Cognitive Impairments in Schizophrenia

Cognition in schizophrenia is not fixed, and describing its time course requires a developmental or life-span perspective [4]. Importantly, cognitive impairment associated with schizophrenia (CIAS) is present before the onset of psychosis, possibly starting during puberty [5] and clearly detectable in prodromal patients and in young people at high-risk for psychosis [6]. Although there might be some worsening around the time of the first episode of psychosis, the deficits plateau after the initial episode and remain stable throughout life until the effects of aging worsen cognition. In other words, the cognitive damage is done once patients present with psychosis. There is no progressive worsening of cognition in established schizophrenia, and in that sense, schizophrenia is not a classic neurodegenerative disorder [7]. Current research efforts attempt to better characterize the varied trajectories and etiologies of abnormal brain development (including putative “toxic” effects of untreated psychosis and medication effects) with the hope to intervene early enough to get abnormally developing brains “back on track” and perhaps prevent the development of schizophrenia, among other neurodevelopmental disorders completely [8].

Even those patients who are unimpaired on testing around the time of their first episode of psychosis probably have an illness-related decrement in their cognitive function, including a decrease in their premorbid IQ [10]. In one study, declining scholastic test scores between the 8th and 11th grade were seen in those adolescent students who later developed schizophrenia [11], consistent with major illness-related brain changes during adolescence. On neuropsychological testing in established schizophrenia, the pattern of impairment is described as both generalized (performance is impaired on a wide variety of tests) and specific (there is a typical pattern of impairment, with some areas more impaired than others) [12]. The biggest impairments are seen in the areas of attention (such as sustained attention or vigilance), verbal learning and memory, and executive function. In these key areas of cognition, patients show impairments between 1 and 1½ and 2 standard deviations below healthy controls. Reasoning, problem-solving, and speed of information processing are other cognitive domains that are usually impaired. Social cognition which encompasses face recognition, emotional processing, and theory of mind, among others [13], is increasingly recognized as an area of functionally highly relevant deficit [14]. Reading social clues like other people’s emotions and intentions and navigating ambiguous and complex social environments are key functions of our social brain that patients with schizophrenia have great difficulties with [15].

A simplified neuroanatomical model of cognition in schizophrenia suggests that almost all patients have some problems with basic memory and learning (temporal-hippocampal system), coupled with executive dysfunction (prefrontal systems). The prefrontal dysfunction, in particular, prevents the use of organizational strategies to learn new material, which is necessary for effective learning. In Alzheimer’s disease, the memory problem is rather basic (the memory stores themselves are degraded); in schizophrenia, some aspects of the memory problem are at a higher level (where strategies and flexibility are needed for better access of memory stores). The cognitive problems of schizophrenia are unlike those of Alzheimer’s dementia or of typical “brain damage” in that the disease is neither progressive nor can the dysfunction be easily localized to one particular brain area, respectively. It is therefore better think of impaired function (e.g., executive dysfunction) as opposed to impaired regions (e.g. frontal lobe dysfunction).

Behavioral disinhibition is another example of a failure of the complex interplay between different brain regions, in this case of a failure of top-down cognitive control. Usually, the prefrontal cortex functions as a break “from above” on other, “lower” brain systems [16] and prevents automatic responses to irrelevant stimuli. This function can be impressively impaired in a subgroup of patients; such patients might have a low frustration tolerance, are impulsive, and act without foresight or regard for social convention. They can display stimulus-bound responses, including broadly inappropriate reactions to the interviewer. They can be quite endearing in their honesty (“Doc, you need a haircut”) and immediacy (“Hey Doc, going home to your wife,” shouted across the subway platform after spotting me) because they lack the brakes (and social wisdom) that prevent most of us from saying what comes to mind without some censorship.

