e-pearls newsletter, November 2009

Introduction

While researching ADHD recently, I came across a couple of papers that detailed some of the psychotherapeutic techniques that have been shown to be effective in clients with ADHD, and I thought I’d share them with you. As usual however, first some background.

ADHD: A Brief Overview

ADHD is a disorder comprised of the core symptoms of inattention and hyperactivity/impulsivity. A DSM-IV diagnosis requires at least 6/9 symptoms in one or both of these symptom categories, resulting in impairment of function. The symptoms must have been present for at least 6 months, they must be present in two or more settings (school, work, home), and they must have begun prior to age 7.

It is important to keep in mind that the home, school, &/or work environment, as well as I.Q., can mitigate the level of disability; some children with symptoms might not be significantly impaired, and may remain undiagnosed (which can make it more challenging to diagnose as an adult).

The most common type in childhood is the combined type (inattentive + hyperactive/impulsive), with a prevalence rate of 61%, followed by inattentive and hyperactive/impulsive subtypes at 30% and 9% respectively. In most studies, ADHD persists into adulthood in 50%-70% of cases. The only clinical feature that has been found to predict persistence of childhood ADHD into adulthood is the occurrence of a major depressive disorder in that child.

ADHD is a familial disorder with a multi-genic inheritance pattern; in other words, many genes are involved in ADHD, and it is necessary to inherit a certain number of them in order for the disorder to appear. For instance, if you have a parent with ADHD, your risk is >50%. Similarly, if you have a sibling, child, or identical twin with the disorder, your risk becomes 20%-25%, 31%-44%, and 80%-90%, respectively.

The only other major points I’ll make before going on to talk about psychotherapy in ADHD have to do with the co-occurrence of mood and substance use disorders (SUD). For every ten adults with a mood disorder, at least one will also have ADHD; for every ten adults that have ADHD, four will also have a mood disorder; and for every ten adults with ADHD, five will also have an anxiety disorder.

This is important to keep in mind, because if underlying ADHD is not recognized and treated, the mood disorder may be resistant to therapy. On the other hand, if the mood disorder is severe (e.g., MDD with suicidal ideation), it would be wise to focus on treating the mood disorder first, even if ADHD is also known to be present.

ADHD is an independent risk factor for SUD; in adolescents with ADHD, 15%-30% will have SUD. In adolescents with SUD, 40%-75% will also have ADHD. Smoking in an adolescent with ADHD increases the risk of future SUD to around 50%.

Why Psychotherapy?

It is now widely accepted that the combination of medication plus psychotherapy yields the best clinical outcome for the client. Keep in mind that although medications alone are frequently helpful (70%-90% show significant improvement; 50%-60% become symptom-free), statistically there may be as many as 30% that do not show significant improvement, and up to 50% that may have residual symptoms.

Furthermore, the improvement in core symptoms brought about by medication alone are not always put into action, so to speak, by the client; clearly, psychotherapists can help in this regard (i.e., helping the client turn symptomatic improvement into improved life functioning). In addition, people that are suffering from ADHD have a number of comorbid disorders for which psychotherapy is also beneficial.

Psychotherapeutic Approach in ADHD

At present, the literature supports a fairly structured, cognitive approach for the treatment of the core symptoms of ADHD, which is summarized below.

Psycho-education:

This is well-established as a useful starting point. Lifelong ADHD can engender a deep-rooted conviction of low self-esteem coupled with a fear of failure; these clients frequently are under-employed, may have received a label of “learning disability,” and have had to work twice as hard to accomplish the same goals as their peers (i.e., impaired working memory and underlying anxiety that occur in ADHD interfere with academic and job performances). Clients often see themselves as failures; learning that a treatable neuro-biological disorder accounts for their difficulties can help overcome this. Their sense of self and world-view may thus be de-pathologized.

Readiness for change:

Many clients with ADHD tend to believe that they can never change; having lived with ADHD for their whole lives, it’s easy to see how this belief may develop. They may see themselves as not needing to change, or being unable to change. This seems to be related to a combination of ambivalence, low self-esteem, and anxiety.

Therapeutic alliance:

It is important for the therapist to take a relatively active and directive stance in therapy with adults; this helps to keep sessions focused on the issues at hand (such as core symptom expression & new coping strategies to deal with them). It is also important to remember again that clients with ADHD have often experienced failure at school, work, and in their relationships; the therapy process may be perceived as yet something else to fail at.

