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Anxiety

Signs and Symptoms

Anxiety disorders encompass excessive anxiety, which is based on the experience of fear, shared with other animals. Fear is the behavior under external, imminent danger: the body experiences a surge of adrenaline in situations requiring escape or defense of oneself, leading to the arousal state of “fight or flight”. Anxiety is the anticipation of future threat, which is an internal stimulus. It can occur in the absence of an identifiable external threat, thus responding only to an internal stimulus. It is an affect characterized by hypervigilance, muscle tension, cautious behavior and avoidance behaviors.

Anxiety that causes significant distress or disability is only normal when it occurs under an extremely stressful situation and is short-lived. Otherwise, when there is not present a substantially stressful situation or when the anxiety continues despite the stressor diminishing, an anxiety disorder is probably present.

Panic attacks are abrupt surges of intense fear or intense discomfort that reach a peak within minutes, accompanied by physical and/or cognitive symptoms. A panic attack is an abrupt surge of intense anxiety in which at least 4 of the following symptoms are experienced:

  • Palpitations, pounding heart, or accelerated heart rate
  • Sweating
  • Trembling or shaking
  • Sensations of shortness of breath or smothering
  • Feelings of choking
  • Chest pain or discomfort
  • Nausea or abdominal distress
  • Feeling dizzy, unsteady, light-headed, or faint
  • Chills or heat sensations.
  • Paresthesias (numbness or tingling sensations)
  • Derealization (feelings of unreality) or depersonalization (being detached from oneself)
  • Fear of losing control or “going crazy.”
  • Fear of dying.

Panic attacks may be expected, such as in response to a typically feared object or situation, or unexpected, meaning that the panic attack occurs for no apparent reason.

Panic Attack Disorder

Panic disorder is a type of anxiety usually emerges in a patient’s twenties and early thirties, characterized by multiple panic attacks and fear of the recurrence of them. While panic disorder has less than 10% prevalence in the population, panic attacks themselves across many psychiatric disorders and are not limited to the anxiety disorders (e.g., substance use, depressive and psychotic disorders). Panic attacks are a symptom that indicate the severity of diagnosis, course, and comorbidity across many psychiatric disorders

In panic disorder, the individual experiences recurrent unexpected panic attacks and is persistently concerned or worried about having more panic attacks or their consequences (e.g., losing control, having a heart attack, “going crazy”). There are subsequent changes his or her behavior in maladaptive ways because of the panic attacks (e.g., avoidance of exercise or of unfamiliar locationss, or leaving home entirely).

Generalized Anxiety Disorder

By far, the type of anxiety that I treat the most of is Generalized Anxiety Disorder. In this disorder, there is excessive anxiety and worry, occurring more days than not for at least 6 months, about a number of events or activities (such as work or school performance). The patient finds it difficult to control the anxiety and at least 6 of the following symptoms are experienced:

  • Restlessness or feeling keyed up or on edge
  • Being easily fatigued
  • Difficulty concentrating or mind going blank
  • Irritability
  • Muscle tension
  • Sleep disturbance (difficulty falling or staying asleep, or restless, unsatisfying sleep).

Separation Anxiety Disorder

Prior to the publication of the latest diagnostic manual in psychiatry, the DSM-5, in 2013, separation anxiety disorder had been included in the section “Disorders Usually First Diagnosed in Infancy, Childhood, or Adolescence.” However, with DSM-5, it has been placed into the “Anxiety Disorders” section. This change implies that Separation Anxiety Disorder can be diagnosed as having an onset in adults.

SepAD is exemplified by developmentally inappropriate and excessive anxiety occurring upon separation (or threat of separation) from significant attachment figures (usually parental figures). In children, this is manifested by excessive crying, tantrums, physical complaints, and other manifestations of fear and avoidance of separation. SepAD is the appropriate diagnosis in many cases of “school phobia”; the other common explanatory diagnosis is social anxiety disorder.

Older children can usually explain their fearfulness that something bad will happen to the parents if they are separated. In adults, the worries about separation from significant others and and about harm befalling them are central to their complaint, though often the pattern of behavior can be so long-standing and ingrained—since childhood—that both the patient and the significant other may rationalize the behaviors. The presentation in adulthood can be one of one of extreme dependence, in which case the diagnosis of dependent personality disorder may be applied apply.

Selective Mutism

Like separation anxiety disorder, selective mutism a disorder that was previously categorized under the section “Disorders Usually First Diagnosed in Infancy, Childhood, or Adolescence” in previous versions of the DSM. In 2013, with the DSM 5, it was moved to the “Anxiety Disorders” section. Is characterized by the failure of the individual (almost almost a child) to speak in nearly all social situations, despite apparently normal language development and abilities, as evidenced by speech with familiar people (usually the parents). Onset is in early childhood; however, precise age-at-onset data are not available, nor are good epidemiological data on the prevalence of selective mutism (although it is considered to be relatively uncommon, affecting approximately 1 in 1,000 children according to some estimates) (Bergman et al. 2002).

Most children with selective mutism are socially anxious and, in fact, meet diagnostic criteria for SAD. This has led most clinical investigators to consider selective mutism as an early-onset, severe subtype of SAD (Bögels et al. 2010; Carbone et al. 2010; Cohan et al. 2006), and in fact, at one point in the development of DSM-5, there was discussion about classifying selective mutism as such (i.e., a subtype of SAD).

Specific Phobia

A specific phobia is the marked fear or anxiety about a specific object or situation. It must be persistent (on exposure or imagined exposure to the object or situation), the fear or anxiety must be intense or severe (sometimes taking the form of a panic attack), and the individual must either be routinely taking steps to actively avoid the situation or object or be intensely distressed in its presence.

As is the case for all phobias, the fear and/or avoidance in specific phobias must be disproportionate to the actual danger posed by the situation (Craske et al. 2009). This is important because people without the specific phobia may still fear the object but not go to extraordinary lengths to avoid it or would tolerate it. For example, people with snake phobias are so frightened by the prospect of encountering a snake that they may refuse to ever go hiking, to go for walks in the park, and even to look at pictures of snakes. People with fear of hypodermic needles may refuse to have blood draws done on them despite a clear medical need to have them. Individuals with this blood-injection-injury specific phobia often demonstrate a vasovagal fainting or near-fainting response; this is one of those rare instances where patients with anxiety disorders can actually “pass out,”

Social Anxiety Disorder

Social anxiety disorder, also known as social phobia, is a condition marked by fear of social and performance situations that typically leads to avoidance. The worry is that the individual will say or do something that will result in embarrassment or humiliation. Thus, the core fear is that of negative evaluation from others. There is an underlying belief that in situations where evaluation is possible, the individual will be judged poorly and not measure up to what is expected.

As with many other anxiety disorders, SAD often occurs early in life, sometimes even before the teen years. It is also frequently comorbid (occurs together with) major depression; in young adults, is a risk factor for depression. It also has a high comorbidity with physical health conditions (Sareen et al. 2006). This comorbidity results in a high burden of functional disability that includes decreased workplace productivity, increased financial costs, and reduced health-related quality of life (Sareen et al. 2006; Stein et al. 2011a).

Clinical Course and Prognosis

Studies show that there are a set of risk factors that are common to all of the anxiety disorders. Like most depressive disorders, most anxiety disorders occur more frequently in females than in males (approximately 2:1 ratio). Younger age, single or divorced marital status, low socioeconomic status, poor social supports, and low education are associated with an increased likelihood of anxiety disorders. Whites are more likely to have anxiety disorders than ethnic minorities. Stressful life events and childhood maltreatment are also strong risk factors for anxiety disorders.

Some of the anxiety disorders typically develop in teenage years (separation anxiety disorder, specific phobia, social anxiety and agoraphobia), while others develop in the twenties and early thirties (panic disorder, generalized anxiety disorder) and tend to persist if not treated.

Prevalence and Public Health Impact

Anxiety disorders are probably the most common of mental disorders to come across the psychiatrist’s office, encompassing 40% of new referrals. In primary care setting, they make up 10%-15% of patients compared to depressive disorders making up 7%-10% of patients. They are in fact the most prevalent conditions in any age category. They are associated with substantial cost to society due to disability and loss of work productivity. Recent evidence shows that anxiety disorders are also associated with increased risk of suicidal behavior (Sareen 2011)

It is estimated that 34% of the population will be afflicted by an anxiety disorder. the phobias—particularly specific phobia and social anxiety disorder (SAD)—are the most common conditions, with specific phobia having a 15.6% lifetime prevalence and social anxiety having a 10.7% prevalence (Kessler et al. 2012). The other anxiety disorders, generalized anxiety (4.3%), panic disorder and agoraphobia (6.3%) to separation anxiety disorder (6.7%) are less prevalent.

An important thing to understand about anxiety disorders are that they are highly comorbid (meaning they occur simultaneously) with other mental disorders, personality disorders, and physical health conditions, with over 90% of persons with an anxiety disorder having lifetime comorbidity with one or more of these disorders (El-Gabalawy et al. 2013). In the presence of other conditions, the treatment of anxiety results in poorer outcomes. The most common comorbidity is the presence of another anxiety disorder. Mood and substance use (including nicotine and alcohol) disorders also commonly co-occur with anxiety disorders. Because anxiety disorders often precede the onset of mood disorders and substance use, early interventions to treat anxiety disorders may prevent mood and substance use disorders. Anxiety disorders are also commonly comorbid with personality disorders, such as borderline, antisocial, and avoidant personality disorders (El-Gabalawy et al. 2013).

Physical health conditions are also common among patients with anxiety disorders (Sareen et al. 2006). Among the comorbid physical health conditions, the most prevalent are cardiovascular disease, respiratory illness (e.g., asthma), arthritis, and migraines. The onset of a serious physical illness might trigger the onset of an anxiety disorder, or conversely, anxiety and avoidance might lead to physical health problems.

