Differential Diagnosis Flashcards
Reactive dysphoria
Relatively low-grade mood changes—sadness, disappointment, despair—that occur in response to minor losses and disappointments. The emotional responses are considered to be normal and appropriate. They are transient, and most importantly, these mood disturbances do not typically interfere with functioning; that is, they have little impact on academic, occupational, or social or interpersonal functioning.
Grief, or uncomplicated bereavement
Is a normal and emotionally necessary response to major losses, such as death of a loved one or divorce. Most normal grief reactions result in significant degrees of emotional distress for a period of six to twelve months, and continued, albeit sometimes less intense, grieving may last for an additional two to four years.
When grief becomes clinical depression?
Marked erosion of self-esteem Agitation* Early morning awakening* Serious weight loss* Psychotic Symptoms* Suicidal ideation or attempts Anhedonia (loss of the ability to experience any pleasure)* Marked impairment of social, interpersonal, academic, or occupational functioning
*Antidepressants recommended
Three types of clinical depression
Major unipolar depressions: reactive, biological, reactive-biological, atypical
Bipolar disorder: manic and depressive episodes
“Minor” depressions: dysthymia, chronic residuals of partially recovered major depressions
Core depression symptoms
Mood of sadness, despair, emptiness Anhedonia (loss of the ability to experience any pleasure) Low self-esteem Apathy, low motivation, and social withdrawal Excessive emotional sensitivity Negative, pessimistic thinking Irritability Suicidal ideas
Biologically based depressive disorders
Are not seen as a reaction to stressors. In fact,
they can emerge apparently spontaneously, “out of the blue”—in individuals encountering little in terms of life
stress. The trigger for biological depressions can be traced to any of a number of conditions that alter
neurotransmitter function in key areas of the limbic system.
Four reasons for biological depressions
Medical illnesses that lead to systemic changes and ultimately to brain dysfunction
Female sex-hormone fluctuation, especially noted postpartum, during meno- pause, and
premenstrually.
Medications and recreational drugs
Endogenous biological depressions
Physiological symptoms of depression
Appetite disturbance—decreased or increased, with accompanying weight loss or gain
Fatigue
Decreased sex drive
Restlessness, agitation, or psychomotor retardation
Diurnal variations in mood—usually feeling worse in the morning
Impaired concentration and forgetfulness
Pronounced anhedonia—total loss of the ability to experience pleasure
Sleep disturbance—early morning awakening, frequent awakenings throughout the night;
occasionally hypersomnia (excessive sleeping).
Note that initial insomnia (difficulty in falling asleep)
may be seen with depression but is not diagnostic of a major depressive disorder. Initial insomnia can
be seen in anyone experiencing stress in general. Initial insomnia alone is more characteristic of
anxiety disorders than of depression.
Atypical depression
Most cases of bipolar depressions present with atypical symptoms
Reactive dysphoria—sadness or despair comes and goes in response to psychological stressors
Profound fatigue, low energy
Hypersomnia (excessive sleeping)
Increased appetite and weight gain
Marked sensitivity to interpersonal rejection or separation
Psychotic depressions
Major depression and bipolar illness can, if extremely severe, manifest psychotic symptoms. Typically, the hallucinations and delusions seen in psychotic mood disorders are said to be “mood congruent,” which means that the themes of these symptoms are congruent with the dominant mood. For example, a psychotically depressed patient might have delusions that she is the most disgusting or evil person in the world and should be executed. This delusional belief embodies the depressive themes of extremely low self-esteem and guilt.
Possible bipolar disorder markers
Depressive symptoms that include hypersomnia (excessive sleeping), severe fatigue, increased appetite, carbohydrate craving, and weight gain. This group of symptoms, as noted earlier, is often referred to as “atypical symptoms.”
Psychotic symptoms (e.g., delusions or hallucinations).
A family history of bipolar disorder.
Physiological consequences to depression
Extraordinarily high, sustained levels of cortisol (hypercortisolemia), seen in about 50 to 60 percent of
those with major depression, have been associated with cell death in the hippocampus, atrophy of the
anterior cingulate (a subcortical frontal-lobe brain structure) and damage to the interior walls of arteries. Hypercortisolemia in depressed mothers during pregnancy may be harmful to the fetus
Abnormal brain metabolic states occur during depressive episodes, including:
Hypometabolism in the frontal lobes (especially the medial-orbital area; anterior cingulate; and lateral, dorsal prefrontal cortex).
