Jump to content
!! Advice given is in no way a substitute for consulting with a competent Veterans law firm, such as one on the NOVA advocate website !! ×
VA Disability Claims Community Forums - Hadit.com

  • veterans-crisis-line.jpg
    The Veterans Crisis Line can help even if you’re not enrolled in VA benefits or health care.


  • question-001.jpeg

    Have Questions? Get Answers.

    Tips on posting on the forums.

    1. Post a clear title like ‘Need help preparing PTSD claim’ or “VA med center won’t schedule my surgery instead of ‘I have a question.
    2. Knowledgeable people who don’t have time to read all posts may skip yours if your need isn’t clear in the title.
      I don’t read all posts every login and will gravitate towards those I have more info on.
    3. Use paragraphs instead of one massive, rambling introduction or story.
      Again – You want to make it easy for others to help. If your question is buried in a monster paragraph, there are fewer who will investigate to dig it out.
    Leading too:

    exclamation-point.pngPost straightforward questions and then post background information.
    • Question A. I was previously denied for apnea – Should I refile a claim?
      • Adding Background information in your post will help members understand what information you are looking for so they can assist you in finding it.
    Rephrase the question: I was diagnosed with apnea in service and received a CPAP machine, but the claim was denied in 2008. Should I refile?
    • Question B. I may have PTSD- how can I be sure?
      • See how the details below give us a better understanding of what you’re claiming.
    Rephrase the question: I was involved in a traumatic incident on base in 1974 and have had nightmares ever since, but I did not go to mental health while enlisted. How can I get help?
    This gives members a starting point to ask clarifying questions like “Can you post the Reasons for Denial of your claim?”
    • Your first posts on the board may be delayed before they appear as they are reviewed. This process does not take long.
    • Your first posts on the board may be delayed before they appear as they are reviewed. The review requirement will usually be removed by the 6th post. However, we reserve the right to keep anyone on moderator preview.
    • This process allows us to remove spam and other junk posts before hitting the board. We want to keep the focus on VA Claims, and this helps us do that.
  • Most Common VA Disabilities Claimed for Compensation:   


  • VA Watchdog

  • Can a 100 percent Disabled Veteran Work and Earn an Income?

    employment 2.jpeg

    You’ve just been rated 100% disabled by the Veterans Affairs. After the excitement of finally having the rating you deserve wears off, you start asking questions. One of the first questions that you might ask is this: It’s a legitimate question – rare is the Veteran that finds themselves sitting on the couch eating bon-bons … Continue reading

  • 0

"secondary Mood Disorder Due To A General Medical Condition."



  • HadIt.com Elder

Clinical Psychopharmacology Seminar 1996-1997

Efficacy of Antidepressants in Medically Ill Patients

Paul J. Perry, Ph.D., Bruce Alexander, Pharm.D., Vicki L. Ellingrod, Pharm.D.

Peer Review Status: Not Peer Reviewed

Diagnosis of Depression in Patients with Medical Illness (DSM-IV, 1993)

Patients with both a medical illness and depression present a diagnostic and treatment challenge. Combined illness is not an uncommon problem for physicians. Surveys of patients seen in medical settings found a majority of depressed patients have a comorbid medical diagnosis. The comorbid illness may effect recovery of the depressed patient. Keitner et al. (1991) studied 78 patients meeting DSM-IIIR criteria for major depression. Forty-one had their major depression compounded by a coexisting axis-I (dysthymia, substance abuse, anxiety disorder, OCD, bulimia), axis-II , or axis-III (cardiovascular disorder, diabetes, epilepsy, asthma, chronic pain) diagnosis. There was no specific mention of the antidepressive treatments applied only that no significant difference existed between the pure depression versus compound depression groups. The patients were monitored for a 12 month period, initially as inpatients and then as outpatients using the HAM-D and GAS. They reported that the patients with compound depression recovery rate of 33% was significantly lower than the "pure" depression recovery rate of 65%. There was no difference in the recovery rates within the groups of patients with compound depression. Thus as patient with MDD and angina had the same probability of recovery as a patient with MDD and OCD, or MDD and schizotypal personality disorder. Instead the authors noted that the limiting factor for a positive antidepressant response was number of life events. Thus the patients with the fewest number of life events such as patients with pure depression were the most likely to response to therapy. Importantly, only the number and not the nature of the life events could predict recovery. Thus it can be hypothesized that in the treatment of depressed patients with concomitant medical illnesses the prognosis for recovery may well decrease the more severe the illness is in the patient. There are numerous medical illnesses below in which the depressed patients have been treated with antidepressants. This review has collated the antidepressant efficacy in the treatment of depressed medically ill patients.

