54. Electroconvulsive Therapy

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    54. ELECTROCONVULSIVE THERAPYKerry L Bloomhgdale,M . D

    1. Has electroconvulsive therapy ECT) become a less clinically advantageous psychiatrictreatment now that such a wide spectrum of psychoactive medications is available?

    No, but its role has changed over the years. In fact, ECT dominated somatic treatment of majormental illness until the introduction of the phenothiazines in the1950s. As neuroleptics, antidepres-sants, and mood stabilizers were m ade increasingly available, the market share of EC T naturallydiminished. However, since the mid1970s refinement in awareness of when an d how to use EC Tsafely has given it an established and respected place alon gside medications in the arm amen tariumof somatic treatments for mental illness.

    2. True or false: ECT is useful primarily in treating the most severe forms of major depres-sive disorder.

    False. It is a misconception that E CT is useful only o r primarily in severe and psychotic forms ofmajor depressive disorder. It is highly effective not only in these disease entities, but also in m oderate andeven mild form s of bona fide major depressive disorder. Confusion sometimes arises because, comparedwith antidepressants alone (without antipsychotic drugs), EC T is m uch more effective in treating psy-chotic depression. Furthermore, m any clinicians find ECT easier touse than combinations of antipsy-chotics and antidepressants. Moreover, whenever significant suicidal ideation, intent, or plann ing occu rs,regardless of the presence or absence of psych otic features, clinicians generally choose the most expedi-tious treatment. Although E CT does no t work immediately, it typically works faster than antidepressants.

    3. For what psychiatric conditions other than major depressive disorder is ECT useful?Mania: ECT probably is not used m ore often for this condition because of the potentially rapid

    effectiveness of mood stabilizers and antipsychotics. However, ECT hasa particularly appropriaterole in the treatment of mania when 1) the patient is in the first trimester of pregnancy (because ofconcerns abo ut the teratogenicityof mood stabilizers) or(2) the patient has a history of neurolepticmalignant syndrome.

    Schizophrenic decompensation: Transient benefit can be obtained in treating acute forms withmany positive symptoms, such as hallucinations, delusions, or floridly bizarre behavior. It may b e par-ticularly appropriate in the context ofa time-limited stressor, such asloss of a loved one or disruptionof a living situation, because of the possible brevity of the schizophren ic patients response to E CT.

    Lethal catatonia: This is a final common-pathway disorder probably caused by various af-fective and psychotic cond itions and marked by extreme rigidity. Such rigidity may lead to musclebreakdown, acute renal failure, and death.

    A variety of other conditions, includingParkinsons disease with significant rigidity andneu-roleptic malignant syndrome, also can benefit from ECT.

    Possible Indicationsfiw ECT

    Major depression (unip olar or bipolar)Mania, especiallyin the context of first-trimesterpregnancy or history of neuroleptic malignant syndrome

    Schizophrenia, especially in the se ttingof floridly positive symptoms and/or a time-limited stressorMiscellaneous cond itions

    Lethal catatoniaParkinsons diseaseNeuroleptic malignant syndrome

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    lectroconvulsive herapy 89

    4 Is ECT useful in depressive conditions marked by features of both axis I major depressivedisorder and axis I1 personality disorders?

    To the extent that the clinician can separate the symptoms of major depressive disorder fromthose o a personality disorder, EC T should be useful in treating the depressive symptom s. However,such discrim inations typically are difficult to make. In practice, the decision of w hether to proceedwith EC T in the face of this combination often is better m ade by using your clinical sen se of w hetheran autonomous, somatically treatable depressive syndrome exists than by counting cookbook crite-ria. Moreover, when considering ECT in patients with symp toms of both major depressive disorderand personality disorder, consider the patients post-treatment subjective sense of well-being as wellas the treatment teams objective criteria for response. For instance, even if the major depressivesym ptoms respond to ECT, the patient may experience almost as much dyspho ria after EC T asbefore because of the relatively refractory problems of personality disorder.

    5. Should psychoactive medications be stopped when ECT is started?The combination of psychoactive drugs with ECT has been the subject of much interest in the

    recent literature. Whereas there has beenno conclusive dem onstration that any medication or classof medication consistently adds to the therapeutic effects of ECT, reports have documented patientswho seemed to d o better clinically with the combination of EC T and a psychoactive medication thanwith either alone.

