Language functions in schizophrenia and N400 [Şizofrenide dil i?şlevleri ve N400]

Abstract

One of the most prominent clinical features of schizophrenia is impaired language function. Clinical studies of schizophrenia have identified poverty of content, tangentiality, distractable speech, derailment, and incoherence as features of schizophrenic language. Cognitive deficits have long been considered to be a central feature of schizophrenia. Bleuler and Kraepelin both noted that cognitive deficits are often most readily apparent in the speech of schizophrenic individuals. The tendency to produce loose and irrevelant associations has been linked recently to dysfunctional processes in lexical memory. Thought-disordered (TD) schizophrenia patients have been showed a priming effect superior to those of normal controls and non-TD patients. It has been considered that language dysfunction in schizophrenia is mediated by overactivation of semantic networks (hyperpriming). Schizophrenic patients typically showed less accurate and slower recognition of target words than normal controls. Schizophrenic patients are unable to take full advantage of contextual information in determining the meaning of target words. Many of the abnormal priming effects in schizophrenia can be explained by either an increase in activation (to loosely related words) or a decrease in inhibition (to unrelated words). One particularly interesting component of event-related potentials is the N400, a negative potential occurring approximately 400 msec poststimulus, elicited by semantically anomalous or unexpected words in a sentence. Data suggest that the N400 reflects aspects of a brain search through the lexicon, as part of the process of recognizing the meaning of a word. The less frequent a word was in the lexicon and nonsensical sentence endings, the larger the N400 it evoked. While only a relatively small number of N400 studies of schizophrenic patients have been performed, these studies have shown abnormal N400 amplitude and a disease-related delay in a N400 latency, suggestive of slow semantic processing. The precise neurobiological mechanisms underlying these N400 abnormalities in schizophrenia are unknown. Prolonged N400 latency may reflect abnormal semantic activation that presumably contributes to associative intrusions in schizophrenic discourse. N400 abnormalities in schizophrenia may be viewed as consistent with the hypothesis of left temporal lobe involvement in patients with schizophrenia. The loose associations, tangentiality, and derailment observed in schizophrenia may be related both to overactivation of the lexical networks and to inefficient context integration.