Schizophrenia: Challenges that arise from Cultural Interpretations of Psychotic Symptoms.

Undoubtedly, our understanding of the biological mechanisms underlying the aetiology and management of schizophrenia has progressed rapidly through the years. Nevertheless, despite convincing evidences gathered from research, cultural explanatory models of illness persist. Social and cultural factors continue to exert a great impact on patients suffering from schizophrenia, particularly those who have not yet been exposed to modern and scientific explanatory models.

Given the prevalence of mental health illness in ethnic minorities especially among migrants from War-torn regions such as Somalia, the importance of cultural competency cannot be understated.  Often, the burden of psychiatric illness such as Schizophrenia is not limited to the biological impairments conferred to patients but also include the social impacts. This is exacerbated by social stigma and cultural beliefs.

In this post, I would like to explain some of the biological and cultural explanatory models, focusing on schizophrenia and the traditional beliefs of Muslim patients whom I frequently encountered in my placement.

Signs and Symptoms of Schizophrenia: from a Biological perspective

Schizophrenia is classically characterised by ‘positive’ and ‘negative’ symptoms. These symptoms insidiously develop, making it difficult to be recognised at their early stages.

Positive symptoms include delusions, hallucinations and formal thought disorder. Delusions could be persecutory (where patients become suspicious of their surrounding and feel that others are trying to harm them), grandiose (excessive beliefs of power and high self-regard) or hypochondriacal. Typically, Hallucinations are aural but could also be tactile, gustatory, olfactory and visual.  Formal thought disorder is characterised by speech incoherence, poverty of speech and sometimes neologism (creating a new word)

Negative symptoms include emotional flattening or inappropriate emotions and cognitive impairments. Patients may show reduced affect – reduced facial expression and detached. In addition, there is an increasing difficulty in planning, concentrating and decision-making.

Biological explanatory models of Schizophrenia 

Various hypothesis and (biological) theories have been emerged to try to explain the pathophysiology:

1. Dopamine Hypothesis of Schizophrenia: two parts to this theory ¹

•  Excessive subcortical dopaminergic activity in mesolimbic pathway is thought to account for various positive symptoms e.g. hallucinations.
• ‘Hypofrontality’: a concept highlighting low dopaminergic activity in mesocortical pathway is suggested to be responsible for the abnormal emotions, impaired executive functions in schizophrenic patients (Figure 1)

Figure 1: Dopamine hypothesis of Schizophrenia

This theory first emerged from the ability of dopamine antagonist to treat psychotic and other positive symptoms. The efficacy of typical antipsychotics such as haloperidol and chlorpromazine is dependent on their antagonist activity on D2-like receptors ² .

However, these are often accompanied by unpleasant side effects e.g weight gain and extra pyramidal symptoms such as Parkinsonism and irreversible tardive dyskinesia. In some cases, neuroleptic malignant syndrome characterised by hyperpyrexia, confusion and rigidity may occur.

Typical antipsychotics have been largely superseded by atypical antipsychotics (APP) as first line treatment. In general, there is a lower incidence of tardive dyskinesias associated with APP use ^3,4. APP has an additional affinity for 5HT_2A ⁵. Besides, atypical antipsychotics such as Quetiapine, Risperidone are better at relieving negative symptoms and cognitive symptoms, possibly due to their affinity for 5HT2A receptors. It is worth noting clozapine, which acts on D4 and 5HT_2A, and is the drug of choice in treatment-resistant schizophrenia. 

2. Glutamate Hypothesis of Schizophrenia

The Hypoglutamate model postulates hypofunction of NMDA receptors in neurolimbic regions as a cause of schizophrenia. This model is supported by the ability of PCP and Ketamine (both are established NMDA antagonists) to induce schizophrenia-like symptoms ^6–8. Besides, genetic predisposition to schizophrenia includes genes e.g. Dysbindin, DAOA that influence glutamatergic signalling ⁹.

This theory does not necessarily oppose the Dopamine hypothesis. In fact, abnormalities in dopaminergic signalling is thought to be secondary to primary hypoglutamate activity, suggesting that glutamate signalling dysfunction is a more upstream process contributing to schizophrenic symptoms ¹⁰.

3. Abnormalities in developmentally timed synaptic pruning

More recently, Sekar et al. published a landmark paper in Nature, identifying complement component 4 (C4) alleles located in chromosome 6 as having the strongest genetic association with schizophrenia ¹¹ (Figure 2). Increased expression of C4A is thought to promote C3 deposition leading to destruction of synapses by microglia ^12,13. The result is an excessive or inappropriate complement-mediated synaptic pruning during neurodevelopment in late teens/early adulthood.

This temporal correspondence with the typical age of presentation of schizophrenia renders great credibility to this theory as an explanatory model. In addition, synaptic loss in prefrontal cortex also accounts for cortical thinning and reduced synaptic structures on cortical pyramidal neurones; which are frequently observed in schizophrenic patients ^14,15.

Figure 2: Genome-wide analysis presents the MHC locus at chromosome 6 as the highest peak associated with Schizophrenia. Within this is identified the high risk C4 alleles.

Cultural Interpretation of Psychotic Symptoms and its implications

Despite the expanding research-based evidence that continues to debunk and elucidate the etiology of schizophrenia, there still exists a deeply entrenched misconception among several ethnic groups. The interpretation of psychotic (and other psychiatric) symptoms among the non-medical community is tightly influenced by cultural, historical and religious beliefs.