    However, there are reasons to be cautious about the concurrent use of ECT and each c lass ofpsychoactive medications. Lithium carbonate, fo r example, may cause increased neurotoxicity whencombined with ECT . Benzodiazepines and anticonvulsant mood-stabilizers, such as carbamazep ineand valproic acid, make the elicitation of seizures more d ifficult. Thus, these medications m ay be ta-pered or discontinued (see Question9). Antidepressants generally lower the seizure threshold, whichmay increase the durationof seizures or the probability of status epilepticus and spontaneou sseizures. Certain antidepressants, such as tricyclics, may increase cardiac irritability w hen com binedwith ECT. Antipsychotic medications lower the seizure threshold and, when combined with ECT,may cause greater neurotoxicity.

    6. Does ECT cause an excessive cardiovascular response e.g., hypertension, tachycardia) ora diminished cardiovascular response e.g., bradycardia)?

    At different stages in the physiologic response to ECT, the procedure may cau se either a height-ened o r an attenuated cardiovascular reaction. Initially, the E CT stimulus may produce a vagally me-diated bradycardia, sometimes associated with a sinus pause. This response is replaced, uponelicitation of the seizure, by a catecholaminergically mediated hypertensive and/or tachycardic reac-tion. Finally, a compensatory b radycardia may then ensue.

    Obviously, each of these stages has different treatment implications (see table). If the patientis refractory to the electrical stimulus and does not ex perience a seizure, he or sh e will be particu-larly susceptible to the original sinus pause and/or bradycardia, because the sinus pause or brady-cardia will not be counterbalanced by the seizure-induced, catecholaminergically mediatedtachycardia.

    Cardiovascular Reactions t ECT

    STAGE OF ECT CARDIOVASCULAR RESPONSE PRETREATMENT OR ACUTE THERAPY~

    Electrical stimulus Sinus pause and/or bradycardia Atropine or similar anticholingeric drug

    Seizure Tachycardia and/or hypertension Short-acting beta blocker (e.g., esm olol)or alpha and beta blocker e.g., abetalol)

    Postictal Com pensatory bradycardia Atropine or similar anticholinergic drug

    7. What are the contraindications to ECT?There are no absolute contraindications to ECT.

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    290 Electroconvulsive Therapy

    Relative Contruindicutions t ECT

    SIGN, FINDING,SYSTEM OR SYMPTOM

    Cardiovascular Ischemic heart disease

    Tachycardia

    HypertensionVentricular ectopy

    Pulmonary Gastroesophageal reflux,surgical history, gastro-paresis-all of which maypredispose to aspiration

    Orthopedic Recent fracture, particularlyvertebral compression

    Neurologic Space-occupying ntracraniallesion see Question 8)

    Seizure disorders seeQuestion 9)

    POSSIBLE INTERVENTIONSFOR SAFE AND EFFECTIVE ECT

    Reduction in anticipated oxygen consumption by heart

    Reduction of heart rate e.g., with preadministration of

    Reduction of blood pressure before and/or during ECTAdministration before and/or just after induced seizure of

    antiarrhythmic agents. Avoid IV lidocaine if possiblebefore seizure because it may raise seizure threshold

    In addition to standard NPO precaution, preadministra-tion of metoclopramide; intraprocedural pressure oncricoid cartilage; intubation

    e.g., with preadministration of beta blocker)

    beta blocker)

    Use of increased dose of muscle relaxant e.g., succinyl

    Neurologic and/or neurosurgical consultation indicatingcholine) andor curare

    that intracranial pressure not likely to rise to dangerouslevel during ECT

    Consider lowering dose of anticonvulsant drug in consul-tation with neurologist

    8. Is a space-occupying intracranial lesion a contraindication to ECT?Yes, but only relatively, not absolutely. At one time they were considered absolute contraindications,

    and clinicians avoided ECT because of concern over the sometimes already elevated intracranial pressure.They anticipated that the pressure would go even higher with ECT-induced seizures, putting the patientat risk of complications such as herniation. However, experience has dictated that such lesions can becompatible with safe and effective ECT; clinicians have administered ECT without complications to pa-tients in whom imaging studies subsequently revealed pre-existing space-occupying intracranial lesions.

    If these lesions are discovered before ECT in patients who are candidates for the proceduree.g., after work-up for a localizing finding on neurologic examination for ECT), appropriate consul-

    tation should be sought. If there is no evidence of a mass effect, such as papilledema on funduscopicexamination, or edema and midline shift on imaging studies, and if the lesion appears relativelysmall, it may be possible to administer ECT safely. In this instance the potential dangers must bebalanced carefully against the potential benefits of ECT.