Hypermetabolism in hypothalamus, amygdala, hippocampus, and infra- limbic cingulate (area 25)
Reductions in secretion of growth hormone that may contribute to osteoporosis, and retarded growth
and failure to thrive in children and elders.
High cortisol levels leach out minerals from bone and contribute to osteoporosis.
Immune-suppression (likely due to multiple factors, including chronic sleep deprivation and hypercortisolemia).
Reduced synthesis of brain-derived neurotropic factor (BDNF), which is essential for neuronal maintenance, repair, and neurogenesis
Possible depression treatments
Electroconvulsive therapy (ECT) High-intensity light therapy Repetitive Transcranial Magnetic Stimulation (rTMS) Vagus nerve stimulation Deep brain stimulation Exercise Psychotherapy Psychosurgery (rarely used)
Bipolar disorders
are mood disorders characterized by the essential diagnostic feature of mania or hypomania. In general, these disorders follow cyclic patterns of mood, energy, behavior, and thought alterations, alternating between mania or hypomania and depression.
Mania
Mania rarely occurs as a primary psychiatric condition by itself, so the presence of a manic episode usually
leads to a diagnosis of bipolar I disorder, even in the absence of depressive history. The manic episode as
defined by DSM-5 is “a distinct period of abnormally and persistently elevated, expansive, or irritable mood
and abnormally and persistently increased goal-directed activity or energy, lasting at least one week and present most of the day, nearly every day (or any duration if hospitalization is necessary)”
Additionally, episodes are defined as mild, moderate, or severe.
Diagnostic critera of mania episode
combinations of: racing thoughts pressured speech grandiosity increased energy and goal-directed activity engaging in pleasurable activities distractibility decreased need for sleep.
Additional diagnostic criteria include
marked social or occupational impairment hospitalization
psychotic features.
Further disorders to rule out in the differential diagnosis include attention-deficit/hyperactivity disorder, chizophrenia, and schizoaffective disorder.
Stages of acute mania
Stage 1 (corresponds with hypomania): Increased psychomotor activity Emotional lability Euphoria or grandiosity Coherent but tangential thinking
Stage 2 (frank mania): Increased psychomotor activity Heightened emotional lability Hostility, anger, impulsivity Assaultive or explosive behavior Flight of ideas, cognitive disorganization Possible grandiose or paranoid delusions
Stage 3 (exhibited by some patients):
Frenzied psychomotor activity
Incoherent thought processes
Ideas of reference, disorientation, delirium
Florid psychosis (indistinguishable from other psychotic disorders, although usually mood congruent)
Medical conditions associated with mania
CNS trauma (eg. post-stroke) Metabolic diseases (hyperthyroidism) Encephalitis Seizure disordes CNS tumor
Drugs that can induce mania
Stimulants (amphetamines) Antidepressants (esp tricyclic) SAM-e Antihypertensives Corticosteroids in higher doses Anticholinergics (benztropine, trihexyphenidyl) Thyroid hormones (levothyroxine)
Bipolar I disorder
One or more manic episodes constitute the diagnosis of bipolar I disorder. There may be preceding or subsequent episodes of hypomania or depression. A depressive episode in bipolar disorder meets diagnostic criteria for major depression.
Between episodes, most bipolar patients are relatively asymptomatic, although many will continue to experience functional impairment after symptom resolution. With increasing age, episodes become more frequent and prolonged.
Bipolar II disorder
Bipolar II disorder is defined as one or more depressive episodes and at least one episode of hypomania.
It has been postulated that bipolar II is difficult to differentiate from major depression, for several reasons. First, many patients subjectively do not recognize periods of elevated mood as dysfunctional—or may even deny the existence of such periods because of the predominate depressive element.
Second, the patient may primarily manifest irritability rather than classic mood and behavior symptoms of hypomania. Finally, there is considerable variation between individual clinicians’ ability to reliably assess for hypomania. Despite the differences in severity between mania and hypomania, bipolar II disorder can be chronic and disabling, and carries a substantial suicide risk.
