Is Schizophrenia Treatable?


Is Schizophrenia Treatable?
What is Schizophrenia?
Schizophrenia includes a range of mental health complications associated with cognitive impairment, disorganized behavior, speech difficulty, hallucinations, and delusions (Patel, Cherian, Gohil, & Atkinson, 2014). The chronicity of schizophrenia leads to negative symptoms that potentially impact executive function, working memory, and attention span of the affected patients. However, the positive symptoms of schizophrenia include hallucinations, delusions, and suspiciousness. The schizophrenia’s inherent heterogeneity pattern is the preliminary cause of differences in opinions regarding its pathophysiology, etiology, and diagnostic parameters. Schizophrenia patients commonly experience the following problems in their day-to-day life. However, these problems variably impact men and women of various age groups (Seeman, 2018).
  1. The schizophrenia patients usually deny their symptoms while resisting to correlate them with their illness. 
  2. Every stimulus leads to the development of a perception that induces hallucinations or delusions in schizophrenia patients. 
  3. The schizophrenia hallucinations predominantly impact the vision, taste, smell, or touch perceptions of the affected patients. 
  4. Most of the schizophrenia patients experience auditory hallucinations that potentially interfere in their daily activities.        
  5. Schizophrenia-based delusions potentially deteriorate the beliefs and perceptions of the affected patients to an unprecedented level. 
  6. The personal themes of delusions are based on the feelings of persecution and passivity. The schizophrenia patients consider themselves as the victims of a stratagem and threatening circumstances. 
  7. The passive thoughts of the schizophrenia patients force them to believe in the existence of an external force that potentially threatens their survival and well-being. 
  8. Schizophrenia patients usually experience religious, sexual, or grandiose delusions. 
  9. The schizophrenia patients’ irrational thinking pattern reflects through their illogical decisions and speech complications. 
  10. The schizophrenia patients abruptly deflect their categorical chain of thoughts and fail to use language coherently. 
  11. Some of the passive behavioral manifestations of schizophrenia include paucity of speech, emotional blunting, loss of initiative/motivation, self-neglect, and social withdrawal. 
What are the Commonly Reported subdivisions of Schizophrenia?
Schizophrenia is divided into the following subtypes (Picchioni & Murray, 2007). 
  1. The paranoid schizophrenia manifests through prominent hallucinations or delusions. 
  2. The hebephrenic schizophrenia manifests through incongruous/sustained flattened affect, irrational behavior, and disturbing thoughts. 
  3. Catatonic schizophrenia leads to the development of rigid behavior. The patients also experience behavioral conflicts based on posturing, excitement, and stupor. 
  4. The simple schizophrenia manifests through the progressive intensification of passive symptoms, absence of personal drive, and cognitive decline. The patients usually reflect a marked reduction in their employment/academic performance and social functioning. 
What are the Commonly Reported Causes of Schizophrenia?
The following attributes predominantly elevate the risk of schizophrenia in predisposed patients (IOM, 2001). However, the pathomechanism of schizophrenia is still not clearly understood until the date (Stępnicki, Kondej, & Kaczor, 2018).   
  1. Reduced self-care
  2. Inappropriate nutrition 
  3. Heavy smoking 
  4. Medical negligence 
  5. Childbirth/pregnancy complications 
  6. Prolonged consumption of psychotropic or psychoactive drugs 
  7. Family history of mental illnesses 
  8. Genetic predisposition 
What are the Complications Faced by Schizophrenia Patients?
The adverse psychosocial outcomes of schizophrenia potentially increase the risk of the following conditions (Mayo Clinic, 2020). 
  1. Aggressive or violent behavior 
  2. Medical comorbidities    
  3. Social isolation 
  4. Homelessness and financial issues 
  5. Unemployment 
  6. Nicotine/drug addiction and alcoholism 
  7. Depression  
  8. Anxiety 
  9. Obsessive-compulsive disorder 
  10. Suicidal ideation 
What is the Pathophysiology of Schizophrenia?