When depression is seen in the medically ill, the following diagnostic possibilities need consideration and investigation:

a. Major depressive episode independent of the medical condition

b. Adjustment Disorder with Depressed Mood from the stress of the medical illness precipitating a depressed mood

c. Secondary Depression Due to the Medical Condition - when the medical illness precedes the depression and is felt to have an etiologic (pathophysiologic) relationship to the depression

d. Substance-induced Depression - alcohol, drug or prescription medication produces a depressed mood

e. Depression symptoms is that are a normal response to the effect of being severely ill

Compounding the problem of assessment is the changing of diagnostic nomenclature from DSM-IIIR to DSM-IV for identifying the relationship between medical illness and depression. DSM-IIIR identified a category of depression called organic mood syndrome, depressed type. The name had been changed from organic affective disorder in DSM-III. This category was defined describing a "prominent and persistent depressed mood" with "evidence from the history, physical examination or laboratory tests of a specific organic factor judged to be etiologically related to the disturbance." In DSM-IV the term organic will be deleted from a variety of conditions. The section "Organic Mood Syndromes and Disorders" is also being deleted. Specific psychiatric syndromes such as depression felt due to organic factors are grouped into the Mood Disorders with a renamed category - "Secondary mood disorder due to a general medical condition." The proposed criteria for this disorder is listed in the table along with the other DSM-IV diagnoses to consider in medical patients presenting with depression.

Proposed DSM-IV Categories for Depression and Medical Illness*

Major Depressive Episode

A. At least five of the following symptoms have been present during the same two-week period and represent a change from previous functioning; at least one of the symptoms is either (1) depressed mood (2) loss of interest or pleasure.

1. depressed mood most of the day, nearly every day as indicated by either subjective report or observation by others

2. markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day

3. significant weight loss or weight gain when not dieting (> 5% body weight in a month) or decrease or increase in appetite nearly every day

4. insomnia or hypersomnia nearly every day

5. psychomotor agitation or retardation nearly every day (observable by others not merely subjective feelings of restlessness or being slowed down

6. fatigue or loss of energy nearly every day

7. feelings of worthlessness or excessive or inappropriate guilt nearly every day

8. diminished ability to think or concentrate, or indecisiveness, nearly every day

9. recurrent thoughts of death, recurrent suicidal ideation without a specific plan, or a suicide attempt or plan for committing suicide

B. The disturbance causes marked distress or significant impairment in social or occupational functioning

C. Not due to a Substance-induced or Secondary Mood Disorder

D. Not within 2 months of the loss of a loved one (except if associated with marked functional impairment, the presence of morbid preoccupation with worthlessness, suicidal ideation, psychotic symptoms or psychomotor retardation).

Secondary Mood Disorder Due to a General Medical Condition (293.83)

A. A prominent and persistent disturbance in mood characterized by either (or both) of the following:

1. depressed mood or markedly diminished interest or pleasure in all, or almost all, activities

2. elevated, expansive, or irritable mood

B. There is evidence from the history, physical examination, or laboratory findings of a general medical condition judged to be etiologically related to the mood disturbance.

C. The disturbance is not better accounted for by another mental disorder (e.g., Adjustment Disorder with Depressed Mood, in response to the stress of having a general medical condition.

D. disturbance causes marked distress or significant impairment in social or occupational functioning.

E. The disturbance does not occur exclusively in the course of delirium or dementia

Specify type: with manic features, with depressed features, with mixed features

Substance-induced Mood Disorder (29x.)

A. A prominent and persistent disturbance in mood characterized by either (or both) of the following:

1. depressed mood or markedly diminished interest or pleasure in all, or almost all, activities

2. elevated, expansive, or irritable mood

B. There is evidence from the history, physical examination, or laboratory findings of substance intoxication or withdrawal, and the symptoms in A developed during intense substance intoxication or withdrawal, or occurred within a month of the cessation of intoxication or withdrawal.

