A myriad of baffling questions foster educated inquiries regarding the types of causes for schizophrenia, in terms of neurological foundations. Psychiatry and neuropsychological research continues to engage professionals in exploring the role of the frontal lobes in schizophrenia. While more questions persist than answers, it appears that the elements of memory and behavior correlate in ways that bond to either a region or function that is important in the disorder. According to medical researcher, Dr. Raphael Bonelli (2007) “schizophrenia, and mood disorders may result from disturbances that have a direct or indirect impact on the integrity or functioning of” various loops in the neurocircuitry pathways (“Frontal-subcortical circuitry”). Based upon his research it appears as though impulsivity and emotional flux demonstrate the hallmarks of dysfunction, rather than point to causes rooted in the region. Therefore, the thesis for this paper is as follows. The role of the frontal lobes in schizophrenia correlates to the bio-neurological function of memory in the disorder, which may be well defended by research findings.
It is important to explain a little bit about what the neuro-bio function of memory within schizophrenia is, and the elements which correlate with it. According to a Science Daily source, in schizophrenia the brain activity in a subject’s memory malfunctions when a network of genes responsible for controlling the neurons fail to close gaps in adequate neural processes (“Memory Schizophrenia Connected”). Mechanism malfunctions contribute to the escalation and advancement in schizophrenia development, primarily affecting functions in the cerebrum and cerebellum parts of the brain. The neurological and biological basis of memory function in schizophrenia concerns impairments in the neuron cells abilities to transmit information adequately to the memory centers of the brain. The problem has to do with circuitry, and since the brain is still quite a mystery involving biological matter, and electrical impulses, not even the greatest medical scientists and doctors understand clearly a single, definitive answer of what the role of neuro-bio function of memory in schizophrenia patients is, and what correlates to it. Therefore, continual research is being conducted.
Simply presenting a description of the processes, and how they have an impact, fails to suffice in determining a cogent argument as to why function is important to the role of the frontal lobes as connected to memory and behavior patterns in patients with schizophrenia. At the outset of this investigation it may be useful to explore counter-arguments to the thesis. Canadian researchers Widjaja, Mahmoodabadi, Snead, Almehdar, and Smith (2011) studied cortex thinning (and thickness) in children for the purpose of uncovering seizure activities connected to the frontal lobe. Their agenda focused upon an identification of regions as an explanation, rather than why function was most critically important to the process of the disorder. Although key findings indicated that a thinning of cortical matter in the 17 children being evaluated for epilepsy-related surgery, Widjaja et al. (2011) concluded and admitted that “Further studies correlating cortical changes with neuro-cognitive measures are needed to determine if the cortical changes relate to cognitive function” (p. 1685). In other words, the results were inconclusive in solidly identifying an absolutely positive medical evidence connecting the structure, or region of the temporal lobe, as the primary role in damages typical of schizophrenia. Obviously, no discourse of memory surfaced in their article since frontal lobe connections to remembrance did not comprise the purpose of their investigative methodology. Likewise, the Highley research team explored schizophrenia from the standpoint of the frontal lobe region, or structure, in a post-mortem review. Their study sought to garner information to support their conjecture about frontal lobe tissue volumes (region) as evidence to explain schizophrenic conditions.
Similar to the basis of the Widjaja team’s focus, the Highley et al. researchers looked at the amount of mass thickness in the frontal lobe in schizophrenic patients. After screening the brain tissue sample for disease, cutting and dissecting away “temporal and occipital” lobe matter Highley et al. (2001) derived clinical implications that “the volumes of the frontal lobes are unchanged in schizophrenia, in contrast with decreased volumes” with comparable temporal lobe asymmetries (p. 342). They also found that “schizophrenia cannot be considered as a simple disorder of the frontal lobes” (Highley et al., 2001, p. 342). The results of this post-mortem brain research study may lend reasonable credibility to theory established in the thesis that memory as a function connects to the role of the frontal lobes. Furthermore it is important not to neglect the factor how emotional responses may uniquely fit into patterns of memory.
