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Статті в журналах з теми "Brain damage - Patients"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 29 липня 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. Most patients with emotionalism are helped by simple education and reassurance. Some severe cases respond dramatically to tricyclic antidepressants, levodopa or fluoxetine.

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3

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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4

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 sub-groups.

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5

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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7

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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8

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 (34.1%) patients had symptomatic stenosis of carotid artery. The following protection systems to avoid the distal microembolism were used during the CAS: (1) Filters: FilterWire EZ (Boston Scientific Corporation); Emboshield NAV (Abbott Vascular); SpideRX (EV3); Defender (Medtronic); FiberNet Filter (Invatec-Medtronic); (2) Occlusion MoMa Baloon System (Invatec-Medtronic). Acute ischemic damages of the brain before and after CAS procedure were diagnosed using magnetic resonance imaging (MRI) with diffusion-weighted imaging (DWI) sequences. Sixty-five (30.8%) patients underwent MRI test. Exact and asymptomatic χ2 criteria were applied for testing the hypothesis of inter-dependency of the symptoms. Results: Forty-six (70.8%) patients had new ischemic foci in the brain on MRI DWI after CAS procedures. Among those patients, focal damage of the brain was diagnosed in 36 (78.3%) cases; linear damage of the brain - in 9 (19.6%) patients; ipsilateral damage of the brain - in 37 (80.4%) patients; bilateral damage of the brain - in 16 (34.8%) patients, 38 (82.6%) patients were diagnosed with forebrain damage; 4 (8.7%) patients were diagnosed with damage of brainstem; 5 (10.9%) patients were diagnosed with cerebellum damage. Clinical symptoms of brain damage were diagnosed only for 2 (4.3%) patients. Focal damage of the brain was significantly less frequent only for aortic arch type 1, if compared with aortic arch type 2 and 3: 64.3%, 93.3% and 100.0%, respectively (p < 0.05). Focal damage of the brain occurred least in patients (28.6%) with Emboshield NAV protection type, if compared to other types of protection (71.4-100.0%). Linear >10mmbrain damage was less frequent when using FilterWire EZ, Emboshield NAV and SpideRX protection type. Ipsilateral ischemic brain damage also occurred less frequent when using Emboshield NAV protection type; bilateral damage occurred less frequent when using FilterWire EZ, Emboshield NAV and SpideRX protection type. Ischemic forebrain damage was also diagnosed less often in patients for whom protection type FilterWire EZ and Emboshield NAV was applied. Conclusions: Most frequent findings by MRI after CAS procedures were focal, ipsilateral and forebrain damage (about 80%), but less than 5% patients had clinical symptoms. In the case of aorta arch type 1 focal ischemic damage of the brain was significantly less frequent, then in aortic arch type 2 and 3. The localization and extent of brain damage was associated with the type of protection systems that have been used.

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9

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 orthostatic test (POT) 0° to 60° to 0° was performed using an electrically driven tilt table (Vario Line). Hemodynamic monitoring during the verticalization was done using a non-invasive oscillometric recording of blood pressure on the brachial artery, stroke volume (SV) and cardiac minute output (CMO) were measured by impedance cardiography with the multifunctional «Task Force Monitor 3010i» (CNSystem, Austria). Data were statistically analyzed using the Statistica 10 software package.Results. Orthostatic hemodynamic stability was found in 26 out of 30 patients with chronic disorders of consciousness after critical brain damage. It was manifested by stable systolic blood pressure (SBP) in tilted orthostatic and horizontal position (120.7±2.2 and 121.1±3.6 mmHg, respectively, P>0.05). Orthostatic hypotension was observed in 3 patients and postural tachycardia syndrome (PTS) in one patient. We compared orthostatic hemodynamic changes in the studied cohort versus published data on orthostatic hemodynamic changes uncluding POT revealed in patients with severe brain damage examined before and after brain death.Conclusion. Orthostatic stability of blood circulation can be maintained for a short period of time in patients surviving after critical diffuse brain damage associated with chronic disorders of consciousness. Critical brain damage resulting in brain death associates with a significant reduction of all hemodynamic parameters and severe orthostatic hypotension with restoration of initial blood pressure values when the patient is returned to the horizontal position.

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10

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 schizophrenia and the brain-damaged patients were significantly impaired on most, but not all tests. The degree of carer-rated memory or executive failure was similar in the two groups, but the schizophrenia patients were rated as having significantly more executive failures than memory failures, whereas the brain-damaged patients showed the reverse pattern. Both groups of patients showed similar consistency of performance across sessions.ConclusionsNeuropsychological impairment in schizophrenia resembles that seen in patients with brain damage, not only in terms of overall severity, but also in terms of stability and the degree to which poor test performance translates into cognitive failures in daily life.

