Electroconvulsive Therapy: A Primer for Mental Health Counselors.

Electroconvulsive therapy is the treatment of choice for severe depressive episodes. Although little definitive research exists to explain its effectiveness, since its development in 1938 it has proven effective for the treatment of depression with psychotic features and suicidal ideation. The procedure is explained and implications for the mental health counselor are discussed.

Changes in professional understanding of mental illness have led to the increasing use of somatic, or biological, therapy as part of the successful treatment of some of the more common disorders. Somatic therapies are physical in nature, and the most commonly used of these are medication and electroconvulsive therapy (ECT). Many psychiatrists returned to the biological model in the 1980s and use both medication and ECT to treat the more severe or serious illnesses: (a) depression, (b) mania, (c) schizophrenia, (d) severe anxiety disorders, and (e) dementia. These disorders are common, handicapping, and often resistant to treatments other than ECT (Rey & Walter, 1997). In addition, they are the most likely disorders to have biological causes, and somatic therapies are seen as correcting an underlying biological imbalance.

Electroconvulsive therapy is widely used today, but continues to attract controversy (Baldwin & Jones, 1998; Johnstone, 1999). Even by the 1970s many standard psychiatric texts did not address ECT with children or adolescents, while others included brief references to possible clinical indications for administration. A paucity of training courses regarding ECT exists for health professionals as well as nonmedical mental health workers, who often hold responsible clinical or administrative positions (Kramer, 1999). Education and experience in the use of ECT result in a more positive attitude toward ECT as a viable treatment option for clients with refractory mood disorders and psychotic disorders (Baldwin & Jones, 1998; Finch, Sobin, Carmody, DeWitt, & Shiwach, 1999; Gass, 1998; Hermann, Ettner, Dowart, Hoover, & Yeung, 1998).

The belief held by many outside the mental health professions that ECT is dangerous, unnecessary, and misused is erroneous. Dr. Daniel Dye was a psychiatric resident with the diagnosis of bipolar disorder. He took lithium regularly after an initial course of ECT for severe depression. He is quoted by Restak (1988) in a case study as saying that ECT is "the gold standard" (p. 188). He felt that ECT broke through his depression and stopped it. Research supports the efficacy, safety, and economic savings of the use of ECT; however, the use of ECT varies widely and depends on geographic location (Irvin, 1997; Olfson, Marcus, Sackeim, Thompson, & Pincus, 1998; Salzman, 1998; Sherman, 2000; Wheeldon, Robertson, Eagles, & Reid, 1999). Rey & Walter (1997) suggest that more research and education of professionals and the public are needed, since information is necessary in order to accept or reject the opinions and criticisms of those who wish to limit the use of ECT. The purpose of this article is to provide basic information on ECT to mental health counselors for use in developing and providing more effective services to clients considering, receiving, or completing a course of ECT.

APPLICATIONS

When ECT was developed it was often given without adequate sedation beforehand and without the use of muscle relaxants to prevent violent seizures. ECT was a frightening and risky procedure. As a result of this, ECT was frequently portrayed inappropriately in films as a form of punishment with which to control unruly patients (Salzman, 1998).

Background

Convulsive therapy as a treatment for schizophrenia was introduced by von Meduna and reported in 1934. His reasoning for such an approach was based on two observations long noted by mental hospital physicians. The first was that patients would suddenly lose their symptoms when they had a convulsion. The second was the belief, now known to be erroneous, that epilepsy and schizophrenia rarely occurred in the same patient (Restak, 1988).

Von Meduna's work followed that of another Hungarian, Nyiro, who treated schizophrenic patients with the blood from epileptic patients (Restak, 1988). This treatment proved unsuccessful, so von Meduna induced actual convulsions in patients with schizophrenia by injecting camphor in oil intramuscularly. This was found to be unreliable, since it was not possible to predict when the first convulsion would occur. Some patients would have several convulsions, and some patients would have no convulsions at all. Von Meduna changed to a soluble synthetic camphor preparation, Metrazol (pentylenetetrazol), which was injected intravenously. In the majority of cases, this produced a convulsion within 30 seconds (Butcher, Carson, & Coleman, 1988). Several pharmacological convulsive agents were used after Metrazol was introduced. Usage of only one continued; hexaflourodiethyl ether, or Indoklin, produces a tonic-clonic seizure when inhaled (Freedman, Kaplan, & Sadock, 1975).

