S K Misser1,2, J W Lotz3, R van Toorn4, N Mchunu5,6,7, M Archary8, A J Barkovich9. 1. Form the Department of Radiology (D.S.K.M.), Faculty of Health Sciences, University of Kwa-Zulu Natal, Nelson R Mandela School of Medicine, Durban, South Africa shalendra.misser@lakesmit.co.za. 2. Lake Smit and Partners Inc (D.S.K.M.), Durban, South Africa. 3. Department of Radiodiagnosis (P.J.W.L.), Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, South Africa. 4. Department of Paediatrics and Child Health (P.R.v.T.), Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, South Africa. 5. Biostatistics Research Unit (M.N.M.), South African Medical Research Council, Durban, South Africa. 6. School of Mathematics, Statistics and Computer Sciences, (M.N.M.), University of KwaZulu-Natal, Pietermaritzburg, South Africa. 7. Centre for the AIDS Programme of Research in South Africa (M.N.M.), Urban, South Africa. 8. Department of Pediatrics (P.M.A.), University of Kwa-Zulu Natal, Faculty of Health Sciences, Nelson R Mandela School of Medicine, Durban, South Africa. 9. School of Medicine (P.A.J.B.), University of California, San Francisco, California.
Abstract
BACKGROUND AND PURPOSE: Considerable overlap exists in the MR imaging features of hypoglycemic injury and hypoxic-ischemic brain injury, with similar predilections for the occipital and parietal lobes. In partial, prolonged hypoxia-ischemia, there is cortical destruction at the interarterial watershed zones, and in concomitant hypoglycemia and hypoxia-ischemia, an exaggerated final common pathway injury occurs. We interrogated secondary white matter tract-based thalamic injury as a tool to separate pure injuries in each group. MATERIALS AND METHODS: A retrospective observational study of the MRIs of 320 children with a history of hypoxia-ischemia and/or hypoglycemia was undertaken with 3 major subgroups: 1) watershed-type hypoxic-ischemic injury, 2) neonatal hypoglycemia, and 3) both perinatal hypoxia-ischemia and proved hypoglycemia. Cerebral and thalamic injuries were assessed, particularly hyperintensity of the posterolateral margin of the thalami. A modified Poisson regression model was used to assess factors associated with such thalamic injury. RESULTS: Parieto-occipital injuries occurred commonly in patients with hypoglycemia and/or hypoxia-ischemia. Eighty-five of 99 (86%) patients with partial, prolonged hypoxia-ischemia exhibited the thalamus L-sign. This sign was also observed in patients who had both hypoglycemia and hypoxia-ischemia, predominantly attributable to the latter. Notably, the risk of a thalamus L-sign injury was 2.79 times higher when both the parietal and occipital lobes were injured compared with when they were not involved (95% CI, 1.25-6.23; P = .012). The thalamus L-sign was not depicted in patients with pure hypoglycemia. CONCLUSIONS: We propose the thalamus L-sign as a biomarker of partial, prolonged hypoxia-ischemia, which is exaggerated in combined hypoglycemic/hypoxic-ischemic injury.
BACKGROUND AND PURPOSE: Considerable overlap exists in the MR imaging features of hypoglycemic injury and hypoxic-ischemic brain injury, with similar predilections for the occipital and parietal lobes. In partial, prolonged hypoxia-ischemia, there is cortical destruction at the interarterial watershed zones, and in concomitant hypoglycemia and hypoxia-ischemia, an exaggerated final common pathway injury occurs. We interrogated secondary white matter tract-based thalamic injury as a tool to separate pure injuries in each group. MATERIALS AND METHODS: A retrospective observational study of the MRIs of 320 children with a history of hypoxia-ischemia and/or hypoglycemia was undertaken with 3 major subgroups: 1) watershed-type hypoxic-ischemic injury, 2) neonatal hypoglycemia, and 3) both perinatal hypoxia-ischemia and proved hypoglycemia. Cerebral and thalamic injuries were assessed, particularly hyperintensity of the posterolateral margin of the thalami. A modified Poisson regression model was used to assess factors associated with such thalamic injury. RESULTS: Parieto-occipital injuries occurred commonly in patients with hypoglycemia and/or hypoxia-ischemia. Eighty-five of 99 (86%) patients with partial, prolonged hypoxia-ischemia exhibited the thalamus L-sign. This sign was also observed in patients who had both hypoglycemia and hypoxia-ischemia, predominantly attributable to the latter. Notably, the risk of a thalamus L-sign injury was 2.79 times higher when both the parietal and occipital lobes were injured compared with when they were not involved (95% CI, 1.25-6.23; P = .012). The thalamus L-sign was not depicted in patients with pure hypoglycemia. CONCLUSIONS: We propose the thalamus L-sign as a biomarker of partial, prolonged hypoxia-ischemia, which is exaggerated in combined hypoglycemic/hypoxic-ischemic injury.
Authors: Emily W Y Tam; Laurel A Haeusslein; Sonia L Bonifacio; Hannah C Glass; Elizabeth E Rogers; Rita J Jeremy; A James Barkovich; Donna M Ferriero Journal: J Pediatr Date: 2012-02-04 Impact factor: 4.406
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