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Characteristics of Paranoid Schizophrenia

Question:

Discuss About The Auditory Variety Perceptual Disturbances?

It is the most common sub-type of schizophrenia whose defining characteristics are auditory hallucinations accompanied with thoughts and beliefs laden with delusions. As per the ICD-10 classification, it is a chronic form of schizophrenia characterised by “relatively stable, often paranoid delusions, usually accompanied by hallucinations, particularly of the auditory variety, and perceptual disturbances. Disturbances of affect, volition, and speech, and catatonic symptoms are either absent or relatively inconspicuous” (World Health Organization (WHO), 2015). According to the definition, the key characteristics that define this form of schizophrenia include perceptual disturbances, hallucination, particularly of auditory nature and delusions (persecutory or grandiose). These characteristics have a significant negative effect on an individual’s quality of life as they affect their functioning. Regardless, compared to other forms of schizophrenia, those presenting with paranoid schizophrenia are able to function better in daily life as they have fewer problems with memory, emotional apathy and concentration (Torgersen, 2012). Paranoid schizophrenia is a lifelong condition but still, an individual can attain a high quality of life with proper treatment. The form of treatment and response to the treatment often varies from patient to patient and it depends on an individual’s clinical picture. It is thus advisable to look at how severe the symptoms are when considering treatment modalities.

Common symptoms characterising paranoid schizophrenia include severe anxiety and agitation, unexplained anger, argumentative habits, emotional disconnect, frequent suicidal thoughts and behaviours, auditory disturbances, delusions and violent tendencies and behaviours (Sadock, Sadock, & Ruiz, 2017). While most of these signs and symptoms are present in persons presenting with other forms of schizophrenia, there are two symptoms (i.e. paranoid delusions and auditory hallucinations) which set paranoid schizophrenia apart from other subtypes of schizophrenia (National Institute of Mental Health, 2016).

Paranoid delusions: Persons suffering from paranoid schizophrenia often feel that other people are conspiring against them. A delusion is a strong perception that something is in a certain way but in reality, the evidence says otherwise. Delusions in paranoid schizophrenia often lead to abnormal behaviours in the patient. This is often as a result of intensifying of the paranoid thoughts which makes one behave in an aggressive manner or commit violence under the guise of self-defence against those persons in the delusions of the patient who wants to cause him/her or their loved ones some form of harm. These delusions also tend to make patients believe that they possess some supernatural abilities, or they are famous persons (delusions of grandeur) (Grohol, 2016). Even though people may present contrary evidence, the patient often holds onto the beliefs.

Pathophysiology of the Disorder

Auditory hallucinations: This symptom involves a person hearing voices or sounds which in reality are not present (Puri & Treasaden, 2013). One may hear multiple voices which may be talking to him/her or voices which may be conversing to one another. Such hallucinations often influence patients to behave in a particular manner as they sometimes criticise, poke or make fun of the patient’s real or perceived flaws, or may persuade the patient to hurt themselves or another person (Mayo Foundation for Medical Education and Research, 2013). Even though the voices are not real, to the patient, they are.

The pathophysiology of paranoid schizophrenia (and schizophrenia as a whole) is widely debated. The most common and respected hypothesis of the pathophysiology is that of the condition resulting as a result of disruptions in the functioning of the neurotransmitters dopamine and glutamate and abnormal neurological structures (Elert, 2014). Evidence from studies suggests that schizophrenia is a disorder resulting from abnormal dopamine signalling (Howes & Nour, 2016).

Dopamine synthesis and release capacity are increased in persons with the condition, specifically in the midbrain origin of the neurons and the striatum (Howes, et al., 2012; Howes, et al., 2013). Despite the hypothesis of dopamine dysregulation being the most common, it still remains clear how it contributes to the symptoms of the condition. Some studies claim that there is the disruption of the auditory thalamocortical projections and this causes hallucinations, whereas the delusions are likely to be as a result of dysregulated corticostriatal circuitry and reward circuitry in the form of aberrant salience (Chun, et al., 2014).

The other hypothesis focuses on the neurotransmitter glutamate. Post-mortem of brains of persons previously diagnosed with the condition has shown diminished levels of glutamate receptors (Rubio, Drummond, & Meador-Woodruff, 2012). Evidence links reduced glutamate function to poor performance on tasks that require the function of the frontal lobe and hippocampal regions (Howes, McCutcheon, & Stone, 2016). Additionally, glutamate also has an effect on dopamine function, and the role of glutamate pathways in schizophrenia has been implicated in the development of the condition (Rubio, Drummond, & Meador-Woodruff, 2012).

Other than the neurotransmitter hypothesis, another proposed hypothesis in the pathophysiology of paranoid schizophrenia is neurological abnormalities. The abnormalities may take different forms including dysfunction of neurons in the brain (Pittman-Polletta, Kocsis, Vijayan, Whittington, & Kopel, 2015), and myelination abnormalities (reduction in the volume of grey matter) (Cassoli, et al., 2015). However, there is no consensus on how this hypothesis contributes to the clinical picture of paranoid schizophrenia.

