A psychotic disorder involves a disconnection from reality (Bowie, et. Al, 2016). Whereas, a psychosis is a group of cohesive symptoms that can shape the way one can feel, think or behave (Fioravanti, et. Al, 2015). Psychotic episodes and the feeling attached to this can interfere with your work, family, friends and everyday tasks. People with psychosis tend to have hallucinations; this can involve seeing or hearing things around you that may seem present and ‘real’ but others are unable to sense this. Whereas, others may have delusions, in which one holds a strong sense of belief on things that aren’t true. Psychosis can be a one-off event, short or long event which is caused by a trigger (Bowie, et. Al, 2016), such as substance misuse or uncomfortable, provoking experiences (Fioravanti, et. Al, 2015).
The most common type of psychotic disorder is known as schizophrenia. Schizophrenia is a complex disorder that is characterised by impairment in a number of domains, all of which contribute to disability (Fioravanti, et. Al, 2015). People with schizophrenia can experience a range of cognitive deficits. These deficits in cognitive functioning are classified as one or two standard deviations below the mean of normal healthy individuals (Fioravanti, et. Al, 2015).
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For healthy functioning, the brain and body work together to exhibit cognition that can make experiences and functioning normal. Abnormalities in cognition can affect the way the brain works and can demonstrate psychosis and psychotic episodes. Cognition has manifested a key role in schizophrenia as it reveals what a lack of or disabled cognition can illustrate. Common symptoms of schizophrenia include hallucinations, delusions, paranoia, and thought disorder (Bowie, et. Al, 2016). These experiences are manifest in multiple sensory modalities and include abnormalities in all aspects of ones thought, cognition and emotion (Gold, et. Al, 2003).
The impact of cognition therefore stages a key role in schizophrenia and normal sensory functioning. This paper aims to analyse cognitive impairment in schizophrenia and the effects this can carry on the brain and body of an individual. In psychosis, functions such as logic, intent and customary association are impaired. It is the malfunction of these roles that characterises psychosis, as opposed to the loss of it. These features can fluctuate in severity and across sensory substrates throughout the illness (Sharma and Antonova, 2013). In various contemporary studies collated, patients who are diagnosed with schizophrenia have reported to perform more poorly on neuropsychology tasks than normal individuals (Insel, 2010). This performance defect can be categorised as a result of two factors: a. ongoing psychotic symptoms and b. a set of specific deficits associated with the pathophysiology of schizophrenia (Medalia, 2008). Individuals with schizophrenia have shown consistent inability when performing tasks that are associated with ones executive function, memory and attention. A recent study depicts in monozygotic twins for discordant for schizophrenia, the schizophrenic twin inevitably has a poorer performance in comparison to the other twin in attention, memory, verbal fluency, and pattern recognition (Insel, 2010).
Another study collectively analysed required sustained attention, which can be referred to as vigilance. Results highlighted that persons diagnosed with schizophrenia consistently performed poorly in these tasks (Insel, 2010). This was concluded by finding that the “working memory” which can often be referred to as the mechanism which keeps task-relevant information active (Gold, et. Al, 2003), for short periods, it is completely deficient in persons with schizophrenia. Multiple studies share common themes and results with the outcome of schizophrenia and the inhibition of cognitive ability in these persons (Polimeni, et. Al, 2016).
A vast majority of contemporary and older studies suggest the same implications and factors. A change in internal representation of the brains background intelligence can suggest the extensive disruptions in attention, memory and language (Fioravanti, et. Al, 2015). Cognitive scientists have suggested that the circuitry of the Central Nervous System (CNS) may be altered, but not the internal organisation of the module itself (Polimeni, et. Al, 2016). Although the cognitive deficits of schizophrenia are coherent with a widespread disturbance in cerebral functions and cognition, it is important to note that symptoms can fluctuate over time and change. This can make it hard to pinpoint permanent cerebral changes that propagate schizophrenia as the basis of cerebral malfunctions can vary from person to person.