Dara Manoach, of the Department of Psychiatry in association with Massachusetts General and the Harvard Medical School announces promising information pertaining to how memory plays a role in the function of the frontal cortex, relative to schizophrenia. Manoach (2002) firmly posits “Working memory (WM) deficits are a persistent, disabling and relatively treatment-resistant feature of schizophrenia that may underlie many cognitive deficits and symptoms. They are associated with prefrontal cortex dysfunction” (p. 285). Manoach believes that the hypothesis presented in her research study is both informative and valid, correlating a deficiency in working memory from data collection in samples. Manoach (2002) found that several other experts suggested, or hypothesized, that memory deficits persisted “throughout the course of the illness,” along with possible hereditary markers in currently “healthy relatives of schizophrenic patients” (p. 285). In agreement with this theory, Conklin et al. (2007) state “It has previously been demonstrated that adult first-degree relatives of schizophrenia patients demonstrate impaired performance,” in terms of performance “on some of the WM tasks included in the current study” (p. 123). While it is true that Conklin et al. focused their research upon child development, they believe that frontal lobe impairment impacts memory delays in cognitive function.
The view of schizophrenia having a functional basis, as opposed to confined explanations focused upon a region, is dramatized by Reichenberg and Harvey in their article entitled, “Neuropsychological Impairments in Schizophrenia: Integration of Performance-Based and Brain Imaging Findings.” Reichenberg et al. (2007) do acknowledge the genetic liability involved with the disorder, they clearly “present quantitative evaluation of the literature demonstrating that the most severe impairments are apparent in episodic memory and executive control processes, evident on a background of a generalized cognitive deficit” (p. 833). Connecting abnormalities in frontal lobe functioning Reichenberg et al. (2007) emphatically propose that “schizophrenia is the result of dysfunction of distributed neural networks and that the prefrontal cortex is an intrinsic part of these networks” (p. 833). After review of a plethora of literature in neuropsychology on schizophrenia functioning, they also sought to examine how higher cognitive functions associated with the prefrontal lobe cortex areas of the brain. Behavioral responses and long-term decision-making in terms of controlling future actions in response to “environmental demands” played a role. The section of their research report on memory was particularly revealing. Reichenberg et al. (2007) insist that “Current researchers see memory impairment as a severe feature of schizophrenia” although it is important to clarify the kinds of memory impairments weigh in on the disorder (p. 838). Findings from several research teams noted that models of neuropsychological disruptions interfered with memory episodes in schizophrenia, serving as a core deficit in the disorder. The research group of Murray, Cheng, Clark, Barnett, Blackwell, Fletcher, Robbins, Bullmore, and Jones posed a study based on a background of reinforcement and reversal learning.
Having studied a 119 initial-episode patients, they used reinforcement learning data to structure their testing methods of cognitive flexibility. Murray et al. (2008) found a definite correlation of “reinforcement learning abnormalities in first-episode psychosis, which correlate with negative symptoms” that suggested perhaps a role in the orbital-frontal cortex involved a pathology in the situation. Apparently the patients they studied were medicated, and the researchers’ suggestions for future studies to allow participants to be unmedicated, to further delve into the reversal learning aspects. Other researchers, such as Hagino et al. (2002) acknowledge that “verbal memory impairment” is a most “consistent” finding “among the neuropsychological deficits in schizophrenia,” connecting frontal lobe involvement as a reason (p. 499). Their brain imaging study results showed consistencies in morphologic abnormalities.
In conclusion, evidence appears to be mounting concerning a valid connection between schizophrenia frontal lobe dysfunction and memory. While it is true that age, gender, or hereditary factors play a role memory as an important aspect of frontal lobe neurological engagement cannot be denied. According to Dr. Jordan Grafman, who has studied brain function for over 25 years, his research indicates “that the human prefrontal cortex is especially designed to store in long-term memory” that helps organize “sets of sequential events” (“Prefrontal Cortex and Lobe Disorders”). While certainly everyone may have greater or lesser degrees of lucidity in their daily lives, those with schizophrenia “may have more extreme inconsistencies” (“Moments of Lucidity”). Perhaps as research progresses a key to unlock a cure, or at least improvement, to the frontal lobe functioning-connection to schizophrenia is on the horizon.
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