In 1938, two Italian workers, Cerletti and Bini, used electrically induced convulsions in place of pharmacological convulsive therapy. Bini built a simple apparatus using alternating current. Most machines used today are still based on his model. Other machines have been introduced over the years, and there is much controversy over whether modified currents produce less confusion and reduce memory impairments seen in patients after a course of electroconvulsive therapy than machines based on Bini's design. Today, ECT machines are classified as Class III devices by the Federal Food and Drug Administration (FDA), which means that ECT is an experimental procedure, classified in the highest risk category by the FDA. The machines have not gone through the rigorous FDA testing required of medical devices, including safety testing and efficacy assessments (Breeding, 2000). Regulation of ECT is done by each state and varies widely. The American Psychiatric Association offers guidelines for the use of ECT, and research is ongoing to determine efficacy, electrode placement, and optimum stimulus intensity (Bailine, Rifkin, Kayne, & Selzer, 2000; Prudic, Haskett, Mulsant, & Malone, 1996; Rey & Walter, 1997).

Treatment Recommendations

Originally used to treat schizophrenia, ECT was largely replaced by the use of antipsychotic drugs in the 1950s. Today, fewer than 20% of the clients given ECT are diagnosed as having schizophrenia. ECT is still used in the emergency treatment of some intractable psychotic patients, but probably does not change the course of the illness (Reid, 1989). It may benefit those with major depression, bipolar disorder, and some forms of schizophrenia, including catatonia (Hermann, Dorwart, Hoover, & Brody, 1995). It is useful for several types of schizophrenic episodes, but most clinicians feel that pharmacological treatment is preferable at all stages of schizophrenia. However, a client who suffers from schizo-affective disorder, with serious suicide risk, morbid withdrawal, or manic or catatonic agitation, who is unresponsive to medication, is a good candidate for ECT. In a review of all studies published in English on the use of electroconvulsive therapy in persons 18 years of age and younger, Rey and Walter (1997) found that rates of improvement or remission of symptoms, based on pre-treatment and post-treatment scores on the Beck Depression Inventory, Hamilton Depression Rating Scales, and autobiographical reports, were 63% for depression, 80% for mania, 42% for schizophrenia, and 80% for catatonia. It has not been found effective with clients with obsessive compulsive disorder (Shusta, 1999).

Electroconvulsive therapy is frequently recommended for life-threatening mania, unless pharmacological regimens can take effect quickly (Walter & Rey, 1999; Willoughby, Hradek, & Richards, 1997). Prior to the development of lithium and the neuroleptics, ECT was the most effective treatment available for the rapid cycling of manic-depressive illnesses and was used quite often.

ECT is probably the safest and most effective treatment for major depression with psychotic features and is the treatment of choice for the client suffering concurrently from depression and heart disease, since tricyclic antidepressants may activate adrenergic mechanisms in the heart in addition to those in the brain and produce dangerous abnormalities in cardiac rhythm (Andreasen, 1984).

Certain signs and symptoms indicate an improved response to electroconvulsive therapy. These include: (a) psychomotor retardation or agitation, (b) early morning insomnia, (c) sustained depression relatively uninfluenced by environmental changes, (d) delusions, (e) feelings of guilt or unworthiness, and (f) diurnal rhythm. Response is also improved if the client possesses a relatively normal personality prior to or between attacks of depression.

The client with (a) neurotic traits, (b) a fluctuating level of depression, (c) initial insomnia, (d) broken sleep, or (e) poorly adjusted personality prior to depression will show a less favorable response to electrotherapy and relapse more often. ECT is not effective for treating antisocial personality disorder and is ineffective and may have adverse effects in anxiety states (Blais, Matthews, Schouten, O'Keefe, & Summergrad, 1998; Butcher et al., 1988).

Expected Improvement

Some clients suffering from depression do not respond to antidepressant medication or cannot take any because of serious side effects (Irvin, 1997). These clients often respond with dramatic improvement after one or two treatments. One study showed that 72% of those treated with ECT improved versus 59% of those who did not receive ECT, and the duration of the depressive episode was cut from an average of 4 and one-half months to 2 and one-third months (Freedman et al., 1975). Recent research by Prudic et al. (1996) concluded that resistance to heterocyclic antidepressants predicted poorer outcome after ECT, while resistance to selective serotonin reuptake inhibitors and monoamine oxidase inhibitors did not show significant predictive relations. However, ECT does not prevent further episodes, and ECT does not substitute for ongoing drug treatment combined with psychotherapy. It is usually reserved for depressive episodes where no treatment works and the patient is dangerously depressed or suicidal (Olfson et al., 1998; Rey & Walter, 1997).

