Treatment for Anxiety Disorders

Can Anxiety Disorders Be Treated?

Fortunately, the vast majority of people with an anxiety disorder can be helped with the right professional care. There are no guarantees, and success rates vary with the circumstances. Treatment periods vary. Some individuals require only a few months of treatment, while others need a year or more. People with anxiety disorders often have more than one disorder, which can complicate treatment. Equally, substance abuse and clinical depression often co-exist in patients with an anxiety disorder.

Treatment Options

Treatment must be specially tailored for each individual, but there are a number of standard approaches. Individuals with anxiety disorders can almost always be treated without being admitted to a hospital.

Generally, therapists use a combination of the following treatments; there is no single correct approach.

NAME

GOAL

HOW IT WORKS

BENEFITS

DRAWBACKS

Behavior Therapy

Modify and gain control over unwanted behavior Learning to cope with difficult situations, often through controlled exposure to them Person actively involved in recovery skills that are useful for a lifetime Can take time to achieve results

Cognitive Therapy

Change unproductive thought patterns Examine feelings and learn to separate realistic from unrealistic thoughts Person actively involved in recovery skills that are useful for a lifetime Can take time to achieve results

Medication

Resolve symptoms Help restore chemical imbalances that lead to symptoms Effective for many people, enables other treatment to move forward Most medications have side effects

Relaxation Techniques

Help resolve stresses that can contribute to anxiety Breathing re- training, exercise and other skills Person actively involved in recovery skills that are useful for a lifetime Can take time to achieve results

Treatment is successful in as many as 90 percent of anxiety disorder patients. Most people respond best to a combination of the four options summarized in this table.

Treatments have been largely developed through research conducted by the National Institute of Mental Health (NIMH) and other research institutions. They are extremely effective and often combine medication or specific types of psychotherapy.

More medications are available than ever before to effectively treat anxiety disorders. These include antidepressants or benzodiazepines. If one medication is not effective, others can be tried. New medications are currently being tested or are under development to treat anxiety symptoms.

The two most effective forms of psychotherapy used to treat anxiety disorders are behavioral therapy and cognitive-behavioral therapy. Behavioral therapy tries to change actions through techniques such as diaphragmatic breathing or through gradual exposure to what is frightening. Cognitive-behavioral therapy teaches patients to understand their thinking patterns so they can react differently to the situations that cause them anxiety.

GAD

In-depth look at options for treatment of anxiety disorders and panic attacks; including benefits and drawbacks of each anxiety treatment.Treatment for Generalized Anxiety Disorder often includes a combination of medication and therapy. Busipirone is frequently prescribed although other drugs are being researched. Therapeutic techniques can include cognitive or behavior therapy (see box), relaxation techniques, and biofeedback to alleviate muscle tension.

PAD

The physical symptoms associated with panic disorder can make diagnosis more difficult. Often, it is mistaken for heart disease, thyroid problems, respiratory disease or hypochondria.

Recent research has shown that the roots of panic disorder are both physical and psychological. The most successful treatment approach for panic disorder combines medication with cognitive and behavior therapy. In particular, medications, such as antidepressants and benzodiazepines, have proven effective for 75 to 90 percent of sufferers.

Phobias

Treatment usually involves desensitization or exposure therapy through which the sufferer is exposed to the source of the phobia and gradually learns to overcome the fear. Exposure therapy can significantly reduce or end phobic reactions for at least seven years. Therapy is often combined with medication, such as antianxiety drugs, antidepressants and, in some cases, tranquilizers.

OCD

Behavior therapy is used to expose individuals to situations that provoke their compulsions and help them learn how to decrease and eventually refrain from performing the rituals. This treatment approach has been successful for 50 to 90 percent of those suffering from OCD. Because OCD may be accompanied by depression, it is important to identify whether this illness is present and treat it concurrently. For some individuals medications, such as chlomipramine or fluoxetine, are effective in alleviating obsessions.

PTSD

Post-traumatic stress disorder can be successfully treated. Individual psychotherapy helps survivors work through their pain and grief. Support groups or peer counseling groups enable survivors of similar traumatic events to share their experiences and reactions. Family therapy may also be an important component of the treatment process. Medications, such as antidepressants, lithium, benzodiazepines, and beta-blockers, can help control the symptoms of PTSD.

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APA Reference
Staff, H. (2007, February 19). Treatment for Anxiety Disorders, HealthyPlace. Retrieved on 2024, December 19 from https://www.healthyplace.com/anxiety-panic/articles/treatment-for-anxiety-disorders

Last Updated: July 1, 2016

The Importance of Breathing Through Your Nose

breathing techniques for anxiety disorders. For sufferers, survivors of anxiety disorders, panic disorders, phobias. Expert information, panic, anxiety, phobias support groups, chat, journals, and support lists.Many of us are habitual mouth breathers--either in our daily life or when we are exercising or stressed out. For most of us, this habit began in childhood and not only diminishes our energy but also undermines our health and well-being.

Except for emergencies, our breathing was designed to take place mainly through our nose. The hairs that line our nostrils filter out particles of dust and dirt that can be injurious to our lungs. When too many particles accumulate on the membranes of the nose, we automatically secret mucus to trap them or sneeze to expel them. The mucous membranes of our septum, which divides the nose into two cavities, further prepare the air for our lungs by warming and humidifying it.

There is another important reason for breathing through the nose, one that was not taught to us in school or by our parents. This has to do with maintaining the correct balance of oxygen and carbon dioxide in our blood. When we breathe through our mouth we usually inhale and exhale air quickly in large volumes. This can lead to hyperventilation (breathing excessively fast for the actual conditions in which we find ourselves). It is important to recognize that it is the amount of carbon dioxide in our blood that generally regulates our breathing. If we release carbon dioxide too quickly, the arteries and vessels carrying blood to our cells constrict and the oxygen in our blood is unable to reach the cells in sufficient quantity. This includes the carotid arteries, which carry blood (and oxygen) to the brain. The lack of sufficient oxygen going to the cells of the brain can turn on our sympathetic nervous system, our "fight or flight" response, and make us tense, anxious, irritable, and depressed.

One researcher, Dr. Konstantin Buteyko of Russia, claim that insufficient carbon dioxide in our blood also leads to the symptoms of asthma, various other breathing disorders, and even angina, as the body struggles to maintain the correct balance of oxygen and carbon dioxide. He states that to keep the right balance in someone whose carbon dioxide level is too low the body automatically tries to increase the amount of carbon dioxide in the blood by constricting the airways, swelling tissues, secreting mucus, and so on--thus making it more difficult to quickly inhale and exhale large volumes of air.

Dr. Buteyko has apparently had great success in treating asthma and other disorders emphasizing nose breathing and using special techniques, including shallow breathing and breath-holding, designed to reduce the volume of air that we breathe and increase the carbon dioxide level in the blood. As promising as this approach may seem in relation to health problems such as asthma, however, breath-holding and intentional shallow breathing are neither healthy nor natural for the majority of us, and any effort to impose them on our breathing to increase our carbon dioxide level would lose many of the benefits of natural breathing, which utilizes, when necessary, the full range of coordinated movement in our diaphragm, belly, and ribcage.

A SIMPLE PRACTICE

Here's a simple, beneficial practice you can try. Over the next few days or weeks, see if you can observe and sense your breathing several times a day in the middle of your activities. Notice whether or not you are breathing through your mouth. Also notice how often you hold your breath. For some of you, mouth breathing or breath holding may be a frequent activity. For others, it may occur mainly in physically, emotionally, or mentally stressful situations. When you notice yourself breathing through your mouth or holding your breath, remind yourself to breathe through your nose and to stop holding your breath.

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APA Reference
Staff, H. (2007, February 19). The Importance of Breathing Through Your Nose, HealthyPlace. Retrieved on 2024, December 19 from https://www.healthyplace.com/anxiety-panic/articles/the-importance-of-breathing-through-your-nose

Last Updated: July 1, 2016

California Figures From the Department of Mental Health

Statistics from the Department of Mental Health about the use and effects of Electroconvulsive Therapy (ECT).Despite the American Psychiatric Association's claim that only 0.5 percent (1 in 200) of electroconvulsive therapy (ECT) patients suffer memory loss, statistics from California show that the actual figure is 40 times that amount. California is one of a small number of states that require reporting of ECT statistics.

It is estimated that between 100,000 and 200,000 patients undergo ECT in the United States every year. Why is it only an estimate? Because only four states (Colorado, California, Texas, Massachusetts) require reporting on ECT statistics.

The National Alliance for the Mentally Ill (NAMI) opposes such reporting, despite the fact that such reporting is anonymous. There is only one reason for such opposition - NAMI apparently wants to silence any revelations such reporting might reveal.

In California, statistics are gathered quarterly and maintained by the California Department of Mental Health. The following statistics are gathered: number of patients receiving treatment, their age, sex and race, number of treatments given, complications, and any "excessive treatments" (any patients receiving more than 15 treatments within a 30-day period, or anyone receiving more than 30 treatments in one year).

Complications are limited to:

a) non-fatal cardiac arrests or arrhythmias which required resuscitative efforts.
b) fractures
c) apnea persisting 20 minutes or more after initiation of treatment
d) memory loss reported by the patient extending more than 3 months following the completed course of treatment.
e) deaths which occur during or within the first 24 hours after a treatment.

The following is from California for a period of six years, 1989 through 1994. 1993 figures were unavailable. (Or you can go directly to the full statistics, directly from CDMH. If your browser does not support tables, you may email me and I'll send them to you directly in an MS Word file.)

During this period, over 12 thousand persons received ECT. Of those, 445 (3.6%) were involuntary patients. Of all persons receiving ECT during these five years in California, 364 (3%) received ECT without consent. Of those who did not consent to treatment, 287 were deemed by the state to be incapable of providing consent, and 77 were judged to have the capacity, but refused to provide consent (the treatment was forced completely against their will).

Approximately 50 percent were age 65 or older. 21 (1.7%) were under the age of 18. 68 percent of all patients were female. Slightly more than 90 percent were white, with 2.3 percent black, and 4.5 percent Hispanic. The remaining were categorized as "other" ethnic groups.

Medicaid/Medicare paid for over half of these patients' treatments, with private insurance and private pay each paying for slightly over 20 percent.

More than one-fifth of all patients had serious complications. The most often reported complication (19.7% of all patients and 93.6% of all complications) was extended memory loss. For reporting purposes, this consisted of memory loss lasting longer than three months. The second most common complication was apnea (cessation of breathing) lasting longer than 20 minutes (1.25% of all patients, and 5.9% of all complications).

Other complications included non-fatal cardiac arrest and fractures. No deaths attributed to ECT were reported in this period, but the conditions of reporting mandate that the death must occur within 24 hours of treatment.

Figures from California Dept. of Mental Health as reported to the California State Legislature 1989-1994 (1993 not available)

Number Of Patients Who Received ECT By Patient Type

Year Total Voluntary Voluntary Involuntary Involuntary
- - With Consent Without Consent With Consent Without Consent
1989 2,503 2,403 4 33 63
1990 2,671 2,566 12 26 67
1991 2,251 2,160 11 34 46
1992 2,356 2,233 9 42 72
1994 2,529 2,426 41 23 39
Totals 12,310 11,788 77 158 287

Number Of Patients By Age, Gender, Ethnicity, Payer

By Age Group

Age 1989 1990 1991 1992 1994 Total
12-15 2
(0.1%)
2
(0.1%)
2
(0.1%)
0 0 6
(0.04%)
16-17 2
(0.1%)
7
(0.3%)
3
(0.1%)
2
(0.1%)
1
(0.04%)
15
(0.1%)
18-24 63
(2.5%)
95
(3.6%)
62
(2.8%)
40
(1.7%)
42
(1.7%)
302
(2.5%)
25-44 627
(25%)
710
(26.6%)
531
(23.6%)
566
(24%)
518
(20.5%)
2,952
(24%)
45-64 607
(24.3%)
583
(21.8%)
515
(22.9%)
599
(25.4%)
677
(26.8%)
2,981
(24.2%)
65+ 1,202
(48%)
1,274
(47.7%)
1,133
(50.3%)
1,149
(48.8%)
1,280
(50.6%)
6,038
(49%)
Unknown 0 0 5
(0.2%)
0 11
(0.4%)
16
(0.1%)

By Gender

Sex 1989 1990 1991 1992 1994 Total
Male 798
(31.9%)
903
(33.8%)
671
(29.8%)
814
(32.2%)
751
(31.9%)
3,937
(32%)
Female 1,705
(68.1%)
1,768
(66.2%)
1,580
(70.2%)
1,715
(67.8%)
1,605
(68.1%)
8,373
(68%)

By Ethnic Group

Ethnicity 1989 1990 1991 1992 1994 Total
White 2,271
(90.7%)
2,394
(89.6%)
2,050
(91.1%)
2,140
(90.8%)
2,279
(90.1%)
11,134
(90.4%)
Black 58
(2.3%)
60
(2.2%)
58
(2.6%)
49
(2.1%)
64
(2.5%)
289
(2.3%)
Hispanic 108
(4.3%)
133
(5%)
82
(3.6%)
104
(4.4%)
122
(4.8%)
549
(4.5%)
Other 66
(2.6%)
84
(3.1%)
61
(2.7%)
63
(2.7%)
64
(2.5%)
338
(2.7%)

