Quantitative MRI Analysis of Brain Volume Changes due to Controlled Cortical Impact

More than 85% of reported brain traumas are classified clinically as "mild" using the Glasgow Coma Scale (GCS); qualitative MRI findings are scarce and provide little correspondence to clinical symptoms. Our goal, therefore, was to establish in vivo sequelae of traumatic brain injury (TBI)...

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Published inJournal of neurotrauma Vol. 27; no. 7; pp. 1265 - 1274
Main Authors Colgan, Niall C., Cronin, Michelle M., Gobbo, Oliviero L., O'Mara, Shane M., O'Connor, William T., Gilchrist, Michael D.
Format Journal Article
LanguageEnglish
Published United States Mary Ann Liebert, Inc 01.07.2010
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Abstract More than 85% of reported brain traumas are classified clinically as "mild" using the Glasgow Coma Scale (GCS); qualitative MRI findings are scarce and provide little correspondence to clinical symptoms. Our goal, therefore, was to establish in vivo sequelae of traumatic brain injury (TBI) following lower and higher levels of impact to the frontal lobe using quantitative MRI analysis and a mechanical model of penetrating impact injury. To investigate time-based morphological and physiological changes of living tissue requires a surrogate for the human central nervous system. The present model for TBI was a systematically varied and controlled cortical impact on deeply-anaesthetized Sprague-Dawley rats, that was designed to mimic different injury severities. Whole-brain MRI scans were performed on each rat prior to either a lower- or a higher-level of impact, and then at hourly intervals for 5 h post-impact. Both brain volume and specific anatomical structures were segmented from MR images for inter-subject comparisons post-registration. Animals subjected to lower and higher impact levels exhibited elevated intracranial pressure (ICP) in the low compensatory reserve (i.e., nearly exhausted), and terminal disturbance (i.e., exhausted) ranges, respectively. There was a statistically significant drop in cerebrospinal fluid (CSF) of 35% in the lower impacts, and 65% in the higher impacts, at 5 h compared to sham controls. There was a corresponding increase in corpus callosum volume starting at 1 h, of 60-110% and 30-40% following the lower- and higher-impact levels, respectively. A statistically significant change in the abnormal tissue from 2 h to 5 h was observed for both impact levels, with greater significance for higher impacts. Furthermore, a statistically significant difference between the lower impacts and the sham controls occurred at 3 h. These results are statistically substantiated by a fluctuation in the physical size of the corpus callosum, a decrease in the volume of CSF, and elevated levels of atrophy in the cerebral cortex.
AbstractList More than 85% of reported brain traumas are classified clinically as "mild" using the Glasgow Coma Scale (GCS); qualitative MRI findings are scarce and provide little correspondence to clinical symptoms. Our goal, therefore, was to establish in vivo sequelae of traumatic brain injury (TBI) following lower and higher levels of impact to the frontal lobe using quantitative MRI analysis and a mechanical model of penetrating impact injury. To investigate time-based morphological and physiological changes of living tissue requires a surrogate for the human central nervous system. The present model for TBI was a systematically varied and controlled cortical impact on deeply-anaesthetized Sprague-Dawley rats, that was designed to mimic different injury severities. Whole-brain MRI scans were performed on each rat prior to either a lower- or a higher-level of impact, and then at hourly intervals for 5 h post-impact. Both brain volume and specific anatomical structures were segmented from MR images for inter-subject comparisons post-registration. Animals subjected to lower and higher impact levels exhibited elevated intracranial pressure (ICP) in the low compensatory reserve (i.e., nearly exhausted), and terminal disturbance (i.e., exhausted) ranges, respectively. There was a statistically significant drop in cerebrospinal fluid (CSF) of 35% in the lower impacts, and 65% in the higher impacts, at 5 h compared to sham controls. There was a corresponding increase in corpus callosum volume starting at 1 h, of 60-110% and 30-40% following the lower- and higher-impact levels, respectively. A statistically significant change in the abnormal tissue from 2 h to 5 h was observed for both impact levels, with greater significance for higher impacts. Furthermore, a statistically significant difference between the lower impacts and the sham controls occurred at 3 h. These results are statistically substantiated by a fluctuation in the physical size of the corpus callosum, a decrease in the volume of CSF, and elevated levels of atrophy in the cerebral cortex.More than 85% of reported brain traumas are classified clinically as "mild" using the Glasgow Coma Scale (GCS); qualitative MRI findings are scarce and provide little correspondence to clinical symptoms. Our goal, therefore, was to establish in vivo sequelae of traumatic brain injury (TBI) following lower and higher levels of impact to the frontal lobe using quantitative MRI analysis and a mechanical model of penetrating impact injury. To investigate time-based morphological and physiological changes of living tissue requires a surrogate for the human central nervous system. The present model for TBI was a systematically varied and