Because of this, clients with ADHD may be especially sensitive to perceived criticism or disapproval from the therapist (such as when they forget or arrive late for an appointment). This sense of not “measuring up” may be enough to re-activate memories of past failures, self-criticism, and emotional distress. If not recognized and discussed in therapy, it might cause the client to drop out.

Cognitive modification:

Although ADHD is not caused by cognitive distortions or negative thoughts, many people with ADHD have automatic, negative thoughts in response to stressful situations. Stress causes anxiety, which further impairs working memory, thereby increasing the chance of failure. Before too long failure is expected; hence their tendency to engage in negative self-talk, resulting in magnification &/or over-generalization, for instance.

It is useful for the client to recognize how this pattern can lead to a number of negative effects on emotion, attention, self-esteem, behaviors, and performance. Helping the client come up with alternative perceptions and explanations results in a more positive and balanced world-view, allowing the client to make more effective use of coping skills and strategies. Cognitive modification also fosters a sense of resilience and empowerment, further contributing to an environment within which positive change and growth may occur.

Maintaining Focus on Specific Problems and Coping Strategies:

Starting “small” and gradually eliciting more significant maladaptive responses &/or behaviors helps keep therapy focused and relevant; it also increases therapist understanding of the inner experience of the client with ADHD.

In addition, it is useful to help clients recognize how their symptoms influence their coping mechanisms (how they deal with disturbances in working memory and selective attention, for example) in order for them to develop and implement new ones (such as taking notes or asking for something to be repeated). This paves the way for clients to become more self-confident and empowered.

References

Neuroscience Education Institute (2009 October 24). Clinical update on ADHD: A one-day symposium. Presented at a meeting of the Neuroscience Education Institute. Seattle, WA.

Ramsey, J.R., Rostain, A.L. (2007). Psychosocial treatments for Attention-Deficit/Hyperactivity Disorder in adults: Current evidence and future directions. Professional Psychology: Research and Practice, 38, 338-346.

Rostain, A.L., Ramsay, J.R. (2006). A combined treatment approach for adults with ADHD: Results of an open study of 43 patients. Journal of Attention Disorders, 10, 150-159.

Burnout was first described in the mid-1970’s by Herbert Freudenberger, who was a psychiatrist working in an alternative health care agency at the time. Because of this, the early writings on burnout focused primarily on the experiences of health-care workers.

According to Freudenberger, mental health professionals may be particularly susceptible, due to the fact that “…we are contending with the ills of society, with the needs of the individuals who come to us for assistance, and with our own personality needs.” However, the burnout syndrome (as we understand it today) is certainly not confined to health-care workers.

Rather than write a very long blog post here, I thought instead I’d supply a link to a pdf file on the syndrome of burnout; it’s taken from an updated powerpoint presentation that I did some time ago. To view it, simply click here.

epearls newsletter, July 2009:

Introduction

In light of my interest in panic disorder, this month’s e-pearls is devoted to the relationship between panic attacks and partial seizures. The fact that partial seizures can present as panic attacks is a perfect example of the overlap between neurology and mental health, and underscores the need for mental-health practitioners to have some basic awareness of medicine and physiology.

A Few Words About Seizures

First of all, I’m sure many of you are wondering what partial seizures are. Perhaps they can best be explained by first contrasting them with generalized seizures.

A true, physiologic seizure is always associated with some sort of abnormal electrical discharge in the brain (as you might recall, the brain works by generating lots of small electrical discharges; we can see these by placing electrodes on the scalp, and routing them through an EEG machine).

Sometimes, and for lots of different reasons, one or another of these electrical discharges may grow and spread abnormally to other parts of the brain, which in turn generate their own abnormal discharges. This has a cascading effect, and within a few seconds, the entire cerebral cortex can be discharging in synchrony. When this happens, a grand mal seizure may result.

As their name suggests, generalized seizures affect the entire brain, and are associated with impairment of consciousness. Grand mal seizures are one example of this type, and consist of full loss of consciousness, jerking of all four limbs, and a period of confusion following the event (the patient is said to be post-ictal during the latter, simply meaning after the ictus, or seizure).