Source of Payment

Source 1989 1990 1991 1992 1994 Total
Private 669
(26.7%)
652
(24.4%)
515
(22.9%)
522
(22.2%)
432
(17.1%)
2,790
(22.6%)
3rd Party 549
(21.9%)
528
(19.8%)
458
(20.3%)
507
(21.5%)
652
(25.8%)
2,694
(21.8%)
Public 1,146
(45.8%)
1,322
(49.5%)
1,192
(53.0%)
1,274
(54.1%)
1,240
(49.0%)
6,174
(50.2%)
Other 139
(5.8%)
169
(6.3%)
86
(3.8%)
53
(2.2%)
205
(8.1%)
652
(5.3%)

Number of Complications Resulting from ECT

For reporting purposes: memory loss lasting longer than three months after final treatment; apnea must last longer than 20 minutes; deaths must occur within 24 hours of treatment

1989

Total Complications: 520, 20% of Patients

Type of Complication Number Percent
Cardiac Arrest 0 0
Memory Loss 498 95.8
Fractures 0 0
Apnea 22 4.2
Deaths 0 0

1990

Total Complications: 656, 24.7% of Patients

Type of Complication Number Percent
Cardiac Arrest 1 0.2
Memory Loss 538 82.0
Fractures 3 0.5
Apnea 114 17.4
Deaths 0 0

1991

Total Complications: 530, 23.5% of Patients

Type of Complication Number Percent
Cardiac Arrest 1 0.2
Memory Loss 510 96.2
Fractures 2 0.4
Apnea 17 3.2
Deaths 0 0

 

1992

Total Complications: 252, 10.7% of Patients

Type of Complication Number Percent
Cardiac Arrest 2 0.8
Memory Loss 249 98.8
Fractures 0 0
Apnea 1 0.4
Deaths 0 0

1994

Total Complications: 631, 25% of Patients

Type of Complication Number Percent
Cardiac Arrest 2 0.3
Memory Loss 629 99.7
Fractures 0 0
Apnea 0 0
Deaths 0 0

Total Complications, 1989-1994

Totals: 2,589, 21% of all patients suffered complications

Complication Number % of all patients % of all complications
Cardiac Arrest 6 0.04 0.23
Memory Loss 2,424 19.7 93.6
Fractures 5 0.04 0.2
Apnea 154 1.25 5.9
Deaths 0 0 0

 

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APA Reference
Staff, H. (2007, February 19). California Figures From the Department of Mental Health, HealthyPlace. Retrieved on 2024, December 19 from https://www.healthyplace.com/depression/articles/california-figures-from-the-department-of-mental-health

Last Updated: April 10, 2013

The Practice of Electroconvulsive Therapy

Recommendations for Treatment, Training, and Privileging

A Task Force Report of the American Psychiatric Association

The APA Task Force on Electroconvulsive Therapy:

Richard D. Weiner, M.D., Ph.D. (Chairperson)
Max Fink, M.D.
Donald W. Hammersley, M.D.
Iver F. Small, M.D.
Louis A. Moench, M.D.
Harold Sackeim, Ph.D. (Consultant)

APA Staff

Harold Alan Pincus, M.D.
Sandy Ferris

Published by the American Psychiatric Association
1400 K Street, N.W.
Washington, DC 20005


11.4.3. Electrical Safety Considerations

a) The device's electrical grounding should not be bypassed. ECT devices should be connected to the same electrical supply circuit as all other electrical devices in contact with the patient, including monitoring equipment (see Section 11.7).

b) Grounding of the patient through the bed or other devices should be avoided, except where required for physiological monitoring (see Section 11.7).

11.5. Stimulus Electrode Placement

11.5.1. Characteristics of Stimulus Electrodes

Stimulus electrode properties should be in conformance with any applicable national device standards.

11.5.2. Maintenance of Adequate Electrode Contact

a) Adequate contact between stimulus electrodes and the scalp should be assured. Scalp areas in contact with stimulus electrodes should be cleansed and gently abraded.

b) The contact area of the stimulus electrodes should be coated with a conducting gel, paste, or solution prior to each use.

c) When stimulus electrodes are placed over an area covered by hair, a conducting medium, such as a saline solution, should be applied; alternatively, the underlying hair may be clipped. Hair beneath the electrodes should be parted prior to application of the stimulus electrodes.

d) Stimulus electrodes should be applied with sufficient pressure to assure good contact during stimulus delivery.

e) Conducting gel or solution should be confined to the area under the stimulus electrodes, and should not spread across the hair or scalp between stimulus electrodes.

f) A means of assuring the electrical continuity of the stimulus path is encouraged (see Section 11.4.1.(g)).

11.5.3. Anatomic Location of Stimulus Electrodes

a) Treating psychiatrists should be familiar with the use of both unilateral and bilateral stimulus electrode placement.

b) The choice of unilateral versus bilateral technique should be made on the basis of an ongoing analysis of applicable risks and benefits. This decision should be made by the treating psychiatrist in consultation with the consentor and the attending physician. Unilateral ECT (at least when involving the right hemisphere) is associated with significantly less verbal memory impairment than is bilateral ECT, but some data suggest that unilateral ECT may not always be as effective. Unilateral ECT is most strongly indicated in cases where it is particularly important to minimize the severity of ECT-related cognitive impairment. On the other hand, some practitioners prefer bilateral ECT in cases where a high degree of urgency is present and/or for patients who have not responded to unilateral ECT.

c) With bilateral ECT, electrodes should be placed on both sides of the head, with the midpoint of each electrode approximately one inch above the midpoint of a line extending from the tragus of the ear to the external canthus of the eye.

d) Unilateral ECT should be applied over a single cerebral hemisphere. Most practitioners using unilateral electrode placement routinely place both electrodes over the right hemisphere, since it is usually nondominant with respect to language even for the majority of left-handed individuals. Stimulus electrodes should be placed far enough apart so that the amount of current shunted across the scalp is minimized. A typical configuration involves one electrode in the standard frontotemporal position used with bilateral ECT, and the midpoint of the second electrode one inch ipsilateral to the vertex of the scalp (d'Elia placement).

e) Care should be taken to avoid stimulating over or adjacent to a skull defect.


11.6. Stimulus Dosing

a) The primary consideration with stimulus dosing is to produce an adequate ictal response (see Sections 11.8.1 and 11.8.2). Regardless of the specific dosing paradigm used, whenever seizure monitoring (see Section 11.7.2) indicates that an adequate ictal response has not occurred, restimulation should be carried out at a higher stimulus intensity.

Informed Consent

Since a considerable time period is involved, however, care should also be taken to ensure that the informed consent process continues across the complete period during which ECT is administered. Patient memories of consent for medical and surgical procedures in general are commonly faulty (Roth et al. 1982; Meisel and Roth 1983). For patients receiving ECT, this difficulty with recall may be exacerbated by both the underlying illness and the treatment itself (Sternberg and Jarvik 1976; Squire 1986). For these reasons, the consentor should be reminded in an ongoing fashion of his/her option to withdraw consent. This reminding process should also include a periodic review of clinical progress and side effects.

The occurrence of a substantial alteration in the treatment procedure or other factor having a major effect upon risk-benefit considerations should be conveyed to the consentor on a timely basis. The need for ECT treatments exceeding the range originally conveyed to the consentor as likely (see Section 11.10) represents one such example. All consent-related discussions with the consentor should be documented by a brief note in the patient's clinical record.

Continuation/maintenance ECT (see Section 13) differs from a course of ECT in that its purpose is the prevention of relapse or recurrence, and that it is characterized by both a greater inter-treatment interval and a less well-defined endpoint. Because the purpose of continuation/maintenance treatment differs from that used in the management of an acute episode, new informed consent should be obtained prior to its implementation. As a series of continuation ECT typically lasts at least 6 months, and because continuation/ maintenance ECT is, by its nature, provided to individuals who are in clinical remission and who are already knowledgeable regarding this treatment modality, a 6-month interval before readministration of the formal consent document is adequate.

There is no clear consensus as to who should obtain consent. Ideally, consent should be obtained by a physician who has both an ongoing therapeutic relationship with the patient and, at the same time, has knowledge of the ECT procedure and its effects. In practice this can be accomplished by the attending physician, treating psychiatrist, or their designees acting individually or in concert.

Information Provided

The use of a formal consent document for ECT ensures the provision of at least a minimum measure of information to the consentor, although consent forms vary considerably in scope, detail, and readability. For this reason, a sample consent form and sample supplementary patient information material are included in Appendix B. If these documents are used, appropriate modifications should be made to reflect local conditions. It is also suggested that any reproductions be in large type, to ensure readability by patients with poor visual acuity.

Earlier task force recommendations (American Psychiatric Association 1978), other professional guidelines, and regulatory requirements (Mills and Avery 1978; Tenenbaum 1983; Winslade et al. 1984; Taub 1987; Winslade 1988), as well as a growing concern regarding professional liability, have encouraged the use of more comprehensive written information as part of the ECT consent process. Such material is often contained wholly within the formal consent document, while others use an additional supplementary patient information sheet. A copy of the major components of such information should be given to the consentor to facilitate learning and understanding of the material and assimilation by significant others.

To rely entirely upon the consent form as the sole informational component of the informed consent process would be ill-founded. Even with considerable attention to readability, many patients understand less than half of what is contained in a consent form (Roth et al. 1982). It is interesting to note, however, that psychiatric patients do not perform more poorly than medical or surgical cases (Meisel and Roth 1983). Besides problems with limited patient comprehension, members of the treatment team may see the consent form as relieving them of any additional responsibility to supply information to the patient/consentor over the ECT course. Alternatively, the consentor may perceive the signing of the consent form as a single, final act in the consent process, after which the matter is "closed." Both of these attitudes should be eschewed.

The written information supplied within and accompanying the consent document should be supplemented by a discussion between the consentor and the attending physician, treating psychiatrist and/or designee, that highlights the main features of the consent document, provides additional case-specific information, and allows an exchange to take place. Examples of case-specific information include: why ECT is recommended, specific applicable benefits and risks, and any planned major alterations in the pre-ECT evaluation or the ECT procedure itself. Again, as with all significant consent related interactions with the patient and/or consentor, such discussions should be briefly summarized in the patient's clinical record.

To improve the understanding of ECT by patients, consentors, and significant others, many practitioners use additional written and audiovisual materials, which have been designed to cover the topic of ECT from the layman's perspective. Videotapes, in particular, may be helpful in providing information to patients with limited comprehension, although they may not serve as a substitute for other aspects of the informed consent process (Baxter et al. 1986). A partial listing of such materials has been included as part of Appendix C.

The scope and depth of informational material provided as part of the consent document should be sufficient to allow a reasonable person to understand and evaluate the pertinent risks and benefits of ECT as compared to treatment alternatives. Since individuals vary considerably in terms of education, intelligence, and cognitive status, efforts should be made to tailor information to the consentor's ability to comprehend such data. The practitioner should be aware that too much technical detail can be as counterproductive as too little.

The specific topics to be covered in the consent document generally include the following: 1) a description of the ECT procedure; 2) why ECT is being recommended and by whom; 3) applicable treatment alternatives; 4) the likelihood and anticipated severity of major risks associated with the procedure, including mortality, adverse effects upon cardiovascular and central nervous systems, and common minor risks; 5) a description of behavioral restrictions that may be necessary during the pre-ECT evaluation period, the ECT course, and the recuperative interval; 6) an acknowledgement that consent for ECT is voluntary and can be withdrawn at any time; and 7) an offer to answer questions regarding the recommended treatment at any time, and the name of whom to contact for such questions.


The description of the ECT procedure should include the times when treatments are given (e.g., Monday, Wednesday, Friday mornings), general location of treatment (i.e., where treatments will take place), and typical range for number of treatments to be administered. In the absence of precise quantitative data, the likelihood of specific adverse effects is generally described in terms such as "extremely rare," "rare," "uncommon," and "common" (see Section 4). Because of ongoing concern regarding cognitive dysfunction with ECT, an estimate of the potential severity and persistence of such effects should be given (see Section 4). In light of the available evidence, "brain damage" need not be included as a potential risk.

Capacity and Voluntariness to Provide Consent

Informed consent is defined as voluntary. In the absence of consensus as to what constitutes "voluntary," it is defined here as the consentor's ability to reach a decision free from coercion or duress.

Since the treatment team, family members, and friends all may have opinions concerning whether or not ECT should be administered, it is reasonable that these opinions and their basis be expressed to the consentor. In practice, the line between "advocacy" and "coercion" may be difficult to establish. Consentors who are either highly ambivalent or are unwilling or unable to take full responsibility for the decision (neither of which are rare occurrences with patients referred for ECT) are particularly susceptible to undue influence. Staff members involved in clinical case management should keep these issues in mind.

Threats of involuntary hospitalization or precipitous discharge from the hospital due to ECT refusal clearly represent a violation of the informed consent process. However, consentors do have the right to be informed of the anticipated effects of their actions on the patient's clinical course and the overall treatment plan. Similarly, since physicians are not expected to follow treatment plans which they believe are ineffective and/or unsafe, an anticipated need to transfer the patient to another attending physician should be discussed in advance with the consentor.

It is important to understand the issues involved in a consentor's decision to refuse or withdraw consent. Such decisions may sometimes be based upon misinformation or may reflect unrelated matters, e.g., anger towards self or others or a need to manifest autonomy. In addition, a patient's mental disorder can itself severely limit the ability to cooperate meaningfully in the informed consent process, even in the absence of psychotic ideation. Patients who are involuntarily hospitalized represent a special case. A number of suggestions have been offered to help guarantee the right of such individuals to accept or refuse specific components of the treatment plan, including ECT. Examples of such recommendations include the use of psychiatric consultants not otherwise involved in the case, appointed lay representatives formal institutional review committees, and legal or judicial determination. While some degree of protection is indicated in such cases, overregulation will serve to limit the patient's right to receive treatment.