C. The disturbance is not better accounted for by a mood disorder that is not substance induced. Evidence that the symptoms are better accounted for by a mood disorder that is not substance induced might include: the symptoms precede the onset of the substance abuse or dependence; persist for a substantial period of time (e.g. about a month) after the cessation of withdrawal or severe intoxication; are substantially in excess of what would be expected given the character, duration, or amount of the substance used; or there is other evidence suggesting the existence of an independent non-substance-induced mood disorder (e.g., history of recurrent mood episodes).

D. The disturbance causes marked distress or significant impairment in social or occupational functioning

E. The disturbance does not occur exclusively during the course of Delirium.

Specify: (Specific Substance) (Intoxication/Withdrawal) Mood Disorder

Specify type: with manic features, with depressed features, with mixed features

Adjustment Disorder with Depressed Mood (309.0)

A. The development of emotional or behavioral symptoms in response to an identifiable stressor(s), which occurs within three months of the onset of the stressor (2).

B. These symptoms or behaviors are clinically significant as evidenced by either of the following:

1. marked distress that is in excess of what would be expected from exposure to the stressor

2. significant impairment in social or occupational (academic) functioning

C. The stress-related disturbance does not meet the criteria for any specific Axis I disorder and is not merely an exacerbation of a preexisting Axis I or Axis II disorder.

D. Does not represent Uncomplicated Bereavement

E. The symptoms do not persist for more than six months after the termination of the stressor. It is not uncommon to experience major depression secondary to a psychiatric disorder or a medical illness


Yates et al.(1991) compared 50 patients with depression secondary to medical illness (MDD/MI) to 50 patients with organic mood disorder (OMD). Organic mood disorder assumes that the pathophysiology of the primary medical illness (e.g., cerebrovascular accident, epilepsy, corticosteroid use, multiple sclerosis, head trauma, brain cancer, cerebral palsy, etc.) directly causes the mood disorder. Depression in the medically ill occurs without a major medical pathophysiologic mechanism (e.g., diabetes, hypertension, coronary artery disease, atypical chest pain, obesity, prostate cancer, hypothyroidism, etc.). Of the OMD group and MDD/MI group 76% and 80% respectively received a trial of a TCA. Trial adequacy was defined as imipramine or its equivalent 150 mg per day for eight weeks. The number of patients who received an adequate trial in the OMD and MDD/MI group was 34% and 34% respectively. For all patients 11% of the OMD and 59% of the MDD/MI experienced a full recovery. Thus it would seem that medical illnesses that affect the CNS by causing clinical depressions are far less likely to respond to antidepressant treatment than depressed patients who have concomitant medical illness that do not affect the CNS. If this hypothesis is correct one should observe negative antidepressant treatment studies for OMD and positive treatment studies for MDD/MI.

Organic Mood Disorder - Treatment Studies


It is estimated that post-stoke depressions occur in 26-50% of patients (Robinson et al 1984, Feible and Springer 1982). Thus the treatment of this disorder is a very practical consideration in the rehabilitation of these patients.

Lingham et al (1988) examined the records of 25 post-stroke patients who met the DSM-III criteria for depression. All were treated with methylphenidate 15-40 mg/d (mean = 26 mg/d). According to the information distilled from the progress notes, the patients were classified as responders or nonresponders. Thirteen (52%) of the patients recovered completely from depression. Mood demonstrated an improvement in the responders usually within 48 hours. Two patients with a history of cardiac disease had cardiac side effects from the drug and one patient had visual hallucinations which stopped after the methylphenidate dose was decreased. Thus although open trials suggest a role for methylphenidate in the treatment of post-stroke depression confirmation with a placebo controlled trial is still necessary.

Balunov et al (1990) contrasted the use of amitriptyline (n = 30) to two minor tranquilizers (n = 30), seduxen and or sibazone, or no pharmacotherapy (n = 30) in the treatment of 90 post-stroke depressed patients. No diagnostic depression criteria were utilized. However, the 90 patients mean HAM-D score was approximately 13 ± 1 suggesting the patients were only mildly depressed. The amitriptyline dose was titrated from 25 mg in week-1, 50 mg week-4 and 4, and 75 mg during week 4. At week-4 of therapy, amitriptyline HAM-D scores were significantly lower when compared to the two other treatments. No significant difference was found between seduxen and placebo.

