The most prudent long-term approach seems to be to keep treatment options flexible, with careful attention to managing symptoms as they wax and wane, rather than rigidly fixing on a single medication or type of medication.

Related resources

  • National Mental Health Association factsheet on schizoaffective disorder www.nmha.org/infoctr/factsheets/52.cfm
  • Reichenberg A, Weiser M, Rabinowitz, J, et al. A population-based cohort study of premorbid intellectual, language, and behavioral functioning in patients with schizophrenia, schizoaffective disorder, and nonpsychotic bipolar disorder. Am J Psychiatry 2002;159(12):2027-35.
  • Robinson DG, Woerner, MG, Alvir JM, et al. Predictors of medication discontinuation by patients with first-episode schizophrenia and schizoaffective disorder. Schizophr Res 2002;57(2-3):209-19.

Psychiatry has used the term “schizoaffective disorder” for more than 60 years, but its specific meaning remains uncertain. Patients who meet its diagnostic criteria typically present with a confusing blend of mood and psychotic symptoms, and we often classify them as being schizoaffective because we don’t know where else to put them.

Much of our difficulty in trying to determine what schizoaffective disorder is can be blamed on insufficient data. We do not know the specific cause of either schizophrenic or mood disorders, and today’s concepts of these broad diagnoses probably encompass multiple etiologies.

Based on the evidence and clinical experience, this article presents:

  • the evolution of schizoaffective disorder as a psychiatric diagnosis
  • the four main concepts that attempt to explain the disorder’s cause
  • and a practical approach for managing these patients’ complicated symptoms.

Origins of schizoaffective disorder

When Jacob Kasanin1 riginated the term schizoaffective disorder in 1933, psychiatry was struggling to integrate Emil Kraepelin’s and Eugene Bleuler’s two competing and complementary schemes for understanding psychotic disorders.

Kraepelin had proposed that the major psychoses could be divided between dementia praecox and manic-depressive insanity (and to a lesser extent, paraphrenia), based on the presenting symptoms and—importantly—course of illness:2

  • Manic-depressive insanity typically included periods of full recovery of mental functions between episodes.
  • Dementia praecox was defined by a steady deterioration of mental function and personality from which patients rarely recovered.

Box

DSM-IV CRITERIA FOR SCHIZOAFFECTIVE DISORDER

  1. An uninterrupted period of illness during which, at some time, there is either a major depressive episode, a manic episode, or a mixed episode concurrent with symptoms that meet Criterion A for schizophrenia:
  2. During the same period of illness, there have been delusions or hallucinations for at least 2 weeks in the absence of prominent mood symptoms.
  3. Symptoms that meet criteria for a mood episode are present for a substantial portion of the total duration of the active and residual periods of the illness.
  4. The disturbance is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition.

Specific type:

Bipolar type: If the disturbance includes a manic or a mixed episode (or a manic or a mixed episode and major depressive episodes)

Depressive type: If the disturbance only includes major depressive episodes.

Source: Diagnostic and statistical manual of mental disorders (4th ed., TR). Washington, DC: American Psychiatric Association, 2000.

This distinction was a landmark in psychiatry but did not offer a specific understanding of the mental or brain dysfunctions underlying these conditions nor a cross-sectional means to diagnose a patient’s condition.

Bleuler was less concerned with predicting course and outcome. Instead, he wished to understand his observations that patients commonly exhibited a disjunction among psychological processes that were integrated in healthy individuals.3 He described the cause of this loss of psychological integration as the “schizophrenias” or, literally, “split mind.” In the schizophrenias, he identified symptoms that seemed to reflect this psychological disjunction, such as flat affect, ambivalence, and splitting of cognition from emotion and behavior.

Because Kraepelin described many of these same symptoms in dementia praecox, clinicians tended to equate the schizophrenias with dementia praecox. However, many more patients with Bleuler’s schizophrenia recovered than did those with Kraepelin’s dementia praecox (essentially by definition). Therefore, some “schizophrenic” patients appeared to meet Kraepelin’s diagnosis of manic-depressive insanity. At this point, Kasanin stepped into the fray with his concept of schizoaffective disorder.