Informed consent requires a patient who is capable of understanding and acting intelligently upon information provided to him/her. For the purpose of these recommendations, the term the chronic dysthymia or whether dysthymic symptomatology also improves. However, some practitioners believe that dysthymic symptoms do improve and that focusing treatment termination on resolution of the major depressive episode alone may result in incomplete treatment, with possible heightened risk of relapse. In contrast, some patients with schizoaffective disorder present with relatively chronic forms of thought disorder (e.g., delusions), upon which is superimposed prominent episodic affective symptomatology. In a number of these patients, ECT may ameliorate the affective component without influencing the chronic thought disorder. Prolonging the ECT course to attempt such resolution may result in unnecessary treatment.

After the start of ECT, clinical assessments should be performed by the attending physician or designee after every one or two treatments. These assessments should preferably be conducted on the day following a treatment to allow for clearing of acute cognitive effects and should be documented. The assessments should include attention to changes in the episode of mental disorder for which ECT has been referred, both in terms of improvement in signs and symptoms present initially and the manifestation of new ones. During the course of ECT, switches from depression to mania may occur on an uncommon basis. In this context, it is important to distinguish between an organic euphoric state and mania (Devanand et al. 1988b) (see also Section 11.9). Formal assessment of changes in cognitive functioning may help in making this differential diagnosis.

In patients treated for prominent catatonic symptomatology, the nature of other symptoms may have been difficult to discern at pretreatment due to mutism or negativism. With introduction of ECT and the clearing of catatonia, other aspects of psychopathology may become evident and should be assessed and documented. Some patients may have experienced delusions or hallucinations prior to or during the ECT course, but, due to patient guardedness or other factors, these symptoms may have been difficult to verify With clinical improvement, the clinician may ascertain their presence, a determination which may impinge on discharge planning and future treatment.

12.2. Adverse Effects

Cognitive changes. The impact of ECT on mental status, particularly regarding orientation and memory functioning, should be assessed both in terms of objective findings and patient report during the ECT course (see Section 4). This assessment should be conducted prior to the start of ECT in order to establish a baseline level of functioning and repeated at least weekly throughout the ECT course. It is suggested that cognitive assessment, like assessment of therapeutic change, be conducted at least 24 hours following an ECT treatment to avoid contamination by acute postictal effects.


The evaluation may include either bedside assessment of orientation and memory and/or more formal test measures. It should include determination of orientation in the three spheres (person, place, and time), as well as immediate memory for newly learned material (e.g., reporting back a list of three to six words) and retention over a brief interval (e.g., reporting back the list 5-10 minutes later). Remote recall might likewise be assessed by determining memory for events in the recent and distant past (e.g., events associated with the hospitalization, memory for personal details: address, phone number, etc.).

Formal testing instruments provide quantitative measures for tracking change. To assess global cognitive functioning, an instrument such as the Mini-Mental State exam (Folstein et al. 1975) may be used. To track orientation and immediate and delayed memory, subtests of the Russell revision of the Weschler Memory Scale could be used (Russell 1988). To formally assess remote memory, tests of recall or recognition of famous people or events can be used (Butters and Albert 1982; Squire 1986). When cognitive status is assessed, the patient's perception of cognitive changes should also be ascertained. This may be done by informally inquiring whether the patient has noticed any changes in his/her abilities to concentrate (e.g., to follow a television program or a magazine article) or to remember visitors, events of the day, or recall of more remote events. Patient perception of memory functioning may also be examined using a quantitative instrument (Squire et al. 1979).

In the event that there has been a substantial deterioration in orientation or memory functioning during the ECT course that has not resolved by discharge from the hospital, a plan should be made for post-ECT follow-up of cognitive status. Most commonly there is marked recovery in cognitive functioning within days of the end of the ECT course (Steif et al. 1986) and patients should be reassured that this will likely be the case. The plan should include a description of when follow-up assessment would be desirable, as well as the specific domains of cognitive function to be assessed. It may be prudent in such cases to conduct additional evaluations, e.g., neurological and electroencephalographic examinations, and if abnormal to repeat until there is resolution.

It should be kept in mind that the cognitive evaluation procedures suggested here provide only gross measures of cognitive status. Furthermore, interpretation of changes in cognitive status may be subject to a number of difficulties. Psychiatric patients frequently have cognitive impairments prior to receiving ECT and a therapeutic response may therefore be associated with improvement in some cognitive domains (Sackeim and Steif 1988). However, while some patients show improved scores relative to their pre-ECT baseline, they still may not have fully returned to their baseline level of cognitive functioning (Steif et al. 1986). This discrepancy may be a basis for complaints about lingering cognitive deficits. In addition, the procedures suggested here only sample limited aspects of cognitive functioning, for example, deliberate learning and retention of information. Patients may also have deficits in incidental learning. Likewise, the suggested procedures concentrate on verbal memory, although both right unilateral and bilateral ECT produce deficits in memory for nonverbal material (Squire 1986).

Other adverse effects. During the ECT course, any onset of new risk factors, or significant worsening of those present at pre-ECT, should be evaluated prior to the next treatment. When such developments alter the risks of administering ECT, the consentor should he informed and the results of this discussion documented. Patient complaints about ECT should be considered adverse effects. The attending physician and/or a member of the ECT treatment team should discuss these complaints with the patient, attempt to determine their source, and ascertain whether corrective measures are indicated.

13. Management of Patient's Post-ECT Course

Continuation therapy, which is defined as the extension of somatic therapy over the 6-month period following induction of a remission in the index episode of mental illness, has become the rule in contemporary psychiatric practice. Exceptions may include patients who are intolerant to such treatment and possibly those with either an absence of prior episodes or a history of extremely long periods of remission (although compelling evidence for the latter is lacking). Unless residual adverse effects necessitate a delay, continuation therapy should be instituted as soon as possible after remission induction, since the risk of relapse is especially high during the first month. Some practitioners believe that the onset of symptoms of impending relapse in patients who are ECT responders may represent an indication for institution of a short series of ECT treatments for a combination of therapeutic and prophylactic purposes, although controlled studies are not vet available to substantiate this practice.

Continuation pharmacotherapy. A course of ECT is usually completed over a 2- to 4-week period. Standard practice, based in part on earlier studies (Seager and Bird 1962; Imlah et al. 1965; Kay et al. 1970), and in part on the parallel between ECT and psychotropic drug therapies, suggests continuation of unipolar depressed patients with antidepressant agents (with the possible addition of an antipsychotic drug in cases of psychotic depression), bipolar depressives with antidepressant and/or antimanic medications; and manics with antimanic and possibly antipsychotic agents. For the most part, dosages are maintained at 50%-100% of the clinically effective dose range for acute treatment, with adjustment up or down depending upon response. Still, the role of continuation therapy with psychotropic drugs after a course of ECT is undergoing assessment, and our recommendations should be considered provisional. Disappointment with high relapse rates, especially in patients with psychotic depression and in those who are medication resistant during the index episode (Sackeim et al., 1990), compels reconsideration of present practice, including a renewed interest in continuation ECT (Fink 1987b).

Continuation ECT. While psychotropic continuation therapy is the prevailing practice. few studies document the efficacy of such use after a course of ECT, and some recent studies report high relapse rates even in patients complying with such regimens (Spiker et al. 1985; Aronson et al. 1987, 1988a, 1988b; Sackeim et al., in press). These high relapse rates have led some practitioners to recommend continuation ECT for selected cases. Recent retrospective reviews of this experience find surprisingly low relapse rates among patients so treated, although controlled studies are not yet available (Kramer 1987; Decina et al. 1987; Clarke et al. 1989; Loo et al. 1988; Matzen et al. 1988; Thornton et al. 1988). Because continuation ECT appears to represent a viable form of continuation management of patients following completion of a successful course of ECT, facilities are encouraged to offer this modality as a treatment option. Patients referred for continuation ECT should meet all of the following criteria: 1) history of recurrent illness that is acutely responsive to ECT; 2) either refractoriness or intolerance to pharmacotherapy alone or a patient preference.


Appendix B

Examples of Consent Forms and Patient Information Sheet for an ECT Course
[Name of Facility Here]

ECT Consent Form

Name of Attending Physician:

Name of Patient: ______________________________________

My doctor has recommended that I receive treatment with electroconvulsive Therapy (ECT). The nature of this treatment, including the risks and benefits that I may experience have been fully described to me and I give my consent to be treated with ECT.

I will receive ECT to treat my psychiatric condition. I understand that there may be other alternative treatments for my condition which may include medications and psychotherapy. Whether ECT or an alternative treatment is most appropriate for me depends on my prior experience with these treatments, the nature of my psychiatric condition, and other considerations. Why ECT has been recommended for my specific case has been explained to me.

ECT involves a series of treatments. To receive each treatment I will be brought to a specially equipped room in this facility. The treatments are usually given in the morning, before breakfast. Because the treatments involve general anesthesia, I will have had nothing to drink or eat for at least six hours before each treatment. When I come to the treatment room, an injection will be made in my vein so that I can be given medications. I will be given an anesthetic drug that will quickly put me to sleep. I will be given a second drug that will relax my muscles. Because I will be asleep, I will not experience pain or discomfort during the procedure. I will not feel the electrical current, and when I wake up I will have no memory of the treatment.

To prepare for the treatments, monitoring sensors will be placed on my head and other parts of my body. A blood pressure cuff will be placed on one of my limbs. This is done to monitor my brain waves, my heart, and my blood pressure. These recordings involve no pain or discomfort. After I am asleep, a small, carefully controlled amount of electricity will be passed between two electrodes that have been placed on my head. Depending on where the electrodes are placed, I may receive either bilateral ECT or unilateral ECT. In bilateral ECT, one electrode is placed on the left side of the head, the other on the right side. In unilateral ECT, both electrodes are placed on the same side of the head, usually on the right side. When the current is passed, a generalized seizure is produced in the brain. Because I will have been given a medication to relax my muscles, muscular contractions in my body that would ordinarily accompany a seizure will be considerably softened. The seizure will last for approximately one minute. Within a few minutes, the anesthetic drug will wear off and I will awaken. During the procedure my heart rate, blood pressure, and other functions will be monitored. I will be given oxygen to breathe. After waking up from the anesthesia, I will be brought to a recovery room, where I will be observed until it is time to leave the ECT area. The number of treatments that I receive cannot be predicted ahead of time. The number of treatments will depend on my psychiatric condition, how quickly I respond to the treatment, and the medical judgment of my psychiatrist. Typically, six to twelve treatments are given. However, some patients respond slowly and more treatments maybe required. Treatments are usually given three times a week, but the frequency of treatment may also vary depending on my needs.

The potential benefit of ECT for me is that it may lead to improvement in my psychiatric condition. ECT has been shown to be a highly effective treatment for a number of conditions. However, not all patients respond equally well. As with all forms of medical treatment, some patients recover quickly; others recover only to relapse again and require further treatment, while still others fail to respond at all.

Like other medical procedures, ECT involves some risks. When I awaken after each treatment, I may experience confusion. The confusion usually goes away within an hour. Shortly after the treatment, I may have a headache, muscle soreness, or nausea. These side effects usually respond to simple treatment. More serious medical complications with ECT are rare. With modern ECT techniques, dislocations or bone fracture, and dental complications very rarely occur. As with any general anesthetic procedure, there is a remote possibility of death. It is estimated that fatality associated with ECT occurs approximately one per 10,000 patients treated. While also rare, the most common medical complications with ECT are irregularities in heart rate and rhythm.

To reduce the risk of medical complications, I will receive a careful medical evaluation prior to starting ECT. However, in spite of precautions there is a small chance that I will experience a medical complication. Should this occur, I understand that medical care and treatment will be instituted immediately and that facilities to handle emergencies are available. I understand, however, that neither the institution nor the treating physicians are required to provide long-term medical treatment. I shall be responsible for the cost of such treatment whether personally or through medical insurance or other medical coverage. I understand that no compensation will be paid for lost wages or other consequential damages.

A common side effect of ECT is poor memory functioning. The degree of disruption of memory is likely to be related to the number of treatments given and their type. A smaller number of treatments is likely to produce less memory impairment than a larger number of treatments. Right unilateral ECT (electrodes on the right-side) is likely to produce milder and shorter-lived memory impairment than that following bilateral ECT (one electrode on each side of the head). The memory difficulties with ECT have a characteristic pattern. Shortly following a treatment, the problems with memory are most pronounced. As time from treatment increases, memory functioning improves. Shortly after the course of ECT, I may experience difficulties remembering events that happened before and while I received ECT. This spottiness in memory for past events may extend back to several months before I received ECT, and in rare instances, to one or two years. Many of these memories will return during the first several months following the ECT course. However, I may be left with some permanent gaps in memory, particularly for events that occurred close in time to the ECT course. In addition, for a short period following ECT, I may experience difficulty in learning and remembering new information. This difficulty in forming new memories should be temporary and will most likely subside within several weeks following the ECT course. Individuals vary considerably in the extent to which they experience confusion and memory problems during and shortly following treatment with ECT. However, in part because psychiatric conditions themselves produce impairments in learning and memory, many patients actually report that their learning and memory functioning is improved after ECT compared to their functioning prior to the treatment course. A small minority of patients, perhaps 1 in 200, report severe problems in memory that remain for months or even years. The reasons for these rare reports of long-lasting impairment are not fully understood.


