Search

Cel pracyW odniesieniu do choroby afektywnej dwubiegunowej (ChAD), dotychczasowe prace wskazują na zaburzenia ruchów sakadycznych, głównie pod postacią wydłużenia czasu reakcji (latencji) w testach prosakad i antysakad. Dotychczas nie przeprowadzono oceny ruchów wergencyjnych gałek ocznych u osób z ChAD. Głównym celem naszego badania jest ocena parametrów konwergencji (zbieżne ruchy gałek ocznych) w tej grupie klinicznej.MetodaDo badania włączono 30 pacjentów z ChAD w stanie remisji objawowej i 23 zdrowych ochotników. Uczestników poddano badaniu optometrycznemu oceniającemu punkt bliski konwergencji przy użyciu pręta fiksacyjnego. Badanie okulometryczne przeprowadzono przy pomocy okulografu wykorzystującego promieniowanie podczerwone z dedykowanym stymulatorem wergencji.WynikiPacjenci z ChAD wykazali istotnie większy średni błąd pozycji konwergencji do celu oraz większą liczbę wtrąceń sakadycznych w porównaniu do grupy kontrolnej. Analiza składowych głównych przeprowadzona na zmiennych okulometrycznych pokazała istotne różnice między pacjentami z ChAD a zdrowymi ochotnikami. Wykazano obecność istotnych korelacji między zaburzeniami ruchów wergencyjnych a liczbą wtrąceń sakadycznych.WnioskiPacjenci z ChAD ujawnili zaburzenia ruchów wergencyjnych gałek ocznych podobne do zaburzeń opisywanych w trakcie śledzenia bodźców poruszających się w płaszczyźnie czołowej. Podczas gdy zaburzenia wergencji były opisywane w innych zaburzeniach psychicznych, nasza praca po raz pierwszy obiektywnie zmierzyła to zjawisko w ChAD.

Magnocellular neurosecretory cells (MNCs) clustered in the hypothalamic paraventricular nucleus (PVN) and supraoptic nucleus constitute a major source of oxytocin (OXT) and arginine vasopressin (AVP) peptides, and are among the best described peptidergic neurons in the brain. OXT and AVP are involved in a range of homeostatic processes, social behaviours, emotional processes, and learning. Notably, their actions can be sex-specific, and several sex differences in the anatomies of the OXT and AVP systems have been reported. Nonetheless, possible sex differences in the detailed distributions of MNCs and in their intrinsic electrical properties ex vivo have not been extensively examined. We addressed these issues utilizing immunostaining and patch-clamp ex vivo recordings. Here, we showed that Sprague-Dawley rat PVN AVP neurons are more numerous than OXT cells and that more neurons of both types are present in males. Furthermore, we identified several previously unreported differences between putative OXT and AVP MNC electrophysiology contributing to their partially unique profiles. Notably, elucidation of the highly specific action potential (AP) shapes, with AVP MNCs having a narrower AP and faster hyperpolarizing after-potential (HAP) kinetics than OXT MNCs, allowed unambiguous discrimination between OXT and AVP MNCs ex vivo for the first time. Moreover, the examined electrophysiological properties of male and female MNCs generally overlapped with the following exceptions: higher membrane resistance in male MNCs and HAP kinetics in putative OXT MNCs, which was slower in males. These reported observations constitute a thorough addition to the knowledge of MNC properties shaping their diverse physiological actions in both sexes.