Kasanin’s conceptualization

Kasanin recognized that many patients exhibited a blending of Bleuler’s schizophrenia symptoms with those of Kraepelin’s manic-depressive (affective) illness.1 Moreover, unlike patients with dementia praecox, these blended patients exhibited:

  • good premorbid adjustment
  • typically a sudden illness onset with marked emotional turmoil
  • few symptoms of withdrawal or passivity
  • and a relatively short course with complete recovery.

In reporting these patients and subsequently originating the term “schizoaffective psychosis,” Kasanin tried to identify a homogeneous patient population that could be distinguished from the more broadly conceptualized Bleulerian schizophrenias and the more narrowly defined Kraepelinian categories.

The term “schizoaffective disorder” has evolved from this beginning. Interestingly, most—if not all—of the nine cases reported by Kasanin would be diagnosed with an affective disorder with psychotic features under today’s diagnostic criteria.4 Nonetheless, the term “schizoaffective disorder” was adopted by psychiatry (particularly in the United States) and has been used to classify patients who present with features of both schizophrenia and affective illness but cannot be clearly described as having either.

Evolutions from DSM-I to DSM-III

In American nosology, schizoaffective disorder was included as a subtype of schizophrenia in DSM-I (1952)5 and DSM-II (1968)6 and then reclassified in DSM-III (1980)7 as a “psychotic disorder not elsewhere classified.” Remarkably, none of these classifications provided criteria for diagnosing schizoaffective disorder.

 

 

Shortly before publication of DSM-III, Robert Spitzer, MD, and colleagues at the New York Neuropsychiatric Institute developed diagnostic criteria for schizoaffective disorder as part of their research diagnostic criteria (RDC).8 The RDC separated patients with affective and certain types of psychotic symptoms, suggestive of schizophrenia at that time, into two types—schizoaffective mania and schizoaffective depression—based on the polarity of the mood symptoms.

The psychotic symptoms identified as “schizophrenic” by the RDC were certain first-rank symptoms designated by Kurt Schneider, such as delusions of being controlled or mood-incongruent hallucinations. [Note: In recent studies, neither first-rank symptoms nor other subtypes of psychotic symptoms (moodincongruent delusions or hallucinations) have been shown to specifically identify patients with schizophrenia.9,10 In fact, no psychotic symptoms are considered pathognomonic for any specific disorder at this time.]

The RDC also introduced the idea that schizoaffective disorder was distinct from psychotic mood disorder in that:

  • psychotic symptoms persisted for a specific period (1 week), during which mood symptoms were absent
  • and mood and psychotic symptoms overlapped at some time during the course of illness.

These criteria were then adopted with modifications in DSM-III-R,11 which provided the first widely-accepted, well-defined criteria for schizoaffective disorder.

DSM-III-R and DSM-IV

DSM-III-R defined schizoaffective disorder based on relationships between affective syndromes and the criteria for schizophrenia. Specifically, the diagnosis required the presence of a full depressive or manic syndrome while the patient also met criteria for schizophrenia. To distinguish schizoaffective disorder from psychotic mood disorders, DSM-III-R required that psychotic symptoms persist for 2 weeks in the absence of “prominent” mood symptoms.

Unfortunately, “prominent” was not defined, leaving a fair amount of discretion to clinicians and making it difficult to standardize research studies. In addition, the predictive utility of 2 weeks of psychosis has not been strongly validated. In fact, the time span at which psychosis without a mood disorder identifies a new syndrome is not known.

To rule out schizophrenia, the mood syndrome could not have been “brief” relative to the psychosis; again, what “brief” meant was difficult to put into practice. Notably, there was no specific requirement to rule out mood disorders (i.e., that the psychosis was not brief relative to the duration of mood symptoms).