Muslim communities frequently attribute psychotic symptoms especially hallucinations to ‘Jinn’ –described in Qur’an as a supernatural malignant creature ^16,17. In areas such as Pakistan, it is shown that faith healers continue to blame Jinn for the presence of psychotic symptoms and epilepsy ¹⁸. Even in UK e.g. Leicester, the attribution of psychiatric symptoms to Jinn is common among the Muslim communities ¹⁷. This interpretation has great ramifications; it affects patients’ coping mechanisms, response to illness, and management of the illness and inevitably leads to stigmatization.

In some countries such as Indonesia, this belief prevents patients suffering from schizophrenia and other psychiatric illnesses from receiving appropriate medical treatments. Clearly, the idea that psychiatric symptoms are manifestations of demonic possession by Jinn and that psychiatric symptoms arise due to religious non-devotion and own misdoings are not extremely helpful. Instead, it is a strong barrier to patients seeking medical help. In these cases, many prefer traditional healing from Imam, their religious leaders. While seeking help from religious leaders is harmless, it is uncommon for patients to seek grossly unsafe ‘treatments’. For instance, traditional Somalian practices believed in the use of hyenas to treat mental illness and oust ‘evil spirits’¹⁹. The bottom line is the attribution of psychotic symptoms to Jinn contributes to patients’ reluctance in accepting help from biomedical evidence-based medicine ¹⁶.

As a result, patients delay or completely ignore and disregard the need for western medications, unless they are directed by their religious leaders to psychiatrists. Nevertheless, Dein et al. showed even those South-Asian psychiatric patients in UK who had agreed on undergoing conventional western medications, might not necessarily have given up their traditional explanatory models of illness ^20,21. Despite seeking medical help, they may still hold onto their cultural beliefs. This mismatch between the perceived cause and the recommended treatment may sometimes lead to low compliance and loss to follow-up. 

The importance of Cultural Competency

Given the trust and faith that Muslims placed in Imam and the prevalence of the cultural idea of Jinn as the aetiology of psychotic symptoms, cultural competency is extremely important. The ability to appreciate their views, understand their cultural backgrounds and explore their beliefs would be important to build a strong foundation for doctors-patients relationship and to work towards a more effective management of schizophrenia in these communities.

To this end, there have been initiatives looking into the possibility of relying more on religious social workers and engaging with community (religious) leaders such as Imam ^16,22. In Tower Hamlets, MIND provides services that are culturally sensitive by working closely with faith and cultural communities ²³. For instance, there are services that target specifically and cater to African Caribbean, Bengali and Somalia communities. In addition to providing more relevant and meaningful advices and educational services, such service promotes social inclusion and becomes a platform to build and expand their social support network. In some cases, patients may go on to advocate for the service and medical treatments. 

Stigma associated with Schizophrenia and its implications

In addition to misattribution of symptoms, other social factor that needs to be considered is social stigma associated with Schizophrenia. Both felt and enacted stigma are detrimental to the quality of life and have direct impact on co-morbidities e.g. suicide tendencies among schizphrenic patients. Besides, associative stigma affecting family members would impair the capability of family members to act as carers.

Enacted stigma refers actual acts of discrimination and treating someone differently due to their condition. Patients with schizophrenic patients were shunned, publicly humiliated, labelled as 'mad' and unfairly disadvantaged in housing, education and employment ²⁴.

Besides, felt stigma indirectly undermines any available or potential social support netweok; the fear of discrimination may modify patient behaviours towards self-isolation. This not only reduces access to neccessary support but also accentuates stigma further. Due to the fear of shaming and disapproval, patients experiencing first episode psychoses tend to feel discouraged from immediately sharing their thoughts with their friends and family. They may decide to isolate themselves during relapses and delay seeking medical help²⁴.

Personally, i suspect that the historical - now defunct and obsolete (at least in some countries)- ways of treating schizophrenia such as locking them up and chaining them or the old-fashioned 'shock therapy' where insulin injection is given to induce coma, had contributed to the ill-feelings surrounding psychiatric treatment and contributed to this stigma. While the management of psychiatric illness has largely changed in some countries, media representations of schizophrenia and its unpleasant treatments continue to perpetuate this stigma.

Conclusion and future developments

The challenges that cultural interpretations of disease and stigma pose are real; they affect the quality of life of patients and affect the effectiveness of clinical practice. They could dictate the availability of social support network – an important social determinant of health in schizophrenia. As such, there is a need to continually search for ways to better engage patients from ethnic minorities.

In addition, there are few and inadequate research-based evidences investigating specific reasons behind stigma in schizophrenia. This is an area of unmet clinical demand that requires further investigations. This would be necessary to form basis for formulation of ways to reduce stigma in the UK and especially among certain ethnic groups in which social stigma is more significant.

References 

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11.       Sekar, A. et al. Schizophrenia risk from complex variation of complement component 4. Nature 530, 177–183 (2016).

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18.       Saeed, K., Gater, R., Hussain, A. & Mubbashar, M. The prevalence, classification and treatment of mental disorders among attenders of native faith healers in rural Pakistan. Soc. Psychiatry Psychiatr. Epidemiol. 35, 480–485 (2000).

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