Diagnostic specifiers for bipolar
Episode severity Remission status With anxious distress With mixed features With rapid cycling With melancholic features With atypical features With mood-congruent psychotic features With mood-incongruent psychotic features With catatonia With peripartum onset With seasonal pattern
Rapid bipolar cycling
Rapid cycling is defined as at least four episodes of mania, hypomania, or major depression in the previous twelve months. The characteristics of rapid cycling are these:
Estimated incidence: 10 to 20 percent of bipolar patients.
Of rapid cyclers, 70 to 90 percent are women (no link to menstrual cycle or menopausal status).
May be associated with hypothyroidism, neurological conditions, head injury, intellectual disability, and/or substance abuse.
Poor lithium response.
Cycle acceleration may be associated with antidepressant use.
Poor long-term prognosis.
Most cases of rapid cycling represent a time-limited complication of bipolar illness that lasts from a
few months to one and one-half years.
Cyclothymic disorder
The features of cyclothymic disorder include numerous periods of alternating depressive symptoms with
hypomanic symptoms, of at least two years’ duration, that do not meet criteria for either major depression or
hypomania.
During this two-year period, symptoms are present at least half the time and never absent for more than two months. Social and occupational impairment may occur during the depressive phase but, typically, not during the hypomanic period.
Cyclothymia disorder criteria
History of numerous periods of alternating depressive and hypomanic symptoms
Symptoms do not meet criteria for a hypomanic, manic, or depressive episode
Not due to organic factors, substance abuse, medical condition, or other psychiatric disorder
Symptoms of anxiety
Trembling, feeling shaky, restlessness, muscle tension
Shortness of breath, smothering sensation
Tachycardia (rapid heartbeat)
Sweating and cold hands and feet
Light-headedness and dizziness
Paresthesias (tingling of the skin)
Diarrhea, frequent urination, or both
Feelings of unreality (derealization)
Initial insomnia (difficulty falling asleep)
Impaired attention and concentration
Nervousness, edginess, or tension
Generalized anxiety disorder
Generalized anxiety disorder is characterized by chronic, low-level anxiety (without panic attacks). Patients with this disorder may have no specific current stressors. Life in general is stressful for them. Such people are often high-strung and are chronic worriers
Anxiety associated with acute psychological stressors
In such disorders, anxiety symptoms are not evident prior to the onslaught of stressors; preclinically the person functioned well. Symptoms emerge in the wake of acute life stress.
Specific phobias
These phobias involve fears of specific objects, such as dogs, places, or heights. Anxiety is seen only in the phobic situation.
Social phobias / anxiety
Social phobias involve serious anxiety symptoms experienced only when the person is in social or interpersonal settings, such as speaking before a group, participating in a social gathering, or asking someone for a date.
Agoraphobia without panic
This disorder is characterized by intense fears of being in situations or places from which escape might be difficult or embarrassing. As in other phobias, the anxiety is accompanied by a strong tendency to avoid being in such feared places. Agoraphobia commonly develops in the course of panic disorder, but in agoraphobia without panic, there is no history of full-blown spontaneous panic attacks (see “Panic disorder,” below).
Experiences of anxiety are always associated either with entry into a feared place or situation, such as entering a crowded store, or with anticipation of such an event.
Neurotic anxiety
Neurotic anxiety arises when an individual is beset by significant emotional issues or conflicts but maintains tight defenses against awareness of these inner issues. In other words, the conflicts are unconscious, and what one sees overtly are anxiety symptoms—often “generalized” and sometimes in the form of occasional panic attacks. Another version of neurotic anxiety is seen in individuals who are plagued by more conscious
conflicts. Often such conflicts take the form of approach-avoidance, such as the person very much wanting to do something but worrying about offending others or violating certain internalized rules or “shoulds.” The person feels inwardly torn and will often experience feelings of generalized anxiety.
Panic disorder
Panic disorder is characterized by recurring, intense panic attacks. Many times these attacks appear to be spontaneous, not provoked by identifiable stressors. As the disorder progresses, most patients begin to develop considerable anticipatory anxiety (a rather continuous, mild-to-moderate generalized anxiety as they come to worry when the next attack will occur) and phobias (agoraphobia is especially common). With time, alcohol
abuse and depression commonly develop.
GAD and medication
In GAD the individual is almost continuously predicting, anticipating, or imagining “dangerous” (unpleasant) events. The limbic system is kept in a perpetual state of alert—on guard for a multitude of “whatifs.” Since daily life rarely presents GAD patients with severely traumatic or life-threatening events, the level of activation does not reach the intensity of threshold of full-blown fight or flight. The result is a low-grade, but chronic, state of anxiety.
