Electroconvulsive Therapy: Physiological Effects of Treating Depression
Electroconvulsive therapy (ECT) is a treatment that uses electrical shocks which are generated in the brain to cause convulsions or seizures for a brief period of time (Read & Bentall, 2010). ECT was used as a therapy for depression 75 years ago by a man named Laszlo Meduna (Read & Bentall, 2010). This therapy has been successfully used in treating disorders, such as depression, since the 1930s (Read & Bentall, 2010). Per the National Alliance for the Mentally Ill, ECT is commonly used three times weekly during a predetermined period of therapy sessions. ECT is given by administering a general anesthesia. Electrodes are then placed above each temple which is known as bilateral ECT. As the electrical current is directed through the brain tissues, the seizure then begins. Though seizures cause the body’s muscles to convulse, the patient’s body is in a relaxed state due to the use of succinylcholine muscle relaxer. An electroencephalography monitors the patient’s seizures while the electrocardiogram is used, simultaneously, to monitor the patient’s heart. The electrical current is administered only for a brief moment, normally less than a few seconds. The seizures may last from a few seconds to minutes after the original electrical currents have taken place (National Alliance for the Mentally Ill (NAMI), 2011).
ECT has been debated for many years, yet studies suggest that this therapy is more effective on depression than the use of antidepressants (NAMI, 2011). Depression is a mental disorder that is characterized by symptoms of low self-esteem, loss of interest or pleasure, and an overall state of gloom (Collins English Dictionary, 2009). Depression has become more common in the United States over the past few decades. According to “How depression affects the brain” written in 2010, approximately 19 million people, in the U.S. alone, struggle with depression and its symptoms. Depression has direct effects on the physiological functions of the brain. Neurotransmitters are the mechanisms that best explain the physiological aspects of depression. Neurotransmitters are the chemicals used to communicate between neurons. These mechanisms can inhibit or activate other neurons that receive the neurotransmitters from the synapse. A below-average level of the neurotransmitters, specifically norepinephrine and serotonin, may lead to depression. These monoamines help to contravene the glutamate efficacy by binding to the receptor sites on the postsynaptic neuron. If low levels of the neurotransmitters impede this process, depression may become a predisposed outcome (Cloe, 2010). ECT is used as a treatment for depression because it acts as a quick relief to symptoms related to depression (Ongur & Heckers, 2004) ECT has helped save the lives of those with suicidal tendencies (Read & Bentall, 2010). Though electroconvulsive therapy is quick to relieve symptoms of depression, antidepressants are normally used as a long-term coaid of therapy. The relevance of ECT in the medical field has continued growing throughout the last 2 decades despite the side effects which may include temporary amnesia, headache, and nausea (Sienaert, 2011). Serious risks have been practically eradicated due to the techniques practiced and the use of medicines such as muscle relaxers (Sienaert, 2011). ECT has been involved in controversy over the effects it may have on the physiological aspects of the brain.
The physiological effects on the brain include both adverse and beneficial outcomes. During bilateral ECT, the electrical waves that are directed into the brain may cause temporary or permanent effects to the limbic system. The limbic system is also known as the medial temporal lobe (Weedman, 1997). This system includes several components of the brain such as the amygdala and the hippocampus (Weedman, 1997). Studies have shown that a decrease of activity of the glia cells in the prefrontal cortex is linked to emotional processing (Kay, 2008). ECT studies have shown an increase in the production of glia cells in these regions (Kay, 2008) The electrical current used in ECT helps stimulate the increase in proliferation of cells in the hippocampus (Kay, 2008). The hippocampus is directly linked to memory and controls the storage of short-term memory to the conversion of long-term memory. Amnesia has been shown as a cognitive effect of electroconvulsive therapy (Neuhaus, Gallinat, Bajbouj, & Reischies, 2005). Retrograde amnesia is the most common cognitive effect and is categorized by the loss of memory for a temporary time after ECT (Neuhaus et al., 2005). This shows a direct correlation between ECT and its effect on the hippocampus. In a study of the hippocampus, the researchers hypothesized that there may be two metabolite changes that may be caused by ECT (Ende, Braus, Walter, Weber-Fahr, & Henn, 2000). The first metabolite change is a decrease in the N-acetyl aspartate (NAA), which is caused by the loss of neurons (Ende et al., 2000). The decrease in NAA may show the correlation associated with the hippocampus and memory loss after ECT (Ende et al., 2000). The second metabolite change is the increase in the signaling from compounds containing choline (Ende et al., 2000). The increased signal may be due to a moss fiber found in the hippocampus. These fibers may be related to the substantial increase of membrane turnover (Ende et al., 2000). Thus, the hippocampus may be directly affected by ECT. Interical slow waves in the left medial temporal lobe have been observed during bilateral ECT (Neuhaus et al., 2005). These brain waves showed a distinct pattern of brain waves that are referred to as theta activity (Neuhaus et al., 2005). The theta activity in the left medial temporal lobe may also represent cause for amnesia during ECT.