Cognitive decline in people with schizophrenia can also be assessed through the measures of brain response to graded external stimuli. Studies indicate what primary eye movements in response to smooth pursuit stimulus should look like; arc slow eye movements used to track a small moving object. Participants of this test who are not diagnosed with schizophrenia are able to locate the moving target on their retinal fovea and move their eye in correspondence with the moving target (Gold, et. Al, 2003). In a normal eye and brain, this is done by using a predicative smooth pursuit movement which allows an individual to keep up with a moving target. Persons with schizophrenia are unable to cascade smooth pursuit eye movements. Many studies hypothesise that the reason for this is motion processing (Fioravanti, et. Al, 2015).
Different studies conclude varying reasons for the abnormal motion processing. However, the prime reasoning can settle to the link between eye movements and motor information and/or in capacity of holding motor information in the short term memory (Polimeni, et. Al, 2016). In addition to this, saccadic eye movements have also been noted to appear irregular in schizophrenia. The context of this irregularity could also translate to potential frontal cortical dysfunction in the illness.
By observing the structures of the brain between a person with schizophrenia, and a healthy individual, cognitive impairment was analysed. Johnstone and Crow (Insel, 2010), discovered these structural abnormalities first and later, Weinberger (Insel, 2010), also noticed this. The structure was described as having large ventricles (Rund, Borg, 2009). With time, this has been confirmed through multiple studies that have used modern imaging technologies to attest this difference. Typically, the ventricular size is an uncommon example that would link cerebral dysfunction to schizophrenia. Nonetheless, this observation has served the notion that people with this illness share this malfunction in common as opposed to those of healthy brain. A more specific example of structural change in the brain for people with schizophrenia is their structure of superior temporal gyrus (STG) (Rund, Borg, 2009). It is reported through high resolution imaging techniques that the volume of this structure in a person with schizophrenia is decreased (Gold, et. Al, 2003). As the STG contains the auditory cortex, it is responsible for the ability to understand and hear sound (Insel, 2010). As people with schizophrenia have an abnormal STG, it can suggest an impairment in cognition, hence the disconnection from reality.
Further, the medial temporal cortex is also reduced in size when compared to a normal brain (Fioravanti, et. Al, 2015). Although the decrease of size is as little at 5% (Polimeni, et. Al, 2016), this is accountable and consistent within multiple subject populations. As the middle temporal cortex plays a vital role in mediating ones memory (Rund, Borg, 2009), an abnormality to this region, corresponds positively to the symptoms of schizophrenia. Regional cerebral blood flow reports in schizophrenia have been used to analyse the CNS areas of irregular processing in this illness. Despite not finding a common single region amongst all laboratories, several clear abnormalities are present in all persons of schizophrenia and can suggest that several systems in the brain constitutes this illness (Rund, Borg, 2009).
Both functioning magnetic resonance imaging and regional cerebral blood flow have formulated a large sum of results that conflict with each other (Rund, Borg, 2009). These differences can occur due to augmented spatial resolution of this methodology. One study conducted an experiment where persons with schizophrenia and healthy individuals both have to perform an auditory recognition task in a practised condition. The results showed discrepancies, concluding to a concept of circuit failure, potential limbic cortex and some areas of the prefrontal cortex. This reinstates the notion of an apparent impairment of cognition in those with schizophrenia.
Reasoning to explain manifestations of schizophrenia have been commonly linked and supported by dopamine. Dopamine is a neurotransmitter that transmits messages in the brain and body (Savilla, et. Al, 2008). Dopamine is linked to schizophrenia as dopamine has a reputation of being blocked when an individual takes antipsychotic drugs (Savilla, et. Al, 2008). The dopamine receptors are blocked by this drug and therefore constitute to the idea that an overactive dopamine system could be the cause for psychotic episodes. Although, multiple studies (Savilla, et. Al, 2008, Rund, Borg, 2009), are unable to conclude if increase dopamine release is broadly influential or negative in cognitive manifestations.