Research

Inheritance

Among genetic and family factors, there is increasing evidence for the familial transmission of anxiety disorders through both genetic transmission and modeling. With panic disorder, generalized anxiety disorder, and social anxiety disorder, research has supported a “stress-diathesis” model, explaining risk as a predispositional vulnerability together combined with stress from life experiences. Studies have suggested that early life trauma or maltreatment (Stein et al. 1996) is an important risk factor, extending to both anxiety and depressive disorders. Twin studies suggest that panic disorder has moderate heritability (~ 40%) (Gelernter and Stein 2009). From a genetic perspective, it is believed that anxiety disorders are complex disorders with multiple genes conferring vulnerability through as-yet largely undetermined pathways (Manolio et al. 2009; Smoller et al. 2009).
Some other promising leads have emerged (Logue et al. 2012). For example, several studies have implicated the adenosine 2A receptor gene (ADORA2A) as having a possible role in panic disorder, consistent with the anxiogenic effects of caffeine, a known antagonist at this receptor (Hohoff et al. 2010). Association studies examining genes involved in other neurotransmitter systems thought to be associated with fear and anxiety (e.g., norepinephrine and serotonin) have produced inconsistent, often non-replicated results. The most consistent results have involved the 22q11 catechol O-methyltransferase gene (COMT) that codes for the enzyme responsible for norepinephrine metabolism.

Learning theory

Beginning in 1967 with Pitt’s observation that sodium lactate provoked panic attacks in patients with panic disorder but not in control subjects (Pitts and McClure 1967), a series of studies showed that agents with disparate mechanisms of action such as caffeine, isoproterenol, yohimbine, carbon dioxide, and cholecystokinin (CCK) had similar abilities to provoke panic in patients with panic disorder but not in control subjects (Roy-Byrne et al. 2006). Many of these neurobiological “challenge” agents have been thought to have specific effects on the brain’s fear circuits, which are believed to function aberrantly in patients with panic disorder. The studies of these challenge agents were originally proposed to indicate specific biochemical abnormalities in panic disorder. However, many investigators now agree that most of the effects elicited by these compounds can be explained on the basis of learning theories of panic disorder, which emphasize that patients with panic disorder misinterpret and are frightened by perceived perturbations in their physiological state.

Elevated anxiety-sensitivity is probably multi-factorial, studies suggesting that it may be acquired from recurrent direct aversive experience such as maltreatment in childhood or physical suffering during illness such as asthma, vicarious observations (e.g. significant illnesses or deaths among family members), or parental reinforcement or modeling of distressed reactions to bodily sensations. This factor may contribute to a heightened state of interoceptive attention (attention to internal sensations) that primes the individual to experience panic attacks and to be intensely frightened by them when they occur. Hence, “fear of fear” develops after the initial panic attacks results in interoceptive conditioning (conditioned fear of internal cues such as pounding heart and shortness of breath) and the subsequent interpretation of these internal cues as indicating something dangerous (e.g., loss of control, heart attck, or stroke), thus further causing strengthening of these cues. (Bouton et al. 2001).

Neuroanatomy

Alterations in the functioning of fear circuitry are generally posited across many of the anxiety disorders, with dysfunction in the amygdala and its connections believed to play an important etiological role in the pathophysiology of an array of fear-based disorders, including panic disorder, social phobia, and PTSD (Etkin and Wager 2007; Figure 5-). Amygdala dysfunction may also be a critical underlying factor in anxiety proneness more generally (Stein et al. 2007). Functional neuroimaging data suggest that a particular brain structure, the insula, is involved in the intense awareness of somatic sensations experienced by patients with panic disorder and related disorders (Paulus and Stein 2010).

SAD seems to involve abnormal responding in anxiety circuitry that includes the amygdala and insular cortex, findings that are shared with several other anxiety and trauma-related disorders (Etkin and Wager 2007). Adults with SAD demonstrate a variety of attentional, interpretative, and other cognitive biases (Ouimet et al. 2009), the origins of which are poorly understood but which nonetheless may be a focus for therapeutic interventions, such as those discussed later in this chapter.

Tempermental Factors

Some specific phobias develop following a traumatic event (e.g., being bitten by a dog), but most patients with specific phobia do not recall any experiential precursor (e.g., most snake phobics have never been bitten by a snake and most flying phobics have never been in a plane crash). Temperamental factors that are a risk factor for specific phobia, such as neuroticism or behavioral inhibition, are shared with other anxiety disorders (Craske et al. 2009).

Treatment for Anxiety

Anxiety disorders tend to respond well to psychological and pharmacological treatments, but the initial assessment is important in order to spell out the direction of the treatment.
The impact on functioning and the suicidal risk are key elements that will guide the intensity or speed of the treatment.

Next, there next to be a consideration of the differential diagnoses (the other possible diagnoses and causes for the symptoms). These can include substance-indeed anxiety or medical condition related anxiety. Along these lines, there should be a physical done and laboratory exams performed.

Following that, there should be an identification of the type of anxiety(ies) that are involved in the individual’s symptoms. (e.g. separation anxiety disorder, selective mutism, social anxiety disorder, panic disorder, generalized anxiety disorder, specific phobia, agoraphobia).

There also needs to be considered whether the patient has other mental disorders, such as a depressive disorder, which is often comborbid with an anxiety disorder.

Finally, there needs to be psychoeducation of the patient, leading to consideration for psychotherapy as well as pharmacological therapy.

Psychotherapy

Cognitive Behavioral Therapy starts with understanding the behavioral model of anxiety, which suggests that individuals respond to external and internal triggers that lead to a sense of danger. The sense of danger leads to a fight-or-flight response and they avoid the triggering situation. Behavioral treatments of anxiety disorders aim to expose the individual to the anxiety-provoking situation and prevent the response of avoidance. Through systematic desensitization, patients gradually but in increasingly more challenging situations face the phobic stimuli that make them feel anxious.

At the core of CBT are the four components: psychoeducation, relaxation training, cognitive restructuring, and exposure therapy. Among the psychosocial interventions for anxiety disorders, CBT has the most robust evidence for efficacy.

As an example, a particular patient may have panic attacks that are triggered by isolated chest pains. These chest pains lead the anxiety-provoking thought that she could be having a heart attack. The patient would learn ways to challenge this thinking through looking at evidence for and against the thought that she is having a heart attack, thus restructuring her cognition.

Exposure therapy would then be used with this patient to reinforce this restructuring; exposure therapy for panic disorder often involves exercises that recreate the panic symptoms (interoceptive exposure). One technique often used to recreate these symptoms is hyperventilation, because this phenomenon is common in panic attacks. When used as a technique in exposure therapy, the patient and the therapist hyperventilate together for brief periods and patients are taught that the physiological symptoms will resolve on their own.

Next, the patient would be asked to make a hierarchical list of situations that she avoids because of anxiety. Over the course of the therapy the patient would slowly face the anxiety-provoking situations and learn that if she stays in the situation long enough, the anxiety resolves.

Other techniques that CBT include to promote relaxation training are deep muscle relaxation and/or breathing management.

CBT techniques can be very empowering for patients. They often feel alone and bewildered, especially if they have not known other who have had anxiety symptoms like their own. The sharing of unbiased high-quality information can greatly lessen this sense of being isolated. Information is available at the Web sites of the National Institutes of Health (www.nih.gov), Anxiety and Depression Association of America (www.adaa.org), or UpToDate (www.uptodate.com; provides free access to medical information in materials written expressly for consumers), among others.

Pharmacotherapy

Pharmacotherapy is a good option for many patients with anxiety disorders, either in combination with cognitive behavior therapy or as a stand-alone treatment. The main medications used for anxiety disorders are the antidepressants and the benzodiazepine anxiolytics. The antidepressants include selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), and monoamine oxidase inhibitors (MAOIs). On occasion, there are several nonbenzodiazepine anxiolytics (e.g., buspirone and pregabalin) and atypical antipsychotics (for refractory anxiety) that are used. Antidepressants are more thoroughly discussed in the antidepressant section of the depression page of this blog.

References

Blanco C, Heimberg RG, Schneier FR, et al: A placebo-controlled trial of phenelzine, cognitive behavioral group therapy, and their combination for social anxiety disorder. Arch Gen Psychiatry 67:286–295, 2010

Bögels SM, Alden L, Beidel DC, et al: Social anxiety disorder: questions and answers for the DSM-V. Depress Anxiety 27:168–189, 2010

Bouton ME, Mineka S, Barlow DH: A modern learning theory perspective on the etiology of panic disorder. Psychol Rev 108:4–32, 2001

Carbone D, Schmidt LA, Cunningham CC, et al: Behavioral and socio-emotional functioning in children with selective mutism: a comparison with anxious and typically developing children across multiple informants. J Abnorm Child Psychol 38:1057–1067, 2010

Cohan SL, Price JM, Stein MB: Suffering in silence: why a developmental psychopathology perspective on selective mutism is needed. J Dev Behav Pediatr 27:341–355, 2006

Craske MG, Rauch SL, Ursano R, et al: What is an anxiety disorder? Depress Anxiety 26:1066–1085, 2009

Craske MG, Stein MB, Sullivan G, et al: Disorder-specific impact of coordinated anxiety learning and management treatment for anxiety disorders in primary care. Arch Gen Psychiatry 68:378–388, 2011

El-Gabalawy R, Tsai J, Harpaz-Rotem I, et al: Predominant typologies of psychopathology in the United States: a latent class analysis. J Psychiatr Res 47:1649–1657, 2013

Etkin A, Wager TD: Functional neuroimaging of anxiety: a meta-analysis of emotional processing in PTSD, social anxiety disorder, and specific phobia. Am J Psychiatry 164:1476–1488, 2007

Kessler RC, Petukhova M, Sampson NA, et al: Twelve-month and lifetime prevalence and lifetime morbid risk of anxiety and mood disorders in the United States. Int J Methods Psychiatr Res 21:169–184, 2012

Ouimet AJ, Gawronski B, Dozois DJ: Cognitive vulnerability to anxiety: a review and an integrative model. Clin Psychol Rev 29:459–470, 2009

Roy-Byrne PP, Craske MG, Stein MB: Panic disorder. Lancet 368:1023–1032, 2006

Sareen J, Jacobi F, Cox BJ, et al: Disability and poor quality of life associated with comorbid anxiety disorders and physical conditions. Arch Intern Med 166:2109–2116, 2006 17060541

Sareen J: Anxiety disorders and risk for suicide: why such controversy? Depress Anxiety 28:941–945, 2011

Stein MB, Simmons AN, Feinstein JS, et al: Increased amygdala and insula activation during emotion processing in anxiety-prone subjects. Am J Psychiatry 164:318–327, 2007

Depression

Signs and Symptoms

Depression is the state of feeling unhappy, “being down in the dumps”, or having “the blues”, with the associated feelings of feeling unmotivated, and not feeling satisfied with things that ordinarily are naturally enjoyable, such as eating, sleeping, concentrating on things, exercising, or positive life events. Other associated feelings are feelings of low self-esteem, excessive guilt, feeling tired moving and thinking, and thinking more about death.