Schizophrenia drastically impacts the neuropsychological performance of the affected patients (Tamminga, 2000). The chronic institutionalization and early onset of the psychotic symptoms potentially impact the patients’ coping skills and performance levels. The schizophrenia patients exhibit reduced performance outcomes based on their deteriorated pattern recognition skills, verbal fluency, attention, memory, and intelligence. They also develop serious language/memory/attention deficits that predominantly impact their contextual information processing abilities. The disruption in cognitive circuitry and cerebral function of the schizophrenia patients impacts their thinking pattern, learning skills, and perceptions. Sensory stimuli in schizophrenia patients impact their eye movements and also lead to deflection in their FRG (electroencephalography) outcomes (Tamminga, 2000). The abnormal smooth pursuit eye movements of schizophrenia patients have an unknown etiology. However, they might have an active genetic cause within their genome. The motion processing problem of schizophrenia patients relates to their sustained cerebral defects. They experience considerable difficulty in linking the movements of their eyes with motion information. They also lack the short-term memory for retaining the motion information (Tamminga, 2000). The abnormal eye movements of the schizophrenia patients also reveal questionable defects in their middle frontal and/or parietal cortices. Some of the schizophrenia patients exhibit saccadic eye movements apart from experiencing smooth pursuit movements. The evoked potentials based on cognitive or sensory episodes lead to signal-averaged abnormal EEG alterations in schizophrenia patients. These alterations predominantly occupy P50 and P300 locations of EEG (Tamminga, 2000). 
The schizophrenia patients variably reflect structural and functional changes in their brains that effectively correlate with their clinical symptoms (Tamminga, 2000). For example, A marked reduction in the volume of the temporal gyrus in schizophrenia patients is a well-defined clinical attribute. Similarly, schizophrenia manifests through a sustained reduction in the volumes of hippocampal, entorhinal, and parahippocampal cortices of the middle temporal cortex. The schizophrenia patients also exhibit a considerable reduction in the vascular supply of their prefrontal cortex. Furthermore, they also encounter metabolic alterations and blood supply reduction in the middle frontal gyrus and anterior cingulate of their frontal cortex. A marked decrease in regional cerebral blood flow predominantly leads to the development of psychosocial manifestations in schizophrenia patients (Tamminga, 2000). These outcomes reveal potential CNS (central nervous system) abnormalities in the schizophrenia patients that lead to the development of their negative symptoms. The fMRI (functional magnetic resonance imagining) reveals a contradictory finding based on regional cerebral blood flow elevation in some of the schizophrenia patients. This variable finding warrants prospective analysis to understand the causative mechanisms associated with schizophrenia phase contributions and performance demands in the affected patients (Tamminga, 2000). The regional cerebral blood flow differences in schizophrenia patients necessitate a comparative clinical assessment of their inferior and middle frontal cortices to understand their contribution to the clinical manifestations.   
Evidence-based clinical literature reveals functional variations in the hippocampus of schizophrenia patients (Tamminga, 2000). Some of the schizophrenia patients do not exhibit any structural or functional hippocampal alteration despite marked variations in their regional cerebral blood flow patterns (rCBF). Contrarily, some of the schizophrenia patients exhibit a considerable reduction in their hippocampus rCBF under the influence of ketamine, which is a non-competitive JV-methyl-D-aspartate (NM'DA) antagonist. Scientists provide several other theories related to the pathophysiology and causative mechanisms of schizophrenia (Tamminga, 2000). Some of them advocate the impact of an overactive dopaminergic system on the psychosocial manifestations of schizophrenia patients. Some of the researchers still believe in the hypothesis that advocates the molecular docking mechanism dominating the interaction between the brain’s dopamine receptors and antipsychotic drugs in schizophrenia patients. This interaction presumably minimizes schizophrenia’s psychotic manifestations (Tamminga, 2000). 
