A Comparison of Schizophrenia and Bipolar Disorder: Important Distinctions and Diagnostic Disparities Based on Race

Although bipolar disorder is a mood disorder while schizophrenia is a psychotic disorder, there are several significant similarities between their diagnostic criteria, etiology, and treatment that suggest similar development. Many psychologists have identified disparities in the diagnosis of both disorders across different racial groups. Research has determined that the underdiagnosis of bipolar disorder in African American populations is caused by an overdiagnosis of schizophrenia in the group. Current work aims to find the cause of the disparity to ensure all patients are given the most accurate diagnosis and appropriate treatment.

Bipolar disorder is characterized by manic episodes which are periods of abnormally and persistently elevated or irritable mood. Alteration in mood must last at least one week for most of the day and three or more specific symptoms (four if the mood is irritable) must be present. These symptoms include grandiosity, decreased need for sleep, talkativeness, flight of ideas, increased goal-directed activity, psychomotor agitation, or engagement in risky activities (American Psychiatric Association, 2013). The majority of people with bipolar disorder also experience depressive episodes, however, they are not a requirement for diagnosis. They may include depressed mood, anhedonia, thoughts of death, fatigue, and changes in sleep and appetite (American Psychiatric Association, 2013). Bipolar has a 1% prevalence and usually develops in late adolescence or early adulthood equally in both genders. Many are people are comorbid for an anxiety or substance abuse disorder (Nolen-Hoeksema & Marroquín, 2017).

Biological theories of bipolar suggest a genetic influence because first degree relatives and identical twins have a greater likelihood of developing bipolar compared to more distant relatives and fraternal twins respectively (Nolen-Hoeksema & Marroquín, 2017). Evidence also points to structural and functional brain abnormalities being implicated as research has shown abnormalities in the amygdala and prefrontal cortex as well as the striatum of the basal ganglia. These parts of the brain are involved in the processing of reward cues and thus it is suggested that those with bipolar may be hypersensitive to rewarding environmental cues (Nolen-Hoeksema & Marroquín, 2017). Research has also suggested that the dysregulation of dopamine contributes to bipolar disorder because high levels lead to greater reward seeking and low levels cause insensitivity to reward (Nolen-Hoeksema & Marroquín, 2017). Psychosocial studies of bipolar disorder have found that stressful events and unsupportive family are associated with the onset of a manic episode and disruptions body rhythms or routines can also trigger a relapse. Additionally, gambling experiments have shown that those with bipolar have a heightened sensitivity to rewarding stimuli (Nolen-Hoeksema & Marroquín, 2017).

Treatments of bipolar disorder are similar to those of other mood disorders, involving both medications and psychotherapy. Antidepressants such as selective serotonin reuptake inhibitors, mood stabilizers such as lithium, and in some cases atypical antipsychotics are prescribed. Atypical antipsychotics decrease dopamine levels to treat mania symptoms but have a greater number of side effects than SSRIs which block the reuptake of dopamine (Nolen-Hoeksema & Marroquín, 2017). Psychological treatments for bipolar include interpersonal and social rhythm therapy which aims to help patients maintain stability and relationships and use behavioral techniques to maintain regular routines. Family-focused therapy is also designed for bipolar disorder and works to reduce interpersonal stress in the familial context. It involves training members in communication and problem solving so that they can better function as a unit (Nolen-Hoeksema & Marroquín, 2017).

Schizophrenia is a psychotic disorder that has a 1-2% prevalence and usually begins in adolescence or early adulthood. The diagnostic requirements are two or more symptoms for at least 1 month, composing the acute phase, and 6 months of symptoms (which may be milder) composing either a prodromal or residual phase (American Psychiatric Association, 2013). The symptoms of schizophrenia can be broken down into several categories of related symptoms. Positive symptoms include delusions, which are beliefs that have no basis in reality and hallucinations which are unreal perceptual experiences (American Psychiatric Association, 2013). Additionally, positive symptoms include disorganized behavior, speech, and thought (American Psychiatric Association, 2013). The negative symptoms of schizophrenia include restricted affect, which is defined as a decrease in emotional expression, and avolition, which is an inability to initiate or persist in goal-directed activity. Finally, the symptoms of schizophrenia may include cognitive deficits such as impairments in mental processes such as attention and memory (Nolen-Hoeksema & Marroquín, 2017).

