Artykuły w czasopismach na temat „Brain damage”

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1

Larsson, L. "BRAIN DAMAGE, BRAIN REPAIR". Brain 125, nr 12 (1.12.2002): 2785–86. http://dx.doi.org/10.1093/brain/awf266.

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2

Raisman, Geoffrey. "Brain Damage, Brain Repair". Journal of the Royal Society of Medicine 96, nr 5 (maj 2003): 249–50. http://dx.doi.org/10.1177/014107680309600517.

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Lanham, Richard A. "Brain Damage, Brain Repair". Journal of Head Trauma Rehabilitation 17, nr 3 (czerwiec 2002): 270–72. http://dx.doi.org/10.1097/00001199-200206000-00012.

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Jellinger, K. A. "Brain Damage, Brain Repair". European Journal of Neurology 10, nr 3 (maj 2003): 335. http://dx.doi.org/10.1046/j.1468-1331.2003.00557.x.

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Raisman, G. "Brain Damage, Brain Repair". JRSM 96, nr 5 (1.05.2003): 249–50. http://dx.doi.org/10.1258/jrsm.96.5.249.

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6

Toledo, C. A. B. "Brain Damage, Brain Repair". Journal of Chemical Neuroanatomy 27, nr 2 (maj 2004): 139. http://dx.doi.org/10.1016/j.jchemneu.2004.01.001.

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Floyd, Pink. "Brain Damage". Academic Medicine 83, nr 8 (sierpień 2008): 742. http://dx.doi.org/10.1097/acm.0b013e318181d965.

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8

Volpe, Joseph J., A. Ernest i Jane G. Stein. "BRAIN DAMAGE". Pediatric Research 20, nr 10 (październik 1986): 1024–25. http://dx.doi.org/10.1203/00006450-198610000-00039.

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9

Rothwell, Nancy J., i Giamal N. Luheshi. "Brain TNF: Damage limitation or damaged reputation?" Nature Medicine 2, nr 7 (lipiec 1996): 746–47. http://dx.doi.org/10.1038/nm0796-746.

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10

Lakatos, Andras. "Brain Damage and Brain Repair". Neuropathology and Applied Neurobiology 27, nr 3 (czerwiec 2001): 252–53. http://dx.doi.org/10.1046/j.1365-2990.2001.00336-2.x.

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11

Antonis, Theofilidis. "The Hypothesis of Unexplained Brain Damage and Learning Difficulties". Neuroscience and Neurological Surgery 8, nr 5 (10.05.2021): 01–08. http://dx.doi.org/10.31579/2578-8868/165.

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Introduction: The term learning disabilities refers to a complex and multidimensional phenomenon that affects many thousands of students. Due to the rich symptomatology of learning difficulties and the increased differences between individuals, it has not been possible to analyze all cases exclusively from the perspective of the neuropsychological approach. Aim. The aim of this study was to present research conducted in the context of theories on the brain function of people with learning disabilities. Supporting the hypothesis of brain dysfunction. Methodology: Literature review was carried out in the web, which referred to researches on Special Learning Disabilities and the brain function associated with them. Results: Review of the literature highlighted key points of the relationship between learning difficulties and brain function. Brain dysfunction and the cognitive functions produced emerged as one of the key factors involved in learning disabilities. Many of the theories developed around the problems of children with learning disabilities have focused on specific areas of the brain that may be dysfunctional. Conclusions: The difficulty of locating obvious brain damage in individuals who have been characterized as dyslexic leads to the strengthening of the hypothesis of the existence of a slight or minimal brain damage that cannot be easily diagnosed and strengthens the hypothesis of an unexplained brain damage that could be heterogeneous groups of learning disabilities.
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12

Montagu, Ashley. "Sociogenetic Brain Damage". Developmental Medicine & Child Neurology 13, nr 5 (12.11.2008): 597–605. http://dx.doi.org/10.1111/j.1469-8749.1971.tb08323.x.

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13

S., L. "Ischemic brain damage". Neurology 41, nr 6 (1.06.1991): 953. http://dx.doi.org/10.1212/wnl.41.6.953.

