Psychological Factors and the Effect on the Memory
This past summer I suffered from a stint of Mononucleosis and Lyme’s Disease. It was a hectic summer of many blood tests, doctor’s appointments, and physical misery. I expected the physical pains, which are known to accompany both illnesses, but what I did not expect was the psychological problems that came along with them. As the illnesses progressed I started to suffer from stress, depression, and anxiety issues that although now resolved, created hell for me. The effect of these psychological problems most alarming to me was the trouble I had remembering things. After recovering, my memory came back to normal. The question that interests me is why can psychological factors, especially depression, in the neurological pathways that cause decreased levels of memory and how is it able to switch back to normal.
Nearly everyone at some point in their life has forgotten something, but there are many reasons for the occurrence of frequent memory loss. Some of these include old age, physiological factors, medications, and psychological factors (Anon). Depression and anxiety are known to create memory problems because they affect one’s ability to encode information taken in and recall what one took in. From first hand experience, I found this to be true because I was unable to concentrate on specific tasks at hand. On the macro level, in Adams’s article “The impact of psychological disturbances on immediate memory”, research suggests that psychological disturbances have a greater impact on memory tasks that require more effort. It can be hypothesized that the deficits seen in performances on memory test are attributable more to impairments in attention than to defective memory. The hypothesized model was supported; it showed that psychological disturbances predict attention and attention predicts general memory.
From a neuro-philosophical standpoint, the effects of the psychological factors on the brain would be looked at differently between Descartes and Emily Dickinson. Dickinson believes that your mind captures the world around one’s self. She would believe that the mind gives a person their self-concept and the brain tells the body how we feel. Therefore, the brain would tell us we were depressed and cause the cognitive defects. In theory, a correction to this could be such treatment as electronic shock therapy to rewire the brain, which would change the outlook on one’s self and life.
On the other hand, Descartes believes that the physical nervous system has to do with how one feels. As a result he would believe that the external factors, such as injury, stress, socioeconomic status, relationships, etc. would cause damage or affect the central nervous system. This in turn would affect the brain’s ability to retain memories through a changing pattern of neurons than that which would have normally affected the individual.
From a biological point of view, memory is generally attributed to synaptic plasticity; with synaptic structures the unit for memory storage (Ito). This is a controversial issue, because, the exact storage unit of memory is not fully understood. One alternative hypothesis is that memory is stored in individual neurons or proteins (Ito). To expand on this, at what level of neurons will memory be stored in. Will it be in a large or a smaller box, or an even smaller box to use our class model as an example? Whichever hypothesis one wants to accept, there is a connection between memory loss and psychological factors. Researchers from the Wake Forest University Baptist Medical Center’s Cardiovascular Health Cognition Study found that 43% of the participants with mild cognitive impairment had psychiatric symptoms in the month before examination (Editor). The research also showed that effective drugs are available for treating most of the symptoms, which are "likely to provide substantial benefits to patients."(Editor)
The problems of depression and anxiety have to do with the pattern of neurons that flow throughout our nervous systems, as we spoke about in class. The input, or psychological factor, that affects the “self” may vary, but the stress response in a micro level is mediated by the hypothalamo–pituitary–adrenal (HPA) system. Corticotropin-releasing hormone (CRH) neurons in the hypothalamus start cortisol release from the adrenal cortex. CRH neurons are released into the brain and all over the body in the blood steam, where they regulate autonomic systems and affect mood (Bao). Increased levels of cortisol contribute to the signs and symptoms of depression. An androgen-responsive element initiates a suppressing effect on CRH expression. This decreases the activity of the hypothalamic clock, which is responsible for the rhythmic changes of the stress system, which is the basis for the disturbances in mood, sleep, memory, and hormonal rhythms found in depression. Neuronal loss was also reported in the hippocampus of stressed or corticosteroid-treated humans (Bao). Further, untreated depression has been shown to decrease the volume of the hippocampus, through studies using magnetic resonance imaging, and can cause structural differences leading to impairment in spatial learning and memory. The hippocampus is the part of the brain that is involved in cognitive function (McEwen).
The HPA system seems to be the final pathway in depression symptomatology. Studies of the hippocampus as a target of stress have revealed a considerable degree of structural plasticity. Repeated stress causes shortening and debranching of dendrites in the hippocampus (McEwen). In addition to this, alternative new research details the active firing of neurons through the middle brain. It is shown that individuals’ neurons, when suffering with depression, have locomotive problems because they exhibits clustering properties at synapses, slowing the patterns of the neurons. This may be an explanation for slow motor reaction and loss of short-term memory (Adams). Because of the high level of plasticity, this pathway seems to be reversible after treatment through restructuring the hippocampus mediated by glucocorticoid hormones, excitatory amino acids, receptors, and transmitters, such as serotonin (McEwen).
Another phenomenon that I found to be intriguing is that patients with major depression often showed disturbances in the HPA function before clinical depression symptoms even occurred (Bao). This is interesting to me because it goes against Dickinson’s theory and reinforces Descartes theory. To explain more, the prior problem to the HPA in the nervous system that is responsible for depression is not detected until the body tells the brain how it feels and not vice versa. The central nervous system in this case is not controlled by the brain’s creation, but by a predetermined disposition to depression in the central nervous system! In my case, I believe this phenomenon could have been a factor because there is a history of incidents of depression in my family.
Through exploring this topic, I was able to learn and expand my view of many of the topics we learned in class and apply them to the effects of psychological factors on memory. Psychological factors, most notably depression, create inputs on the body that creates a cascade of changes to neuron patterns in the central nervous system. While these psychological problems directly affect the central nervous system, reinforcing Descartes, I believe Emily Dickinson is also correct because after the onset of the psychological problems, the mind changes into an altered state, directly stimulating the body. I want to finally agree with Descartes because the neuron synapses exhibit properties of plasticity. Once the problems are treated in the central nervous system, the synapses are able to convert back to normal and the person can retain their memory again.
Adams, Robert A., and Et. al. "The impact of psychological disturbances on immediate memory." Archives of Clinical Neuropsychology 16 (2001): 605-18. Pergamon.
Anon. "The meaning of memory loss." Health News 16 (1999): 9.
Bao, A. M., G. Meynen, and D. F. Swaab. "The stress system in depression and neurodegeneration: Focus on the human hypothalamus." Brain Research Reviews 57 (2008): 531-553. Science Direct.
Bershadskii, A., E. Dremencov, and G. Yadid. "Short-term memory and critical clusterization in brain neurons spike series." Physics Letters A 313 (2003): 158-61. Science Direct.
Editors. "Memory; Treatable depression often accompanies even mild memory loss." Pain & Central Nervous System Week Oct (2002): 6. Proquest.
Ito, Masao. "Cerebellar circuitry as a neuronal machine." Progress in Neurobiology 78 (2006): 272-303. Elsevier.
McEwen, Bruce S. "Effects of Adverse Experiences for Brain Structure and Function." Society of Biological Psychiatry 48 (2000): 721-31.