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11

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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12

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 network organization. Critically, this network dysfunction extended into the structurally intact hemisphere. Thus, focal brain damage can have a widespread, nonlocal impact on brain network organization when there is damage to regions important for the communication between networks. These findings fundamentally revise our understanding of the remote effects of focal brain damage and may explain numerous puzzling cases of functional deficits that are observed following brain injury.

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13

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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14

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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15

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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16

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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17

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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18

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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19

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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20

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 bacterial dissemination contributed to damage progression in brain tissue, increased brain edema and intracranial pressure. The association between gene expression of SOCS3 which is effective in repressing the JAK/STAT signal transduction pathway and meningitis disease were investigated in this study. Gene expression levels of SOCS3 in leukocytes leaked to CSF were investigated by using real-time PCR method in this study. As a result of our study, there was no difference in blood SOCS3 gene expression levels between meningitis patients and healthy controls (p>0.05). Additionally, there was no meaningful difference between SOC3 gene expression of blood and CSF samples in meningitis patients (p>0.05). Our data suggests that further molecular studies are needed and important in meningitis disease diagnosis and treatment, and in the other genes responsible for repressing of inflammatory development.

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21

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 dysregulation of all systems in the body, dependent on its degree and extent. In most cases, the brain injury increases the risk of developing epilepsy and neurodegenerative diseases such as Alzheimers disease, arkinsons disease and chronic traumatic encephalopathy (CTE), with mental health disorders. TBI is a long-term symptomatic process in patients with functional and structural damage. In response to a traumatic event, the damage-associated molecular patterns (DAMPs) encountered upon tissue damage are expressed, which cause activation of the resident brain tissue cells, and secretion of multiple chemokine and cytokine by distinct cell populations. Neutrophils migrate to focal lesions, which remove damaged cells and debris. Migration of T and B cells is observed 3-7 days after the trauma. Hence, following primary injury, due to a cascade of immune reactions, a more extensive lesion, the so-called secondary trauma, is developed. The aim of our study was to evaluate the role of immune response in pathogenesis of mild traumatic brain injury. An increased number of Bm2 cells, IgDdimCD27low naive B cells and B cells with the IgDlowCD27hi (plasmablasts) phenotype was found in patients with mild brain contusion, compared to comparison group. Moreover, the number of naive mature B cells with the CD27lowCD38dim phenotype was significantly decreased compared with the controls.

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22

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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23

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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24

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 neuropsychological disorders, where damage to the frontal lobes or to their interconnections has been implicated, on hand movement sequencing performance in adults. The three groups studied included patients diagnosed with alcohol-related brain damage (n = 57), patients diagnosed with mild traumatic brain injury (n = 21), and patients diagnosed with age-related dementia (n = 30). HMT performance was significantly poorer in all three clinical groups relative to controls, supporting the addition of this brief, paediatric test in neuropsychological evaluations assessing these disorders.

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25

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 procedures for these patients. In the near future, biomarkers will become one of the prime driving forces of cancer treatment. In this minireview, we analyze the documented work on the acute brain damage and late consequences induced by radiotherapy, identify the biomarkers, in particular, the predictive biomarkers for the damage, and summarize the biological significance of the biomarkers. It is expected that translation of these research advance to radiotherapy would assist stratifying patients for optimized treatment and improving therapeutic efficacy and the quality of life.

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26

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, 30 left brain-damaged patients and 30 healthy controls were given the Happy–Sad Chimeric Faces Test.Results. Right hemisphere damaged and unipolar depressed patients both showed a significantly reduced left hemispatial bias (LHB) compared to controls, bipolars and left brain-damaged patients. No significant difference in mean LHB between controls and both hypomanics and left brain-damaged patients was found. There was no significant association between LHB and clinical variables.Conclusions. The results suggest a physiological distinction between bipolar and unipolar depression. The significantly diminished left hemifacial bias in depressed patients suggests right hemisphere dysfunction.

