Discussing Psychiatric Comorbidities and Treatment Options for Schizophrenia

In Part 1 of this video, Heather Flint, senior digital managing editor, Psych Congress Network, sits down with Psych Congress Steering Committee Member Craig Chepke, MD, FAPA, Medical Director, Excel Psychiatric Associates, Huntersville, NC, to discuss psychiatric comorbidities in schizophrenia, adverse events in medication, and the potential for future treatments.

In the upcoming Part 2, Dr Chepke discusses challenges in treating patients with schizophrenia. 

Read the Transcript:

Heather Flint:  Hello, Psych Congress Network. I am thrilled to be here today interviewing Dr. Craig Chepke. Dr. Chepke, can you please introduce yourself?

Dr. Chepke:  Sure thing. Thanks for having me here, Heather. My name is Dr. Craig Chepke. I'm a psychiatrist in Charlotte, North Carolina. As an adjunct faculty appointments with universities and I'm also a steering committee member of Psych Congress.

Heather:  Excellent. Dr. Chepke is going to join us today to talk about schizophrenia and talk about his sessions that he's been presenting at Psych Congress. What are the most common psychiatric comorbidities seen with schizophrenia?

Dr. Chepke:  Schizophrenia is such a complex in and of itself, but it does have a lot of comorbidities as well. The top three statistically are found to be substance-use disorders, anxiety, and depression.

That makes complex disorder even more complex, unfortunately. We have to consider the treatment of those comorbidities when treating people with schizophrenia.

Heather:  Can you briefly describe some medication-related adverse events for patients with schizophrenia?

Dr. Chepke:  Sure. Unfortunately, there's far too many. In terms of EPS, it's actually a term that I really can't stand. Extrapyramidal symptoms is a term only used by psychiatrists. Neurologists don't like that term because it's very vague and generic. Anything that is extrapyramidal is anything other than the voluntary movement that the body has.

I would actually prefer that all of us in psychiatry call it acute motor side effects if we have to but being more specific. The specific ones would be akathisia, an inner sense or restlessness. The person feels they have to keep moving. Dystonia, a sustained muscle contraction or Parkinsonism where like Parkinsons disease, there's a slowness and stiffness of the movement.

Those are some of the common acute motor side effects. Later on, in the treatment of dopamine-blocking antipsychotics, there can be tardive dyskinesia that can occur months to years after treatment with the dopamine-blocking antipsychotics or other dopamine-blocking meds as well.

That is a permanent situation that the patient gets into where they have extra involuntary movements. In addition to the neurologic side effects, there's endocrine side effects. Prolactin levels can be increased by antipsychotics. Diabetes can occur or other hyperglycemia, but metabolic consequences as well on top of the potential for diabetes.

Hyperlipidemia, hypertension, weight gain. There's a tremendous amount of potential side effects and these are powerful medications. They can be powerful in terms of their efficacy, but, unfortunately, also powerful in terms of their propensity to cause adverse reactions.

Heather:  In your session, you talked about TAAR1. Can you tell us how that has impacted the treatment of schizophrenia?

Dr. Chepke:  So far, it's not impacted it yet because there's still only in investigation products. There is one TAAR antagonist that is in Phase 3 clinical trials, but that still can be several years off. It is incredibly exciting for me though.

The TAAR1 mechanism has been only discovered in the past few decades. It's been around as long as humans have been around, but we had no knowledge of it. The TAAR stands for Trace Amino-Associated Receptor.

As you can guess from the name trace, they are found in very small quantities in the body, much lower than any of the traditional neurotransmitters like dopamine, serotonin, norepinephrine, etc. They were at such small levels, we really couldn’t detect them or detect their significance especially because they're intracellular.

It's a lot easier to find receptors that are on the outside of a neuron than inside of a neuron. They've been there probably having some significant effects on pathophysiology and treatment of the disease. We've been completely oblivious to it.

With the advance in technology, we've been able to find these receptors and develop medications that can modulate them. TAAR1 is able to, when bound by an agonist, form a dimer that it comes together with a dopamine receptor. It modulates the way that dopamine receptor acts both presynaptically and postsynaptically.

Both sides of the neuron, it can affect the process of psychosis. It's really exciting. The agonist that they've add preclinically and now in clinical trials have shown early signs of antipsychotic activity. Most importantly, possibly, the adverse event profile is stunningly different.

There's not any motor side effects seen. There was not weight gain seen. There was not any problem with the endocrine system like the prolactin as well. It almost feels too good to be true that it can have good efficacy on par with the current antipsychotics that we have and potentially, without a lot of the adverse reactions that people with schizophrenia suffer with many of these drugs.

Of course, it's yet to be seen, is it going to play out over the Phase 3 clinical trial program. The Phase 2 was very promising and encouraging, but you never want to put too much hope on something until it's replicated in those large scale Phase 3 trials.