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Abstract
Researchers found that patients with mental illness improved after fever and that epileptic patients were less liable to develop schizophrenia, so the idea that fits improve mental illness was elaborated. Subsequently attempts were made to induce fits by various methods including malaria, insulin and Metrazol until discovery of ECT in 1937.
Multiple studies, done on young patients, revealed the efficiency of ECT in treating unipolar or bipolar mood disorders, catatonia, acute delusional psychosis, schizoaffective and, less often, schizophrenia.
The aim of the technique is to decrease cognitive impairment hence the brief pulse wave is recommended, unilateral electrode placement than bilateral and bifrontal more than bitemporal, use of a twice per week frequency rather than three times.
EEG monitoring is necessary and the aim of successful sessions is to achieve generalized epileptic activity in both hemispheres. However if ictal activity persists more than 180 seconds or the fit became recurrent, neurological evaluation is needed.
For ethical reasons, there are scarce ECT studies concerning children, hence, the decision to give ECT to children and adolescents is a complicated one, not only because of brain immaturity but also due to lack of solid scientific evidence. Thus, the decision is taken by both the psychiatrist and the family.
The exact mode of action is unknown. However there are multiple theories including augmentation of 5HT receptors and increased release of norepinphrine and dopamine. Another theory is decrease in cortisol level, thus adjusting hypothalamic-pituitary-adrenal axis; decrease in metabolic rate of glucose in frontal cortex contributing to its therapeutic effect. Other possible theories include changes in blood levels of different neuromodulators. However, the specific effect of each is still unknown.
Despite the absence of absolute contraindications for ECT, neurological assessment is needed in cases of acute stroke, space occupying lesions, as seizure related brain injury increases in those cases. On other hand longitudinal brain imaging studies showed that there was no structural brain damage caused by ECT.
Side effects include cognitive affection in form of prolonged confusion, anterograde and retrograde amnesia due to reversible affection of protein synthesis in hippocampus and temporal lobe. This was associated with cognitive deterioration in those with lower cognitive reserves. The studies done on adolescents to asses cognitive side effects revealed that cognitive functioning with ECT is similar to psychiatric controls and that cognitive functioning is likely to return to its baseline level several months after ECT. The main cause of mortality from ECT is cardiovascular complications, as ECT sessions stimulate autonomic nervous system and may precipitate arrhythmia or ischemic changes.