The Dark side of Hypomania

The Dark Side of Hypomania

While working on the American Psychiatric Association’s latest DSM version of bipolar disorder (IV-TR), Trisha Suppes MD, PhD of the University of Texas Medical Center in Dallas carefully read its criteria for hypomania, and had an epiphany. “I said, wait,” she told a UCLA grand rounds lecture in April 2003, “where are all those patients of mine who are hypomanic and say they don’t feel good?”

The DSM defines hypomania as “a distinct period of persistently elevated, expansive, or irritable mood,” but the overwhelmingly standard misconception is one of unadulterated exuberance. Ask your typical patient about hypomania and he or she will fondly recall those life-of-the-party and unbelievably productive moments and reply, “if only I could put it in a bottle and sell it.” And a psychiatrist off the record may add, with a hint of envy, “if only I could buy it.”

But what about road rage and other destructive behaviors? The DSM recognizes “mixed” states in mania where highs and lows simultaneously run riot in the brain, but nowhere does it acknowledge a parallel phenomenon in hypomania. Does mixed hypomania exist and how common is it? Dr Suppes decided to find out. The results of her seven-year investigation appear in the October Archives of General Psychiatry.

Drawing from patients in seven clinics associated with the Stanley Foundation Bipolar Treatment Network, Dr Suppes and her colleagues gathered prospective data on 908 bipolar patients (most by far with bipolar I). Of 14,328 visits by patients, 1,044 involved hypomania. Examinations of the patients in this state found that the majority (57 percent) “met criteria for mixed hypomania.”

By “mixed hypomania,” patients must have met the researchers’ threshold for at least mild hypomania (corresponding to a YMRS score of 12 or greater) combined with at least mild depression (corresponding to an IDS-C score of 15 or greater).

Patients with bipolar I were far more likely to experience hypomania than those with bipolar II, though the likelihood of mixed states within each diagnosis remained about the same. Women were significantly more likely to experience mixed states than men (72 percent vs 42 percent). Women in the study with no hypomania had a 41 percent probability of experiencing depression. This increased to 66 percent with mild hypomania and 81 percent with moderate hypomania, then dipped back to 67 percent with severe hypomania.

Although there was no association between hypomanic and depressive symptoms in men, the authors of the study concluded that “men are far more likely to be irritable and agitated when hypomanic.”

Dr Suppes and her colleagues observe that one reason bipolar II patients are misdiagnosed with depression is “the expectation that hypomania is predominantly euphoric.” Patients tend not to report mixed episodes and psychiatrists often fail to ask the right questions. The result, they say, may lead to inappropriate treatments, such as antidepressant monotherapy which may induce increased cycling.

Read on …

Dysphoric Hypomania

The unofficial title of Dr Mood Spectrum belongs to Hagop Akiskal MD of the University of California, San Diego. Entering “mixed” to his name on PubMed turns up 47 published articles. His latest one, in the October Bipolar Disorders, reinforces Dr Suppes’ study and adds new insights.

From a sample of 320 bipolar II patients, Dr Akiskal and frequent collaborator, Franco Benazzi MD of the Hecker Outpatient Center (Ravenna) focused on 45 who presented with both hypomania and major depression. This meant that euphoric mood was absent. Instead, hypomania was based on the often overlooked DSM criteria for irritable mood plus four hypomanic symptoms.

The authors define this hypomania-major depression double-whammy as “dysphoric hypomania,” which roughly corresponds to Dr Suppes “mixed hypomania,” but sets a higher threshold involving more severely ill patients.

Comparing these patients to the “pure” bipolar II patients in the study found that those with dysphoric hypomania experienced more agitated depressions by a wide margin (86.6 percent vs 5.8 percent) and evidenced more atypical features (such as mood reactivity). Hypomanic symptoms included racing thoughts, distractibility, being more talkative, excessive risky activities, and increased goal-directed activity. Women were more likely to experience dysphoric hypomania than men.

Clearly, these individuals require urgent attention. Unfortunately, say the authors of the study, this “dark facet” of hypomania “is likely to be relegated to the domain of erratic personality disorders.”

Based on their previous work and the work of others, the authors propose a continuum of mixed states that includes:

DSM-IV mixed state (dysphoric mania).
Mixed mania (mania with a few depressive symptoms).
Dysphoric hypomania (hypomanic episode plus full major depression).
Depressive mixed state (major depressive episode plus a few hypomanic behaviors. A landmark 2001 study by the same authors found at least two hypomanic symptoms in 73.1 percent of bipolar II depressions and 42.1 percent of unipolar major depressions. Three or more hypomanic symptoms were found in 46.3 percent of bipolar depressions and 7.8 percent of unipolar depressions.).
Agitated depression.
Think road rage, tall, venti, and grande, potentially dangerous in any brew. How safe are you?