Some of the research studies reveal sustained defects in the long-tract mechanisms dominating the interactions between subcortical regions and the frontal cortex in schizophrenia patients (Tamminga, 2000). These defects potentially impact the functionality of thalamus and basal ganglia that eventually increases the intensity of functional and cognitive abnormalities. The modulation of the frontal cortical function in schizophrenia patients could occur under the influence of functional alterations in neuromodulators, neurotransmitters, and their innervations. Furthermore, thalamic dysfunction in schizophrenia patients could also induce functional alterations in their frontal cortex. The neurodevelopmental factors of schizophrenia correlate with the genetic predisposition of the high-risk populations (Tamminga, 2000). This indicates that schizophrenia’s pathobiology is already programmed since birth and intensifies with age under the influence of environmental factors. The premorbid cognitive predictors and their interactions with prenatal or perinatal episodes in many scenarios explain the development of psychotic manifestations in schizophrenia patients. The dysfunction of the neural apparatus of the schizophrenia patients, however, reflects during the late teenage. Interestingly, not all schizophrenia patients could experience neurodevelopmental changes despite the existence of similar pathophysiology (Tamminga, 2000). The etiological variations in schizophrenia patients require clinical investigation in the context of developing novel treatment approaches for mitigating the psychotic episodes. Research studies also reveal the limbic system disruptions in schizophrenia patients. The postmortem examinations of some of the schizophrenia patients reveal the elevated expression of TRG genes under the impact of phencyclidine. The expression of these genes reveals the neuronal responses recorded after the administration of phencyclidine. Some of the studies reveal a marked elevation in the NMDA-sensitive glutamate receptor’s NR subunit under the influence of phencyclidine. The NR elevation typically occurs in the hippocampus of schizophrenia patients. Furthermore, the failure of the GABA-ergic (inhibitory gamma-aminobutyric acid) system’s glutamatergic excitation leads to the feed-forward inhibition in schizophrenia patients (Tamminga, 2000). This eventually elevates resting regional cerebral blood flow inside the hippocampus of the schizophrenia patients. However, researchers still require conducting extensive studies to evaluate the inconclusive pathophysiological evidence in the context of schizophrenia.
What are the Unmet Clinical Demands and Treatment Options for Schizophrenia Management?
The clinicians require customizing therapeutic interventions for schizophrenia patients while considering the following therapeutic options/targets (Fellner, 2017).
  1. Evidence-based strategies for enhancing pharmacotherapeutic compliance
  2. Meaningful utilization of safe and effective drugs 
  3. Selection of novel and approved treatment methods for the health care management of treatment-resistant individuals 
  4. Mitigation of negative symptoms including social withdrawal, apathy, and lethargy 
  5. Cognitive enhancement through pharmacotherapy 
Pharmacotherapy for Schizophrenia patients is based on the following interventions. However, these approaches are associated with potential side-effects (Chein & Yip, 2013) (Muench & Hamer, 2010).
  1. The utilization of 1st and 2nd generation antipsychotics 
  2. The typical or 1st generation antipsychotics include haloperidol, fluphenazine, and chlorpromazine 
  3. The 2nd generation antipsychotics include risperidone, olanzapine, and clozapine
  4. The 2nd generation antipsychotics assist in controlling the positive symptoms of schizophrenia
  5. The 2nd generation antipsychotics associate with fewer side-effects including sedative complications, cardiovascular disease, and movement disorders
  6. Multivitamin therapy based on vitamins B12, B6, E, and C in addition to the baseline drug therapy helps in reducing schizophrenia manifestations
  7. The 1st generation antipsychotics elevate the risk of the following conditions
    • Weight gain 
    • Type 2 diabetes mellitus 
    • Sexual dysfunction 
    • Seizures 
    • Sedation 
    • QT interval prolongation 
    • Postural hypotension 
    • Neuroleptic malignant syndrome 
    • Hyperprolactinemia 
    • Extrapyramidal symptoms 
    • Dyslipidemia 
    • Anticholinergic effects 
What are the Nonpharmacological Schizophrenia Management Options?

The clinicians recommend the use of integrative management approaches based on pharmacotherapeutic and non-pharmacological interventions for controlling the negative and positive symptoms of schizophrenia. Some of these interventions are listed below (Ganguly, Soliman, & Moustafa, 2018) (Matei, Mihailescu, & Davidson, 2014). 
  1. The administration of CBT (cognitive behavioral therapy) along with conservative management helps in mitigating delusions, hallucinations, suicidal ideation, sedentary, and aggression of the schizophrenia patients. 
  2. CBT potentially helps in improving the health-related behavior, feelings, and thinking pattern of the schizophrenia patients 
  3. CBT focusses on mitigating the social impairments of the schizophrenia patients 
  4. The cognitive restructuring technique challenges the patients to falsify their illusions and irrational beliefs 
  5. CBT-based enhancement of conversational skills assists the schizophrenia patients to improve their interpersonal relations with family members 
  6. CBT also assists in controlling the disorganized behavior of the schizophrenia patients 
  7. Dietary management with increased consumption of vitamin D and folic acid helps in minimizing the negative symptoms of schizophrenia. 