Because depression can range in intensity from a low grade state to one that overtakes the person’s existence, there are different levels of depression, categorized as major depressive disorder and dysthymia. There are different types of depression, some due to “unipolar” depression, and bipolar depression, in which the person has experienced not only depression, but also hypomania and mania. The descriptions in this page are of unipolar depression; bipolar depression is similar in signs and symptoms but will be discussed further in the page on bipolar disorder.

Major Depressive Disorder

One of the major reasons seek out psychiatrists is to treat depression. According to the DSM-V, (the Diagnostic and Statistical Manual of Mental Disorders, edition 5), the rule book professionals use to diagnose mental conditions, the most serious type of depression is Major Depressive Disorder. In this condition, at least five of the following symptoms have been present during a 2-week period; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure.

  1. Depressed mood most of the time, demonstrated in subjective report (e.g., feels sad, empty, hopeless) or observation made by others (e.g., appears tearful). (Note: In children and adolescents, can be irritable mood.)
  2. Decreased interest or pleasure in all, or almost all, activities most of the time (as indicated by either subjective report or observation).
  3. Significant weight loss when not dieting or weight gain or decrease or increase in appetite nearly every day.
  4. Insomnia or increased sleeping nearly every day.
  5. Psychomotor agitation or retardation most of the time, observable by others (increased restlessness, or the opposite, acting or speaking too slowly or after long pauses).
  6. Fatigue or loss of energy nearly every day.
  7. Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) most of the time, but not just being sad about being sick.
  8. Diminished ability to think or concentrate, or indecisiveness, most of the time.
  9. Recurrent thoughts about death, recurrent suicidal thoughts with or without a specific plan, or a suicide attempt.

Dysthymia

Other than major depressive disorder, other forms of depression include Persistent Depressive Disorder (Dysthymia), a more more persistent but often lower grade form of depression. In this condition, there is depressed mood most of the time over 2 years, with the addition of 2 of the following 6 criteria:

  • low self-esteem
  • Hopelessness
  • Insomnia or hypersomnia (oversleeping)
  • Poor appetite or overeating
  • Low energy or fatigue
  • Poor concentration or difficulty making decisions

Premenstrual Dysphoric Disorder

Another type of depressive disorder is Premenstrual Dysphoric Disorder. In the majority of menstrual cycles, at least five symptoms must be present in the final week before the onset of menses, start to improve within a few days after the onset of menses, and become minimal or absent in the week after the menses occurs.
One (or more) of the following symptoms must be present:

Marked affective lability (instability) occurs (e.g., mood swings; feeling suddenly sad or tearful, or increased sensitivity to rejection).
Marked irritability or anger or increased interpersonal conflicts.
Marked depressed mood, feelings of hopelessness, or self-deprecating thoughts.
Marked anxiety, tension, and/or feelings of being keyed up or on edge.

One (or more) of the following symptoms must additionally be present, to reach a total of five symptoms when combined with mood symptoms above.

  • Decreased interest in usual activities (e.g., work, school, friends, hobbies).
  • Subjective difficulty in concentration.
  • Lethargy, easy fatigability, or marked lack of energy.
  • Marked change in appetite; overeating; or specific food cravings.
  • Hypersomnia or insomnia.
  • A sense of being overwhelmed or out of control.
  • Physical symptoms such as breast tenderness or swelling, joint or muscle pain, a sensation of “bloating,” or weight gain.

Clinical Course and Prognosis

For every patient,, the illness begins with a single episode; however, in most cases, the episodes eventually become recurrent (estimates of recurrence range from ~ 50% within the first year to up to 85% during a lifetime; Mueller et al. 1999).

Most scenarios of major depressive disorder tend to be cyclical. The length of a depressive episode is in the range of 5–6 months, with approximately 20% of episodes becoming chronic (i.e., lasting beyond 2 years).

Genetic and physiological factors

First-degree family members of individuals with MDD have a risk for MDD that is 2 to 4 times higher than that of the general population. Relative risks appear to be higher for early-onset and recurrent forms. Heritability is approximately 40%, with the personality trait neuroticism (defined as a predisposition toward negative affective states such as depression, anxiety, anger, and shame) accounting for a substantial portion of this genetic liability (Sullivan et al. 2000).

Temperament factors

Neuroticism (is a well-established risk factor for the onset of MDD, and high levels appear to render individuals more likely to develop depressive episodes in response to stressful life events.

Course modifiers

Features associated with lower recovery rates include long course duration, severity of symptoms, including psychotic symptoms, prominent anxiety, and co-existing personality disorders. The risk for recurrence falls slowly as time in remission increases and is higher when the preceding episode was severe, especially in younger individuals and in those who have already experienced multiple episodes (Kanai et al. 2003). The persistence of even mild depressive symptoms during remission is a powerful predictor of recurrence.

Essentially, all major non-mood-related psychiatric disorders increase the risk of an individual’s developing depression (Kessler et al. 1997). Major depressive episodes that develop against the background of another disorder often follow a more refractory course. Substance use, anxiety, and borderline personality disorders are among the most common of these, and the presenting depressive symptoms may obscure and delay their recognition (Kessler et al. 2005). However, sustained clinical improvement in depressive symptoms may depend on the appropriate treatment of underlying illnesses. Chronic or disabling medical conditions also increase risks for major depressive episodes. Such prevalent illnesses as diabetes, morbid obesity, and cardiovascular disease are often complicated by depressive episodes, which are more likely to become chronic than are depressive episodes in medically healthy individuals (McIntyre et al. 2012).

Risk and Prognostic Factors and Environmental factors

Adverse childhood experiences, particularly when there are multiple experiences of diverse types, comprise a set of potent risk factors for MDD. Stressful life events are well recognized as precipitants of major depressive episodes, but the presence or absence of adverse life events near the onset of episodes does not appear to provide a useful guide to prognosis or treatment selection.

Despite consistent differences between genders in prevalence rates for depressive disorders, there appear to be no clear differences by gender in phenomenology, course, or treatment response. The higher prevalence in females is the most reproducible finding in the epidemiology of MDD. Risks for suicide attempts are higher in women; however, risks for completion of suicides in women are lower. There are no consistent differences between genders in symptoms, course, treatment response, or functional consequences.

Similarly, there are no clear effects of current age on the course or treatment response of MDD. Some symptom differences exist, however, such that reverse vegetative symptoms are more likely in younger individuals, and melancholic symptoms, particularly psychomotor disturbances, are more common in older individuals. The likelihood of suicide attempts lessens in middle and late life, although the risk of completed suicide does not. Depressions with earlier ages at onset are more familial and are more likely to involve personality disturbances. The course of MDD within individuals does not generally change with aging. Mean times to recovery appear to be stable over long periods, and the likelihood of being in an episode does not generally increase or decrease with time.

Prevalence and Public Health Impact

Estimates of the lifetime prevalence of MDD vary from 4% to 30%. In the Western culture, the most generally accepted figure is 16%, with an range of variability between 15%–17% (Kessler et al. 2003). The 1-month prevalence in the National Comorbidity Study was estimated to be 6%.

Research

Etiological Factors

Although over 90,000 references are identified when etiology and depression are searched in Medline, the etiology of major depression remains an enigma. Much is known and is being researched, yet consistently reproducible results remain on the horizon. One of the most helpful discussions for beginning an understanding of the complex etiologies behind a heterogeneous disorder such as major depression is in Perspectives of Psychiatry by McHugh and Slavney 1998).

There can be (at least) four perspectives to approaching and understanding depressive illnesses and phenomena. The biological perspective considers the increased genetic risk in affected family members, as well as biochemical and immunological factors such as inflammatory molecules and stress-related markers of the endocrine system. The behavioral perspective takes into account the role of motivated behaviors contributing to the clinical picture, including unhealthy lifestyle choices and related behaviors; smoking, drinking, unhealthy eating habits leading to obesity, and gambling are examples of behaviors that compromise moods and contribute to the etiology of major depression. Personality features and temperament contributing to mood disorders are captured in the dimensional perspective. Finally, the life-story perspective describes the influences that life events and environmental influences may have on the development of the disorder.

Bipolar Disorder

BIPOLAR DISORDER

Signs and Symptoms

At the center of the illness is at least one manic or hypomanic episode. A manic episode is a distinct period of unusually elevated, expansive, or irritable mood accompanied by increased goal-directed activity or energy, lasting at least 1 week and present most of the time. During the period of mood disturbance and increased energy or activity, about half of the associated symptoms must be noted and must be different from baseline.

  • Inflated self-esteem or grandiosity.
  • Decreased need for sleep
  • More talkative than usual or pressure to keep talking.
  • Flight of ideas or subjective experience that thoughts are racing.
  • Distractibility (overly rapid shifting of focus)
  • Increase in goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation (i.e., purposeless non-goal-directed activity).
  • Excessive involvement in activities that have a high potential for painful consequences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments).