controlled cortical impact on deeply-anaesthetized Sprague-Dawley rats, that was designed to mimic different injury severities. Whole-brain MRI scans were performed on each rat prior to either a lower- or a higher-level of impact, and then at hourly intervals for 5 h post-impact. Both brain volume and specific anatomical structures were segmented from MR images for inter-subject comparisons post-registration. Animals subjected to lower and higher impact levels exhibited elevated intracranial pressure (ICP) in the low compensatory reserve (i.e., nearly exhausted), and terminal disturbance (i.e., exhausted) ranges, respectively. There was a statistically significant drop in cerebrospinal fluid (CSF) of 35% in the lower impacts, and 65% in the higher impacts, at 5 h compared to sham controls. There was a corresponding increase in corpus callosum volume starting at 1 h, of 60-110% and 30-40% following the lower- and higher-impact levels, respectively. A statistically significant change in the abnormal tissue from 2 h to 5 h was observed for both impact levels, with greater significance for higher impacts. Furthermore, a statistically significant difference between the lower impacts and the sham controls occurred at 3 h. These results are statistically substantiated by a fluctuation in the physical size of the corpus callosum, a decrease in the volume of CSF, and elevated levels of atrophy in the cerebral cortex.
More than 85% of reported brain traumas are classified clinically as "mild" using the Glasgow Coma Scale (GCS); qualitative MRI findings are scarce and provide little correspondence to clinical symptoms. Our goal, therefore, was to establish in vivo sequelae of traumatic brain injury (TBI) following lower and higher levels of impact to the frontal lobe using quantitative MRI analysis and a mechanical model of penetrating impact injury. To investigate time-based morphological and physiological changes of living tissue requires a surrogate for the human central nervous system. The present model for TBI was a systematically varied and controlled cortical impact on deeply-anaesthetized Sprague-Dawley rats, that was designed to mimic different injury severities. Whole-brain MRI scans were performed on each rat prior to either a lower- or a higher-level of impact, and then at hourly intervals for 5 h post-impact. Both brain volume and specific anatomical structures were segmented from MR images for inter-subject comparisons post-registration. Animals subjected to lower and higher impact levels exhibited elevated intracranial pressure (ICP) in the low compensatory reserve (i.e., nearly exhausted), and terminal disturbance (i.e., exhausted) ranges, respectively. There was a statistically significant drop in cerebrospinal fluid (CSF) of 35% in the lower impacts, and 65% in the higher impacts, at 5 h compared to sham controls. There was a corresponding increase in corpus callosum volume starting at 1 h, of 60-110% and 30-40% following the lower- and higher-impact levels, respectively. A statistically significant change in the abnormal tissue from 2 h to 5 h was observed for both impact levels, with greater significance for higher impacts. Furthermore, a statistically significant difference between the lower impacts and the sham controls occurred at 3 h. These results are statistically substantiated by a fluctuation in the physical size of the corpus callosum, a decrease in the volume of CSF, and elevated levels of atrophy in the cerebral cortex. [PUBLICATION ABSTRACT]
More than 85% of reported brain traumas are classified clinically as "mild" using the Glasgow Coma Scale (GCS); qualitative MRI findings are scarce and provide little correspondence to clinical symptoms. Our goal, therefore, was to establish in vivo sequelae of traumatic brain injury (TBI) following lower and higher levels of impact to the frontal lobe using quantitative MRI analysis and a mechanical model of penetrating impact injury. To investigate time-based morphological and physiological changes of living tissue requires a surrogate for the human central nervous system. The present model for TBI was a systematically varied and controlled cortical impact on deeply-anaesthetized Sprague-Dawley rats, that was designed to mimic different injury severities. Whole-brain MRI scans were performed on each rat prior to either a lower- or a higher-level of impact, and then at hourly intervals for 5 h post-impact. Both brain volume and specific anatomical structures were segmented from MR images for inter-subject comparisons post-registration. Animals subjected to lower and higher impact levels exhibited elevated intracranial pressure (ICP) in the low compensatory reserve (i.e., nearly exhausted), and terminal disturbance (i.e., exhausted) ranges, respectively. There was a statistically significant drop in cerebrospinal fluid (CSF) of 35% in the lower impacts, and 65% in the higher impacts, at 5h compared to sham controls. There was a corresponding increase in corpus callosum volume starting at 1 h, of 60-110% and 30-40% following the lower- and higher-impact levels, respectively. A statistically significant change in the abnormal tissue from 2h to 5h was observed for both impact levels, with greater significance for higher impacts. Furthermore, a statistically significant difference between the lower impacts and the sham controls occurred at 3 h. These results are statistically substantiated by a fluctuation in the physical size of the corpus callosum, a decrease in the volume of CSF, and elevated levels of atrophy in the cerebral cortex.
