Tools for Assessing Cognition in Patients With Schizophrenia

Leslie Citrome, MD, MPH, clinical professor of psychiatry and behavioral sciences at New York Medical College, Valhalla, New York, discusses cognition in schizophrenia. Dr Citrome breaks down the regions of the brain responsible for symptoms and tools for assessing cognition.

Dr Citrome also reviews the the Personal and Social Performance Scale (PSP) and the MATRICS Consensus Cognitive Battery (MCCB).

In the upcoming parts 2 and 3, Dr Citrome examines the severity of functional deficits in schizophrenia, medical benefits, and neurobiological targets.

Read the transcript:

Hello, I'm Dr Leslie Citrome, clinical professor of psychiatry and behavioral sciences at New York Medical College in Valhalla, New York. Today, we're going to talk about cognition in schizophrenia.

Cognition in schizophrenia has gotten a lot of attention these days, specifically because we're on the cusp of doing something about it. Let's talk about what we mean by cognition. First, let me put it into perspective.

We've known for quite some time about the positive symptoms of schizophrenia, such as delusions and hallucinations, and the negative symptoms of schizophrenia, such as the lack of motivation, lack of interest, and difficulty in expressing emotion.

We've also learned to acknowledge the existence of cognitive dysfunction. Problems, for example, with verbal fluency, with paying attention, with problem-solving. At the same time, we've also paid more attention to the effective symptoms of schizophrenia. These overlap somewhat with negative symptoms.

It turns out that there are different regions of the brain that might be explanatory for all these different symptoms. We think about the ventral striatum, or the psychiatrist's striatum, as the source of positive symptoms of delusions and hallucinations.

It is really the dorsolateral prefrontal cortex that is the source of problems with cognitive dysfunction, and the ventral medial prefrontal cortex, which is the source of problems with effective symptoms. Different sets of symptoms originate in different parts of the brain.

With the dorsolateral prefrontal cortex, we need to better understand those neurotransmitters that perhaps affect cognitive function. That can include norepinephrine, acetylcholine, serotonin, dysbindin—by the way, has also been looked at, and neuregulin is another different neurotransmitter that has been looked at, not as well known as the monoamines or acetylcholine—and of course, dopamine.

Now, I mention dopamine because dopamine seems to be the final common pathway to many kinds of symptoms, but as we shall see, not all dopamine receptors are the same.

Now, cognitive impairment is quite common. It can be encountered in about 85% of people with schizophrenia, and this has been demonstrated in a number of different studies. Cognitive impairment occurs in first episode and chronic schizophrenia.

We can observe that people with schizophrenia have a lower degree of cognitive abilities, relative to the general population, right from the beginning. One to two, to three standard deviations different from the general population.

This can be apparent at the very first episode. In fact, can predate the first episode of psychosis. People who are in the prodrome, or even in their childhood or adolescent, can exhibit some

Now, the course of cognitive impairment with schizophrenia can worsen, improve slightly, or stay the same. Even we those who improve, they don't quite reach the level generally observed with the people who are unafflicted with schizophrenia.

How do we assess cognition? It's actually challenging. Cognition in clinical trials with schizophrenia can be formally assessed using neuropsychological testing. The standard today is to use a battery of tests called the MATRICS Consensus Cognitive Battery or MCCB.

The MCCB consists of 10 tests designed to evaluate performance across seven different domains. These include speed of processing, attention or vigilance, working memory, verbal learning, visual learning, reasoning and problem-solving, and social cognition.

At present, there is no clinician-friendly bedside tests that can be easily and quickly administered to assess cognition, other than gross measures of cognitive ability, such as the Mini-Mental State Examination.

Something we do all the time in a mental status examination, such as ask patients to remember three words and to repeat them at 5 minutes, or to spell “world” forwards and backwards, or to do some simple calculations, such as serial sevens. Like 100 minus 7, and then keep on subtracting 7, or 40, took away 4, keep on subtracting 4. We do this as a substitute. It's a very gross measure, but it's surprising how often you do pick up some deficits that way, too.

Cognitive deficits do predict functional outcomes. If we can measure impairments in learning and memory, executive function, and attention, that correlates with school and occupational function, social function, and activities of daily living.

Measuring cognition actually has a purpose. It helps us predict how well someone will function. Now, there are various scales to assess functioning, and I'm going to describe a couple of them for you.

The PSP, the Personal and Social Performance Scale is one that has been around for a long time. Functional impairment is probably more clinically relevant than focusing exclusively on psychopathology or on the results of cognitive testing alone. This allows us to get a sense of how someone is doing in the real world.

Now, the research tools that are available include this personal and social performance scale. I'm going to also talk about another one called the University of California and San Diego Performance-Based Skills Assessment or UPBSA, but let's talk about the PSP first.

It's been used as a prespecified secondary outcome measure for several agents that have gone through FDA approval. We'll see the PSP actually in product labeling. It's described as such.

What does it measure? It actually measures socially useful activities, including work and study, personal and social relationships, self-care, as well as disturbing and aggressive behaviors.

We actually have information about functioning already available for several agents that we use every day, but perhaps a better approach would be the UPBSA. The UPBSA is a performance-based scale with 5 domains of functioning.

Here, patients are assessed regarding household chores, communication, finance, transportation, and planning recreational activities. All these things we take for granted for ourselves, we need to actually measure how well our patients can do.

The administration of the UPBSA takes about 30 minutes. It's currently only a research tool. It does correlate with the severity of negative symptoms and cognitive impairment, but not with positive or depressive symptoms.

This is actually quite interesting. This means that the existence of positive symptoms may not necessarily impair functioning, but impairment of cognition can lead to impairment in functioning, as well as negative symptoms can impair functioning.

Hallucinations and delusions by themselves aren't going to be the determinants whether someone can work or have social relationships. It's going to be negative symptoms and cognitive impairment.

Studies have been done correlating various aspects of cognition, such as recall memory, and success in employment in a rehabilitation program, for example. This has been done numerous times. Every time it's done, we can see this relationship.

The functional importance of cognition in schizophrenia basically is that, let me repeat, control of positive symptoms alone does not necessarily lead to good outcomes, and improving cognitive symptoms does lead to better outcomes.