Non-pharmacological somatic treatments
6.2.10.1 Electroconvulsive therapy
Max Fink
Introduction
Convulsive therapy (ECT or electroshock) is an effective treatment for those with severe and persistent emotional disorders. It is safe for patients of all ages, for those with debilitating systemic illnesses and during pregnancy. It relieves symptoms in a briefer time than do psychotropic drugs. To achieve remission, treatments are usually given three times a week for two to seven weeks. To sustain recovery, treatments are continued either weekly or biweekly for several months. The overall duration of the treatment course is similar to that of the psychotropic medications frequently used for the same conditions.
The treatment is severely stigmatized and its use is discouraged, even interdicted, in the belief that the electricity or the seizures irreversibly damage the brain.(1,2,3,4,5) Few physicians are tutored in its use and facilities are limited making ECT unavailable to many who would benefit. The ease in the use of psychotropic medications, and neither greater efficacy nor greater safety, encourages their preferential use as ECT is relegated to the ‘last resort.’ In countries where psychotropic medications are expensive, ECT is prescribed, but the expense for anesthetics limits its use to its unmodified form.
Despite these hurdles of stigma, expense and lack of training, its use has persisted for more than 70 years. Indeed, its use is increasing. Whole societies where it was interdicted at the end of the 20th century, as in the Netherlands, Germany, Austria, Italy, and Japan, interest and usage has increased, texts have been written or translated, and local psychiatric societies formed to encourage its use.(4,5,6)
Origins
At the turn of the century when malarial fevers were used to treat patients with neurosyphilis, it was deemed possible to treat one illness by developing another. Reports that patients with dementia praecox were relieved of their psychosis after suffering convulsions supported a concept of an antagonism between epilepsy and psychosis. An explanation was seen in the reports that the concentrations of brain glial cells in patients with dementia praecox were low and in those with epilepsy were high.(7) Was it possible that the root of schizophrenia lay in the paucity of glia and would their increase relieve the illness?
After testing ways to induce a grand mal seizure in animals, Ladislas Meduna, a Hungarian neuropathologist and psychiatrist, on January 24, 1934, injected camphor-in-oil into a man with the catatonic form of schizophrenia. The patient seized and recovered without incident. Following the model of malarial fever therapy, Meduna repeated the injections every three days, and after the fifth seizure, the patient, for the first time in four years, talked spontaneously and fed and cared for himself. After three additional treatments he was discharged home, returned to work, and was well when Meduna left Hungary in 1939.(7)
Chemically induced seizures, either with camphor or pentylenetetrazol (Metrazol), were rapidly adopted worldwide as the treatment for dementia praecox, but the treatments were painful and
frightening, so alternative means were sought. In 1938, the Roman psychiatrists Ugo Cerletti and Luigi Bini demonstrated the ease of administration and the efficiency of electrically induced seizures. Quickly, ‘electroconvulsive therapy’ (ECT, electroshock) became the commonest method of inducing seizures and is the standard induction today.(4,5,8)
frightening, so alternative means were sought. In 1938, the Roman psychiatrists Ugo Cerletti and Luigi Bini demonstrated the ease of administration and the efficiency of electrically induced seizures. Quickly, ‘electroconvulsive therapy’ (ECT, electroshock) became the commonest method of inducing seizures and is the standard induction today.(4,5,8)
For whom is ECT effective?
Established DSM diagnoses are usually cited as the indications for ECT. The diagnoses are imprecise, however, offering heterogeneous population samples. A syndromic view offers more homogeneous populations for treatment.(9,10,11)
Defined by DSM Classification. The DSM defined conditions for which ECT is prescribed are cited in established texts(12,13,14,15) (Table 6.2.10.1.1). The breadth of its clinical efficacy across major DSM diagnostic classes is striking, reflecting commonalities in the pathophysiology of different disorders. This experience challenges the concept that DSM classified disorders are distinct biological abnormalities, and supports the 19th century concept of a unitary psychosis.(16)
ECT is not useful for a patient with neurosis, situational maladjustment, personality disorder (character pathology), or drug dependence. It is of limited benefit for anyone with a lifelong history of mental and emotional dysfunction, unless the onset of the present illness is acute and well defined, or affective, psychotic, or catatonic features dominate the presentation(12,13,14,15) (Table 6.2.10.1.2).