Murray et al (1986) reviewed the charts of 14 patients who received ECT after post-stroke depression (13). Between 3-18 treatments were administered. Twelve of the patients were characterized as markedly improved. One patient was described as showing little improvement while the other patient response was unknown. One patient with CV disease developed a transitory arrhythmia during ECT. No patients were noted to have any worsening of their neurologic status. Finklestein et al (1987) also conducted a retrospective chart review to contrast the effectiveness of antidepressants in the treatment (doxepin, maprotiline, trazodone, desipramine, amitriptyline, imipramine, and nortriptyline) of 42 depressed post-stroke patients to 18 post-stroke patients receiving no treatment for 6 weeks. Patients met criteria for major depression (DSM-III). Seventeen (33%) of the antidepressant responded to pharmacotherapy. However, there was no difference in the final depression scores between the two treatment groups. The antidepressant doses between the responders and nonresponders according to imipramine equivalents differed from 68 mg/d in the responders versus 50 mg/d (p < 0.07) in the nonresponders. These findings may be biased by the fact that the antidepressant doses were by subtherapeutic.

There are two controlled double-blind trials that have evaluated the effectiveness of antidepressant therapy in stroke patients. Lipsey et al (1984) compared 4 or 6 weeks of nortriptyline treatment to placebo in 39 patients with post-stroke depression (Lipsey et al 1984). The nortriptyline dose was titrated to 100 mg/d over a 4-week period. Twenty-six patients (11 nortriptyline and 15 placebo) completed the entire study. Patients who given nortriptyline showed a significantly greater improvement in both the HAM-D scores (p = 0.06) and the Zung scores (p = 0.02) than patients who were on placebo. Unlike the previous negative study were antidepressant dose was a potentially confounding issue these patients received therapeutic doses which may be why the study was positive. Reding et al (1986) studied 27 post-stroke with either major depression or dysthymia (DSM-III) patients in a double blind study comparing trazodone to placebo. Barthel ADL scores improved significantly only in the patients with the abnormal DST treated with trazodone 32 days of treatment.

Summary. Depression following stroke is not fully explained as a psychological response to the associated impairment. There appear to be subgroups of depressed post-stroke patients whose depression is causally related to the injury, possibly including its strategic location in the brain (left dorsal lateral frontal cortex or left basal ganglia); a family history of depression; premorbid subcortical atrophy; and premorbid or ongoing social factors. When a patient with a recent stroke meets the criteria for major depressive episode, organic (secondary) mood disorder is diagnosed.

Multiple Sclerosis

Schiffer and Wineman (1990) designed a double-blind placebo controlled study to assess whether desipramine plus psychotherapy would be more effective than placebo plus psychotherapy in the treatment of 28 multiple sclerosis patients who met criteria for major depressive disorder (RDC). Patients were randomized to desipramine or placebo. During the first week of treatment, the desipramine dose was titrated to 150 mg/d or to the maximum tolerable dose. The aim was to obtain serum levels of 125-150 ng/ml. Half of the group treated with desipramine was unable to tolerate doses that would enable them to reach serum levels of 125 ng/ml. However, when the low level group (< 125 ng/ml) was compared to the therapeutic level group (> or = 125 ng/ml), the same number of patients improved within each group, i.e., 6 of 7. According to results of blind clinical judgment 11 of 13 patients in the desipramine group and 6 of 14 patients in the placebo group showed an improvement in their depressive symptoms. This difference in clinical improvement was significant.


Robertson and Trimble (1985) conducted a double blind controlled study of two antidepressants, nomifensine and amitriptyline compared to placebo in 39 epileptics meeting RDC criteria for depression. At the end of a six-week trial in which the drugs were administered at a fixed dose of 75 mg/d, patients were assessed and there were no significant differences in the clinical improvement among the three groups. It was also noted that there was no significant relationship between serum level and clinical response to antidepressants. This was an important issue because of the possibility of drug-drug interactions occurring between the antidepressants and anticonvulsants. Non-responders at the end of the six-week period had their antidepressant doses doubled and continued the study for another six weeks. At the end of the second 6-week trial, a significant difference between the drugs emerged. Nomifensine was the more effective antidepressant. Despite doubling the dose, there was no correlation between serum levels and therapeutic response. Because of the risk of antidepressant-anticonvulsant interactions it probably reasonable to confine the selection of antidepressants to those known to have a therapeutic blood level. For the tricyclics, a nortriptyline dose producing a therapeutic plasma concentration between 50-150 ng/ml is advisable.