Research indicates that ECT is at least as effective as antidepressant medications for the treatment of major depression (Olfson et al., 1998). Clients respond to antidepressant medication in 2 to 4 weeks, and maximal effects are produced by the medications in 4 to 8 weeks. The possibility of relapse is reduced with the addition of psychological treatment. Clients who undergo ECT also respond with symptom ratings returning to normal within 5 to 6 weeks if the treatment is successful. However, complete recovery may take up to 1 year after treatment, and mental health counseling aids recovery and helps to prevent relapse (Blazer, 1996).

Procedure

Before instituting ECT, consent should be obtained as for a surgical procedure, since anesthesia will be involved. At the same time, a video-tape showing an actual treatment can be viewed by the client (and family, if applicable) to allay any fears regarding ECT. The procedure is much less distressing than fantasy or movie portrayals.

A pre-ECT workup should be done, which includes a complete history and physical examination, including chest X-rays and an electrocardiogram for clients over 40. A complete blood count, serum chemistries and electrolytes, sickle cell screening for African-American patients, and urinalysis should also be done (Reid, 1989). At this time, the only contraindication for ECT is increased cranial pressure in the patient or sensitivity to transient increases in intracranial pressure. The presence of physical illness does not appear to be a contraindication (Rey & Walter, 1997).

Monoamine oxidase inhibitors should be discontinued 2 weeks prior to ECT because of possible interference with anesthetics or emergency medications. There is some disagreement about whether or not the use of phenothiazines should be stopped. Some physicians believe use should be stopped because of possible transient impairment of autonomic regulatory mechanisms when used to treat catatonic stupor while others are of the theory that ECT is more effective if medication is continued (Krystal, Dean, Weiner, & Tramontozzi, 2000). If a patient is taking Lithium, a level should be drawn before treatment and twice a week during ECT.

The treatment is performed on an inpatient or outpatient basis, with the client first receiving an anesthetic to put him or her to sleep. A muscle relaxant is then given to prevent sprains and fractures as a result of the convulsions induced by the therapy. An electric current lasting one-half to one and one-half seconds is passed between electrodes placed on the scalp, which causes a motor seizure called a grand mal seizure or convulsion that lasts 25 to 120 seconds. The popular term shock therapy is misleading, since the client feels no shock.

The client should ingest nothing for 4 hours before treatment. He or she should empty his or her bladder if possible. Dentures should be removed except in the case of partial dentures. Tightening of the jaw muscles may result in the breakage of teeth in clients who have had partial dentures removed, so these appliances should be left in. Emergency drugs and equipment should be readily available for use during ECT if necessary, since the danger of complications due to use of anesthesia are the same as they are during surgery. The treatment table must be insulated.

An anesthesiologist should be present to administer the anesthesia. This can be done either intravenously or with syringes. The anesthesiologist will first give the patient 100% oxygen by mask for several minutes. This is done because the muscle relaxant that is needed to prevent sprains and fractures during convulsions also will suppress respiration. The anesthetic is then administered followed immediately by a muscle relaxant. It is advisable not to mix the two, since the client will feel the muscle relaxant acting on his or her respiration before falling asleep. To minimize discomfort and subsequent fear, the anesthetic must be administered first.

Paralysis will be manifested by tremors, loss of knee reflexes, and finally complete paralysis. At this point, a gag or bite block is inserted and two electrodes are placed unilaterally or bilaterally on the temples.

The electrical stimulus used should be just enough to produce an adequate seizure. This will increase with each treatment. The amount of current varies with each person, with males having a lower threshold than females. There is concern that the seizure threshold may be lower in children and adolescents; however, research results have not supported this. Originally the amount of current applied was 70 to 130 volts for one-tenth to one-half second. Now 70 to 100 volts are passed through the brain for a period of one to two seconds (Gazzaninga, 1988).

The presence of a seizure can be ascertained by electroencephalogram (EEG) readings, by monitoring heart rate, or by careful observation of any convulsive muscle contractions not entirely suppressed. If the amount of current is not sufficient, the patient will have a petit mal response, which is not sufficient for the therapeutic effect. The stimulus may be increased and repeated after one to two minutes until a seizure is achieved in which the tonic phase lasts about 10 seconds and the clonic phase 30 to 40 seconds. After the seizure is over, oxygen is administered until normal respiration resumes.