Defined by syndrome. DSM-III and DSM-IV classify illnesses based on the check-off of symptoms modified by duration criteria. The DSM criteria identify heterogeneous populations that do not support useful treatment algorithms or the search for biological roots of the illnesses. Clinical syndromes describe more homogeneous populations, often substantiated by biological tests and/or a high specificity of interventions. Melancholia, psychotic depression, catatonia, delirious mania, and acute schizophrenia are syndromes that are particularly responsive to ECT (Table 6.2.10.1.3). These syndromes are not readily identified in the established classification systems. Summary descriptions are offered here; the interested reader will find more extensive descriptions in the cited literature.
(a) Depressive mood disorders
Convulsive therapy is most effective against mood disorders, depression and mania. Depressive mood disorders are dominated by sadness, hopelessness, fears, and thoughts that life is no longer worth-living. Variants are recognized, dominated by vegetative and motor abnormality (melancholia), by delusions (psychotic depression), by severe cognitive deficit (pseudodementia), or by catatonia.(14)
While all variants respond to induced seizures, some also respond to other specific treatments. Melancholic and pseudodementia patients respond to tricyclic antidepressants. Psychotic depressed patients require high doses of both antidepressant and antipsychotic medications.(11) Anticonvulsant sedative drugs, the barbiturates and the benzodiazepines, are useful in catatonic patients.(9)
(i) Melancholia
Motor signs (retardation or agitation) and vegetative symptoms of inability to sleep, feeding, and weight loss are its features. Work, sex, and family are disregarded. Thoughts of suicide are prominent.(10,11)
Table 6.2.10.1.1 DSM defined clinical diagnoses in which ECT is effective(11) | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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Hypercortisolemia is characteristic of the syndrome.(17) Cortisol metabolism is influenced by hypothalamic, pituitary, and adrenal interactions. Melancholic patients exhibit elevated serum levels of cortisol, obtunded diurnal rhythmicity, and serum levels remain elevated despite an administered dose of dexamethasone. The abnormality is measurable by the dexamethasone suppression test (DST) or its variant, the dexamethasone/corticotrophin releasing factor test (Dex/CRH). Elevated cortisol levels normalize with treatment and become abnormal again with relapse. In the 1980s, the specificity of the DST was considered poor for the major depressions defined by DSM-III and the test was discarded. But the re-assessment of the literature and recent reports find the test as
both sensitive and specific for melancholic depression, where it has a positive predictive value.(11,18)
both sensitive and specific for melancholic depression, where it has a positive predictive value.(11,18)
Table 6.2.10.1.2 DSM diagnoses in which ECT is ineffective11 | ||||||||||||||||||||
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Table 6.2.10.1.3 ECT responsive syndromes | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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After an extensive review of the literature, Taylor and Fink (2006) concluded that classifying mood disorder patients as either melancholic or non-melancholic offered more homogeneous populations with better outcomes with TCAs and ECT than did the DSM classification of major depression and bipolar disorder.(11) In their formulation, melancholia is a syndrome of depressive mood, with motor and vegetative abnormalities and with evidence of cortisol abnormality.
(ii) Delusional (psychotic) depression
Overwhelmed by feelings of helplessness, hopelessness, and worthlessness, the patient believes others are watching or talking about him, reporting voices when no one is present. He imagines that events depicted on a television or movie screen apply directly to him. This form is labelled psychotic depression and is remarkably responsive to ECT.
In 1975, Glassman and his associates at Columbia University reported that only three of 13 delusional depressed patients (23 per cent) improved when they were treated with high doses of imipramine, while 14 of 21 non-delusional patients (66 per cent) improved under the same treatment.(18) Nine of the 10 unimproved delusional patients responded well to ECT. These findings have been repeatedly verified.(11,12)
In a study of 437 depressed hospitalized patients treated with imipramine in doses of 200 to 350 mg/day for 25 days or longer, 247 (57 per cent) were evaluated as recovered and were discharged.(19) When the 190 unimproved patients were treated with bilateral ECT, 156 (72 per cent) were recovered. Most of the depressed patients who had not improved with imipramine were delusional as well as depressed.
Only a third of delusional depressed patients recover when treated with antidepressant drugs alone and half recover with antipsychotic drugs alone.(11, 19,20) Two-thirds of those treated with ECT or with high doses of both antidepressant and antipsychotic drugs regain their health.
