Discussing prevention of relapse or recurrence of major depression is beyond the scope of this paper but is clearly important. Long-term use of antidepressants is sometimes necessary particularly if patients have two or more episodes. Compliance becomes absolutely necessary, but side effects often cause patients to stop taking medications. Tricyclics and, to a lesser degree, traditional monoamine oxidase inhibitors (MAOIs) have many side effects because they act on the muscarinic, α₁-adrenergic, and histamine H₁ receptors. If an antidepressant is effective, the side effects can be managed.

The new antidepressants have become the agents of choice because they have fewer side effects. Sexual dysfunction is the most common reason for noncompliance and unfortunately is a relatively frequent problem with all antidepressants. Moclobemide and nefazodone seem to have the fewest sexual side effects.

For long-term therapy, doses that were effective for the acute episode should be continued. Clinical experience suggests a need for lifelong maintenance on antidepressants for patients older than 50 years at the time of first episode, for patients 40 years or older who have had two episodes, or for all patients with three or more episodes. If an antidepressant is discontinued, it should be withdrawn very gradually and signs of recurring depression monitored. Long-term use of lithium for prophylaxis of both bipolar disorder and major depression has also been shown to be very effective. There is a very high rate of attempted suicide among patients with major depression following lithium discontinuation.

Conclusion

Treatment-resistant depression is a relative term and depends on how far a physician is willing to go in treating a particular patient. Appropriate use of antidepressants can relieve symptoms in at least two thirds of cases. Drug combinations, electroconvulsive therapy (ECT), and augmentation strategies can, if vigorously applied, reduce the proportion of patients truly treatment resistant to about 7%. Considering the morbidity and mortality associated with depression, a vigorous approach to therapy is worthwhile. Long-term maintenance, once success is achieved, is essential.

Many less commonly used antidepressant therapies are supported by anecdotal evidence only. They include light therapy (non-seasonal affective disorder), high-dose TCA or MAOI therapy (only if serum levels can be monitored), intravenous clomipramine or maprotiline (allows for rapid perfusion, avoids first pass liver metabolism), bromocriptine, high-dose selegiline, and psychosurgery. Modern stereotaxic psychosurgical procedures offer symptom relief with minimal risk, and reports of large trials indicate that up to 60% of truly treatment-resistant patients either recover or are considerably improved.

Absolute treatment resistance

Very few patients show absolute treatment resistance. In specialized clinics, only about 7% of patients remain depressed after 1 year of extensive investigations and treatment. Extensive treatment involves many drug trials singly and in combination as well as one or more courses of electroconvulsive therapy (ECT). Patients with absolute treatment-resistant depression (TRD) are older (mean age about 55), have been depressed longer, and usually have insoluble life problems.

Even patients with absolute TRD can be helped. Antidepressants often give some relief, and carefully prescribed psychostimulants can improve mood and psychoenergize.

Supportive psychotherapy and CBT can also be of benefit. Supportive psychotherapy helps depressed patients to carry on and CBT allows patients to view the world more positively. Regular exercise and reduction of alcohol consumption also help.

Electroconvulsive therapy

An important and effective treatment for depression, electroconvulsive therapy (ECT) is effective in about 90% of cases of major depression. The success rate drops when it is used for drug-refractory cases. Using ECT depends on patient-related factors: it clearly is the treatment of choice for depression with psychomotor slowing, stupor, psychotic symptoms, or depression requiring rapid response because of suicidal risk or malnutrition. Use of ECT should be considered whenever therapeutic management is being reviewed and revised.

Triiodothyronine (T₃) augmentation

Thyroid hormone potentiation of tricyclic antidepressants (TCAs) can be useful. The thyrotropin-releasing hormone stimulation test should be done first, if available and convenient, to rule out grade three (subclinical) hypo thy roidism. If hypo thy roidism is present, it should be treated with thyroid replacement therapy. If the patient is euthyroid, low doses of T₃ (25 to 50 µg/d) can be given with the antidepressant for 10 to 14 days. Up to a third of depressed patients, particularly women, respond. Most experience with this approach has involved tricyclic antidepressants (TCAs), and the effect on the selective serotonin reuptake inhibitors (SSRIs) or other new agents is not well studied.

