Alexithymia is a personal trait characterized by a reduced ability to identify and describe one's own feelings and is known to contribute to a variety of physical and behavioural disorders. To elucidate the pathogenesis of stress-related disorders and the normal functions of emotion, it is important to investigate the neurobiology of alexithymia. Although several neurological models of alexithymia have been proposed, there is very little direct evidence for the neural correlates of alexithymia. Using PET, we studied brain activity in subjects with alexithymia when viewing a range of emotional face expressions. Twelve alexithymic and 12 non-alexithymic volunteers (all right-handed males) were selected from 247 applicants on the basis of the 20-item Toronto Alexithymia Scale (TAS-20). Regional cerebral blood flow (rCBF) was measured with H(2)(15)O-PET while the subjects looked at angry, sad and happy faces with varying emotional intensity, as well as neutral faces. Brain response in the subjects with alexithymia significantly differed from that in the subjects without alexithymia. The alexithymics exhibited lower rCBF in the inferior and middle frontal cortex, orbitofrontal cortex, inferior parietal cortex and occipital cortex in the right hemisphere than the non-alexithymics. Additionally, the alexithymics showed higher rCBF in the superior frontal cortex, inferior parietal cortex and cerebellum in the left hemisphere when compared with the non-alexithymics. A covariance analysis revealed that rCBF in the inferior and superior frontal cortex, orbitofrontal cortex and parietal cortex in the right hemisphere correlated negatively with individual TAS-20 scores when viewing angry and sad facial expressions, and that no rCBF correlated positively with TAS-20 scores. Moreover, the anterior cingulate cortex and insula were less activated in the alexithymics' response to angry faces than their response to neutral faces. These results suggest that people with alexithymia process facial expressions differently from people without alexithymia, and that this difference may account for the disorder of affect regulation and consequent peculiar behaviour in people with alexithymia.

The unpleasantness of itching is reduced by cooling. Although previous research suggests the presence of a central itch modulation system, there is little documentation about the modulation system in the brain. In the present study, we investigated the modulating system of the itching sensation in human brains using positron emission tomography and H(2) (15)O. The significant increases of regional cerebral blood flow caused by histamine stimuli using iontophoresis were observed in the anterior cingulate cortex (BA24), the thalamus, the parietal cortex (BA40 and BA7), the dorsolateral prefrontal cortex (BA46) and the premotor cortex (BA6). We did not observe any changes in the secondary somatosensory cortex (S2) during the itching stimulus, corresponding to the previous imaging studies concerning itching. Activation in these areas related to itching stimuli was decreased by a simultaneous stimulation of itching and cold pain (the dual stimuli), as compared to itching alone. Interestingly, the midbrain, including periaqueductal gray matter (PAG), was only activated during the dual stimuli. PAG is well known to be a modulating noxious stimulus. Here we hypothesize that the activation of PAG may also be related to the itch modulation. These findings indicate that the modified brain activities in the PAG, the cingulate, the frontal and the parietal cortex might be associated with the itch modulation in the central nervous system and that the S2 might not be primarily involved in processing the itching perception in the brain since the activity of S2 was not observed in any concentration of itching stimuli.

Histamine H1-receptor (H1R) antagonists, or antihistamines, often induce sedative side effects when used for the treatment of allergic disorders. This study compared the sedative profiles of the second-generation antihistamines, fexofenadine and cetirizine, using 3 different criteria: subjective sleepiness evaluated by the Stanford Sleepiness Scale, objective psychomotor tests (simple and choice reaction time tests and visual discrimination tests at 4 different exposure durations), and measurement of histamine H1-receptor occupancy (H1RO) in the brain. Subjective sleepiness and psychomotor performance were measured in 20 healthy Japanese volunteers at baseline and 90 min after administration of fexofenadine 120 mg or cetirizine 20 mg in a double-blind, placebo-controlled crossover study. Hydroxyzine 30 mg was included as a positive control. H1RO was measured using positron emission tomography (PET) with (11)C-doxepin in 12 of the 20 subjects, and a further 11 volunteers were recruited to act as controls. In psychomotor tests, fexofenadine was not significantly different from placebo and significantly less impairing than cetirizine on some tasks, as well as significantly less impairing than hydroxyzine on all tasks. For subjective sleepiness, fexofenadine was not significantly different from placebo, whereas cetirizine showed a trend toward increased sleepiness compared with fexofenadine and placebo. H1RO was negligible with fexofenadine (-0.1%) but moderately high with cetirizine (26.0%). In conclusion, fexofenadine 120 mg is distinguishable from cetirizine 20 mg, as assessed by H1RO and psychomotor testing.

Alcohol is one of the most widely used recreational drugs, yet it is associated with undesirable social behaviour. It is used primarily for its psychoactive properties, increasing sociability and talkativeness. We hypothesize that low doses of alcohol can improve the performance related to positive emotional cognition. In this experiment, we examined the effect of low doses of alcohol on the processing of emotional facial expressions. Fifteen young male volunteers drank alcohol at volumes of 30, 60, 120 ml (0.14, 0.28, 0.56 g/kg) and performed discrimination tasks on morphed facial emotion expressions of anger, happiness, sadness and surprise-neutral. One-way ANOVA co-varying pretreatment performances revealed significant differences between alcohol levels in happy face discrimination ( p<0.01). Bonferroni correction demonstrated that low doses of alcohol caused a significantly better discrimination of happy faces, and that the performances were worse with higher doses ( p<0.001). No significance was observed with the other three emotional faces. These results indicate that low doses of alcohol affect positive emotional cognition of happy facial expressions.

Low-frequency stimulation via the optimal contacts is effective in improving overall motor function of patients with PD.