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.

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.

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.

e-pearls newsletter, March 2009:

There has been increasing evidence over the years showing a strong association between psychological stress, depression, and physical illness. This rather direct link has been well-established in the literature; this month’s focus is on the relationship between stress and heart disease, which is just one aspect of the so-called mind-body connection.

As counselors, we are in an excellent position to help our clients deal with stress. By so doing, we may be helping them not only from a psychological standpoint, but from a physical one as well. I have been fascinated by the relationship between the mind and body for a long time; look for more on this in future editions!

Background 

When subjected to psychological (or physical) stress, there is a rise in serum cortisol and adrenaline, which are produced by the adrenal gland. Both of these are so-called “stress hormones;” taken together, they cause an increase in heart rate, blood pressure, and blood glucose. This essentially gets us “primed” to act quickly in response to a given situation. Cortisol also stimulates the immune system to manufacture small proteins called pro-inflammatory cytokines, which serve to increase inflammation in the body.

These same cytokines also trigger a key enzyme that breaks down tryptophan, an amino acid that is necessary for the manufacture of serotonin. The result is a depletion of serotonin, often leading to the development of depression. Because these cytokines also promote inflammation, they may lead to an increased risk of many inflammatory diseases such as diabetes and arthritis (among others) as well as coronary heart disease.

Chronic Stress, Depression, and Coronary Heart Disease (CHD) 

Before getting much further, it is necessary to define a few terms here. “Coronary heart disease,” or CHD, refers to heart disease related to narrowing of the arteries that supply blood to the heart, namely the coronary arteries. When far enough advanced, CHD results in a heart attack because the heart muscle cells are deprived of oxygen and other nutrients.

This narrowing of the coronary arteries often involves so-called “plaque,” which is the build-up of cholesterol (and sometimes calcium as well) in the wall of the artery, causing it to become narrowed (think of a pipe with a glob of gunk stuck on the inside; you get the picture). Anyway, there’s lots of evidence in the literature that these plaques often become inflamed, causing them to become fragile and prone to breakage. When that happens, this “gunk” breaks off and may completely block the artery.

This is what happens in a heart attack. The thinking is that chronic psychological stress causes increased cytokine production by the immune system, resulting not only in depression, but also in an ongoing inflammatory process that in this case involves the coronary arteries. In fact, depression is a major risk factor for CHD, right up there along with smoking, high blood pressure, and diabetes.

Sudden Psychological Stress and the Sympathetic Nervous System 

In addition to the release of cortisol and the subsequent rise in blood levels of cytokines, adrenaline is also released by the adrenal gland in response to a sudden emotional stress. Adrenaline causes something called the sympathetic nervous system (which is part of the nervous system that controls heart rate and blood pressure) to become activated. When this happens, heart rate and blood pressure rise. Usually this is transient, and does not result in any physical impairment. 

However, in some cases, actual physical changes can take place. For instance, there have been reports of sudden enlargement of the heart (“congestive heart failure,” in medical lingo) with the resulting buildup of fluid in the lungs (“pulmonary edema”) in response to receiving the unexpected news of the death of a loved one. Granted, this is rare, but nonetheless is a powerful example of just how intimately the mind and body are connected.

Panic Disorder and Cardiac Risk

People who suffer from panic disorder often experience cardiac symptoms such as chest pain or a sensation of a rapid heartbeat. Medical testing usually reveals no abnormality, and patients are typically reassured that there is no risk of physical harm.

However, this turns out not to be the case. There is in fact an increased risk of sudden death from heart attack and/or heart rhythm disturbances during panic attacks. This is caused by the sudden increase of sympathetic nervous system activity discussed above, which in this case causes spasm of the coronary arteries (resulting in severe narrowing) and/or an irregular heart beat (causing a fatal drop in blood pressure). This can happen even in people who have no known history of cardiac disease, and serves as yet another example of how powerful the mind-body connection can be.

References

Anda, R., et al. (1993). Depressed affect, hopelessness, and the risk of ischemic heart disease in a cohort of U.S. adults. Epidemiology, 4, 285-294.

Esler, M., Schwarz, R., Alvarenga, M. (2008). Mental stress is a cause of cardiovascular diseases: From scepticism to certainty. Stress and Health, 24, 175-180.

Maes, M., et al. (1997). Serotonin-immune interactions in major depression: Lower serum tryptophan as a marker of an immune-inflammatory response. European Archives of Psychiatry and Clinical Neuroscience, 247, 154-161.