Partial seizures, on the other hand, do not spread very far. In these types of spells, the electrical discharges are pretty much confined to whatever area they are first generated in; depending upon where they originate, many different types of symptoms can result. For instance, when they occur in the temporal lobe, fear, dizziness, elevated heart rate, and flushing of the skin, among others, may occur. In other words, there is considerable overlap between the symptoms that may occur in partial seizures and the symptoms that typically occur during panic attacks.

Partial Seizures Presenting as Panic Attacks: Two Case Summaries

Case 1–A 68 year old man with a four-year history of attacks:

These attacks were stereotyped, or similar each time, consisting of “pins and needles” in the head, spreading to torso and limbs, followed by dry mouth, nausea, and a feeling of unease. The patient would appear pale, sweaty, agitated, and tearful. The spells would appear and disappear gradually. Referral was made first to a cardiologist, then a psychiatrist, and panic disorder was diagnosed. Over three years, group psychotherapy and medication did not help. EEG and video monitoring were ultimately performed, which showed the spells to be due to a partial seizure emanating from the right hemisphere. The spells responded to treatment with an anti-epileptic drug.

Case 2–A 30 year old woman presents with 10 years of stereotyped spells:

The spells began with pain in the head, hyperventilation, and palpitations (a feeling of rapid or irregular heartbeat), followed by tingling of the left face and arm, diminished hearing, pain in the left side of the chest, fear, and a dry mouth. The symptoms built up and diminished gradually, lasting for 15-30 minutes. Initial treatment for seizures was not successful, and panic disorder was then diagnosed. Further testing six years later including EEG monitoring showed the spells to be associated with seizure activity in the left hemisphere; the patient’s husband reported that the patient had repetitive chewing and swallowing movements during the spells just prior to her re-evaluation. Scarring of the left hippocampus was seen on MRI. The spells abated after a different anti-epileptic drug was begun.

Discussion

From the above cases, it should be evident that indeed partial seizures can be mistaken for panic attacks. What clues, if any, might there be in the case descriptions that these spells might be seizures and not panic attacks?

In the first case, the development of panic attacks for the first time at the age of 64 is worrisome. Panic disorder is only rarely first diagnosed after age 45; this fact alone suggests the need for further medical investigation. Secondly, even though numbness and tingling are included in the DSM-IV description of panic, I would be concerned when these symptoms are prominent (as they were in this case) and occur in a certain order. In other words, the fact that the tingling developed in a stereotyped pattern, always preceding the other symptoms, would be worrisome to me.

In the second case, I would again be concerned about the patient’s complaints of numbness, this time involving the left side, and diminished hearing. I get worried whenever someone tells me that a particular sensory symptom always occurs on one side only. In addition, the description of repetitive motor activity (swallowing and chewing movements) is a huge red flag. Whenever these kinds of movements are present, it is very suggestive of a seizure.

In conclusion, one should always be looking for anything in the client’s description of their panic attacks that is atypical; to that end, it might also help to get the description of a witness, if possible. Finally, when in doubt, do not hesitate to refer the client for a neurological evaluation.

Reference

Thompson, S. A., Duncan, J. S., & Smith, S. J.M. (2000). Partial seizures presenting as panic attacks. The British Medical Journal, 321, 1002-1003.

I’m sure many of you have come across this situation: Your father or mother retires at age 65 or so and spends the rest of his or her days “relaxing.” After several years of puttering around the yard, visiting the grandchildren, and watching “Wheel of Fortune,” you notice that their mental abilities aren’t quite as “sharp” as they were in the years before retirement. After a few more years, they are on the road toward needing assisted living. Sound familiar? It is to me. It’s pretty much exactly what happened to my own father.

It is a fact of our biology that the brain begins to lose neurons (nerve cells) pretty steadily after we reach early adulthood. That means that over time, one’s memory and reasoning power gradually decline. This process accelerates after the age of around 60; by that time, the brain is losing approximately 0.5-1% of its volume each year. As time goes on, many people develop so-called mild cognitive impairment, which is often the first step along the way to a full-blown dementia. In decades past, it was believed that there was little to be done about this.

However, we now know that this is no longer the case. Beginning in the 1970’s, scientists discovered that the brain has the ability to form new neurons and make new connections with existing neurons. This was the first hint that the brain is really a “plastic” organ; that is, it is capable of dynamic change. Instead of being cast in “stone,” the brain actually has the capacity to reshape itself in a very real sense. The whole idea of a dynamic and changing brain was revolutionary.

