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Thematische Bibliographien / Brain damage - Patients / Zeitschriftenartikel

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Zeitschriftenartikel zum Thema „Brain damage - Patients“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 29. Juli 2024

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1

Dabrowski, Wojciech, Ziemowit Rzecki, Jacek Pilat, and Marek Czajkowski. "Brain damage in cardiac surgery patients." Current Opinion in Pharmacology 12, no. 2 (April 2012): 189–94. http://dx.doi.org/10.1016/j.coph.2012.01.013.

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2

Allman, Peter. "Emotionalism Following Brain Damage." Behavioural Neurology 4, no. 1 (1991): 57–62. http://dx.doi.org/10.1155/1991/209837.

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Emotionalism is an heightened tendency to cry, or more rarely, laugh. It is commonly associated with brain damage and is often distressing to both patients and carers. Emotionalism is easily confused with depression, and when severe it can interfere with treatment. The aetiology is poorly understood but its response to drugs with different modes of action suggests that there is more than one underlying mechanism. When the components of emotionalism are studied separately a wide range is observed and they combine in a more complex and varied way than commonly held stereotyped views suggest. Mos

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Nazarova, J. A., and N. K. Kayumova. "DAMAGE TO THE AUTONOMIC NERVOUS SYSTEM IN PATIENTS WITH HYPOTHYROIDISM." Oriental Journal of Medicine and Pharmacology 03, no. 05 (September 8, 2023): 15–20. http://dx.doi.org/10.37547/supsci-ojmp-03-05-03.

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The most studied in hypothyroidism (HT) in this regard are neuromuscular disorders (hypothyroid myopathy and myotonic phenomenon) and damage to peripheral nerves, the prevalence of which is highly variable. Among the signs of organic brain damage, vestibulocerebellar disorders and, less frequently, extrapyramidal disorders are mentioned. In the structure of chronic encephalopathy in hypothyroidism, psycho-emotional and intellectual disorders are most often described (2,3,4,5).

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Asthana, Hari S., Manas K. Mandal, Shiv C. Tandon, and Sanjay Asthana. "Matching Top–Bottom Parts of Facial Expressions by Brain-Damaged Patients." Behavioural Neurology 4, no. 4 (1991): 255–63. http://dx.doi.org/10.1155/1991/485672.

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Patients with focal brain-damage, right/left hemisphere-damage (RHD/LHD) and anterior/posterior region-damage (ARD/PRD), and normal controls (NC) were asked to match photographs of top–bottom facial parts expressing different emotions, positive (happy, surprise), negative–aroused (fear, anger), negative–nonaroused (sad, disgust). The LHD patients performed significantly worse than the RHD patients, and the ARD patients were significantly worse than the PRD patients, in the perceptual-matching task with affective stimuli. NC subjects performed significantly better than any of the brain damaged

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Grigoryeva, V. N., and G. V. Tikhomirov. "Topographic Disorientation in Patients with Brain Damage." Neuroscience and Behavioral Physiology 49, no. 7 (August 13, 2019): 929–36. http://dx.doi.org/10.1007/s11055-019-00821-0.

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6

Lee, Joon, Sang-Hyeon Hwang, Ji-Hye Park, and Won-Serk Kim. "Dermatological conditions in patients with brain damage." Dermatologica Sinica 32, no. 3 (September 2014): 133–36. http://dx.doi.org/10.1016/j.dsi.2013.11.003.

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Lavrentieva, A., M. Giannakou, G. Tsaousi, A. Amaniti, and E. Sofianos. "Serum markers of brain damage in patients with brain death." European Journal of Anaesthesiology 18, Supplement 21 (2001): 70. http://dx.doi.org/10.1097/00003643-200100001-00247.

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Misonis, Nerijus, Darius Palionis, Algirdas Tamošiūnas, Vaidotas Zabulis, Kristina Ryliškienė, and Dalius Jatužis. "Early ischemic brain lesions after carotid angioplasty and stenting on diffusion-weighted magnetic resonance imaging study." Seminars in Cardiovascular Medicine 19, no. 2 (December 1, 2013): 13–20. http://dx.doi.org/10.2478/semcard-2013-0003.