 

Because of the possible problems with confusion and memory, it is important that I not make any important personal or business decisions during the ECT course or immediately following the course. This may mean postponing decisions regarding financial or family matters. After the treatment course, I will begin a "convalescence period," usually one to three weeks, but which varies from patient to patient. During this period I should refrain from driving, transacting business, or other activities for which impairment of memory may be problematic, until so advised by my doctor.

The conduct of ECT at this facility is under the direction of Dr. _________________. I may contact him/her at (phone number: ________________) if I have further questions.

I understand that I should feel free to ask questions about ECT at this time or at any time during the ECT course or thereafter from my doctor or from any other member of the ECT treatment team. I also understand that my decision to agree to ECT is being made on a voluntary basis, and that I may withdraw my consent and have the treatments stopped at any time.

I have been given a copy of this consent form to keep.

Patient:

Date Signature

Person Obtaining Consent:

Date Signature

Sample Patient Information Sheet

Electroconvulsive Therapy

Electroconvulsive therapy (ECT) is a safe and effective treatment for certain psychiatric disorders. ECT is most commonly used to treat patients with severe depression. It is often the safest, fastest, and most effective treatment available for this illness. ECT is also sometimes used in the treatment of patients with manic illness and patients with schizophrenia. Treatment for depression has improved remarkably over the past 25 years. The techniques of administering ECT have also improved considerably since its introduction. During ECT, a small amount of electrical current is sent to the brain. This current induces a seizure that affects the entire brain, including the parts that control mood, appetite, and sleep. ECT is believed to correct biochemical abnormalities that underlie severe depressive illness. We know that ECT works: 80% to 90% of depressed people who receive it respond favorably, making it the most effective treatment for severe depression.

Your physician suggests that you be treated with ECT because you have a disorder that (s) he believes will respond to ECT. Discuss this with your doctor. Before ECT begins, your medical condition will be carefully assessed with a complete medical history, physical examination and laboratory tests including blood tests and an electrocardiogram (ECG).

ECT is given as a course of treatments. The number needed to successfully treat a severe depression ranges from 4 to 20. The treatments are usually given 3 times a week: Monday, Wednesday, and Friday. You must not eat or drink anything after midnight prior to your scheduled treatment. If you smoke, please try to refrain from smoking on the morning prior to your treatment.

Before your receive the treatment, a needle will be injected into a vein so that medications can be given. Although you will be asleep during the treatment, it is necessary to begin to prepare you while you are still awake. Electrodes are placed on your head for recording your EEG (electroencephalogram or brain waves). Electrodes are placed on your chest for monitoring your ECG (cardiogram or heart rhythm). A blood pressure cuff is wrapped around your wrist or ankle for monitoring your blood pressure during the treatment. When everything is connected, the ECT machine is tested to ensure that it is set properly for you.

CONTINUING EDUCATION COURSES

FOR PSYCHIATRISTS Duke University

Visiting Fellowship: 5-day course for one or two students, designed to provide advanced training and skills in modern ECT administration. 40 CME credits.

Mini-Course: 1.5 day course designed to enable practicing clinicians to upgrade their skills in ECT. 9 CME credits.
Director: C. Edward Coffey, M.D. 919-684-5673

SUNY at Stony Brook

5-day course for four to six students, designed to provide advanced training and skills in modern ECT. 27 CME credits.
Director: Max Fink, M.D. 516-444-2929

American Psychiatric Association

At annual meetings of the APA, one-day courses are usually presented for classes of students up to 125. These are lecture/demonstrations and aim to provide discussions of such topics as treating the high-risk patient, technical aspects of treatment, and theories of ECT action. For details, see annual course offerings of APA.

Individual preceptorships

From time to time, other experienced clinicians accept visitors for varying lengths of stay at their clinics.

FOR NURSES

Courses for nurses are available at both Duke University and SUNY at Stony Brook. For information, contact Martha Cress, R.N., or Dr. Edward Coffey at Duke University, or Dr. Max Fink at SUNY at Stony Brook.

FOR ANESTHESIOLOGISTS

The courses for psychiatrists at SUNY at Stony Brook include special sessions for anesthesiologists.

Appendix D

Addresses of Present ECT Device Manufacturers in the United States and Major Characteristics of Models Offered as of February 1990

The present devices of these manufacturers meet the recommended standards of the APA Task Force on Electroconvulsive Therapy. In addition, the manufacturers distribute educational materials (books and videotapes), which are useful in learning about ECT.

ELCOT Sales, Inc.
14 East 60th Street
New York, NY 10022
212-688-0900

MECTA Corp.
7015 SW. McEwan Road
Lake Oswego, OR 97035
503-624-8778

Medcraft
433 Boston Post Road
Darien, CT 06820
800-638-2896

Somatics, Inc.
910 Sherwood Drive
Unit 17
Lake Bluff, IL 60044
800-642-6761

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APA Reference
Staff, H. (2007, February 19). The Practice of Electroconvulsive Therapy, HealthyPlace. Retrieved on 2024, December 19 from https://www.healthyplace.com/depression/articles/the-practice-of-electroconvulsive-therapy

Last Updated: June 23, 2016

Electroconvulsive Therapy (ECT)

An article from the American Psychiatric Association website about Electroconvulsive Therapy (ECT).note: I have put this article on the Shocked! ECT web site, rather than a link to the APA site, after many complaints that the APA site is difficult to access (i.e. busy and slow). However, this article is provided by the American Psychiatric Association and is from the APA website.

Electroconvulsive Therapy, more commonly known as "ECT," is a medical treatment performed only by highly skilled health professionals including doctors and nurses under the direct supervision of a psychiatrist, who is a medical doctor trained in diagnosing and treating mental illnesses. Its effectiveness in treating severe mental illnesses is recognized by the American Psychiatric Association, the American Medical Association, the National Institute of Mental Health and similar organizations in Canada, Great Britain and many other countries.

A course of treatment with ECT usually consists of six to twelve treatments given three times a week for a month or less. The patient is given general anesthesia and a muscle relaxant. When these have taken full effect, the patient's brain is stimulated, using electrodes placed at precise locations on the patient's head, with a brief controlled series of electrical pulses. This stimulus causes a seizure within the brain which lasts for approximately a minute. Because of the muscle relaxants and anesthesia, the patient's body does not convulse and the patient feels no pain. The patient awakens after five to ten minutes, much as he or she would from minor surgery.

How ECT Works

The brain is an organ that functions through complex electrochemical processes, which may be impaired by certain types of mental illnesses. Scientists believe ECT acts by temporarily altering some of these processes.

Indications for Use

Electroconvulsive therapy is generally used with severely depressed patients when other forms of therapy such as medications or psychotherapy have not been effective, cannot be tolerated, or (in life threatening cases) will not help the patient quickly enough. ECT also helps patients who suffer with most forms of mania (a mood disorder which is associated with grandiose, hyperactive, irrational and destructive behavior), some forms of schizophrenia, and a few other mental and neurological disorders. ECT is also useful in treating these mental illnesses in older patients for whom a particular medication may be unadvisable.

Extent of Use

Psychiatrists are very selective in their use of electroconvulsive therapy. According to the National Institute of Mental Health, approximately 33,000 hospitalized Americans received ECT in 1980, the last year for which NIMH has figures. That comes out to only about two tenths of one percent of the 9.4 million who suffer with depression, the four million who suffer with schizophrenia and the more than one million who suffer with mania during any given year. Some patients a minority also undergo ECT as an outpatient procedure.

Effectiveness

Numerous studies since the 1940s have demonstrated ECT's effectiveness. Clinical evidence indicates that for uncomplicated cases of severe major depression, ECT will produce a substantial improvement in at least 80 percent of patients (1). ECT has also been shown to be effective in depressed patients who do not respond to other forms of treatment (2). Medication is usually the treatment of choice for mania, but here too certain patients don't respond. Many of these patients have been successfully treated with ECT (3).

Risks

Any medical procedure entails a certain amount of risk. However ECT is no more dangerous than minor surgery under general anesthesia, and may at times be less dangerous than treatment with antidepressant medications. This is in spite of its frequent use with the elderly and those with coexisting medical illnesses (1,4). A small number of other medical disorders increase the risk associated with ECT, and patients are carefully screened for these conditions before a psychiatrist will recommend them for the treatment.

Side Effects

Immediate side effects from ECT are rare except for headaches, muscle ache or soreness, nausea and confusion, usually occurring during the first few hours following the procedure. Over the course of ECT, it may be more difficult for patients to remember newly learned information, though this difficulty disappears over the days and weeks following completion of the ECT course. Some patients also report a partial loss of memory for events that occurred during the days, weeks, and months preceding ECT. While most of these memories typically return over a period of days to months following ECT, some patients have reported longer lasting problems with recall of these memories. However, other individuals actually report improved memory ability following ECT, because of its ability to remove the amnesia that is sometimes associated with severe depression. The amount and duration of memory problems with ECT vary with the type of ECT that is used and are less a concern with unilateral ECT (where one side of the head is stimulated electrically) than with bilateral ECT.

Myths About Brain Damage

Researchers have found no evidence that ECT damages the brain (5,6). There are medical conditions such as epilepsy that cause spontaneous seizures which, unless prolonged or otherwise complicated, do not harm the brain. ECT artificially stimulates a seizure; but ECT induced seizures occur under much more controlled conditions than those that are "naturally occurring" and are safe. A recent study by Coffey and colleagues (7) found no changes in brain anatomy with ECT, as measured by very sensitive scans of the brain using magnetic resonance imaging (MRI) equipment. Other research has established that the amount of electricity which actually enters the brain, (only a small fraction of what is applied to the scalp) is much lower in intensity and shorter in duration than that which would be necessary to damage brain tissue (5).


Restrictions

The idea of ECT is frightening to many people, thanks in part to its depiction in the film "One Flew Over the Cuckoo's Nest." Some may not know that muscle relaxants and anesthesia make it a safe, practically painless procedure.

Some people who advocate legislative bans against ECT are former psychiatric patients who have undergone the procedure and believe they have been harmed by it and that the treatment is used to punish patients' misbehavior and make them more docile. This is untrue.

It is true that many years ago, when psychiatric knowledge was less advanced, ECT was used for a wide range of psychiatric problems, sometimes even to control troublesome patients. The procedure was frightening for patients because it was then administered without anesthesia or muscle relaxants, and the uncontrolled seizures sometimes broke bones.

Today, the American Psychiatric Association has very strict guidelines for ECT administration. This organization supports use of ECT only to treat severe, disabling mental disorders; never to control behavior.

Patient Rights

No psychiatrist simply "decides" to treat a patient with ECT. Before he or she can administer ECT, he or she must first obtain written consent from the patient or (in most states), if the patient is too ill to make decisions for him or herself, from a court appointed guardian (usually one of the patient's family members).

Under the APA's recommended "informed consent" protocol, permission to administer ECT comes after a careful review of the treatment. This review is not a simple recitation of dry, confusing facts; the psychiatrist explains in clear language what ECT involves, what other treatments might be available, and the benefits and risks these procedures may entail. The patient or family member is informed of when, where, and by whom the treatment will be administered and the number of treatments expected. Questions are encouraged. The person consenting to the procedure is kept informed of progress as the treatment continues, and may withdraw consent at any time.

Costs

The costs for any psychiatric treatment vary widely, depending on the state and the facility administering it. Usually, however, ECT costs between $300 and $800 per treatment, an amount which covers the psychiatrist, anesthetist, and a variety of hospital charges. With eight as the average number of treatments, this means a course of ECT treatment will usually cost between $2,400 and $6,400. The cost of ECT is at least partially reimbursed by most insurance plans offering coverage for mental disorders. In cases where the use of ECT shortens the duration of a hospital stay, its net cost may be substantially less.

Bibliography

1. Weiner RD, Coffey CE: Indications for use of electroconvulsive therapy, in Review of Psychiatry, Vol 7. Edited by Frances AJ, Hales RE. Washington, DC: American Psychiatric Press Inc., pp 45881, 1988

2. Sackheim, HA, Prudic J, Devanand DP: Treatment of medication resistant depression with electroconvulsive therapy, in Review of Psychiatry, Vol. 9. Edited by Tasman A, Goldfinger SM, Kaufman CA, Washington, DC: American Psychiatric Press, Inc., pp 91115, 1990

3. Small JG, Klapper MH, Kellams JJ, Miller MJ, Milstein V, Sharpley PH, Small IF: Electroconvulsive treatment compared with lithium in the management of manic states. Arch Gen Psychiatry 45:72732, 1988

4. Weiner RD, Coffey CE: Electroconvulsive therapy in the medical and neurological patient, in Psychiatric Care of the Medical Patient. Edited by Stoudemire A, Fogel B. New York: Oxford University Press, pp 207224, 1993

5. Weiner RD: Does ECT cause brain damage? Brain Behav Sci 7:153, 1984

6. Meldrum BS: Neuropathological consequences of chemically and electrically induced seizures. Ann NY Acad Sci 462:18693, 1986

7. Coffey CE, Weiner RD, Djang WT, Figiel GS, Soady SAR, Patterson LJ, Holt PD, Spritzer CE, Wilkinson WE: Brain anatomic effects of ECT: A prospective Magnetic resonance imaging study. Archives of General Psychiatry 115:10131021, 1991

8. American Psychiatric Association: The Practice of ECT: Recommendations for Treatment, Training, and Privileging. Washington, DC: American Psychiatric Press Inc., 1990

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APA Reference
Staff, H. (2007, February 19). Electroconvulsive Therapy (ECT), HealthyPlace. Retrieved on 2024, December 19 from https://www.healthyplace.com/depression/articles/electroconvulsive-therapy-ect

Last Updated: June 22, 2016

Breathing Techniques to Calm Anxiety and Panic

Significant help for those anxious moments

Panic disorder can be frightening, disabling, and difficult to treat. It's usually mistreated by well-meaning health professionals for years. Recent research and practice supports the use of several steps. The most important focus is breathing. Slow, abdominal breathing alone has been shown to abort panic attacks and prevent them. But for a person with panic disorder, learning slow abdominal breathing can be quite difficult. People with panic disorder are almost always chest breathers. The worst thing you can tell a person during a panic attack is to breathe deeply. I have seen clients who simply could not breathe with their diaphragm without a great deal of training. If they can learn to breathe slowly with their diaphragms, they will not panic!