Tricyclic-fluoxetine combination

Some reports indicate that fluoxetine, when added to a TCA such as desipramine, can produce a robust and rapid response in many patients. This augmentation effect could be a result of increased TCA levels due to fluoxetine inhibition of the cytochrome P 450 system. Because fluoxetine can raise blood levels of tricyclic antidepressants (TCAs), routine serum levels of TCAs are recommended. Other TCA-SSRI combinations can also be tried. All selective serotonin reuptake inhibitors (SSRIs), however, effect the cytochrome P 450 System by raising TCA levels.

Tricyclic-MAOI combination

Some evidence suggests that this combination is more effective than either drug used alone for some patients. Ideally both drugs should be started simultaneously or the MAOI added to a TCA regimen. The safest combination seems to be phenelzine with either amitriptyline or doxepin. Clomipramine, imipramine, and the new agents, such as fluoxetine, should be avoided. Give low doses initially and pay rigid attention to dietary restrictions.

The SSRI combinations

Although no literature supports the practice, clinical experience suggests that lower doses of two selective serotonin reuptake inhibitors (SSRIs) together might work better than either alone.

Augmentation with L-tryptophan

L-tryptophan is the dietary precursor of brain serotonin. Reports confirm that L-tryptophan can enhance the antidepressant effect of monoamine oxidase inhibitors (MAOIs) as well as tricyclic antidepressants (TCAs) and lithium. This might apply to the new antidepressant agents as well. The high doses required (more than 3 to 4 g/d) make this approach cumbersome because the tablets are quite large.

Psychostimulants

Dextroamphetamine, methylphenidate, and to a lesser degree magnesium pemoline all have mood-elevating, psychoenergizing properties and have a place in the management of mood disorders. These drugs can be used alone or combined with antidepressants. Apathetic, elderly, and medically ill depressed patients often respond to psychostimulants when they cannot tolerate the side effects of antidepressants or a rapid response is necessary.

Psychostimulants are also useful for patients who do not respond to any antidepressant and are truly treatment resistant. Non-response to one psychostimulant does not predict non-response to another. There is no evidence of addiction or dose escalation although clearly this class of drugs needs to be prescribed cautiously and monitored carefully. Using psychostimulants is somewhat similar to prescribing analgesics for chronic pain conditions and can be justified considering the morbidity associated with major depression.

Cognitive behavioural therapy (CBT)

This therapy can be very useful for treating chronic depression, such as dysthymia, and can be helpful as an augmentation strategy in conjunction with pharmacotherapy for treatment-resistant patients. Several studies have demonstrated the effectiveness of CBT, a technique that family physicians can easily learn.

If lithium augmentation is ineffective, it should be discontinued and the antidepressant changed (Table 5). A lack of response to one of the newer agents in a class, such as the selective serotonin reuptake inhibitors (SSRIs), does not predict lack of response to others in that class. If the first drug used was a reversible inhibitors of monoamine oxidase A (RIMA) with only one drug in the class, the switch should be to an SSRI. If the original drug was an SSRI, a second SSRI, a RIMA, or other newer agents should be tried. If a TCA or MAOI was used first, the switch should also be to one of the new classes of antidepressants.

The tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs) should be kept as third-line antidepressants. Evidence shows that response to an SSRI does not determine response to a TCA. One study has shown that 60.5% of patients who failed to respond to SSRI monotherapy responded when switched to a noradrenergic TCA. Most tricyclic antidepressants (TCAs) have both serotonergic and noradrenergic properties. Desipramine and nortriptyline are somewhat more noradrenergic than the others. Venlafaxine, a new selective serotonin and noradrenaline reuptake inhibitor (SSNRI) might also be considered.

If atypical symptoms, such as panic attacks or anxiety, are present, an MAOI or reversible inhibitors of monoamine oxidase A (RIMA) should be considered after a suitable washout period for the previously used antidepressant (10 to 14 days for most antidepressants; up to 5 weeks for fluoxetine because of an active metabolite).

