Proton MR Spectroscopy and MRI-Volumetry in Mild Traumatic Brain Injury
More than 85% of brain traumas are classified as "mild"; MR imaging findings are minimal if any and do not correspond to clinical symptoms. Our goal, therefore, was to quantify the global decline of the neuronal marker N-acetylaspartate (NAA), as well as gray (GM) and white matter (WM) atr...
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| Veröffentlicht in: | American Journal of Neuroradiology 2007-05, Vol.28 (5), p.907-913 |
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| creator | Cohen, B.A Inglese, M Rusinek, H Babb, J.S Grossman, R.I Gonen, O |
| description | More than 85% of brain traumas are classified as "mild"; MR imaging findings are minimal if any and do not correspond to clinical symptoms. Our goal, therefore, was to quantify the global decline of the neuronal marker N-acetylaspartate (NAA), as well as gray (GM) and white matter (WM) atrophy after mild traumatic brain injury (mTBI).
Twenty patients (11 male, 9 female; age range, 19-57 years; median, 35 years) with mTBI (Glasgow Coma Scale score 13-15 with loss of consciousness for at least 30 seconds) and 19 age- and sex-matched control subjects were studied. Seven patients were studied within 9 days of TBI; the other 13 ranged from 1.2 months to 31.5 years (average and median of 4.6 and 1.7 years, respectively) after injury. Whole-brain NAA (WBNAA) concentration was obtained in all subjects with nonlocalizing proton MR spectroscopy. Brain volume and GM and WM fractions were segmented from T1-weighted MR imaging and normalized to the total intracranial volume, suitable for intersubject comparisons. The data were analyzed with least squares regression.
Patients with mTBI exhibited, on average, a 12% WBNAA deficit that increased with age, compared with the control subjects (p |
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Twenty patients (11 male, 9 female; age range, 19-57 years; median, 35 years) with mTBI (Glasgow Coma Scale score 13-15 with loss of consciousness for at least 30 seconds) and 19 age- and sex-matched control subjects were studied. Seven patients were studied within 9 days of TBI; the other 13 ranged from 1.2 months to 31.5 years (average and median of 4.6 and 1.7 years, respectively) after injury. Whole-brain NAA (WBNAA) concentration was obtained in all subjects with nonlocalizing proton MR spectroscopy. Brain volume and GM and WM fractions were segmented from T1-weighted MR imaging and normalized to the total intracranial volume, suitable for intersubject comparisons. The data were analyzed with least squares regression.
Patients with mTBI exhibited, on average, a 12% WBNAA deficit that increased with age, compared with the control subjects (p<.05). Adjusted for age effects, patients also suffered both global atrophy (-1.09%/year; P=.029) and GM atrophy (-0.89%/year; P=.042). Patients with and without visible MR imaging pathology, typically punctate foci of suspected shearing injury, were indistinguishable in both atrophy and WBNAA.
WBNAA detected neuronal/axonal injury beyond the minimal focal MR-visible lesions in mTBI. Combined with GM atrophy, the findings may provide further, noninvasive insight into the nature and progression of mTBI.</description><identifier>ISSN: 0195-6108</identifier><identifier>EISSN: 1936-959X</identifier><identifier>EISSN: 1432-1920</identifier><identifier>PMID: 17494667</identifier><language>eng</language><publisher>United States: Am Soc Neuroradiology</publisher><subject>Adult ; Age Factors ; Aspartic Acid - analogs & derivatives ; Aspartic Acid - metabolism ; Atrophy ; Axons - pathology ; Brain ; Brain - metabolism ; Brain - pathology ; Brain Injuries - metabolism ; Brain Injuries - pathology ; Female ; Glasgow Coma Scale ; Humans ; Magnetic Resonance Spectroscopy - methods ; Male ; Middle Aged ; Neurons - pathology ; Protons</subject><ispartof>American Journal of Neuroradiology, 2007-05, Vol.28 (5), p.907-913</ispartof><rights>Copyright © American Society of Neuroradiology 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8134347/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8134347/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17494667$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cohen, B.A</creatorcontrib><creatorcontrib>Inglese, M</creatorcontrib><creatorcontrib>Rusinek, H</creatorcontrib><creatorcontrib>Babb, J.S</creatorcontrib><creatorcontrib>Grossman, R.I</creatorcontrib><creatorcontrib>Gonen, O</creatorcontrib><title>Proton MR Spectroscopy and MRI-Volumetry in Mild Traumatic Brain Injury</title><title>American Journal of Neuroradiology</title><addtitle>AJNR Am J Neuroradiol</addtitle><description>More than 85% of brain traumas are classified as "mild"; MR imaging findings are minimal if any and do not correspond to clinical symptoms. Our goal, therefore, was to quantify the global decline of the neuronal marker N-acetylaspartate (NAA), as well as gray (GM) and white matter (WM) atrophy after mild traumatic brain injury (mTBI).
