Platelet activation plays an important role in atherothrombotic disease. Several glycoproteins are expressed on the platelet surface during platelet activation. One of them is P-selectin (CD62P), the more important platelet activation marker. P-selectin is transmembrane protein of the α-granules, which is translocated to the cell surface following activation. The interaction between platetel P-selectin and the specific ligand for P-selectin on leukocytes, P-selectin glycoprotein ligand-1 (PSGL-1), resulting in the formation of platelet-leukocyte complexes, and secretion cytokines and chemokines leading to aggravate the inflammatory processes. Glycoprotein 53 (CD63) which is present in lysosomal membranes also translocates to the plasma membrane during platelet activation. Platelet hyperactivation has been reported in patients with ischemic stroke. Several studies have suggested that platelets are excessively activated in the acute and chronic phases after cerebral ischemia. Therefore, finding platelet function test, could be the first step toward identifying patients who would benefit from antiplatelet treatment.
The International Panel presented in December 2005 revised and modified diagnostic criteria for multiple sclerosis of McDonald used since 2001. New diagnostic criteria maintain basic principles of the classical McDonald criteria, integrating adequate sensitivity and specificity. The core requirements of diagnosis is still the concept of dissemination of central nervous system lesions in space and time. Constant developing of the use and interpretation of neurological examinations and tests, especially of new imaging technologies allow now for a more rapid diagnosis, in practice making diagnosis more simple and speed. The Panel stated that T2 lesions can be useful for demonstrating dissemination in time more rapidly than before – at least 30 days after the onset of the initial clinical event. Other newness of current criteria is broader incorporation of spinal cord lesions into the imaging requirements. The revisions simplify criteria for primary progressive multiple sclerosis; a positive cerebrospinal fluid finding is no longer required for diagnosis when clinical and imaging specific criteria are fulfilled. Beyond all doubt it’s worth reading original article while present comment encourages only to do it.
The 2-year outcomes of three non-parallel, prospective, placebo-controlled studies (BENEFIT, CHAMPS, ETOMS) have shown that IFN beta-1b s.c. (Betaferon®), IFN beta-1a i.m. (Avonex®) and IFN beta-1a s.c. (Rebif®) similarly prevented conversion of clinically isolated syndromes (CIS) into clinically definite multiple sclerosis (CDMS). Smaller proportions of CIS patients in the Betaferon®, Avonex® and Rebif® groups converted to CDMS as compared with fractions in the placebo groups (28%, 21%, 34% vs. 45%, 35%, 45%); p from 0.047 to 0.00007. The mean number of days to CDMS development was prolonged by three products of IFN beta (363, 375, 569 days), but not by placebo (255, 309, 252 days); p between <0.05 and 0.00007. The mean or median number of new T2-related brain lesions was more strongly reduced in all studies by the verum than by placebo (1.0 vs. 2.0, 2.1 vs. 5.0, 2.0 vs. 3.0); the differences were significant. The mean or median number of new, enhancing lesions was also significantly reduced in the BENEFIT and in the CHAMPS studies, but not in the ETOMS study. An indirect comparison proved that three products of IFN beta partially prevented or delayed conversion of CIS into CDMS and hampered the evolution of new brain lesions on magnetic resonance images.
Status epilepticus or continuous seizures occur as a result of many hard disorders and complications in epilepsy which appear in brain on different backgrounds. Most often these cases may become serious danger for the patient’s life, so they demand immediate intervention and appropriate treatment. Particularly it concerns convulsion epilepsy seizure, appearing with metabolic disorders, which lead to acidosis and brain oedema. The aim of pharmacological treatment of status epilepticus is to stop its clinical symptoms (seizures and its other forms) as quickly as possible and to normalize its bioelectric exponent EEG. Giving the classic drugs (benzodiazepines, phenytoin, phenobarbital – phenobarbiturates, sodium valproate) not always helps to take control over this state. In case of the lack of results of this treatment one may try to use the drugs of new generation. Last days there have appeared some information concerning the efficiency of topiramate treatment in status epilepticus unresponsive to traditional pharmacological therapies. The authors present a case of a 26-year-old patient with partial epileptic attack with secondary generalization, in whom there occurred status epilepticus resistant to treatment with commonly applied drugs. Only the administration of topiramate did allow to control the status epilepticus.