More than 85% of reported brain traumas are classified clinically as "mild" using the Glasgow Coma Scale (GCS); qualitative MRI findings are scarce and provide little correspondence to clinical symptoms. Our goal, therefore, was to establish in vivo sequelae of traumatic brain injury (TBI) following lower and higher levels of impact to the frontal lobe using quantitative MRI analysis and a mechanical model of penetrating impact injury. To investigate time-based morphological and physiological changes of living tissue requires a surrogate for the human central nervous system. The present model for TBI was a systematically varied and controlled cortical impact on deeply-anaesthetized Sprague-Dawley rats, that was designed to mimic different injury severities. Whole-brain MRI scans were performed on each rat prior to either a lower- or a higher-level of impact, and then at hourly intervals for 5 h post-impact. Both brain volume and specific anatomical structures were segmented from MR images for inter-subject comparisons post-registration. Animals subjected to lower and higher impact levels exhibited elevated intracranial pressure (ICP) in the low compensatory reserve (i.e., nearly exhausted), and terminal disturbance (i.e., exhausted) ranges, respectively. There was a statistically significant drop in cerebrospinal fluid (CSF) of 35% in the lower impacts, and 65% in the higher impacts, at 5h compared to sham controls. There was a corresponding increase in corpus callosum volume starting at 1 h, of 60-110% and 30-40% following the lower- and higher-impact levels, respectively. A statistically significant change in the abnormal tissue from 2h to 5h was observed for both impact levels, with greater significance for higher impacts. Furthermore, a statistically significant difference between the lower impacts and the sham controls occurred at 3 h. These results are statistically substantiated by a fluctuation in the physical size of the corpus callosum, a decrease in the volume of CSF, and elevated levels of atrophy in the cerebral cortex. Key words: animal studies; MRI; rat; traumatic brain injury
More than 85% of reported brain traumas are classified clinically as "mild" using the Glasgow Coma Scale (GCS); qualitative MRI findings are scarce and provide little correspondence to clinical symptoms. Our goal, therefore, was to establish in vivo sequelae of traumatic brain injury (TBI) following lower and higher levels of impact to the frontal lobe using quantitative MRI analysis and a mechanical model of penetrating impact injury. To investigate time-based morphological and physiological changes of living tissue requires a surrogate for the human central nervous system. The present model for TBI was a systematically varied and controlled cortical impact on deeply-anaesthetized Sprague-Dawley rats, that was designed to mimic different injury severities. Whole-brain MRI scans were performed on each rat prior to either a lower- or a higher-level of impact, and then at hourly intervals for 5 h post-impact. Both brain volume and specific anatomical structures were segmented from MR images for inter-subject comparisons post-registration. Animals subjected to lower and higher impact levels exhibited elevated intracranial pressure (ICP) in the low compensatory reserve (i.e., nearly exhausted), and terminal disturbance (i.e., exhausted) ranges, respectively. There was a statistically significant drop in cerebrospinal fluid (CSF) of 35% in the lower impacts, and 65% in the higher impacts, at 5 h compared to sham controls. There was a corresponding increase in corpus callosum volume starting at 1 h, of 60-110% and 30-40% following the lower- and higher-impact levels, respectively. A statistically significant change in the abnormal tissue from 2 h to 5 h was observed for both impact levels, with greater significance for higher impacts. Furthermore, a statistically significant difference between the lower impacts and the sham controls occurred at 3 h. These results are statistically substantiated by a fluctuation in the physical size of the corpus callosum, a decrease in the volume of CSF, and elevated levels of atrophy in the cerebral cortex.
Audience Academic
Author Cronin, Michelle M.
Colgan, Niall C.
O'Mara, Shane M.
O'Connor, William T.
Gobbo, Oliviero L.
Gilchrist, Michael D.