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Summary Aim: The aim of the paper is to evaluate the appearance of the new early ischemic lesions in the brain after carotid angioplasty and stenting on diffusion-weighted magnetic resonance imaging, and their relationship with clinical and procedural factors. Methods: Carotid artery stenting (CAS) procedures performed by a single interventional cardiologist in years November 2006 to January 2013 were evaluated retrospectively. In total, 227 procedures for 211 patients (mean age 69.8 ± 8.5 years) were performed, from which 171 (75.3%) for male and 56 (24.7%) for female patients. Seventy-two (3

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Dorogovtsev, V. N., I. V. Molchanov, and D. S. Yankevich. "Orthostatic Hemodynamic Changes in Brain Damage." General Reanimatology 16, no. 2 (April 24, 2020): 22–29. http://dx.doi.org/10.15360/1813-9779-2020-2-22-29.

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Aim: to study orthostatic hemodynamic changes in patients with chronic disorders of consciousness after critical brain damage.Materials and methods. We studied 30 patients (10 women and 20 men) with chronic disorders of consciousness after severe brain damage aged 45±7 years, 10 of which were in the vegetative state (VS) and 20 had the minimally conscious state (MCS). The main causes of brain damage were traumatic brain injury (53% of patients) and cerebrovascular accidents (CVA) (23.3%). The rest of the patients had posthypoxic encephalopathy or were after brain tumor removal surgery. Passive

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Ornstein, T. J., B. J. Sahakian, and P. J. McKenna. "Memory and executive impairment in schizophrenia: comparison with frontal and temporal brain damage." Psychological Medicine 38, no. 6 (September 10, 2007): 833–42. http://dx.doi.org/10.1017/s0033291707001468.

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BackgroundAlthough poor neuropsychological test performance is well documented in schizophrenia, how closely it resembles that seen in patients with brain damage in terms of cognitive failures in daily life and stability over time has been little studied.MethodThirty patients with chronic schizophrenia, 24 patients with frontal or temporal brain damage and 30 healthy controls were given a battery of memory and executive tests. Carers of the two patient groups also completed questionnaires rating memory and executive failures in daily life. Testing was repeated 6 weeks later.ResultsThe schizoph

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Zaidel, Dahlia W. "Overall intelligence and localized brain damage." Behavioral and Brain Sciences 30, no. 2 (April 2007): 173–74. http://dx.doi.org/10.1017/s0140525x07001331.

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AbstractOverall mean performance on intelligence tests by brain-damaged patients with focal lesions can be misleading in regard to localization of intelligence. The widely used WAIS has many subtests that together recruit spatially distant neural “centers,” but individually the subtests reveal localized functions. Moreover, there are kinds of intelligence that defy the localizationist approach inferred from brain damage.

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Gratton, Caterina, Emi M. Nomura, Fernando Pérez, and Mark D'Esposito. "Focal Brain Lesions to Critical Locations Cause Widespread Disruption of the Modular Organization of the Brain." Journal of Cognitive Neuroscience 24, no. 6 (June 2012): 1275–85. http://dx.doi.org/10.1162/jocn_a_00222.

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Although it is generally assumed that brain damage predominantly affects only the function of the damaged region, here we show that focal damage to critical locations causes disruption of network organization throughout the brain. Using resting state fMRI, we assessed whole-brain network structure in patients with focal brain lesions. Only damage to those brain regions important for communication between subnetworks (e.g., “connectors”)—but not to those brain regions important for communication within sub-networks (e.g., “hubs”)—led to decreases in modularity, a measure of the integrity of net

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ZIHL, J., and D. VON CRAMON. "VISUAL FIELD RECOVERY FROM SCOTOMA IN PATIENTS WITH POSTGENICULATE DAMAGE." Brain 108, no. 2 (1985): 335–65. http://dx.doi.org/10.1093/brain/108.2.335.