Since the eighties of the 20th century, studies have been carried out on the health state of children of epileptic mothers. These studies indicated quite high percentage of children with mental retardation and inborn defects. They are thought to be associated with less effective treatment in pregnancy, application of antiepileptic drugs of marked teratogenic properties (phenobarbital, phenytoin) and also with polytherapy as the principle of antiepileptic management. Then, the groups of pregnant women with epilepsy were not subjected to specialistic care of a neurologist and obstetrician. Current studies evaluating neuropsychological state of offspring of epileptic mothers point to the occurrence of psychomotor retardation, increased risk of manifestation of central nervous system significant and insignificant dysfunction, epilepsy as well as lower than on the average global intellectual ability and insignificant neurological dysfunction. Psychomotor retardation concerns mainly visual and auditory coordination, speech and social contacts. The latest prospective studies of epileptic mothers’ offspring indicate that epilepsy is significantly more frequently manifested among them (7% till the end of the first decade) than it was reported in earlier retrospective studies. In this period, generalized epilepsy (different syndromes) is more often revealed in offspring of mothers with early manifestation of epilepsy with attacks of unconsciousness. Polytherapy and monotherapy with walproine acid is a very important factor of the risk of decreased intelligence quotient and less beneficial results of learning. The importance of other risk factors including environmental has not been recognized sufficiently. Low socioeconomic level and the child’s male gender modify distinctly unbeneficially the effect of antiepileptic drugs administered in pregnancy. However, the so far carried out studies have not comprised sufficiently numerous groups of offspring of epileptic mothers and the methods of assessment applied by particular authors differ significantly. Furthermore, majority of mechanisms of the way different genetic and environmental factors affect the development of cognitive functions in offspring of epileptic patients are not known.
The paper presents current views concerning the role of stem cells in neoplasia, with particular emphasis of CNS tumors. First, some arguments are presented supporting the thesis that at the first stage of neoplasia, the cellular target for carcinogens are normal stem cells or progenitor cells. Also, discussed are important problems associated with attempts at identification of cellular sources of neoplasms. One of these is the difficulty encountered with distinguishing stem cells and non-differentiated cells. Second, data are presented allowing the conclusion that within neoplastic tissue exist neoplastic stem cells – cells enabling regeneration of this pathological tissue. In the context of discussion concerning the role of stem cells in the pathogenesis of neoplasms, a new theory about physiologic and pathologic role of normal and damaged proteins, e.g. APC, SUFU, EGFR, c-MYC, P53 is presented. Discussed is also the role of proteins controlling modification of chromatin, e.g. the Polycomb protein. These proteins are extremely important for the differentiation process. The paper presents also own preliminary experience with the role of stem cells in the pathogenesis of CNS tumors. Finally, presented are premises providing hope for application of knowledge concerning neoplastic stem cells in designing novel modalities of oncologic therapies. Development of such therapies may be based on the search for chemotherapeutic agents which would selectively eliminate neoplastic stem cells. It is also possible to use normal but genetically modified stem cells to detect neoplastic stem cells and to eliminate them.