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/20486804$$D View this record in MEDLINE/PubMed
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Cites_doi 10.3171/jns.1975.43.5.0523
10.1136/emj.17.6.392
10.1007/s00134-004-2376-4
10.1176/appi.neuropsych.16.1.1
10.1016/S0973-0508(05)80005-X
10.1097/00001199-199106000-00003
10.1111/j.1469-8749.1997.tb08199.x
10.1016/S0193-953X(18)30245-4
10.1523/JNEUROSCI.18-15-05663.1998
10.1002/mrm.10142
10.1089/neu.1999.16.109
10.1016/S0733-8619(05)70266-8
10.3171/jns.1977.47.5.0670
10.1093/bja/62.6.694
10.1177/107385840000600611
10.1126/science.7569924
10.1111/j.1475-1305.2004.00168.x
10.1089/neu.1997.14.715
10.1002/hbm.460030303
10.1136/jnnp.73.3.330
10.1002/0470869526
10.1016/0165-0270(91)90104-8
10.1097/00006123-198311000-00008
10.1089/neu.1994.11.573
10.1111/j.1600-0404.1973.tb01330.x
10.1093/bja/ael110
10.1016/S0006-8993(96)00819-0
10.1007/PL00007414
10.1089/neu.2005.22.947
10.1007/BF01405862
10.1016/j.brainres.2009.06.067
10.1089/neu.2007.0383
10.1089/089771503770802853
10.1097/01.yco.0000165601.29047.ae
10.1089/neu.1993.10.135
10.1097/00006123-199802000-00047
10.1097/00001199-200104000-00003
10.1038/jcbfm.1990.115
10.3171/jns.1977.47.1.0019
10.1089/neu.2006.23.1828
10.3171/foc.2007.22.5.12
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References B20
B21
B22
B23
B24
B25
B26
B27
B28
B29
Bowen J.M. (B4) 1997; 39
Cope D.N. (B13) 1982; 63
B30
B32
B36
B37
Mackay L.E. (B33) 1992; 73
B38
B39
Tofts P. (B52) 2003
B1
B2
B3
Cronin M. (B14) 2008; 177
Evans R.W. (B18) 1996
B6
B7
B8
Tofts P.D. (B53) 2003
B40
Ryder H.W. (B41) 1953; 41
Van Zomeren A.H. (B54) 1985; 48
B44
B45
Self Learning Packet (B43) 2004
B46
B47
B48
B49
Langlois J.A. (B31) 2004
Mackenzie J.D. (B34) 2002; 23
Salvado O. (B42) 2004
B50
B51
B10
B11
B55
B12
B57
B58
B15
B16
B19
Cohen B.A. (B9) 2007; 28
Bramlett H.M. (B5) 2002; 103
Marmarou A. (B35) 1991; 75
Whiting M.D. (B56) 2006
References_xml – ident: B36
  doi: 10.3171/jns.1975.43.5.0523
– ident: B6
  doi: 10.1136/emj.17.6.392
– ident: B1
  doi: 10.1007/s00134-004-2376-4
– ident: B26
  doi: 10.1176/appi.neuropsych.16.1.1
– ident: B7
  doi: 10.1016/S0973-0508(05)80005-X
– volume-title: Animal Models of Cognitive Impairment
  year: 2006
  ident: B56
– volume-title: Neurology and Trauma
  year: 1996
  ident: B18
– volume: 41
  start-page: 428
  year: 1953
  ident: B41
  publication-title: J. Lab. Clin. Med.
– ident: B47
  doi: 10.1097/00001199-199106000-00003
– volume: 39
  start-page: 17
  year: 1997
  ident: B4
  publication-title: Dev. Med. Child Neurol.
  doi: 10.1111/j.1469-8749.1997.tb08199.x
– volume: 75
  start-page: 59
  year: 1991
  ident: B35
  publication-title: American Association of Neurological Surgeons
– volume: 73
  start-page: 635
  year: 1992
  ident: B33
  publication-title: Arch. Phys. Med. Rehabil.
– ident: B37
  doi: 10.1016/S0193-953X(18)30245-4
– ident: B12
  doi: 10.1523/JNEUROSCI.18-15-05663.1998
– start-page: 1
  volume-title: Centers for Disease Control and Prevention
  year: 2004
  ident: B31
– volume: 23
  start-page: 1509
  year: 2002
  ident: B34
  publication-title: Am. J. Neuroradiol.
