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OBJECTIVE: Patients with fibromyalgia (FM) syndrome often report a cluster of cognitive disorders that strongly interferes with their work and daily life, but the relationship between impaired cognitive function and self-reported dysfunction remains unclear. We aimed to investigate the presence of cognitive impairments in patients with FM and to analyze the relationship between the impairments and their evaluation by the patients through a comparison with a group of healthy controls. METHODS: In total, 30 FM patients and 30 healthy controls performed a neuropsychological and clinical evaluation of short-term, long-term, and working memory; executive function; and self-evaluation of cognitive impairment and depressive and anxiety symptoms. To thoroughly investigate executive function, we adopted the Miyake model that identifies 4 domains: shifting, inhibition, updating, and access. RESULTS: Our results confirmed the presence of impairments of attention, long-term memory, working memory, and shifting and updating executive functions in FM patients compared with healthy controls. These impairments are reflected in patient reports independently of depressive symptoms. CONCLUSION: The use of a self-reported questionnaire in clinical practice would provide a first and easy screen for the presence of cognitive impairment in FM patients and, in most cases, obviate the need for a time-consuming full neuropsychological test battery.

Crossing the hands over the body midline reduces the perceived intensity of nociceptive stimuli applied to the hands by impairing the ability to localize somatosensory stimuli. The neural basis of this "crossed-hands analgesia" has not been investigated previously, although it has been proposed that the effect may be modulated by multimodal areas. We used functional magnetic resonance imaging to test the hypothesis that crossed-hands analgesia is mediated by higher-order multimodal areas rather than by specific somatosensory ones. Participants lay in the scanner while mechanical painful stimuli were applied to their hands held in either a crossed or uncrossed position. They reported significantly lower perceived intensity of pain when their hands were crossed. Although activations elicited by stimuli applied to the crossed hands revealed significantly greater blood oxygen level-dependent responses in the anterior cingulate cortex, the insula, and the medial frontal gyrus, the blood oxygen level-dependent responses in the superior parietal lobe were greater with the hands uncrossed. Our results provide evidence that crossed-hands analgesia is mediated by higher-order frontoparietal multimodal areas involved in sustaining and updating body and spatial representations.

Unawareness of deficits is a symptom of Alzheimer's disease that can be observed even in the early stages of the disease. The frontal hypoperfusion associated with reduced awareness of deficits has led to suggestions of the existence of a hypofunctioning prefrontal pathway involving the right dorsolateral prefrontal cortex, inferior parietal lobe, anterior cingulate gyri and limbic structures. Since this network plays an important role in response inhibition competence and patients with Alzheimer's disease who are unaware of their deficits exhibit impaired performance in response inhibition tasks, we predicted a relationship between unawareness of deficits and cingulate hypofunctionality. We tested this hypothesis in a sample of 29 patients with Alzheimer's disease (15 aware and 14 unaware of their disturbances), rating unawareness according to the Awareness of Deficit Questionnaire-Dementia scale. The cognitive domain was investigated by means of a wide battery including tests on executive functioning, memory and language. Neuropsychiatric aspects were investigated using batteries on behavioural mood changes, such as apathy and disinhibition. Cingulate functionality was assessed with functional magnetic resonance imaging, while patients performed a go/no-go task. In accordance with our hypotheses, unaware patients showed reduced task-sensitive activity in the right anterior cingulate area (Brodmann area 24) and in the rostral prefrontal cortex (Brodmann area 10). Unaware patients also showed reduced activity in the right post-central gyrus (Brodmann area 2), in the associative cortical areas such as the right parietotemporal-occipital junction (Brodmann area 39) and the left temporal gyrus (Brodmann areas 21 and 38), in the striatum and in the cerebellum. These findings suggest that the unawareness of deficits in early Alzheimer's disease is associated with reduced functional recruitment of the cingulofrontal and parietotemporal regions. Furthermore, in line with p