If the second antidepressant is not effective, lithium augmentation should be tried once more before the antidepressant is changed again.

Strategies before changing antidepressants

Higher dose

For the new antidepressant compounds, most manufacturers recommend standard doses. If side effects are minimal, doses usually can be increased and tolerated well. Increasing the dose should be tried before adding other antidepressants or switching drugs.

Lithium augmentation

For patients who have failed to respond to an adequate course of an antidepressant, lithium augmentation is the most reasonable next step (Table 4 summarizes augmentation strategies). About 30% to 50% of patients respond to this technique, and it seems to work with all of the antidepressants (although less is known about how it works with the newer agents). Lithium, an antidepressant and mood stabilizer when used alone, appears to augment other drugs by enhancing postsynaptic receptor sensitivity.

To use this technique, the antidepressant should be continued at the current dose and lithium started at a dose of 300 mg three times a day. A positive response can occur in 5 to 12 days. If the response is positive, patients should continue to receive lithium for at least 6 months and in some cases for the duration of antidepressant therapy. Lithium levels should be monitored and kept within the therapeutic range of 0.6 to 1.0 mmol/L, and thyroid status should be closely followed.

Many physical diseases present with depressive symptoms or complicate depressive illness (Table 2). Some of these illnesses remain undetected for years and account for an apparent treatment-resistant depression (TRD). Normal thyroid function is particularly important; even mild or subclinical hypothyroidism can impair response to antidepressants. Hypothyroidism can be induced by lithium therapy, and many drugs, both medical and nonmedical, can cause depression or complicate treatment (Table 3).

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Are there underlying psychosocial factors?

Psychological and social factors, such as unresolved neurotic conflicts, a history of sexual abuse, current marital or work conflicts, unemployment, and poverty, can exacerbate mood disorders. Psychotherapy must be part of the treatment plan.

Is the current course of treatment adequate?

The most frequent reason for patients not responding to treatment is inadequate use of antidepressants. Surveys have shown that two thirds of correctly diagnosed patients do not receive adequate treatment, even under specialist care. Inadequate dose is the most common reason for treatment failure. One third of patients do not respond to the first course of antidepressants; this proportion decreases with use of consecutive antidepressant trials.

The dose and duration of an antidepressant drug trial must be adequate. For most antidepressants, this means the maximum recommended daily dose for at least 3 to 5 weeks. Unpleasant side effects sometimes lead to noncompliance, and serum levels are sometimes subtherapeutic despite what seems to be an adequate dose. Other factors, such as alcohol or drug use or abuse, might affect serum levels.

If the antidepressant is a tricyclic (TCA), determining serum levels could be important for management; tests are readily available at most centres. Nortriptyline has a therapeutic range of 50 to 140 ng/mL (178 to 499 nmol/L). Other tricyclic antidepressants (TCAs) have a less precise range (about 150 to 200 ng/mL or 535 to 1070 nmol/L). Establishing serum levels can help to ensure compliance; ensure adequate absorption; and assist in dose adjustment for special groups such as the elderly or medically ill, when severe or unusual side effects are present or during apparent treatment failure. Serum levels unfortunately have not been established for other classes of antidepressants.

The most common causes of noncompliance are disabling or unpleasant side effects, particularly those that cause sexual dysfunction. Most side effects are transient; if persistent, they usually can be easily managed.

Many patients are reluctant to take antidepressants. They sometimes feel they are relying on a pharmacologic “crutch,” or that they are unworthy of receiving help. They fear addiction, worry about side effects, or could have delusional beliefs about being poisoned.

Inadequate response to therapy can be iatrogenic. Lack of understanding of the biologic basis of depression, failure to educate patients and families, failure to conduct adequate treatment trials, or reluctance to prescribe the newer antidepressants, monoamine oxidase inhibitors (MAOIs), or electroconvulsive therapy (ECT) are factors.