Bipolar I disorder involves manic symptoms while Bipolar II disorder involves only hypomanic episode(s). A hypomanic episode is similar to a manic episode but is of a lower level of intensity. It too is a distinct period of elevated, expansive, or irritable mood and abnormally increased activity or energy, but lasting at least only 4 consecutive days. Hypomanic episodes are defined similarly to manic episodes with one important difference being that they are not severe—that is, they do not entail psychosis, hospitalization, or severe impairment. Similarly, in a hypomanic episode, as in a manic episode, during the period of mood disturbance and increased energy, there are at least three associated symptoms (four if the mood is only irritable): inflated self esteem, decreased need for sleep, more talkative than usual, increase in goal-directed activity or psychomotor agitation, distractibility, racing thoughts or flight of ideas, excessive involvement in pleasurable activities with painful consequences.

Cyclothymic disorder involves manic symptoms and depressive symptoms of at least 2 years that do not meet the criteria of Bipolar I or II or Major Depressive Disorder.

Clinical Course and Prognosis

Bipolar disorder is one of the most disabling mental illnesses, potentially including symptoms of depression, mania, and psychoses (disconnection with reality). Clinical samples suggest that patients with bipolar and related disorders are commonly not able to maintain full-time employment, even if they have at least some college education (Kogan et al. 2004).

Prevalence and Public Health Impact

Bipolar and related disorders, although less common than depressive disorders, may have a lifetime prevalence as high as 4% (1% bipolar I disorder, 1% bipolar II disorder, and 2% bipolar disorder with symptoms that do not meet the criteria for bipolar I or II disorders) (Merikangas et al. 2007). The peak age at onset for bipolar and related disorders is in the late teens to early 20s, with the mean onset age being earliest in bipolar I disorder, intermediate in bipolar II disorder, and latest in major depressive disorder.

Depressive episodes are common in bipolar disorder and are described in Major Depressive Disorder section. When manic or hypomanic episodes coincide with major depressive episodes, we say that they have “mixed features”.

Research

Treatment

The treatment of bipolar disorder involves treatment of both manic or manic symptoms and depressive symptoms. While the occurrence of depressive symptoms are not necessary in meeting the criteria for bipolar disorder, they are actually the most common and disabling symptoms in bipolar disorder.

The foundation of treating bipolar has been the mood stabilizers valproate, lamotrigine, and carbamazepine. They treat mania and lamotrigine treats depressive symptoms as well. In addition, antidepressants, anxiolytics/hypnotics, other anticonvulsants, and other medications are commonly combined with mood stabilizers and SGAs in clinical settings (Ketter 2010).

In the past 10 years, however, second-generation antipsychotics (SGAs) have been increasingly used and many are approved by the FDA for treating symptoms of bipolar disorder.

Lithium

Lithium is an established treatment for acute mania and bipolar maintenance therapy that with chronic treatment appears to decrease suicidal behavior and suicide (Baldessarini et al. 2006; Bauer et al. 2006; Jefferson et al. 1987). As stated in the section on depression, it is also used in major depressive disorder as an augmentation strategy to enhance an antidepressant.

Lithium is especially effective in classic bipolar disorder (euphoric manias, not rapid cycling) but appears less effective in patients with manic episodes with mixed features; patients with rapid cycling (at least four episodes per year); and patients with substance abuse.

Lithium’s usefulness, however, is limited by its adverse effects, which undermine compliance. The prescribing information for lithium include boxed warnings about the toxicity of lithium that can occur at blood levels of the drug close to therapeutic levels. Symptoms can result in the central nervous system, cardiovascular, renal, and gastrointestinal systems. In severe cases, these symptoms may be irreversible. Those most at risk for toxicity include patients with significant renal or cardiovascular disease, those with severe debilitation, those with dehydration, those with sodium depletion, or those taking diuretics or angiotensin-converting enzyme (ACE) inhibitors. However, in medically healthy individuals, at dosages of 900 mg/day or less, lithium is usually well tolerated, and even with low serum levels it may yield benefit in milder forms of bipolar disorders

Lithium can cause common benign as well as rare serious renal adverse effects. Frequent urination is a common benign side effect. Known as nephrogenic diabetes insipidus, the condition involves the kidneys not retaining water as well as at baseline and may occur in as many as 10% of patients with chronic lithium therapy. (Although diabetes is in its name, it does not involve sugar dysregulation, as occurs with the the more common condition diabetes mellitus). Chronic lithium less commonly causes more long-standing and serious renal complications that are apparently more prevalent in cases with repeated lithium toxicity, advanced age, and concurrent nonsteroidal anti-inflammatory drug (NSAID) therapy or chronic medical illness. Patients need to maintain adequate fluid and sodium intake, as fluid and sodium depletion can cause lithium blood levels to rise. Caution is indicated in the setting of protracted sweating, diarrhea, infection, and fever.

Tremor often occurs with lithium treatment and is dose-related. If troublesome, the dose can be lowered or a beta blocker such as propranolol can be prescribed. This medication often relieves the tremor with few side effects.

Weight gain appears to be more of an issue with lithium than with lamotrigine, but less of a problem than with valproate or olanzapine.

Gastrointestinal effects include dyspepsia and diarrhea, but may be relieved by using the extended-release formulation instead of the instant-release formulation.

Dermatological side effects with lithium therapy include acneiform and maculopapular eruptions, psoriasis, and folliculitis. Lithium can also cause thyroid problems.

Lithium can have adverse cardiac effects, ranging from benign electrocardiographic T wave changes to clinically significant sinus node dysfunction or sinoatrial block and irritation to the cardiac ventricular rhythm. Therefore, any cardiac disorders should be reported the the prescribing physician and cardiac symptoms promptly reported.

Like the other mood stabilizers, lithium is a teratogen so female patients should have ensure that they will not become pregnant while being prescribed lithium. (FDA Pregnancy Category D).

Clinical assessments with lithium therapy includes a baseline physical examination and routinely querying patients at baseline and during treatment regarding CNS (sedation, tremor, ataxia), gastrointestinal (nausea, vomiting, diarrhea), metabolic (weight gain), and renal (polyuria, polydipsia) disorders and adverse effects. Laboratory monitoring includes a baseline electrocardiogram (in patients over 40 years of age), and renal (blood urea nitrogen, serum creatinine, and electrolytes) and thyroid (thyroid-stimulating hormone [TSH]) indices, with reevaluation of renal and thyroid indices at 3 and 6 months and then every 6–12 months thereafter, and as clinically indicated (American Psychiatric Association 2002). Serum lithium concentrations are commonly assessed at steady state, which occurs at about 5 days after a dosage change, and then as indicated by inefficacy or adverse effects. More frequent laboratory monitoring is prudent in the medically ill and in patients with abnormal indices.

Valproate

Valproate has shown effectiveness in treating both manic and mixed (concurrently having symptoms of depression and mania/hypomania) episodes, but not in patients under 18 years of age.

The U.S. prescribing information for valproate includes boxed warnings regarding the risks of hepatotoxicity, teratogenicity, and pancreatitis (Physicians’ Desk Reference 2012). Valproate, like the other mood stabilizers, is a teratogen (FDA Pregnancy Category D), and rates of major congenital malformations with valproate exposure could be higher compared with lamotrigine, carbamazepine, or no anticonvulsant exposure. Other warnings include the risks of hyperammonemic encephalopathy in patients with urea cycle disorders, somnolence in older adults, thrombocytopenia, hypothermia, multiorgan hypersensitivity reactions, and suicidality (an anticonvulsant class warning). Valproate therapy has also been associated with polycystic ovarian syndrome.

Dose-related adverse effects with valproate include gastrointestinal (nausea, vomiting, dyspepsia, diarrhea), hepatic (transaminase elevations), CNS (tremor, sedation, dizziness), and metabolic (weight gain, osteoporosis) problems and hair loss. CNS adverse effects may be lessened by weighting the dose toward bedtime or reducing the dose. The divalproex extended-release and the delayed-release formulation may cause fewer gastrointestinal side effects than valproic acid. Valproate can cause weight gain, which appears to be more problematic than with lithium, but less problematic than with olanzapine.

Valproate inhibits liver enzymes that break down other medications, and thus can increase serum concentrations of other medications

Patients need to be advised of valproate adverse effects and drug interactions. Clinical assessments with valproate therapy include a baseline physical examination and routinely querying patients at baseline and during treatment regarding hepatic and hematological disorders and adverse effects. Laboratory monitoring during valproate therapy commonly includes baseline complete blood count, differential, platelets, and hepatic indices, and reevaluation every 6–12 months and as clinically indicated (American Psychiatric Association 2002). Serum valproate concentrations are typically assessed at steady state and then as clinically indicated by inefficacy or adverse effects.

Lamotrigine

Lamotrigine is approved for bipolar maintenance treatment in adults and is generally well tolerated, particularly in comparison with other treatment options. The most common adverse events in patients with bipolar disorders in clinical trials were headache, benign rash, dizziness, diarrhea, dream abnormality, and pruritus.

The U.S. prescribing information for lamotrigine includes a boxed warning regarding the risk of serious rashes requiring hospitalization, which have included Stevens-Johnson syndrome (Physicians’ Desk Reference 2012). The risk of rash is higher in patients under age 16 years, and may be higher when lamotrigine is coadministered with valproate, when exceeding the recommended initial lamotrigine dose, and when exceeding the recommended lamotrigine dose escalation. Benign rash may be seen in 10% of patients, but because any rash is potentially serious, discontinuation of lamotrigine is required unless the rash is clearly not drug related. Other warnings in the prescribing information include the following risks:

Lamotrigine can cause CNS (headache, somnolence, insomnia, dizziness, tremor) and gastrointestinal (nausea, diarrhea) adverse effects. In most instances these problems lessen or resolve with time or lamotrigine dosage adjustment, but in some patients may require lamotrigine discontinuation. Unlike other mood stabilizers, lamotrigine has not been associated with weight gain.