In a two-year study of late-life depression, 47 per cent of the delusional depressed patients treated with medication relapsed earlier and more often than the nondelusional depressed (15 per cent), indicating that delusional depression is particularly resistant to medication.(21) It is, however, so amenable to ECT that it is considered a primary indication for its use.(11,12,13,14) But the condition is difficult to diagnose making inadequate treatment common. In a three-hospital research study of ECT and continuation medications, only 2 of 52 delusional depressed patients had adequate courses of medication treatment before they were referred for ECT.(22) The same failure was found in another multi-center study with only 5 of 106 patients failing adequate courses of treatment before referral to ECT.(23)
Many reviews find psychotic depression to have a more severe pathophysiology and just using the same treatments as for nonpsychotic depression, even at much higher doses is not adequate.(11,12) Yet, bilateral ECT is remarkably effective. In a multi-site collaborative ECT study, of 253 patients with unipolar major depression, 77 were psychotic depressed. Their remission rate was 95 per cent compared to 83 per cent for the non-psychotic depressed, with the speed of response faster for the psychotic depressed patients.(24, 25)
(iii) Pseudodementia (reversible dementia)
Because the depressed patient ignores daily events, little of what happens to him is registered and memory is compromised. The condition is hardly distinguishable from Alzheimer’s dementia. The onset is usually more rapid and severe compared to the onset of a structural dementia, and patients often report a history of prior depressive episodes.(11,14)
Because the syndrome is not well known, patients are often sent to nursing home care. An example of a 58-year old woman who developed a reversible dementia and was not adequately treated for eight years is reported. Once the diagnosis was considered, antidepressant treatment relieved the syndrome and returned the patient to a more normal family life.(14)
(iv) Catatonia
When the patient is mute, sitting rigidly in a chair or lying motionless on his bed, and unresponsive to questions and commands, he appears as in a stupor. The state is called catatonia or depressive stupor. Catatonia is seen among patients with many DSM diagnoses.(9) It is discussed in detail below.
(b) Manic mood disorders
A mood disorder dominated by grandiosity, expansiveness, feelings of increased power and energy, and excitement, can last for hours, days, weeks, or months. Even after it is relieved, it may recur or alternate or combine with episodes of depression. When the switches occur within one or a few days, the experience is labelled rapid cycling, a malignant form of the illness. Bipolar disorder is the label applied to both mania and mixed forms of the illness.(11,26)
Disturbances in eating and sleeping, thinking, memory, and movement are features of mania. The patient does not sleep, eats poorly, loses weight, and concentrates thoughts poorly. Memory is impaired, often severely; he may be so disorganized as to appear demented and delirious. Melancholia, psychosis, pseudodementia, and catatonia variations are commonly seen.
Delirious mania is a striking form of mania. A normal person suddenly becomes excited, restless, and sleeps poorly, fears that neighbors are watching him, and is easily frightened. He may hide in the house or leave it abruptly, dressed inappropriately, sometimes naked, and wander about the streets. His hallucinations are vivid, his thoughts disorganized. Confusion alternates with mutism, posturing, rigidity, and stereotyped repetitive movements. Physical exhaustion even to the point of death occurs.(11,27)
Before ECT, patients were sedated with opiates, bromides, or chloral and many died of poor care, inanition, and pneumonia. A 1994 summary of the reports of manic patients treated with ECT finds 371/562 (66 per cent) remitted or showed marked clinical improvement.(28) The introduction of chlorpromazine and other sedative drugs quickly replaced ECT for efficacy and ease of use. But when chlorpromazine and other antipsychotic drugs were used in place of ECT, the doses often carried the risks of sudden death and neuroleptic malignant syndrome, as well as tardive dyskinesia and tardive dystonia.(9)
Anticonvulsant drugs are now preferentially recommended, even though the evidence for their efficacy is poor. Many authors encourage the use of lithium for immediate relief and for prophylaxis. In 438 manic patients treated with ECT or lithium, 78 per cent of the ECT treated group showed marked improvement compared to 62 per cent of those treated with adequate doses of lithium and 56 per cent of those treated with inadequate doses.(29) The group receiving neither ECT nor lithium fared least favourably with only 37 per cent improved.
No matter the array of medications and polypharmacy for mania, ECT is an effective alternative.
(c) Catatonia
Muscular rigidity, posturing, negativism, mutism, echolalia, echopraxia, and stereotyped mannerisms, the signs of catatonia, appear suddenly and immobilize patients.(9) When the disorder is transient, it may be disregarded, but when it persists, it threatens life. Patients undergo forced feeding and develop bedsores, muscular atrophy and pulmonary embolization. Repeated bladder catheterizations induce infections.