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14

Riva, Daria, Silvana Franceschetti, Alessandra Erbetta, Giovanni Baranello, Silvia Esposito i Sara Bulgheroni. "Congenital Brain Damage". Journal of Child Neurology 28, nr 4 (29.06.2012): 446–54. http://dx.doi.org/10.1177/0883073812447684.

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15

Auer, Roland N. "Hypoglycemic Brain Damage". Metabolic Brain Disease 19, nr 3/4 (grudzień 2004): 169–75. http://dx.doi.org/10.1023/b:mebr.0000043967.78763.5b.

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16

RUTH, VINETA J., i KARL O. RAIVIO. "Perinatal Brain Damage". Obstetrical & Gynecological Survey 44, nr 4 (kwiecień 1989): 267–68. http://dx.doi.org/10.1097/00006254-198904000-00014.

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17

ROVNER, SOPHIE. "UNDOING BRAIN DAMAGE". Chemical & Engineering News 85, nr 7 (12.02.2007): 18. http://dx.doi.org/10.1021/cen-v085n007.p018a.

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18

Hinton, Geoffrey E., David C. Plaut i Tim Shallice. "Simulating Brain Damage". Scientific American 269, nr 4 (październik 1993): 76–82. http://dx.doi.org/10.1038/scientificamerican1093-76.

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19

Auer, Roland N. "Hypoglycemic brain damage". Forensic Science International 146, nr 2-3 (grudzień 2004): 105–10. http://dx.doi.org/10.1016/j.forsciint.2004.08.001.

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20

Wasterlain, Claude G., i Yukiyoshi Shirasaka. "Seizures, brain damage and brain development". Brain and Development 16, nr 4 (lipiec 1994): 279–95. http://dx.doi.org/10.1016/0387-7604(94)90025-6.

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21

Siesjö, Bo K. "Hypoglycemia, brain metabolism, and brain damage". Diabetes / Metabolism Reviews 4, nr 2 (marzec 1988): 113–44. http://dx.doi.org/10.1002/dmr.5610040203.

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22

Ladavas, E. "RIGHT HEMISPHERE DAMAGE." Brain 123, nr 3 (1.03.2000): 650–51. http://dx.doi.org/10.1093/brain/123.3.650.

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23

Iwadate, Kimiharu, Nagahisa Matsuyama, Miwako Aoyagi, Ryo Shimada i Yohko Ito. "A case of generalized hypoxic brain damage following traumatic brain damage". Legal Medicine 7, nr 2 (marzec 2005): 117–21. http://dx.doi.org/10.1016/j.legalmed.2004.10.003.

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24

Gratton, Caterina, Emi M. Nomura, Fernando Pérez i Mark D'Esposito. "Focal Brain Lesions to Critical Locations Cause Widespread Disruption of the Modular Organization of the Brain". Journal of Cognitive Neuroscience 24, nr 6 (czerwiec 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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25

Lv, Yuan, Ling-Ling Zhu i Gui-Hua Shu. "Relationship between Blood Glucose Fluctuation and Brain Damage in the Hypoglycemia Neonates". American Journal of Perinatology 35, nr 10 (14.02.2018): 946–50. http://dx.doi.org/10.1055/s-0038-1626706.

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Objective To investigate the relationship between blood glucose fluctuation and brain damage in the hypoglycemia neonates. Study Design A retrospective study including all neonates hospitalized due to hypoglycemia from September 2013 to August 2016 was performed. All the 58 hypoglycemia infants were divided into two groups—the brain-damaged group and the nonbrain-damaged group, according to head magnetic resonance imaging and/or amplitude-integrated electroencephalogram. Relationship between glucose variability and brain damage and whether these variation indexes could act as early indicators for hypoglycemic brain damage were investigated. Results Of the 13 brain-damaged cases, the lowest blood glucose (LBG) level was lower, while duration of hypoglycemia was longer compared with the 45 nonbrain-damaged cases (p < 0.001). The largest amplitude of glycemic excursions, standard deviation of blood glucose, and mean amplitude of glycemic excursions (MAGE) of the brain-damaged group were higher (p < 0.001). Under receiver-operating characteristic curve, values of area under the curve of MAGE were 0.892, duration of hypoglycemia was 0.921, and LBG was 0.109 (p < 0.0001). Conclusion Brain damage of the hypoglycemia neonates relates not only with LBG and duration of hypoglycemia but also with the blood glucose variation indexes; MAGE and duration of hypoglycemia could act as predictors for brain damage.
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26