The most important part of recovering from panic attacks is proper breathing. Learn breathing techniques to help you deal with your next panic attack.Some tips on learning diaphragmatic breathing. Start while lying on your back. Place one hand on your chest and one hand on your belly (between navel and ribs). Focus on allowing the belly to rise easily when inhaling and fall when exhaling. HOLD THE CHEST STILL with your hand on your chest. The objective is to breathe all the time with the belly (diaphragm) and not the chest. You are aiming at about 6 breaths per minute. This is a slow relaxed process. There should be no sense of effort.

If the belly won't move and the chest continues to move, put a weight on the belly between the navel and ribs (where their hand was). A heavy book will do, but a sandbag that weighs 3 - 5 pounds is best. Focus on "allowing" the weight to rise on inhale and sink on exhale. Again - no effort!

If still no success, kneel on all fours, ie., assume a position of a four-legged animal. In this position, the chest tends to be locked in place, forcing the diaphragm to take over the breathing task. Slow and easy, no effort.

In some stubborn cases, biofeedback of the diaphragm, chest, and various muscles involved can unstick a stuck diaphragm. This requires someone with the proper equipment and trained in the technique.

Once the person learns to breathe with their belly, they must practice, practice, practice. The first week, they should practice for only a few breaths at a time while lying on their back. Then gradually extend the practice time to 15 minutes. When this can be done comfortably, they should start to practice while sitting. Then standing. Then walking.

After they can breathe with the belly in all positions, they are to practice in different situations. Start with easy situations like sitting in a car. Then sitting in a restaurant. Progress until they can breathe with the belly in situations that previously provoked a panic attack. See phase 3 below.

IMPORTANT: If at any time during the breathing training, they feel dizzy or light-headed, they are to stop the exercise, rest, and try again in a few minutes. The breathing training is not about being tough or facing your fear. It is about learning to breathe to normalize the bodily functions.

The second phase of treatment runs concurrently with phase one (after abdominal breathing is learned). In a therapy session with a well-trained professional, the person learns that the symptoms that seem to signal imminent death are actually quite harmless. The client is instructed to hyperventilate by breathing with the mouth open and taking deep breaths for about a minute or two. This usually instantly produces panic symptoms (lending support to the theory that panic is a hyperventilation phenomenon). Once the dreaded symptoms are produced, the client notes that they feel just like a panic attack. Then the client switches to abdominal breathing and learns that within a minute or two, these symptoms disappear. This is repeated weekly in session until the client is quite comfortable that they can not only produce the symptoms of panic at any time, but that they can stop them at will.

They can also practice other disturbing sensations in session such as dizziness. A safe way is to spin in a chair until dizzy. Then switch to abdominal breathing and wait until the symptoms subside.

The objective of this phase is to allow the client to experience the terrifying symptoms, learn that they are not lethal, and that they can control them.

The third phase is started after some comfort with phase one and two is obtained. This phase is systematic desensitization. A list of feared situations is made and ordered from least feared to most feared. In session, the least feared situation is imagined and distress noted. The slow belly breathing is used to reduce the distress until the person can imagine the situation with no distress. Then the next situation is imagined, etc. After in-session desensitization, the person goes out into the actual situations starting with the least feared and practices again. They proceed down the list until they can go into any situation with no fear. This phase could take weeks or months.

In my opinion (supported by the research), phases 2 and 3 can reduce panic, but relapse is likely when the person experiences major stressors. With breathing training, the client has a procedure to quickly regain equilibrium if a stressor should trigger the beginning a panic attack, preventing relapse.

If the above steps are not done, the client could get worse. The reason: they are experiencing symptoms that feel life-threatening. They go to numerous doctors and are told there is nothing wrong. They conclude that they have some mysterious condition that will kill them any day and the doctors aren't smart enough to find it. With each treatment that is unsuccessful, their conclusion is strengthened and their fear - and panic attacks - get worse. This can lead to house-bound agoraphobia.

If the health professional knows energy psychology, a simple EFT routine can be added to the above procedures at each step to help reduce the fear.

In my experience, phase one alone (breathing training) can stop panic attacks. But phase 2 and 3 are necessary for complete control. In my opinion, panic disorder has nothing to do with killing or harming oneself or anyone else. If that were true, the above treatment steps wouldn't work.

The person in India might be able to do some of this on his own, but for the average client, that would be very difficult. Phase two can be quite frightening the first time and requires a calm, confident professional to guide one through it.

Please note : Always inhale through the nose, never through the mouth. You can exhale through nose or mouth, although nose is better. Or, even better, inhale through the nose and exhale through pursed lips as if trying to blow through a drinking straw.

Please get advice from your Doctor before using any of these techniques.

Why is it important to breath through your nose?

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APA Reference
Staff, H. (2007, February 19). Breathing Techniques to Calm Anxiety and Panic, HealthyPlace. Retrieved on 2024, December 19 from https://www.healthyplace.com/anxiety-panic/articles/breathing-techniques-to-calm-anxiety-and-panic

Last Updated: July 1, 2016

Letters from 2 Shock Doctors/Researchers in the Country

University of Health Sciences/The Chicago Medical School
Department of Psychiatry and Behavioral Sciences
3333 Green Bay Road
North Chicago, Illinois 60064-3095
Telephone 708.578.3331

October 10, 1990

Dockets Management Branch
FDA
Room 4-62
5600 Fishers Lane
Rockville MD 20857

Re: 21 CFR Part 882 (Docket No. 82P-0316): Neurological devices; proposed rule to reclassify the electroconvulsive therapy device intended for use in treating severe depression

Gentlemen:

I have the following comments concerning the above-referenced
proposed rule, which appeared in the Federal Register, vol. 55,
No. 172, pp. 36578-36590, Wednesday, September 5, 1990.

1. Limitation of intended use to severe depression, as defined by DSM-III-R criteria for major depressive episode with melancholia. (section IV, p. 36580)

a. Exclusion of non-melancholic major depressives.

The 5 references cited in support of this proposed limitation are mostly outdated--4 of them appeared between 1953 and 1965--especially in view of the several random-assignment, double-blind, sham ECT-controlled studies demonstrating the efficacy of ECT in depressed patients who do not meet DSM-III-R criteria for major depressive episode with melancholia, as follows.

Freeman, Basson and Crighton (1978) found genuine ECT (N=20) superior to sham ECT (N=20) in patients suffering from "depressive illness", which the authors defined only as a persistent mood change exceeding customary sadness, accompanied by at least one of the symptoms of guilt, insomnia, retardation, or agitation. This definition is substantially less restrictive than that for DSM-III-R major depressive episode with melancholia, which requires a minimum of 10 depressive features: at least 5 for major depressive episode plus at least 5 more for melancholia.

West (1981) demonstrated the superiority of genuine (N=11) over sham (N=11) ECT in patients with "primary depressive illness" diagnosed according to the Feighner criteria, which are substantially less restrictive than those of DSM-III-R for major depressive episode with melancholia because they require only 5 depressive features for a "definite" or 4 for a "probable" diagnosis.

Brandon et al (1984) found an advantage for genuine (N=38) vs. sham (N=31) ECT in patients described only as having "major depression", without any specification as to endogenicity, psychosis, melancholia, or number or type of symptoms required.

Gregory et al (1985) reported an advantage for genuine (N=40) vs. sham (N=20) ECT in patients who met ICD-9 criteria for major depressive disorder (296.2/3), which are very simply and broadly defined as "a widespread depressed mood of gloom and wretchedness with some degree of anxiety", often with reduced activity or agitation and restlessness, and much less restrictive than DSM-III-R criteria for major depressive episode with melancholia.

Moreover, the FDA's own summary of data in support of the proposed reclassification (section IV para. A, p. 36580) relies heavily on the 1976 study of Avery and Winokur (FDA reference #7) to support the claim that ECT exerts more potent antidepressant effects than tricyclic antidepressants. The Avery and Winokur (1976) study, however, employed only a Feighner "probable" diagnosis of depression--that is, at least four depressive symptoms--which is far less restrictive than DSM-III-R requirements for a major depressive episode with melancholia.

Thus, the proposed rule to limit the use of ECT devices in the treatment of major depression to patients who meet DSM-III-R criteria for major depressive episode with melancholia is unjustifiably restrictive, and should be broadened by dropping the "with melancholia" qualifier.

b. Exclusion of patients with schizophrenia.

The FDA's position (p. 36582) that the evidence regarding the efficacy of ECT in schizophrenia is inconclusive because it is based on mainly anecdotal and uncontrolled studies omits consideration of two important double-blind, random assignment, sham-ECT controlled studies:

Bagadia et al (1983) found a course of 6 genuine ECTs plus placebo (N=20) to be therapeutically equal to a course of 6 sham ECTs plus 600 mg/day chlorpromazine (N=18) in a sample of 38 patients who met the stringent Research Diagnostic Criteria for schizophrenia. This study is notable for excluding patients with prominent affective symptoms.

Brandon et al (1985) found a course of 8 genuine ECTs (N=9) significantly more effective than 8 sham ECTs (N=8) in lowering Montgomery-Asherg Schizophrenia Scale scores in a sample of 17 patients diagnosed as schizophrenic according to the PSE-based CATEGO program.

Taken together with the Taylor and Fleminger (1980) sham-ECT controlled study cited by the FDA, these reports provide strong scientific evidence for the efficacy of ECT in schizophrenia.


c. Exclusion of patients with the diagnosis of mania.

In taking the position (p. 36585) that further scientific study is needed to demonstrate the effectiveness of ECT in mania, the FDA notes that it is already aware of the "well-designed prospective study" by J.G. Small et al (1988) . Perhaps because it is the only controlled study on the subject, the FDA apparently decided not to give it much weight; it is necessary, however, to place this study in a perspective that includes the fact that virtually every textbook on ECT, and every clinician experienced with using ECT, agrees that ECT is no less effective in mania than in melancholia. Moreover, the Small et al (1988) study must also be viewed in the context of a series of carefully-conducted retrospective chart review studies drawn from very large patient samples treated over many years (McCabe, 1976; McCabe and Norris, 1977; Thomas and Reddy, 1982; Black, Winokur, and Nasrallah, 1987), that provide compelling if not definitive evidence for a substantial anti-manic effect of ECT--in fact, no contradictory data exist. In this sense, the case was already considered proved by most experts, and lacked only the "formality" of confirmation by a controlled trial such as that of Small et al (1988)

It is further noteworthy that the recent chart review study of Black, Winokur, and Nasrallah (1987), which shows a much greater efficacy of ECT than lithium in the treatment of mania, was done at the same institution and with the same methodology as the study of Avery and Winokur (1976) that is so prominently cited by the FDA in support of the greater efficacy of ECT than antidepressant drugs. Moreover, Avery and Winokur (1976) reported that only 49% of depressives receiving ECT enjoyed "marked improvement", whereas Black, Winokur and Nasrallah (1987) found that 78% of manics who received ECT achieved this degree of improvement.

These considerations all strongly suggest that FDA should include mania as a prime indication for ECT in the proposed labeling requirement.

2. The proposed labeling requirement that the use of ECT should progress from unilateral to bilateral placement, from pulse to sine wave energy, and from subcritical to minimum amount of energy needed to induce seizure activity.

The unfortunate result of this well-intended but antitherapeutic requirement is that all patients must intially receive brief pulse right -unilateral ECT administered with near-threshold dosing, ignoring the elegant study of Sackeim et al (1987) , which conclusively demonstrates that just-above-threshold brief pulse right unilateral ECT lacks significant therapeutic benefit in depression. The requirement also ignores the fact that the only one out of 6 genuine vs. sham ECT studies that failed to show an advantage for genuine ECT (Lambourn & Gill, 1978) employed low- dose (1OJ energy) brief pulse unilateral ECT as the "active" treatment.

Finally, my colleagues and I (Abrams, Swartz and Vedak, Arch. Gen. Psychiat., in press, copy enclosed) have recently demonstrated that high-dose (markedly suprathreshold) brief pulse right unilateral ECT is equal in therapeutic efficacy to bilateral ECT, in contrast to an earlier study at the same site (Abrams et al, 1983) that found conventional-dose unilateral ECT to be much less effective than bilateral ECT.

Sincerely yours,

Richard Abrams, M.D.
Professor of Psychiatry

 

STATE UNIVERSITY OF NEW YORK AT STONY BROOK
SCHOOL OF MEDICINE - DEPARTMENT OF PSYCHIATRY
P.O. BOX 457
ST. JAMES, N. Y. 11780
PHONE: 516-444-2929

October 26, 1990

Dockets Management Branch (HFA-305)
Food and Drug Administration
5600 Fishers Lane, Room 4-62
Rockville, MD 20857

Ref: 21 CFR Part 882 Docket # 82P-0316

Gentlemen:

The FDA proposed reclassification of ECT (electroconvulsive therapy) devices to class II is commendable. The restriction in labelling for patients with "Major Depression with Melancholia" is inconsistent, however, with present practice, international experience since 1934, and numerous recent expert reviews, notable that of the Royal College of Psychiatrists of Great Britain in 1989 (1) and the American Psychiatric Association in 1990 (2). Nor is it consistent with the changing diagnostic schemes which are now beginning to view major mental illnesses as varying manifestations of a single endogenous disorder. In the proposed rule and in its in-house Task Force Review of the Literature on ECT. 1982 to 1988, dated June 10, 1988, the FDA failed to fully consider the scientific literature, failed to comprehend the meaning of the studies, and ignored well designed studies, some of which they cited and derogated.