Wellen, K.E., Hotamisligil, G.S. (2005). Inflammation, stress, and diabetes. The Journal of Clinical Investigation, 115, 1111-1119.

Wittstein, I.S., et al. (2005). Neurohumoral features of myocardial stunning due to sudden emotional stress. The New England Journal of Medicine, 352, 539-548.

e-pearls newsletter, February 2009:

I chose this month’s topic because of a strong personal interest in schizophrenia (in which hallucinations are most often of anauditory nature; however, visual hallucinations may occur in a significant percentage of patients over the course of their illness). In addition, therapists will likely come across clients suffering from hallucinations from time to time, and I believe it may be helpful, as mental health providers, to know something about their medical basis. I chose to focus on visual hallucinations because of the different varieties, which are important to distinguish.

Background

Hallucinations have many physical causes including disturbances of the brain structure itself (such as a brain tumor), delirium (which itself has many causes including substance withdrawal, infections, substance intoxication, among others), migraine, and even epilepsy. In fact, up to 75% of delirious patients have hallucinations. They are also commonly seen in psychiatric disorders.

The key fact to keep in mind is to always be suspicious that a client’s hallucinations may be due to a so-called “organic” cause (this is a bit of a misnomer, since even psychotic disorders such as schizophrenia have as their basis some physical mechanism). However, for purposes of discussion, organic illness here refers to non-psychiatric disease.

Formed vs. Unformed Visual Hallucinations

There are basically two main types of visual hallucinations: formed and unformed. Unformed hallucinations consist of blotches of color, geometric shapes, flashing lights, or some other ill-defined image. Formed hallucinations, on the other hand, consist of well-defined objects, people, animals, or anything else. It is easy to figure out what type is being experienced by a client, simply from their description. As one might guess, formed and unformed visual hallucinations have very different sites of origin in the nervous system.

The presence of formed visual hallucinations is generally consistent with psychiatric disease; they are believed to originate in the temporal lobe. If they occur in the presence of auditory hallucinations in a young adult, it goes along with a diagnosis of a primary psychiatric disorder (organic causes must still be excluded; this is an important point). On the other hand, unformed visual hallucinations are believed to originate outside of the temporal lobe. They may be the result of a brain disturbance in the occipital lobe (which is in the back of the brain, and is the area that receives visual information from the eyes), retina (the light-sensitive part of the eyes), optic nerves (which convey the visual signal from the retina back into the brain), or other areas of the brain. The point here is not to necessarily know all the details, but to keep in mind that unformed visual hallucinations should always make one very concerned about an underlying organic, nonpsychiatric process.

References 

Adams, R. D., & Victor, M. (1993). Principles of Neurology (5th ed.). New York: McGraw-Hill, Inc.

Cummings, J. L., & Miller, B. L. (1987). Visual hallucinations: Clinical occurrence and use in

differential diagnosis. Western Journal of Medicine, 146, 46-51.

e-pearls newsletter, January 2009:

As we all know, SSRI’s (as well as SSNRI’s) are often used in the treatment of serious depression. These agents act by inhibiting the re-uptake of serotonin into nerve cells in the brain. This causes serotonin molecules to linger in their synapses (spaces between nerve cells), which in turn allows serotonin to remain in contact with nerve cells that are being stimulated. This results in an enhanced serotonin signal being transmitted.

Problems may arise in people who are also taking another class of drugs, called triptans, for their migraine headaches. Ordinarily, triptans are meant to be taken sparingly, and only at the first sign of a migraine, in order to abort that particular headache occurrence. However, it is not uncommon for people either to take this medication on a regular basis in order to prevent their headaches in the first place, or exceed the recommended per-headache dosage. This causes a further increase in serotonin transmission, because triptans enhance the effects of serotonin by binding to its receptors in the brain. This may easily result in a serious over-enhancement of the effects of serotonin on the brain, due to the combined actions of the client’s triptan and SSRI (or SSNRI).

When this occurs, it is referred to as the so-called serotonin syndrome and is characterized by stupor (reduced alertness), coma (unresponsiveness), seizures, and hyperthermia (markedly elevated body temperature). If not recognized, it can be fatal.

Therefore, it might be wise to ask your migraine-suffering clients that are taking an SSRI or SSNRI whether they are also taking a triptan. You just might be doing them a great service.