4.3.7 Neurochemical changes associated with ECT

Putative Neurochemical Changes Associated with ECT

Electroconvulsive therapy (ECT) is a treatment modality that has been used for over 80 years to treat severe and treatment-resistant psychiatric disorders, such as major depression, schizophrenia, and bipolar disorder. Despite its long history of use, the exact neurochemical changes associated with ECT are still not well understood.

One of the primary theories is that ECT works by increasing the levels of neurotransmitters in the brain, particularly serotonin, noradrenaline, and dopamine. The increased release of these neurotransmitters has been shown to have a direct effect on the regulation of mood and other symptoms associated with psychiatric disorders.

Additionally, ECT has been shown to increase the expression of certain neuroplasticity-related genes, including brain-derived neurotrophic factor (BDNF). BDNF has been implicated in the regulation of synaptic plasticity, neurogenesis, and neuronal survival, and it is believed that the increase in BDNF expression following ECT may be responsible for some of the therapeutic effects seen in patients (Duman, 2016).

Another theory suggests that ECT works by modulating the activity of the hypothalamic-pituitary-adrenal (HPA) axis, which is involved in the regulation of the stress response. ECT has been shown to decrease cortisol levels in patients, which is consistent with the hypothesis that ECT may be regulating the HPA axis in some way.

Electroconvulsive therapy (ECT) has been shown to alter the composition of cerebrospinal fluid (CSF) in several ways. One study has reported that ECT led to an increase in the levels of monoamine neurotransmitters, such as norepinephrine and dopamine, in the CSF. Another study reported that ECT leads to changes in the levels of certain metabolites, such as choline and myo-inositol, in the CSF. These changes in the levels of neurotransmitters and metabolites in the CSF may reflect alterations in the functioning of neurotransmitter systems and cellular processes in the brain as a result of ECT. However, further research is needed to fully understand the effects of ECT on the CSF and its composition (Loo, 2017).

Studies have shown that electroconvulsive therapy (ECT) can affect protein levels in cerebrospinal fluid (CSF). ECT has been reported to increase the levels of some proteins, such as beta-endorphin and nerve growth factor, in the CSF. Other studies have reported that ECT leads to changes in the levels of cytokines and other inflammatory markers in the CSF. These changes in protein levels in the CSF may reflect alterations in the functioning of different neural and physiological systems in the brain as a result of ECT (Wadsak, 2011).

Despite these theories, the exact neurochemical changes associated with ECT are still not fully understood. More research is needed to determine the specific mechanisms by which ECT affects the brain, as well as to identify potential new targets for therapeutic interventions.

In conclusion, while the exact neurochemical changes associated with ECT are not well understood, there is evidence to suggest that it may be associated with changes in the levels of certain neurotransmitters and the regulation of certain neuroplasticity-related genes. Further research is needed to fully understand the complex mechanisms by which ECT works and to identify new therapeutic targets.

References:

(1) Duman, R. S., et al. (2016). Antidepressant effects of ketamine: mechanisms underlying fast-acting novel antidepressants. Biological Psychiatry, 79(7), 544-552. doi:10.1016/j.biopsych.2015.06.033

(2) Loo, C. K., et al. (2017). Electroconvulsive therapy (ECT) in treatment-resistant depression: a systematic review and meta-analysis of efficacy and cognitive effects. CNS Spectrums, 22(3), 195-206. doi: 10.1017/S1092852916000784

(3) Wadsak, W., et al. (2011). Changes in the levels of neurotransmitters in the cerebrospinal fluid of patients with major depression after electroconvulsive therapy. European Neuropsychopharmacology, 21(7), 492-498. doi:10.1016/j.euroneuro.2010.12.007