Kevin Patrick Barman*
Received: May 22, 2023; Published: May 26, 2023
*Corresponding author: Kevin Patrick Barman, Drug Studies Coordinator/Associate Professor Human Services, Rio Hondo College, USA
DOI: 10.26717/BJSTR.2023.50.007989
In the disciplines of the neurological and psychiatric sciences, false memories are referred to as autobiographic or semantic memories that did not happen (Mendez & Fras [1]). In the case of true memories, they are defined as correctly recalled long term memories (Jeye, Karanian & Slotnick [2]). While confabulations are like false memories but are the result of some type of neurological disorder or illness (Mendez & Fras [1]). This essay will discuss the study of the relationship between false memories and confabulation, to identify which parts of the brain are activated by them separately or together. According to (Jeye, et al. [2]) , false memories routinely are activated by the hippocampus and the anterior/dorsolateral prefrontal cortex ( A/DLPFC ) .There is also evidence that the A/DLPFC may inhibit the hippocampus , that can expect a negative association in the severity of action in these regions of the brain (Jeye, et al. [2]) .In regard to true memories , it has been demonstrated that they are a result of activity in the hippocampus .It is also important to report that the hippocampus and the A/DLPC have been both implicated in false and true memories (Jeye, et al. [2]) . While it has also been found that false memories and confabulations equally have reduced activity in the ventromedial frontal lobe area of the brain (Mendez & Fras [1]). It is also important to be able to distinguish between false memories, true memories, and confabulation, to explore any clinical implications that can help clinicians who work with patients that have issues with what they remember or do not remember [3-10].
Keywords: False Memories; True Memories; Confabulation
The study of false memories, true memories, and confabulation is essential, in order to identify the areas of the brain that are activated. So, the basic structure and function of memory can be identified and explained. In the past, it has been argued that the hippocampus plays a major factor in the recall of true memories (Jeye, et al. [2]). It has also been shown that the hippocampus influences the creation of memories that never happened, which are false memories (Jeya, et al. [2]). In a recent functional magnetic resonance imaging (fMRI) study, it was found that there was overlapping neural action in the hippocampus in both true and false memory (Jeya, et al. [2]). Therefore, there is ample evidence that the hippocampus contributes to the construction of both false and true memories. While confabulations are like false memories but are the result of some type of neurological disorder or illness (Mendez & Fras [1]). It has also been shown that false memories and confabulations equally have reduced activity in the ventromedial frontal lobe area of the brain (Mendez & Fras [1]) (Figure 1).
Note: HIPPOCAMPUS
Source: https://www.jneurosci.org/content/27/45/12190
False memories are defined as autobiographic or semantic memories that did not happen (Mendez & Fras, 2010). It has been demonstrated that the A/PLPFC and the hippocampus are activated by false memories (Jeya et al. [2]). According to (Jeya, et al. [2]), the A/ PLPFC may inhibit the hippocampus while recalling false memories, that may suggest a positive association with the strength of activity in these areas of the brain when working with subjects. It has been shown that the A/PLPFC may inhibit the hippocampus during memory retrieval, like in the process of motivated forgetting and retrievalinduced forgetting (Jeya, et al. [2]) What these studies suggest is that participants in these studies select either the hippocampus or A/ PLPFC while accessing false memories (Jeya, et al. [2]) (Figure 2).
Note: HIPPOCAMPUS
Source: file:///C:/Users/rome/Downloads/jeye17_brain_sci.pdf
While experts in neurology and psychiatry study how disorders or maladies of the brain result in confabulations, which are false memories (Mendez & Fras [1]). It is important to explain that confabulations, are not intentional nor is the subject cognizant of trying to mislead anyone (Mendez & Fras [1]). Some routine confabulations are triggered by basic or trivial questions from the subjects past (Mendez & Fras [1]). In fact, some confabulations may be extreme exaggerations, strange, or hard to believe memories of something that may not be possible to have happened (Mendez & Fras [1]). The common neurological or psychiatric causes of confabulation are Wernicke-Korsakoff’s syndrome, arterial aneurysms, strategic diencephalic strokes, traumatic brain injury (TBI), herpes, multiple sclerosis, and frontotemporal dementia (Mendez & Fras [1]). It has been widely believed that confabulations are most often the consequence of both memory damage and frontal executive dysfunction in a brain disorder (Mendez & Fras [1]).Since subjects believe that their confabulations are real , the impairment is found in the frontal-executive dysfunction in self-monitoring that is guided by the medial and orbital frontal areas of the brain (Mendez & Fras [1]). In terms of neuroanatomy , it has been shown that confabulation is much like false memories ,which focuses on the prefrontal regions of the brain that are implicated (Mendez & Fras [1]) (Figure 3).
Note: DORSAL STRIATUM
Source: https://link.springer.com/content/pdf/10.3758/CABN.3.4.323.pdf
Regarding similarities between false memories and confabulations, they both have a necessity for united and comprehensive memories, the awareness of the content, and the inclusion of personal information (Mendez & Fras [1]). In terms of neuroanatomy, both false memories and confabulation appear to have dysfunction in the ventromedial prefrontal cortex (VMPFC) and reduced activity in the ventromedial frontal lobe area of the brain (Mendez & Fras [1]). While some of the differences between false memories and confabulations, are that emotional activity is more influential in false memories than confabulation (Mendez & Fras [1]). Another difference is that subjects may be more open to suggestions for false memories but not for confabulations (Mendez & Fras [1]). It is also important to mention that episodes of confabulation may often include [11-16] (Figures 4-9).
Note: HIPPOCAMPUS
Source: https://memlab.yale.edu/sites/default/files/files/2011_Johnson-etal_NebraskaChapter.pdf
Note: HIPPOCAMPUS
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5297302/
Note: HIPPOCAMPUS
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5297302/
Source: https://memlab.yale.edu/sites/default/files/files/2011_Johnson-etal_NebraskaChapter.pdf
Note: HIPPOCAMPUS
Source: http://learnmem.cshlp.org/content/12/1/3/F3.expansion.html
Note: HIPPOCAMPUS
Source: https://academic.oup.com/cercor/article/18/12/2811/360672
Note: DORSAL STRIATUM
Source: https://www.researchgate.net/figure/Event-Related-fMRI-Analyses-Sensory-Neocortex-and-MTL-A-DM-effects-voxels-for-which_
fig2_234063346
It has been reported in this paper that confabulations are like false memories but are the result of some type of neurological disorder or illness like (i.e., Wernicke’s-Korsakoff’s syndrome, aneurysms traumatic brain injury (TBI), herpes, multiple sclerosis, and frontotemporal dementia) (Mendez & Fras [1]). Even though it has been long recognized that true memories are a result of activity in the hippocampus (Jeya, et al. [2]). It is also important to report that the hippocampus and the A/DLPC have been both implicated in false and true memories (Jeya, et al. [2]). One of the factors that sets the two apart, is that the anterior prefrontal cortex may impede the hippocampus in the duration of false memories and that subjects selected either the anterior prefrontal cortex or the hippocampus during false memories (Jeya, et al. [2]). There is also evidence that the A/DLPFC may inhibit the hippocampus, that can expect a negative association in the severity of action in these regions of the brain (Jeya, et al. [2]). While it has also been found that false memories and confabulations equally have reduced activity in the ventromedial frontal lobe area of the brain (Mendez & Fras [1]).