Diseases and Disorders

Episodic Memory Loss In Depression

Sydney Jobson


Introduction

This article is a review of selected literature which have explored the factors associated with the link between episodic memory deterioration and Major Depressive Disorder (MDD).   It has been definitively established that a direct association between an individual’s episodic memory and the hippocampus, a small organ within the limbic system, exists [22]. Episodic memory, or the brain’s ability to recreate a specific event, is often coupled with contextual emotions [12]. The limbic system, responsible for emotional regulation, is therefore associated with one’s memory.  However, it is an impairment of episodic memory, specifically overgeneral memory (OGM), or the inability to recall precise memories from one's autobiographical memory (AM), which is often evident in individuals with MDD [25]. Meta-analyses, MaQueen et al., [14] and Videbech & Ravnkilde [27]show a reduced volume of the hippocampus in depressed individuals, firmly demonstrating that the hippocampus is linked to MDD [27].  Finally, Lemogne et al., [10], and Bäckman, & Forsell, [3] found direct links between MDD and the deterioration of episodic memory. It can therefore be concluded that depression may cause a deterioration of the episodic memory.  

 

Background on Major Depressive Disorder

    Major depressive disorder (MDD) or depression is a common but serious mood disorder, affecting 16 million people in the United States and 350 million people internationally  [8]. According to Nutt [15] and Andréasson [1], depression produces severe symptoms that may affect the way one thinks, feels, and carries out daily activities such as sleeping, eating, or working.  Although the cause of depression is unknown, current research suggests that a combination of genetic, biological, environmental, and psychological factors are likely contributors [2]. Definitive links between depression and episodic memory loss exist [10].  Procedural (implicit) and declarative (explicit) memory are the two forms of long-term memory; procedural memory is the unconscious memory of skills e.g., knowing how to ride a bicycle, and declarative memory is the memory of events and facts, or memories which can be retrieved consciously, e.g. recalling your wedding day [5]. Declarative memory is comprised of both semantic memory and episodic memory [17]. Semantic memory allows one to recall basic facts learned during one’s lifetime, such as knowing the names of countries. Episodic memory complements knowledge recall with explicit memories of experiences and events in a sequential order; in other words, it provides an ability to recreate a specific event from a time in one’s life. During recollection, episodic memory generally includes contextual emotions one experienced contemporaneously as opposed to merely explicit facts of the event.

 

Overgeneral Autobiographical Memory

    Overgeneral memory (OGM) refers to the inability to recall particular memories from one's autobiographical memory. While attempting to retrieve a memory of a specific event, general memories, the recollection of repeated events, or events lasting long periods of time , are recalled instead [23].  Research shows an association between OGM and certain mental illnesses, including posttraumatic stress disorder (PTSD) and MDD. Although research has been conducted to determine a relationship between OGM, anxiety disorders, and personality disorders, none have been found.  Yet, OGM has been found to be associated with PTSD and depression. OGM is thought to be exclusive to emotional disorders [25]. In Lemogne et al., [10] 21 depressed participants and 21 control subjects without a history of depression were recruited for the study. The depressed participants had no history of bipolar disorder, psychotic disorder, PTSD, substance use disorder, borderline and schizotypal personality disorder, or any other illness linked with memory loss.  At the time of the study, the depressed participants received antidepressants and/or antipsychotics and were presented with a task used to evaluate episodic memory. In the task, participants were requested to recall and describe one positive event and one negative event. To determine if OGM was evident in the participants, the interviewer asked the participants to recall a specific memory that had a duration of less than 1 day and to recall as many details as possible, including: facts, emotional recollections, and the event relative to time and space. The participants were then asked to provide additional responses if the subjects perceived the recalled memory as subjective or objective. They were also asked to provide details that could discriminate between two alike events.  Researchers found that each depressed subject scored lower on the task than his non-depressed counterpart [9]. The study suggests that depression negatively affects episodic memory.