Colchester: Portland Press, 1991, 516 pp

ISBN 1-869868-74-9

The Royal College of Psychiatrists and the Royal College of General Practitioners launched a 5-year Defeat Depression Campaign on 30 January 1992. The first year of the campaign is intended to educate health professionals in the recognition and treatment of depression.

This book, which is the proceedings of the Conference of the British Society for Psycho-Pharmacology held in Ireland in September 1988, provides an overview of the current pharmacological options in the treatment of depression. Thirty years have elapsed since the almost simultaneous discovery of the therapeutic effect of MOA inhibitors and Imipramine in a substantial percentage of patients with severe depression. Antidepressants are the leading category of CNS drugs in research and development, occupying 11th place of all therapeutic categories, with more than 100 new chemical entities at various stages of development at the time of the Conference. One hundred and nineteen contributors helped to place the current use of antidepressants in context and the nine sections of the book cover a wide range: biochemical mechanisms thought to underlie drug action; animal models of depression and laboratory methods of discovering new drugs; biochemical markers of depression and the discussion of toxicity and side effects of both older and new antidepressants. The section with clinical emphasis covers treatment issues, in particular the problem of resistant depression, with advice on management and indications for psycho-surgery. There is also advice on drug treatment for the depressed elderly, depression as seen in general practice with particular reference to the side effects of treatment and the corresponding problems with patient compliance.

This book will be of wide interest both to researchers concerned with the development of future antidepressants and to clinicians wishing to have a fuller understanding of the mechanism of action of these frequently prescribed drugs.

Since the 1983 report, many of the original study subjects have experienced multiple recurrences of major depressive disorder (MDD). In a study published in the Feb. issue of The American Journal of Psychiatry, David A. Solomon, M.D., and colleagues prospectively focused on the time to recurrence of MDD across multiple episodes. They predicted that the risk of recurrence would decrease as time of recovery increased. They also predicted that each recurrence would increase the risk of a subsequent recurrence.

The original collaborative depression group had a total of 955 patients. Of those, 318 recovered from their intake episode of major depression and were at risk of recurrence during the 10-year follow-up period. The study group for the Solomon et al. analysis consisted of these 318 subjects. Recovery was defined as at least eight consecutive weeks “with either no symptoms of major depressive disorder or only one or two symptoms at a mild level of severity”. Recurrence, which could occur only after recovery from the preceding depressive episode, was defined as the reappearance of major depressive disorder (MDD) meeting the full criteria for at least two consecutive weeks, beginning with the first of these two weeks. Episodes meeting criteria for minor depression and chronic intermittent depression were not included.

For the first five years of the follow-up study, patients were assessed every six months, and annually after that, using the Longitudinal Interval Follow-Up Evaluation. The analyses encompass data for up to 520 weeks of follow-up. As an observational study, treatment was not randomized or in any way controlled by anyone connected to the study.

Of the 318 subjects, 263 (83%) were followed for at least five years, and 208 (65%) were followed for the entire 10-year period. During those 10 years, 481 recurrences were observed. The mean number of episodes of major depressive disorder (MDD) per year of follow-up was 0.21 (SD=0.24).

Once the first eight-week recovery period was completed for the 318 subjects, 202 suffered a recurrence. Of those subjects, 172 recovered and remained healthy for the following eight-week period. A second recurrence was suffered by 115 of those patients. The median time to recurrence for the first episode was 150 weeks; for the second, 83 weeks; and for the third 77 weeks. These intervals were significantly longer than the time to recurrence for subsequent recurrences.

The investigators were also interested in the probability of a well patient experiencing a recurrence during a six-month period (the patient having began that period still well). They found the mean probability for recurrence during the first six months after recovery was 20% (SD=6) across the five prospectively observed recurrences. They wrote, “This indicates that, on average, of the subjects at risk for recurrence, 20% had a recurrence in the first 6 months after the onset of recovery from the preceding depressive episode”.