Baumann, Kim. "Brain DNA damage hotspots". Nature Reviews Molecular Cell Biology 22, nr 5 (7.04.2021): 304–5. http://dx.doi.org/10.1038/s41580-021-00367-5.

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27

Wright, N. P., J. K. H. Wales; i T. M. O'Shea. "Brain Damage and Dexamethasone?" PEDIATRICS 106, nr 4 (1.10.2000): 864. http://dx.doi.org/10.1542/peds.106.4.864.

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28

Millichap, J. Gordon. "Hypoglycemia and Brain Damage". Pediatric Neurology Briefs 2, nr 11 (1.11.1988): 83. http://dx.doi.org/10.15844/pedneurbriefs-2-11-3.

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29

Millichap, J. Gordon. "Brain Damage and Violence". Pediatric Neurology Briefs 7, nr 8 (1.08.1993): 57. http://dx.doi.org/10.15844/pedneurbriefs-7-8-1.

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30

Dueñas, Alejandro. "Avoiding the Brain Damage". JOURNAL OF ADVANCES IN PHYSICS 10, nr 3 (6.10.2015): 2871–73. http://dx.doi.org/10.24297/jap.v10i3.1325.

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The pursuit of low losses and low distortion are necessary conditions to improve the signal integrity. As mentioned in [1], it is sometimes said that thereare two types of engineers—those who have signal integrityproblems and those who will.As clock frequencies increase,magnifying signal integrityproblems, this saying willbecome even more accurate.On the other hand, the usage of the technology is now a day unavoidable. Thus, to avoid the electromagnetic radiationdirectly on the brain, should be recomendablethe useof the hand off device since the integrated inalambric amplifiers of new generation genertea lot of energy (power). Besides, it is convenient that the user of that technology be aware to the activities he is doing to avoid accidents mainly when he is manipulating some kind of equipment or driving a vehicle.As mentioned in[2], the power amplifier (PA) is a critical component whitin a WLAN transmitter because PA performance affects wireless coverage area, data rate capacity, and battery life.Â
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31

Fine, Ronald D. "Treatment of brain damage". Medical Journal of Australia 152, nr 8 (kwiecień 1990): 441. http://dx.doi.org/10.5694/j.1326-5377.1990.tb125276.x.

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32

Frisoni, G. B., A. Scuratti, A. Bianchetti i M. Trabucchi. "Hypergraphia and brain damage." Journal of Neurology, Neurosurgery & Psychiatry 56, nr 5 (1.05.1993): 576–77. http://dx.doi.org/10.1136/jnnp.56.5.576-b.

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33

Dammann, Olaf, i Alan Leviton. "Perinatal Brain Damage Causation". Developmental Neuroscience 29, nr 4-5 (2007): 280–88. http://dx.doi.org/10.1159/000105469.

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34

Isaacson, Robert L. "Brain Plasticity Alter Damage". Clinics in Perinatology 17, nr 1 (marzec 1990): 67–75. http://dx.doi.org/10.1016/s0095-5108(18)30589-x.

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35

Shieff, Colin. "BRAIN DAMAGE AND HYPONATRAEMIA". Lancet 332, nr 8624 (grudzień 1988): 1373–74. http://dx.doi.org/10.1016/s0140-6736(88)90919-1.

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36

Lebrun, Yvan. "Cluttering after brain damage". Journal of Fluency Disorders 21, nr 3-4 (wrzesień 1996): 289–95. http://dx.doi.org/10.1016/s0094-730x(96)00031-9.