DSM-IV slightly modified these criteria,12 but their basic flavor from DSM-III-R was retained. Despite their limitations, the diagnostic criteria in DSM-III-R and DSM-IV at least provided clinicians and scientists the means to consistently identify schizoaffective disorder. The diagnostic criteria (Box) are still considered reliable today.13

Four concepts of schizoaffective disorder

Relatively few studies of schizoaffective disorder exist, so the diagnosis remains poorly validated. At least four concepts have been developed (Figure).4

Concept 1: Schizoaffective disorder is a variant of schizophrenia. Many of the characteristics of schizoaffective disorder that Kasanin first described, such as rapid onset and confusion, were identified as good prognostic indicators in later concepts of schizophrenia. Some family history studies also suggest a link between schizophrenic and schizoaffective disorders.15

Concept 2: Schizoaffective disorder is a variant of mood disorder. 9 Schizoaffective disorder represents a pernicious type of mood disorder in which psychotic symptoms persist and the course of illness is worse than in other variants (although better than in schizophrenia).16 Family studies are unclear about links between mood and schizoaffective disorders.17

Figure FOUR CONCEPTS THAT SEEK TO EXPLAIN SCHIZOAFFECTIVE DISORDER


Figure. Four conceptualizations explain schizoaffective disorder as (1) a type of schizophrenia; (2) a type of mood disorder; (3) a heterogeneous combination of patients with schizophrenia, mood disorder, and “real” schizoaffective disorder; and (4) as part of a continuum of psychotic disorders from worst prognosis (schizophrenia) to best prognosis (major depression).Concept 3: Schizoaffective disorder represents a heterogeneous combination of schizophrenia and mood disorder. Specifically, schizoaffective disorder may comprise a group of patients with severe psychotic mood disorders and either good-prognosis schizophrenia or schizophrenia with numerous affective symptoms.

A subgroup of patients with “true” schizoaffective disorder (distinct from schizophrenic or mood disorders) might also exist.18 As a twist on this idea, others have suggested that schizoaffective disorder, bipolar type is simply a variant of bipolar disorder, whereas schizoaffective disorder, depressed type is more closely akin to schizophrenia. The fact that depression occurs at some time in most patients with schizophrenia supports this view.

Concept 4: Psychotic disorders share a genetic vulnerability and exist on a continuum (from worst to best prognosis) from schizophrenia, to schizoaffective disorder, to psychotic then nonpsychotic bipolar and major depressive disorders.19

A lack of definitive evidence prevents us from choosing among these concepts; good studies support and discount each possibility.

 

 

Patient management

When faced with a patient who meets criteria for schizoaffective disorder, I believe practical considerations can guide treatment. The label “schizoaffective disorder” reminds us to consider treatment of these patients broadly (in contrast, for example, to the label “schizophreniform disorder,” which implies a stronger link to schizophrenia than outcome studies support21).

Treat the mood component first. In most patients with schizoaffective disorder, it is difficult to distinguish between diagnoses of schizophrenia or mood disorder. It is prudent to begin by aggressively treating the mood component, because psychotic mood disorders generally respond more favorably to treatment than does schizophrenia. Use mood stabilizers for patients with a history of mania and antidepressants in depressed patients with no history of mania.

As is true for psychotic mood disorders, concurrent administration of an antipsychotic is often warranted. Recent studies strongly suggest that atypical antipsychotics are preferred over traditional neuroleptics to treat psychotic patients in general, and this preference extends to patients with schizoaffective disorder.4,14,20

Some—if not most—atypical antipsychotics may have mood-stabilizing or antidepressant properties and may permit monotherapy of patients with schizoaffective disorder. Controlled clinical trials have not examined these agents as long-term maintenance therapy for the mood component of schizoaffective disorder, however. Until such studies are completed, many patients may require long-term mood-stabilizer or antidepressant therapy, with or without ongoing antipsychotic treatment.4,14

The next step. Alternate treatments should be considered for patients in whom trials of atypical antipsychotics have failed, both in combination with thymoleptics and in monotherapy. Conventional antipsychotics, particularly depot formulations, are a reasonable intervention, particularly in schizoaffective patients with minimal mood symptoms.

Clozapine remains a first-line choice for patients with treatment-resistant psychotic disorders and should be considered in patients with treatment-resistant schizoaffective disorder as well.

Conclusion

Patients meeting criteria for schizoaffective disorder typically present with a complex and confusing combination of affective and psychotic symptoms. The diagnosis continues to be applied predominantly to patients who are otherwise difficult to classify, and the diagnostic criteria supporting the presence of a distinct condition remain poorly validated.