ECT may have an adverse physiological effect on the brain such as amnesia, yet this therapy has beneficial physiological effects such as a stimulation of neuronal rebirth known as neurogenesis (Ongur & Heckers, 2004). When patients are struggling with depression, the brain tissue shows signs of significant decrease in glia cells (Ongur & Heckers, 2004). Among the autonomic nervous system and the endocrine dysregulation, abnormalities are suggested to play a role in the pathophysiology of depression (Ongur & Heckers, 2004). The conclusion of this statement would be that ECT may help reverse the effects of neuronal death by stimulating neurogenesis in the brain and central nervous system. The mechanism active in the treatment of ECT has been hypothesized, yet none have been proven. The glia cells are known to be able to proliferate, under injury or infection, specifically in the central nervous system of the human body (Ongur & Heckers, 2004). The new neurons, from the act of neurogenesis, are known to travel to the hippocampus and olfactory bulb to possibly become fully functional (Ongur & Heckers, 2004). ECT has increased the levels of NAA, which as stated before, is shown to be of decreased levels in those with depression.
ECT has been shown to help stimulate neurogenesis, increase levels of NAA, and lower the rate of suicide in patients with depression. Although ECT is still controversial, it has shown to treat the symptoms of depression in a manner that is quick and effective. The scientific field still has much to learn about neurogenesis and proliferation of the glia cells. The discovery of these mechanisms gives hope to further research of neurogenesis and the proliferation of glia cells in the human body.
References
Cloe, A. (2010). How depression affects the brain. Retrieved June 8, 2011, from Live Strong: http://www.livestrong.com/article/71478-depression-affects-brain/
Collins English Dictionary - Complete & Unabridged 10th Edition. (2009) Depression. Retrieved June 21, 2011, from Dictionary.com website: http://dictionary.reference.com/browse/depression
Ende, G., Braus, D., Walter, S., Weber-Fahr, W., & Henn, F. (2000). The hippocampus in patients treated with electroconvulsive therapy. Arch Gen Psychiatry, 57, 937-943. http://archpsyc.ama-assn.org
Kay, L. (2008). Why electroconvulsive therapy works. Retrieved June 10, 2011, from Brain Blogger: http://brainblogger.com/2008/02/10/why-electroconvulsive-therapy-works/
National Alliance for the Mentally Ill. (2011). All about ECT. Retrieved June 10, 2011, from MedHelp: http://www.medhelp.org/lib/ect.htm
Neuhaus, A. H., Gallinat, J., Bajbouj, M., & Reischies, F. M. (2005). Interictal slow-wave focus in left medial temporal lobe during bilateral electroconvulsive therapy. Neuropsychobiology, 52(4), 183-189. doi:10.1159/000088861
Ongur, D., & Heckers, S. (2004). A role for glia in the action of electroconvulsive therapy. Harvard Review of Psychiatry, 12(5), 253-262. doi:10.1080/1067322049886185
Read, J., & Bentall, R. (2010). The effectiveness of electroconvulsive therapy: A literature review. Epidemiol Psichiatria Sociale, 19(4), 333-347. Retrieved from http://www.pensiero.it/
Sienaert, P. (2011). What we have learned about electroconvulsive therapy and its relevance for the practising psychiatrist. Canadian Journal of Psychiatry, 56(1), 5-12. http://publications.cpa-apc.org/browse/sections/0