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Kotchoubey, B., S. Lang, R. Baales, E. Herb, P. Maurer, G. Mezger, D. Schmalohr, V. Bostanov, and N. Birbaumer. "Brain potentials in human patients with extremely severe diffuse brain damage." Neuroscience Letters 301, no. 1 (March 2001): 37–40. http://dx.doi.org/10.1016/s0304-3940(01)01600-7.

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Cavinato, M., C. Volpato, S. Silvoni, M. Sacchetto, A. Merico, and F. Piccione. "Event-related brain potential modulation in patients with severe brain damage." Clinical Neurophysiology 122, no. 4 (April 2011): 719–24. http://dx.doi.org/10.1016/j.clinph.2010.08.024.

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Tomassini, Valentina, Heidi Johansen-Berg, Saad Jbabdi, Richard G. Wise, Carlo Pozzilli, Jacqueline Palace, and Paul M. Matthews. "Relating Brain Damage to Brain Plasticity in Patients With Multiple Sclerosis." Neurorehabilitation and Neural Repair 26, no. 6 (February 9, 2012): 581–93. http://dx.doi.org/10.1177/1545968311433208.

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Bogolepova, A. N., and O. S. Levin. "Cognitive rehabilitation of patients with focal brain damage." Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova 120, no. 4 (2020): 115. http://dx.doi.org/10.17116/jnevro2020120041115.

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Matsuo, K., M. Ayabe, H. Kuwahara, T. Hoshino, and M. M. Yokoyama. "Immune function in patients with chronic brain damage." Journal of Neuroimmunology 35 (January 1991): 27. http://dx.doi.org/10.1016/0165-5728(91)90879-c.

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Leggio, M. G., A. M. Tedesco, F. R. Chiricozzi, S. Clausi, A. Orsini, and M. Molinari. "Cognitive sequencing impairment in patients with focal or atrophic cerebellar damage." Brain 131, no. 5 (March 11, 2008): 1332–43. http://dx.doi.org/10.1093/brain/awn040.

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Öztuzcu, Serdar, Ahmet Arslan, Ercan Sivaslı, Mustafa Namıduru, Yusuf Ziya İğci, Esma Özkara, Mehri İğci, et al. "mRNA Expressions of SOCS3 Gene in Meningitis Patients." European Journal of Therapeutics 17, no. 1 (January 1, 2011): 29–32. http://dx.doi.org/10.58600/eurjther.2011-17-1-747-arch.

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Meningitis is an inflammatory disease caused by microorganisms and viruses with various clinical symptoms, which damages the brain tissue and membranes, and which induces biochemical and cellular changes in cerebrospinal fluid (CSF). Meningitis is an infectious disease with higher rates of mortality and morbidity. The possibility of death or permanent damage to patient is considerable, mortality rate is one in ten patients and permanent damages like deafness or various brain damages are one in seven patients. Experimental animal meningitis revealed that the leukocytes infiltrated in CSF due to

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Norka, Anna O., S. V. Vorobyev, R. N. Kuznetsova, M. K. Serebriakova, I. V. Kudryavtsev, S. N. Kovalenko, D. N. Monashenko, and Z. R. Korobova. "Features of humoral immunity in patients with mild traumatic brain injury." Russian Journal of Immunology 25, no. 4 (October 7, 2022): 471–76. http://dx.doi.org/10.46235/1028-7221-1182-foh.

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Traumatic brain injury (TBI) is an important problem of the healthcare system. A lPeading role in pathogenesis belongs to the action of shock wave upon skull and brain integuments, extending from the impacted site, as well as displacement and rotation of the cerebral hemispheres relative to the fixed brain stem. As a result, a cascade of metabolic, biochemical and inflammatory changes is initiated, leading to secondary damage. TBI, depending on its mechanism, severity and type, causes various primary structural and functional brain lesions at molecular, cellular, tissue and organ levels with d

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GOLDENBERG, GEORG. "THE ABILITY OF PATIENTS WITH BRAIN DAMAGE TO GENERATE MENTAL VISUAL IMAGES." Brain 112, no. 2 (1989): 305–25. http://dx.doi.org/10.1093/brain/112.2.305.