GAD is primarily believed to be a psychogenic disorder. However, there is some speculation that at least some GAD patients may suffer from a biologically mediated disorder. One hypothesis is that mentioned above: a deficiency of neurochemicals. Another model has emerged more recently. Treatment with serotonin agonists such as buspirone and 5-HT antidepressants (SSRIs and SNRIs) has been shown to reduce “whatifing” (worry) in GAD patients. However, the mechanism of action and underlying pathophysiology are not well understood.
Stress-induced anxiety disorders and medication
In stress-induced anxiety disorders, actual psychological stressors have evoked another version of ongoing limbic alert. And in the wake of severe stress, such patients often may have occasional full-blown panic attacks. These disorders emerge in response to life-threatening stressors (natural disasters, combat, assaults, automobile accidents) and in response to a host of emotional stressors (loss of a job, serious illness in a relative, marital separation). In many cases, the anxiety symptoms can be seen as normal responses; that is, they are not pathological. However, the symptoms can be severe enough to warrant treatment.
Phobias and medication
Phobias such as the fear of snakes, closed-in spaces, heights, and so on, are generally considered to be associated either with age-appropriate fears (fears that subside with maturation) or conditioned responses. There is little evidence that these disorders are due to biological dysfunction, and medication treatment is generally not warranted
Social phobias and medication
One view is that the underlying fear in many social phobias is that the person will be embarrassed, humiliated, and ultimately rejected, which is equivalent to separation. This fear of rejection is also seen in avoidant personalities, so-called hysteroid-dysphorics, and many people suffering from borderline personality disorders. Animals treated with antidepressants or MAO inhibitors (drugs shown to reduce excitation in the LC) exhibit markedly decreased distress in the face of separation stresses. And during the past decade, clinical trials with antidepressants and MAO inhibitors have shown improvement in broad groups of patients with social phobias and rejection sensitivity. The theory contends that such patients may be chronically experiencing very low thresholds of arousal at the level of the LC—accounting for their exquisite sensitivity to humiliation, separation, and rejection.
Agoraphobia without panic and medication
The anxiety experienced with this disorder occurs only when the patient must go into feared situations (such as a store) or in the moments before entering the phobic situation (anticipating anxiety). Although such experiences of anxiety ultimately do involve an activation of the limbic system, the primary disorder is felt to be largely psychogenic, a conditioned fear response. Medications are sometimes used to treat agoraphobia without panic; however, this disorder is not believed to be primarily biologically based.
Panic disorder and medication
Antipanic medications (especially antidepressants) are hypothesized to have their effect by normalizing the operation of LC inhibitory receptors. Other molecules that also have been found to exert inhibitory effects on LC neurons include: serotonin, GABA, adenosine, and opiates. This helps to explain how SSRIs are often useful in treating panic disorder, and how certain minor tranquilizers may reduce panic symptoms (e.g., alprazolam, lorazepam, and clonazepam along with GABA activate chloride ion channels). Although opiates are not approved or indicated for use in treating anxiety disorders, many narcotic addicts may be self-medicating with opiates to reduce anxiety symptoms. Caffeine blocks adenosinic receptors, which also reduces inhibitions.
Neurotic anxiety and medication
Although the term neurosis has fallen out of favor in some professional circles, the concept still has merit. As conceived of here, neurotic anxiety is a condition in which manifest symptoms of anxiety are evident but the underlying problem can ultimately be traced to unconscious conflicts or unrecognized inner emotional issues.
GAD treatments
Benzodiazepines (the class of drugs often termed minor tranquilizers or anti-anxiety medications) can be used in severe cases of GAD. The vast majority of chronically anxious patients do not abuse or become addicted to these medications and rarely require progressive increases in doses. The individuals who do, in fact, present a significant risk of abuse are people with a personal or family history of alcohol or other substance abuse. With such individuals, benzodiazepines are not appropriate.
The atypical antianxiety medication buspirone has been used with some success with GAD patients. This medication offers the benefits of reduced rumination and worry, but without the problems of sedation and potential drug dependence seen with benzodiazepines. Buspirone is not addictive and thus provides a treatment option for GAD patients with substance abuse risk.
Both tricyclic and serotonergic antidepressants (SSRIs and SNRIs) are being used increasingly to treat chronically anxious patients.
