Those who are at risk of potentially developing schizophrenia could receive an early diagnosis if the early use of brain scans were implemented. Those who have schizophrenia, on average, differ in terms of the total tissue volume and brain activity (Cahn, Hilleke, Hulshoff, & Elleke, 2002). Early intervention of the disease has become important in order to know how best to treat the disorder, therefore a two-hit theory has been established in order to attempt to diagnose the condition sooner rather than later. The two (third) hit theory which is used in physical disorders and has been propounded for the diagnosis of schizophrenia early on, describes damage such as infection during the perinatal period is added as an original genetic weakness (Huttunen, Machon, & Mednick, 1994). This would be described as the first hit which impairs neuronal development, therefore creating the potential basis for onset, throughout adolescence and early adulthood, psychological stressors would cause the second hit as symptoms would be manifesting. Subsequently, exacerbation and recurrence will be repeated making negative symptoms more prominent (Iritani, 2013). These processes are called the critical period, it is believed that the prognosis of the disease could have a different outcome if this period is missed. Missing opportunities for the appropriate intervention during the critical period or being unable to provide appropriate responses is called the third hit, which is believed to accelerate the progression of the disease due to the lack of appropriate support. The theory attempts to explain that a combination of genetic susceptibility together with a distinct developmental problem can potentially prime an individual for a later event that ultimately leads to the onset of a full clinical diagnosis of schizophrenia. It also relates to the hypothesis that thinking and cognitive impairments in schizophrenia are related to abnormalities of the neural network which is composed of axons, dendrites, and synapses (Davis, et al., 2016). Brain structural changes in both grey and white matter prior to illness can indicate where the brain structural anomalies can be seen in chronic schizophrenia and which structures in the brain are affected will be beneficial with MRI predictors on who will develop schizophrenia later on in life. Although, as yet it is not possible to have medication that targets certain areas for treatment, continued research and an understanding of the illness will be able to determine whether early pharmacological treatment, will be able to prevent, the cortical progressive brain changes and if they will have a significant effect on future clinical outcomes (Szöke, Pignon, & Schürhoff, 2019).
In the treatment of cognitive dysfunction in schizophrenia, it is being investigated whether cognitive training can remediate impairments. Through the use of a progressive series of computer-based game-like exercises, the principle around cognitive training aims to help those with schizophrenia by targeting the deficits in neuro-cognition. By training areas such as attention, memory, executive functioning, processing speed, and abstraction it is believed that this will significantly improve changes in the functional connectivity, neurophysiological activity and improve the neuroplasticity of specific brain regions of the frontal lobe, occipital cortex, and cingulate cortex (Tripathi, Kar, & Shukla, 2018). Those who have participated in studies in order to develop further cognitive improvement have demonstrated an increased functional capacity with the ability to perform critical everyday living skills (Kar & Singh, 2019). Functional capacity and cognitive performance are strongly related and are considered as an intermediate step between neurocognition and everyday functioning, therefore improving quality of life and the ability to enjoy social and familial interactions. Because cognitive science assumes that skills can develop at any age and can help advance or restore the brain’s capacity for improving cognitive or social performance more detailed knowledge of the meaning and the role of cognitive deficits in schizophrenia has become a relevant target in the care and clinical management of schizophrenia (Bowie, Mcgurk, Mausbach, Patterson, & Harvey, 2012) and to help lower the use of pharmacological treatments.
Typically, the main treatment used for schizophrenia is antipsychotic and antidepressants in order to reduce the psychotic symptoms to allow the patient to function more appropriately (Rogers & Pilgrim, 2014). The use of antipsychotic medicines was introduced in the 1950s, since then new antipsychotics have been regularly introduced. Except for one, clozapine, which is more effective in treatment-resistant schizophrenia, they all share the ability to block D2 receptors and reduce postsynaptic dopamine transmission. Initially, the introduction of antipsychotic drugs brought a revolutionary change in the treatment of schizophrenia. However, despite all the positivity, there was not a significant improvement in the negative symptoms or cognitive impairment. The drugs also caused a variety of adverse reactions such as physical symptoms and over-sedation. This then led to the second generation of antipsychotics (atypical) drugs in the 1970s which were less likely to cause such drastic side effects (Zhang, Mao, & Song, 2018). The new antipsychotics were described as atypical due to them targeting other neuroreceptors other than only dopamine. Normal dopamine transmissions predict the novel rewards and marks and respond to motivationally salient stimuli. Abnormal dopamine transmissions alter these processes and results in an abnormal sense of normality and an inappropriate sense of self which can lead to the experience of psychosis (Kapur, Agid, Mizrahi, & Li, 2006). The use of antipsychotics aims to improve psychosis by diminishing the abnormal transmission by blocking the dopamine D2/3 receptor. By diminishing the dopamine transmission, reduces the salience of the preoccupying symptoms causing the patient to experience a detachment of symptoms and a decrease of the delusions and hallucinations, rather than complete erasure of the symptoms. Significant improvement of symptoms is made within the first two weeks of treatment than in any subsequent two-week period thereafter (Ginovart & Kapur, 2009).