There are stark similarities in the symptoms and prevalence of schizophrenia across both time and different cultures which implicates biological risk factors. Research has suggested that schizophrenia risk is polygenic, with different genes responsible for different symptoms. Family, twin, and adoption studies have identified that the risk of schizophrenia increases as relatedness increases (Nolen-Hoeksema & Marroquín, 2017). Additionally, structural abnormalities such as a reduction in grey matter and abnormally enlarged ventricles are seen and indicate atrophy in other areas of brain tissue (Nolen-Hoeksema & Marroquín, 2017). Imbalances in dopamine also play a role in schizophrenia. Studies have found low dopamine in the prefrontal cortex, leading to negative symptoms but at the same time excess dopamine in the mesolimbic pathway which leads to the development of positive symptoms. (Nolen-Hoeksema & Marroquín, 2017). Finally, birth complications and prenatal exposure to infectious agents increase the risk for schizophrenia (Nolen-Hoeksema & Marroquín, 2017). Psychological theories indicate that people with schizophrenia are more likely to experience chronically stressful events and stressful circumstances may trigger psychotic episodes (Nolen-Hoeksema & Marroquín, 2017). On the other hand, cognitive theorists have suggested that delusions arise from an attempt to explain perceptual experiences and hallucinations arise from hypersensitivity to perceptual input (Nolen-Hoeksema & Marroquín, 2017).

Treatments for schizophrenia include antipsychotic drugs such as typical antipsychotics which treat positive symptoms but not the negative ones. Newer antipsychotics treat both the positive and negative symptoms by targeting dopamine regulation different in different parts of the brain and have fewer adverse side effects. They increase dopamine in the prefrontal cortex, where it is low, and increase dopamine in the mesolimbic pathway, where it is elevated, by inhibiting glutamate (Nolen-Hoeksema & Marroquín, 2017). Cognitive therapy helps to decrease positive symptoms, and decrease social problems by helping patients recognize demoralizing attitudes toward illness so they will seek help. Behavioral therapies may involve a token economy and family therapy has also been successful because it targets expressed emotion regulation (Nolen-Hoeksema & Marroquín, 2017).

Although schizophrenia is a psychotic disorder and bipolar disorder is a mood disorder, there are several significant similarities between their diagnostic criteria, etiology, and treatments. First, both are very rare disorders, affecting 1-2% of the population (Nolen-Hoeksema & Marroquín, 2017). With regards to diagnosis, although the two disorders have different symptoms, they have some criteria in common. Both must contribute to clinically significant distress or impairment in functioning as this is a requirement of all psychological disorders in the DSM 5. (American Psychological Association, 2013). Additionally, symptoms of schizophrenia and bipolar disorder cannot be due to the effects of a substance (American Psychological Association, 2013). Psychosocial theories of both schizophrenia and bipolar suggest that stressful events and family situations can trigger episodes of either mania or psychosis (Nolen-Hoeksema & Marroquín, 2017). Both disorders also often develop in adolescence or early adulthood, which is known to be a stressful period. This theory has led to family-focused therapies which target the regulation of expressed emotion and work to reduce familial stress. This helps resolve issues that may arise in the context of a patient’s family so that they can better cope with their disorder and educates the family about the disorder so they can better handle their patient. Their common biological etiology involves dysregulation of dopamine (Nolen-Hoeksema & Marroquín, 2017).