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Godefroy, Olivier, Chantal Lhullier, and Marc Rousseaux. "Non-spatial attention disorders in patients with frontal or posterior brain damage." Brain 119, no. 1 (1996): 191–202. http://dx.doi.org/10.1093/brain/119.1.191.

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Fox, Geoffrey A., and Allison M. Fox. "The Effects of Brain Damage on the Performance of Hand Movement Sequences." Brain Impairment 2, no. 2 (December 1, 2001): 140–44. http://dx.doi.org/10.1375/brim.2.2.140.

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AbstractThe frontal lobes, if damaged, may lead to a host of divergent abnormalities, depending on the extent, site, depth, and laterality of the damage. Because of the extensive connections which exist between the frontal lobes and the other systems of the brain, damage to a more remote system may cause frontal system disorder through disconnection. The Hand Movement Test (HMT, Kaufman & Kaufman, 1983) is thought to be sensitive to damage affecting these systems, although the test was developed for use with children rather than adults. This paper examines the effects of three diverse neur

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Sultana, Nahida, Chao Sun, Takanori Katsube, and Bing Wang. "Biomarkers of Brain Damage Induced by Radiotherapy." Dose-Response 18, no. 3 (July 1, 2020): 155932582093827. http://dx.doi.org/10.1177/1559325820938279.

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Radiotherapy remains currently a critical component for both primary and metastatic brain tumors either alone or in combination with surgery, chemotherapy, and molecularly targeted agents, while it could cause simultaneously normal brain tissue injury leading to serious health consequences, that is, development of cognitive impairments following cranial radiotherapy is considered as a critical clinical disadvantage especially for the whole brain radiotherapy. Biomarkers can help to detect the accurate physiology or conditions of patients with brain tumor and develop effective treatment procedu

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KUCHARSKA-PIETURA, KATARZYNA, and ANTHONY S. DAVID. "The perception of emotional chimeric faces in patients with depression, mania and unilateral brain damage." Psychological Medicine 33, no. 4 (May 2003): 739–45. http://dx.doi.org/10.1017/s0033291702007316.

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Background. Judgements made on chimeric faces elicit reliably a perceptual bias to the left hemispace, presumed to be due to right hemisphere dominance for emotional processes. Major depressive illness has been shown to attenuate this bias. The aim of this work was to examine lateral perceptual bias in bipolar I and II patients in a hypomanic state and unipolar depressed patients and those with unilateral hemisphere damage following stroke.Method. Sixty patients with DSM-IV affective disorder (30 bipolar I or II, currently hypomanic, 30 unipolar depressives), 30 right brain-damaged patients, 3

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ANDERSSON, S., J. M. KROGSTAD, and A. FINSET. "Apathy and depressed mood in acquired brain damage: relationship to lesion localization and psychophysiological reactivity." Psychological Medicine 29, no. 2 (March 1999): 447–56. http://dx.doi.org/10.1017/s0033291798008046.

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Background. Apathy is a frequent neurobehavioural sequel in patients with acquired brain damage and it may seriously affect outcome of rehabilitation.Methods. Patients with traumatic brain injury, cerebrovascular insults and hypoxic brain injury, categorized into four lesion localization groups: left hemisphere damage (LHD); right hemisphere damage (RHD); bilateral hemispheric damage (BHD); and subcortical damage (SCD) were assessed with the Apathy Evaluation Scale (AES) and Montgomery and Åsberg Depression Rating Scale (MADRS). Heart rate and electrodermal activity were recorded in an experim

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Horton, Macneill,, and Steven A. Sobelman. "The General Neuropsychological Deficit Scale and Halstead Impairment Index: Comparison of Severity." Perceptual and Motor Skills 78, no. 3 (June 1994): 888–90. http://dx.doi.org/10.1177/003151259407800342.