For normal brain functioning, the neural systems in the body work complexly to ensure body functioning is maintained. A study by DeLong suggests that the frontal cortex and the subcortical areas comprise of long-tract pathways in which the basal ganglia and thalamus use to influence the function of the frontal cortex (Polimeni, et. Al, 2016). In schizophrenia, it is apparent that a majority of the abnormalities that occur involve the frontal cortex. Multiple papers suggest that a change in these pathways/feedback systems can account for partial symptoms in schizophrenia (Sharma and Antonova, 2013). As the basal ganglia contains multiple neurotransmitters, its importance in normal functioning is vital. If there is any active malfunction in dopamine levels or the neurotransmitters in the basal ganglia, it can suggest a possible alteration to the functions of the frontal lobe; propagating conclusions for cognitive impairment in schizophrenia.
Although a majority of studies are in favour for cognitive decline in schizophrenia, there are counter studies to suggest schizophrenia and cognition are not related. In a paper by Alptekin, he designed a study in which healthy individuals were compared to persons with schizophrenia. The study involved examining possible changes in cognition, behavioural changes, social changes and an overall quality of life. The results of this study concluded that majority of the participants with schizophrenia matched equally to the healthier participants in cognition. The study found that the cognitive results were not as drastic in relation to the social and overall quality of life. Results showed, that those with schizophrenia had a more likely chance social decline and social exclusion. It is clear that there will be a gap between current studies and papers due to different variables present, history of patients and the validity of the study. Ultimately, these papers can only notify researchers of continuous trends that are occurring in people of schizophrenia, rather than justifying the ultimate underlying cause.
This paper aims to identify the relation of cognition to schizophrenia and analyse if there is a decline in cognitive ability. In majority of the relevant studies discussed, it can be assumed that schizophrenia does have an impact on the cognition of a human being to a great extent. This is supported through the noticeable changes impairment in logic, executive functions, working memory and attention. Although the root of these abnormalities could derive from other causes, these effects were common in all persons with schizophrenia. This allows researchers to conclude that in fact, there is a cognitive decline for people with schizophrenia.
References
- Bowie, C. R., & Harvey, P. D. (2016). Cognitive deficits and functional outcome in schizophrenia. Neuropsychiatric disease and treatment, 2(4), 531.
- Fioravanti, M., Carlone, O., Vitale, B., Cinti, M. E., & Clare, L. (2015). A meta-analysis of cognitive deficits in adults with a diagnosis of schizophrenia. Neuropsychology review, 15(2), 73-95.
- Gold, J. M., & Harvey, P. D. (2003). Cognitive deficits in schizophrenia. Psychiatric Clinics, 16(2), 295-312.
- Insel, T. R. (2010). Rethinking schizophrenia. Nature, 468(7321), 187.
- Medalia, A., Thysen, J., & Freilich, B. (2008). Do people with schizophrenia who have objective cognitive impairment identify cognitive deficits on a self report measure?. Schizophrenia Research, 105(1-3), 156-164.
- Polimeni, J., & Reiss, J. P. (2016). Humor perception deficits in schizophrenia. Psychiatry Research, 141(2), 229-232.
- Rund, B. R., & Borg, N. E. (2009). Cognitive deficits and cognitive training in schizophrenic patients: a review. Acta Psychiatrica Scandinavica, 100(2), 85-95.
- Savilla, K., Kettler, L., & Galletly, C. (2008). Relationships between cognitive deficits, symptoms and quality of life in schizophrenia. Australian & New Zealand Journal of Psychiatry, 42(6), 496-504.
- Sharma, T., & Antonova, L. (2013). Cognitive function in schizophrenia. Deficits, functional consequences, and future treatment. Psychiatric Clinics of North America.
- Singh, T., Kurki, M. I., Curtis, D., Purcell, S. M., Crooks, L., McRae, J., ... & Pietiläinen, O. (2016). Rare loss-of-function variants in SETD1A are associated with schizophrenia and developmental disorders. Nature neuroscience, 19(4), 571. (Singh, et. Al, 2016)
- Sitskoorn, M. M., Aleman, A., Ebisch, S. J., Appels, M. C., & Kahn, R. S. (2014). Cognitive deficits in relatives of patients with schizophrenia: a meta-analysis. Schizophrenia research, 71(2-3), 285-295. (Sitskoom, et. Al, 2014)
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