[During the past decade, several disease-modifying agents have been established and have become available for the treatment of multiple sclerosis. The disease-modifying agents could be grouped into immunomodulatory and immunosuppressive therapies altering the long-term course of multiple sclerosis. Therapy is now available for relapsing-remitting, secondary progressive and progressive-relapsing multiple sclerosis. Different disease-modifying agents became also available for the treatment of relapsing-remitting multiple sclerosis in Hungary which makes the therapeutic decision difficult. This overview might help to give an answer for different questions in the management of multiple sclerosis: Which agent to choose? When to initiate the therapy? Which dose to apply? Are the drugs safe? How long to treat the patients with immunomodulatory drugs? We give a review from the literature to assess the efficacy of disease-modifying therapies and to compare the data from phase three trials of interferon β1b, two preparations of interferon β1a or glatiramer acetate for the treatment of multiple sclerosis. We analyzed the efficacy and safety of these agents on physical, inflammatory and cognitive measures of disease activity. Comparison of study results indicated similar effects of immunomodulatory agents on relapse-related and inflammatory measures in relapsing multiple sclerosis. Interferon β1a slowed the progression of disability in relapsing multiple sclerosis. One interferon β1a preparation (intramuscularly injected) demonstrated efficacy in slowing progression of cognitive dysfunction. The interferons reduced relapses at early phase of secondary progressive multiple sclerosis, but their efficacy have not yet been proven in the later phase of secondary progressive multiple sclerosis without relapses. Mitoxantrone demonstrated efficacy in slowing the progression of disability in secondary progressive multiple sclerosis. All of the disease modifying agents are safe and tolerable, if the indication is correct and the patients are strictly controlled.]

[Objective - In our case report we present the treatment of a female patient suffering from therapy resistant depression. This procedure is not in practice in Hungary at present, the aim of our work to reproduce the findigs of international studies in domestic circumstances. Matter - Major depression is a common, chronic and severe mental disorder, with 16.2% lifetime prevalence. Many international randomized, placebo controlled trials found administration of ketamine infusion effective in depressed patients. Methods - Since ketamine is an anesthetic agent, its administration was performed in the post-operative monitoring room of our hospital operating-room, supervised by an anesthesiologist. According to formerly published data, a dose of 0.5 mg/kg of body weight was administered intravenously in 40 minutes by perfusor. The drug was administered in a same manner fifteen days later. Subject - The patient was admitted to our inpatient ward with severe depression. During two months of combined antidepressant therapy her condition has not improved significantly. Approval for off label drug indication was granted with urgency by the National Institute of Quality and Organizational Development in Healthcare and Medicines. Results - During the two treatments the Hamilton Depression Rating Scale 21 items rating scale score was reduced to 8 from the baseline 28, the Hamilton Anxiety Rating Scale score was reduced to 6 from 25, Beck Depression Inventory was reduced to 9 from 20. Upon administration of the drug no severe adverse event was detected, the mild dissociative state related to ketamine was ceased in a short period of time. Discussion - With administration of 0.5 mg/kg ketamine the authors managed to achieve rapid improvement in a therapy resistant depressed patient, without permanent side effects. Our future plan is to repeat the use of the drug within a double-blind, placebo controlled trial in order to prove its efficacy in hospital settings. ]

[It is well known that glutamate receptors have significant role in the pain transmission. The activation of N-methyl-Daspartate receptors causes persistent pain, therefore the antagonists acting on these receptors cause antinociception in chronic pain states. As the synthetic N-methyl-D-aspartate receptor antagonists have several side effects, they are not used generally in the clinical therapy. The tryptophan metabolite kynurenic acid is an endogenous antagonist of N-methyl-D-aspartate receptors. Although some data proved its neuroprotective effect, only a few studies suggest the antinociceptive potential of kynurenic acid. The goal of this review to summarise the possible role of kynurenic acid in the pain therapy based on the results of animal studies. Data available concerning this subject demonstrated that kynurenic acid is not an appropriate agent for antinociception neither in single nor in continuous administration because of its side-effect resulting in motor deficiency. On the other hand the combination of low doses of kynurenic acid and endomorphin-1 provides effective antinociception without side-effects on inflammatory pain test, thus may offer a new treatment modality in human pain therapy.]

[There has been a very significant reduction in morbidity and mortality associated with the use of antibiotics since they were first introduced, but, there has also been a concomitant rise in resistance among pathogens over the past 50 years. Moreover, antibiotics are sometimes associated with adverse events and their use can account for a significant proportion of the cost of treatment of some conditions. To ensure the optimal use of antibiotics doctors should use the most appropriate antibiotics to stop the spread of infection. In choosing the appropriate antimicrobial agent for the therapy of a certain infection several key factors must be considered: the most likely identity of the infecting organism, the potential antimicrobial susceptibility of the infecting organism and the host factors that influence the response to therapy. This publication is designed to introduce the concept of appropriate antibiotic therapy and how it can minimise the emergence of antimicrobial resistance while ensuring optimal patient management.]

[Here one case report of the posterior ischaemic optic neuropathy, a rare and underdiagnosed form of the non arteritic ischaemic optic neuropathy is presented, to underline the value of the MRI in the diagnosis. The ischaemic optic neuropathy is the infarction of the optic nerve. Depending on the affected segment of optic nerve (optic nerve head or retrobulbar segment) two subclasses exist: the anterior (AION) and the posterior (PION) ischaemic optic neuropathy. Ischaemic optic neuropathy characterized by sudden, painless, mononuclear loss of vision, and/or visual field defect, that is accompanied by a diagnostic picture of the optic disc fundus only in the case of the AION. The diagnosis of the PION is based on a diagnosis of exclusion described by Hayreh in 1981. The macular and retinal laesions, the etiological role of toxic agent, the compression and the inflammation of the optic nerve all have to be excluded. The differential diagnosis between the PION and the retrobulbar neuritis is more difficult. Nowadays, in addition to the case history and the clinical data the diagnosis of the PION could be confirmed with help of VEP (visual evoked potential) and MRI. In the case of an old woman who had a sudden, painless visual loss of left eye we confirmed the diagnosis of PION with MRI which was presumed after had excluding other etiological factors.]