Finally, genetics are highly implicated in both disorders. In fact, recent studies have found there is significant overlap of abnormal genes in schizophrenia and bipolar disorder. Shao and Vawter (2008) found 78 altered genes that were shared between those with the disorders. Particularly, genes AGXT2L1 and SLC1A2, which are involved in amino acid catalyzation and glutamate transportation, were highly dysregulated in the brains of bipolar and schizophrenia patients (Shao & Vawter, 2008). Furthermore, the International Schizophrenia Consortium (2009) found several single nucleotide polymorphisms shared between bipolar and schizophrenia and developed a polygenic model for the interaction of genetic differences as a risk factor for both disorders. Overall, these studies suggest a common gene expression profile of schizophrenia and bipolar disorder which provides a starting point for further examination of genes that might contribute to psychopathology.

Even though there are several similarities between the two disorders, there are important distinctions that set them apart. With regards to diagnosis, it is important to assert that these two disorders are distinct and do not co-occur. If symptoms do co-occur, the patient is given the separate diagnosis of a schizoaffective disorder (American Psychological Association, 2013). In other words, the disorders can be distinguished because of the fact that psychotic symptoms are not characteristic of bipolar disorder and if affective symptoms are seen in a schizophrenic patient, the diagnosis changes to schizoaffective disorder. Another difference is the change in goal-directed activity due to the disorders. Avolition is a negative symptom of schizophrenia involving an inability to begin or carry out goal-directed activity, but in a manic episode of bipolar, there is often an increase in goal-directed activity (American Psychological Association, 2013). Finally, the disorders differ in the time that is required for diagnosis. A bipolar disorder may be diagnosed if one fits the criteria for an alteration in mood that lasts a week for most of the time (American Psychological Association, 2013). On the other hand, diagnosis of schizophrenia is given after an acute phase of at least a month which is preceded or followed by 6 months of disturbance (American Psychological Association, 2013). This time difference may be due to the fact that with schizophrenia, clinicians may want to ensure the diagnosis is correct by ruling out others and this takes an extended period of time.

Schizophrenia and bipolar disorder differ in their etiology because birth complications and prenatal exposure are highly implicated in the development of schizophrenia. These can include brain damage due to hypoxia, prenatal viral exposure, stress during the 2nd trimester, and nutritional deficiency (Nolen-Hoeksema & Marroquín, 2017). However, these biological risk factors are not implicated in bipolar disorder. Additionally, they differ in the treatment because selective serotonin reuptake inhibitors are often used in the treatment of bipolar disorder, but antipsychotics are more often used to treat schizophrenia (Nolen-Hoeksema & Marroquín, 2017). This is done because they each treat the symptoms of the disorder while posing the least risk for side effects. For example, antipsychotics can be effective in treating acute mania but have a higher incidence of mood destabilization and side effects, therefore they’re not the first choice for treatment of bipolar disorder.

An ongoing issue with many psychological disorders are unexplained racial disparities in the prevalence. Studies have shown that both bipolar disorder and schizophrenia are diagnosed unequally across different racial groups. First, mood disorders, in general, are underdiagnosed in African American populations. Several studies, including Barnes (2008), have found that bipolar disorder is diagnosed more often in Caucasians and underdiagnosed in African Americans. The disparities in the diagnosis of schizophrenia based on race are reversed. People of color are diagnosed with schizophrenia at a disproportionately higher rate than Caucasian populations (Schwarz & Blankenship, 2014). More specifically, African Americans are 4 times as likely to receive a diagnosis of schizophrenia than Caucasians (Schwarz & Blankenship, 2014). These results are evident even after controlling for demographics and drug use. Additionally, disparities are still seen when a diagnostic interview is highly structured using standardized criteria (Akinhanmi et al., 2018). Numerous studies over many years are consistent in showing this trend (Barnes, 2008).