They found that rate of recurrence decreased in subsequent six-month intervals. In the second six months the probability of recurrence was 19% (SD=7), in the third six months it was 15% (SD=6), in the fourth six months it was 13% (SD=3), in the fifth six months it was 11% (SD=3). In the final six months after the onset of recovery from the preceding depressive episode the probability of recurrence was 9% (SD=6).

Solomon et al. found that the risk for recurrence increased by 16% for each successive episode of major depression. The number of lifetime episodes of major depressive disorder (MDD) was significantly associated with recurrence during this 10-year follow-up period. Analysis showed that there was very little consistency in the time to recurrence within the subject group.

When the researchers looked at treatment of these subjects, they called the low level of maintenance pharmacotherapy during any of the four weeks immediately preceding any of the prospectively observed recurrences striking. Up to 47% to 50% of subjects received no pharmacotherapy during the four weeks immediately preceding the first three recurrences. One-third received no pharmacotherapy in the four weeks immediately preceding the fourth and fifth recurrences. During any of the preceding four-week periods, only 33% to 45% of subjects received at least 100 mg/d of imipramine (Tofranil) or its equivalent. Only 18% to 30% of subjects received at least 200 mg/d of imipramine or its equivalent during the same time period prior to any of the five prospectively observed recurrences.

Solomon et al. wrote that, as predicted, “as the duration of recovery increases, the risk of recurrences decreases or decays.” Also as predicted, “With each successive recurrence, the risk of a subsequent recurrence increases by 16%.” Consistency in time to recurrence, however, was highly variable among this group, indicating that time to recurrence is also highly variable for any individual.

Limitations of this study, the researchers pointed out, included the progressively smaller group size following each recurrence. They speculate that this caused the data analyses to underestimate rates of recurrence over a patient lifetime. Another limitation was the exclusion of minor or intermittent depression, causing a possible underreporting of the extent of psychopathology in the subject group. Finally, the researchers suggest that variability in treatment may have influenced the findings. Patients may have discontinued treatment following recovery, putting themselves at greater risk of recurrence. Recurrence may have caused other patients to discontinue treatment due to discouragement, putting these patients at risk for further recurrence as well. Solomon et al. found the lack of maintenance pharmacotherapy unfortunate, given its role in preventing recurrences

Patient Presentation and History

JS is a 37-year-old female who comes to the pharmacy intending to purchase St. John’s wort. She has heard that it can relieve depression, and she firmly believes in “natural” treatments. She reports that, for the past three weeks, she has been feeling depressed, has had a decreased appetite with a 15-pound weight loss, has had little energy, no longer enjoys the many recreational activities that pleased her in the past, and finds herself waking up each morning three hours earlier than expected with an inability to fall back to sleep. She is unable to identify any significant, recent stressors in her life, but says that it is becoming increasingly difficult to perform adequately at work and home. She had her annual, routine physical exam one month ago, and all physical and laboratory findings were within normal limits. Aside from her current complaints, she has been in good physical health with no medical problems, alcohol or substance abuse, allergies, or regular use of prescription or nonprescription drugs.

St. John’s Wort

Botanical and Chemical Properties: St. John’s wort (Hypericum perforatum L.), belonging to the family Hypericaceae and also known as klamath weed, amber touch-and-heal, goatweed and rosin rose, is an aromatic shrubby perennial plant with numerous bright yellow flowers that bloom from June to September. The blooms are said to be at their brightest and most abundant around the day traditionally celebrated as the birthday of John the Baptist (June 24).

The plant is native to Europe and can be found as well in the United States and Canada. It is an aggressive weed found in the dry ground of roadsides, meadows, woods and hedges, where it generally grows to a height of one to two feet. Historically, St. John’s wort has been used as an herbal remedy, not only for depression, but also to treat anxiety, diuresis, gastritis and insomnia. In addition, it has been investigated as a treatment for cancer and AIDS.

Low concentrations of hypericin and pseudohypericin are found in the leaves and flowers of St. John’s wort. Other active ingredients are flavonoids, xanthones, phenolic carboxylic acids, essential oils, carotenoids, alkanes, phloroglucinol derivatives, phytosterols, and medium-chain fatty acid alcohols. Tannin, in a concentration of approximately 10%, is most likely responsible for St. John’s wort’s astringent and protein-precipitating effects, contributing to the plant’s traditional, topical use as a wound-healing agent.