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To examine how the severity of brain damage is evaluated by a summary neuropsychological measure, the General Neuropsychological Deficit Scale, 25 brain-damaged patients completed the Halstead-Reitan Neuropsychological Test Battery. From the test scores, both the General Neuropsychological Deficit Scale and the Halstead Impairment Index were calculated for each patient. Hit rates for agreement on severity were 60%, i.e., 15/25. Examination of the data suggested the General Neuropsychological Deficit Scale better reflects severity of brain damage at greater severity.

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Borsche, Max, Inke R. König, Sylvie Delcambre, Simona Petrucci, Alexander Balck, Norbert Brüggemann, Alexander Zimprich, et al. "Mitochondrial damage-associated inflammation highlights biomarkers in PRKN/PINK1 parkinsonism." Brain 143, no. 10 (October 1, 2020): 3041–51. http://dx.doi.org/10.1093/brain/awaa246.

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Abstract There is increasing evidence for a role of inflammation in Parkinson’s disease. Recent research in murine models suggests that parkin and PINK1 deficiency leads to impaired mitophagy, which causes the release of mitochondrial DNA (mtDNA), thereby triggering inflammation. Specifically, the CGAS (cyclic GMP-AMP synthase)-STING (stimulator of interferon genes) pathway mitigates activation of the innate immune system, quantifiable as increased interleukin-6 (IL6) levels. However, the role of IL6 and circulating cell-free mtDNA in unaffected and affected individuals harbouring mutations in

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Guerrini, Irene, and Rosie Mundt-Leach. "Preventing long-term brain damage in alcohol-dependent patients." Nursing Standard 27, no. 19 (January 9, 2013): 43–46. http://dx.doi.org/10.7748/ns2013.01.27.19.43.c9498.

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Anonymous. "Brain damage may be reversible in patients with Alzheimer's." Journal of Psychosocial Nursing and Mental Health Services 36, no. 1 (January 1998): 12. http://dx.doi.org/10.3928/0279-3695-19980101-03.

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Glass, Ilana B. "Alcoholic brain damage: what does it mean to patients?" Addiction 86, no. 7 (July 1991): 819–21. http://dx.doi.org/10.1111/j.1360-0443.1991.tb01830.x.

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Lennane, K. Jean. "Patients with Alcohol-Related Brain Damage: Therapy and Outcome." Australian Drug and Alcohol Review 7, no. 1 (January 1988): 89–92. http://dx.doi.org/10.1080/09595238880000201.

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Viggiano, Maria Pia, and Sabrina Pitzalis. "Identification of Fragmented Pictures in Patients With Brain Damage." Applied Neuropsychology 5, no. 2 (June 1998): 93–99. http://dx.doi.org/10.1207/s15324826an0502_5.

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Ursino, M., C. A. Lodi, S. Rossi, and N. Stocchetti. "Intracranial pressure dynamics in patients with acute brain damage." Journal of Applied Physiology 82, no. 4 (April 1, 1997): 1270–82. http://dx.doi.org/10.1152/jappl.1997.82.4.1270.

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Ursino, M., C. A. Lodi, S. Rossi, and N. Stocchetti.Intracranial pressure dynamics in patients with acute brain damage. J. Appl. Physiol. 82(4): 1270–1282, 1997.—The time pattern of intracranial pressure (ICP) during pressure-volume index (PVI) tests was analyzed in 20 patients with severe acute brain damage by means of a simple mathematical model. In most cases, a satisfactory fitting between model response and patient data was achieved by adjusting only four parameters: the cerebrospinal fluid (CSF) outflow resistance, the intracranial elastance coefficient, and the gain and time constant of

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Pérez de la Ossa, Natalia, Tomás Sobrino, Yolanda Silva, Miguel Blanco, Monica Millán, Meritxell Gomis, Jesús Agulla, et al. "Iron-Related Brain Damage in Patients With Intracerebral Hemorrhage." Stroke 41, no. 4 (April 2010): 810–13. http://dx.doi.org/10.1161/strokeaha.109.570168.

