Schizophrenia is a complex disorder with a large heterogeneity within its clinical handbook. Categorized as a disorder of psychosis, it remains an abstract chronic illness that affects one percent of the global population (Nordqvist, C. 2017). With a vast variety of clinical presentations, the exact nature of the neuropsychology of schizophrenia continues to remain elusive. Ongoing research and continuous technological advances, however, bring clarity to a multifactorial etiology and the spectrum of symptoms the patient displayss. Divided into two categories, schizophrenia manifests into positive and negative symptoms, and arises as to the fundamental aspects of the disorder.
Positive symptoms, the addition of behavior, thought or feeling seemingly coincides with emotional and social reactivity in schizophrenia (Mueser & Jeste, 2011). This is presented phenotypically as delusions and hallucinations where the patient often is perceived to have a loss of contact with reality. Negative symptoms, which take away a behavior thought or feeling can include cognitive impairment, specifically impaired motivation, drop in spontaneous speech, and social withdrawal (Fatani, Aldawod & Alhawaj, 2017).
In this review, cognitive dysfunction has been highlighted as a core domain of schizophrenia, reported to affect 40% to 95% (Velligan DI, Bow-Thomas CC ) of schizophrenic patients. Reflected through the host of cognitive impairments it is exhibited across multiple domains of real word functioning for the individual. Negative schizophrenic symptoms are often linked to symptoms of patients with lesions of the dorsomedial PFC and related structures (Freedman and Brown, 2011). Impairments can include disorganized speech, attention and thought poor memory, and higher-order functions eventually impairing the capacity to communicate effectively (Fatani, Aldawod & Alhawaj, 2017).
In this review, we will explore a possible pathway to explain executive dysfunction and more specifically working memory in schizophrenia. Disrupted component processes and underlying abnormalities in neural architecture and connectivity in combination with altered functional activity form the basis to explain such changes (Daniel Paul Eisenberg and Karen Faith Berman). However due to its heterogeneous nature, sometimes selective and specific, and manifested by different patterns of associated and dissociated performance on different cognitive tasks (Kuperberg and Heckers, 2000) there is no general consensus.
Supported by converging research examined in the post-mortem, regional blood flow studies, neuroimaging techniques, and reviews of functional tasks, these studies continue to unravel and understand the complexity of schizophrenia.
Executive function refers to the ability to coordinate thought and action and directing it toward obtaining a set of goals. Simply it allows us to invoke voluntary control of our behavioral responses to allow human beings to develop and carry out plans, makeup analogies, obey social rules, solve problems, adapt to unexpected circumstances, multitask and locate episodes in time and place (Gricel Orellana1 and Andrea Slachevsky). For these functions to occur they depend on three cognitive actions: shifting among different tasks or mental sets, inhibiting irrelevant automatic responses, and updating mental representations held in working memory (WM) (Miyake et al., 2000; Van der Linden et al., 2000), while taking the environment and the consequences of actions into account. Deficits in executive function can occur in various stages over the progression of schizophrenia. Adolescents at risk of developing the disease, patients with their first outbreak of schizophrenia, first-degree relatives, and aged patients with more severe cognitive impairment all showcase signs of executive dysfunction (Kuperberg and Heckers, 2000; Breton et al., 2011; Freedman and Brown, 2011).
Based on the traditional medical model, executive function was construed as a single construct as a central executive in charge of multi-modal processing and high-level cognitive skills (Della Sala et al., 1998; Shallice, 1990). However, as our understanding continues to evolve, executive function is a model of multiple process-related systems that are inter-related, inter-dependent, and work together as an integrated supervisory or control system (Alexander & Stuss, 2000; Stuss & Alexander, 2000). The prefrontal cortex however plays a key role, supervision. In order for the PFC to coordinate operations of multiple neural systems, it must simultaneously monitor and signal commands for activities within other cortical and subcortical structures. Specifically, top-down processes underlie our critical ability to selectively focus our attention on relevant stimuli and ignore distractions. It is a bi-directional process, accomplished by enhancing and suppressing neural activity in regions based on the significance of the information to our goals.(Zanto, Rubens, Thangavel, & Gazzaley, 2011). Studies have provided evidence that the prefrontal cortex sends top-down signals to the posterior cortices to control information processing (Funahashi & Andreau, 2013).