The antiseizure medication gabapentin, primarily used to treat anxiety in bipolar disorder, is a nonhabit-forming drug. In England, Lyrica is approved for treating GAD
Acute stress treatments
For most individuals, psychological approaches are best suited for treating acute stress reactions. However, antianxiety medications can be an important adjunct to treatment, especially when the patient is experiencing considerable amounts of agitation or insomnia. The classic form of anxiety-related insomnia is initial insomnia (difficulty falling asleep). Middle insomnia or early morning awakening should alert the clinician to a diagnosis of depression. Medications used to treat daytime anxiety include the whole range of benzodiazepines, and for sleep, the so-called sedative-hypnotics.
Typically, drug treatment for acute stress is short-term (one to four weeks), in combination with crisis intervention and other psychological
treatments.
Social phobias treatment
Specific phobias generally are not treated with psychotropic medications. Social phobias often respond well to cognitive-behavioral treatment.
When medications are used, the clinician has two main alternatives: For occasional use—for example, to reduce anxiety associated with theatrical performances or public speaking —the beta blocker propranolol has been shown to be quite effective. This drug does little to alter the cognitive
aspects of anxiety (worry) but effectively reduces many physiological symptoms, such as rapid heart rate. Anxious patients treated with propranolol take the medication only prior to the stressful event, ingesting 10 to 80 mg about one hour before.
More pervasive forms of social anxiety (and avoidant personality disorder) may be treated with MAO inhibitors, SSRIs, or SNRIs, in addition to psychotherapy and social-skills training.
Agoraphobia without panic treatment
Medication treatment as a sole therapy generally is not effective. However, patients are often treated with psychotropic medications in the early phase of graded exposure therapy. Minor tranquilizers (benzodiazepines) and beta blockers (such as propranolol) can be used to somewhat reduce the level of anxiety as the patient begins gradually to reenter anxiety-provoking situations. As the patient starts to experience success and a sense of mastery, the medications can be gradually phased out.
Neurotic anxiety treatment
In neurotic anxiety, medication treatment is generally contraindicated, since the reduction of overt anxiety symptoms can serve to further block awareness of core emotional conflicts. The exceptions are these:
If the patient has inadequate ego strength to tolerate a more “uncovering” psychological approach.
If the patient is not psychologically minded or has a low level of cognitive functioning.
If the clinician must work with a highly symptomatic client in very brief therapy.
If manifest anxiety symptoms are severe. In such cases, short-term treatment with benzodiazepines may help reduce suffering, restore functioning in daily life, and help the patient stabilize. This can then be followed by medication reduction and psychotherapy
Panic disorder
Panic disorder is the anxiety disorder for which medication treatment plays its most important role. This often-devastating illness is quite responsive to combined medication and psychological treatment. It is helpful to focus on four somewhat discrete aspects of this disorder, each of which requires targeted treatments:
Panic attacks
Anticipatory anxiety
Phobias
Associated features—alcohol abuse, depression
Panic attacks must be either eliminated or greatly reduced in the initial phase of treatment. Some behavioral and cognitive techniques have been developed to reduce panic attacks, although antipanic medications take effect more rapidly and have a solid track record as safe and highly effective drugs. Antipanic medications fall into three groups:
High-potency benzodiazepines, such as alprazolam, clonazepam, and lorazepam
Antidepressants (tricyclics, SNRIs, and SSRIs)1
MAO inhibitors
The first goal of treatment is to stop or reduce attacks. However, even when this is successful, anticipatory anxiety and phobias can, and often do, continue unabated. Thus, the second step is to reduce anticipatory anxiety and phobic avoidance using behavioral techniques, especially graded exposure and desensitization. These techniques are highly effective but only after there is good containment of panic symptoms.
Often, especially in more chronic cases, major depression and alcohol abuse/dependency, or both develop along with primary panic symptoms. In that event, appropriate antidepressant medication treatment and/or involvement in Alcoholics Anonymous or a chemical-dependency treatment program becomes necessary.
Finally, when primary anxiety or panic symptoms are resolved, many panic disorder patients often choose to pursue more traditional psychotherapy. As mentioned earlier, a number of panic patients have encountered major losses and must begin the journey of working through these major life changes. In our experience, however, insight-oriented treatment typically must await the resolution of primary panic symptoms.