Treatment of Paranoid Schizophrenia

The acute phase of paranoid schizophrenia occurs when a patient experiences the first episode of psychosis or when a patient with prior history experiences a psychotic relapse. Therefore, the focus of treatment in this phase is to reduce the severity of psychotic thoughts and behaviours. In this phase, antipsychotic drugs are the first-line of treatment. Antipsychotics have demonstrated to reduce symptoms such as hallucinations and delusions (Patel, Cherian, Gohil, & Atkinson, 2014). With the exception of clozapine, evidence suggests that any antipsychotic is more effective than other drugs in the management of hallucinations and delusions in acute paranoid schizophrenia (Patel, Cherian, Gohil, & Atkinson, 2014). Clozapine is more effective in those patients whose response to antipsychotics is poor, but owing to the increased risk of agranulocytosis, Clozapine is reserved to those with poor response or cannot tolerate antipsychotics (Fabrazzo, et al., 2017). Other symptoms in this phase which may include lack of motivation and supressed emotional expression have however proven difficult to treat, with only Cariprazine showing positive results (Németh, et al., 2017).The selection of an antipsychotic is based on both severity of presentation, efficacy, side effects and available formulation.

The primary non-pharmacological intervention in the acute phase is electroconvulsive therapy (ECT) (Kerner & Prudic, 2014). ECT is recommended in schizophrenia (Cassels, 2016).  ECT involves the use of electricity to induce a therapeutic seizure to treat delusions and incoherence. Its efficacy is supported by evidence by Kenner and Prudic (2014) who claim that ECT has demonstrated comparable efficacy with antipsychotics.

The non-acute phase follows a patient’s recovery from an acute psychotic phase. In the non-acute phase, the symptoms are reasonably well controlled. Management in this phase aims at minimising symptoms and functional impairments, preventing relapses, and promoting recovery which will allow the patient have self-determination, can be fully integrated into the society, and can also pursue personal goals (Stroup & Marder, 2017). Regardless, it is recommended that antipsychotic medication should be continued indefinitely even in those who have achieved remission from the first psychotic episode (Acto, 2013). However, the dose used should be the lowest effective dose that achieves the therapeutic goals. In this phase, patients are also involved in the clinical decision-making pertaining to how long they will be on the antipsychotic drug therapy.

Alongside pharmacotherapy, nonpharmacological interventions that can be applied in this phase include a combination of family and psychological interventions. Family interventions have shown to manage the condition successfully and cost-effectively (Chien, Leung, Yeung, & Wong, 2013). This is evidenced in a reduction in relapse rates. Other interventions are targeted at substance misuse and motivational interventions. The risk of relapses is increased in drug misuse. Patients with paranoid schizophrenia who misuse substances are a special challenge, and the most suited intervention in the community setting is psychological interventions.

Pharmacological Treatment

Notably, the most suited non-pharmacological intervention in this phase is cognitive-behavioural therapy (CBT). It is a second frontline treatment in most western countries whose main aim is to allow patients assume more control of their lives and also facilitate a return to the previously-lost functionality (Trach & Mardon, 2016). In CBT, a therapist works with a client to change their thinking behaviour and emotional responses. This gives the patient more control of their lives. Researchers who have compared CBT with other psychosocial interventions have found it to be quite effective compared to others (Rector & Beck, 2012). Other alternatives include skills training and assertive community treatment.

The multidisciplinary nursing care management has five key goals which include reducing the severity of the symptoms, preventing recurrence of the acute episodes, meeting the patient’s needs (physical and psychosocial), helping the patient regain the optimal level of functioning, and increasing the patient's compliance to treatment (Dewit, Stromberg, & Dallred, 2016). There are various routine clinical nursing care and interventions performed so as to attain these goals.

  1. Maximizing level of functioning: Promote independence while discouraging dependence. Reward positive behaviours demonstrated and also work with the patient to improve his/her sense of responsibility to improve function.
  2. Promoting social skills
  3. Ensuring adequate nutrition by monitoring the patient’s nutritional status
  4. Ensuring a safe environment for the patient.
  5. Promoting compliance with medication; This includes administration of the prescribed drugs and encouraging patient compliance. Also, check for adverse events and reactions. Dealing with hallucinations; This includes counteracting it with reality. Also, explore the nature of hallucinations and explain to the patient that they are not real.
  6. Encouraging family involvement; This also includes involving them in the treatment and teaching them in early recognition of impending relapse. Also, teach them on how to manage the symptoms

References

Acto, A. (2013). Issues in Mental Health Research and Practice. Atlanta: ScholarlyEditions.

Cassels, C. (2016, MAy 19). ECT an Effective Treatment Option for Schizophrenia. Retrieved from MedScape: https://www.medscape.com/viewarticle/863547

Cassoli, J. S., Guest, P. C., Malchow, B., Schmitt, A., Falkai, P., & Martins-de-Souza, D. (2015). Disturbed macro-connectivity in schizophrenia linked to oligodendrocyte dysfunction: from structural findings to molecules. NPJ Schizophr, 1-10.