Over the last ten years or so, the concept that the brain is capable of such change has become well-accepted. From a practical standpoint, this means that the steady and inevitable decline of brain function in old age may not be so inevitable after all. It addition, there are some things that can be done to stave off this gradual decline in our intellectual capacity.

As we get older, the areas of the brain that seem to suffer the most are the prefrontal cortex, which is involved in judgment, reasoning, and planning as well as our working memory (which is what we use when we need to keep some piece of information readily retrievable while we’re doing something else). Another part of the brain that suffers is the hippocampus, which is important in long-term memory. After age 50, for instance, recall becomes slower (it may take a few minutes to recall something) and it may be harder to solve a complex problem. By the age of 70 or 80, a significant proportion of the population is cognitively impaired (up to 25% of people in their 80’s are demented).

It turns out that aerobic exercise (running or walking are examples of aerobic exercises, as opposed to lifting weights, which is a form of anaerobic exercise) is one of the most effective ways to ward off this age-related decline in brain function. Regular exercise not only increases blood flow to the brain, but also stimulates the production of so-called “brain-derived neurotrophic factor,” which promotes the growth of new brain cells.

What seems to be happening is that the increase in blood flow to the brain has long-lasting benefits; brain cells get stimulated and over time, blood flow to the brain is increased even in the absence of physical activity. In a sense, aerobic exercise appears to serve an important “maintenance” function for both the blood vessels that supply the brain and the brain itself. This enables existing neurons to maintain their connections with each other (and form new connections) more effectively; over time, their numbers may increase as well. As a result, the brain is “protected” to some degree against the aging process.

The take-home message here is simple; if you are medically able to engage in regular aerobic exercise (and always check with your health-care provider before beginning any exercise regimen) the time to start is now. As someone once said: “no pain, no (mental) gain.”

Fibromyalgia is a disorder that is often associated with severe, ongoing musculo-skeletal pain and stiffness, (pain and stiffness in muscles and joints), and an increased perception of pain in response to stimuli that ordinarily would not be painful (such as gentle pressure). Obviously this can be, and often is, quite disabling. It is also frequently accompanied by psychological symptoms such as depression, anxiety, insomnia (difficulty sleeping), and fatigue, among others. Although it has been around since the 1600’s, it remains poorly understood.

Because of the vagueness of some of its symptoms and the lack of any definitive test or procedure to diagnose it, its sufferers were often marginalized in terms of treatment. Physicians thought of it as primarily a psychological problem rather than a distinct physical disorder, and patient complaints of sometimes disabling pain and fatigue were often not taken seriously. However, this has begun to change in recent years, and the medical establishment now views it as a distinct and legitimate physical syndrome.

Of course, this is good news; however, if it is due to some physical disturbance, what might that be? As you might guess from the title of today’s post, there is some evidence in favor of it being due, at least in part, to altered brain function.

Altered Blood Flow

For instance, it is possible to measure blood flow to the brain very precisely, so that researchers can tell how much blood is being supplied to any given brain region at a specific time. When this was looked at in people with fibromyalgia, it was found that a region of the brain known as the thalamus, which is a structure deep within the brain, received reduced blood flow compared to people without fibromyalgia. This finding has been linked to a disturbance of pain sensitivity, and might correlate with some of the pain sensations that can occur in fibromyalgia.

It has also been shown that certain brain regions show abnormally increased activity in response to a pressure stimulus; in other words, when gentle pressure is applied to various areas of the body, these brain regions became more active than they should be. This increased activity (as measured by blood flow, which gives us an indirect measure of brain activity by the amount of blood it’s “using”) involves a number of areas, including that part of the brain that records sensation from the body, called the sensory cortex.

Neurotransmitters

The brain uses a number of chemical substances, called neurotransmitters, that enable nerve cells (neurons) to communicate with each other. Something called dopamine is one of these neurotransmitters, and there is evidence that there is a disturbance in dopamine in people that are suffering from fibromyalgia.

For example, drugs that increase dopamine activity can be effective in treating the pain associated with fibromyalgia, implying that a relative lack of dopamine activity is at least partially responsible. In addition, certain areas of the brain that are known to contain a lot of dopamine have been shown to have a lower-than-normal blood flow (which means those areas are less active than they should be), again implying that a disturbance of dopamine function is playing a role. In addition, dopamine is linked to motivation and feelings of pleasure, which might explain some of the psychological symptoms that are so common in fibromyalgia.