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37

Lecours, AndréRoch, Jacques Mehler, Maria Alice Parente, Luis Roberto Aguiar, Amauri Batista da Silva, Manoel Caetano, Henriqueta Camarotti i in. "Illiteracy and brain damage". Brain and Cognition 6, nr 3 (lipiec 1987): 243–65. http://dx.doi.org/10.1016/0278-2626(87)90126-6.

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38

Miller, Jimmy D. "Recovery from Brain Damage". Neurosurgery 36, nr 6 (1.06.1995): 1230–33. http://dx.doi.org/10.1227/00006123-199506000-00031.

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39

Bach-y-Rita, P. "Recovery from Brain Damage". Neurorehabilitation and Neural Repair 6, nr 4 (1.01.1992): 191–99. http://dx.doi.org/10.1177/136140969200600404.

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40

Miller, Jimmy D. "Recovery from Brain Damage". Neurosurgery 36, nr 6 (czerwiec 1995): 1231. http://dx.doi.org/10.1097/00006123-199506000-00031.

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41

Wilmshurst, P. "Brain damage in divers". BMJ 314, nr 7082 (8.03.1997): 689. http://dx.doi.org/10.1136/bmj.314.7082.689.

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42

Yates, P. O., J. R. Broome, A. D. Pitkin, M. Knauth i S. Ries. "Brain damage in divers". BMJ 314, nr 7096 (14.06.1997): 1761. http://dx.doi.org/10.1136/bmj.314.7096.1761.

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43

Barltrop, Donald. "Lead and Brain Damage". Human Toxicology 4, nr 2 (marzec 1985): 121. http://dx.doi.org/10.1177/096032718500400201.

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44

Thomson, A. D., O. E. Pratt, M. Jeyasingham i G. K. Shaw. "Alcohol and Brain Damage". Human Toxicology 7, nr 5 (wrzesień 1988): 455–63. http://dx.doi.org/10.1177/096032718800700513.

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The safe limits of alcohol intake are difficult to define because of individual variations in susceptibility to damage. The present recommendations are based largely on epidemiological studies of liver damage. Recent investigations indicate that alcoholic brain damage is much more common than previously suspected. More information is required about its natural history and the characteristics of individuals most likely to suffer damage. Thiamin (vitamin B 1) deficiency has long been associated with brain damage and may result from a number of additive causes in the alcoholic patient. New information indicating damage to the protein moeity of some of the thiamin-using enzymes has been reviewed, as have possible mechanisms of brain cell necrosis.
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45

Allman, Peter. "Emotionalism Following Brain Damage". Behavioural Neurology 4, nr 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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46

Hachinski, V. "Brain Damage and Violence". Archives of Neurology 50, nr 8 (1.08.1993): 871. http://dx.doi.org/10.1001/archneur.1993.00540080074019.

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47

Harper, Clive, i Izuru Matsumoto. "Ethanol and brain damage". Current Opinion in Pharmacology 5, nr 1 (luty 2005): 73–78. http://dx.doi.org/10.1016/j.coph.2004.06.011.

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48

Molnar, Gabriella E., Jessie K. M. Easton, Angeles Badell, Helga Binder, Dennis D. Dykstra, Dennis J. Matthews, Stephen F. Noll i Jane C. S. Perrin. "Brain damage causing disability". Archives of Physical Medicine and Rehabilitation 70, nr 5 (maj 1989): S166—S169. http://dx.doi.org/10.1016/0003-9993(89)90023-3.

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49

Miall, R. Chris, i Joseph Galea. "Cerebellar damage limits reinforcement learning". Brain 139, nr 1 (styczeń 2016): 4–7. http://dx.doi.org/10.1093/brain/awv343.

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50

HARPER, CLIVE. "The Neuropathology of Alcohol-specific Brain Damage, or Does Alcohol Damage the Brain?" Journal of Neuropathology and Experimental Neurology 57, nr 2 (luty 1998): 101–10. http://dx.doi.org/10.1097/00005072-199802000-00001.

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