Catatonia is recognized in patients with affective illnesses, both depression and mania, in patients with systemic disorders, and in those with toxic brain states caused by hallucinogenic drugs. For decades, the prevailing belief was that each instance of catatonia represented schizophrenia. The major classification systems in psychiatry — DSM-III and IIIR of the American Psychiatric Association and the International Classification of Diseases (ICD-IX, ICD-X) — assigned patients with catatonia to the diagnosis of schizophrenia, catatonic type. Few patients were treated with anticonvulsant sedatives or ECT, despite their known efficacy, because neither was recommended for schizophrenia. This short-sighted view was somewhat corrected in the 1994 classification system of the American Psychiatric Association (DSM-IV), which recognized catatonia as secondary to systemic illness in the class of “Catatonic disorder due to … . (Indicate the General Medical Condition) [293.89]”;.(30) The experience that catatonia is not limited to patients with “schizophrenia”; has led to the call for a separate category in DSM-V.(9,31)
Catatonia is defined by the persistence of two or more characteristic motor signs for more than 24 h in a patient with a mental disorder.(9,31) Posturing and staring can be observed, but most signs require elicitation in the examination. The accepted motor signs and a formal examination are cited in catatonia rating scales.(9) An intravenous challenge of lorazepam or amobarbital verifies the diagnosis in more than 2/3 patients with catatonia, and a positive test response augurs well for high dose benzodiazepine therapy. When this treatment fails, ECT is effective, although the treatment schedule may require daily treatments.
Catatonia may be transitory or may persist for months or years. It appears in many guises.(9,32) Prominent examples are malignant (pernicious) catatonia (MC) with a high risk of death and the neuroleptic malignant syndrome (NMS) that follows on the administration of neuroleptic drugs.
(i) Malignant catatonia
Descriptions of patients who develop an acute febrile delirium with excitement or stupor dot the literature. They often exhibit signs of catatonia. Vegetative dysregulation is often severe and death was a frequent feature before the introduction of ECT. Descriptions by Bell (1849), Stauder (1934), and Bond (1950) highlight the lethal nature of the syndrome. In 1952, Arnold and Stepan described patients in whom ECT rapidly relieved malignant catatonia, but to avoid mortality it had to be used within the first five days.(9)
(ii) Neuroleptic malignant syndrome (NMS)
A toxic response to neuroleptic drugs evinced by fever, motor rigidity, negativism, mutism, and cardiovascular and respiratory instability is a toxic response to neuroleptic drugs. It is indistinguishable from malignant catatonia.(9, 32) It is an MC variant as the diagnostic criteria and effective treatments are the same as for MC. MC occurs with almost all neuroleptics, most commonly with the high-potency agents like haloperidol, fluphenazine, and thiothixene, but also with atypical neuroleptics.
One hypothesis explains the syndrome as a consequence of an excessive reduction in the amount of brain dopamine. Those who believe this association prescribe the dopamine agonists bromocriptine or levodopa and relieve muscular rigidity by prescribing the muscle relaxant dantrolene. Neither of these treatments has proved effective and dantrolene use is associated with considerable toxicity.(33) These are best not used and patients are best treated with sedative anticonvulsants and ECT.
