Neurocognitive Testing of Patients with Schizophrenia - Why?

Doctor psychol Merete Øie, Child and Adolescent Psychiatry Clinic, Oppland Central Hospital, Lillehammer, Norway

Introduction

After nearly a century of research it has been firmly established that neurocognitive deficits are a core feature of schizophrenia. Patients with schizophrenia show deficits in areas such as memory, attention and executive functions (Green, 1998). Waldo and colleges (1994) claim that 94% of patients with schizophrenia have neurocognitive deficits compared to non psychiatric controls. However, if you ask someone treating people with schizophrenia what the disorder is, the answer will often take the form of a listing of psychotic symptoms.

Sometimes the answer will be more comprehensive and will include a brief description of negative symptoms. But rarely will neurocognitive deficits be mentioned. Compared to psychotic symptoms, neurocognitive deficits are not as noticeable, not as odd, and they are not part of any formal diagnostic system. But, the deficits are still there and have a great impact on the subject's life.

In actively psychotic phases patients are often hospitalised. When the positive symptoms such as delusions, hallucinations and thought disorders are under control, the patients are often sent home. However, a majority of patients experience relapses. There could be many explanations for this, but one important issue is that although neuroleptics have an impact on symptoms, they do not appear to enhance neurocognition. However, functional outcome appears to be more closely related to neurocognitive abilities than symptoms.

The research of Michael Green (1998) and others has shown that verbal memory, executive functioning and visual vigilance predicts functional outcome in schizophrenia.

While it has been established that adults with chronic schizophrenia demonstrate cognitive deficits, little effort has been directed at examining cognitive functioning in adolescents with schizophrenia. There has been an increasing interest in cognitive training for patients with schizophrenia the past years, and currently such a cognitive training program is being undertaken at the Center for Child and Adolescent Psychiatry in Oslo. If cognitive training is to be employed in adolescents with schizophrenia, it has to be clear in which cognitive area they have deficits. In this presentation I will present data to answer the this question.

Methods

In a study at the National Centre for Child and Adolescent Psychiatry in Oslo 19 adolescents with a DSM-III-R diagnosis of a schizophrenia (five females and 14 males) and 30 healthy controls (14 females and 16 males) were included (Øie & Rund, 1999; Øie et al., 1999). The groups were compared on a comprehensive neurocognitive testbattery consisting of 13 separate tests. The subjects were between 12 and 18 years old. Most of the patients were drug naive.

Results

Consistent with previous neuropsychological studies of patients with chronic schizophrenia (Goldberg et al., 1987; McKenna et
al., 1990; Saykin et al., 1994), our group of adolescents with schizophrenia demonstrated impairments compared to normals on executive functions, visual memory, verbal memory and psychomotor function. Thus, the present results show that these cognitive dysfunction's are also apparent early in the course of schizophrenia. The adolescents with schizophrenia did not perform impaired compared to the normal group on a measure of auditory selective attention and auditory laterality (Dichotic Listening Test) and vigilance (Degraded Stimulus-Continuous Performance Test) (Øie et al., 1998).

Discussion

Impairments on auditory selective attention and auditory laterality and vigilance have frequently been observed in adults with schizophrenia (Green et al., 1994; Nuechterlein et al., 1994). A hypothesis based on the present results is that the deficits observed in patients with chronic schizophrenia using these tests, are a result of having schizophrenia for many years. The adolescent patients in the present study were in an early phase of the illness when psychosis had not yet become established. Further, they were mostly neuroleptic naive and had been hospitalised only for a short period. Thus, it is possible that results from studies with more chronic patients demonstrate the effect of neuroleptic medication and hospitalisation.

It has been proposed that schizophrenia is a neurodevelopmental disorder in which a fixed brain lesion from early in life remains relatively quiet until early adulthood when the normal maturation of certain brain structures occurs (Weinberger, 1987). Thus, it could be possible that the deficits in selective attention, vigilance and in left hemisphere functioning are apparent only after such neurodevelopmental changes in adolescence. MRI research may clarify if there is a different pathophysiology between adult onset and adolescent onset schizophrenia.
Further, longitudinal studies of adolescents with schizophrenia may clarify if the deficits seen in adults with schizophrenia will be apparent later in the illness process.

Conclusion

Neurocognitive deficits are a core feature of schizophrenia and are predictors of course and outcome. The fact that deviance in cognitive functioning is a core deficit in schizophrenia and that the impairment has a strong influence on patients social functioning in the community makes them an appropriate target for treatment and rehabilitation. Although there has been an increasing interest in cognitive training the past years, neuropsychological examinations are seldom included in the patients assessment.

In the future cognitive function should be taken into consideration when planning the patients rehabilitation program. More specifically cognitive training programmes may be valuable for this patient group. Those functions which are most affected and influence the persons social functioning should be emphasised. For adult patients this includes areas such as verbal memory, executive functioning and vigilance. In adolescents visual and verbal memory as well as executive functioning appears to be dysfunctional and should be emphasised in cognitive training programmes.

References

• Goldberg TE, Weinberger DR, Berman KF, Pliskin NH, Podd MH. Further evidence for dementia of the prefrontal type in schizophrenia? Archives of General Psychiatry 1987;44:1008-1014.
  
• Green MF. Schizophrenia from a Neurocognitive Perspective: Probing the Impenetrable Darkness. Boston: Allyn and Bacon, 1998.
  
• Green MF, Hugdahl K, Mitchell S. Dichotic listening during auditory hallucinations in patients with schizophrenia. American Journal of Psychiatry 1994; 151:357-362.
  
• McKenna PJ, Tamlyn D, Lund CE, Mortime AM, Hammond S, Baddeley AD. Amnestic syndrome in schizophrenia. Psychological Medicine 1990; 20: 967-972.
  
• Nuechterlein KH, Buchbaum MS, Dawson ME. Neuropsychological vulnerability to schizophrenia. In AS David JC Cutting (Eds.), The Neuropsychologia of Schizophrenia (pp.53-77).Hillsdale:Laurence Erlbaum, 1994.
  
• Saykin AJ, Shtasel DL, Gur RE, Kester DB, Mozley LH, Stafiniak P, Gur RC. Neuropsychological deficits in neuroleptic naive patients with first episode schizophrenia. Archives of General Psychiatry 1994;51:124-131.
  
• Waldo MC, Cawthra E, Adler LE, Dubster S, Staunton M, Nagamoto H, et.al. Auditory seneory gating, hippocampal volume, and catecholamine metabolism in schizophrenics and their siblings. Schizophrenia Research 1994;12:93-106.
  
• Weinberger DR. Implications of normal brain development of the pathogenesis of schizophrenia. Archives of General Psychiatry 1987; 44:660-669.
  
• Øie, M., and Rund, B.R. Neuropsychological deficits in adolescent-onset schizophrenia compared with attention deficit hyperactivity disorder. American Journal of Psychiatry 1999; 156:1216-1222.
  
• Øie, M., Rund, B.R., Sundet, K., Bryhn, G. (1998). Auditory laterality and selective attention: Normal performance in patients with early-onset schizophrenia.
  
• Schizophrenia Bulletin 1998; 24:643-652.
  
• Øie, M., Sundet, K., Rund, B.R. (1999) Contrast in memory functions between adolescents with schizophrenia or ADHD. Neuropsychologia 1999;1351-1358.

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