Brain Structure

The brain is made up of billions of neurons, along with their connections. A typical neuron consists of what is called a cell body and something called an axon. The axon functions as a signal carrier, physically conducting a message from one neuron to another. These axons are contained in the so-called white matter, so named because it appears white to the naked eye. Groupings of nerve cell bodies, on the other hand, appear gray; collectively, they are referred to as making up the so-called gray matter.

In fibromyalgia, it seems that the amount of gray matter is reduced, and the longer the duration of fibromyalgia, the greater the reduction in gray matter. Furthermore, loss of gray matter is seen in areas that are involved in the regulation of pain.

Concluding Thoughts

In conclusion, fibromyalgia appears to represent a real physical disorder; fortunately for its sufferers, this concept appears to be widely accepted by the medical community. Its cause, however, is still uncertain, in spite of what I’ve written about here. But I think it is fair to say that there is some good evidence that a disturbance of brain function may be playing a role.

References

Schweinhardt, P., Sauro, K. M., & Bushnell, M. C. (2008). Fibromyalgia: A disorder of the brain? Neuroscientist, 14, 415-421.

As I mentioned in my last post, happiness is no doubt the central goal of every sentient creature on the planet. I also talked some about ways to increase our level of happiness, namely in expressing positive emotion and being altruistic toward others. In today’s post, I’d like to introduce and briefly outline a relatively new movement within psychology.

Introduction to Positive Psychology

Psychology has historically focused its energies on illness, and it has been largely successful in this regard. Many, if not most types of mental illness are now amenable to some sort of treatment, whether it be psychotherapy, medications, or a combination of these. The focus of mental health professionals has long been limited to relieving mental illness; the goal of optimizing individual strengths and positivity has not received as much attention.

This illness-oriented model remained the focus of psychologists and psychiatrists until the late 1990’s, when a psychologist by the name of Martin Seligman wrote of the need to shift our focus toward helping people become more fulfilled. This movement, which was cofounded by Martin Seligman and Mihaly Csikszentmihalyi, has come to be known as positive psychology. It’s mission, simply put, is to foster the development of virtues such as “…courage, optimism, interpersonal skill, work ethic, hope, honesty, and perseverance..” (Seligman, 1998) as protective buffers against mental illness. In other words, positive psychology aims to discover and nurture within us that which makes us happy, strong, and resilient.

There appear to be three general categories of human experience that are important in living a happy and fulfilling life. These are:

1)    The pleasant life: living in the present, experiencing positive emotions about the past, and being hopeful for the future

2)    The engaged life: using our so-called “signature strengths” in our life’s work (recognizing our talents and finding a career that allows us to use them)

3)    The meaningful life: becoming involved in something that is greater than ourselves, such as a movement, institution, or group that promotes some greater goal within society

In other words, positive psychology looks not so much at what’s wrong with us so much as it searches for strengths and personal resources in order to alleviate or even prevent the development of psychological problems. However, it is not enough to simply remove the negative; on the contrary, it is necessary to look for and encourage the positive that is within all of us in order to achieve the goal of a happy and meaningful life.

Positive emotions not only make us feel good; they also instill us with greater psychological resiliency in the face of adversity. They appear to make negative emotions disappear more readily, and serve to reduce stress and promote physical health and longevity.

From a therapy standpoint, therefore, instilling hope, enhancing interpersonal skills, fostering the capacity for pleasure, increasing personal responsibility, and helping people become more genuine (among others) are ways in which we can help others experience positive emotions, develop different and more optimistic views of the world and of themselves, and perhaps live more meaningful and fulfilled lives.

Read more about Positive Psychology

References

Duckworth, A. L., Steen, T. A., & Seligman, M.  E.P. (2005). Positive psychology in clinical practice. Annual Review of Clinical Psychology, 1, 629-651.

Seligman, M. E.P., & Csikszentmihalyi, M. (2000). Positive psychology: An introduction. American Psychologist, 55, 5-14.

I think most of us have had the experience of being amazed at how happy some people can be, even when faced with very unpleasant life circumstances. On the other hand, there are many people (some well-known celebrities come to mind) that appear to be blessed with “everything” in life, yet are plagued by personal difficulties. In this post, I’ll look at some of the current ideas about happiness, why some people seem to be happier than others, and ways to increase one’s personal level of happiness.