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27

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 experimental situation that exposed the patients to mental stressors in order to measure psychophysiological reactivity.Results. Significant differences in level of apathy were found between diagnostic groups as well as between localization subgroups. SCD and RHD patients displayed most apathy. Factor analysis of MADRS revealed a three-factor solution; depressed mood, somatic symptoms and negative symptoms. Apathy was significantly correlated with negative symptoms in all localization subgroups, except among the BHD patients. Apathy was not correlated with depressed mood or somatic symptoms. Moreover, apathy was significantly correlated with heart rate reactivity, but not with electrodermal reactivity.Conclusion. Apathy is common, its severity depending on diagnosis and localization of lesion. Apathy and depression in brain damaged patients share common features, but may be differentiated. The significant relationship between apathy and heart rate may provide a psychophysiological correlation of the disengagement, lack of interest and absence of emotional responsivity typically seen in apathy. The results have implications for the theoretical understanding of apathy and related negative symptoms, and for rehabilitation practice.

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28

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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29

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 PRKN/PINK1 and idiopathic Parkinson’s disease patients remain elusive. We investigated IL6, C-reactive protein, and circulating cell-free mtDNA in serum of 245 participants in two cohorts from tertiary movement disorder centres. We performed a hypothesis-driven rank-based statistical approach adjusting for multiple testing. We detected (i) elevated IL6 levels in patients with biallelic PRKN/PINK1 mutations compared to healthy control subjects in a German cohort, supporting the concept of a role for inflammation in PRKN/PINK1-linked Parkinson’s disease. In addition, the comparison of patients with biallelic and heterozygous mutations in PRKN/PINK1 suggests a gene dosage effect. The differences in IL6 levels were validated in a second independent Italian cohort; (ii) a correlation between IL6 levels and disease duration in carriers of PRKN/PINK1 mutations, while no such association was observed for idiopathic Parkinson’s disease patients. These results highlight the potential of IL6 as progression marker in Parkinson’s disease due to PRKN/PINK1 mutations; (iii) increased circulating cell-free mtDNA serum levels in both patients with biallelic or with heterozygous PRKN/PINK1 mutations compared to idiopathic Parkinson’s disease, which is in line with previous findings in murine models. By contrast, circulating cell-free mtDNA concentrations in unaffected heterozygous carriers of PRKN/PINK1 mutations were comparable to control levels; and (iv) that circulating cell-free mtDNA levels have good predictive potential to discriminate between idiopathic Parkinson’s disease and Parkinson’s disease linked to heterozygous PRKN/PINK1 mutations, providing functional evidence for a role of heterozygous mutations in PRKN or PINK1 as Parkinson’s disease risk factor. Taken together, our study further implicates inflammation due to impaired mitophagy and subsequent mtDNA release in the pathogenesis of PRKN/PINK1-linked Parkinson’s disease. In individuals carrying mutations in PRKN/PINK1, IL6 and circulating cell-free mtDNA levels may serve as markers of Parkinson’s disease state and progression, respectively. Finally, our study suggests that targeting the immune system with anti-inflammatory medication holds the potential to influence the disease course of Parkinson’s disease, at least in this subset of patients.

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30

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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31

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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32

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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33

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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34

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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35

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 cerebral autoregulation. The correlation between the parameter estimates was also analyzed to elucidate the main mechanisms responsible for ICP changes in each patient. Starting from information on the estimated parameter values and their correlation, the patients were classified into two main classes: those with weak autoregulation (8 of 20 patients) and those with strong autoregulation (12 of 20 patients). In the first group of patients, ICP mainly reflects CSF circulation and passive cerebral blood volume changes. In the second group, ICP exhibits paradoxical responses attributable to active changes in cerebral blood volume. Moreover, in two patients of the second group, the time constant of autoregulation is significantly increased (>40 s). The correlation between the parameter estimates was significantly different in the two groups of patients, suggesting the existence of different mechanisms responsible for ICP changes. Moreover, analysis of the correlation between the parameter estimates might give information on the directions of parameter changes that have a greater impact on ICP.

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36

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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37

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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38

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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39

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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40

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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41

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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42

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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43

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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44

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 vascular brain damage. An important aspect of selecting effective therapy is the competent diagnosis of the causes of dizziness and instability, which can be caused not only by brain damage, but also by peripheral vestibular system diseases. Early diagnosis of vascular CI, selection of adequate therapy, and prevention of their further progression are of great importance. The studies performed have shown the high efficacy of vinpocetine (Cavinton®) that has a multifactorial mechanism of action in the treatment and prevention of CI, dizziness, and instability caused by cerebrovascular disease.

