[Neurophobia is the fear of neurological diseases. Its main symptom is that medical students and young doctors are not able to utilize their basic neurological knowledge at the bedside. According to statistics, every second student suffers from neurophobia. This attitude could explain why in the last two decades less and less young doctors wanted to become neurologist. Medical students complain that they receive no instructions, and are afraid of loosing their interest and of facing the failure of their competency. The hardship of neurology was explained by the insufficient knowledge of anatomy and the infrequent encounter with patients. Even general practitioners have anxiety about neurological patients. The loss of interest in neurosciences seems to associate with insensitivity of human-centered culture and corruption of empathic thinking. The burnout syndrome of medical doctors and students can be explained by stress, loss of respect, permanent competition, independency that interferes with responsibility, stiff hierarchy of medical society, fear of diagnostic failures and of economical difficulties. The scores of depression in female students were higher than in male. The idea of the “good neurologist” has been changed. The business oriented care, the shortage of time, and the financial restrictions corroded the conventional practice and ceased the vocational idealism. At present, personal teaching is going to transform into impersonal multimedia learning. Because of the drastic change of values, the age of inner-oriented professionals has terminated also in the medicine. Medical doctors follow even less the traditional troll of professional behavior, but according the social demands, they choose their specialization for subsistence. The highly esteemed social status of neurologists and psychiatrists is going to sink in Europe. To reduce neurophobia it would be desirable 1. to introduce neurology training in the early years of medical school; 2. to teach neurology in all semesters, 3. to assure the effective teaching of neuro-anatomy and physiology, 4. to organize more one-to-one teacher-student communication. In the United States, residents participate in teaching during their residency training. To master neurology dedicated teachers are necessary whom neurology residents ought to meet personally with optimal frequency. However, these requirements seem to fail because of the chiefly technical characters of the actual reforms.]

[Parkinson’s disease is a promising target of applying personalized medicine. For this purpose it is crucial to reveal the genetic and environmental factors, which contribute to the disease, also to collect epidemiologic data and to preserve the patients samples and data in a proper biobank. In our investigation we examined the prevalence of the most frequent Parkinson’s disease causing LRRK2 G2019S mutation in a Hungarian Parkinson-patient group. From 120 patients, we haven’t detected this substitution in anyone. Our investigation suggest that the mutation LRRK2 G2019S may be a rare cause of Parkinson disease in the Hungarian population.]

[Background - Bilateral pallidal deep brain stimulation (DBS) is an established treatment option for primary generalized and segmental dystonia. In the present study we evaluated the results of our dystonia patients treated by DBS. Methods - The surgical results of forty consecutive dystonia patients underwent DBS implantation were analyzed (age: 43.7±17.7 years; sex: 22 men; etiology: 24 primary and 16 secondary dystonia; topography: 24 generalized, 12 segmental and four hemidystonia; disease duration: 16.1±9.3 years). Severity of dystonia measured by Burke-Fahn-Marsden Dystonia Rating Scale (BFMDRS) and health-related quality of life measured by EQ-5D scale were obtained preoperatively and compared to the scores obtained at postoperative six months and subsequent yearly follow-ups. The average follow-up lasted 2.5 years (median, 0.5-8 years). In all cases the BFMDRS scores were re-evaluated by a rater blinded to the treatment. Treatment responsiveness was defined as an at least 25% improvement on the BFMDRS scores. Non-parametric Mann-Whitney, McNemar and Kruskal-Wallis tests were applied to test statistical significance. Results - Severity of dystonia improved from 31 to 10 points (median, 68% improvement, p<0.01) in the primary dystonia group, whereas in secondary dystonia these changes were statistically insignificant (improvement from 40 to 31.5 points, 21.2%, p>0.05). However, the health-related quality of life significantly improved in both groups (primary dystonia: 0.378 vs. 0.788 and secondary dystonia: 0.110 vs. 0.388, p<0.01). Significantly more patients in the primary dystonia group responded to DBS treatment than those in the secondary dystonia group (83.3% vs. 37.5%, p<0.01). Conclusion - Our results are in accordance with previously published international findings demonstrating that DBS is a highly effective and long-lasting treatment option for primary dystonia. DBS is considerably less efficient in secondary dystonia; however, it still has a high impact on the quality of life presumably due to its pain-relieving effect.]

[Background and purpose - It has been reported that multiple sclerosis has four different neuropathological subtypes, and two of them (type III and IV) are characterized by primary oligodendrocyte loss. However, the exact pathomechanism that lead to oligodendrocyte apoptosis in human demyelinating diseases is still elusive. The copper chelator cuprizone induces primary oligodendrocyte apoptosis and consequent demyelination in well defined areas of the mouse brain. Nevertheless, the precise subcellular events that result in oligodendrocyte cell death in the cuprizone model are still unknown. We aimed to study the ultrastructural alterations that might induce oligodendrocyte apoptosis in the cuprizone experimental demyelination model. Methods - C57BL/6 mice were given cuprizone for two, 21 and 35 days to induce demyelination to investigate early pathological events, and different stages of demyelination. In addition, mice were given cuprizone for 35 days and were allowed to recover for two or 14 days to study early and late remyelination. After the cuprizone treatment, mice were sacrificed and the corpus callosum, the superior cerebellar peduncle, the optic nerve and the sciatic nerve were studied by electron microscopy. Results - The ultrastructural analysis revealed that cuprizone induced oligodendrocyte apoptosis is accompanied by the formation of giant mitochondria in the affected cells in the corpus callosum and in the superior cerebellar peduncle. Apoptosis of the myelin producing cells was present through the whole cuprizone challenge. Severe demyelination occurred after three weeks of cuprizone administration associated with massive macrophage infiltration and astrocytosis of the demyelinated areas. Axons and neurons remained unaffected. Conclusion - The formation of giant mitochondria in myelin producing oligodendrocytes is the first pathological sign in the cuprizone experimental demyelination. Mitochondrium pathology in the cuprizone challenge might serve as a useful model to study the pathomechanism of multiple sclerosis subtypes (III and IV) characterized by primary oligodendrocyte degeneration.]