 

Memory Bias in Depression

    Not only does research suggest that depressed individuals have more OGM, but also that their memories may also be more negative in nature. Williams and Scott [26], produced similar results when studying this same topic. In their study, 20 depressed participants and 20 controls were prompted to recall positive and negative events. The participants were asked to be specific in their description of the memories. The outcome of this study showed that depressed participants took more time to respond to positive prompts than to negative prompts. The depressed participants were also less specific when describing their memories, particularly when retrieving positive memories.  In Bradley et al. [4], explicit and implicit memory biases were evaluated in 19 depressed participants, 17 anxious participants, and 18 control participants. A memory bias is a cognitive preference that may improve or weaken recollection. The bias may affect the time it takes to recall or modify the substance of a memory. The participants were given tasks designed to assess the presence of mood-congruent biases in any of the groups. Mood congruent memory is a process that discernibly retrieves memories that are consistent with one's mood.  When certain moods were stimulated, the depressed participants recalled more depressive words than the other groups in the study. The results indicate that depression is associated with mood-congruent biases in memory processes. These negative memory biases can cause further depression [21].

    Research continues with the goal of determining additional likely causes of depression, including causes of OGM.  Theories on potential causes of OGM concentrate on the role of memory retrieval. Subsequently, these theories have materialized into a model known as Capture and Rumination, Functional Avoidance, and Impairment in Executive Capacity (CaR-FA-X) [19]. The first aspect of this model, Capture and Rumination, pertains to the notion that people with a negative self-image access general memories that they conflate with negative perceptions of themselves, during memory retrieval. This behavior prevents people from progressing to more specific areas of the memory [25].  The second aspect addresses Functional Avoidance which suggests that people who have depression or PTSD symptoms utilize a coping mechanism in which these individuals avoid specific memories that may elicit emotional distress. However, over time with repeated use, this mechanism becomes ingrained in the retrieval of memories. Because of this, one may not be able to easily access specific memories. The third aspect is based upon impairment in Executive Capacity. This theory posits that autobiographical memory retrieval requires certain cognitive resources including working memory capacity and executive control. People with emotional disorders such as PTSD or depression are shown to have diminished cognitive resources [7].

    Likewise, it is commonly known that elderly people often have diminished cognitive abilities [9].  Bäckman and Forsell [3] showed additional cognitive deficiencies in elderly people with depression.  In their study, Bäckman and Forsell [3] analyzed 17 depressed people with a mean age of 83.29 years and 51 non-depressed people with a mean age of 83.29 years. The participants were tested on an array of episodic recall and recognition assignments. The study found that depressed elderly adults had greater deficits in recall in comparison to the controls.  The study also suggested that elderly people with depression are associated with having a decreased capacity to utilize cognitive resources to improve episodic memory. The results showed that the process of encoding and retrieval are diminished in elderly people with depression. The CaR-FA-X model shows that diminished capabilities of retrieval are strongly associated with OGM [19]. Liu et al. [11] in a meta-analysis studied the results of 22 studies of people with depressive disorders in relation to AM.  The study showed that participants with depressive disorders communicated more overgeneralized memories than the controls. The depressed participants also exhibited lengthier recollection times.  The study suggests that the participants with depressive disorders had AM deficiency due to the overgeneralization of the memories, as well as longer response times.

 

The Hippocampus and Depression

    OGM, an impairment of episodic memory, is associated with contextual emotion and can be better understood through examination of selected organs in the limbic system.  In people suffering from depression, the well-established link between episodic memory and the hippocampus further reveals a reduction in the physiological volume of the hippocampus. [6], [22]. Sheline, et al., [18] suggests that recurrent episodes of depression may lead to hippocampal volume reduction.  Tulving and Markowitsch [22] maintain that it is widely recognized that the hippocampus is a crucial component in declarative memory. Their study suggests that the hippocampus is not necessary for the functioning of semantic memory, but is critical in the processes of episodic memory.  Bremner et al., [6] states that episodes of depression are associated with heightened levels of glucocorticoids, which have further been associated with damage to hippocampal neurons. The study further found that damage to the hippocampus may also result in episodic memory deficits in depressed people. In the study, 16 depressed participants were treated with an antidepressant. No participant received medication other than an antidepressant. Additionally, no subject had any history of PTSD. The study found that participants with MDD had a statistically significant 19% smaller left hippocampal volume than the controls, without a reduction in whole brain volume.