Lamotrigine dosage is initially titrated very slowly to decrease the risk of rash. When given without valproate, the prescribing information recommends starting lamotrigine at 25 mg/day for 2 weeks, increasing to 50 mg/day for the next 2 weeks, then increasing to 100 mg/day for 1 week, and finally increasing to 200 mg/day in a single daily dose. Dosages exceeding 200 mg/day are not recommended unless concurrent hormonal contraceptives (which decrease serum lamotrigine concentrations) are administered. Even in the absence of hormonal contraceptives, selected patients may benefit from further gradual lamotrigine titration to final dosages as high as 400–500 mg/day.

Carbamazepine

Carbamazepine has demonstrated efficacy for acute manic and mixed episodes in adults, but complexity of use (related to drug interactions and side effects) and lack of a maintenance indication make it less commonly used than other mood stabilizers.

Carbamazepine therapy is associated with common, benign adverse events as well as rare, serious adverse events. The most common dose-related adverse effects with carbamazepine involve CNS (diplopia, blurred vision, fatigue, sedation, dizziness, and ataxia) or gastrointestinal system (nausea, vomiting) problems. Gradual initial dosing and careful attention to potential drug-drug interactions can help attenuate such problems.

The U.S. prescribing information for carbamazepine includes boxed warnings regarding the risks of serious dermatological reactions in patients with the genetic HLA-B*1502 allele (Asians should be genetically tested and, if HLA-B*1502 positive, should not be treated with carbamazepine unless benefit clearly outweighs risk), aplastic anemia (16/million patient-years), and agranulocytosis (48/million patient-years) (Physicians’ Desk Reference 2012). Other warnings in the prescribing information include the risks of teratogenicity, increased intraocular pressure due to mild anticholinergic activity, and suicidality (an anticonvulsant class warning). Carbamazepine can cause hematological (benign leukopenia, benign thrombocytopenia), dermatological (benign rash), electrolyte (asymptomatic hyponatremia), and hepatic (benign transaminase elevations) problems. Much less commonly, carbamazepine can cause analogous serious problems. Rash presenting with systemic illness or involving the eyes, mouth, or bladder (dysuria) constitutes a medical emergency; in this situation, carbamazepine should be immediately discontinued and the patient assessed emergently.

Although carbamazepine can cause modest TSH increases, frank hypothyroidism is very uncommon. Carbamazepine may affect cardiac conduction and should be used with caution in patients with cardiac disorders. Carbamazepine appears less likely than lithium or valproate to cause weight gain. Carbamazepine-induced hyponatremia is often tolerated in young physically well individuals, but can cause obtundation and other serious sequelae in medically frail older adult patients. Carbamazepine, like the other mood stabilizers, is a teratogen (FDA Pregnancy Category D).

In acute settings, such as the inpatient treatment of mania, carbamazepine therapy is commonly initiated at 200–400 mg/day and increased as necessary and tolerated by 200 mg/day every 2–4 days. Euthymic or depressed patients tend to tolerate aggressive initiation less well than manic patients. In less acute situations, such as the initiation of prophylaxis or adjunctive use, carbamazepine is often started at 100–200 mg/day and increased as necessary and tolerated by 200 mg/day every 4–7 days. Even this gradual initiation may cause adverse effects. Starting with 50 mg (half of a chewable 100-mg tablet) at bedtime and increasing by 50 mg every 4 days can yield a better-tolerated initiation. Because of autoinduction, doses after 2–4 weeks of therapy may need to be twice as high as in the first week to yield comparable serum levels. Target dosages are commonly between 600 and 1,200 mg/day, yielding serum levels from 6 to 12 μg/mL (20–60 mM/L), with the higher portion of the range used acutely and lower dosages used in prophylaxis or adjunctive therapy.

Carbamazepine has multiple problematic drug-drug interactions (in excess of those seen with lithium or valproate). These interactions are predominantly related to it being a potent hepatic inducer that can decrease serum concentrations and efficacy of psychotropic (including valproate, lamotrigine, most SGAs, and multiple antidepressants and anxiolytics) and nonpsychotropic medications, and to the ability of certain enzyme inhibitors to increase carbamazepine serum concentrations and cause toxicity. Detailed reviews of carbamazepine drug-drug interactions may be found in articles by Ketter et al. 1991a, Ketter et al. 1991b).

Patients need to be advised of carbamazepine adverse effects and drug interactions. Clinical assessments with carbamazepine therapy include a baseline physical examination and routinely querying patients at baseline and during treatment regarding hepatic and hematological disorders and adverse effects. In the past, recommended laboratory monitoring during carbamazepine therapy has included baseline complete blood count, differential, platelets, hepatic indices, and serum sodium, with reevaluation at 2, 4, 6, and 8 weeks, and then every 3 months and as clinically indicated (American Psychiatric Association 2002). In contemporary clinical practice, somewhat less focus is placed on scheduled monitoring, and clinically indicated (e.g., when a patient becomes ill with a fever) monitoring is emphasized. Patients who have abnormal or marginal indices at any point merit careful scheduled and clinically indicated monitoring. Serum carbamazepine concentrations are typically assessed at steady state, and then as indicated by inefficacy or adverse effects.

Second-Generation Antipsychotics

Based on their efficacy profiles and lower risks of extrapyramidal symptoms and tardive dyskinesia, SGAs have displaced first-generation antipsychotics in the management of bipolar and related disorders. Multiple SGAs have FDA indications for monotherapy and adjunctive (combined with lithium or valproate) therapy for acute mania and bipolar maintenance in adults. In addition, risperidone, aripiprazole, olanzapine, and quetiapine have pediatric mania monotherapy indications. Aripiprazole also has a pediatric mania adjunctive (to lithium or valproate) indication and a pediatric bipolar maintenance monotherapy indication. Olanzapine (combined with fluoxetine) and quetiapine monotherapy have acute bipolar depression indications in adults. Although (as of early 2013) cariprazine and lurasidone lack FDA indications for bipolar disorders, controlled trials suggest their efficacy in acute mania and bipolar depression, respectively, and clozapine may be effective in treatment-refractory patients. Short-acting injectable formulations of SGAs such as olanzapine, ziprasidone, and aripiprazole appear useful in the treatment of agitation, and a long-acting injectable (LAI, depot) formulation of risperidone may prove useful in patients with bipolar disorders who have poor medication compliance. Olanzapine LAI, although approved for the treatment of schizophrenia, is not approved for the treatment of bipolar and related disorders.

Second-generation antipsychotics compared with mood stabilizers entail more safety and tolerability challenges that can attenuate their efficacy benefits (e.g., weight gain with olanzapine, extrapyramidal symptoms with risperidone, sedation with quetiapine, and akathisia with ziprasidone and aripiprazole). The U.S. prescribing information includes multiple warnings and precautions for these agents (Physicians’ Desk Reference 2012). Indeed, the six SGAs (olanzapine, risperidone, quetiapine, ziprasidone, aripiprazole, and asenapine) with FDA indications for bipolar disorders (as well as lurasidone, which as of early 2013 was approved for schizophrenia but not yet for bipolar depression) have in common 12 such warnings and precautions:

Increased mortality in elderly patients with dementia-related psychosis; this is a boxed warning, with a reminder that SGAs are not approved for dementia-related psychosis

Neuroleptic malignant syndrome; the drug should be discontinued and the patient should be monitored closely

Tardive dyskinesia; the drug should be discontinued if clinically appropriate

Hyperglycemia and diabetes mellitus; the patient should be monitored for hyperglycemia symptoms such as polydipsia, polyuria, polyphagia, and weakness, and glucose should be monitored if there is a diabetes risk

Orthostatic hypotension with or without syncope; the drug should be used with caution if the patient has cardiovascular or cerebrovascular disease

Leukopenia, neutropenia, and agranulocytosis; the patient should be monitored if there is prior or baseline leukopenia, and the drug should be discontinued if there is a decrease in white blood cells in the absence of other causative factors

Seizures; the drug should be used with caution if the patient has a seizure disorder or seizure risk

Potential for cognitive and motor impairment; the patient should use caution when operating machinery

Body temperature regulation (pyrexia, feeling hot); caution should be used when prescribing the drug to a patient who may be doing strenuous exercise, may be exposed to extreme heat, may become dehydrated, or is taking an anticholinergic medication)

Suicide (risk related to bipolar disorders and schizophrenia); high-risk patients should be closely supervised

Dysphagia; the drug should be used with caution if there is a risk of aspiration pneumonia

Use in patients with concomitant illness; the drug should be used with caution if the patient has cardiovascular or another systemic disease

The presence or absence of additional warnings and precautions indicates within-class safety and tolerability differences between individual SGAs. For example, to date, the U.S. prescribing information includes four additional warnings and precautions for all of the above SGAs, with exceptions as noted:

Weight gain (ziprasidone excepted); the patient’s weight should be monitored

Hyperprolactinemia (aripiprazole excepted); includes risk of galactorrhea, amenorrhea, gynecomastia, and impotence

Hyperlipidemia/dyslipidemia (ziprasidone and asenapine excepted); the patient’s lipids should be monitored

Cerebrovascular accidents, including stroke, in elderly patients with dementia-related psychosis (quetiapine and ziprasidone excepted); SGAs are not approved for dementia-related psychosis

Other, less widespread warnings and precautions distinguishing individual SGAs from one another are noted in the following subsections on specific drugs.

Obsessive-Compulsive Disorder

Symptoms and Signs

Obsessive-compulsive disorder (OCD) is characterized by either obsessions or compulsions. Obsessions are unwanted repetitive thoughts, images, or impulses that the patient has, often themes of threat or danger, and which cause significant distress. Common obsessional content includes fear of impurity, violence, forbidden sexual thoughts, disease, or religious blasphemy. Examples include thoughts of having contracted a deadly illness, or picking up germs, of having run someone over while driving, of having left the stove on, or having molested a child.

