Dr. Ikwunga Wonodi: "If you can break down barriers of stigma, then more people will seek care." (Provided photo)

Long before I moved to Baltimore and became a writer, I was a social worker in New York City. I worked primarily with clients with severe and persistent mental illnesses, such as schizophrenia.

Back in those years, from 1985 to1996, a diagnosis of schizophrenia was absolutely devastating. Most of my clients were poor and unable to hold down a job. Many were homeless, and the majority were addicted to or abusing substances such as alcohol and crack cocaine. The prognosis for these clients was bleak.

Recently, I spoke with Dr. Ikwunga Wonodi, service chief of the Thought Disorders Day Hospital at Sheppard Pratt’s Baltimore/Washington Campus in Elkridge, to learn about new outcomes and innovations in the treatment of schizophrenia.

There are still a lot of misconceptions about schizophrenia. Many people believe schizophrenia means having split personality. Can you explain what the diagnosis means?

Dr. Wonodi: Schizophrenia is not split personality. The term was coined in 1908 by Eugen Bleuler, a renowned Swiss psychiatrist and humanist. I think the fact that schizophrenia, when translated into Greek, means ‘split mind’ somehow has gotten into popular culture.

But what Eugen Bleuler was referring to in introducing that term was a split of the mind from reality. The schizophrenias are a heterogeneous group of brain diseases that typically hit in the late teens and early 20s. They are characterized by fixed, false delusions or beliefs; hallucinations, typically auditory but [sometimes] other types of hallucinations; and disorganized speech and behaviors that are driven by thought disorders.

In schizophrenia, we speak about positive and negative symptom domains. The positive ones would be delusions, hallucinations, thought disorder and bizarre behavior. And the negative are symptoms like blunted affect [diminished emotional expression], a reduction in quantity of words, not being social and anhedonia [the inability to experience pleasure].

This is a severe mental illness, and it’s as costly as cancer. But whereas cancer costs are driven by the cost of treatment, the costs in schizophrenia are driven by lost productivity [because of] an illness that hits early and is chronic. There’s really no cure.

What are the current theories about why people become schizophrenic?

Schizophrenia is a complex syndrome that is multifactorial and highly genetic. Twin studies have shown a heritability of 50-80%, and there have been multiple risk genes identified.

But it’s also substantially environmental. So there’s an interplay with many genes of small effect interacting with environmental factors, and things that have been identified environmentally like season of birth — late winter, early spring, rainy season, December to March.

Another hypothesis is viral infections during pregnancy have a role to play in people going on to develop schizophrenia. We’ve listed influenza, cytomegalovirus, Toxoplasma, gondii — any of these that the mother gets infected with in the first and second trimester results in increased chance of the child having schizophrenia. Obstetric complications and advanced maternal age are also factors.

There are lots of family studies that were done and shown that a certain type of communication in the family called high expressed emotions [can cause children to develop schizophrenia]. Other [factors include] immigration status. If immigrants are dispersed, they’re more vulnerable, but if you immigrate into Chinatown and you’re Chinese or Little Italy and you’re Italian, then there’s less stress [and you’re less vulnerable to schizophrenia]. Those who live in urban environments with high stress [are also more vulnerable].

What about medications?

In the 1950s there was a serendipitous discovery of the anti-psychotic benefit of chlorpromazine [aka Thorazine]. Thorazine was being used as an anesthetic agent, and the surgeons found out that people who had psychosis when they came out from surgery had also improvement in the psychosis. The theory that followed was that the effect of Thorazine was driven by blockade of dopamine receptors. We classify Thorazine, Haldol and Prolixin as first-generation antipsychotic medications. And they’re quite effective.

Then came the second-generation antipsychotics — Abilify, Zyprexa, Invega, Risperdal. They have the advantage because they have a reduced liability to cause tardive dyskinesia [a movement disorder], though we now have effective treatments for tardive dyskinesia as well. Back in the day, it was only after significant chronicity that individuals would be offered long-acting injections like Haldol and Prolixin. Haldol was monthly; Prolixin was biweekly. Now we’ve learned that you can put people on long-acting injections early on.

What big pharma has done — which is helpful — is they’re creating long-acting injectables with widening intervals. So if someone was on Invega, which is a metabolite of risperidone, so to speak, first you put them on Invega Cisterna, which is monthly. After two or three months, you could move them to Invega Trenza, which is every three months. And then if they tolerated it for six months, you can convert them to Invega Javiera, which is six months. Imagine just two shots a year!

Other than drug treatments, are there any other innovations?

There are the psychotherapies. There’s individual therapy, which is usually supportive, cognitive behavioral therapy and a new one called cognitive enhancement therapy, also called cognitive remediation, which combines computer-based brain training and group sessions.

It’s training on social cues because people with schizophrenia have difficulty deciphering emotions and emotional expression, and that affects their functioning in social settings. There are also psychosocial therapies — you know, social skills training, rehabilitation, and then other psychosocial interventions like community support services.

If you come into a system like Sheppard Pratt, you see how it’s set up [to serve] highly acute patients in the inpatient unit here, [less acutely ill patients] in day hospitals and [more stable patients] in outpatient settings. [Another critical service is] getting people into supportive housing, community and case management services, supportive employment. We have to get insurance companies to understand that it costs less when you have this continuum of care.

What is the overall prognostic outlook for schizophrenia these days?

The first thing we use to prognosticate for the schizophrenias is previous functioning. How were they doing academically? How social were they? Were they married? When was their first psychotic break? We can use pre-morbid functioning to prognosticate on who does well.

[Prognosis is] better than it was 10, 20, 30 years ago because there are more treatment options that are more tolerable. Folks like NAMI [National Alliance for the Mentally Ill] and SAMHSA [Substance Abuse and Mental Health Services Administration] are out there every day breaking down barriers of stigma. If you can break down barriers of stigma, then more people will seek care.

Is it true that the fewer psychotic breaks, the better prognosis?

Yes, and that’s something that’s changed — how quickly we offer long acting injectables. Now we can do it even after the first break. If we do it after the first break and get this 19-year-old [for example] on a medication that is taken every three months [the prognosis is better]. Every six months he stays out of the hospital, there’s less deterioration in functioning.

What do you see as the future of treatment for people with schizophrenia?

I spoke about computer brain training for social skills and emotional intelligence already. We also need cognitive remediation through pharmacology. We’re looking for [medications that] target cognition – the functions we use to process information — because it’s the most predictive symptom that determines functional outcome. The medications we have right now, they treat the psychosis, the delusions, hallucinations, thought disorder but not the cognitive deficits.

When people have their first psychotic breaks [in young adulthood] when they’re in college, [medication that targets cognition] could make it possible for them to finish college and go on to have a career.

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