The manifold, widespread, and varied cognitive difficulties seen in schizophrenia patients seem to be the result of a failure of the coordinated activity between distributed brain regions (brain networks) and not the result of a nonfunctioning brain modules with a specific function (e.g., a stroke taking out Broca’s area). (This is not to say that a failure in a critical brain region like the thalamus could not result in widespread network disruptions [17].) In such a network model, the exact clinical expression of connectivity abnormalities would depend on which networks are affected, how severely out-of-sync the circuits are, and how much the impaired brain can compensate. Often, the cognitive impairment in schizophrenia only becomes apparent when the brain is sufficiently challenged (cognitively overtaxed) as compensatory mechanisms cover up what can be viewed as reduced brain efficiency as opposed to frank deficits. Sometimes, superimposed traditional “brain damage” (e.g., a head injury) further complicates the clinical picture.

Clinical Assessment

It should have become clear that any examination of a patient with schizophrenia is incomplete if you assess only positive and negative symptoms: you must also assess cognition. I stress this because, as noted earlier, cognition (despite being a core feature of the illness) is not included in current diagnostic criteria as a specific and explicit diagnostic criterion and might be overlooked, particularly because the deficits can be rather subtle and overshadowed by more obvious positive or negative symptoms.

You should also know that the relationship between symptoms and cognition is not strong. Although there is some connection between negative symptoms and cognition (those with significant negative symptoms tend to have worse cognition), the correlation is rather weak (r = 0.13–0.27 in the Clinical Antipsychotic Trials of Intervention Effectiveness [CATIE] baseline data) [19]. Positive symptoms have essentially no correlation with cognition. In other words, you cannot really judge the severity of cognitive problems from the severity of clinical symptoms.

Unfortunately, such a standardized and comprehensive assessment of cognition is time-consuming and not easy as some areas of cognition require a computer or other equipment (and many tests are copyrighted). For some key domains (e.g., social cognition), no easy-to-use bedside tests is clinically available. Even shorter assessment batteries like the Brief Assessment of Cognition in Schizophrenia (BACS) [22] take too long (the BACS takes 30 minutes) to be incorporated in routine clinical visits. (Do not forget, however, that you could always spread out your cognitive assessment: there is no need to complete everything in one visit.) Performance-based measures of functional capacity to better explain a patient’s disability add additional assessment complexity [23], including who to obtain reliable information from.

I suggest that you get your hands on some of the tests used in the various cognitive batteries to look at the principle behind them and then create your own poor man’s versions of them. For example, look at the Hopkins Verbal learning Test (HVLT) and then create your own word list – you will need 12 words from 3 taxonomic categories – give a patient 3 trials to learn the list, and see how the patient organizes learning.

For a bedside assessment of cognition, I suggest you examine the following key areas of cognition:

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  Assess sustained attention/vigilance – Hard to test without a computer but a fundamental problem in schizophrenia; I use the digit span forward to make sure basic attention is okay.

  
  
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  Assess working memory – Digit span backward and Trails B.

  
  
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  Assess verbal learning and memory – Have patient learn a word list (e.g., based on HVLT, as mentioned above); look for poor memorization strategies that ignore semantic relationships, not absolute performance.

  
  
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  Assess frontal lobe functions – This is a very important area to examine. At a minimum, have patient draw a clock [25]. Table 29.2 presents other screening tests that you could use.

  
  
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  Estimate processing speed – Trails A.

  
  
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  The digit symbol substitution test (DSST) is an excellent screening test for cognitive difficulties that stem from deficits in multiple domains which is typical for schizophrenia [26] – The DSST is a highly sensitive but not specific measure for the efficiency of brain function (processing speed) that relies on the intactness of several related systems, including working memory [27].

  
  
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  Complete the Mini-Mental State Examination (MMSE) – Note that the MMSE is not sufficient to assess cognition in patients with schizophrenia per se. A normal MMSE is useful information, as are the items on the MMSE that pose problems for the patient.

  
  
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  If you have the time, substitute the Montreal Cognitive Assessment (MoCA) for the MMSE – The MoCA is more involved than the MMSE but covers more areas, including some tests of frontal lobe function, and correlates well with specific tests that assess cognition in schizophrenia [28]. Drawing a clock is included in the MoCA.

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