Compulsions are the repetitive behaviors that the sufferer performs either in response to the distress associated with the content of the obsessions, or in response to an unwanted drive . Common compulsive behaviors include excessive cleaning (e.g., hand washing), checking, ordering, rearranging, counting, repeating, and mental rituals..

Most patients with OCD have both obsessions and compulsions. In order to have the OCD diagnosis, the patient must find the obsessions or compulsions time-consuming (e.g., take more than 1 hour per day) or cause clinically significant distress or problems in social, occupational, or other important areas of functioning.

Similar Disorders

The new DSM-V published in 2013 has a new section titled “Obsessive-Compulsive and Related Disorders,” which encompasses the disorders OCD, hoarding disorder, body dysmorphic disorder, trichotillomania (hair-pulling disorder) and excoriation (skin-picking) disorder.

Obsessive-compulsive personality disorder (OCPD) is a separate condition, defined as a rigid, perfectionistic personality type. Although patients with OCPD display recurrent themes in their thinking such as over scrupulousness and inflexibility, they do not perceive their traits as being unwanted. Instead they identify with them, which is the opposite of what patients with OCD do.

The symptoms of OCD can occur in patients with other mental disorders, such as with patients depression who have ruminations, psychotic patients who have delusions, and in anxious patients preoccupied by their symptoms, and others. Psychiatric comorbidity is common in OCD,

Clinical Course and Prognosis

The average age at onset of OCD is 21 years, with average onset age varying by gender (19 years for men; 22 years for women (Rasmussen and Eisen 1992). However, 21% of patients report symptoms before puberty. Although onset may occur during other periods of the life span, late-onset OCD is unusual and may be the result of an organic (non-psychiatric) illness

The clinical course of OCD is typically lifelong with waxing and waning symptomatology. Some patients with OCD may experience symptoms during phases, with periods of complete or partial remission in between. Women are at particular risk during pregnancy and the postpartum period. One report found that 57% of women experiencing postpartum depression also experienced obsessional thoughts (Wisner et al. 1999).

Rates of full remission over different time lengths (although all are over years, not months) in different studies have ranged from 6% to 43%. Rates of partial remission reported in these same studies have ranged from 17% to 75% (Eisen et al. 2010). The longest-term follow-up study ever conducted (mean follow-up period of 47 years) found that almost half (48%) of patients reported clinical recovery (defined as no clinically relevant symptoms for at least 5 years). However, only 20% experienced full remission (i.e., complete absence of symptoms for at least 5 years) (Skoog and Skoog 1999).

Prevalence and Public Health Impact

Although OCD was once considered a rare disorder, data from the ECA study found a lifetime prevalence of OCD of between 1.9% and 3.3% in a large sample of U.S. households (Goodman 1999). Epidemiological studies from other countries throughout the world have generally found comparable lifetime prevalence rates of OCD.

Psychiatric comorbidity (having an additional psychiatric diagnosis) is common in OCD, with the Epidemiologic Catchment Area study (1980-1985) finding that two-thirds of patients with OCD met criteria for at least one other psychiatric illness during their lifetime (Karno et al. 1988). The most common comorbid psychiatric diagnosis is major depressive disorder. Approximately one-third of individuals with OCD are currently experiencing a major depressive episode, and two-thirds will have a major depressive episode during their lifetime. Other commonly comorbid psychiatric illnesses include anxiety disorders, eating disorders, and substance abuse/dependence.(Hales et al. 2014)

The disability associated with OCD is severe enough that the World Health Organization has listed OCD among the 10 medical illnesses most likely to cause disability (Murray and Lopez 1996).

Research

Freud (1909-1973) theorized that obsessions were defensive reactions to unconscious impulses, especially sexual and aggressive impulses. Obsessions functioned to mask these impulses and control them. However, even though psychodynamic therapy can reveal underlying origins to the obsessions, doing so has not been shown to relieve OCD symptoms.

The analysis of twin studies found that there is a strong inheritable component to OCD, including a concordance rate (odds of finding the disorder in both twins) of between 80% and 87% in monozygotic twins (genetically identical twins) and between 47%-50% in dizygotic twins (fraternal twins). (van Grootheest et al. 2005) OCD tends to run in families with a study of 1,209 first-degree relatives of an OCD subject (called the proband) showing an increased risk of OCD (8.2%) compared to control subjects (2%). (Hettema et al. 2001). Genetic studies have focused on a number of genes that may be associated with OCD, including serotonin, dopamine, and glutamate.

Neuroanatomical studies have been focused on a major set of circuits in the brain connecting multiple brain centers, named the cortico-striato-thalamo-cortical (CSTC) circuits. These parallel circuits promote different functions from eye movement to cognitive function and affective functions. One of these CSTC circuits, termed the ventral cognitive loop, includes the orbitofrontal cortex, the caudate nucleus, and the dorsomedial thalamus. Functional neuroimaging studies have found functional abnormalities within all nodes of this circuit. These brain regions are hyperactive at rest in patients with OCD compared with healthy volunteers, this hyperactivity is amplified during OCD symptom exacerbation, and the hyperactivity is decreased with successful treatment (Dougherty et al. 2010).

Treatment

Behavioral Therapy

A specific type of behavioral therapy, exposure and response prevention (ERP), has been developed since the 1960s for the treatment of OCD. Patients are first exposed to stimuli that trigger their specific OCD symptoms. For patients with contamination fears, this may involve touching a doorknob or a faucet handle that they perceive as being contaminated. Patients then prevent themselves from responding to the stimuli as they usually would (e.g., a patient who now feels contaminated will avoid washing his hands after touching the contaminated stimulus). Initially patients experience marked anxiety, and it can take a significant amount of time for the anxiety to decrease. As patients repeat their ERP exercises, both the intensity of the anxiety and the time required for it to diminish will gradually decrease until patients become habituated to the stimuli.

ERP is an effective treatment for some patients with OCD and is considered to be a first-line intervention for OCD. Meta-analysis of the many clinical trials for ERP has provided a general estimate of the response rates associated with ERP. Foa and Kozak (1996), using the cutoff for “response” as a 30% or more improvement of OCD symptoms found that across more than a dozen studies the response rate was 76%–83%.

It is worth noting that a few studies comparing ERP with pharmacotherapy have found that ERP is superior to pharmacotherapy (e.g., Foa et al. 2005). Additionally, some studies suggest that combining ERP and pharmacotherapy results in lower relapse rates in patients with OCD when they discontinue pharmacotherapy.

Cognitive Therapy

Cognitive therapy (CT) is a form of psychotherapy that seeks to identify and modify distortions and other maladaptive beliefs. A recent meta-analysis of psychotherapies in OCD (Rosa-Alcázar et al. 2008) found very similar effect size estimates for CT and ERP; however, the CT effect size was only based on three studies. Several recent CT studies not included in the meta-analysis (e.g., Wilhelm et al. 2009) also showed promising results. However, given that the number of CT studies is still relatively small, ERP is currently considered the psychotherapy of choice for OCD.

Pharmacotherapy

The serotonin reuptake inhibitors (SRIs) are usually the first-line medication treatment for OCD (Bandelow et al. 2008). The SRIs include all of the selective serotonin reuptake inhibitors (SSRIs) as well as clomipramine. Meta-analyses have generally found that 40%–60% of patients with OCD achieve response (defined as at least a 25%–35% decrease in OCD symptoms) when treated with SRIs (Greist et al. 1995).

When SRIs are used for treating OCD, it is important that high dosages be achieved (clomipramine up to 250 mg/day, fluoxetine up to 80 mg/day, paroxetine up to 60 mg/day, fluvoxamine up to 300 mg/day, sertraline up to 200 mg/day, citalopram up to 40 mg/day, and escitalopram up to 30 mg/day) because response rates are higher compared with treatment with low doses. Additionally, it is important to note that response may not be achieved until after 8–12 weeks of treatment, which is longer than the time necessary to see a response in treating depression.

Other potential monotherapy approaches to the treatment of OCD generally involve other classes of antidepressants that affect the serotonergic system. Serotonin-norepinephrine reuptake inhibitors (SNRIs) and, possibly, the monoamine oxidase inhibitors (MAOIs) although there is less data for their use. There is no evidence supporting the use of dopaminergic antidepressants (e.g., bupropion) for the treatment of OCD.

There have long been data supporting the use of dopaminergic antagonists to augment the effects of SRIs in the treatment of OCD. Although the initial studies, by included only conventional antipsychotics, newer studies since the advent of the atypical antipsychotics also support their use as augmenting agents with the SRIs.

Because of the lower extrapyramidal side-effect (movement disorder) burden, most clinicians now use the atypical antipsychotics to augment SRIs for the treatment of OCD rather than the older generation antipsychotics. However, it can be argued that the gains of lower extrapyramidal side-effect burden with the atypical antipsychotics are somewhat mitigated by the higher rates of metabolic syndrome (increase in glucose and lipid levels, and weight gain) with many of the atypical antipsychotics, so risks and benefits should be carefully discussed with the physician. Dosages are usually in the low to moderate range (e.g., risperidone 1–4 mg/day), and response after augmentation is typically seen within 1–4 weeks.

More recent pharmacological approaches to OCD treatment include agents that affect the glutamatergic system. Preliminary studies involving memantine, riluzole, and N-acetylcysteine show some promise.

Neurosurgery

Neurosurgical approaches may be effective for patients with severe, intractable OCD that have not responded to all conventional therapies. These approaches include ablative limbic system procedures such as anterior cingulotomy, anterior capsulotomy, subcaudate tractotomy, and limbic leucotomy as well as deep brain stimulation (DBS) electrodes placed at a number of different brain targets. The U.S. Food and Drug Administration (FDA) approved the use of DBS at the ventral capsule/ventral striatum target for treatment-refractory OCD in 2009.