During the treatment of compound depressions it is important to note that conventional dosing and monitoring parameters of antidepressive agents are not always adequate. Though antidepressants are effective in all of the comorbid illnesses discussed, their efficacy is not dependent on adherence to standard treatment protocols. In choosing an antidepressive agent the potential for side effects and how these side effects impact on the comorbid illness must be considered. When treating depression in patients with chronic fatigue syndrome and multiple sclerosis it is best to start at a lower initial dose and increase the dose gradually based on clinical improvement and the appearance of side effects. Patients with seizure disorders may experience an improvement in their depressive symptoms by employing carbamazepine as an anticonvulsant agent. MAOIs and tricyclics have been effective in the treatment of epileptic depressions. When making adjustments in the treatment of depression with comorbid illnesses standard treatments and target blood levels should be de-emphasized and clinical response should be monitored closely.

Dementia/Alzheimer's Disease

Of patients meeting diagnostic criteria for dementia, one-half are afflicted with Alzheimer's Disease. Prevalence of this disease in the United States in 1988 was estimated to be 3 million cases (Pary et al 1990.) Depression is frequently associated with dementia (40%) and with Alzheimer's Disease (25%) (Lazarus et al 1987, Reifler 1988). While much of Alzheimer's research is directed towards reducing or slowing impairment of cognitive function, the significant presence of concurrent major depression and possible treatments could have some impact on the overall progression of the disease.

Pary et al (1990) recommend a antidepressant trials in dementia patients who meet criteria for the diagnosis of depression. Antidepressants whose adverse effect profiles are especially useful in this population are nortriptyline and fluoxetine. Reifler et al (1989) conducted a prospective, double-blind, randomized, placebo-controlled 8-week trial using a parallel design of imipramine in Alzheimer's Disease patients with and without depression. Of the 61 outpatients (mean age = 72, 25 male, 36 female) with primary degenerative dementia of the Alzheimer's type, 28 met the criteria (DSM-III) for major depression. The investigators included non-depressed patients to examine effect on cognitive function in addition to antidepressant effect. Imipramine was slowly titrated upward to a mean dose of 83 mg/d (total imipramine = 119 ng/ml) for the depressed patients and 82 mg/d (total imipramine = 132 ng/ml). A therapeutic imipramine concentration in an adult is usually considered a total concentration of imipramine plus desipramine of greater than 242 ng/ml. It was noted that side effects of drowsiness and dizziness in the depressed versus non-depressed groups were essentially equal. HAM-D ratings of both the depressed and non-depressed patients improved over time with both imipramine and placebo. Two tests of cognitive function (mini-mental state exam and the dementia rating scale) were used to compare depressed versus non-depressed patients and imipramine versus placebo with differing results. Imipramine produced greater improvement on the cognitive measures than placebo regardless of the diagnostic group. It is difficult to judge the significance of this study since the investigators choice of an antidepressant precluded dosing into a therapeutic range due to the adverse effect profile of the drug.

Summary. In patients presenting with signs of both depression and dementia, if symptoms suggestive of dementia are significantly more prominent than depressive symptoms, the diagnosis is dementia with depressive symptoms. If symptoms suggesting a major depressive episode are at least as prominent as those consistent with dementia, the diagnosis is major depressive disorder. In selecting treatment, it is prudent to assume that symptoms suggesting dementia may be manifestations of the depressive disorder until proven otherwise. When the depressive episode ends. so should the symptoms suggestive of dementia. If they do not, the diagnosis of early dementia should be considered.


Chronic Obstructive Pulmonary Disease

Gordon et al (1985) studied the effects of desipramine on 13 patients with severe chronic COPD in a double blind, crossover study using desipramine and placebo for 8 weeks each. Patients were not diagnostically depressed. However, it was the investigators hypothesis that desipramine would enhance the patients ventilatory drive and improve the arterial blood gases. The desipramine was titrated over 4 weeks to a maximum dose of 100 mg/d. The authors hypothesized that the tricyclic would improve both depression and spirometry scores in these patients. The Beck Depression Inventory (BDI) scale scores showed significant improvement from baseline for both the desipramine and the placebo while the Zung scores showed no significant change following either placebo or desipramine. At baseline the mean ± sd scores were 14 ± 4 for the BDI and 39 ± 9 for the Zung scale. At the end of 8 weeks of desipramine, mean BDI scores were 10 ± 7 (significant improvement, p < 0.05) and mean Zung scales were 36 ± 11 (p = NS). Neither desipramine nor placebo had either a beneficial or adverse effect on the patients' pulmonary function tests which included FEV1, FVC, PaO2, PaCO2 and pH. Thus all the could be concluded from this study is that tricyclic antidepressants are not contraindicated in patients with COPD.

