Everything About ECT and Ablation Neurosurgery

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Detailed information on ECT and Ablation Neurosurgery.
  INTRODUCTION — Electroconvulsive therapy (ECT) uses a small electric current to produce a generalized cerebral seizure under general anesthesia. ECT is used mainly to treat severe depression, but is also indicated for patients with other conditions, including bipolar disorder, schizophrenia, schizoaffective disorder, delirium, and neuroleptic malignant syndrome.There is no question about the efficacy and safety of ECT, which is practiced widely in the United States and the rest of the world . Nevertheless, it remains controversial and stigmatized because of misinformation and outmoded perceptions about how the treatment is performed.This topic provides an overview of ECT. The indications for treating unipolar major depression with ECT, the efficacy of ECT for treating unipolar depression, technique for performing ECT, and medical consultation for ECT are discussed separately.HISTORY OF ECT — The use of seizures to treat psychiatric disorders has progressed over time, and began with observations that schizophrenic patients often improved temporarily after a spontaneous seizure. Initially, physicians induced seizures with medications. In 1938, Italian psychiatrists used an electric current to induce seizures as a treatment for schizophrenia. ECT quickly spread around Europe and the rest of the world, and was first used in the United States in 1939. Patients suffered bone fractures occasionally and considerable anticipatory anxiety, but advances in anesthesia techniques in the 1950s allowed for the use of general anesthesia and muscle relaxation for ECT, which reduced the incidence of these problems.The use of ECT in the United States has fluctuated. Use of ECT declined in the 1970s, and subsequently increased, possibly as a result of greater treatment resistance to pharmacotherapy in depressed patients, increased recognition of the limitations of pharmacotherapy, and better public acceptance. A practice survey from 1988-89 estimated that at least 100,000 patients received ECT annually. The typical ECT patient today is relatively affluent and receives ECT in a private sector psychiatric facility. State hospitals rarely offer the treatment, even though many of the patients would meet indications for ECT.MECHANISM OF ACTION — The mechanism of action for ECT is unknown, but there are a myriad of well-documented changes in the central nervous system:Human and animal studies show that ECT increases release of monoamine neurotransmitters, particularly dopamine and serotonin. ECT also enhances monoamine transmission by desensitizing presynaptic adrenergic autoreceptors.One theory postulates that ECT exerts its beneficial effects by increasing release of central neuropeptides, including corticotrophin releasing factor, somatostatin (STS), and neuropeptide Y .The neuroendocrine hypothesis is based upon the diabetes/insulin model and suggests that mood disorders are caused by insufficiency of a hypothalamic mood-maintaining peptide. Repeated seizures enhance the production and release of the putative hypothalamic peptide  antidepression, which relieves both neuroendocrine and behavioral abnormalities.ECT has anticonvulsant properties, which has led to the suggestion that these properties are responsible for the therapeutic effects of the treatment.Positron emission tomography (PET) studies demonstrate decreased metabolic activity in frontal and cingulate cortex after ECT.Functional magnetic resonance imaging before and after successful treatment with ECT reveals a reduction in global connectivity within the left dorsal lateral prefrontal cortex. Quantitative electroencephalogram (EEG) studies demonstrate increased slow (delta) wave activity in the prefrontal cortex after ECT, which is associated with clinical response.Several human and animal studies indicate that ECT has trophic effects on the central nervous system. ECT increases brain derived neurotrophic factor (BDNF) in patients and electroconvulsive stimulation induces neurogenesis and mossy fibre sprouting from granule cells in rat hippocampus.PRE-ECT EVALUATION — The goals of the pre-ECT evaluation are to: ã Determine whether ECT is indicated. ã Establish baseline psychiatric and cognitive status to serve as reference points for evaluating response and cognitive effects. ã Identify and treat any nonpsychiatric medical conditions that might be associated with an increased risk of adverse events from ECT. ã Initiate and continue the informed consent process. ã A complete medical history should be taken. Medical consultation prior to ECT is indicated for most patients 40 years or older, and is frequently obtained in younger patients as well. Particular attention should be paid to any history of cardiopulmonary disease and prior surgeries (with inquiry about type of anesthesia and any complications). A history of skull fractures should be determined, as this may affect electrode placement. ã Appropriate physical examination and laboratory evaluation, guided by the relevant history, should be performed. The patient's handedness and any dental problems should be noted. Specific laboratory tests are not indicated for patients without known medical comorbidities. SPECIFIC MEDICAL CONDITIONS — Inducing a seizure causes transient increases in blood pressure, pulse, and