Search Results

1 - 10 of 23 items :

  • "deep brain stimulation" x
Clear All

References 1. Graat I., Figee M. & Denys D. The application of deep brain stimulation in the treatment of psychiatric disorders, International Review of Psychiatry, 2017;29:2, 178-190, DOI: 10.1080/09540261.2017.1282439 2. Zrinzo L, Foltynie T, Limousin P, Hariz MI: Reducing hemorrhagic complications in functional neurosurgery: a large case series and systematic literature review. J Neurosurg. 2012; 116: 84-94. 10.3171/2011.8.JNS101407. 3. Pool JL. Psychosurgery in older people. J Am Geriatr Soc 1954;2:456-66. U.S. Department of Health and Human Services. 4. FDA

, Dzierzęcki S, Ząbek M. Głęboka stymulacja mózgu w leczeniu depresji i zaburzeń obsesyjno-kompulsyjnych. Neurol. Neurochir. Pol. 2009; 43:6. 9. Denys D, Mantione M, Figee M, van den Munckhof P, Koerselman F, Westenberg H, et al. Deep brain stimulation of the nucleus accumbens for treatment-refractory obsessive-compulsive disorder. Arch Gen Psychiatry. 2010; 67:1061–1068. 10. De Hemptinne C, Swann NC, Ostrem JL, Ryapolova-Webb ES, San Luciano M, Galifianakis NB, Starr PA. Therapeutic deep brainstimulation reduces cortical phase-amplitude coupling in Parkinson’s disease. Nat

Introduction Neuromodulation is among the fastest growing areas in medicine. It involves cortical and sub-cortical electrical stimulation for the treatment of an increasing number of neurological and psychiatric diseases. Among interventions that use electrical stimulation to treat movement disorders, such as Parkinson’s disease (PD), deep brain stimulation (DBS) is probably the most successful approach [ 1 ]. High-frequency (approx. 130 Hz, 60-μs needle pulses) DBS of the subthalamic nucleus (STN) is an effective therapeutic option for PD patients, particularly

References [1] Bouton, C. (2017). Cracking the neural code, treating paralysis and the future of bioelectronic medicine. Journal of Internal Medicine , 282 (1), 37-45. [2] Wichmann, T., DeLong, M.R. (2016). Deep brain stimulation for movement disorders of basal ganglia origin: Restoring function or functionality? Neurotherapeutics , 13 (2), 264-283. [3] Kocabicak, E., Alptekin, O., Ackermans, L., Kubben, P., Kuijf, M., Kurt, E., et al. (2015). Is there still need for microelectrode recording now the subthalamic nucleus can be well visualized with high field and

Abstract

New achievements within structural and functional imaging of central nervous system offer a basis for better understanding of the mechanisms underlying many mental disorders. In everyday clinical practice, we encounter many difficulties in the therapy of eating disorders. They are caused by a complex psychopathological picture, varied grounds of the problems experienced by patients, often poor motivation for active participation in the treatment process, difficulties in communication between patients and therapeutic staff, and various biological conditions of eating disorders. In this paper, the latest reports on new concepts and methods of diagnosis and treatment of anorexia nervosa have been analyzed. The selection of the analyzed publications was based on the criteria taking into account the time of publication, the size of research cohorts, as well as the experience of research teams in the field of nutritional disorders, confirmed by the number of works and their citations. The work aims to spread current information on anorexia nervosa neurobiology that would allow for determining the brain regions involved in the regulation of food intake, and consequently that may be a potential place where neurobiochemical processes responsible for eating disorders occur. In addition, using modern methods of structural imaging, the authors want to show some of the morphometric variations, particularly within white matter, occurring in patients suffering from anorexia nervosa, as well as those evaluated with magnetoencephalography of processes associated with the neuronal processing of information related to food intake. For example as regards anorexia nervosa, it was possible to localize the areas associated with eating disorders and broaden our knowledge about the changes in these areas that cause and accompany the illness. The described in this paper research studies using diffusion MRI fiber tractography showed the presence of changes in the white matter pathways of the brain, especially in the corpus callosum, which indicate a reduced content of myelin. These changes probably reflect malnutrition, and directly represent the effect of lipid deficiency. This leads to a weakening of the structure, and even cell death. In addition, there are more and more reports that show the normal volume of brain cells in patients with long-term remission of anorexia. It was also shown that in patients in remission stage there are functional changes within the amygdala in response to a task not related symptomatologically with anorexia nervosa. The appearing in the scientific literature data stating that in patients with anorexia nervosa there is a reduced density of GFAP + cells of the hippocampus and increased expression of vimentin and nestin, is also worth noting.