Light et al (1986) contrasted the antidepressant efficacy of six weeks of doxepin (mean = 105 mg/d) to placebo in 12 with severe chronic COPD patients in using a double-blind crossover design. Each treatment was administered for 6 weeks with a 2 week washout period between therapies. Although patients were required to have a score of > 15 on the Beck Depression Inventory and > 50 on the State-Trait Anxiety Inventory, they were not required to meet any diagnostic criteria for depression. There was no significant difference (p < 0.05) in the BDI score when doxepin and placebo therapy were compared. Three of the 12 patients in the study dropped out due to side effects such as drowsiness, blurred vision, and nausea. Pulmonary function tests were not affected either beneficially or detrimentally by doxepin. Neither doxepin nor placebo had either a beneficial or adverse effect on the patients' pulmonary function tests which included FEV1, FVC, PaO2, PaCO2 and pH.

Borson et al (1992) randomly administered nortriptyline 1 mg/kg/d or placebo to 30 COPD for a 12-week treatment trial in the treatment of their depression. All patients had a primary diagnosis of moderate to severe COPD (FEV1 and FEVa/FVC < 60% of predicted and a coexistent diagnosis of depressive disorder. The criteria for diagnosing depressive disorder were not specified. Responders were defined as patients who had a score of 1 or 2 on the Clinical Global Impression, i.e., markedly or moderately improved respectively. Ten (77%) patients responded to nortriptyline in contrast to only 2 receiving placebo (12%) (X2 = 13.0, p < 0.0003). Patients' ratings on the Hamilton Depression Rating Scale (HAM-D) improved by 60% (29.6 ± 7.6 to 12.6 ± 6.9) while placebo improved ratings by 17% (29.5 ± 6.4 to 22.8 ± 11.3) (F = 7.72, df =1, p = 0.01). A 45% reduction in mean score on the Patient Related Anxiety Scale was seen with patients on nortriptyline (54.3 ± 17.0 to 29.9 ± 11.4) while a 4% improvement was seen with patients on a placebo (47.4 ± 21.5 to 45.3 ± 28.6, p < 0.005). Nortriptyline did not affect shortness of breath in day to day activities or during structured exercise. As in the two previous studies the antidepressant had no effect on pulmonary function tests.

Myocardial Infarction

Because of the side effects of tricyclic antidepressants such as conduction disturbances, tachycardia, and orthostatic hypotension, they are contraindicated for the first 6 weeks following a myocardial infarction (Kavan et al 1991, Stern 1985). According to Schleiffer et al (1989), 45% of patient admitted to the hospital for an MI will develop symptoms of major or minor depression within 8-10 days. Since the tricyclic antidepressants and monoamine oxidase inhibitors are contraindicated, the clinical question still remains which antidepressant pharmacologic treatment are acceptable for a post-MI depressed patient. Potential alternative pharmacologic treatments include the benzodiazepine, alprazolam and fluoxetine (Kavan et al 1991). No studies have been found concerning the safety and efficacy of other antidepressants such as fluoxetine or bupropion in the treatment of post-MI depression, but they appear to have minimal significant effects on blood pressure, heart rate, and conduction. ECT, relatively contraindicated in the first three months post-MI, has been used successfully to treat severely depressed patients in the immediate post-MI period.

Summary. The relationship between depression and increased morbidity and mortality is well documented in both post-myocardial infarction patients and in coronary artery disease patients without myocardial infarction. Give the higher morbidity and the fact that most of these patients do not develop a major depression, the practitioner is advised to screen assess fully, and treat major depression when present in these patients groups.

