Some patients are no longer able to communicate effectively or even interact with the outside world in ways that most of us take for granted. In the most severe cases, tetraplegic or post-stroke patients are literally 'locked in' their bodies, unable to exert any motor control after, for example, a spinal cord injury or a brainstem stroke, requiring alternative methods of communication and control. But we suggest that, in the near future, their brains may offer them a way out. Non-invasive electroencephalogram (EEG)-based brain-computer interfaces (BCI) can be characterized by the technique used to measure brain activity and by the way that different brain signals are translated into commands that control an effector (e.g., SYNOPSIScontrolling a computer cursor for word processing and accessing the internet). This review focuses on the basic concepts of EEGbased BCI, the main advances in communication, motor control restoration and the downregulation of cortical activity, and the mirror neuron system (MNS) in the context of BCI. The latter appears to be relevant for clinical applications in the coming years, particularly for severely limited patients. Hypothetically, MNS could provide a robust way to map neural activity to behavior, representing the high-level information about goals and intentions of these patients. Non-invasive EEG-based BCIs allow brain-derived communication in patients with amyotrophic lateral sclerosis and motor control restoration in patients after spinal cord injury and stroke. Epilepsy and attention deficit and hyperactive disorder patients were able to downregulate their cortical activity. Given the rapid progression of EEG-based BCI research over the last few years and the swift ascent of computer processing speeds and signal analysis techniques, we suggest that emerging ideas (e.g., MNS in the context of BCI) related to clinical neurorehabilitation of severely limited patients will generate viable clinical applications in the near future. VOLUME 21, NO. 6,2010 451 Brought to you by | provisional account Unauthenticated Download Date | 6/7/15 7:42 AM 452 S. MACHADO ET AL. KEY WORDSAmyotrophic Lateral Sclerosis, attention deficit and hyperactive disorder, EEG-based braincomputer interface, epilepsy, mirror neurons system, sensorimotor integration, spinal cord, stroke

The present study aims to conduct a systematic review of the literature by checking the impact of positive emotion in the treatment of depression and on the use of strategies of positive psychology which involves positive emotion to treat and reduce symptoms of depression. For this purpose, we conducted searches in databases ISI Web of Knowledge, PsycINFO and PubMed and found a total of 3400 studies. After inclusion application and exclusion criteria, 28 articles remained, presented and discussed in this study. The studies have important relations between humor and positive emotion as well as a significant improvement in signs and symptoms of depression using differents strategies of positive psychology. Another relevant aspect is the preventative character of the proposed interventions by positive psychology by the fact that increase well-being and produce elements such as resilience and coping resources that reduce the recurrent relapses in the treatment of depression. The strategies of positive psychology, such as increasing positive emotions, develop personal strengths: seeking direction, meaning and engagement for the day-to-day life of the patients, appear as potentially tools for the prophylaxis and treatment of depression, helping to reduce signs and symptoms as well as for prevention of relapses.

There is no sense organ specifically dedicated to time perception, as there is for other senses such as hearing and vision. However, this subjective sense of time is fundamental to our conception of reality and it creates the temporal course of events in our lives. Here, we explored neurobiological relations from the clinical perspective, examining timing ability in patients with different neurological and psychiatric conditions (e.g. Parkinson's disease, depression, bipolar disorder, anxiety disorders and schizophrenia). The neural bases of present distortions in time perception and temporal information processing still remain poorly understood. We reviewed: a) how the brain is capable of encoding time in different environments and multiple tasks, b) different models of interval timing, c) brain structures and neurotransmitters associated with time perception, d) the relationship between memory and time perception, e) neural mechanisms underlying different theories in neural and mental processes, and f) the relationship between different mental diseases and time perception. Bibliographic research was conducted based on publications over the past thirteen years written in English in the databases Scielo, Pubmed/MEDLINE, ISI Web of Knowledge. The time perceptions research are executed to evaluate time perception in mental diseases and can provide evidence for future clinical applications.