Twenty patients (11 male, 9 female; age range, 19-57 years; median, 35 years) with mTBI (Glasgow Coma Scale score 13-15 with loss of consciousness for at least 30 seconds) and 19 age- and sex-matched control subjects were studied. Seven patients were studied within 9 days of TBI; the other 13 ranged from 1.2 months to 31.5 years (average and median of 4.6 and 1.7 years, respectively) after injury. Whole-brain NAA (WBNAA) concentration was obtained in all subjects with nonlocalizing proton MR spectroscopy. Brain volume and GM and WM fractions were segmented from T1-weighted MR imaging and normalized to the total intracranial volume, suitable for intersubject comparisons. The data were analyzed with least squares regression.
Patients with mTBI exhibited, on average, a 12% WBNAA deficit that increased with age, compared with the control subjects (p<.05). Adjusted for age effects, patients also suffered both global atrophy (-1.09%/year; P=.029) and GM atrophy (-0.89%/year; P=.042). Patients with and without visible MR imaging pathology, typically punctate foci of suspected shearing injury, were indistinguishable in both atrophy and WBNAA.
WBNAA detected neuronal/axonal injury beyond the minimal focal MR-visible lesions in mTBI. Combined with GM atrophy, the findings may provide further, noninvasive insight into the nature and progression of mTBI.</description><subject>Adult</subject><subject>Age Factors</subject><subject>Aspartic Acid - analogs & derivatives</subject><subject>Aspartic Acid - metabolism</subject><subject>Atrophy</subject><subject>Axons - pathology</subject><subject>Brain</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Brain Injuries - metabolism</subject><subject>Brain Injuries - pathology</subject><subject>Female</subject><subject>Glasgow Coma Scale</subject><subject>Humans</subject><subject>Magnetic Resonance Spectroscopy - methods</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Neurons - pathology</subject><subject>Protons</subject><issn>0195-6108</issn><issn>1936-959X</issn><issn>1432-1920</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEtLw0AUhYMoWqt_QbLRXeBO5r0RVHwUFEWruBtukkk7kmTqJLHk3xuoiq5cXTjn4-Nwt6IJ0VQkmuvX7WgCRPNEEFB70X7bvgEA1zLdjfaIZJoJISfR9UPwnW_iu8f4aWXzLvg296shxqYYs1ny4qu-tl0YYjdCririecC-xs7l8XnAMZw1b30YDqKdEqvWHn7dafR8dTm_uElu769nF2e3yZKmvEsEQMbLUqBGnUEKQhUlVSxThZKQIiUcCNNcKCWYzAmKNGUMM8wpWJQIdBqdbryrPqttkdumC1iZVXA1hsF4dOZv07ilWfgPowhllMlRcPIlCP69t21natfmtqqwsb5vjQSmdArsX5BowTVwMoJHvyf9bPl-8ggcb4ClWyzXLljT1lhVI07Mer1OleFGg6SfeI-GTA</recordid><startdate>20070501</startdate><enddate>20070501</enddate><creator>Cohen, B.A</creator><creator>Inglese, M</creator><creator>Rusinek, H</creator><creator>Babb, J.S</creator><creator>Grossman, R.I</creator><creator>Gonen, O</creator><general>Am Soc Neuroradiology</general><general>American Society of Neuroradiology</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7TK</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20070501</creationdate><title>Proton MR Spectroscopy and MRI-Volumetry in Mild Traumatic Brain Injury</title><author>Cohen, B.A ; Inglese, M ; Rusinek, H ; Babb, J.S ; Grossman, R.I ; Gonen, O</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h325t-600b5ff6a9a9b02068df384b8d8702a31501495688647c1a62244abac30ea7a03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adult</topic><topic>Age Factors</topic><topic>Aspartic Acid - analogs & derivatives</topic><topic>Aspartic Acid - metabolism</topic><topic>Atrophy</topic><topic>Axons - pathology</topic><topic>Brain</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>Brain Injuries - metabolism</topic><topic>Brain Injuries - pathology</topic><topic>Female</topic><topic>Glasgow Coma Scale</topic><topic>Humans</topic><topic>Magnetic Resonance Spectroscopy - methods</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Neurons - pathology</topic><topic>Protons</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cohen, B.A</creatorcontrib><creatorcontrib>Inglese, M</creatorcontrib><creatorcontrib>Rusinek, H</creatorcontrib><creatorcontrib>Babb, J.S</creatorcontrib><creatorcontrib>Grossman, R.I</creatorcontrib><creatorcontrib>Gonen, O</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American Journal of Neuroradiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cohen, B.A</au><au>Inglese, M</au><au>Rusinek, H</au><au>Babb, J.S</au><au>Grossman, R.I</au><au>Gonen, O</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Proton MR Spectroscopy and MRI-Volumetry in Mild Traumatic Brain Injury</atitle><jtitle>American Journal of Neuroradiology</jtitle><addtitle>AJNR Am J Neuroradiol</addtitle><date>2007-05-01</date><risdate>2007</risdate><volume>28</volume><issue>5</issue><spage>907</spage><epage>913</epage><pages>907-913</pages><issn>0195-6108</issn><eissn>1936-959X</eissn><eissn>1432-1920</eissn><abstract>More than 85% of brain traumas are classified as "mild"; MR imaging findings are minimal if any and do not correspond to clinical symptoms. Our goal, therefore, was to quantify the global decline of the neuronal marker N-acetylaspartate (NAA), as well as gray (GM) and white matter (WM) atrophy after mild traumatic brain injury (mTBI).
Twenty patients (11 male, 9 female; age range, 19-57 years; median, 35 years) with mTBI (Glasgow Coma Scale score 13-15 with loss of consciousness for at least 30 seconds) and 19 age- and sex-matched control subjects were studied. Seven patients were studied within 9 days of TBI; the other 13 ranged from 1.2 months to 31.5 years (average and median of 4.6 and 1.7 years, respectively) after injury. Whole-brain NAA (WBNAA) concentration was obtained in all subjects with nonlocalizing proton MR spectroscopy. Brain volume and GM and WM fractions were segmented from T1-weighted MR imaging and normalized to the total intracranial volume, suitable for intersubject comparisons. The data were analyzed with least squares regression.
Patients with mTBI exhibited, on average, a 12% WBNAA deficit that increased with age, compared with the control subjects (p<.05). Adjusted for age effects, patients also suffered both global atrophy (-1.09%/year; P=.029) and GM atrophy (-0.89%/year; P=.042). Patients with and without visible MR imaging pathology, typically punctate foci of suspected shearing injury, were indistinguishable in both atrophy and WBNAA.
WBNAA detected neuronal/axonal injury beyond the minimal focal MR-visible lesions in mTBI. Combined with GM atrophy, the findings may provide further, noninvasive insight into the nature and progression of mTBI.</abstract><cop>United States</cop><pub>Am Soc Neuroradiology</pub><pmid>17494667</pmid><tpages>7</tpages></addata></record> |
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| subjects | Adult Age Factors Aspartic Acid - analogs & derivatives Aspartic Acid - metabolism Atrophy Axons - pathology Brain Brain - metabolism Brain - pathology Brain Injuries - metabolism Brain Injuries - pathology Female Glasgow Coma Scale Humans Magnetic Resonance Spectroscopy - methods Male Middle Aged Neurons - pathology Protons |
| title | Proton MR Spectroscopy and MRI-Volumetry in Mild Traumatic Brain Injury |
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