(iii) Toxic serotonin syndrome (TSS)
A toxic syndrome is occasionally described in association with the SSRI antidepressant drugs. TSS is similar to MC with prominent gastrointestinal symptoms. The diagnosis and treatment follows the protocol for MC.(9)
(d) Psychosis
A severe impairment of thought characterized by delusions is a feature of many psychiatric conditions, notably manic delirium, psychotic depression, post partum depression, and toxic psychosis. It is broadly defined as a psychosis and diagnosed within the major class of psychoses as schizophrenia. In this class ECT is hardly considered. But when we consider the efficacy of ECT in the psychotic variants of the mood disorders, we appreciate that ECT is an effective treatment of psychosis.(34)
Convulsive therapy was introduced for the treatment of dementia praecox and was widely and quickly adopted. Comparisons with chlorpromazine found both treatments effective in acute and severe short-term illnesses, but neither was useful in chronic states. Chlorpromazine was favoured since its cost is considerably less and
its image better. As more patients failed to respond to medications, however, a cadre of ‘medication resistant’ psychotic patients developed. Families asked whether anything else could be done to better the patients’ lives. Friedel (1986) augmented a failed course of thiothixene therapy with ECT, returning each of nine patients to community life. The finding was replicated in the successful augmentation in 8/9 psychotic patients.(34)
its image better. As more patients failed to respond to medications, however, a cadre of ‘medication resistant’ psychotic patients developed. Families asked whether anything else could be done to better the patients’ lives. Friedel (1986) augmented a failed course of thiothixene therapy with ECT, returning each of nine patients to community life. The finding was replicated in the successful augmentation in 8/9 psychotic patients.(34)
Clozapine was described as a treatment for psychotic patients who had failed to respond to two different antipsychotics. As the experience with this treatment grew, clinicians were again faced with treatment failures and ECT augmentation was tried. A synergy for ECT and clozapine was described and offers an effective treatment for patients who have failed conventional antipsychotics and clozapine.(34)
It is reasonable to consider ECT in the treatment of psychosis, whether in an affective illness or in schizophrenia. For the affective illnesses, ECT is used alone. In schizophrenia, ECT is effective alone or in augmenting neuroleptics.(34)
(e) Delirium
Acutely ill psychotic patients often exhibit disturbances in consciousness and are confused. Delirium is common in toxic states, either drug induced (alcohol being the most common), or secondary to drug withdrawal, or associated with systemic illnesses. Delirium is a feature of acute manic states (e.g. delirious mania) and the confusional state described as oneirophrenia. With few resources to treat acute psychoses, ECT was applied with favourable results.(14,35) The relief of delirium by ECT is an unrecognized effect that warrants consideration as an alternative to the risks of high potency neuroleptic drugs inducing NMS (MC).
(f) Neurological syndromes
ECT is well appreciated in catatonia, but it is also useful in status epilepticus (SE), non-convulsive status epilepticus (NCSE), and Parkinsonism.
(i) Status epilepticus
SE and NCSE are emergency conditions with high mortality rates. The pathophysiology is the persistence of seizures as biochemical inhibitory mechanisms fail to terminate a seizure.(36) Despite ever larger doses of anticonvulsant medications, proceeding from lorazepam to phenytoin, phenobarbital, and general anesthesia with midazolam, propofol, or barbiturates, patients persist in SE and NCSE.
ECT is another effective intervention. During the course of electroconvulsive therapy, the seizure threshold rises, encouraging seizure termination. The first report of the relief of intractable epilepsy by ECT in 1943 has been sporadically verified.(37)
An explanation for this application is physiologically interesting. The strength of a seizure can be judged by the immediate rise in serum prolactin after a sustained epileptic seizure. Within the hour after a seizure, the level of serum prolactin indicates whether the seizure is a cerebral grand mal event or a pseudoseizure. Serum prolactin levels do not rise in SE but remain normal. This suggests that the SE seizures are partial or incomplete and that they fail to stimulate an inhibitory termination process. But even in patients in SE, ECT elicits maximal seizures, making it a reasonable alternative to general anesthesia as a treatment for intractable seizures.
(ii) Parkinsonism
In treating older depressed patients with concurrent Parkinsonism with ECT, motor and facial rigidity were also relieved. In Parkinsonism, brain dopamine levels are reduced, making dopamine agonists effective treatments. In ECT, brain and CSF levels of dopamine increase. Experiments in Parkinsonian patients without mood disorder found motor rigidity to be relieved.(38) For those patients who are not relieved by conventional treatments, periodic ECT has been helpful. Continuation treatments, like continuation pharmacotherapy, are necessary to sustain the benefit.
(g) Suicide
All psychiatric disorders carry the risk of suicide. ECT reduces this drive. The impact of medications on suicide risk is not well defined but compared to ECT, the efficacy is less favourable.(6,11) Comparisons of ECT and TCAs across different treatment eras find the frequency of suicides decreased in the ECT era. A study of the psychiatric status of 519 patients six months after discharge from hospital treatment for depression found 0.8 per cent of the ECT treated patients had made a subsequent suicide attempt compared to 4.2 per cent for those rated as receiving adequate and 7 per cent of those receiving inadequate courses of antidepressant drugs. At the 6-month follow-up no suicides were reported in 34 women treated with ECT, but two suicides occurred in the 84 patients treated with antidepressants (2.4 per cent).(39)
In a study of the expressed suicide intent (changes in Item 3 of the HAMD rating scale) in 148 patients treated with ECT, the baseline average score was 1.8. It reduced to 0.1 in 72 responders and to 0.9 in 76 non-responders. For the total sample, there was a greater decrease in the suicide item scores than in the overall HAMD scores.(40)
In another study of 444 patients referred for ECT, 131 had high expressed suicide intent scores.(6) The scores dropped to zero in 106 (80.9 per cent) with treatment, occurring in 38.2 per cent (50/131) after 3 ECT (one week), in 61.1 per cent (80/131) after 6 ECT (two weeks); and in 76.3 per cent (100/131) after nine ECT (three weeks).