During the last decade dozens of papers have been published, whose approval for printing signifies a consent for changes in some biology handbooks. Stem cells have found their way to newspaper headlines and even became an element of presidential campaign in the United States. Indeed, an important issue on scientific and medical ground is that recently several paradigms in hitherto force in developmental biology have been challenged. First, the paradigm of barrier between embryonal layers has been questioned. Second, it has been demonstrated that even in such structures as the central nervous system and heart muscle there is a steady but distinct renovation, even in adult mammals. Third, new models of cell differentiation have been proposed. For many years, developmental biology was based on instructional models of differentiation. At present, the instructional model is increasingly frequently replaced by the stochastic model. Furthermore, the question of debate is whether there is still any rationale for further propagation of hierarchic models. Current dispute concerning the above mentioned concepts and paradigms, which is currently taking place among biologists studying the development of organisms, has a direct transmission onto practical applications thereof. For example, lack of barrier between embryonal layers (or its permeability) paves the way for the use of mesenchymal stem cells from bone marrow as “progenitors” of neurons, whose deficit is seen in persons with Parkinson disease. In other words, if inter-embryonal layer barrier does not exist or may be transgressed, then therapeutic cloning may be substituted by simple aspiration of bone marrow or sampling of skin fibroblasts. After a few years of negation, it is accepted again that in mammals take place processes of dedifferentiation and transdifferentiation. This paper presents old paradigms as well as arguments of partisans of challenging or even to refute these paradigms.
Oculomotor nerves (III, IV, VI) paralysis after cranial injury is not an exceptional case. However, bilateral abducens nerves injury following cranial trauma without fracture is a very rare occurrence. The abducens nerve (n. VI) is relatively long in its intracranial passage, during injury has relatively high elasticity and its mechanical avulsion is more difficult. In literature, we did not find any case describing bilateral abducens nerve injury as the only symptom of head trauma. There were described cases of unilateral injury of these nerves as an isolated symptom or in combination with the damage of other cerebral nerves mainly third and facial nerve. The authors present a case of a 67-year old man, in whom only bilateral abducens nerves injury was detected after cranial trauma. Neuroimaging examinations did not reveal the location of the injury. Lack of improvement of abducens nerves function in 4-month follow-up indicates, that most probably there came to neurotmesis as a result of injury. The authors consider the possible cause of VI nerve injury basing on various cases mentioned in literature.
We present a case of 66-year old male patient with history of hypertension, atrial fibrillation, ischaemic heart disease and diabetes mellitus. The patient was admitted to the Department of Neurology Medical University of Bialystok because of an ischaemic lesion of the right cerebral hemisphere. Besides left-sided hemiparesis, symptoms of unilateral neglect syndrome were observed. Term “unilateral neglect” is used to describe specific behavioural disturbances. It can be defined as a failure to respond and turn towards stimuli present in the contralesional hemispace. The lesion is usually located in cortical and subcortical structures of the right cerebral hemisphere. Left-sided cerebral lesions are seldom observed. In our patient, symptoms of perceptive variant of unilateral neglect syndrome (without any motor features of neglect) were observed. Features of the syndrome noticed shown in visual, auditory and tactile modalities. Cases of perceptive variant of the unilateral neglect syndrome, in particular incomplete ones (limited to one or two sensory modalities), could be easily overlooked in medical practice. Authors emphasize an importance of correct diagnosis of the unilateral neglect syndrome and early introduction of rehabilitation in improvement of neurological condition.
Models of neuropoiesis make it possible to determine at what stage of differentiation are neuronal cells. These models reflect our current knowledge about neuropoiesis, but they have also practical significance. In vitro determination whether neuronal stem cells differentiate to neuronal, astrocytic or oligodendrocytic progenitors is of utmost importance for cellular transplantologists. It seems that the use of progenitor cells and not fully differentiated cells or stem cells provides transplantologists with the greatest chance for therapeutic success: stem cells may choose a differentiation pathway other than planned by transplantologist, while mature cell, e.g. neurons, are quite sensitive to environmental changes. Determination of the progenitor type currently requires screening of expression of markers recognized as specific for particular cell type. Studies conducted for several years indicate that in the case of many markers this strategy is not appropriate. For example, the GFAP protein considered until recently a specific marker of astrocytes is also expressed in some neuronal stem cells. This discovery has led to a considerable chaos in the way cells are being defined. Furthermore, results of studies of the team where the author of this publication belongs indicate that stem cells may show coexpression of glial and neuronal markers. For the neuropoiesis model constructed upon this kind of data, a name “model of suppression of discordant phenotypes'’ has been proposed.