Chien, W. T., Leung, S. F., Yeung, F. K., & Wong, W. K. (2013). Current approaches to treatments for schizophrenia spectrum disorders, part II: psychosocial interventions and patient-focused perspectives in psychiatric care. Neuropsychiatr Dis Treat, 1463–148.

Chun, S., Westmoreland, J. J., Bayazitov, I. T., Eddins, D., Pani, A. K., Smeyne, R. J., . . . Zakharenko, S. S. (2014). Specific disruption of thalamic inputs to the auditory cortex in schizophrenia models. Science, 1178-1182.

Dewit, S. C., Stromberg, H., & Dallred, C. (2016). Medical-surgical Nursing: Concepts & Practice. Amsterdam: Elsevier Health Sciences.

Elert, E. (2014). Aetiology: Searching for schizophrenia's roots. Nature , S2-S3.

Fabrazzo, M., Prisco, V., Sampogna, G., Perris, F., Catapano, F., Monteleone, A., & Maj, M. (2017). Clozapine versus other antipsychotics during the first 18 weeks of treatment: A retrospective study on risk factor increase of blood dyscrasias. Psychiatry Res, 275-282.

Grohol, J. M. (2016, July 17). Delusion of Grandeur. Retrieved from PschCentral: https://psychcentral.com/encyclopedia/delusion-of-grandeur/

Howes, O. D., & Nour, M. M. (2016). Dopamine and the aberrant salience hypothesis of schizophrenia. World Psychiatry, 3-4.

Howes, O., Kambeitz, J., Kim, E., Stahl, D., Slifstein, M., Abi-Dargham, A., & Kapur, S. (2012). The nature of dopamine dysfunction in schizophrenia and what this means for treatment. Arch Gen Psychiatry, 776-86.

Howes, O., McCutcheon, R., & Stone, J. (2016). Glutamate and dopamine in schizophrenia: an update for the 21st century. J Psychopharmacol, 97-115.

Howes, O., Williams, M., Ibrahim, K., Leung, G., Egerton, A., McGuire, P., & Turkheimer, F. (2013). Midbrain dopamine function in schizophrenia and depression: a post-mortem and positron emission tomographic imaging study. Brain.

Kerner, N., & Prudic, J. (2014). Current electroconvulsive therapy practice and research in the geriatric population. Neuropsychiatry (London), 33–54.

Mayo Foundation for Medical Education and Research. (2013, June 18). Paranoid Schizophrenia. Retrieved from Mayo Clinic: https://web.archive.org/web/20130618045057/https://www.mayoclinic.com/health/paranoid-schizophrenia/DS00862/DSECTION%3Dsymptoms

National Institute of Mental Health. (2016, February). Schizophrenia. Retrieved from https://www.nimh.nih.gov/health/publications/schizophrenia/what-are-the-symptoms-of-schizophrenia.shtml

Németh, G., Laszlovszky, I., Czobor, P., Szalai, E., Szatmári, B., Harsányi, J., . . . Fleischhacker, W. (2017). Cariprazine versus risperidone monotherapy for treatment of predominant negative symptoms in patients with schizophrenia: a randomised, double-blind, controlled trial. Lancet, Epub 2017 Feb 7.

Patel, K. R., Cherian, J., Gohil, K., & Atkinson, D. (2014). Schizophrenia: Overview and Treatment Options. P T, 638-645.

Pittman-Polletta, B. R., Kocsis, B., Vijayan, S., Whittington, M. A., & Kopel, N. J. (2015). Brain Rhythms Connect Impaired Inhibition to Altered Cognition in Schizophrenia. Biol Psychiatry, 1020-1030.

Puri, B., & Treasaden, I. (2013). Textbook of Psychiatry. Philadelphia: Churchill Livingstone.

Rector, N., & Beck, A. (2012). Cognitive Behavioral Therapy for Schizophrenia: An Empirical Review. The Journal Of Nervous And Mental Disease, 832-839.

Rubio, M. D., Drummond, J. B., & Meador-Woodruff, J. H. (2012). Glutamate Receptor Abnormalities in Schizophrenia: Implications for Innovative Treatments. Biomol Ther (Seoul), 1-18.

Sadock, B. J., Sadock, V. A., & Ruiz, P. (2017). Kaplan and Sadock's Comprehensive Textbook of Psychiatry. Alphen aan den Rijn: Wolters Kluwer Health.

Stroup, S. T., & Marder, S. (2017, May 23). Pharmacotherapy for schizophrenia: Acute and maintenance phase treatment View in Chinese. Retrieved from UpToDate: https://www.uptodate.com/contents/pharmacotherapy-for-schizophrenia-acute-and-maintenance-phase-treatment

Torgersen, S. (2012). Paranoid schizophrenia, paranoid psychoses, and personality disorders. Journal for the Norwegian Medicine Association, 851-852.

Trach, N., & Mardon, A. (2016). Cognitive-Behavioral Therapy for Schizophrenia. Retrieved from PsychCentral: https://psychcentral.com/lib/cognitive-behavioral-therapy-for-schizophrenia/

World Health Organization (WHO). (2015). International Statistical Classification of Diseases and Related Health Problems. Geneva: World Health Organization.

Signs and Symptoms

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