  8. The positive modifications in the home environment and compassionate or empathetic dealing by family members also help in controlling schizophrenia complications to a measurable extent 
What are the Recommended Diagnostic Measures and Evaluation Strategies for Schizophrenia Patients?
The following comprehensive interventions assist in evaluating the causes, treatment response, and prognostic outcomes of schizophrenia symptoms (Grover, Chakrabarti, Kulhara, & Avasthi, 2017).
  1. Neuroimaging for the assessment of treatment response, neurological signs, and psychotic episodes 
  2. Mental status examination 
  3. Comprehensive psychological assessment of executive functions 
  4. The utilization of standardized rating scales for evaluating the entire facets of schizophrenia manifestations 
  5. Comprehensive assessment of medication accessibility, family care paradigm, environmental issues, and treatment compliance/side-effects 
  6. The assessment of the family members’ beliefs, perceptions, attitudes, knowledge, and awareness of schizophrenia symptoms 
  7. Basic clinical investigations including electrocardiogram, renal function test, liver function test, lipid profile, Blood glucose level, HbA1C, and hemogram 
  8. Assessment of sociocultural milieu 
  9. Assessment of psychosocial and physical functioning levels  
  10. Evaluation of the risk of suicidal tendency and self-harm 
  11. Assessment of substance abuse pattern, psychiatric complications, physical comorbidities, cognitive manifestations, and symptom dimensions/severity  
  12. Physical examination based on waist circumference, body mass index, and vital signs 
  13. Complete clinical history, including medication use patterns and family history 
  14. A comprehensive evaluation of caregivers and patients 
References

Chein, W. T., & Yip, A. L. (2013). Current approaches to treatments for schizophrenia spectrum disorders, part I: an overview and medical treatments. Neuropsychiatric Disease and Treatment, 1311-1332. doi:10.2147/NDT.S37485
Fellner, C. (2017). New Schizophrenia Treatments Address Unmet Clinical Needs. Pharmacy and Therapeutics , 42(2), 130–134. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5265239/
Ganguly, P., Soliman, A., & Moustafa , A. A. (2018). Holistic Management of Schizophrenia Symptoms Using Pharmacological and Non-pharmacological Treatment. Frontiers in Public Health, 6(166). doi:10.3389/fpubh.2018.00166
Grover, S., Chakrabarti, S., Kulhara , P., & Avasthi, A. (2017). Clinical Practice Guidelines for Management of Schizophrenia. Indian Journal of Psychiatry, 59(1), S19-S33. doi:10.4103/0019-5545.196972
IOM. (2001). Schizophrenia. In Neurological, Psychiatric, and Developmental Disorders: Meeting the Challenge in the Developing World. Washington (DC): National Academies Press (US). Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK223456/
Matei, V. P., Mihailescu , A. I., & Davidson , M. (2014). Is non-pharmacological treatment an option for certain schizophrenia patients? Psychiatria Danubina, 26(4), 308-313. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/25377364
Mayo Clinic. (2020). Schizophrenia. Retrieved from https://www.mayoclinic.org/diseases-conditions/schizophrenia/symptoms-causes/syc-20354443
Muench, J., & Hamer , A. M. (2010). Adverse Effects of Antipsychotic Medications. American Family Physician, 81(5), 617-622. Retrieved from https://www.aafp.org/afp/2010/0301/p617.html
Patel, K. R., Cherian, J., Gohil, K., & Atkinson, D. (2014). Schizophrenia: Overview and Treatment Options. Pharmacy and Therapeutics, 39(9), 638-645. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159061/
Picchioni, M. M., & Murray, R. M. (2007). Schizophrenia. BMJ, 335(7610), 91-95. doi:10.1136/bmj.39227.616447.BE
Seeman, M. V. (2018). Women who suffer from schizophrenia: Critical issues. World Journal of Psychiatry, 8(5), 125-136. doi:10.5498/wjp.v8.i5.125
Stępnicki, P., Kondej, M., & Kaczor, A. A. (2018). Current Concepts and Treatments of Schizophrenia. Molecules. doi:10.3390/molecules23082087
Tamminga, C. A., & Medoff, D. R. (2000). The biology of schizophrenia. Dialogues in Clinical Neuroscience, 2(4), 339-348. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181617/





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