Numerous researchers have drawn a connection between the overdiagnosis of schizophrenia and underdiagnosis of bipolar in African Americans. Mukherjee, Shukla, Woodle, Rosen, and Olarte (1983) was the first to identify that ethnicity is statistically significantly associated with misdiagnosis of bipolar as schizophrenia. In particular, African Americans with bipolar were at the highest risk for misdiagnosed as schizophrenic if they were young and reported hallucinations during a manic episode (Mukherjee et al., 1983). Newer studies have found that these disparities still exist today. Akinhanmi et al., (2018) found that African Americans are misdiagnosed with schizophrenia even when they have no clinical history of psychosis. These researchers have all pointed to the fact that the underdiagnosis of mood disorders and overdiagnosis of schizophrenia in African American populations is caused by a connection of misdiagnosis between the two disorders.

Many researchers who have recognized the disparities have postulated why the disparities are seen. There is the idea that the disparities are true, however, there is an absence of genetic evidence that would indicate a greater prevalence of schizophrenia in African Americans (Perlman, Kotov, Fu, Bromet, Fochtmann, & Medeiros, 2016). There is also a lack of differences in positive and negative symptoms severity between Caucasian and African American patients (Akinhanmi, Biernacka, & Strakowski, 2018). These results indicate that the disparities are not likely attributable to biology. Perlman et al. (2016) suggested that social and economic variables that are correlated with race may contribute to risk for psychosis although this issue has not yet been supported by the literature. There is not much evidence to suggest that the disparities seen reflect a true difference in prevalence.

If the differences are not true, they must be caused by an actual misdiagnosis. One study postulated that mania may be misdiagnosed as a psychotic episode due to the delay in treatment. As a manic episode progresses untreated, euphoria decreases and the risk of psychosis increases. This indicates that perhaps African Americans with who delay seeking treatment more than Caucasians with the disorder may be more likely to present with symptoms that look psychotic and thus are misdiagnosed (Akinhanmi et al., 2018). An alternative explanation is that mental disorder diagnoses are influenced by personal perceptions and stereotypes. Although bias or misinterpretation may be an unconscious process, it is causing stark differences in diagnostic rates (Schwarz & Blankenship, 2014). There are unremarkable differences in symptoms across racial groups, so the same symptoms are likely causing different clinical interpretations due to the race of patient (Akinhanmi, Biernacka, & Strakowski, 2018). Perlman et al. (2016) used methods to assess racial bias and found it to be present in the assessment of psychosis in different racial groups.

This issue is very significant because a misdiagnosis can have severe consequences. Lasting negative effects that are associated with misidentification of one disorder for another include an inaccurate health record, complications with insurance, and even death (Schwarz & Blankenship, 2014). This is caused by the fact that misdiagnosis impedes treatment and has many negative consequences. First, misdiagnosis delays the application of the effective treatment because patients may not have the most effective treatment if they didn’t even have the correct diagnosis. Second, there may be adverse consequences of applying an inappropriate treatment. For instance, treatment with inappropriate medications may be detrimental to a patient (Barnes, 2008). Now that these disparities have been identified, more research is needed to determine their underlying cause so that they may be resolved to ensure that everyone receives the same level of care.

References

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Barnes, A. (2008). Race and hospital diagnoses of schizophrenia and mood disorders. Social Work, 53(1), 77–83. https://doi.org/10.1093/sw/53.... Schizophrenia Consortium. (2009). Common polygenic variation contributes to risk of schizophrenia and bipolar disorder, Nature, 42(6), 748. https://doi.org/10.1038/nature...

Mukherjee, S., Shukla, S., Woodle, J., Rosen, A.M., & Olarte, S. (1983). Misdiagnosis of schizophrenia in bipolar patients: A multiethnic comparison. The American Journal of Psychiatry, 140(12), 1571-1574. http://dx.doi.org/10.1176/ajp.140.12.1571

Nolen-Hoeksema, S., & Marroquín, B. (2017). Abnormal psychology (7th ed.). New York, NY: McGraw Hill Education.

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