Hippocampal sulcus - Wikipedia

    Similar to the research of Bremner, et al., [6], a meta-analysis by Videbech and Ravnkilde (2004) examined studies totaling 351 participants with MDD or bipolar disorder and 279 control participants. In comparison to controls, depressed participants showed an 8% reduction of volume on the left side of the hippocampus and a 10% reduction of volume on the right side. The study found that hippocampal volume is diminished in participants with MDD, but not in participants with bipolar disorder. MaQueen, McKinnon, Yucel, and Nazarov [14], in a meta-analytical study, used data for 32 magnetic resonance imaging studies of hippocampal volume in participants with MDD. The study found that among participants who have had MDD for longer than two years, or experienced more than one depressive episode, a disparity in the volume of the hippocampus exists between test and control subjects. The depressed participants had smaller hippocampal volumes than those of the controls. However, in participants with less than two episodes of MDD, no difference in hippocampal volume exists.  It is apparent that the study suggests that a reduction of the hippocampus occurs in people with recurrent depression or depression lasting longer than two years.

 

Antidepressants and Other Medications

    Additionally, Sheline et al. [18] studied the effect of antidepressants on hippocampal volume in participants with MDD. 38 depressed participants were tested, some received antidepressants and some did not. The results showed there was no significant decrease in hippocampal volume in depressed participants receiving antidepressants. However, participants who had not received antidepressants experienced a reduction in volume of the hippocampus. Sheline et al. [18] and Lemogne et al., [10] both used antidepressants as a variable. Lemogne et al., [10] found a reduction of the hippocampus in depressed participants taking antidepressants. However, Sheline, Gado, and Kraemer [18] found that depressed participants taking antidepressants did not experience a reduction of the hippocampus.

    Sheline et al. [18] used magnetic resonance imaging (MRI) to quantify hippocampal volumes in people with a history of depression as compared to controls.  24 participants with a history of depression, and 24 controls completed MRI scanning. Participants with a history of depression had lesser hippocampal volumes than the controls.  Moreover, the depressed participants scored lower in a verbal memory test. This verbal test measured neuropsychological hippocampal function.

    To mediate decreased neurological functions in people with MDD, interventions such as mindfulness-based cognitive therapy (MBCT) and memory specificity training (MEST) have been used, and furthermore, have been shown to decrease OGM and symptoms of MDD [24]. MEST instructs people to be more attentive to their environments. This results in the person being more attentive to their thoughts and their thought processes. When the depressed person is more attentive to his or her surroundings, the memories of that time period become encoded with greater detail. Multiple studies, including Neshat-Doost et al. [20], and Raes et al. (2009) showed that MEST could decrease OGM in depressed individuals.

    It is promising to note that OGM has been shown to be reduced after specific interventions in depressed individuals Neshat et al., (2012). These results could reduce the likelihood that individuals with depression or PTSD would experience OGM. Research shows that modifying this memory style could inhibit OGM as well as certain symptoms of depression from recurring [16].

 

Conclusion

    Behavioral studies, including Lemogne et al., [10], and Bäckman and Forsell, [3] have found direct links between MDD and the deterioration of the episodic memory.  It has been firmly established that the hippocampus controls episodic memory [22]. Physiological meta-analytical studies such as MaQueen et al., [14] and Videbech & Ravnkilde [27] showed a reduced volume of the hippocampus in depressed people. Because of these findings, it can be concluded that depression may cause a deterioration of the episodic memory. Research accomplished by Raes, Williams, and Hermans [16] is significant in its findings of a successful intervention processes addressing OGM.  Additional research should be explored, to analyze the effects of antidepressants and episodic memory.


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Sydney Jobson

Sydney Jobson


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