 


I urge the FDA to recognize that ECT devices, when properly used to induce seizures, are effective for a range of disorders broader than that cited in the rule: ECT is effective for endogenous psychiatric illnesses in which psychosis can occur. In the present classification scheme (DSM-IIIR), these include (but are not limited to) the mood disorders of major depression, bipolar disorder (manic or depressed or mixed phases), with or without psychosis (296.xx); and schizophrenia, catatonic type (295.2x). Since it is highly likely that these labels will be changed in the next few years (DSM-IV is in preparation), a description of the populations suitable for ECT which define the labelling of these devices should be as broad as the prevailing evidence of efficacy and safety allow.

It is often difficult to separate these diagnoses, and many patients exhibit a variety of syndromes in the course of their lifelong illness. It is not unusual for patients to be depressed in one admission, psychotic and depressed in a second, and manic in a third. And these states may or may not be associated by melancholic signs and symptoms. Limiting the use of a treatment to the melancholic phase of an illness as if such a phase is unique is in error and will do a disservice to large numbers of patients.

Others have argued persuasively the merits of ECT in the treatment of a wide range of depressive disorders, notably psychotic depression (3); bipolar disorder with mania (4); and schizophrenia (5). Their arguments have been persuasive for the Task Force of the American Psychiatric Association (2) and the Royal College of Psychiatrists (1). It would be redundant for me to reiterate their persuasive arguments, when the agency staff can read those arguments directly.

I wish to comment on three issues in the recommended rule: the use of ECT in the syndrome of catatonia, in mania, and the recommendations for a sequence in treatment parameters.

Catatonia: When convulsive therapy was developed by Prof. Ladislas Meduna in Budapest in 1934, it was first used (and most successfully) in a patient with catatonia. When the first electrical inductions were made by Professors Ugo Cerletti and Luigi Bini in Rome in 1938, it was for a patient with catatonia. Catatonia is an uncommon psychiatric syndrome, but one which occurs in patients with psychosis (catatonic schizophrenia), in mania and depression (6), and secondary to medical disorders, such as lupus erythematosus and typhoid fever (7). Catatonia is also seen as a manifestations of a toxic reaction to antipsychotic drugs -- the syndrome is known as neuroleptic malignant syndrome. Finally, catatonia has a form known as malignant catatonia, a disorder that is rapidly fatal. In each of these conditions, ECT has been found to be life-saving (8).

For example, in our hospital last year, we were called to treat a young woman with lupus erythematosus who developed a malignant form of catatonia. She was cachectic, was unable to stand or feed herself, and had lost 25% of her body weight. All medical treatments having failed, after five weeks she was treated successfully and rapidly with ECT, and was well in one year follow-up (9).

I recognize that the APA classification schemes, DSM-III and DSM-IIIR do not specifically recognize this syndrome except as a type of schizophrenia (295.2x). Nevertheless, ECT has been life-saving in this syndrome and it is essential that this application be made a feature of labelling (9).

Mania: The syndrome of mania appears in many guises, that of excitement and overactivity, psychosis, psychosis with melancholia, and delirium. It is often thought of as the obverse of depressive mood. In the history of convulsive therapy, manic conditions were identified as suitable for ECT at the same time that depressive states were identified. The development of lithium and its use with antipsychotic drugs replaced the use of ECT for a time -- long enough to determine that therapy resistant and rapid cycling manic patients of may not respond to medication. In such cases, ECT is life-saving. In our recent experience, we have treated two patients in manic delirium who had been continually hospitalized for 2 and for 3 years. Further, a severely manic woman with sickle cell disease, in her second trimester of pregnancy, could not be treated with medication; ECT was highly successful (10).

Treatment Parameters: The FDA proposed rule states that "ECT use should progress from unilateral to bilateral electrode placement and from brief-pulse to sine wave stimulation and from subcritical to minimum amounts of energy needed to induce seizure activity." This recommendation is wholly inconsistent with present practice and with the recommendations of national task forces (1, 2). By making such a recommendation, the FDA is engaging in the practice of medicine, a stipulation from which the agency is clearly enjoined.

The choice of electrode placement is determined by the type of syndrome, medical status, need for urgency in response, and individual psychology and employment. The 1990 APA report does not recommend unilateral placement as the initial choice for all cases; nor does it reserve bilateral placement as a secondary use. It stipulates that each case must be treated individually. In clinical practice, for patients who have concurrent medical illness where each anesthesia exposure must be considered, bilateral electrode placement is clearly preferred. In patients who are severely suicidal, or severely manic (especially where restraints are a consideration), bilateral placement is preferred. For severely catatonic patients, especially if mute and requiring tube-feeding, bilateral placement is preferred. The use of unilateral electrode placements, with their associated 15% response failure rate, is clearly dangerous to these patients (11).

Stimulation currents at subthreshold energy levels are associated with failed or inadequate seizures. Seizures which have been induced at marginal doses of energy are clearly less efficient than those with suprathreshold currents (12), especially when brief-pulse currents and unilateral electrode placements are used (13). Recent research led the two national reviews (1,2) to argue for moderately suprathreshold currents to induce seizures and to monitor seizure duration as an index of treatment efficacy. Comparisons of U.S. experience with fixed dose brief pulse currents with Scandinavian/German experience with variable dose, modified sinusoidal currents finds a greater number of treatment failures in the fixed dose methodology.

Since the definition of an adequate treatment is under active study, the prescription of a defined sequence of treatment parameters is clearly premature and prejudicial to medical practice.

I commend the FDA in seeking to clarify the status of ECT devices, and I urge the agency to simplify the classification and labelling requirements by assigning these devices to Class II. The labelling should be consistent with more than half a century of experience and research, and must include a wider range of endogenous psychiatric illnesses, including the affective illnesses of severe depression and mania, catatonic schizophrenia, and the special syndrome of primary and secondary catatonia.


But the agency should resist interfering in medical practice by seeking to define the technical details of electrode placement, energy level, and current type and dose, leaving these details to the continuing developments of the profession and departures from prevailing practice to case law.

I have been a licensed physician since 1945; certified in neurology in 1952, in psychiatry in 1954, and in psychoanalysis in 1953. I have been a practitioner of ECT since 1952; a researcher in ECT since 1954 with more than 200 publications in convulsive therapy; editor (with Seymour Kety and James McGaugh) of the volume Psychobiology of Convulsive Therapy (Winston/Wiley, New York, 1974); author of the textbook Convulsive Therapy: Theory and Practice (Raven Press, New York, 1979); and Editor-in-Chief of Convulsive Therapy, a quarterly scientific journal published by Raven Press, since its inception in 1985. I have been a Professor of Psychiatry at various medical schools since 1962.

Sincerely yours,

Max Fink, M.D. Professor of Psychiatry

Citations:

1. Royal College of Psychiatrists. The Practical Administration of Electroconvulsive Therapy (ECT). Gaskell, London, 30 pp., 1989.

2. American Psychiatric Association. The Practice of ECT: Recommendations for Treatment. Training and Privileging. American Psychiatric Press, Washington, D.C., 1990.

3. Avery, D. and Lubrano, A.: Depression treated with imipramine and ECT: the DeCarolis study reconsidered. Am. J. Psychiatry 136: 559-62, 1979.

Kantor, S.J. and Glassman, A.H.: Delusional depressions: natural history and response to treatment. Br. J. Psychiatry 131: 351-60, 1977.

Kroessler, D.: Relative efficacy rates for therapies of delusional depression. Convulsive Ther. 1:173-182,1985.

4. Milstein, V., Small, J.G., Klapper, M.H., Small, I.F., and Kellams, J.J.: Uni-versus bilateral ECT in the treatment of mania. Convulsive Ther. 3: 1-9, 1987.

Mukherjee, S., Sackeim, H.A., Lee, C., Prohovnik, I., and Warmflash, V.: ECT in treatment resistant mania. In; C. Shagass et al. (Eds.): Biological Psychiatry 1985. Elsevier, New York, 732-4, 1986.

Berman, E. and Wolpert, E.A.: Intractable manic-depressive psychosis with rapid cycling in an 18-year-old woman successfully treated with electroconvulsive therapy. J.N.M.D. 175: 236-239,1987.

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APA Reference
Staff, H. (2007, February 19). Letters from 2 Shock Doctors/Researchers in the Country, HealthyPlace. Retrieved on 2024, December 19 from https://www.healthyplace.com/depression/articles/letters-from-2-shock-doctorsresearchers-in-the-country

Last Updated: June 22, 2016

Time to Abandon Electroconvulsion as a Treatment in Modern Psychiatry

Advances In Therapy
Volume 16 No. 1
January/February 1999

Hanafy A. Youssef, D.M. D.P.M., FRC Psych.
Medway Hospital
Gillingham, Kent, United Kingdom

Fatma A. Youssef, D.NSc, M.P.H, R.N.
School of Health Professions
Marymount University
Arlington, Virginia, USA

ABSTRACT

This review examines the evidence for the current use of electroconvulsive therapy (ECT) in psychiatry. The history of ECT is discussed because ECT emerged with no scientific evidence, and the absence of other suitable therapy for psychiatric illness was decisive in its adoption as a treatment. Evidence for the current recommendation of ECT in psychiatry is reconsidered. We suggest that ECT is an unscientific treatment and a symbol of authority of the old psychiatry. ECT is not necessary as a treatment modality in the modern practice of psychiatry.

INTRODUCTION

Time to abandon Electroconvulsion as a treatment in modern psychiatry. A review of the evidence for the current use of electroconvulsive therapy (ECT)Berrios (1) has thoroughly documented the history of electroconvulsive therapy (ECT). We suggest that in both the 19th and 20th centuries the social context in which ECT emerged, rather than the quality of the scientific evidence, was decisive in determining its adoption as a treatment.

The medical literature is a virtual graveyard for inadequately tested preparations that die ignominiously after a brief moment of glory. Egas Moniz won a Nobel Prize in medicine for the prefrontal lobotomy, targeted at patients in whom ECT had failed. Clearly, psychiatrists abandoned all forms of shock treatment except ECT because of the empiric nature of such therapy and the lack of a credible explanation why it should work.

The prime bases of validation for ECT are vague statements about "clinical experience." Since the introduction of antipsychotics and antidepressants, the number of people subjected to ECT has undoubtedly declined, yet it is still used by some psychiatrists as the ultimate weapon. The proponents of ECT have to preserve the integrity of its use by having more training and better technology and claiming that ECT has proved its worth in clinical "experience." Thomas Szasz wrote that electricity as a form of treatment is "based on force and fraud and justified by 'medical necessity'." "The cost of this fictionalization runs high," he continued. "It requires the sacrifice of the patient as a person, of the psychiatrist as a clinical thinker and moral agent." Some people who have had ECT believe that they were cured by it; this fact indicates that they have so little self-control over the conditions of their lives that they must be shocked by an electric current to discharge their responsibilities.

When ECT became an emotional issue in psychiatry because of pressure groups, various bills were introduced by legislators in the United States. Professional societies and colleges - the task force of the American Psychiatric Association (3) and the Royal College of Psychiatrists memoranda (4-6) - have tried to study the subject and survey ECT use. Despite these efforts, ECT is and will remain controversial.

SHOCK AND TERROR AS THERAPY

Terror as a therapy for insanity has been used since antiquity, and as late as the 19th century, the insane were submerged in cold water to terrify them with the prospect of inevitable death.

While using insulin as a sedative in Viennese drug addicts, Sakel (8) observed that accidental overdose resulted in coma or epileptic fits. In a burst of nonscientific theorizing, he wrote: "I began with the addict. I observed improvements after severe epileptic fits.... Those patients who had previously been excited and irritable suddenly became contented and quiet after this shock.... The success I had achieved in treating addicts and neurotics encouraged me to use it in the treatment of schizophrenia or major psychoses."

Meduna used camphor-induced fits on psychiatric patients in a Hungarian state mental hospital after unsuccessful attempts by Nyiro, his superior, to treat schizophrenia by injections of blood from epileptics. Meduna later employed Cardiazol-induced shock. Nyiro's and Meduna's convulsive therapies were based on the view that a neurobiologic opposition existed between epilepsy and schizophrenia. Meduna abandoned his theory of schizophrenia and epilepsy and later wrote "We are undertaking a violent onslaught...because at present nothing less than a shock to the organism is powerful enough to break the chain of noxious processes that lead to schizophrenia."

Psychiatrists of that era who used this form of shock therapy believed that the fear and terror produced were therapeutic because the "feeling of horror" before the onset of convulsion following injection of camphor, pentetrazol, triazole, picrotoxin, or ammonium chloride rendered the patients different after the experience. (10)

ELECTRICITY AS THERAPY

Extensive literature is available on the use of electricity as a therapy and the induction of epilepsy by electric current. (11) In ancient Rome, Scriborus Largus tried to cure the emperor's headache with an electric eel. In the 16th century, a Catholic missionary reported that the Abyssinians used a similar method to "expel devils out of human body." Aldini treated two cases of melancholia in 1804 by passing galvanic current through the brain. In 1872, Clifford Allbutt in England applied electric current to the head for treatment of mania, dementia, and melancholia.