intracranial pressure, which can have deleterious effects. Organ systems of most concern are: ã Cardiovascular ã Pulmonary ã Central nervous system ã Seizures increase cardiac workload and oxygen demand. Thus, it is important to try to  maximize the patient's cardiovascular status before ECT. Additionally, medication to blunt increases in heart rate and blood pressure is indicated prior to ECT and during the procedure in patients for whom these increases would be detrimental. ã Coronary heart disease — Cardiac complications are the most common cause of serious morbidity and mortality during ECT. ã Patients with coronary heart disease should be evaluated prior to ECT with a careful cardiac history and ECG. Additional cardiovascular diagnostic testing and evaluation by a cardiology consultant may be indicated for selected patients, and for any patient with unstable disease. ã History of myocardial infarction — History of myocardial infarction and current unstable angina present increased risk. Careful consideration of the risk/benefit ratio of ECT in such cases is essential. The key factors in this assessment are the extent of myocardial damage and subsequent healing, and the residual functional cardiac status. ã In general, the longer one waits after a myocardial infarction, the safer it is to perform ECT. For patients who have had a myocardial infarction and are not at imminent risk from their depressive episode, we suggest waiting a minimum of three months prior to starting a course of ECT. However, patients at high risk of death due to their depression can be treated sooner. For severely depressed patients, treatment with ECT on an emergent basis may be indicated. ã Hypertension — The patient's blood pressure should be well controlled prior to ECT. The patient should take his or her currently prescribed antihypertensive medications (with the exception of diuretics) with a small sip of water, prior to each ECT treatment. ã Use of prophylactic beta blockers to prevent treatment-induced hypertension is discussed separately. ã Heart failure and valvular disease — The use of ECT in patients with heart failure or valvular disease is discussed separately. ã Pacemakers and implantable defibrillators — The use of ECT in patients with pacemakers or implantable defibrillators is discussed separately. ã Pulmonary disease — Optimizing pulmonary status before ECT is important. The anesthesiologist manipulates the patient's airway during ECT using a bag and mask circuit and there is a risk of inducing bronchoconstriction. All patients should receive supplemental oxygen via nasal cannula, initiated a few minutes prior to each treatment.  ã Elective intubation is not indicated for ECT, except in rare circumstances in which the anesthesiologist assesses that intubation would be exceptionally difficult should the airway become compromised. ã Neurologic disease — The use of ECT for patients with brain tumors, history of stroke, dementia, and neuromuscular disease is discussed separatelyCONCURRENT MEDICATIONS — The patient's current medications, including prescription, over-the-counter, and complementary or alternative drugs should be reviewed prior to ECT. The ECT psychiatrist, anesthesiologist, or medical consultant should decide which to continue and which to taper and discontinue.Psychotropic drugs — Many psychotropic medications may be continued during a course of ECT for their synergistic effect without compromising safety, including antidepressants, antipsychotics, and lithium. Morning doses on the day of ECT are given after the patient has recovered from that day's procedure. Anticonvulsants and benzodiazepines often interfere with ECT and may need to be tapered and discontinued.Antidepressants improve the efficacy of ECT. A review of 10 systematic reviews, 7 meta-analyses, and 3 practice guidelines found that for depressed patients, a tricyclic may improve the antidepressant effect of ECT. As an example, a randomized trial assigned 319 depressed patients receiving an acute course of ECT to concomitant nortriptyline, venlafaxine, or placebo. Remission occurred in more patients who received nortriptyline or venlafaxine compared with placebo (63 and 60 versus 49 percent) with a significant difference between nortriptyline and placebo.Antidepressants are generally safe to use with ECT and do not affect its tolerability. As an example, a randomized trial of depressed patients receiving an acute course of ECT with concomitant nortriptyline, venlafaxine, or placebo found the number of adverse events did not differ significantly between the three groups . Other types of antidepressants are also well tolerated during ECT, including selective serotonin reuptake inhibitors, tetracyclics, and monoamine oxidase inhibitors.Antipsychotic medications are often continued during ECT and may provide a synergistic antipsychotic effect, especially second generation antipsychotics. In addition, antipsychotics generally do not appear to affect the tolerability of ECT. Second generation antipsychotics and high potency first generation antipsychotics are thought to be safe. A review found that early reports warned of hypotension and cardiac complications from combining chlorpromazine and ECT, but later reports did not substantiate these problems . Nonetheless, combining of low potency, first generation antipsychotics with ECT should be done cautiously.
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