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Georgopoulos, D., I. Mitrouska, K. Koletsos, K. Markopoulou, D. Riggos, D. Patakas, and N. R. Anthonisen. "Ventilatory post-stimulus potentiation in patients with brain damage." American Journal of Respiratory and Critical Care Medicine 152, no. 5 (November 1995): 1627–32. http://dx.doi.org/10.1164/ajrccm.152.5.7582306.

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Stocchetti, N., A. Parma, V. Songa, A. Colombo, M. Lamperti, and L. Tognini. "Early translaryngeal tracheostomy in patients with severe brain damage." Intensive Care Medicine 26, no. 8 (August 21, 2000): 1101–7. http://dx.doi.org/10.1007/s001340051324.

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Go, Tohshin, and Yukuo Konishi. "Neonatal Oral Imitation in Patients with Severe Brain Damage." PLoS ONE 3, no. 11 (November 7, 2008): e3668. http://dx.doi.org/10.1371/journal.pone.0003668.

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Josefson, D. "Cooling patients after cardiac arrest may prevent brain damage." BMJ 323, no. 7318 (October 20, 2001): 889. http://dx.doi.org/10.1136/bmj.323.7318.889b.

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Odell, Katharine, James Wollack, and Marge Flynn. "Functional outcomes in patients with right hemisphere brain damage." Aphasiology 19, no. 9 (September 2005): 807–30. http://dx.doi.org/10.1080/02687030500239226.

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Zaidel, Dahlia W. "Neuronal connectivity, regional differentiation, and brain damage in humans." Behavioral and Brain Sciences 22, no. 5 (October 1999): 854–55. http://dx.doi.org/10.1017/s0140525x99502197.

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When circumscribed brain regions are damaged in humans, highly specific impairments in language, memory, problem solving, and cognition are observed. Neurosurgery such as “split brain” or hemispherectomy, for example, has shown that encompassing regions, the left and right cerebral hemispheres, each control human behavior in unique ways. Observations stretching over 100 years of patients with unilateral focal brain damage have revealed, without the theoretical benefits of “cognitive neuroscience” or “cognitive psychology,” that human behavior is indeed controlled by the brain and its neurons.

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Cristinzio, C., K. N'Diaye, M. Seeck, P. Vuilleumier, and D. Sander. "Integration of gaze direction and facial expression in patients with unilateral amygdala damage." Brain 133, no. 1 (October 14, 2009): 248–61. http://dx.doi.org/10.1093/brain/awp255.

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Antonenko, L. M., N. V. Vakhnina, and D. O. Gromova. "Cognitive impairment, dizziness, and unsteadiness in hypertensive patients." Neurology, Neuropsychiatry, Psychosomatics 12, no. 5 (October 25, 2020): 92–97. http://dx.doi.org/10.14412/2074-2711-2020-5-92-97.

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Hypertension is a widespread disease related to modifiable vascular risk factors for stroke and chronic cerebrovascular diseases. The pathogenetic basis of brain damage in hypertension is cerebral microangiopathy that leads to vascular cognitive impairment (CI), instability, and falls. Microcirculatory changes in the presence of hypertension at the initial stages of cerebrovascular disease occur without visible clinical manifestations of brain damage. Pathogenetically justified treatment used at an early stage of the disease makes it possible to achieve good results in the prevention of vascul

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Suzuki, Noboru, Nagisa Arimitsu, Jun Shimizu, Kenji Takai, Chieko Hirotsu, Yuji Ueda, Sueshige Wakisaka, Naruyoshi Fujiwara, and Tomoko Suzuki. "Neuronal Cell Sheets of Cortical Motor Neuron Phenotype Derived from Human iPSCs." Cell Transplantation 26, no. 8 (August 2017): 1355–64. http://dx.doi.org/10.1177/0963689717720280.