Anatomically these functions are linked to the prefrontal cortex as deficits in executive skills often are correlated to damage to the prefrontal cortex (Grattan & Eslinger, 1991; Stuss & Benson, 1986). Supporting this comes a plethora of functional neuroimaging studies that have observed increased activation of the prefrontal cortex when performing tasks specifically designed for executive functioning (Baker et al., 1996; Morris, Ahmed, Syed, & Toone, 1993; Rezai et al., 1993). However, despite the innumerable replications of these findings, the exact nature of frontal lobe circuit disturbances contributing to executive dysfunction remains elusive. (Funahashi & Andreau, 2013) .
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The PFC is subdivided into four main regions, the ventromedial PFC, largely involved in the integration of emotional information kept in memory and external stimuli, the dorsolateral PFC related to working memory, reasoning, and thematic understanding, the medial PFC (superomedial areas) involved in attentional control and planning and the frontal pole involved in adaptive planning and self-awareness (Orellana & Slachevsky, 2013).
Schizophrenic patients most commonly show deficits in tasks related to the dorsolateral PFC. Described not as an anatomical structure, but rather defined by its functional attributions it is located in the middle of the frontal gyrus of the cortex (Brodmann’s 9 and 46) with its main functions including conceptualization, cognitive flexibility, and working memory.
Numerous lines of evidence continue to point towards abnormalities of the dorsolateral prefrontal lobe, but not to degeneration or possible lesion, instead highlighting alterations in neuronal density, decreased neuronal size, and/or decreases in the neuropil (axons+dendrites+glia) may account for the reductions in grey matter and functional outcomes in executive tasks(Boksa, 2012).
Synaptic pruning referring to the process of elimination of excess neuronal synapses often occurs during early adolescence. Feinberg8 speculated that schizophrenia might result “from a defect of synaptic elimination programmed to occur during adolescence.” Consistent with this hypothesis, are at least 2 lines of evidence suggesting that the brains of adult patients with schizophrenia have fewer synaptic connections in multiple brain regions. Post-mortem brain studies have similarly reported decreased spine density on cortical pyramidal cells from patients with schizophrenia compared with controls. Where it is mainly this type of spine that is eliminated during developmental synaptic pruning. In combination with the pronounced loss of grey matter occurring in the early years after the onset of schizophrenia, described by Andreasen and colleagues,1coincides with the time in normal human development when synaptic pruning is prominent.
Post-mortem studies form the majority of evidence, investigating at the anatomical level more insight is brought on the pathophysiology of schizophrenia. Through a direct three-dimensional counting in a post-mortem study, it was found there was increased neuronal density in the prefrontal area 9 of cortical layers 3 and 6 (Selemon, Rajkowska, & Goldman-Rakic, 1995). But with limited support and repetition, the findings remain inconclusive.
Similarly, a significant reduction in the numerical density of dendritic spines (Garey et al., 1998) has been reported in several cases and may explain the loss of cortical volume without loss of neurons. It also highlights the case of disturbances in neuronal connectivity as a contributor to psychiatric disorders. (Obi-Nagata, Temma, & Hayashi-Takagi, 2019). The advent of newly developed techniques has revealed a correlation between spine size and the efficiency of synaptic transmission. For example, electron microscopic studies have demonstrated a positive correlation between the volume of a spine and postsynaptic density (PSD).
The majority of excitatory synapses, which facilitate the transmission of an action potential, are formed on the dendritic spine. Hence the evaluation of dendritic spines explicitly assesses the synaptic function in post-mortem brains. With 2 independent research groups undergoing parallel studies, both reported that small spine density was significantly reduced in layer 3 pyramidal neurons in the prefrontal cortex in schizophrenic brains. Small spines correlate with neural plasticity and are related to learning and behavioral flexibility.
In order for this to occur, neural networks are formed between various brain cortices. Often plentiful, complex, and intertwined in nature, the efferent and afferent projections connect the PFC with the brain stem, occipital, temporal, and parietal loves, limbic, subcortical regions, and many other structures (Stuss & Benson, 1984). Therefore, as a result of this complex neural network, executive dysfunction is not indefinitely associated with the prefrontal cortex directly but related to network disruptions such as white matter damage