Pharmacology

Historically, people thought that the tranquilizing effects of St. John’s wort were secondary to increased capillary blood flow. More recent studies demonstrate that the extract, primarily hypericin, is a strong, and nearly irreversible, inhibitor of monoamine oxidase types A and B. In addition, the extract enhances sleep, extends narcotic-induced sleeping time in a dose-dependent manner, antagonizes the effects of reserpine and decreases aggressive behavior in socially isolated male mice. The Food and Drug Administration has designated hypericin as an investigational new drug. In Germany, it has been approved by the regulatory authorities for the treatment of depression.

Clinical Trials

Hypericum has been tested in over 3,000 patients against placebo and various active medications.2 Linde et al. conducted a meta-analysis of 23 randomized trials (15 in which hypericum was compared with placebo and 8 in which it was compared with another drug treatment); 1,757 outpatients with mainly mild or moderately severe depressive disorders were included. Overall, results of this analysis indicated that extracts of hypericum are more effective than placebo and equal in efficacy compared to standard antidepressants for the treatment of mild to moderately severe depressive disorders. In addition, fewer side effects were seen in patients treated with hypericum (19.8%) than in those treated with standard antidepressants (52.8%).

In a four-week, double-blind trial of 105 outpatients with mild depression of short duration, 67% of patients taking hypericum extract (300 mg three times daily) improved, compared with 28% of patients taking placebo. No significant side effects were noted.

In two studies, hypericum was compared with a standard heterocyclic antidepressant. In one, lasting six weeks, the dose of hypericum extract was 300 mg three times daily and that of imipramine was 25 mg three times daily. Hamilton Depression Rating Scale scores decreased from 20.2 to 8.8 in the hypericum group and from 19.4 to 10.7 in the imipramine group. In addition, fewer and milder side effects were noted in the patients treated with hypericum than in those treated with imipramine. In the other study, lasting four weeks, hypericum extract was compared with maprotiline in 102 depressed patients. The dose of hypericum extract was 300 mg three times daily and that of maprotiline was 25 mg three times daily. At the end of the study, no significant differences in either group were noticed. Overall, the relatively low doses of imipramine and maprotiline and short treatment periods make the results of these studies difficult to interpret.

No trials have been published comparing hypericum with any of the selective serotonin reuptake inhibitors (e.g., fluoxetine, sertraline, paroxetine), nor has there been systematic investigation of its efficacy over the long-term (i.e., six or more months) treatment period required for a major depressive episode. In addition, it has not been studied in patients with severe depression.

Adverse Effects and Toxicity

No adverse effects (e.g., changes in EEG, ECG, or laboratory test parameters) have been reported following treatment for up to six weeks with a standardized hypericum extract in controlled human studies. However, St. John’s wort has been associated with severe photosensitivity in animals grazing extensively on the plant. Photosensitization in humans is characterized by inflammation of the skin and mucous membranes following exposure to light. Toxicity in humans seems unlikely if the agent is used at recommended medicinal doses. Although not reported, orthostatic hypotension is theoretically possible in light of the drug’s monoamine oxidase-inhibiting properties.

Drug Interactions

Although no systematic studies of drug interactions have been conducted, patients taking St. John’s wort should observe the same precautions followed by those taking monoamine oxidase inhibitors (e.g., phenelzine and tranylcypromine). Foods containing large amounts of tyramine (e.g., aged meats and cheeses) and sympathomimetic amines (e.g., amphetamine, phenylpropanolamine, and pseudoephedrine) should be avoided in order to minimize any risk of a hypertensive crisis. In addition, serotonergic agents (e.g., selective serotonin reuptake inhibi-tors, such as venlafaxine, nefazodone, mirtazapine and buspirone, as well as trazodone, some tricyclic antidepressants, lithium, meperidine and possibly dextromethorphan) should be avoided to minimize the risk of a serotonin syndrome, a potentially life-threatening excess in serotonergic activity characterized by confusion, agitation, shivering, fever, diaphoresis, diarrhea, myoclonus, hyperreflexia and tremor.