The client regains consciousness after a few minutes, but remains in a clouded state for 15 to 30 minutes. Many clients remain somewhat confused, reportedly for up to 6 hours, with the period of disorientation increasing with each treatment but ending 36 hours after the final treatment (Johnstone, 1999). Disorientation is very frightening for the client, who experiences it as a loss of identity and may experience increasing anxiety regarding further treatment as a result. The client will need constant reassurance and support during these periods.

Treatments are given every 2 or 3 days, for a total of 8 to 15 sessions. Improvement may occur within the first few days, but a complete series should be given. After ECT, maintenance dosages of antidepressant and antianxiety drugs ordinarily are given to maintain the treatment gains achieved until the depression has run its course.

Adverse Effects and Side Effects

Prolonged seizures and post-ECT seizures have been reported in patients who were concurrently taking desipramine and trifluoperazine (Rey & Walter, 1997). Generally, administration of medication stops and time is allowed for the medication to clear the body before beginning ECT.

Clients frequently complain of headaches and neck and muscle soreness, particularly after the first few treatments. The muscle soreness diminishes with subsequent treatment.

Transient anterograde and retrograde amnesia occur during treatment and may last for up to several weeks after termination of treatment. It is suspected that minor, transient side effects have often been underreported or overlooked (Rey & Walter, 1997). The longer the period of post-traumatic amnesia the greater the severity of the brain damage. However, investigations by psychologists have shown that no lasting memory impairment occurs (Barnes, Hussein, Anderson, & Powell, 1997; Cohen et al., 2000).

Other cognitive impairment is unusual, and many expected complications do not occur. The electrically induced convulsion is not different from a spontaneous one. No pre-existing disease becomes worse when a patient experiences a convulsion induced by ECT. For this reason, the only definite contraindications to ECT are brain tumors. The sudden increase in intracranial pressure during a convulsion can cause severe neurological symptoms and death in cases where a brain tumor simulates a depression and ECT is applied for this reason.

Some clinicians argue that the application of ECT to the left hemisphere of the brain is more injurious to speech in right-handed people than a similar application to the right hemisphere and that all such results are much more variable with left-handers (Smith, 1984). Post-traumatic amnesia is the most reliable form of measurement of what is happening internally in either case.

After ECT, EEG monitoring indicates brain wave activity is slowed. This is a highly individual factor. EEG slow-wave abnormalities result after a series of ECT treatments and are associated with organic mental signs. This persists for several days or weeks. Occasionally it never returns to normal, but clinical evidence of organic cerebral disease usually does not persist. Bender's study (as cited in Rey & Walter, 1997) showed evidence of a correlation between EEG abnormalities after ECT and success of the treatment.

The most serious complication appears to be associated with the risk of anesthesia. Some hospitals still consider this risk to be too high and perform unmodified ECT. In these cases, the risks of sprains and fractures associated with convulsions increases. Sprains and fractures do not occur in spontaneous epileptic seizures, probably because epileptics go into a seizure slowly, while therapeutic convulsions start suddenly.

IMPLICATIONS FOR COUNSELORS

Various kinds of psychological stress may initiate a physical response in the body that may eventually trigger depressive symptoms. Mental health counselors, particularly those working closely with psychiatrists, are aware that biological treatment is an important first line intervention, but psychosocial aspects must not be omitted or underestimated. After ECT is applied, mental health counseling should accompany pharmacological treatment, since 30% to 50% of patients who have had a depressive episode at one time are likely to have another at some time later in life (Blazer, 1996). Severe episodes are treated with a full series of ECT until the presenting symptoms have been relieved.

Client Consideration of ECT

When the possibility of ECT is initially presented to the client, it has been suggested that there is frequent denial and minimization of harmful effects (Breeding, 2000). The counselor can describe the procedure in detail and answer questions regarding the procedure, including risks, benefits, and the possible cognitive and psychological consequences (Baldwin & Jones, 1998; Breeding, 2000). Information should be given to the client in writing that is free of jargon and easily read and understood by the patient. It should be stressed that although most people appear to find ECT helpful, they also report side-effects, with memory impairment most frequently reported, followed by headaches and confusion (Johnstone, 1999).

The counselor will need to be sensitive to the perceived threat of involuntary treatment, since clients may believe that they must do what their physician tells them regardless of their feelings about the matter (Breeding, 2000; Johnstone, 1999). Encourage the client to express his or her feelings regarding the treatment and the possible side effects. The client may need assurance from the counselor that it is acceptable and to his or her benefit to be actively involved in the decision-making process. It should also be made clear to the client that consent can be withdrawn at any stage, even after signing the consent form.

