For example, self-generated eye movements do not result in the percept of visual motion even though an image moves across

the retina. If corollary discharges associated with speech acts (1) are used to distinguish self- from externally-generated speech, and (2) if this system is imprecise in schizophrenia, self-generated speech (perhaps even subvocal speech) may be perceived as externally generated, i.e., hallucinations. Consistent with this hypothesis, a recent study found that hallucinating patients do not show the normal suppression of auditory response to self-generated speech and the degree of abnormality correlated both with severity of hallucinations and misattributions of self-generated speech (Heinks-Maldonado et al., 2007). Schizophrenics also have anatomical abnormalities of the plaunum temporale, particularly in the upper cortical layers (I-III, the cortico-cortical layers) of the see more caudal region (likely corresponding to the location of Spt) in the left hemisphere, which show a reduced fractional volume relative to controls (Smiley et al., 2009). Thus, in Selleck PF01367338 schizophrenia the nature of the behavioral and physiological effects (implicating sensorimotor

integration), the location of anatomical abnormalities (left posterior PT), and the level of cortical processing implicated (cortico-cortical) are all consistent with dysfunction involving area Spt. As with stuttering, a research emphasis on this functional circuit is warranted in understanding aspects of schizophrenia. One would not have expected a connection between disorders as apparently varied as conduction aphasia,

stuttering, and schizophrenia, yet they all seem to involve, in part, dysfunction of the same region and functional circuit. A closer look at these syndromes reveals other similarities. For example, all three disorders show atypical responses to delayed auditory feedback. Fluency of speech in both stutterers and conduction aphasics is not negatively affected by delayed auditory feedback and may show paradoxical improvement (Boller et al., 1978, Martin and Haroldson, 1979 and Stuart et al., 2008), whereas in schizophrenia delayed auditory feedback induces the reverse effect: greater than normal Megestrol Acetate speech dysfluency (Goldberg et al., 1997). Further, both stuttering and schizophrenia appear to be associated with dopamine abnormalities: dopamine antagonists such as risperidone and olanzapine (atypical antipsychotics commonly used to treat schizophrenia) have recently been shown to improve stuttering (Maguire et al., 2004). Although on first consideration it seems problematic to have such varied symptoms associated with disruption of the same circuit, having the opportunity to study a variety of breakdown scenarios may prove to be particularly instructive in working out the details of the circuit.