Schizoaffective disorder probably defines a heterogeneous group of patients, but—practically speaking—they can often be managed by following algorithms for psychotic mood disorders.4,13 The most prudent long-term approach seems to be to keep treatment options flexible, with careful attention to managing symptoms as they wax and wane, rather than rigidly fixing on a single medication or type of medication.

Related resources

  • National Mental Health Association factsheet on schizoaffective disorder www.nmha.org/infoctr/factsheets/52.cfm
  • Reichenberg A, Weiser M, Rabinowitz, J, et al. A population-based cohort study of premorbid intellectual, language, and behavioral functioning in patients with schizophrenia, schizoaffective disorder, and nonpsychotic bipolar disorder. Am J Psychiatry 2002;159(12):2027-35.
  • Robinson DG, Woerner, MG, Alvir JM, et al. Predictors of medication discontinuation by patients with first-episode schizophrenia and schizoaffective disorder. Schizophr Res 2002;57(2-3):209-19.
References

1. Kasanin J. The acute schizoaffective psychoses. Am J Psychiatry 1933;113:97-126.

2. Kraepelin E. Dementia praecox and paraphrenia, together with manic depressive insanity. Translated from original texts by The Classics of Psychiatry and Behavioral Sciences Library. Delran, NJ; Gryphon Editions, 1993.

3. Bleuler E. Text-book of psychiatry. Translated from original texts by The Classics of Psychiatry and Behavioral Sciences Library. Delran, NJ: Gryphon Editions, 1994.

4. Keck PE, Jr, McElroy SL, Strakowski SM/, West SA. Pharmacologic treatment of schizoaffective disorder. Psychopharmacology 1994;114:529-38.

5. Diagnostic and statistical manual of mental disorders. Washington, DC: American Psychiatric Association, 1952.

6. Diagnostic and statistical manual of mental disorders (2nd ed). Washington, DC: American Psychiatric Association, 1968.

7. Diagnostic and statistical manual of mental disorders (3rd ed). Washington, DC: American Psychiatric Association, 1980.

8. Spitzer RL, Endicott J, Robins E. Research diagnostic criteria. Rationale and reliability. Arch Gen Psychiatry 1978;35:773-82.

9. Pope HG, Jr, Lipinski JF. Diagnosis of schizophrenia and manic-depressive illness: a reassessment of the specificity of ‘schizophrenic’ symptoms in the light of current research. Arch Gen Psychiatry 1978;35:811-28.

10. Strakowski SM, McElroy SL, Keck PE, Jr, West SA. Racial influence on diagnosis in psychotic mania. J Affect Disord 1996;39:157-62.

11. Diagnostic and statistical manual of mental disorders (3rd ed, rev). Washington, DC: American Psychiatric Press, 1987.

12. Diagnostic and statistical manual of mental disorders (4th ed). Washington, DC: American Psychiatric Press, 1994.

13. Keck PE, Jr., McElroy SL, Strakowski SM. New developments in the pharmacologic treatment of schizoaffective disorder. J Clin Psychiatry 1996;57S:41-8.

14. Clayton PJ. Schizoaffective disorders. J Nerv Ment Dis 1982;170:646-50.

15. Kendler KS, Spitzer RL, Williams JBW. Psychotic disorders in DSM-III-R. Am J Psychiatry 1989;146:953-62.

16. Strakowski SM, Keck PE, Jr, Sax KW, McElroy SL, Hawkins JM. Twelve-month outcome of patients with DSM-III-R schizoaffective disorder: comparisons to matched patients with bipolar disorder. Schizophrenia Res 1999;35:167-74.

17. Maier W, Lichtermann D, Minges J, Heun R, Hallmayer J, Benkert O. Schizoaffective disorder and affective disorders with mood-incongruent psychotic feathers: keep separate or combine? Evidence from a family study. Am J Psychiatry 1992;149:1666-73.

