Neural activation of swallowing and swallowing‐related tasks in healthy young adults: An attempt to separate the components of deglutition

Understanding the underlying neural pathways that govern the highly complex neuromuscular action of swallowing is considered crucial in the process of correctly identifying and treating swallowing disorders. The aim of the present investigation was to identify the neural activations of the different components of deglutition in healthy young adults using functional magnetic resonance imaging (fMRI). Ten right‐handed young healthy individuals were scanned in a 3‐Tesla Siemens Allegra MRI scanner. Participants were visually cued for both a “Swallow” task and for component/control tasks (“Prepare to swallow”, “Tap your tongue”, and “Clear your throat”) in a randomized order (event‐related design). Behavioral interleaved gradient (BIG) methodology was used to address movement‐related artifacts. Areas activated during each of the three component tasks enabled a partial differentiation of the neural localization for various components of the swallow. Areas that were more activated during throat clearing than other components included the posterior insula and small portions of the post‐ and pre‐central gyri bilaterally. Tongue tapping showed higher activation in portions of the primary sensorimotor and premotor cortices and the parietal lobules. Planning did not show any areas that were more activated than in the other component tasks. When swallowing was compared with all other tasks, there was significantly more activation in the cerebellum, thalamus, cingulate gyrus, and all areas of the primary sensorimotor cortex bilaterally. Hum Brain Mapp 2009. © 2009 Wiley‐Liss, Inc.     

Maternal Adnexal Torsion in Pregnancy Is Associated with Significant Risk of Recurrence

Study ObjectivesTo investigate the phenomenon of recurrent adnexal torsion during the same pregnancy, describe its risk factors, and suggest possible management of this entity.DesignRetrospective case-control study (Canadian Task Force classification II-3).SettingGynecologic endoscopy unit in a university hospital.Patients and interventionsPregnant women with surgically proved adnexal torsion were retrospectively identified from 1993 to 2007. Details of clinical presentation, method of conception, preoperative ultrasound findings, and operative findings were analyzed.InterventionComparison of characteristics of patients with recurrent episodes of adnexal torsion during the same pregnancy vs a single episode of torsion.Measurements and Main ResultsThirty-three pregnant women with 38 episodes of adnexal torsion were included in the study. Seventeen pregnancies (51.5%) were spontaneously conceived. Twenty-eight women had a single episode of torsion, and 5 women (15.1%) had recurrent episodes of torsion during the same pregnancy. No significant differences were found between the 2 groups in age, method of conception, and gestational age at time of torsion. However, ultrasound studies demonstrated that multicystic ovaries were significantly more common in women with recurrent torsion compared with women with a single episode of torsion (80% vs 25%; p = .02). The interval between the first and second episodes of torsion ranged from 1 to 4 weeks.ConclusionPregnant women are at risk for recurrent torsion, especially when the ovaries are enlarged and ultrasound studies demonstrate multiple cysts. Cyst aspiration may prevent recurrent torsion during the same pregnancy.     

Short‐term plasticity following motor sequence learning revealed by diffusion magnetic resonance imaging

Current noninvasive methods to detect structural plasticity in humans are mainly used to study long‐term changes. Diffusion magnetic resonance imaging (MRI) was recently proposed as a novel approach to reveal gray matter changes following spatial navigation learning and object‐location memory tasks. In the present work, we used diffusion MRI to investigate the short‐term neuroplasticity that accompanies motor sequence learning. Following a 45‐min training session in which participants learned to accurately play a short sequence on a piano keyboard, changes in diffusion properties were revealed mainly in motor system regions such as the premotor cortex and cerebellum. In a second learning session taking place immediately afterward, feedback was given on the timing of key pressing instead of accuracy, while participants continued to learn. This second session induced a different plasticity pattern, demonstrating the dynamic nature of learning‐induced plasticity, formerly thought to require months of training in order to be detectable. These results provide us with an important reminder that the brain is an extremely dynamic structure. Furthermore, diffusion MRI offers a novel measure to follow tissue plasticity particularly over short timescales, allowing new insights into the dynamics of structural brain plasticity.     