Happiness is defined in the dictionary as “feeling or showing pleasure or contentment,” and it’s something we all strive for. In fact, the right to pursue it is even written into the Declaration of Independence: “…certain inalienable rights, that among these are Life, Liberty, and the pursuit of Happiness.”

Happiness is not only important to Americans however; to paraphrase Aristotle, it is perhaps the central goal of human existence. Clearly, the attainment of happiness is important to all of us. And just as clearly, it seems, material wealth does not necessarily lead to a happier life. How can this be?

It turns out that the factors that mostly influence how happy we’ll be are our personality and temperament; in other words, how we tend to interpret and relate to the world at large. These characteristics are based upon our genetics, plus our early childhood years. These are determined either at birth or at a very early stage of life (the personality is pretty much “set” by age 2), and we can’t do much about either of them.

The other two major determinants of future happiness are the circumstances in which we find ourselves at any given time (things like health, income, and geographical locale) and current life activities (such as engagement with others; eating right; exercising regularly; and from a cognitive standpoint, trying to look at the “bright side” of life).

Of the two of these, that is life circumstances and life activities, the former does not really have a significant long-term effect on happiness. Yes, it’s true that if you win the lottery, you will experience a significant boost in happiness; however, it turns out that this is short-lived. Studies have been done that look at lottery winners, for instance, and found that within a couple of years, they have reverted to their pre-winning level of happiness. (This is why people who have focused their energies solely on material gain remain personally troubled. Simply put, material wealth is not a cure for unhappiness).

Conversely, if you look at people that have suffered a disabling injury or illness, there is a temporary decline in their reported level of happiness (as you might expect). Over time, their level of happiness rises, back to its former baseline.

How then, can we pursue this elusive state of bliss? Are we as powerless as we seem to be? Don’t give up hope just yet! Remember, I haven’t talked much about how life activities may be factoring in to the happiness equation. As you might have guessed by now, it is by changing our life activities that we can achieve a significantly greater level of happiness that does persist.

This kind of makes sense, if you think about it. Life circumstances are just that, circumstances. They may change from time to time (getting a raise, moving to an expensive home, buying a luxury car) but they tend to remain relatively static over time, and do not require any ongoing personal effort once we have attained them. In a sense, we get used to the idea of having more creature comforts available to us. This is referred to in the literature as “hedonic decay,” which is the tendency for the effects of either positive or negative changes in our life circumstances to fade over time.

Life activities, on the other hand, require the ongoing expenditure of effort and energy on our parts (starting a new project, going back to graduate school, embarking on a new career path). In turn, these kinds of changes will most likely result in new experiences, new social ties to other people and the community, and a different way of viewing oneself. Exposure to new circumstances leads to new opportunities and possibilities presenting themselves, which in turn may very well lead to long-term positive benefits.

Of these life activities, those considered to be altruistic are among the most powerful agents of change. It seems that by expressing positive emotions and helping others (without being emotionally overwhelmed) we can ultimately achieve not only a greater sense of personal well-being and happiness, but also improved health and longevity.

References
Post, S. G. (2005). Altruism, happiness, and health: It’s good to be good. International Journal of Behavioral Medicine, 12, 66-77.

Sheldon, K. M., & Lyubomirsky, S. (2006). Achieving sustainable gains in happiness: Change your actions, not your circumstances. Journal of Happiness Studies, 7, 55-86.

epearls newsletter, April 2009:

I was struck not long ago by the clinical similarities between obsessive-compulsive disorder and schizophrenia (referred to in the literature as so-called schizophrenia spectrum disorders, or SSD’s), so much so that I went to the literature to learn more about their relationship.  I hereby present to you the results of my brief investigation.

Background

Let me start off by saying that the clinical significance of the association between obsessive-compulsive disorder and obsessive-compulsive symptoms (OCD and OCS, respectively) and schizophrenia is not without controversy.  Hold that thought for now; I’ll get to it a bit later. 

It has been known for over a century that such an association exists; for instance, in 1878 Westphal postulated that OCD was a variant or prodrome of schizophrenia.  Although the literature does not seem to support such a direct relationship, there is evidence that individuals with anxiety disorders in general (e.g., OCD, panic disorder, social phobia) have an increased risk of developing schizophrenia.  This varies according to the study cited, but long-term follow-up studies of patients with OCD often show incidence rates of SSD’s to be in the 5-12% range.  This is much higher than the average incidence of schizophrenia worldwide of approximately 0.5%-1%. 