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Transplantation of stem cells that differentiate into more mature neural cells brings about functional improvement in preclinical studies of stroke. Previous transplant approaches in the diseased brain utilized injection of the cells in a cell suspension. In addition, neural stem cells were preferentially used for grafting. However, these cells had no specific relationship to the damaged tissue of stroke and brain injury patients. The injection of cells in a suspension destroyed the cell–cell interactions that are suggested to be important for promoting functional integrity of cortical motor n

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Białaszek, Wojciech, Bartłomiej Swebodziński, and Paweł Ostaszewski. "Intertemporal Decision Making After Brain Injury: Amount-Dependent Steeper Discounting after Frontal Cortex Damage." Polish Psychological Bulletin 48, no. 4 (December 20, 2017): 456–63. http://dx.doi.org/10.1515/ppb-2017-0052.

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Abstract Traumatic brain injuries to the frontal lobes are associated with many maladaptive forms of behavior. We investigated the association between brain damage and impulsivity, as measured by the rate of delay discounting (i.e., the extent to which future outcomes are devalued in time). The main aim of this study was to test the hypothesis of steeper discounting of different amounts in a group of patients with frontal lobe damage. We used a delay discounting task in the form of a structured interview. A total of 117 participants were divided into five groups: three neurological groups and

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Rahmanzadeh, Reza, Po-Jui Lu, Muhamed Barakovic, Matthias Weigel, Pietro Maggi, Thanh D. Nguyen, Simona Schiavi, et al. "Myelin and axon pathology in multiple sclerosis assessed by myelin water and multi-shell diffusion imaging." Brain 144, no. 6 (March 9, 2021): 1684–96. http://dx.doi.org/10.1093/brain/awab088.

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Abstract Damage to the myelin sheath and the neuroaxonal unit is a cardinal feature of multiple sclerosis; however, a detailed characterization of the interaction between myelin and axon damage in vivo remains challenging. We applied myelin water and multi-shell diffusion imaging to quantify the relative damage to myelin and axons (i) among different lesion types; (ii) in normal-appearing tissue; and (iii) across multiple sclerosis clinical subtypes and healthy controls. We also assessed the relation of focal myelin/axon damage with disability and serum neurofilament light chain as a global bi

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Serra, Laura, Matteo Mancini, Gabriella Silvestri, Antonio Petrucci, Marcella Masciullo, Barbara Spanò, Mario Torso, et al. "Brain Connectomics’ Modification to Clarify Motor and Nonmotor Features of Myotonic Dystrophy Type 1." Neural Plasticity 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/2696085.

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The adult form of myotonic dystrophy type 1 (DM1) presents with paradoxical inconsistencies between severity of brain damage, relative preservation of cognition, and failure in everyday life. This study, based on the assessment of brain connectivity and mechanisms of plasticity, aimed at reconciling these conflicting issues. Resting-state functional MRI and graph theoretical methods of analysis were used to assess brain topological features in a large cohort of patients with DM1. Patients, compared to controls, revealed reduced connectivity in a large frontoparietal network that correlated wit

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Nyakale, Nozipho, Ralf Clauss, Wally Nel, and Mike Sathekge. "Clinical and brain SPECT scan response to zolpidem in patients after brain damage." Arzneimittelforschung 60, no. 04 (December 2, 2011): 177–81. http://dx.doi.org/10.1055/s-0031-1296269.

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Granziera, Cristina, Jens Wuerfel, Frederik Barkhof, Massimiliano Calabrese, Nicola De Stefano, Christian Enzinger, Nikos Evangelou, et al. "Quantitative magnetic resonance imaging towards clinical application in multiple sclerosis." Brain 144, no. 5 (May 1, 2021): 1296–311. http://dx.doi.org/10.1093/brain/awab029.

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Abstract Quantitative MRI provides biophysical measures of the microstructural integrity of the CNS, which can be compared across CNS regions, patients, and centres. In patients with multiple sclerosis, quantitative MRI techniques such as relaxometry, myelin imaging, magnetization transfer, diffusion MRI, quantitative susceptibility mapping, and perfusion MRI, complement conventional MRI techniques by providing insight into disease mechanisms. These include: (i) presence and extent of diffuse damage in CNS tissue outside lesions (normal-appearing tissue); (ii) heterogeneity of damage and repai

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