References Anderson, P.B. and Rogers, M.H. (2009). Deep Brain Stimulation: Applications, Complications and Side Effects , Nova Biomedical Books, New York, NY. Apostolidis-Afentoulis, V. and Lioufi, K.I. (2015). classification with linear and RBF kernels, http://www.academia.edu/13811676/SVM_Classification_with_Linear_and_RBF_kernels . Cagnan, H., Dolan, K., He, X., Contarino, M.F., Schuurman, R., Van Den Munckhof, P., Wadman, W.J., Bour, L. and Martens, H.C. (2011). Automatic subthalamic nucleus detection from microelectrode recordings based on noise level and

treatment of a severe tardive dyskinesia: A case report. SAGE Open Med Case Rep. 2019;7:2050313X19833254. doi:10.1177/2050313X19833254 9. Caroff SN, Aggarwal S, Yonan C. Treatment of tardive dyskinesia with tetrabenazine or valbenazine: a systematic review. J Comp Eff Res. 2018;7(2):135-148. doi:10.2217/cer-2017-0065 10. Caroff SN. Overcoming barriers to effective management of tardive dyskinesia. Neuropsychiatr Dis Treat. 2019;15:785-794. doi:10.2147/NDT.S196541 11. Macerollo A, Deuschl G. Deep brain stimulation for tardive syndromes: Systematic review and meta

, M. H., Tsiokos, C., Matlack, C., Chizeck, H. J., & Pouratian, N. (2014). Creating the Feedback Loop. Neurosurgery Clinics of North America , 25 (1), 187–204. doi: 10.1016/j.nec.2013.08.006 Hell, F., Köglsperger, T., Mehrkens, J., & Boetzel, K. (2018). Improving the Standard for Deep Brain Stimulation Therapy: Target Structures and Feedback Signals for Adaptive Stimulation. Current Perspectives and Future Directions. Cureus , 10 (4). doi: 10.7759/cureus.2468 Kuhner, A., Schubert, T., Cenciarini, M., Wiesmeier, I. K., Coenen, V. A., Burgard, W., Weiller, C., et

References 1. Amtage F. et al. Hypokinesia upon pallidal deep brain stimulation of dystonia: support of a GABAergic mechanism. Front. Neurol., 1-6, 4, 2013. DOI: 10.3389/fneur.2013.00198 2. Contarteze R.V. et al. Stress biomarkers in rats submitted to swimming and treadmill running exercises. Comp. Biochem. Physiol. Part A: Mol. Integr. Physiol., 415-22, 151, 2008. DOI: dx.doi. org/10.1016/j.cbpa.2007.03.005 3. Kim H. G. et al. Effects of treadmillexercise on hypoactivity of the hypothalamo-pituitary-adrenal axis induced bychronic administration of corticosterone

enhancement and deep-brain stimulation of the entorhinal area. N Engl J Med 2012, 6 , 502-510. 25. Suzuki W.A., Porteros A.: Distribution of calbindin D-28k in the entorhinal, perirhinal, and parahippocampal cortices of the macaque monkey. Comp Neurol Sep 2002, 4 , 392-412. 26. Skrebitskiĭ V.G., Shtark M.B.: The fundaments of neuronal plasticity. Vestn Ross Akad Med Nauk 2012, 9, 39-44. 27. Szalak R.: The morphology of neurons and topography of gyrus parahippocampalis in the chinchilla. Med Weter 2008, 64 , 1240-1243. 28. Szalak R., Jaworska-Adamu J.: Intracellular