18. Kendler KS, McGuire M, Gruenberg AM, Walsh D. Examining the validity of DSM-III-R schizoaffective disorder and its putative subtypes in the Roscommon Family Study. Am J Psychiatry 1995;152:755-64.

19. Crow TJ. A continuum of psychosis, one human gene and not much else—the case for homogeneity. Schizophrenia Res 1995;17:135-45.

20. Strakowski SM, DelBello MP, Adler CM. Comparative tolerability of drug treatments for bipolar disorder. CNS Drugs 2001;15:701-18.

21. Strakowski SM. Diagnostic validity of schizophreniform disorder. Am J Psychiatry 1994;151:815-24.

References

1. Kasanin J. The acute schizoaffective psychoses. Am J Psychiatry 1933;113:97-126.

2. Kraepelin E. Dementia praecox and paraphrenia, together with manic depressive insanity. Translated from original texts by The Classics of Psychiatry and Behavioral Sciences Library. Delran, NJ; Gryphon Editions, 1993.

3. Bleuler E. Text-book of psychiatry. Translated from original texts by The Classics of Psychiatry and Behavioral Sciences Library. Delran, NJ: Gryphon Editions, 1994.

4. Keck PE, Jr, McElroy SL, Strakowski SM/, West SA. Pharmacologic treatment of schizoaffective disorder. Psychopharmacology 1994;114:529-38.

5. Diagnostic and statistical manual of mental disorders. Washington, DC: American Psychiatric Association, 1952.

6. Diagnostic and statistical manual of mental disorders (2nd ed). Washington, DC: American Psychiatric Association, 1968.

7. Diagnostic and statistical manual of mental disorders (3rd ed). Washington, DC: American Psychiatric Association, 1980.

8. Spitzer RL, Endicott J, Robins E. Research diagnostic criteria. Rationale and reliability. Arch Gen Psychiatry 1978;35:773-82.

9. Pope HG, Jr, Lipinski JF. Diagnosis of schizophrenia and manic-depressive illness: a reassessment of the specificity of ‘schizophrenic’ symptoms in the light of current research. Arch Gen Psychiatry 1978;35:811-28.

10. Strakowski SM, McElroy SL, Keck PE, Jr, West SA. Racial influence on diagnosis in psychotic mania. J Affect Disord 1996;39:157-62.

11. Diagnostic and statistical manual of mental disorders (3rd ed, rev). Washington, DC: American Psychiatric Press, 1987.

12. Diagnostic and statistical manual of mental disorders (4th ed). Washington, DC: American Psychiatric Press, 1994.

13. Keck PE, Jr., McElroy SL, Strakowski SM. New developments in the pharmacologic treatment of schizoaffective disorder. J Clin Psychiatry 1996;57S:41-8.

14. Clayton PJ. Schizoaffective disorders. J Nerv Ment Dis 1982;170:646-50.

15. Kendler KS, Spitzer RL, Williams JBW. Psychotic disorders in DSM-III-R. Am J Psychiatry 1989;146:953-62.

16. Strakowski SM, Keck PE, Jr, Sax KW, McElroy SL, Hawkins JM. Twelve-month outcome of patients with DSM-III-R schizoaffective disorder: comparisons to matched patients with bipolar disorder. Schizophrenia Res 1999;35:167-74.

17. Maier W, Lichtermann D, Minges J, Heun R, Hallmayer J, Benkert O. Schizoaffective disorder and affective disorders with mood-incongruent psychotic feathers: keep separate or combine? Evidence from a family study. Am J Psychiatry 1992;149:1666-73.

18. Kendler KS, McGuire M, Gruenberg AM, Walsh D. Examining the validity of DSM-III-R schizoaffective disorder and its putative subtypes in the Roscommon Family Study. Am J Psychiatry 1995;152:755-64.

19. Crow TJ. A continuum of psychosis, one human gene and not much else—the case for homogeneity. Schizophrenia Res 1995;17:135-45.

20. Strakowski SM, DelBello MP, Adler CM. Comparative tolerability of drug treatments for bipolar disorder. CNS Drugs 2001;15:701-18.

21. Strakowski SM. Diagnostic validity of schizophreniform disorder. Am J Psychiatry 1994;151:815-24.

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