Dosage

When used for its antidepressant action, St. John’s wort has generally been used as an extract, standardized to contain 0.3% hypericin, taken in a dosage of 300 mg three times daily. Significant effectiveness may not be seen for several weeks, and two or three months of continuous use may be needed to achieve a full effect.

Conclusion

St. John’s wort, in the form of an extract, seems to offer an intriguing option for the treatment of depression, especially in patients with mild to moderately severe depression who insist upon “natural” treatments. In short-term trials, it appears to be effective and, at the same time, relatively safe and well tolerated. However, the potential risks associated with its monoamine oxidase inhibiting activity and ability to induce photosensitivity require a degree of caution. Further studies are needed to assess the role of St. John’s wort in the treatment of severe depression, its long-term efficacy and side effects, as well as to compare it with full therapeutic doses of heterocyclic and newer antidepressants.

Pharmacist Intervention

The symptoms described by JS are classic for a major depression; there does not appear to be a medical or psychosocial etiology. Her preference for a “natural” remedy and her moderate depression make her a good candidate for St. John’s wort. However, the pharmacist must inform the patient of the limitations in our current knowledge regarding this treatment, as well as the significant morbidity and mortality associated with inadequately treated depression. The relative risks and benefits of both standard antidepressants and St. John’s wort should be reviewed. Since JS is of child-bearing age, she must be informed of our lack of information regarding possible teratogenic effects of St. John’s wort.

If JS still wishes to try this “natural” alternative, the pharmacist should become involved in monitoring the therapeutic response and any emergent side effects, as well as advising her to avoid certain foods and drugs and to protect herself against photosensitivity while using St. John’s wort. Finally, the patient should be referred back to her primary care provider or to a local institution or clinic that specializes in the evaluation and treatment of depressive disorders, especially if she does not show a positive response within a few weeks of use. Patient counseling and monitoring, of course, should also be provided to all other patients who wish to try this and other herbal medicines.

Helping Your Depressed Teenager. A Guide for Parents and Caregivers

Helping Your Depressed Teenager.

A Guide for Parents and Caregivers

Gerald D. Oster, Sarah S. Montgomery
John Wiley & Sons Canada, Ltd, 5353 Dundas St W, 4th Floor, Etobicoke, ON M9B 6H8
1995/184 pp

Strengths

Very informative, logical presentation, useful bibliography and resource list

Weaknesses

Support groups mostly in the United States

Adolescents are not just “big children” or “little adults.” They represent a separate stage in the transition from infancy to old age. The authors have written an informative guide on the teenage years to help parents and caregivers understand the normal and abnormal transitional stages and emotional experiences of adolescents. They identify the feelings and symptoms of clinical depression, as distinct from the “ups and downs” that we take for granted in this age group. Signs and symptoms of suicidal thoughts and actions are given and what treatment approaches to take. Overall, the emphasis in this handbook is for parents to listen to, understand, communicate with, and take their teenagers seriously.

Most material is presented logically, with case studies and tables describing danger signs of depression, as well as guidelines on how to talk to teenagers. Key points are highlighted at the end of each chapter. Information is given on the indications and use of antidepressant medication, available therapies and how to access them, and the need for and process of hospitalization. An appendix provides resources for parents with depressed and suicidal adolescents and a useful bibliography of books and pamphlets for parents and caregivers.

The preface states, “most parents have the opportunity to watch their teens successfully move through the adolescent years without extended emotional upheaval.” It also states that the book is directed toward parents of a distinct “subgroup of teens who do suffer from clinical depression.” Although the book is directed to this particular group, it provides some excellent general insights into teenage developmental tasks in general.

Support organizations and groups, however, are relevant largely in the United States. Nevertheless, a better understanding can be gained, especially by parents, about the very real existence of depression in teenagers, how to recognize it, and how to react to it.