[11C]5-HTP and microPET are not suitable for pharmacodynamic studies in the rodent brain

The PET tracer [¹¹C]5-hydroxytryptophan ([¹¹C]5-HTP), which is converted to [¹¹C]5-hydroxytryptamine ([¹¹C]5-HT) by aromatic amino acid decarboxylase (AADC), is thought to measure 5-HT synthesis rates. But can we measure these synthesis rates by kinetic modeling of [¹¹C]5-HTP in rat? Male rats were scanned with [¹¹C]5-HTP (60 minutes) after different treatments. Scans included arterial blood sampling and metabolite analysis. 5-HT synthesis rates were calculated by a two-tissue compartment model (2TCM) with irreversible tracer trapping or Patlak analysis. Carbidopa (inhibitor peripheral AADC) dose-dependently increased [¹¹C]5-HTP brain uptake, but did not influence 2TCM parameters. Therefore, 10 mg/kg carbidopa was applied in all subsequent study groups. These groups included treatment with NSD 1015 (general AADC inhibitor) or p-chlorophenylalanine (PCPA, inhibitor of tryptophan hydroxylase, TPH). In addition, the effect of a low-tryptophan (Trp) diet was investigated. NSD 1015 or Trp depletion did not affect any model parameters, but PCPA reduced [¹¹C]5-HTP uptake, and the k₃. This was unexpected as NSD 1015 directly inhibits the enzyme converting [¹¹C]5-HTP to [¹¹C]5-HT, suggesting that trapping of radioactivity does not distinguish between parent tracer and its metabolites. As different results have been acquired in monkeys and humans, [¹¹C]5-HTP-PET may be suitable for measuring 5-HT synthesis in primates, but not in rodents.     

On the positive side of error processing: error-awareness positivity revisited

Performance errors are indexed in the brain even if they are not consciously registered, as demonstrated by the error-related negativity (ERN or Ne) event-related potential. It has recently been shown that another response-locked potential, the error positivity (Pe), follows the Ne, but only in those trials in which the participants consciously detect making the error ('Aware Errors'). In the present study we generalize these findings to an auditory task and investigate possible caveats in the interpretation of the Pe as an index of error awareness. In an auditory Go/No-Go error-awareness task (auditory EAT) participants pressed an additional 'fix error' button after noticing that they had made an error. As in visual tasks, the Ne was similar for aware ('fixed') and unaware ('unfixed') errors, while the Pe was enhanced only for Aware Errors. Within subjects, the Ne and Pe behaved in similar fashions for auditory and visual errors. A control condition confirmed that the awareness effect was not due to the requirement to report error awareness. These results reinforce the evidence in favor of the Pe as a correlate of conscious error processing, and imply that this process is not modality-specific. Nevertheless, single-trial analysis suggested that the Pe may be a delayed P3b related to stimulus processing rather than to response monitoring.     

Predicting individual variability in task‐evoked brain activity in schizophrenia

What goes wrong in a schizophrenia patient''s brain that makes it so different from a healthy brain? In this study, we tested the hypothesis that the abnormal brain activity in schizophrenia is tightly related to alterations in brain connectivity. Using functional magnetic resonance imaging (fMRI), we demonstrated that both resting‐state functional connectivity and brain activity during the well‐validated N‐back task differed significantly between schizophrenia patients and healthy controls. Nevertheless, using a machine‐learning approach we were able to use resting‐state functional connectivity measures extracted from healthy controls to accurately predict individual variability in the task‐evoked brain activation in the schizophrenia patients. The predictions were highly accurate, sensitive, and specific, offering novel insights regarding the strong coupling between brain connectivity and activity in schizophrenia. On a practical perspective, these findings may allow to generate task activity maps for clinical populations without the need to actually perform any tasks, thereby reducing patients inconvenience while saving time and money.     

A review of friedreich ataxia clinical trial results

There are now 21 agents or classes of therapeutic agents in the Friedreich ataxia research pipeline (http://www.curefa.org/pipeline.html) that have been developed in the 15 years since the discovery of the frataxin gene, with the ongoing characterization of its mutations and the resulting molecular pathology. Twenty-four studies are currently posted on ClinicalTrials.gov. Twenty-seven works discussing the results of clinical trials in Friedreich ataxia have been published. In 2010, 42 public (National Institutes of Health) and private (Friedreich Ataxia Research Alliance, Muscular Dystrophy Association, and National Ataxia Foundation) grants were funded for translational and clinical research in Friedreich ataxia. Millions of dollars from public, private, and industry-based initiatives have been dedicated to research in Friedreich ataxia therapeutics. Despite this vigorous international effort, there is as yet no proven disease-modifying therapy for Friedreich ataxia.