ECT’s effect on the death rate in the mentally ill, particularly those with mood disorders, must be a major consideration in treatment recommendations.
Principles of treatment
When to consider ECT? Psychotropic drugs and psychotherapy are the first treatments of the psychiatrically ill, with referral to ECT when these treatments fail. Since ECT is effective in medication treatment failures, would it not be wise to spare patients a prolonged illness and risks of suicide by offering ECT as the initial treatment? ECT is indeed considered the first treatment when there is a need for a rapid, definitive response, as in suicidal patients who require constant observation and restraint, in hyperactive patients who may be at risk of harm to themselves or others, in those with malignant disorders as malignant catatonia, neuroleptic malignant syndrome, or delirious mania, or in those whose lives are in jeopardy from systemic illness. It is also preferred in those patients who have had a prior illness that responded well to ECT or who have had a poor experience with medications.(11,12,13,14,15)
How many failed trials of medications are reasonable before ECT is considered? For some patients, especially those whose practitioners are not knowledgeable about ECT, medication trials
become interminable and ECT is considered only when the patient seeks care elsewhere. A reasonable guideline is derived from the experimental trials with clozapine, an agent with life-threatening risks.(41) To put patients at risk and yet obtain the possible benefits of clozapine, the researchers decided that patients should not be offered clozapine unless they had experienced two unsuccessful courses of neuroleptic treatment. A similar standard seems reasonable for recommending ECT. After patients have failed two different courses of medications at adequate doses and for adequate periods, ECT is to be considered.
become interminable and ECT is considered only when the patient seeks care elsewhere. A reasonable guideline is derived from the experimental trials with clozapine, an agent with life-threatening risks.(41) To put patients at risk and yet obtain the possible benefits of clozapine, the researchers decided that patients should not be offered clozapine unless they had experienced two unsuccessful courses of neuroleptic treatment. A similar standard seems reasonable for recommending ECT. After patients have failed two different courses of medications at adequate doses and for adequate periods, ECT is to be considered.
Financial considerations affect the decision. If the patient is severely ill and has only a limited ability to pay for extended care, repeated unsuccessful medication trials are unwarranted. All practitioners should balance the cost of medication trials and the effective use of ECT.
Consideration of age. ECT is an accepted treatment for adults. For decades, the attitudes of child and adolescent psychiatrists precluded consideration of ECT for their patients except the most devastatingly ill. The acknowledged safety of ECT in adults relaxed prejudices against its use and led to more treatment trials. Once it became clear that the response of adolescents was similar to that of adults, the attitude changed and ECT is now an accepted treatment for adolescents with the same illnesses that are successfully treated in adults.(42)
ECT is probably effective in similar conditions in children, but their expression of mood and psychotic disorders is different than in adults and difficult to interpret. The published experience in the few children treated with ECT finds that conditions that respond in adults and adolescents also respond in children.
ECT is widely used in geriatric patients. Indeed, it is increasingly called on when the side effects of medications become intolerable and when medication trials fail. The safety of modern ECT is such that even the frailest and systemically ill elderly can be safely treated with ECT. We acknowledge no absolute contraindication to ECT other than the lack of skill of the clinicians.(11,12,13,14,15)
The treatment process
Consent. The referral of a patient to an ECT service starts the treatment process. As in surgical treatment, the patient and family members are educated as to the risks and processes of the treatment course, and a signed voluntary consent, witnessed by a family member if possible, is obtained. In response to the turmoil of the 1970s when a draft for an unwelcome war led to widespread questioning of authority, attacks on ECT as a forced involuntary treatment led the profession to suggest procedures for informed voluntary consent. These procedures are well established.(1, 2, 4, 12)
An explanation of why the treatment is recommended, specific anticipated benefits and risks, the names of the responsible physicians, and a statement that the patient may, at any time, discontinue the treatment are elements of a valid consent.(4,13,14) Although voluntary consent is the basis for ECT in almost all Western countries, provisions for involuntary treatment for patients who may not be able to understand the severity of their illness nor the need for treatment is provided in state laws with courts authorizing treatment. In a few venues, surrogate consent by family members is accepted. Educational videotapes and books for laymen support the consent process.(4, 12, 43)
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