This long-term extension of an 8-week randomized, naturalistic study in patients with panic disorder with or without agoraphobia compared the efficacy and safety of clonazepam (n = 47) and paroxetine (n = 37) over a 3-year total treatment duration. Target doses for all patients were 2 mg/d clonazepam and 40 mg/d paroxetine (both taken at bedtime). This study reports data from the long-term period (34 months), following the initial 8-week treatment phase. Thus, total treatment duration was 36 months. Patients with a good primary outcome during acute treatment continued monotherapy with clonazepam or paroxetine, but patients with partial primary treatment success were switched to the combination therapy. At initiation of the long-term study, the mean doses of clonazepam and paroxetine were 1.9 (SD, 0.30) and 38.4 (SD, 3.74) mg/d, respectively. These doses were maintained until month 36 (clonazepam 1.9 [SD, 0.29] mg/d and paroxetine 38.2 [SD, 3.87] mg/d). Long-term treatment with clonazepam led to a small but significantly better Clinical Global Impression (CGI)-Improvement rating than treatment with paroxetine (mean difference: CGI-Severity scale -3.48 vs -3.24, respectively, P = 0.02; CGI-Improvement scale 1.06 vs 1.11, respectively, P = 0.04). Both treatments similarly reduced the number of panic attacks and severity of anxiety. Patients treated with clonazepam had significantly fewer adverse events than those treated with paroxetine (28.9% vs 70.6%, P < 0.001). The efficacy of clonazepam and paroxetine for the treatment of panic disorder was maintained over the long-term course. There was a significant advantage with clonazepam over paroxetine with respect to the frequency and nature of adverse events.

Unlike for depression, only few studies are available today investigating the therapeutic effects of repetitive transcranial magnetic stimulation (rTMS) for anxiety disorders. This review aims to provide information on the current research approaches and main findings regarding the therapeutic use of rTMS in the context of various anxiety disorders. Although positive results have frequently been reported in both open and randomized controlled studies, our review of all identified studies indicates that at present no conclusive evidence of the efficacy of rTMS for the treatment for anxiety disorders is provided. Several treatment parameters have been used, making the interpretation of the results difficult. Moreover, sham-controlled research has often been unable to distinguish between response to rTMS and sham treatment. However, there is a limitation in the rTMS methods that likely impacts only the superficial cortical layers. It is not possible to directly stimulate more distant cortical areas, and also subcortical areas, relevant to the pathogenesis of anxiety disorders, though such effects in subcortical areas are thought to be indirect, via trans-synaptic connections. We thus recommend further studies to clearly determine the role of rTMS in the treatment of anxiety disorders. Key advances in combining TMS with neuroimaging technology may aid in such future developments.

, FÁTIMA AZEVEDO IGNÁCIO 7 , ROGÉRIO PAYSANO MARROCOS 8 ABSTRACT -We tested the hypothesis that Part B of the Trail Making Test (TMT) is a measure of cognitive setshifting ability in 55 normal subjects with the conventional (written) TMT and a verbal adaptation, the "verbal TMT" (vTMT). The finding of a significant association between Parts B of TMT and vTMT (r = 0,59, p < 0,001), after correcting for age and education, supports the view that Part B of TMT is a valid measure of the ability to alternate between cognitive categories.KEY WORDS: trail making test, verbal trail making test, set-shifting cognition. . In Part A, the circles are numbered from 1 to 25, whereas in Part B numbers from 1 to 13 and letters from A to M must be connected in alternating fashion, beginning at 1-A and ending at M-13. Total score is given by time spent to complete each part. Factor analysis has shown that the TMT loads on both a rapid visual search and a visuospatial sequencing factor 3 . Whether it also superimposes on a third, "cognitive set-shifting", factor has been debated [4][5][6] . If true, however, this would be an important attribute of the test, as the ability to switch between categories is one of the most reliable indexes of normal neurobehavioral functioning 7 .In this study we administered a verbal adaptation of TMT-the "verbal Trail Making Test" (vTMT)-to normal individuals to see whether Part B of Trail Making Test (TMTB) also gauges the ability to shift between cognitive sets. Since in vTMT the visuospatial and visuomotor factors intrinsic to the conventional (written) TMT are reduced to a minimum, a lack of correlation between Parts B

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The Brain-Derived Neurotrofic Factor (BDNF) is one of the most important neurotrophins in the brain and it is suggested influences the activity of the serotonergic, noradrenergic and dopaminergic pathways. In the last few years, it has been hypothesized that BDNF level is related with depression and sleep. Several studies show that depressive subjects present low levels of BDNF in the brain. Poor sleep quality is also related with alterations in the BDNF concentration. Some authors argue that most of the cases show that impaired sleep quality increases the stress and, consequently, the vulnerability to depressive disorders, suggesting that there is a relationship between sleep, depression and BDNF levels.