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Treatment of A Typical Depression with cognitive Therapy

Abstract

BACKGROUND:

Patients with atypical depression are more likely to respond to monoamine oxidase inhibitors than to tricyclic antidepressants. They are frequently offered psychotherapy in the absence of controlled tests. There are no prospective, randomized, controlled trials, to our knowledge, of psychotherapy for atypical depression or of cognitive therapy compared with a monoamine oxidase inhibitor. Since there is only 1 placebo-controlled trial of cognitive therapy, this trial fills a gap in the literature on psychotherapy for depression.

METHODS:

Outpatients with DSM-III-R major depressive disorder and atypical features (N = 108) were treated in a 10-week, double-blind, randomized, controlled trial comparing acute-phase cognitive therapy or clinical management plus either phenelzine sulfate or placebo. Atypical features were defined as reactive mood plus at least 2 additional symptoms: hypersomnia, hyperphagia, leaden paralysis, or lifetime sensitivity to rejection.

RESULTS:

With the use of an intention-to-treat strategy, the response rates (21-item Hamilton Rating Scale for Depression score, < or =9) were significantly greater after cognitive therapy (58%) and phenelzine (58%) than after pill placebo (28%). Phenelzine and cognitive therapy also reduced symptoms significantly more than placebo according to contrasts after a repeated-measures analysis of covariance and random regression with the use of the blind evaluator's final Hamilton Rating Scale for Depression score. The scores between cognitive therapy and phenelzine did not differ significantly. Supplemental analyses of other symptom severity measures confirm the finding.

CONCLUSIONS:

Cognitive therapy may offer an effective alternative to standard acute-phase treatment with a monoamine oxidase inhibitor for outpatients with major depressive disorder and atypical features

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How common is A Typical Depression

In addition to the core symptoms of depression, atypical depression is defined by the ability to feel better temporarily in response to a positive life event, plus any two of the following criteria: excessive sleep, overeating, a feeling of heaviness in the limbs and a sensitivity to rejection.

Patients with atypical depression tend to have an earlier age of onset than those with other subtypes (it often first appears in the teenage years). These patients are also likely to have a history of social phobia, avoidant personalities and a history of body dysmorphic disorder.1

How Common Is Atypical Depression?

Despite the name, atypical depression is actually the most common subtype, according to Dr. Andrew A. Nierenberg, associate director of the depression clinical and research program at Massachusetts General Hospital, Boston. In a 1998 study, he and his associates found that 42% of participants had atypical depression, 12% had melancholic depression, 14% had both depression subtypes, and the rest had neither. “It’s more common than we all think. There’s no doubt we underrecognize it,”said Dr. Nierenberg.2

Making a correct diagnosis of this subtype is critical in providing the patient with effective treatment. Although SSRIs and other newer medications are often the first line choice for depression treatment due to their favorable side-effect profiles, very little is yet known about how well these work for the patient with atypical depression. What is known is that patients respond well to MAOIs, but not to tricyclics. Data on newer medications is sparse and inconclusive.3 How many patients out there may be suffering through drug trial after drug trial simply because their physician does not know which medication best treats atypical depressions or does not recognize this distinct subtype?

How Is Atypical Depression Treated?

Current data suggests that those with atypical depression will respond better to MAOIs (monoamine oxidase inhibitors) like phenelzine than they will to imipramine (a tricyclic). Dietary restrictions and side-effects remain a problem. At the present time, research is concentrating on finding newer medications with better side-effect profiles to which these patients will also get a good response.4

Although more research is needed, it seems that patients may also obtain an adequate response with the SSRIs, but not all studies seem to back up this assertion. In one study, the SSRI Prozac was found to have a response only equal to imipramine, a tricyclic whose comparative response to phenelzine is well-known.5

Interestingly, however, drug treatment may not be necessary at all. A study conducted in 1999 found that patients receiving cognitive behavioral therapy responded just as well as patients receiving the MAOI phenelzine. 58% of patients in both groups responded, in comparison to only 28% of patients in the placebo group.6

Implications for the Patient

It is important to see a psychiatrist rather than your primary care physician for treatment. Not all depressions are alike nor do they respond to the same medications. A physician in general practice is not likely to have the experience necessary to differentiate between subtypes of depression or to know which treatment choices are more likely to work. A patient may suffer unnecessarily as his doctor tries all the wrong medications. Given the very nature of depression, this only complicates the patient’s already depressed feelings. If the patient is forced by insurance or financial circumstances to see a primary care physician for their treatment, they must do the leg work to make up the deficit in their physician’s knowledge. This is not as it should be, certainly, but until there is a radical change in our healthcare systems, it is necessary. The educated healthcare consumer who takes an active role in his or her treatment is less likely to slip through the diagnostic cracks.

