This is the first study to examine attentional control capacities in generalized anxiety disorder (GAD). GAD is characterized by uncontrollable worry. Individuals diagnosed with GAD and healthy participants (HPs) performed a random key-pressing task while thinking about a worrisome or a positive future event, to assess the extent to which attentional control resources are used by worry. Attentional control was also assessed when participants were not instructed to think about a specific topic using the N-back task, which varies in task difficulty, and therefore is sensitive to subtle differences in ability to handle increasing demands on attentional control within the same paradigm. GAD participants (but not HPs) were less random while worrying than thinking about a positive event during the key-pressing task, suggesting that worry consumed more attentional control resources in this population. During the N-Back task, GAD participants performed worse than HPs during the high load conditions only, indicating greater difficulty in sustaining focus on conditions requiring a higher degree of attentional control, even without concurrent task activity. Poor attentional control might underpin the difficulty of GAD individuals to stop worrying and switch to thinking more benign information. Further research could investigate whether worry consumes attentional control resources in other psychological disorders with high rates of worry (e.g., panic disorder, psychosis), as well as the extent to which attentional control is used by other forms of repetitive thinking, such as depressive rumination.
There is considerable evidence for cognitive dysfunction in schizophrenia and affective disorders, but the pattern of potential similarities or differences between diagnostic groups remains uncertain. The objective of this study was to conduct a quantitative review of studies on cognitive performance in schizophrenia and affective disorders. Relevant articles were identified through literature search in major databases for the period between January 1980 and December 2005. Meta-analytic treatment of the original studies revealed widespread cognitive deficits in patients with schizophrenia and affective disorders in intellectual ability and speed of information processing, in encoding and retrieval, rule discovery and in response generation and response inhibition. Differences between diagnostic groups were quantitative rather than qualitative.
Neurokinin B (NKB) is a hypothalamic neuropeptide binding preferentially to the neurokinin 3 receptor. Expression of the gene encoding NKB is elevated in postmenopausal women. Furthermore, rodent studies suggest that NKB signalling may mediate menopausal hot flushes. However, the effects of NKB administration on hot flushes have not been investigated in humans. To address this, we performed a randomised, double-blinded, placebo-controlled, 2-way cross-over study. Ten healthy women were admitted to a temperature and humidity-controlled research unit. Participants received 30 minute intravenous infusions of NKB and vehicle in random order. Symptoms, heart rate, blood pressure, sweating and skin temperature were compared between NKB and vehicle in a double-blinded manner. Eight of ten participants experienced flushing during NKB infusion with none experiencing flushing during vehicle infusion (P = 0.0007). Significant elevations in heart rate (P = 0.0106 vs. pre-symptoms), and skin temperature measured using skin probe (P = 0.0258 vs. pre-symptoms) and thermal imaging (P = 0.0491 vs. pre-symptoms) characteristic of menopausal flushing were observed during hot flush episodes. Our findings provide evidence that NKB administration can cause hot flushes in women. Further studies are required to determine if pharmacological blockade of NKB signalling could inhibit hot flushes during the menopause and during treatment for sex-steroid dependent cancers.
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