During the Course of ECT

Fears that have been reported by clients regarding ECT include worries about brain damage, death, personality change, and being anaesthetized. The counselor may need to spend some time with the client in the alleviation of anxiety, which is often a result of the lack of knowledge regarding the procedure. Uken (cited in Johnstone, 1999) found that psychological after-effects of ECT may include loss of confidence, dignity, and self-esteem; fear of hospitals and psychiatry; anger and aggression; loss of self; and nightmares.

Reaction to treatment may be very strong, necessitating periodic debriefing of the client by the counselor. Johnstone (1999) found that 20 out of 22 clients interviewed found ECT to be upsetting or distressing, although each had experienced full recovery, and none had experienced relapse. Debriefing during the course of treatment can help to alleviate fear and prevent flashbacks and nightmares in the future.

Following ECT

Supportive counseling on a follow-up basis can be a substantial contributor to total recovery for clients attempting to reintegrate themselves into their former social networks. Visits of 25 minutes each may be scheduled at extended intervals, during which the counselor can recognize and reflect to the client the difficulties faced by someone who has had an embarrassing, if not stigmatizing, psychiatric illness.

Although most of the depressive symptoms may appear to decline with outpatient ECT, rating scales should be complemented with a qualitative assessment of the perceptions of the client. Johnstone (1999) surveyed clients who had received ECT and found that the most optimistic outcomes were for those who were able to reverse previous patterns of powerlessness and compliance by directing their anger outwards and taking control of their lives again. Group counseling may be beneficial. Such groups may combine psychotherapeutic and psychoeducational interventions to help clients develop realistic expectations regarding their recovery period, learn new coping methods, and relieve fears of further loss of power and control. The support of others who have had a similar experience can bolster confidence, increase compliance with pharmacotherapy, and relieve loneliness.

Counseling Family Members

Family counseling (often of a short-term, psychoeducational nature) may be utilized to help family members and address any concerns they may have regarding the diagnosis, the treatment, and the prognosis. Family members may experience concern regarding adverse treatment effects, and the counselor can offer assurance that adverse effects are not long-lasting.

In addition, some clients may improve and return to their normal mood and functional state while still in the hospital, while others may improve more slowly (Blazer, 1996). Risk for relapse during the months after recovery is high, particularly when client anxiety is high (Flint & Rifat, 2000), and family members may be hypervigilant during this period. They may benefit from supportive counseling individually as well as with the client and other family members. Group counseling with other clients' family members may provide assurance and support and relieve anxiety and feelings of isolation.

Counselors can also use follow-up sessions to monitor the client and stress the importance of reporting any increase of symptoms that may suggest another depressive episode.

Cautions are more than warranted regarding ECT (Woody, 1981). However, somatic therapy can be successfully combined with individual and group counseling directed at helping the client develop a more stable, long-range adjustment. Blazer (1996) reported that clearly explaining the procedure and the possible ramifications, supportive counseling during the procedure, and supportive counseling for up to one year after ending ECT were helpful for an elderly client in achieving full recovery. Mental health counselors can educate themselves about ECT and provide supportive interventions to their clients.

REFERENCES

Andreasen, N. C. (1984). The broken brain--the biological revolution in psychiatry. New York: Harper & Row.

Bailine, S. H., Rifkin, A., Kayne, E., & Selzer, J. (2000). Comparison of bifrontal and bitemporal ECT for major depression. The American Journal of Psychiatry, 157, 121-123.

Baldwin, S., & Jones, Y. (1998). Is electroconvulsive therapy unsuitable for children and adolescents? Adolescence, 33, 645-655.

Barnes, R. C., Hussein, A., Anderson, D. N., & Powell, D. (1997). Maintenance electroconvulsive therapy and cognitive function. British Journal of Psychiatry, 170, 285-287.

Blais, M. A., Matthews, J., Schouten, R., O'Keefe, S. M., & Summergrad, P. (1998). Stability and predictive value of self-report personality traits pre- and post-electroconvulsive therapy: A preliminary study. Comprehensive Psychiatry, 39, 231-235.

Blazer, D. G. (1996). Severe episode of depression in late life: The long road to recovery. The American Journal of Psychiatry, 153, 1620-1623.

Breeding, J. (2000). Electroshock and informed consent. Journal of Humanistic Psychology, 40, 65-79.

Butcher, J., Carson, R., & Coleman, J., (Eds.). (1988). Abnormal psychology and modern life (2nd ed.). Glenview: Scott, Foresman.