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45

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 neurons. In order to obtain suitable cell types for grafting in patients with stroke and brain damage, a protocol was modified for differentiating human induced pluripotent stem cells from cells phenotypically related to cortical motor neurons. Moreover, cell sheet technology was applied to neural cell transplantation, as maintaining the cell–cell communications is regarded important for the repair of host brain architecture. Accordingly, neuronal cell sheets that were positive Forebrain Embryonic Zinc Finger (Fez) family zinc finger 2 (FEZF2), COUP-TF-interacting protein 2, insulin-like growth factor–binding protein 4 (IGFBP4), cysteine-rich motor neuron 1 protein precursor (CRIM1), and forkhead box p2 (FOXP2) were developed. These markers are associated with cortical motoneurons that are appropriate for the transplant location in the lesions. The sheets allowed preservation of cell–cell interactions shown by synapsin1 staining after transplantation to damaged mouse brains. The sheet transplantation brought about partial structural restoration and the improvement of motor functions in hemiplegic mice. Collectively, the novel neuronal cell sheets were transplanted into damaged motor cortices; the cell sheets maintained cell–cell interactions and improved the motor functions in the hemiplegic model mice. The motoneuron cell sheets are possibly applicable for stroke patients and patients with brain damage by using patient-specific induced pluripotent stem cells.

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46

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 two groups without brain damage. Our analyses showed that patients with focal damage to the frontal lobes demonstrated steeper delay discounting than other participants. Other clinical groups demonstrated similar discounting rates. The data pattern related to the magnitude effect on the group level suggested that the magnitude effect is absent in the group of patients with damage to the frontal lobes; however, results were less consistent on an individual level. Amount-dependent discounting was observed in only two groups, the healthy control group and the neurological group with other cortical areas damaged.

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47

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 biological measure of neuroaxonal damage. Ninety-one multiple sclerosis patients (62 relapsing-remitting, 29 progressive) and 72 healthy controls were enrolled in the study. Differences in myelin water fraction and neurite density index were substantial when lesions were compared to healthy control subjects and normal-appearing multiple sclerosis tissue: both white matter and cortical lesions exhibited a decreased myelin water fraction and neurite density index compared with healthy (P < 0.0001) and peri-plaque white matter (P < 0.0001). Periventricular lesions showed decreased myelin water fraction and neurite density index compared with lesions in the juxtacortical region (P < 0.0001 and P < 0.05). Similarly, lesions with paramagnetic rims showed decreased myelin water fraction and neurite density index relative to lesions without a rim (P < 0.0001). Also, in 75% of white matter lesions, the reduction in neurite density index was higher than the reduction in the myelin water fraction. Besides, normal-appearing white and grey matter revealed diffuse reduction of myelin water fraction and neurite density index in multiple sclerosis compared to healthy controls (P < 0.01). Further, a more extensive reduction in myelin water fraction and neurite density index in normal-appearing cortex was observed in progressive versus relapsing-remitting participants. Neurite density index in white matter lesions correlated with disability in patients with clinical deficits (P < 0.01, beta = −10.00); and neurite density index and myelin water fraction in white matter lesions were associated to serum neurofilament light chain in the entire patient cohort (P < 0.01, beta = −3.60 and P < 0.01, beta = 0.13, respectively). These findings suggest that (i) myelin and axon pathology in multiple sclerosis is extensive in both lesions and normal-appearing tissue; (ii) particular types of lesions exhibit more damage to myelin and axons than others; (iii) progressive patients differ from relapsing-remitting patients because of more extensive axon/myelin damage in the cortex; and (iv) myelin and axon pathology in lesions is related to disability in patients with clinical deficits and global measures of neuroaxonal damage.

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48

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 with their isolated impairment in visuospatial reasoning. Despite a global preservation of the topological properties, peculiar patterns of frontal disconnection and increased parietal-cerebellar connectivity were also identified in patients’ brains. The balance between loss of connectivity and compensatory mechanisms in different brain networks might explain the paradoxical mismatch between structural brain damage and minimal cognitive deficits observed in these patients. This study provides a comprehensive assessment of brain abnormalities that fit well with both motor and nonmotor clinical features experienced by patients in their everyday life. The current findings suggest that measures of functional connectivity may offer the possibility of characterizing individual patients with the potential to become a clinical tool.

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49

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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50

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 repair in focal lesions; and (iii) specific damage to CNS tissue components. This review summarizes recent technical advances in quantitative MRI, existing pathological validation of quantitative MRI techniques, and emerging applications of quantitative MRI to patients with multiple sclerosis in both research and clinical settings. The current level of clinical maturity of each quantitative MRI technique, especially regarding its integration into clinical routine, is discussed. We aim to provide a better understanding of how quantitative MRI may help clinical practice by improving stratification of patients with multiple sclerosis, and assessment of disease progression, and evaluation of treatment response.

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