In 1938, Ugo Cerletti obtained permission to experiment with electricity on pigs in a slaughterhouse. "Except for the fortuitous and fortunate circumstances of pigs' pseudo-butchery," he wrote, electroshock would not have been born." (12) Cerletti did not bother to obtain permission to experiment on the first human subject, a schizophrenic who after the initial shock said "Non una seconda! Mortifere." (not again; it will kill me). Cerletti nevertheless proceeded to a higher level and a longer time, and so ECT was born. Cerletti admitted that he was frightened at first and thought that ECT should be abolished, but later he started to use it indiscriminately.

In 1942, Cerletti and his colleague Bini advocated the method of "annihilation," which consisted of a series of (unmodified) ECTs many times a day for many days. They claimed good results in obsessive and paranoid states and in psychogenic depression. In fact, Cerletti had discovered nothing, as both electricity and fits were already known. No scientist, he believed that he discovered a panacea, reporting success with ECT in toxemia, progressive paralysis, parkinsonism, asthma, multiple sclerosis, itch, alopecia, and psoriasis. (12) By the time of his death in 1963, neither Cerletti nor his contemporaries had learned how ECT worked. The inheritors of ECT continue the same lack of understanding today.

Insulin coma and pentetrazol-induced fits, heretofore treatments of choice for schizophrenia, are not therapies any longer, and ECT is not a treatment for schizophrenia. The fact of the matter is that the pioneers of all these shock treatments contributed nothing to the understanding of mental illness, which contemporary psychiatrists are still trying to comprehend and treat on a scientific basis.

ELECTRICITY, CONVULSIONS, THE BODY, AND THE BRAIN

For its proponents, ECT is a relatively simple procedure. Electrodes are attached to the subject's head, either at the temples (bilateral ECT) or at the front and back of one side (unilateral ECT). When the current is turned on for 1 second, at 70 to 150 volts and 500 to 900 milliamperes, the power produced is roughly that required to light a 100-watt bulb. In a human being, the consequence of this electricity is an artificially induced epileptic fit. Modified ECT was introduced as a humane improvement on earlier versions of convulsive therapy to eliminate the elements of fear and terror. In modified ECT, muscle relaxant and general anesthesia are supposed to make the patient less fearful and feel nothing. Nonetheless, 39% of patients thought it was a frightening treatment. (13) These induced fits are associated with many physiologic events, including electroencephalographic (EEG) changes, increased cerebral blood flow, bradycardia followed by tachycardia and hypertension, and throbbing headache. Many patients report temporary or prolonged loss of memory, a sign of acute brain syndrome.

Since early in the history of ECT, we have known that insulin coma or pentetrazol shock can cause brain damage. (14) Bini reported severe and widespread brain damage in experimental animals treated with electroshock. (15) EEG studies showed generalized slowing following ECT that takes weeks to disappear and may persist even longer in rare cases. (16) Calloway and Dolan raised the issue of frontal lobe atrophy in patients previously treated with ECT. (17) The memory deficits after ECT may persist in some patients. (18)

Fink, an advocate of ECT, argues that the risks of ECT amnesia and organic brain syndrome are "trivial" (19) and can be reduced by hyperoxygenation, unilateral ECT over the nondominant hemisphere, and the use of minimal induction currents. (20) Earlier, Fink had indicated that post-ECT amnesia and organic brain syndrome were "not trivial." ECT advocates blame the modification for decreasing the efficacy of the treatment. (21) In the United States, the issue of unilateral ECT reflected class differences. In Massachusetts in 1980, ECT was bilateral in 90% of patients in public hospitals and in only 39% of patients in private hospitals. (22)

Templer compared the issue of ECT brain damage to that of boxing. He wrote that "ECT is not the only domain in which change to the human brain is denied or de-emphasised on the grounds that this damage is minor, occurs in a very small percentage of cases or is primarily a matter of the past." (23)

There has been less scientific investigation into the effect of ECT on other body functions and morbidity. Various animal studies showed significant results that may be important in psychoimmunology-an area of investigation that is more neglected in psychiatry than in any other field of medicine. Although it is difficult to move from an animal model to the human system, animal models frequently demonstrate the role of a range of variables in disease onset. Rats subjected to electrical stress showed significant diminution in the strength of their lymphocyte response that could not be explained by an elevation in adrenal corticosteroids. Even adrenalectomized rats had a similar decrease in lymphocyte response after electric shock (24) ; other studies have confirmed immunologic change following electric shock in animals.

USE AND ABUSE OF ECT IN SCHIZOPHRENIA

Initial claims that cardiazol convulsions and insulin coma were successful in the treatment of schizophrenia were not universally shared. Some researchers found that these interventions were worse than no treatment. (26)

For more than 50 years, psychiatrists used ECT as therapy for schizophrenia, even though there is no evidence that ECT alters the schizophrenic process. (27) In the 1950s, ECT was reported to be no better than hospitalization alone (28) or anesthesia alone. (29) At the beginning of the 1960s, the era of ECT in schizophrenia was fast drawing to a close as ECT abuses were brought to light by patients and pressure groups. In 1967, however, Cotter described symptomatic improvement in 130 schizophrenic Vietnamese men who refused to work in a psychiatric hospital and received ECT at a rate of three shocks per week. (30) Cotter concluded that "the result may simply be due to patients' dislike and fear of ECT," but he further claimed that "the objective of motivating these patients to work was achieved." (30)

Most contemporary psychiatrists consider the use of ECT in schizophrenia as inappropriate, but some believe that ECT is at least equal to other therapies in this illness. (31)


ECT in Depression

In the 1960s, advocates of ECT were not able to provide evidence that it is therapeutic in schizophrenia but were nevertheless convinced that electricity and fits are therapeutic in mental illness and vigorously defended the use of ECT in depression. Their rationale came from studies in the United States (32) and Britain. (33)

In the US study, 32 patients were pooled from three hospitals. In hospitals A and C, ECT was as good as imipramine; in hospitals B and C, ECT equaled placebo. The results showed that ECT was universally effective in depression, regardless of type: 70% to 80% of depressed patients improved. The study also showed, however, a 69% improvement rate after 8 weeks of placebo. Indeed, Lowinger and Dobie (34) reported that improvement rates as high as 70% to 80% can be expected with placebo alone.

In the British study, (33) hospitalized patients separated into four treatment groups: ECT, phenelzine, imipramine, and placebos. No differences were observed in male patients at the end of 5 weeks, and more men who received placebo were discharged from the hospital than those treated with ECT. Skrabanek (35) commented about this most quoted study: "One wonders how many psychiatrists read more than the abstract of these studies."

The Royal College of Psychiatrists memorandum mentioned earlier was in response to a report of ECT abuse in depression. The memorandum declared that ECT is effective in depressive illness and that in "depressed patients" there is suggestive, if not yet unequivocal, evidence that the convulsion is a necessary element of the therapeutic effect. Crow, (36) on the other hand, questioned this widely held view.

In the late 1970s and in the 1980s, with uncertainty continuing and further work needed, seven controlled trials were carried out in Britain.

Lambourn and Gill (37) used unilateral simulated ECT and unilateral real ECT in depressed patients and found no significant difference between the two.

Freeman and associates (38) used ECT in 20 patients and achieved a satisfactory response in 6; a control group of 20 patients received the first two of six ECT treatments as simulated ECT, and 2 patients responded satisfactorily. (38)

The Northwick Park Trial showed no difference between real and simulated ECT. (39)

Gangadhar and coworkers (40) compared ECT and placebo with simulated ECT and imipramine; both treatments produced equally significant improvements over 6 months follow-up.

In a double-blind controlled trial, West (41) showed that real ECT was superior to simulated ECT, but it is not clear how a single author carried out a double-blinding procedure.

Brandon et al (42) demonstrated significant improvements in depression with both simulated and real ECT. More important, at the end of 4 weeks of ECT, consultants were unable to guess who received real or simulated treatment. The initial differences with real ECT disappeared at 12 and 28 weeks.

Finally, Gregory and colleagues (43) compared simulated ECT with actual unilateral or bilateral ECT. Real ECT produced faster improvement but no difference between the treatments was apparent 1, 3, and 6 months after the trial. Only 64% of patients completed this study; 16% of the patients withdrew from bilateral ECT and 17% from simulated ECT.

From the West and the Northwick Park trials, it appears that only delusional depression responded more to real ECT, and this view is held by ECT proponents today. A study by Spiker et al, showed that in delusional depression amitriptyline and perphenazine were at least as good as ECT. After a series of ECT for his depression and just before committing suicide, Ernest Hemingway said, "Well, what is the sense of ruining my head and erasing my memory, which is my capital, and putting me out of business." His biographer remarked that "it was a brilliant cure but we lost the patient." (45)

ECT AS AN ANTISUICIDAL

Despite the lack of an acceptable theory as to how it works, Avery and Winokur (46) regard ECT as a suicide preventive, although Fernando and Storm (47) later found no significant difference in suicide rates between patients who received ECT and those who did not. Babigian and Guttmacher (48) found that the mortality risk after ECT was higher soon after hospitalization than in patients who did not receive ECT. Our own study (49) of 30 Irish suicides from 1980 to 1989 showed that 22 patients (73%) had received a mean of 5.6 ECTs in the past. The explanation that "ECT induces a transient form of death and thus perhaps satisfies an unconscious desire on the part of the patient, but this has no preventative effect on suicide; indeed it reinforces suicide in the future." (49) Many psychiatrists today concur that ECT as a suicide preventive does not hold up.

THE PSYCHIATRIST'S DILEMMA: TO USE OR NOT USE ECT

Some psychiatrists jusitify the use of ECT on "humanistic grounds and as a means of controlling behaviour" against the wishes of the patient and family. (50) Even Fink admits that the catalogue of ECT misuses is depressing but suggests that the guilt lies with the abusers and not the instrument. (51) The editor of the British Journal of Psychiatry considered it "inhuman" to administer ECT without asking the patient or the relative, even though Pippard and Ellam showed that this was common practice in Britain. Not long ago, ECT administration in Great Britain was described as "deeply disturbing" by a Lancet editorial writer, who commented that "it is not ECT which brought psychiatry into disrepute; psychiatry has done just that for ECT". (53) Despite efforts to preserve the integrity of the treatment, in Great Britain and in most public hospitals worldwide consultant psychiatrists order ECT and a junior doctor administers it. This maintains the belief of institutional psychiatry that electricity is a form of treatment and prevents the junior psychiatrist from being a clinical thinker.


Levenson and Willett (54) explain that to the therapist using ECT it may seem unconsciously like an overwhelming assault, which may resonate with the therapist's aggressive and libidinal conflict."

Studies that examined attitudes of psychiatrists toward ECT found marked disagreement among clinicians about the value of this procedure. (55,56) Thompson et al (57) reported that ECT use decreased 46% between 1975 to 1980 in the United States, with no significant changes between 1980 to 1986. Fewer than 8% of all US psychiatrists use ECT, however. (58) A very recent study (59) on the characteristics of psychiatrists who use ECT found that female practitioners were only one-third as likely to administer it as were their male counterparts. (59) The proportion of female psychiatrists has been rising steadily and if the gender gap continues, this could hasten the end of ECT.

CONCLUSION

When ECT was introduced in 1938, psychiatry was ripe for a new therapy. Psychopharmacology offered two approaches to the pathogenesis of mental disorders: to investigate the mechanism of action of drugs that ameliorate the disorder and to examine the actions of drugs that reduce or mimic the disorder. In the case of ECT, both approaches have been pursued without success. Chemically or electrically induced fits have profound but short-lived effects on brain function, ie, acute organic brain syndrome. Shocking the brain causes increases in levels of dopamine, cortisol, and corticotropin for 1 to 2 hours after the convulsion. These findings are pseudoscientific, as there is no evidence that these biochemical changes, specifically or fundamentally, affect the underlying psychopathology of depression or other psychoses. Much of the improvement attributed to ECT is an effect of placebo or, possibly, anesthesia.

From the earliest uses of convulsive therapy, it was recognized that the treatment is unspecific and only shortens the duration of psychiatric illness rather than improves the outcome. (60) Convulsive therapy based on the old belief of shocking the patient into sanity is primitive and unspecific. The claim that ECT has proved its usefulness, despite the lack of an acceptable theory as to how it works, has also been made for all the unproven therapies of the past, such as bloodletting, which are reported to produce great cures until they are abandoned as useless. Insulin coma, cardiazol shock, and ECT were treatments of choice in schizophrenia, until they, too, were abandoned. For ECT to remain as an option in other psychoses transcends clinical and common sense.

When an electrical current is applied to the body by tyrannical rulers, we call this electrical torture; however, an electrical current applied to the brain in public and private hospitals by professional psychiatrists is called therapy. Modifying the ECT machine to reduce memory loss and giving muscle relaxants and anesthesia to make the fit less painful and more humane only dehumanize users of ECT.

Even if ECT were relatively safe, it is not absolutely so, and it has not been shown to be superior to drugs. This history of ECT, its abuse, and resultant public pressure are responsible for its increasingly lower use.

Is ECT necessary as a treatment modality in psychiatry? The answer is absolutely not. In the United States, 92% of psychiatrists do not use it despite the existence of an established journal entirely devoted to the subject to give it scientific respectability. ECT is and always will be a controversial treatment and an example of shameful science. Even though some 60 years have been spent defending the treatment, ECT remains a revered symbol of authority in psychiatry. By promoting ECT, the new psychiatry reveals its ties to the old psychiatry and sanctions this assault on the patient's brain. Modern psychiatry has no need of an instrument that allows the operator to zap a patient by pressing a button. Before inducing a fit in a fellow human being, the psychiatrist as clinician and moral thinker needs to recall the writings of a fellow psychiatrist, Frantz Fanon (61) : "Have I not, because of what I have done or failed to do, contributed to an impoverishment of human reality?"

