توهم شنوایی کلامی و عملکرد شناختی در افراد سالم
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|34821||2011||5 صفحه PDF||سفارش دهید||4494 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Schizophrenia Research, Volume 132, Issues 2–3, November 2011, Pages 203–207
Auditory verbal hallucinations (AVH) are a characteristic symptom in schizophrenia, and also occur in the general, non-clinical population. In schizophrenia patients, several specific cognitive deficits, such as in speech processing, working memory, source memory, attention, inhibition, episodic memory and self-monitoring have been associated with auditory verbal hallucinations. Such associations are interesting, as they may identify specific cognitive traits that constitute a predisposition for AVH. However, it is difficult to disentangle a specific relation with AVH in patients with schizophrenia, as so many other factors can affect the performance on cognitive tests. Examining the cognitive profile of healthy individuals experiencing AVH may reveal a more direct association between AVH and aberrant cognitive functioning in a specific domain. For the current study, performance in executive functioning, memory (both short- and long-term), processing speed, spatial ability, lexical access, abstract reasoning, language and intelligence performance was compared between 101 healthy individuals with AVH and 101 healthy controls, matched for gender, age, handedness and education. Although performance of both groups was within the normal range, not clinically impaired, significant differences between the groups were found in the verbal domain as well as in executive functioning. Performance on all other cognitive domains was similar in both groups. The predisposition to experience AVH is associated with lower performance in executive functioning and aberrant language performance. This association might be related to difficulties in the inhibition of irrelevant verbal information.
Auditory verbal hallucinations (AVH) are a characteristic symptom of schizophrenia but have also been described in the general population (Tien, 1991 and Verdoux and van Os, 2002). Thus far, the pathophysiology of AVH is still largely unknown. Many theories concerning the origin of AVH have been postulated of which several have implicated specific cognitive dysfunctions as the core abnormality to cause AVH. For example, Frith and Done (1988) hypothesized a failure in self-monitoring as the basic deficit in AVH whereas Verkammen et al. (2008) stated that increased top-down processing plays an important role in the vulnerability to experience AVH. In support of such cognitive deficits or traits, hypothesized to underlie AVH, a number of studies found prominent impairments in several cognitive functions such as speech processing (Hoffman et al., 1999), working memory (Hoffman et al., 1999), episodic memory (Berenbaum et al., 2008), source memory (Brébion et al., 2007), attention (Berman et al., 1997), inhibition (Waters et al., 2003) and self-monitoring (Seal et al., 2004 and Waters et al., 2010). However, patients with schizophrenia suffer from various other symptoms besides AVH, among which avolition, lack of motivation and a general decline in cognitive functioning. Therefore, decreased performance on specific tests is not necessarily a reflection of their tendency to hallucinate. A more specific reflection of AVH may be provided by cognitive differences that occur in non-psychotic individuals with AVH, who are free of negative symptoms and have only sub-clinical levels of positive symptoms (Sommer et al., 2010a and Sommer et al., 2010b). The fact that that these healthy individuals with AVH function at a normal level, were able to finish their education, are medication naïve and have no history of admission to hospital is an additional advantage. Although differences in AVH have been found between healthy individuals and psychotic patients, regarding for instance frequency and emotional content, several similarities remain: no differences were found between location of AVH, loudness, number of voices and personification (Daalman et al., 2011). Based on these results one cannot conclude that both types of AVH are different. Furthermore, Diederen et al. (2011) found no significant differences in brain activation during the experience of AVH between healthy individuals with AVH and patients. In order to measure cognitive functioning in non-psychotic individuals with AVH, a group of 101 persons with AVH who were screened for axis I or II pathology was compared to a matched control group with a battery of neuropsychological tests. These tests focus primarily on cognitive domains that were previously found to be affected in patients with a psychotic disorder experiencing AVH. The most important cognitive domains in that perspective were included: memory, language, executive functioning, processing speed, spatial ability, verbal and non-verbal reasoning. The aim of the present study was to establish a cognitive profile of healthy individuals with AVH. Compared to healthy individuals without AVH, this group might show deviant cognitive performance. These cognitive differences will then provide clues for a potential cognitive mechanism that could underlie AVH since these individuals are otherwise healthy.