    9. Is a patient taking anticonvulsants for seizure disorder a viable candidate for ECT?Yes, in many cases. Consult with a neurologist. The seizure disorder itself is not an absolute

    contraindication to ECT, although careful consideration should be given to the possibilities that ECTmay destabilize an epileptic condition or precipitate status epilepticus. Conversely, of course, ECTmay make a patient with epilepsy temporarily more refractory to spontaneous seizures.Anticonvulsants typically do not interfere with ECT, although they may require higher electricaldosing. If it is impossible to elicit adequate seizures in patients taking anticonvulsants for seizuredisorder, consult with the patients treating neurologist about cautious titration downward of the an-

    ticonvulsant dose. If the patient is taking anticonvulsants purely for their mood-stabilizing effects,the decision to taper them before ECT is less weighty.

    In addition, before proceeding with ECT, consider tapering and discontinuing drugs such asbenzodiazepines that are not used for anticonvulsant purposes, but raise the seizure threshold.

    10. Does ECT cause permanent structural or functional brain damage?No compelling evidence indicates that ECT causes structural brain damage. When animals are

    given electroconvulsive shock usmg parameters analogous to those used in ECT, histopathologic

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    studies reveal no structural neuronal dam age. Im aging studies b efore and after patients h ave receivedECT also reveal no structural brain damag e. Moreover, autopsies of patients who received ECT d onot suggest a pattern of CN S dam age caused by ECT .

    It is mo re difficult to rule out permanentfunction al CN S damag e resulting f rom ECT. In fact,limited numbers of patients note cognitive changes persisting for extended periods. Studies based onneuropsychological testing of EC T patients show that interferenc e with the ability to form newmemories (anterograde amnesia) can persist for at least3 months after a course of ECT. Patientshave difficulty laying down permanent mem oriesof some events that take place just before, during,and immediately aftera course of ECT. Neuropsychologically docum ented retrograde amnesia forevents that took place more than several weeks before the start of E CT is rare. In g eneral, then, it isdifficult to docum ent EC T interference with memory for events that take place m ore than a fewmonths before or more thana few months aftera course of ECT.

    11. Is the suprathreshold approach to dosing in ECT the best way to administer the treatment?Suprathreshold ECT is definedas the use of electrical charge or energy in excess of the am ount

    minimally needed to elicit a seizure. The parameters fo r suprathreshold EC T are established by firsttitrating upward to the minimal electrical charge or energy necessary to elicit a seizure; for subse-quent seizures that amount is multiplied bya factor greater than 1 such as 1.5. The universal appro-priateness of sup rathres hold EC T is not fully clear. Clinical research seem s to indicate thathigher-than-necessary quan tities of charge or energy are often more effective than thresholdamounts, particularly in unilateral ECT.It has not yet been firmly established whether the cognitiveside effects of suprathreshold ECT are greater than those of threshold ECT .

    12. Should electrode placement in ECT be unilateral or bilateral?The cho ice of which electrode placement to use for ECTis controversial. In un ilate ralECT one

    electrode is placed mid line and the other is placed temporally ov er the non dom inant hem isphe re(generally presumed to be the right). In bilateralECT both electrodes are placed temporally, oneover each hemisphere. B ilateral EC T often seem s to work m ore effectively and rapidly than u nilat-eral ECT, but it also may produce more cognitive side effects. Some practitioners believe that bilat-eral ECT is universally advantageous, if cognitive impairment does not preclude its use. Otherclinicians believe that it is appropriate in many casesto initiate ECT treatment with a unilateral ap-proach and then switch to bilateral ECT in patients with poor or sluggish clinical response.

    13. What is the optimal number of treatments in a course of ECT?There is no magic num ber of EC T adm inistrations per course of treatment. In treating patients

    who m anifest a prompt and full responseto ECT for m ajor depressive disorder, experienced practi-tioners may administer5-10 treatments, generally at the rate of3 per week.

    If patients with m ajor depressive disorder do not respond prom ptly or adequately to ECT, clini-cians may give 10-20 treatments, assuming that each treatment results in an adequate seizure.However, in giving such an extended course of treatment, theECT practitioner also is likely to ma-nipulate key variables such as electrode placement o r amount of electrical charge o r energy. If theseizure durations are inadequate, the clinician administering the ECT should:I ) if possible, makesure that the patient isoff all drugs that could raise the seizure threshold;2) adjust the dose or typeof anesthetic agent;(3) hyperventilate the patient; andlor 4) use agents such as intravenous caffeineto lower the seizure threshold.