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Bipolar #1 and Bipolar #2 Substance Abuse Disorders

Abstract

OBJECTIVE:

To evaluate the prevalence of substance abuse dependence and/or alcohol abuse dependence among subjects with bipolar I versus bipolar II disorder in a voluntary registry.

METHOD:

One hundred randomly selected registrants in a voluntary case registry for bipolar disorder were interviewed, using the Structured Clinical Interview for DSM-IV Axis I Disorders, to validate the diagnosis of this registry. Corroborative information was obtained from medical records, family members and the treating psychiatrist. Eighty-nine adults (18-65 years) met criteria for bipolar disorder (bipolar I = 71, bipolar II = 18) and were included in this analysis.

RESULTS:

Forty-one (57.8%) subjects with bipolar I disorder abused, or were dependent on one or more substances or alcohol, 28.2% abused, or were dependent on, two substances or alcohol, and 11.3% abused or were dependent on three or more substances or alcohol. Nearly 39% of bipolar II subjects abused or were dependent on one or more substances, nearly 17% were dependent on two or more substances or alcohol, and 11% were dependent on three or more substances or alcohol. Alcohol was the most commonly abused drug among either bipolar I or II subjects.

CONCLUSIONS:

Consistent with other epidemiologic and hospital population studies, this voluntary bipolar disorder registry suggests a high prevalence of comorbidity with alcohol and/or substance abuse dependence. Bipolar I subjects appear to have higher rates of these comorbid conditions than bipolar II subjects; however, as the number of bipolar II subjects was rather small, this suggestion needs confirmation.

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Part # 3 Mood Stablizers and Novel Anti Pshychotics in the treatment of Borderline Personality Disorder

Conclusions

Recent investigations of mood stabilizers in the treatment of BPD are promising and suggest that these drugs can be useful in clinical practice, particularly for controlling affective instability and impulsive aggression. However, further studies are needed to confirm the initial results and to ascertain whether some novel antipsychotics can be used for their mood-stabilizing effects in patients with BPD.

Future investigations should focus on a list of relevant topics: pilot studies of new drugs; controlled trials of drugs already tested in open case series; comparisons of new anticonvulsant agents with better-known mood stabilizers, such as lithium or valproate; head-to-head comparisons of novel and traditional antipsychotics to verify which differences in clinical effects and adverse events specifically occur in patients with BPD; maintenance studies to assess persistence of therapeutic effects in longlasting disorders such as BPD; add-on trials of mood stabilizers and novel antipsychotics in samples of patients with BPD who do not respond to firstline therapy with serotonergic antidepressants; and the relationship of clinical subtypes of patients with BPD (eg, affective labile, self-injurious, psychotoform) with response to drug treatment.

Dr Bellino is assistant professor of psychiatry, Dr Paradiso is a resident in psychiatry, and Dr Bogetto is professor of psychiatry and chairman in the department of neuroscience at the University of Turin in Italy.

Drs Bellino, Paradiso, and Bogetto report that they have no conflicts of interest with the subject matter of this article.

Drugs Mentioned in This Article

Carbamazepine (Carbatrol, Tegretol, others)
Clonazepam (Klonopin, Rivotril)
Clozapine (Clozaril)
Divalproex (Epival, Depakote)
Fluoxetine (Prozac)
Lamotrigine (Lamictal)
Lithium (Eskalith)
Olanzapine (Zyprexa)
Oxcarbazepine (Trileptal)
Phenytoin (Dilantin)
Quetiapine (Seroquel)
Risperidone (Risperdal)
Tranylcypromine (Parnate)
Trifluoperazine (Stelazine)
Valproate/valproic acid (Depakote, others)
– See more at: http://www.psychiatrictimes.com/articles/mood-stabilizers-and-novel-antipsychotics-treatment-borderline-personality-disorder/page/0/3#sthash.fn2Sab7Y.dpuf

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