ELECTROCONVULSIVE THERAPY

Electroconvulsive therapy (ECT) was introduced in the 1930s as a treatment of schizophrenia. Although use of this therapy declined through the 1970s because of negative publicity, interest in and use of ECT have increased over the past 20 years. Current acceptance of this procedure is in part due to the use of general anesthesia to reduce the physical and psychological trauma associated with ECT. Indications for ECT include major depression, mania, certain forms of schizophrenia, and perhaps Parkinson's syndrome.^{[140] [141]} Pheochromocytoma is a contraindication to ECT. Relative contraindications include increased intracranial pressure, recent cerebrovascular accident, cardiovascular conduction defects, high-risk pregnancy, and aortic and cerebral aneurysms.^{[142] [143]} In these conditions, the risk of the patient's psychiatric illness and the side effects of antidepressant medications must be weighed against the risk associated with ECT and anesthesia.

ECT consists of programmed electrical stimulation of the central nervous system to initiate seizure activity. The precise mechanism of the therapeutic effect of ECT remains unknown despite increasing research in this area.^[144] After induction of general anesthesia and muscle relaxation to prevent traumatic injury during generalized seizure activity, two stimulus electrodes are applied to the patient's scalp. A series of programmed electrical pulses at precise energy levels are then delivered to induce a generalized seizure. The energy level for a given patient is based on an initial titration of increasingly powerful pulses. The seizure is monitored both by observation of the patient and by monitoring of an electroencephalogram on the ECT machine. Seizure duration is recorded. Treatment efficacy is believed to be related to a minimum seizure duration of 25 seconds and to the total seizure duration over the course of treatment. Energy delivery is thus minimized and tailored to the condition of each patient. Treatments continue two to three times per week until either improvement is seen or the treatment is deemed unsuccessful. Successful treatment may be supported by continuation of ECT at weekly to monthly intervals for up to 6 months and by similar maintenance ECT continuing more than 6 months past initiation of treatment.^[140]

Physiologic Effects

Direct brain effects of the stimulus and seizure include large increases in cerebral blood flow and intracranial pressure.^[145] Seizure activity causes an initial parasympathetic discharge manifested by bradycardia, occasional asystole, premature atrial and ventricular contractions, or a combination of these abnormalities. Hypotension and salivation may be noted. The parasympathetic discharge is followed by sympathetic discharge associated with tachycardia, hypertension, premature ventricular contractions, and rarely, ventricular tachycardia. The tachycardia peaks at 2 minutes after the stimulus and is normally self-limited.^{[146] [147]} ECG changes, including ST-segment depression and T-wave inversion, may also be seen after ECT without any of the myocardial enzyme changes consistent with myocardial infarction. These ECG changes are presumed to be secondary to the sympathetic discharge.^{[148] [149]} Arrhythmias associated with ECT, even in patients with preexisting arrhythmias, are self-limited and not in themselves a contraindication to treatment. ECT has been found to be relatively safe even in high-risk cardiac patients, provided that careful management is provided.^{[150] [151]}

Neuroendocrine responses to ECT include increased levels of stress hormones, including adrenocorticotropic hormone, cortisol, and arginine vasopressin, as well as prolactin and growth hormone.^{[142] [152]} Norepinephrine and epinephrine increase immediately after ECT, and epinephrine levels decrease more rapidly thereafter. Glucose homeostasis is variably affected by ECT. Improvement in control of non-insulin-dependent diabetes is generally noted, whereas hyperglycemia may be seen when the diabetes is insulin dependent. A single report noted hyperglycemia in a patient with no previous history of diabetes.^[153]