Auditory event related potentials in schizophrenic patients
The use of P3 as a diagnostic marker for schizophrenia was examined in a qualitative and quantitative review of the literature, as well as with an auditory discrimination task involving 21 schizophrenics, 16 patients with idiopathic Parkinson's disease and 50 matched controls. Although some studies have reported a lack of significant group differences between schizophrenics (or Parkinson's disease) and controls, both the quantitative reviews and the experimental studies suggest that this is probably due to a type 2 error. The band pass employed in experimental studies modifies results in that high pass filters with high frequency cut-off are usually associated with a greater effect size. This hypothesis was confirmed by meta-analytic techniques, by filtering of wave forms with analogue and digital filters, and can be modelled by simple compound sine-wave forms. Such a simple model for wave forms observed in schizophrenics involves the reduction of a low frequency (slow) wave, super-imposed with a higher frequency sine wave. Neither the putative genetic marker impaired smooth eye pursuit, nor a positive family history of psychiatric illness were associated with abnormal P3 in schizophrenics. In controls, abnormal P3 was associated with a positive family history. In Parkinsonian patients P3 latency was correlated with clinical markers of dopaminergic hypofunction like rigidity and bradykinesia. This is in agreement with more recent studies suggesting that delayed P3 in Parkinson's disease normalises with treatment with L-DOPE. In the absence of accurate clinical markers of dopaminergic activity in schizophrenics, no direct comparisons have been made. The role of dopaminergic alterations in the generation of P3 changes in schizophrenics can be examined with in-vivo imaging of receptor binding.