In fact, some modern authors have postulated that OCD and schizophrenia represent a psychopathological spectrum, determined by the degree of insight that is present.  The thinking here is that patients at the more severe end (SSD) possess little or no insight; the clinical shift from obsessions to delusions may take place when insight is lost. 

In addition, it is not hard to imagine that some compulsive behaviors, along with the stated reasons for them, might seem bizarre even to a sophisticated observer, resulting in a mistaken diagnosis of schizophrenia.  This is obviously of great importance, since the treatment of schizophrenia is quite different from that of OCD, to say nothing of the emotional consequences both to the affected individual and his or her family of such a mistaken diagnosis.

OCD and Schizophrenia: Significant Comorbidity

As alluded to above, it has been known for some time that there seems to be some association between OCD and SSD’s.  Whether this actually represents a clinical spectrum is still controversial, but the fact that OCD and/or OCS co-exist with schizophrenia in a significant number of patients is well-established.

There is some variation in OCD prevalence reported in the literature between those patients with recent-onset as opposed to chronic schizophrenia.  For the former, the prevalence of OCD ranges between 3.5% to 47.6%, with most reports ranging somewhere between 11 and 15%.  In the latter, more chronic patients, the prevalence of OCD is somewhat higher, ranging between 18% and 37.5%, with most studies reporting a prevalence of between 22% and 30%.  The average rate may be somewhat higher during the prodrome of childhood schizophrenia (41%) and in adolescents with SSD’s (26%).  This variability may in part be accounted for by different reporting techniques (self-rating scales vs. structured clinical interviews, for example) as well as by demographic variations in the respective study populations.      

Based on their significant comorbidity, some authors even have gone so far as to advocate for the establishment of a new diagnostic sub-category of schizophrenia, a so-called “obsessive-compulsive” type.

Okay, so OCD/OCS and SSD’s are often co-morbid.  What does that mean clinically?  Indeed, there appears to be considerable variation in the literature on this very point.  Some authors have reported that the presence of OCD/OCS in schizophrenia predicts a more favorable outlook, with greater insight and fewer negative symptoms.  Others report exactly the opposite: a greater incidence of negative symptoms and a worse clinical course both in terms of treatment response and impairment of functioning.  In other words, the clinical significance of OCD or OCS in schizophrenia remains uncertain.

Concluding Thoughts

This discussion is certainly not, and is by no means intended to be, an exhaustive review of the subject.  However, the literature does seem to justify several conclusions:

1) OCD appears to occur in patients with schizophrenia/SSD’s at a higher rate than in the general population.

2) Comorbid anxiety disorders, such as OCD, may precede the onset of SSD’s in some patients.

3) The presence of OCD may offer some insight into the course of schizophrenia, although the literature is quite variable on this point.

4) The relationship between OCD and schizophrenia/SSD’s merits further investigation.

References

Hwang, M. Y., & Losonczy, M. F. (1997). Schizophrenia with obsessive-compulsive features. Medscape Psychiatry and Mental Health eJournal, 2,4 . Retrieved April 1, 2009, from Medscape database.

Kayahan, B., Ozturk, O., Veznedaroglu, B., & Eraslan, D. (2005). Obsessive-compulsive disorder in schizophrenia: Prevalence and clinical correlates. Psychiatry and Clinical Neurosciences, 59, 291-295.

Pokos, V., & Castle, D. (2006). Prevalence of comorbid anxiety disorders in schizophrenia spectrum disorders: A literature review. Current Psychiatry Reviews, 2, 285-307.

Reznik, I., Mester, R., Kotler, M., & Weizman, A. (Winter 2001). Obsessive-compulsive schizophrenia: A new diagnostic entity? [Letter to the editor]. Journal of Neuropsychiatry and Clinical Neuroscience, 13, 115-116.

Rodowski, M. F., Cagande, C. C., & Riddle, M. A. (2008). Childhood obsessive-compulsive disorder presenting as schizophrenia spectrum disorders. Journal of Child and Adolescent Psychopharmacology, 18, 395-401.