References

Dougherty DD, Rauch SL, Greenberg BD: Pathophysiology of obsessive-compulsive disorders, in Textbook of Anxiety Disorders, 2nd Edition. Edited by Stein DJ, Hollander E, Rothbaum BO. Washington, DC, American Psychiatric Publishing, 2010, pp 287–309
Foa EB, Kozak MJ: Psychological treatment for obsessive-compulsive disorder, in Long-Term Treatments for Anxiety Disorders. Edited by Mavissakalian MR, Prien RF. Washington, DC, American Psychiatric Press, 1996, pp 285–309

Foa EB, Liebowitz MR, Kozak MJ, et al: Randomized, placebo-controlled trial of exposure and ritual prevention, clomipramine, and their combination in the treatment of obsessive-compulsive disorder. Am J Psychiatry 162:151–161, 2005

Goodman WK: Obsessive-compulsive disorder: diagnosis and treatment. J Clin Psychiatry 60 (suppl 18):27–32, 1999

Hales RE, Yudofsky SC, Roberts LW, et al. The American Psychiatric Publishing Textbook of Psychiatry, Sixth Edition, 2014

Hettema JM, Neale MC, Kendler KS: A review and meta-analysis of the genetic epidemiology of anxiety disorders. Am J Psychiatry 158:1568–1578, 2001

Karno M, Golding JM, Sorenson SB, et al: The epidemiology of obsessive-compulsive disorder in five US communities. Arch Gen Psychiatry 45:1094–1099, 1988

Murray CJ, Lopez AD: The Global Burden of Disease. Boston, MA, Harvard University Press, 1996

Rasmussen SA, Eisen JL: The epidemiology and differential diagnosis of obsessive-compulsive disorder. J Clin Psychiatry 55 (suppl):4–10, 1992

Rosa-Alcázar AI, Sánchez-Meca J, Gómez-Conesa A, et al: Psychological treatment of obsessive-compulsive disorder: a meta-analysis. Clin Psychol Rev 28:1310–1325, 2008

Skoog G, Skoog I: A 40-year follow-up of patients with obsessive-compulsive disorder. Arch Gen Psychiatry 56:121–127, 1999

van Grootheest DS, Cath DC, Beekman AT, et al: Twin studies on obsessive-compulsive disorder: a review. Twin Res Hum Genet 8:450–458, 2005

Wilhelm S, Steketee G, Fama JM, et al: Modular cognitive therapy for obsessive-compulsive disorder: a wait-list controlled trial. J Cogn Psychother 23:294–305, 2009

Wisner KL, Peindl KS, Gigliotti T, et al: Obsessions and compulsions in women with postpartum depression. J Clin Psychiatry 60:176–180, 1999

Obstructive Sleep Apnea

Overview

Obstructive sleep apnea (OSA) is a condition characterized by multiple episodes of sleep-related  apnea or hypopnea (loss or decrease in breathing) during sleep, resulting in symptoms such as   snoring, snorting/gasping, or breathing pauses during sleep; and daytime sleepiness, fatigue, or unrefreshing sleep despite sufficient opportunities to sleep.  It occurs in a significant number of people and is associated with major health risks.  Along with an increased risk of drowsy driving and motor vehicle accidents, there is a higher rate of hypertension, stroke, coronary artery disease, insulin resistance, type 2 diabetes mellitus, and perioperative complications.  Individuals with OSA have a 2- to 3-fold increased risk of all-cause mortality compared with those who do not have OSA. 1

Now, recent studies show that OSA and Major Depressive Disorder also tend to co-occur. A 4-year study with controls, run by Peppard and colleagues that included 1400 community-dwelling patients revealed a 2-fold increase in depression with mild OSA and a 2.6-fold increase in depression with moderate to severe OSA.

A large national study by Wheaton and associates 3 showed a high association of sleep apnea and an elevated Patient Health Questionnaire-9 (PHQ-9) score of more than 10 (indicative of moderate depression) with over double of the normal risk.

The prevalence of OSA in the general population differs by age and gender. In men aged 30 to 49 years, the prevalence is 10%; in older men (aged 50 to 70), it is 17% among the general population. The prevalence in women aged 30 to 49 is 3%, and in women aged 50 to 70 it is 9%. 4 it is estimated that 82% of men and 92% of women with moderate-to-severe sleep apnoea have not been diagnosed. 5

The reasons for the co-occurrence of OSA and MDD is not well established. Possible reasons are the fragmentation of sleep, low oxygen states, and disruption of the sleep-wake cycle. It has also been hypothesized that depression may exacerbate or impede recovery of the neuronal injury caused by OSA, specifically in sensitive brain regions responsible for affect and cognition.6 There may also be confounding risks or root causes for both MDD and OSA. These include age, gender, obesity, hypertension, diabetes, and cerebrovascular disease.

There are also neurotransmitters for both sleep and mood regulation, such as serotonin, dopamine, norepinephrine, and g-aminobutyric acid. Serotonin in particular is interesting given its role in depression and also the fact that it influences the strength of muscles in the upper airway that contribute to OSA and plays an important role in causing arousals from sleep.7

Diagnosis

In a general clinical setting, the diagnoses of OSA and MDD can be difficult to diagnose and differentiate from each other due to overlapping symptoms.  Symptoms and signs suggestive of OSA, such as snoring, insomnia, unrefreshing sleep, and excessive daytime sleepiness are often present. In general, patients with comorbid depression tend to report more sleepiness, which is also evidenced by higher Epworth Sleepiness Scale scores.8 A diagnostic polysomnograph (overnight sleep study) is necessary to complete the diagnosis.

Psychological scales that can effectively be used to screen for OSA are the STOP Bang9 questions or the Berlin Questionnaire.10

Treatment

Once the patient completes the PSG, the information from it can be empowering.  It indicates the amount of time spent in a low or zero breathing (apnea-hyponea index), the lowest oxygen saturation during the course of the night, the loudness of snoring, the presence of REM sleep, and periodic limb movements.

The treatment of choice for OSA is positive airway pressure (PAP) therapy, including continuous positive airway pressure (CPAP), bi-level PAP (BPAP), or auto-PAP (APAP). For those who are unable to tolerate PAP therapy, alternative treatments—such as a mandibular advancement device, upper airway surgery, or hypoglossal nerve stimulation therapy—might be considered. Improvement in depressive symptoms has been reported after the treatment of OSA.11-14

CPAP delivers a constant pressure based on a pressure titration study. The pressure keeps the airway open as a pressure column. BPAP delivers 2 different levels of pressure—one for inspiration and the other for expiration (IPAP and EPAP). With APAP the machine can automatically adjust the pressure slowly within a prescribed range based on the patient’s need.

The mandibular advancement device is an oral device that the patient wears inside of the mouth while asleep. This device pulls the mandible forward and opens up the airway in the back of the tongue. Hypoglossal nerve stimulation therapy uses an implanted device to stimulate cranial nerve XII (the hypoglossal nerve); the result is tongue protrusion, which opens up the airway in the back of the tongue as well.  Improvement in depressive symptoms has been reported after the treatment of OSA.8,14-16

References

  1. Young T, Palta M, Dempsey J, et al. Burden of sleep apnea: rationale, design, and major findings of the Wisconsin Sleep Cohort study. WMJ. 2009;108:246-249.
  2. Peppard PE, Szklo-Coxe M, Hla KM, Young T. Longitudinal association of sleep-related breathing disorder and depression. Arch Intern Med. 2006;166:1709-1715.
  3. Wheaton AG, Perry GS, Chapman DP, Croft JB. Sleep disordered breathing and depression among U.S. adults: National Health and Nutrition Examination Survey, 2005-2008. Sleep. 2012;35:461-467.
  4. Peppard PE, Young T, Barnet JH, et al. Increased prevalence of sleep-disordered breathing in adults. Am J Epidemiol. 2013;177:1006-1014.
  5. Ancoli-Israel S, Kripke DF, Klauber MR, et al. Sleep-disordered breathing in community-dwelling elderly. Sleep. 1991;14:486–95.
  6. Cross RL, Kumar R, Macey PM, et al. Neural alterations and depressive symptoms in obstructive sleep apnea patients. Sleep. 2008;31:1103-1109.
  7. Buchanan GF, Smith HR, Macaskill A, Richerson GB. 5-HT2A receptor activation is necessary for CO2-induced arousal. J Neurophysiol. 2015;114:233-243.
  8. Ishman SL, Cavey RM, Mettel TL, Gourin CG. Depression, sleepiness, and disease severity in patients with obstructive sleep apnea. Laryngoscope. 2010;120:2331-2335.)
  9. Farney RJ, Walker BS, Farney RM, et al. The STOP-Bang equivalent model and prediction of severity of obstructive sleep apnea: relationship to polysomnographic measurements of the apnea/hypopnea index. J Clin Sleep Med. 2011;7:459-465.
  10. Netzer NC, Stoohs RA, Netzer CM, et al. Using the Berlin Questionnaire to identify patients at risk for the sleep apnea syndrome. Ann Intern Med. 1999;131:485-491.
  11. Chung F, Yegneswaran B, Liao P, et al. STOP questionnaire: a tool to screen patients for obstructive sleep apnea. Anesthesiology. 2008;108:812–21.
  12. Chung F, Yegneswaran B, Liao P, et al. Validation of the Berlin questionnaire and American Society of Anesthesiologists checklist as screening tools for obstructive sleep apnea in surgical patients. Anesthesiology. 2008;108:822–30..
  13. Finkel KJ, Searleman AC, Tymkew H, et al. Prevalence of undiagnosed obstructive sleep apnea among adult surgical patients in an academic medical center. Sleep Med. 2009;10:753–8.
  14. Habukawa M, Uchimura N, Kakuma T, et al. Effect of CPAP treatment on residual depressive symptoms in patients with major depression and coexisting sleep apnea: contribution of daytime sleepiness to residual depressive symptoms. Sleep Med. 2010;11:552-557.
  15. Povitz M, Bolo CE, Heitman SJ, et al. Effect of treatment of obstructive sleep apnea on depressive symptoms: systematic review and meta-analysis. PLoS Med. 2014;11:e1001762.
  16. Ejaz SM, Khawaja IS, Bhatia S, Hurwitz TD. Obstructive sleep apnea and depression: a review. Innov Clin Neurosci. 2011;8:17-25.