Background: Schizophrenia (SZ) and bipolar disorder (BD) patients share deficits in motor functions in the form of neurological (NSS) and cerebellar soft signs (CSS), and implicit motor learning disturbances. Here, we use cluster analysis method to assess (1) the relationship between those abnormalities in SZ and BD and (2) the differences between those groups. Methods: 33 SZ patients, 33 BD patients as well as 31 healthy controls (HC) took part in the study. We assessed CSS with the International Cooperative Ataxia Rating Scale (ICARS) and NSS with the Neurological Evaluation Scale (NES). Implicit motor learning was evaluated with the Serial Reaction Time Task (SRTT). Participants were divided into clusters (Ward's method) based on the mean response time and mean error rate in SRTT. The difference in ICARS and NES scores, and SRTT variables between clusters were evaluated. We have measured associations between SRTT parameters and both ICARS and NES total scores and subscores. Results: Cluster analysis based on the SRTT parameters allowed to extract three clusters. Those were characterized by the increasing disruption of motor functioning (psychomotor retardation, the severity of NSS and CSS) regardless of the diagnosis. Cluster 1 covered almost all of HC and was characterized by faster reaction times and small number of errors. BD and SZ patients represented in cluster 1, although fully functional in performing the SRTT, showed higher rates of NSS and CSS. Patients with BD and SZ were set apart in clusters 2 and 3 in a similar proportion. Cluster 2 presented significantly slower reaction times but with the comparable number of errors to cluster 1. Cluster 3 consisted of participants with normal or decreased reaction time and significantly increased number of errors. None of the clusters were predominantly composed of the patients representing one psychiatric diagnosis. Conclusions: To our best knowledge, we are presenting the first data indicating the relationship between implicit motor learning and NSS and CSS in SZ and BD patients' groups. Lack of clusters predominantly represented by patients with the diagnosis of SZ or BD may refer to the model of schizophrenia-bipolar disorder boundary, pointing out the similarities between those two disorders.

Malformations of cortical development (MCDs), such as cortical dysplasia and tuberous sclerosis complex, are common causes of intractable epilepsy, especially in paediatric patients. Recently, mounting evidence points to a common pathology of these disorders. Hyperactivation of mammalian target of rapamycin (mTOR) has been proposed as a central mechanism in most, if not all, MCDs. The transition from mTOR hyperactivation and cellular abnormalities to large-scale functional changes and seizure is, however, not fully understood. In this article we set out to review currently available information regarding MCD pathology, focusing on glial cells - especially astrocytes - and their interactions with the brain vascular system. A large body of evidence points to these elements as potential targets in MCD. Here, we attempt to provide a review of this evidence and propose some hypotheses regarding the possible chain of events linking primary glial dysfunction and epilepsy. We focus on extracellular matrix remodelling, blood-brain barrier leakage and failure of astrocyte-dependent removal of extracellular debris. We posit that the failure of these systems results in a chronically pro-inflammatory environment, maintaining local astrocytes in a state of gliosis, with increased susceptibility to seizures as a consequence.

Aim: Without taking into consideration the pedagogical justification for doing the strength training by prisoners, the authors of this study discuss the problem of the consequences of allowing prisoners to do the strength training freely. The study was conducted to determine the frequency and the location of the overload changes in the musculoskeletal system of prisoners who do the strength training as well as the presumable reasons for such changes. Methods: The study was conducted with the use of an interview technique among 44 men, repeat offenders serving a sentence of imprisonment in a prison in Inowrocław, regularly engaged in strength training in their free time. Results: The respondents trained quite often (more than 5 times a week), slightly more than a half of them started the training with the warm up, and 64% did not do any stretching exercises after the training. The overload changes associated with strength training affected 30% of the respondents. Conclusion: The high level of injury among prisoners who do the strength training is due to: too many sessions a week, the lack of warm up and stretching exercises, as well as the insufficient level of knowledge on the prevention from sports injuries.

Pregnant Wistar rats were exposed to a single 1.0 Gy dose of gamma-irradiation on gestational day 13, 15, 17 or 19. Thirty-day-old male offspring received a mechanical lesion in the left cerebral hemisphere. One, 2 or 4 days after the injury the rats were injected with [3H]thymidine and sacrificed 4 h after the injection. Thereafter, brain sections were immunostained for GFAP or S100 beta protein, subjected to autoradiography and examined microscopically to record immunopositive astrocytes labelled with [3H]thymidine. Statistically significant elevation of the reactive astrocyte proliferation was revealed on the 2nd day following injury in brains irradiated on gestational day 15. The results represent the first in vivo evidence that a low-dose prenatal gamma-irradiation can induce a long-term increase in the ability of astroglia to proliferate in response to injury.