Particularly over the last several years, the intimate connection between our emotions and our physical bodies has become more and more evident. Today, the power of this so-called mind-body connection is both well-recognized and widely accepted by the healthcare and scientific communities; there is no longer any question that our feelings and emotions can influence our physical health. It turns out that psychological stress is one of the most powerful of these influences. In this post, I’ll talk about psychological stress and some of the effects it can have on our bodies.

One can think of stress as something our body is doing to prepare for some imminent “action,” whether it be fleeing from danger, fighting an infection, or healing from an injury. These are common physical stresses that we all experience from time to time. Once the stressor is removed or healing has taken place, our bodies “stand down” from this process.

Ongoing, or chronic psychological stress, as it turns out, can have major physical consequences. Whatever its cause, our bodies react to the negative emotions caused by psychological stress by making excess amounts of substances known as inflammatory cytokines. These are protein molecules that are made widely in the body which in turn signal the body and immune system to do nasty things to us.

For instance, these inflammatory cytokines interfere with the normal functioning of insulin receptors (insulin “pushes” glucose from the blood into cells, where it is available for energy production; to do this properly, it has to bind to its receptor). When these receptors are impaired, blood sugar (glucose) rises and can lead to diabetes. Interestingly, adipose tissue (fat) is one of the places in the body where inflammatory cytokines are produced; this may be one mechanism by which obesity can lead to diabetes.

In addition, inflammatory cytokines act to reduce serotonin in the brain, which may lead to a serious depression (serotonin is one of many so-called neurotransmitters used by the brain to allow nerve cells, or neurons, to communicate with each other). In fact, some studies have shown that it is possible to predict whether someone’s depression will be resistant to treatment simply by measuring the blood levels of inflammatory cytokines that are present.

Look for more on the mind-body connection in an upcoming post!

Recently I came across a couple of articles that present a slightly different “take” on trauma, and I thought it was worth summarizing here. It piqued my interest because they examine the effects of chronic interpersonal abuse, which is not really captured in the classic DSM-IV definition of PTSD in which a person is: (1)“…confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others… “ and (2) “the person’s response involved intense fear, helplessness, or horror.”

Victims of chronic interpersonal abuse are often subjected to repeated traumatization, often in the form of physical or sexual assaults. Indeed, it has been found that recurrent interpersonal trauma can have significant psychological consequences that go beyond the standard DSM-IV-defined symptoms of re-experiencing, avoidance and numbing, and increased arousal.

Its victims are at risk for difficulties in mood regulation (and mood disorders), attachment disorders in childhood, anxiety, aggressive behavior towards the self and others, personality disorders, and more. Chronic interpersonal abuse also leads to an increased risk of chronic medical illnesses including heart disease, immune disorders, disturbances of metabolism, substance abuse, and obesity.

Taken together, these symptoms have been classified under the rubric of “Disorders of Extreme Stress, Not Otherwise Specified,” or simply DESNOS for short. It is not uncommon for victims of interpersonal trauma to also suffer from PTSD in addition to DESNOS; the longer the duration of the trauma, the more likely it is that both will co-occur.

DESNOS symptoms cover seven broad categories of psycho-social functioning and regulation of the self including impulse control and mood, biological self-regulation (such as somatization, which consists of multiple physical complaints that cannot be explained on a medical basis), alterations of attention and/or consciousness, dysfunctional attitudes toward the perpetrator(s) of the trauma (such as idealization), disturbed perceptions of the self, disturbances in interpersonal relationships, and alterations of previously held belief systems (such as loss of faith).

This distinction between DESNOS and PTSD becomes important in terms of treatment implications; the treatment of PTSD focuses on the memories of past events in order to reduce the impact of traumatic experiences. On the other hand, when confronted by a client that has experienced interpersonal abuse, it is imperative to look for the presence of symptoms compatible with DESNOS. For in clients with this syndrome, one must focus on much more than just the memories of their traumatic events.

References

Ford, J. D., Stockton, P., Kaltman, S., & Green, B. L. (2006). Disorders of extreme stress (DESNOS) symptoms are associated with type and severity of interpersonal trauma exposure in a sample of healthy young women. Journal of Interpersonal Violence, 21, 1399-1416.

Van Der Kolk, B. A., Roth, S., Pelcovitz, D., Sunday, S., & Spinazzola, J. (2005). Disorders of extreme stress: the empirical foundation of a complex adaptation to trauma. Journal of Traumatic Stress, 18, 389-399.