Marta Bianciardi1, Saef Izzy2, Bruce R Rosen2, Lawrence L Wald2, Brian L Edlow2. 1. From the Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging (M.B., B.R.R., L.L.W., B.L.E.), and Center for Neurotechnology and Neurorecovery, Department of Neurology (B.L.E.), Massachusetts General Hospital and Harvard Medical School; Division of Sleep Medicine (M.B.), Harvard University; and Department of Neurology (S.I.), Brigham and Women's Hospital and Harvard Medical School, Boston, MA. martab@mgh.harvard.edu. 2. From the Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging (M.B., B.R.R., L.L.W., B.L.E.), and Center for Neurotechnology and Neurorecovery, Department of Neurology (B.L.E.), Massachusetts General Hospital and Harvard Medical School; Division of Sleep Medicine (M.B.), Harvard University; and Department of Neurology (S.I.), Brigham and Women's Hospital and Harvard Medical School, Boston, MA.
Abstract
BACKGROUND: In patients with severe traumatic brain injury (TBI), coma is associated with impaired subcortical arousal mechanisms. However, it is unknown which nuclei involved in arousal (arousal nuclei) are implicated in coma pathogenesis and are compatible with coma recovery. METHODS: We mapped an atlas of arousal nuclei in the brainstem, thalamus, hypothalamus, and basal forebrain onto 3 tesla susceptibility-weighted images (SWI) in 12 patients with acute severe TBI who presented in coma and recovered consciousness within 6 months. We assessed the spatial distribution and volume of SWI microbleeds and evaluated the association of microbleed volume with the duration of unresponsiveness and functional recovery at 6 months. RESULTS: There was no single arousal nucleus affected by microbleeds in all patients. Rather, multiple combinations of microbleeds in brainstem, thalamic, and hypothalamic arousal nuclei were associated with coma and were compatible with recovery of consciousness. Microbleeds were frequently detected in the midbrain (100%), thalamus (83%), and pons (75%). Within the brainstem, the microbleed incidence was largest within the mesopontine tegmentum (e.g., pedunculotegmental nucleus, mesencephalic reticular formation) and ventral midbrain (e.g., substantia nigra, ventral tegmental area). Brainstem arousal nuclei were partially affected by microbleeds, with microbleed volume not exceeding 35% of brainstem nucleus volume on average. Compared to microbleed volume within nonarousal brainstem regions, the microbleed volume within arousal brainstem nuclei accounted for a larger proportion of variance in the duration of unresponsiveness and 6-month Glasgow Outcome Scale-Extended scores. CONCLUSION: These results suggest resilience of arousal mechanisms in the human brain after severe TBI.
BACKGROUND: In patients with severe traumatic brain injury (TBI), coma is associated with impaired subcortical arousal mechanisms. However, it is unknown which nuclei involved in arousal (arousal nuclei) are implicated in coma pathogenesis and are compatible with coma recovery. METHODS: We mapped an atlas of arousal nuclei in the brainstem, thalamus, hypothalamus, and basal forebrain onto 3 tesla susceptibility-weighted images (SWI) in 12 patients with acute severe TBI who presented in coma and recovered consciousness within 6 months. We assessed the spatial distribution and volume of SWI microbleeds and evaluated the association of microbleed volume with the duration of unresponsiveness and functional recovery at 6 months. RESULTS: There was no single arousal nucleus affected by microbleeds in all patients. Rather, multiple combinations of microbleeds in brainstem, thalamic, and hypothalamic arousal nuclei were associated with coma and were compatible with recovery of consciousness. Microbleeds were frequently detected in the midbrain (100%), thalamus (83%), and pons (75%). Within the brainstem, the microbleed incidence was largest within the mesopontine tegmentum (e.g., pedunculotegmental nucleus, mesencephalic reticular formation) and ventral midbrain (e.g., substantia nigra, ventral tegmental area). Brainstem arousal nuclei were partially affected by microbleeds, with microbleed volume not exceeding 35% of brainstem nucleus volume on average. Compared to microbleed volume within nonarousal brainstem regions, the microbleed volume within arousal brainstem nuclei accounted for a larger proportion of variance in the duration of unresponsiveness and 6-month Glasgow Outcome Scale-Extended scores. CONCLUSION: These results suggest resilience of arousal mechanisms in the human brain after severe TBI.
Authors: Marta Bianciardi; Christian Strong; Nicola Toschi; Brian L Edlow; Bruce Fischl; Emery N Brown; Bruce R Rosen; Lawrence L Wald Journal: Neuroimage Date: 2017-05-03 Impact factor: 6.556
Authors: Marta Bianciardi; Nicola Toschi; Brian L Edlow; Cornelius Eichner; Kawin Setsompop; Jonathan R Polimeni; Emery N Brown; Hannah C Kinney; Bruce R Rosen; Lawrence L Wald Journal: Brain Connect Date: 2015-08-11
Authors: Nicole L Mazwi; Saef Izzy; Can Ozan Tan; Sergi Martinez; Mel B Glenn; Joseph T Giacino; Ona Wu; Ross Zafonte; Brian L Edlow Journal: J Head Trauma Rehabil Date: 2019 Nov/Dec Impact factor: 2.710