1999
DOI: 10.1016/s0010-9452(08)70803-7
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Corpus Callosum Damage and InterhemispherIc Transfer of Information following Closed Head Injury in Children

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Cited by 62 publications
(48 citation statements)
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“…Although research examining the cognitive sequelae to callosal damage following TBI is limited, there are reports of callosal disconnection following severe TBI (Levander & Sonesson, 1998;Rubens et al, 1977;Vuilleumier & Assal, 1995), with patients displaying gross deficits in their ability to transfer and integrate information between hemispheres (e.g., apraxia, finger localization, dichotic listening), consistent with the deficits shown by patients who have had commissurotomies (e.g., Benavidez et al, 1999;Bentin et al, 1984;Damasio et al, 1980;Geffen et al, 1985). However, there do not appear to be any studies that have used information processing measures in order to detect more subtle deficits that may arise from less severe damage.…”
Section: Mild Traumatic Brain Injurymentioning
confidence: 79%
“…Although research examining the cognitive sequelae to callosal damage following TBI is limited, there are reports of callosal disconnection following severe TBI (Levander & Sonesson, 1998;Rubens et al, 1977;Vuilleumier & Assal, 1995), with patients displaying gross deficits in their ability to transfer and integrate information between hemispheres (e.g., apraxia, finger localization, dichotic listening), consistent with the deficits shown by patients who have had commissurotomies (e.g., Benavidez et al, 1999;Bentin et al, 1984;Damasio et al, 1980;Geffen et al, 1985). However, there do not appear to be any studies that have used information processing measures in order to detect more subtle deficits that may arise from less severe damage.…”
Section: Mild Traumatic Brain Injurymentioning
confidence: 79%
“…7 The reduction over time in CC volume, along with thinning of the CC, are thought to result from Wallerian degeneration following TBI. 9 The posterior region, or splenium, of the CC is especially vulnerable to TBI 10,11,12,13 Atrophy of the splenium of the CC has been observed following TBI. 14,15,16 Lesions in the posterior half of the CC accounted for 80% of all CC injuries in a study of 92 patients (i.e., ages 2-77, mean age 28) with severe TBI.…”
Section: Event-related Potential Measure Of Interhemispheric Transfermentioning
confidence: 99%
“…The hypothesis that the posterior CC is responsible for the interhemispheric transfer of visual information is supported by other studies, including a study examining commissurotomies in non-epileptic patients 25 and case studies of two patients with posterior CC sectioning for tumor removal, 26 as well as in a case study of one patient with hemialexia following posterior CC surgical sectioning. 27 Some evidence for impaired IHTT in TBI is provided by the performance of children with severe TBIs on a verbal dichotic listening task 10 and adults on visual and tactile reaction time tasks 20 that required IHTT. Although white matter atrophy was moderately related to visual and tactile reaction time task performance in adults, total CC area was not significantly related to performance on these tasks.…”
Section: Event-related Potential Measure Of Interhemispheric Transfermentioning
confidence: 99%
“…44,45 WM and the CC after pediatric TBI The CC, the largest commissural white-matter bundle in the human brain, is the main route for interhemispheric transfer of information and is implicated in a large number of cognitive processes. [46][47][48][49][50] The CC is particularly vulnerable to injury in TBI. 46,51,52 DTI studies have shown lower FA and higher diffusivity metrics in all callosal subregions, relative to TD comparison groups, after TBI in both children and adults at subacute and chronic stages of recovery.…”
Section: 32mentioning
confidence: 99%
“…[46][47][48][49][50] The CC is particularly vulnerable to injury in TBI. 46,51,52 DTI studies have shown lower FA and higher diffusivity metrics in all callosal subregions, relative to TD comparison groups, after TBI in both children and adults at subacute and chronic stages of recovery. 44,45,[53][54][55][56] Given the proposed involvement of the CC in the bilateral frontoparietal neural networks underlying WM, 31,32 and its particular vulnerability to injury, reduced microstructural integrity of the CC may act as a neuropathological mechanism, possibly contributing to long-term WM deficits after pediatric TBI.…”
Section: 32mentioning
confidence: 99%