REFERENCES

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13. Freeman CP, Kendall RE. ECT, I: Patients' experience and attitude. Br J Psychiatry. 1980;137:8-16.
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16. Weiner RD. The persistence of electroconvulsive therapy-induced changes in the electroencepha-logram. J Nerv Ment Dis. 1980;168:224-228.
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18. Weiner RD. Does electroconvulsive therapy cause brain damage? Behav Brain Sci. 1984;7:54.
19. Fink M. ECT-Verdict: not guilty. Behav Brain Sci. 1984;7:26-27.
20. Fink M. Convulsive and drug therapy of depression. Ann Rev Med. 1981;32:405-412.
21. d'Elia G, Rothma H. Is unilateral ECT less effective than bilateral ECT? Br J Psychiatry. 1975; 126:83-89.
22. Mills MJ, Pearsall DT, Yesarage JA, Salzman C. Electroconvulsive therapy in Massachusetts. Am J Psychiatry. 1984;141:534-538.
23. Templer DI. ECT and brain damage: how much risk is acceptable? Behav Brain Sci. 1884;7:39.
24. Keller S, Weiss J, Schleifer S, Miller N, Stein M. Suppression of immunity by stress: effect of graded series stressor on lymphocyte stimulation in the rat. Science. 1981;213:1397-1400.
25. Laudenslager ML, Ryan SM. Coping and immunosuppression: inescapable but not escapable shock suppresses lymphocyte proliferation. Science. 1985;221:568-570.
26. Stalker H, Millar W, Jacobs H. Remission in schizophrenia. Insulin and convulsion therapies compared with ordinary treatment. Lancet. 1939;i:437-439.
27. Salzman C. The use of ECT in the treatment of schizophrenia. Am J Psychiatry. 1980;137:1032-1041.
28. Appel KE, Myers MJ, Scheflen AE. Prognosis in psychiatry: results of psychiatric treatment. Arch Neurol Psychiatry. 1953;70:459-468.
29. Brill H, Crampton E, Eiduson S, Grayston H, Hellman L, Richard R. Relative effectiveness of various components of electroconvulsive therapy. Arch Neurol Psychiatry. 1959;81:627-635.
30. Lloyd H, Cotter A. Operant Conditioning in a Vietnamese Mental Hospital. Am J Psychiatry. 1967;124:25-29.
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32. Greenblatt M, Grosser GH, Wechsler H. Differential response of hospitalized depressed patients to somatic therapy. Am J Psychiatry. 1964;120:935-943.
33. Medical Research Council Psychiatric Committee. Clinical trial of the treatment of depressive illness. Br Med J. 1965;131:881-886.
34. Lowinger P, Dobie SA. Study of placebo response rates. Arch Gen Psychiatry. 1969:20:84-88.
35. Skrabanek P. Convulsive therapy: a critical appraisal of its origin and value. Irish Med J. 1986; 79:157-165.
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37. Lambourn J, Gill DA. A controlled comparison of simulated and real ECT. Br J Psychiatry. 1978; 133:514-519.
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53. ECT in Britain: a shameful state of affairs. Lancet. 1981;ii:1207.
54. Levenson JL, Willet AB. Milieu reactions to ECT. Psychiatry. 1982;45:298-306.
55. Kalayam B, Steinhard M. A survey of attitude on the use of electroconvulsive therapy. Hosp Com Psychiatry. 1981;32:185-188.
56. Janicak P, Mask J, Timakas K, Gibbons R. ECT: an assessment of mental health professionals' knowledge and attitude. J Clin Psychiatry. 1985;46:262-266.
57. Thompson JW, Weiner RD, Myers CP. Use of ECT in the United States in 1975, 1980 and 1986. Am J Psychiatry. 1994;151:1657-1661.
58. Koran LM. Electroconvulsive therapy. Psychiatr Serv. 1996;47:23.
59. Hermann RC, Ettner SL, Dorwart RA, Hoover CW, Yeung AB. Characteristics of psychiatrists who perform ECT. Am J Psychiatry. 1998;155:889-894.
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APA Reference
Staff, H. (2007, February 19). Time to Abandon Electroconvulsion as a Treatment in Modern Psychiatry, HealthyPlace. Retrieved on 2024, December 19 from https://www.healthyplace.com/depression/articles/time-to-abandon-electroconvulsion-as-a-treatment-in-modern-psychiatry

Last Updated: June 23, 2016

Support for Anxiety Sufferers

Page Contents:

We Are All Connected

Understand the anxiety sufferer and learn how to provide support to someone with an anxiety disorder or panic attacks.Illnesses happen to individuals, but one person's disease can take a toll on everyone in the patient's life. If one member of the family becomes sick, the routine of the entire household can be disrupted. If the illness is short-lived, the family can return to its normal activities quickly and without lasting impact. But a chronic illness or one that is disabling permanently may affect the way family members interact with one another and with the world.

Anxiety disorders can be as disruptive as physical ailments, sometimes more so. Many normal family activities may become difficult or impossible. Economic loss may occur if the anxiety disorder limits a person's ability to work. Anxiety disorders may exact a significant emotional toll on all members of the family because the individual with the disorder may be reluctant to participate in typical social activities.

Relationships can be further complicated by the failure of family members to honestly confront the existence of an anxiety disorder. Individuals with a phobia or obsessive-compulsive disorder (OCD) may be too ashamed or embarrassed to ask for help. They may try to hide their anxieties and, at the same time, expect members of the household to be sensitive to their needs and concerns.

Providing Support

The family can play a major supporting role in combating one member's anxiety disorder. Although ultimate responsibility lies with the patient, family members can help by taking part in the treatment program. With training they can accompany the patient into anxiety-producing situations, offer support and encouragement, and create an environment that promotes healing. Family members should:

  • recognize and praise small accomplishments
  • modify expectations during stressful periods
  • measure progress on the basis of individual improvement, not against some absolute standard
  • be flexible and try to maintain a normal routine

Family members often can play an active role in anxiety disorder treatment. The precise nature of the assistance will vary depending on the disorder and the family member's relationship with the patient. In addition to providing psychological therapy and medication, mental health professionals increasingly are recommending treatment programs that include family members. As a rule, the more severe the disorder the more likely that family and/or marital issues will need to be addressed by the therapy program.

In one common approach to family therapy, mental health professionals enlist a spouse or other family member as a co-therapist. Making the family member part of the treatment team tends to reduce the possibility of tension concerning the therapy program. Reading educational materials also promotes understanding.

Helping The Patient With Homework

Family members can play an extremely valuable and supportive role by assisting the patient in "homework" that has been agreed upon in consultation with the therapist. Most typically, at-home assignments for patients with phobias involve controlled exposure to situations that trigger anxiety. Exposure therapy works by gradually bringing patients into contact with a feared object or situation to teach them that they can face their anxieties without harm.

Achievement and progress, no matter how small, should be acknowledged. The patient, using anxiety reduction techniques taught by the therapist, should be encouraged to remain in the situation even when anxiety increases. But the patient should not be forced or humiliated into staying.

All goals and rewards should be clearly spelled out and agreed upon before the home practice sessions get underway.

Families and patients must recognize that the recovery process can itself become a source of tension by changing existing relationships. Patients' emotional needs may change during treatment. They may become more assertive or independent. Working through such changes will require patience and understanding by all members of the family, but they should ultimately lead to more stable and more satisfactory lives for all.

Special Concerns of Older Patients

Diagnosis of an anxiety disorder can be difficult at any age, but particularly in the elderly patient. Many of the signs of an anxiety disorder are identical to the symptoms of illnesses common in older people. And some anxiety disorder symptoms may also mimic side effects of medication. Compounding this is the fact that, for a variety of reasons, older people tend to avoid treatment by mental health professionals.

Mental health specialists report success in treating elderly patients.

Medications have proven effective in reducing or eliminating many of the symptoms of anxiety disorders and tend to be many therapists' treatment of choice for the elderly. But there are several unique considerations that must be weighed when prescribing drugs for older patients.

For example, metabolism, liver and kidney function, and the working of the central nervous system decline with age. Physicians also must take into account the patient's ability to remember to take medication, and other drugs they may be taking. Some doctors insist that another member of the household take responsibility for monitoring the elderly patient's adherence to the medication schedule and any adverse reaction to the drug.

next: The Importance of Breathing Through Your Nose
~ all articles on anxiety self-help
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APA Reference
Staff, H. (2007, February 19). Support for Anxiety Sufferers, HealthyPlace. Retrieved on 2024, December 19 from https://www.healthyplace.com/anxiety-panic/articles/support-for-anxiety-sufferers

Last Updated: July 1, 2016

My Story of Panic

My story of anxiety and my self-help therapy. Visit my Anxiety Self-Help site.Hello and welcome to my website! My name is Christine Evans I live in Bathurst, Australia, I'm 43 years old, and was diagnosed as having Panic Disorder in the year of 85'.

I'm married to a wonderful man and I have 3 wonderful children, who all bring joy and meaning in my life. I believe my disorder to be genetic in nature, as I also have other family members with the same affliction.

I was young and in the prime of my life, it was 1985 and life was about going out and having fun. But my life was about to change!

My friends had called me to tell me they were going out night clubbing, I quickly got ready to go with them. We started the evening at a nightclub not to far from my home, and were enjoying a few drinks when BANG something hit me! What the hell is going on?? My ears are ringing, and I feel like I'm going to pass out! Oh my God...my heart! I think I'm having a heart attack...I have to get OUT of here!!

I left my friends and headed for home...I don't remember how I got there. I went straight to bed, but could not sleep. The room was spinning and I thought I was going to throw up. Ohhh Please God let me get through this night!

The next morning I woke up with the ringing still in my ears. Ohhh no! I definitely have some awful condition! I woke my sister early that morning (I was living with her and her husband). "You need to take me to the Doctors, something is terribly wrong with me!" We arrived at the Doctors and he examined me, he said I was suffering from tinnitus and it should pass in 24 hrs. With that he told me to go home and relax. How could I "relax" when I KNEW I was dying!

Weeks past and nothing changed and I was now a virtual prisoner in my own home, just sitting there in a state of total panic and waiting to die!

My family decided it was best for me to start seeing psychiatrist, I agreed to go but I knew he could not help me. All he did was prescribe drugs each week...drugs that I would NEVER take. Why would I want to feel more dizzy and sick? I knew I didn't need these drugs...I knew there was some mysterious, deathly illness that the doctors had overlooked.

I went on like this for 3 years, I don't know how I got better back then...but it did slowly start to diminish and I started to live an almost "normal" life again.

Just over 2 years ago the panic, fear and anxiety returned. I have done much research and now know I do not need to suffer, and with the combination of the techniques I describe on this site, and with the help of medication (which I'm no longer terrified to take) I'm no longer living in a world of terror. I have found an inner peace, and I thank God for allowing me to experience these "bad" times, because without them I probably would not have grown into the kind and caring person I am today. We really do learn the most about ourselves in our "down times".

I believe everything happens for a reason, and I'm now becoming a stronger, more loving, and spiritual person. I have started a journey to find out my purpose and meaning in life, and on this journey I'm discovering the true meaning to "Inner Peace". These are the symptoms that I'm striving to achieve:

My Symptoms Of Inner Peace

  • Tendency to think and act spontaneously rather than from fear based on past experience.
  • Loss of interest in judging other people.
  • An unmistakable ability to enjoy each moment.
  • Loss of interest in judging self.
  • Loss of interest in interpreting the actions of others.
  • Loss of interest in conflict.
  • Loss of ability to worry (a very serious symptom).
  • Frequent, overwhelming episodes of appreciation.
  • Contented feelings of connectedness with others and with nature.
  • Frequent attacks of smiling through the eyes and heart.
  • Increasing tendency to let things happen rather than make them happen.
  • Increased susceptibility to love extended from others as well as the uncontrollable urge to extend it.
  • Wouldn't it be nice to achieve all of those qualities?

Common Questions And Answers

Q -You mentioned this runs in your family. Who else has it?

A -My Aunt, My Mother and My Daughter.

Q -Were you working/in school when the panic started?

A -I had a child at the age of 17...so I was a stay at home Mum.

Q -What are your interests?

A -I am a nail artist and I enjoy creating unusual nail art designs. I like reading (books about self development), meditating, listening to music.

Q -When you found out you had a panic disorder, were your friends understanding about it?

A -No..and I found it hard to explain...of course I never admitted having Panic Disorder...as I myself did not believe it.

Q -In your story, you said you used a combination of techniques to help you deal with the anxiety. I know they're on your website, but can you mention which ones were most helpful to you?

A -Meditation, breathing and positive affirmations.

Q -Are you able to go out now?

A -Yes...I'm no longer agoraphobic and life is wonderful. I do still have some phobias ...such as claustrophobia and fear of flying.

Q -What is your life like now?

A -My life is wonderful and every new day is a blessing.

next: Relaxation Techniques for Relief of Anxiety and Stress
~ all articles on anxiety self-help
~ anxiety-panic library articles
~ all anxiety disorders articles

APA Reference
Staff, H. (2007, February 19). My Story of Panic, HealthyPlace. Retrieved on 2024, December 19 from https://www.healthyplace.com/anxiety-panic/articles/my-story-of-panic

Last Updated: July 1, 2016