Chronic Fatigue Syndrome

Manu et al. (1989) evaluated 44 patients for depressive disorder (DSM-III-R) secondary to chronic fatigue syndrome. Twenty-four patients were treated with antidepressant medication (19 TCAs, 4 phenelzine, 1 TCA/lithium). Twenty reported significant improvement of their fatigue symptoms and their depressive disorder. The importance of this study is that it confirmed the hypothesis that approximately half the patients with chronic fatigue syndrome are depressed and will have their symptoms improved by antidepressant medication. There are anecdotal reports that in some cases of chronic fatigue syndrome patients poorly tolerate the first generation tricylic antidepressants due to the sedating side effects that may exacerbate fatigue symptoms. However, 7 of the 24 patients were treated with sedating TCAs (doxepin, imipramine, and amitriptyline). Lynch et al. (1991) suggests that sedating TCAs can be tolerated and adverse effects minimized by using lower doses initially and slowly titrating the dosage upward. The antidepressant drug used should be chosen based on the level of fatigue and the level of anxiety. When fatigue is mild but anxiety severe, a more sedating drug such as amitriptyline could be used. When fatigue is severe and anxiety mild, a less sedating drug would be a better choice. In a systematic follow up of 50 patients with chronic fatigue syndrome 30 patients responded to treatment with either lofepramine, a TCA, or fluoxetine (Lynch et al 1991). A third of the responders showed a 50% or greater decrease in the severity of depressive symptoms. Another third showed a 25-50% reduction in symptom severity. Twenty-five of thirty responders discontinued treatment without relapse for a six month period.

Summary. Nearly all depressed patients complain of fatigue and low energy. This symptom is associated with a 46-75% lifetime rate of major depressive disorder. Complaints of chronic fatigue must be differentiated from the formal chronic fatigue syndrome.

Post-Partum Depression

Because post-partum depression affects approximately 10% of all childbearing women (Robinson and Stewart 1986, Butler and Leonard BE 1986), the importance and effects of therapy decisions are far-reaching. Relief from despondency, emotional lability, guilt, anorexia, sleep disorders, feelings of inadequacy, fatigue, and irritability provide the mother, the infant, and their family with a healthier environment. Current literature supports the use of both drug therapy and psychotherapy for post partum depression.

Butler and Leonard (1986) treated eight cases of post-partum depression with nomofensine 150 mg/d. Seven of the eight cases were patients who had experienced depression previously with pregnancy. The patients medical and psychiatric parameters were compared to 8 non-depressed mothers. Treatment and control subjects were matched for age and obstetrical status which included parameters such as postpartum time, number of previous children, and use of anaesthetic during delivery. In addition to assessing efficacy of drug treatment in the depressed group, the study also examined hormonal status in depressed mothers vs. control non-depressed mothers, and biochemical markers of depression in the depressed group. Following six weeks of antidepressant treatment, the HAM-D depression ratings decreased to scores equal to the non-depressed controls. Robinson and Stewart (1986) suggest the use of tricyclic antidepressants at their usual recommended therapeutic doses to alleviate difficulty sleeping and persistent post partum depression. However, they do not document these assertions.

HIV Seropositivity

In a retrospective chart review, Hintz et al (1990) reviewed charts of 90 male outpatients, mean age 37 (21-61) who had been treated with antidepressants. One group of 45 were seropositive for HIV while the second group of 45, matched by sex, age, and treatment criteria, HIV-negative with no known risk factors for the illness. The response rate for antidepressant treatment was contrasted in the two groups. A large percentage of both groups (89% of HIV-positives, 94% of HIV-negatives) met DSM-III-R criteria for an affective disorder, i.e., major depression, dysthymia, schizoaffective, or bipolar depressed. The only other diagnoses included organic mood disorder and adjustment disorder with depressed mood. The HIV-positive group was most commonly treated with either amitriptyline, imipramine, or desipramine while the HIV-negative group were more commonly treated with fluoxetine or trazodone. All the antidepressants appeared to produce a beneficial antidepressant effect in the HIV-positive patients with the exception of trazodone, in whom only subtherapeutic doses of 50-100 mg/d were prescribed. The efficacy of treatment for the HIV negative group was determined to be slightly higher the efficacy for the HIV positive patients, however some treatment response was noted for both groups. It was noted that antidepressant dosages tended to be higher in the HIV-negative patients. Of the HIV positive group, the asymptomatic patients achieved higher efficacy ratings than the AIDS and ARC patients. It was postulated that health factors could alter treatment response and that immune function and CNS alterations common to advanced HIV infection play an interactive role in response to drug therapy of any nature. Not surprisingly, side effect incidence and severity was also greater in the symptomatic group of HIV positive patients. Although the retrospective design of this study limits its usefulness as a therapeutic guide, it does suggest benefit can be derived from antidepressant therapy for HIV seropositive patients who meet criteria for major depression.