Cohen, D., Taieb, O., Flament, M., Benoit, N., Chevret, S., Corcos, M., Fossati, P., Jeammet, P., Allilaire, J. F., & Basquin, M. (2000). Absence of cognitive impairment at long-term follow-up in adolescents treated with ECT for severe mood disorder. American Journal of Psychiatry, 157, 460-462.

Finch, J. M., Sobin, P. B., Carmody, T. J., DeWitt, A. P., & Shiwach, R. S. (1999). A survey of psychiatrists' attitudes toward electroconvulsive therapy. Psychiatric Services, 50, 264-265.

Flint, A. J., & Rifat, S. L. (2000). Maintenance treatment for recurrent depression in late life. A four-year outcome study. American Journal of Geriatrics Psychiatry 8, 112-116.

Freedman, A., Kaplan, H., & Sadock, B. (Eds.). (1975). Comprehensive textbook of psychiatry (2nd ed.). Baltimore, MD: Williams & Wilkins.

Gass, J P. (1998). The knowledge and attitudes of mental health nurses to electroconvulsive therapy. Journal of Advanced Nursing, 27, 83-90.

Gazzaninga, M. (1988). Mind matters: How the mind and brain interact to create our conscious lives. Boston: Houghton Mifflin.

Hermann, R. C., Dorwart, R. A., Hoover, C. W., & Brody, J. (1995). Variation in ECT use in the United States. American Journal of Psychiatry, 152, 868-874.

Hermann, R. C., Ettner, S. L., Dorwart, R. A., Hoover, C. W., & Yeung, E. (1998). Characteristics of psychiatrists who perform ECT. American Journal of Psychiatry, 155, 889-894.

Irvin, S. M. (1997). Treatment of depression with outpatient electroconvulsive therapy. AORN Journal, 65, 573-578, 581-582.

Johnstone, L. (1999). Adverse psychological effects of ECT. Journal of Mental Health, 8, 69-85.

Kramer, B. A. (1999). A teaching guide for electroconvulsive therapy. Comprehensive Psychiatry, 40, 327-331.

Krystal, A. D., Dean, M. D., Weiner, R. D., & Tramontozzi, L. A., III. (2000). ECT stimulus intensity: Are present ECT devices too limited? American Journal of Psychiatry, 157, 963-967.

Olfson, M., Marcus, S., Sackeim, H. A., Thompson, J., & Pincus, H. A. (1998). Use of ECT for the inpatient treatment of recurrent major depression. American Journal of Psychiatry, 155, 22-29.

Prudic, J., Haskett, R. F., Mulsant, B., & Malone, K.M. (1996). Resistance to antidepressant medications and short-term clinical response to ECT. American Journal of Psychiatry, 153, 985-995.

Reid, W. (1989). The treatment of psychiatric disorders revised for the DSM-III-R. New York: Brunner/Mazel.

Restak, R. (1988). The mind. New York: Bantam Books.

Rey, J. M., & Walter, G. (1997). Half a century of ECT use in young people. American Journal of Psychiatry, 154, 594-602.

Salzman, C. (1998). ECT, research, and professional ambivalence. American Journal of Psychiatry, 155, 1-2.

Sherman, C. (2000). Adjust dose, schedule to smooth ECT in elderly. Clinical Psychiatry News, 28, 24.

Shusta, S. R. (1999). Successful treatment of refractory obsessive-compulsive disorder. American Journal of Psychotherapy, 53, 377-391.

Smith, A. (1984). The mind. New York: Viking Press.

Walter, G., & Rey, J. M. (1999). Practitioner review: Electroconvulsive therapy in adolescents. Journal of Child Psychology and Psychiatry and Allied Disciplines; 40, 325-334.

Wheeldon, T. J., Robertson, C., Eagles, J. M., & Reid, I. C. (1999). The views and outcomes of consenting and non-consenting patients receiving ECT. Psychological Medicine, 29, 221-223.

Willoughby, C. L., Hradek, E. A., & Richards, N. R. (1997). Use of electroconvulsive therapy with children: An overview and case report. Journal of Child and Adolescent Psychiatric Nursing, 10, 11-17.

Woody, R. H. (Ed.). (1981). Encyclopedia of clinical assessment. San Francisco: Bass.

Tracy C. Leinbaugh, Ph.D., is an assistant professor, Department of Counseling and Higher Education, Ohio University, Athens, OH Email [e-mail]