    14. How does the clinician know that a patient is responding to ECT?Generally, objective signsof improvement precede subjective signs. For example, if the pa-

    tient is treated for m ajor depressive order, other inpatients on the psychiatric unit or, if on an out-patient basis, the family m ay report that the patient acts more spontaneously, eats more, or sleepsbetter before doctors or nursing staff observe changes. Clinical staff then may notice similar neu-rovegetative change s. Finally, the patient may note imp roved self-esteem , hopefu lness, or physicalwell-being.

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    Occasionally, the clinician encounters a difficult and awkward period in his or her alliance withthe patient, perhaps between app roxim ately the third an d seventh treatm ents, in which objectivesigns of improvement are relatively clearcut, but the patient is discouraged about the lack of per-ceived improvement and wants to stop E CT. At suc h a time, the E CT practitioners alliance with the

    patients family or friends may prove critical in ensuring the continuation of treatment.15. Is the electroencephalograph EEG) the best way to assess the duration of a seizure in ECT?

    If accessible, an EEG printout readily provides a way to quantify the duration of the seizure.However, a two-lead EEG produced by an E CT apparatus may be difficult to interpret, especially indocumenting an exact seizure duration. Accordingly, the EEG printout should be used in conjunc-tion with visual monitoring of s eizure duration , especially if th e cuff method is used. This tech-nique consists of inflating a blood pressure cuff to a greater than systolic pressure around anextremity b efore infusion of the mu scle relaxant, to prevent the extremity from being paralyzedduring the seizure. The visually monitored duration of the convulsion in the extremity generally pro-vides an accurate measure of seizure length.

    Another way to corrobo rate seizure duration is to record the rate of change in heart rate. If IVbeta blockers are not used, the heart rate w ill peak in approx imate conjunction with the visually andEEG -monitored durations of the seizure.

    16. What are continuation ECT and maintenance ECT?ontinuation E T is administered after a successful, acute course of ECT, but during the inter-

    val when the patient would still be su ffering from the index episo de of illness if the treatment hadbeen unsuccessful. Sucha period may be presum ed to last for at least several months.MaintenanceECT is administered after the patient is no longer suffering from the underlying episode of illnessoriginally treated acutely with ECT. Continuation and m aintenance EC T treatments usually are

    given less frequently than ECT to treat an acute episode of illness. Preferred schedules of mainte-nance EC T vary considerably: som e experienced clinicians use a fixed schedule, such as w eekly,then biweekly, then mon thly, assum ing that the patient remains symptom-free; others plan follow-upECT on a less frequent basis, but increase the frequencyif symptoms recur.

    17 Are continuation and maintenance ECT always indicated when a patient responds acutelyto ECT?

    They are only o ne follow-up treatment option for the patient who responds acutely to ECT. Ifthe patient was treated for major depressive disorder, antidepressant or mood-stabilizing medica-tions typically are used for follow-up. S om e form of supportive or insight-oriented psychotherapyusually should accompany follow-up E CT o r medications.

    The decision about the form of follow-up treatment after a successful acute courseof ECT iscomplicated. It should be m ade on the basisof anticipated safety and efficacy as well as patientpreference. On e strategy for patients treated effectively w ith EC T for an episode of m ajor depres-sive disorder is to con sider med ication follo w-u p after the first episod e of illness; if the patientbreaks through such follow-up, ECT m ay be offered again. Follow-up EC T is instituted if the break-through, relapse, or recurrence is treated successfully with further acute ECT.

    18. Is ECT too complicated from a medical standpoint to be done on an outpatient basis?Excep t in limited cases, EC T can be do ne safely and effectively on an ou tpatient basis. In fact,

    outpatient ECT may be preferable to inpatient ECT, because the patient is able to remain in his or

    her home environment and the cos ts are lower. Obviously, the severity ofa patients psychiatric con-dition may preclude outpatient ECT.Note that the period s of greate st physical risk from E C T are usually the treatment a nd post-

    treatment recovery phases. Assuming that the patient is carefully monitored d uring these phases,outpatient E CT may be considered even for mild-to-moderate medical risk factors. The clinicianshould give specified pre- and post-treatment suggestions to the patient and responsible family mem -bers, such as avoiding oral ingestion before ECT and refraining from activities such as driving, oper-ating machinery, and making major decisions.

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