Balunov OA, Sadov, OG, Alemasova AY (1990). Therapy of depressions in post-stroke patients. Alaska Medicine 32:27-9.

Borson S, McDonald GJ, Gayle T, et al (1992). Improvement in mood, physical symptoms, and function with nortriptyline for depression in patients with COPD. Psychosomatics 33:190-201.

Butler J, Leonard BE (1986). Postpartum depression and the effect of nomifensine treatment Int Clin Psychopharmacol. 1:244-52.

Task Force on DSM-IV (Work In Progress 1/8/93). DSM-IV Draft Criteria. American Psychiatric Association, Washington, DC.

Finklestein SP, Weintraub RJ, Davar G, et al (1987). Antidepressant drug treatment for post-stroke depression: Retrospective study. Arch Phys Med Rehabil 68: 772-6.

Gordon GH, Michiels TM, Mahutte CK, et al (1985). Effect of desipramine on control of ventilation and depression scores in patients with severe COPD. Psychiatry Res. 15:25-32.

Hintz S, Kuck J, Peterkin JJ, et al (1990). Depression in the context of Human Immunodeficiency Virus infection: implications for treatment. J Clin Psychiatry 51:497-501.

Kavan MG, Elsasser GN, Hurd RH (1991). Depression after acute myocardial infarction. Post Grad Med 89:83-9.

Keitner GI, Ryan CE, Miller IW et al (1991). 12-Month outcome of patients with major depression and comorbid psychiatric or medical illness (compound depression). Am J Psychiatry 148:345-50.

Lazarus L, Newton N, Cohler B, et al (1987). Frequency and presentation of depressive symptoms in patients with primary degenerative dementia. Am J Psychiatry 144:41-5.

Light RW, Merrill EJ, Despars J, et al (1986). Doxepin treatment of depressed patients with chronic obstructive pulmonary disease. Arch Intern Med 146: 1377-80.

Lingham VR, Lazarus LW, Groves L, et al (1988). Methylphenidate in treating post-stroke depression. J Clin Psychiatry 49: 151-3.

Lipsey JR, Robinson RG, Pearlson GD (1984). Nortriptyline treatment of post-stroke depression: a double-blind study . Lancet 1:297-300.

Lynch S, Seth R, Montgomery S (1991). Antidepressant therapy in the chronic fatigue syndrome. B J Gen Prac 41:339-342.

Manu P, Matthews DA, Lane TJ et al (1989). Depression among patients with a chief complaint of chronic fatigue. J Affective Disord 17:165-172.

Murray GB, Shea V, Conn DK (1986). Electroconvulsive therapy for post-stroke depression. J Clin Psychiatry 47:258-60.

Pary R, Tobias CR, Lippmann S (1990). Dementia: what to do. Southern Medical Journal. 83:1182-88.

Reding MJ, Orto LA, Winter, et al (1986). Antidepressant therapy after stroke. A double-blind trial. Arch Neurol 43:763-5.

Reifler BV (1988). Clinical problems in geriatric psychiatry. NC Med J. 49:536-8.

Reifler BV, Teri L, Raskind M, et al (1989). Double-blind trial of imipramine in Alzheimer's Disease patients with and without depression. Am J Psychiatry. 146:45-9.

Robertson MM, Trimble MR (1985). The treatment of depression in patients with epilepsy a double-blind trial. J Affective Disord 9:127-136.

Robinson GE, Stewart DE (1986). Postpartum psychiatric disorders. Can Med Assoc J. 134:31-7.

Schiffer RB, Wineman NM (1990). Antidepressant pharmacotherapy of depression associated with multiple sclerosis. Am J Psychiatry 147:1493-7.

Schliefer SJ, Macari-Hinson MM, Coyle DA et al (1989). The nature and course of depression following myocardial infarction. Atch Intern Med 149:1785-9.

Stern TA (1985). Management of depression and anxiety following myocardial infarction. Mt. Sinai J Med 52:623-33.

Yates WR, Wesner RB, Thompson R (1991). Organic mood disorder: a valid psychiatry consultation diagnosis? J Affective Disord 22:37-42.

Link to comment
Share on other sites

  • Answers 0
  • Created
  • Last Reply

Top Posters For This Question

Popular Days

Top Posters For This Question

0 answers to this question

Recommended Posts

There have been no answers to this question yet

This topic is now closed to further replies.
  • Create New...

Important Information

Guidelines and Terms of Use