– ident: B23
  doi: 10.1002/mrm.10142
– ident: B16
  doi: 10.1089/neu.1999.16.109
– ident: B30
  doi: 10.1016/S0733-8619(05)70266-8
– volume-title: Overview of adult traumatic brain injuries
  year: 2004
  ident: B43
– ident: B44
  doi: 10.3171/jns.1977.47.5.0670
– ident: B55
  doi: 10.1093/bja/62.6.694
– ident: B45
  doi: 10.1177/107385840000600611
– ident: B38
  doi: 10.1126/science.7569924
– start-page: 539
  year: 2004
  ident: B42
  publication-title: IEEE Eng. Med. Biol. Soc.
– volume: 177
  start-page: 17
  issue: 1
  year: 2008
  ident: B14
  publication-title: Irish J. Med. Sci.
– volume: 63
  start-page: 433
  year: 1982
  ident: B13
  publication-title: Arch. of Phys. Med. Rehabil.
– ident: B21
  doi: 10.1111/j.1475-1305.2004.00168.x
– ident: B46
  doi: 10.1089/neu.1997.14.715
– ident: B19
  doi: 10.1002/hbm.460030303
– ident: B40
  doi: 10.1136/jnnp.73.3.330
– volume-title: Histograms: Measuring subtle diffuse disease, in: Quantitative MRI of the Brain: Measuring Changes Caused by Disease
  year: 2003
  ident: B52
  doi: 10.1002/0470869526
– ident: B10
– ident: B15
  doi: 10.1016/0165-0270(91)90104-8
– ident: B2
  doi: 10.1097/00006123-198311000-00008
– volume-title: Proton density of tissue water, in: Quantitative MRI of the Brain: Measuring Changes Caused by Disease
  year: 2003
  ident: B53
  doi: 10.1002/0470869526
– ident: B8
  doi: 10.1089/neu.1994.11.573
– ident: B32
  doi: 10.1111/j.1600-0404.1973.tb01330.x
– ident: B48
  doi: 10.1093/bja/ael110
– ident: B11
  doi: 10.1016/S0006-8993(96)00819-0
– volume: 103
  start-page: 607
  year: 2002
  ident: B5
  publication-title: Acta Neurochirurgica
– ident: B22
  doi: 10.1007/PL00007414
– ident: B28
  doi: 10.1089/neu.2005.22.947
– ident: B51
  doi: 10.1007/BF01405862
– ident: B58
  doi: 10.1016/j.brainres.2009.06.067
– ident: B24
  doi: 10.1089/neu.2007.0383
– ident: B20
  doi: 10.1089/089771503770802853
– ident: B27
  doi: 10.1097/01.yco.0000165601.29047.ae
– ident: B49
  doi: 10.1089/neu.1993.10.135
– volume: 48
  start-page: 21
  year: 1985
  ident: B54
  publication-title: Br. Med. J.
– ident: B25
  doi: 10.1097/00006123-199802000-00047
– ident: B3
  doi: 10.1097/00001199-200104000-00003
– ident: B39
  doi: 10.1038/jcbfm.1990.115
– volume: 28
  start-page: 907
  year: 2007
  ident: B9
  publication-title: Am. J. Neuroradiol.
– ident: B50
  doi: 10.3171/jns.1977.47.1.0019
– ident: B57
  doi: 10.1089/neu.2006.23.1828
– ident: B29
  doi: 10.3171/foc.2007.22.5.12
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Snippet More than 85% of reported brain traumas are classified clinically as "mild" using the Glasgow Coma Scale (GCS); qualitative MRI findings are scarce and provide...
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SubjectTerms Animals
Brain
Brain - physiopathology
Brain damage
Brain Edema - diagnosis
Brain Edema - etiology
Brain Edema - physiopathology
Brain Injuries - diagnosis
Brain Injuries - etiology
Brain Injuries - physiopathology
Cerebral Cortex - injuries
Cerebral Cortex - physiopathology
Disease Models, Animal
Disease Progression
Health aspects
Injuries
Magnetic resonance imaging
Magnetic Resonance Imaging - methods
Male
Neurology
NMR
Nuclear magnetic resonance
Organ Size - physiology
Rats
Rats, Sprague-Dawley
Rodents
Time Factors
Title Quantitative MRI Analysis of Brain Volume Changes due to Controlled Cortical Impact
URI https://www.ncbi.nlm.nih.gov/pubmed/20486804
https://www.proquest.com/docview/706550771
https://www.proquest.com/docview/734032634
Volume 27
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