Uses for antidepressants

Given their broad utility, antidepressants are the first line treatments for multiple conditions, especially depression of different kinds and recurrent anxiety.   Most patients (up to 95%) with depression have significant anxiety as well, so antidepressants are the best ongoing treatment for both issues.  Another significant condition for which antidepressants are useful is obsessive condition. Continue reading Uses for antidepressants

Augmentation with other medications: second generation antipsychotics, lithium, thyroid hormone, stimulants

  1. Augmenting with medications that may be antidepressants or antianxiety medications, but possibly not.  This ability to add to the effectiveness of an antidepressant is augmentation
  2. Wellbutrin and Buspar were mentioned earlier.  In addition to possibly relieving chronic side effects, they can sometimes improve the chances of a mildly effective SSRI being more effective (each is also used as a sole medication for some patients).   
  3. Serotonin enhancing antidepressants:  SNRIs, Remeron, TCAs, even MAOIs, be mixed and matched.  The main side effects to be monitored when doing this are i) liver enzyme interactions: some of these medications are metabolized (broken down) by liver enzymes that are inhibited by newer antidepressants, causing the blood levels of older ones like the TCAs to possibly rise to dangerous levels ii)
  4. Second generation antipsychotic medications, or SGAs.  These medications are named for their use in treating psychotic disorders; however they have found usefulness for treating anxiety and depression as well.  Like the SSRI’s, they are offshoots of older medications first used in the 1950’s, in this case the first generation antipsychotics, drugs such as haloperidol and fluphenazine.  Like the first antidepressants, the FGAs were discovered serendipitously in the course of testing drugs used for other indications.  The understanding of their chemical activity would drive the “dopamine blockage hypothesis” of treating psychosis.  In short, delusions and hallucinations, which form the elements of psychosis, originate from aberrant signals traveling along specific neural pathways that use dopamine as a neurotransmitter.  By blocking the dopamine receptors there, antipsychotics are able to inhibit psychotic thought processes.
     

    However, just as TCA’s and MAOIs had heavy side effects limiting their use, so did the first generation antipsychotics: most prominent of these were severe movement disorders and impaired cognition.  Over the past 3 decades, however, a new generation of antipsychotics have been developed with reduced motor effects, leading to a greater acceptance of their use, similar to what happened with the SSRIs.  The SGA, or second generation antipsychotics, have fewer movement and cognitive side effects but also enhancement in mood.  These new drugs modulate not only dopamine signals in the brain but also serotonin signals.  As a result, they found a use for a new population of patients who did not necessarily have psychotic symptoms.  In conjunction with antidepressants, they were found to increase their efficacy of the antidepressant for an unresponsive patient.   One reason they are thought to be particularly effective is that they modulate 2 particular serotonin receptors in a unique way.  

    They increase the signal strength through the 5HT-1a receptor mentioned earlier, thought to be responsible for largely responsible for the antidepressant and antianxiety effects of serotonin-enhancing medications.  They also inhibit signals through the 5HT-2a receptor, thought to be a receptor that counteracts the effects of 5HT-1a.  This one-two punch is thought to allow SGAs to work quickly, sometimes within 1-2 weeks, to relieve depression and anxiety.   As one can imagine, this makes SGAs particularly useful in urgent cases of depression.  Often, SGAs and benzodiazepines are used in the initially stages of severe anxiety and depression.  Dose titrations are simple with SGAs since they are used at lower doses than are used when treating as a psychotic disorder like schizophrenia.  However, caution needs to be heeded.  Although they have fewer motor effects, they are not the FGA’s because they increase the risk of a “metabolic syndrome”: hyperlipidemia (high triglycerides and LDL cholesterol) diabetes, and high blood pressure.

  5. Lithium:  There is a solid body of evidence supporting lithium as an effective and generally well tolerated augmentation medication. Of all the adjunctive medications, lithium is the most extensively studied and may also reduce the long-term risk of suicide. The manner in which lithium augmentation is effective is unclear but has been hypothesized to be due to sensitisation of serotonin receptors. Other neurotransmitter systems such as noradrenergic transmission and other messenger systems have also been theorized. Lithium plasma concentrations are drawn to achieve therapeutic levels (0.4 to 1 mmol/L).  Side effects include nausea, diarrhoea, abdominal pain, muscle weakness and fine tremor.  The interval before full response to adjunctive lithium is said to be in the range of several days to 6 weeks.  The main concern over chronic treatment with lithium is that thyroid and kidney function be monitored at least yearly.  

    In a small percentage of patients, usually bipolar patients, who require higher doses of lithium, there will be a decline in functioning of these 2 body systems.  While this often does not cause a pragmatic issue with the majority of patients, even the ones who show a decline, the biggest concern is with a small number of patients who eventually go on to develop renal failure and require dialysis.  It is unclear who will have that complication, but it often is associated with patients who have been exposed to high levels, e.g. In older patients who do not drink enough fluids and become dehydrated.

  6. Thyroid hormone: Thyroid hormone supplementation, even in patients with normal thyroid function, may increase the effectiveness of antidepressant medication treatment, whether used as an augmentation agent (445, 446) or in combination with an antidepressant from the outset of therapy (447). The dose typically used for this purpose is 25 mcg/day of triiodothyronine, in- creased to 50 mcg/day if the response is inadequate after about a week. The duration of treatment required has not been well studied.  The risk in patients without a pre-existing cardiac condition is fairly low.
  7. Stimulants: Many clinicians find that augmentation of antidepressants with low doses of stimulants such as methylphenidate or dextroamphetamine may help improve otherwise suboptimally responsive depression, although not all clinical trials have shown benefits from this strategy.  What stimulants can do is restore functionality to patients, allowing them to mobilize and complete tasks that would otherwise hang over them and cause them further stress if left undone.  They may also lead to patients becoming involved in social or therapeutic activities that can improve mood.  Stimulants can worsen or exacerbate cardiac problems and can be addictive in certain patients, so a history of addictive disorders and a cardiac history should be ruled out..

Making the decision to take an antidepressant_former

When patients seek treatment for emotional or mental problems, it often comes after a long delay, after patients have had repeated episodes of feeling distraught and out of control.  It can be years.  Unlike the denial associated with having physical symptoms, associated with the fear of finding out that there is something serious going on, the denial with mental conditions triggers a deeper denial about there being anything wrong with oneself.  We accept our reactions to the world to be rational, attributing cause of symptoms to external factors.  As an example, if our heart races and we feel fear after hearing something critical from another person, our immediate instinct is that they are threatening to us and not on our side.  Sometimes a person can live that way for years, feeling misunderstood and menaced by others.  If insight later comes, it is a chance for the perpetual chain of misunderstanding to be broken.  It often takes the form of a vague sense of recognition after the fact that our reactions were inappropriate or excessive and that the anxiety was self-generated, albeit triggered by hearing something.

 

If that patients goes to talk therapy, there may be relief; having another person witness and hear the details of our suffering allows that person to provide both support and objective reflection.  Through support patients previously suffering alone in shame finds someone who validates them. Through the therapist’s reflection, patients see dysfunctional parts of themselves as foreign to the image of who they are.  Change then naturally follows.  Resistance to talk therapy takes different forms.  There may be shame from the thought that a person must be worthless or unloveable to have to pay another person to listen to him/her.  Resistance to  talk therapy can also stem from the feeling of humiliation, from the belief that  opening oneself up to be questioned is like an interrogation, leading to brainwashing to occur in their service of another person’s motives.  

 

When talk therapy is not enough, when patients have gone over the same themes and subjects over and over again, patients may be advised to consider psychiatric medication.  Here there is resistance again.  There may be shame because the patient feels she/he can longer be helped by others, that one is so damaged that chemical alteration of who we are is necessary.  There is the fear of alteration of our thoughts, fear of changing our thoughts not to a therapist’s choosing, but to a pill that can take away our feelings or sense of ourselves, leading to the fear of loss of control.  We all depend on our internal self-image and our feelings as an internal compass to make decisions and take care of ourselves.  

 

There is another sort of patient who is reluctant to try psychiatric medications, not fearing the unknown, but because they think they know what the drugs do and that it is not a good thing.  They associate antidepressants with opiates and seem them as pain-relieving medications with the same numbing effects towards emotions as opiates have towards physical pain.  Thus like opiates can cover up true pathology if taken irresponsibly, they see antidepressants as covering up the perception of reality.  They also see antidepressants can causing dependency and drug-seeking behavior as opiates.  This returns us to a previous paragraph in which I discussed how benzodiazepines treat the sensations of anxiety, while antidepressants treat the symptoms by treating the disordered thinking behind anxiety and depression.  Patients think antidepressants act like benzodiazepines.

 

What they do not appreciate is that antidepressants, when working correctly is supposed to relieve emotional pain in more than an immediate sense.  Yes, in the immediate sense, they can take away tearfulness, the pain of loss, loss of pleasure, poor sleep and appetite.  Plus, they also address thoughts like helplessness and hopelessness that define a dismal world view that gives us feelings of depression.  This second fact is what is unexpected and maybe counterintuitive.

Hello world!

Welcome!  This is the premiere of my website, designed for my patients, colleagues and others interested.  My hope is that over time, the information will be a source of knowledge I’ve gained working with my generous patients,  and may spark further discussion about future directions in mental health treatment.