Arnold Toth1, Noemi Kovacs2, Viktoria Tamas3, Balint Kornyei4, Mate Nagy5, Andrea Horvath6, Tamas Rostas7, Peter Bogner8, Jozsef Janszky9, Tamas Doczi10, Andras Buki11, Attila Schwarcz12. 1. Department of Neurosurgery, Pécs Medical School, H-7623, Rét. u. 2., Pécs, Hungary. Electronic address: prsarn@gmail.com. 2. Department of Neurosurgery, Pécs Medical School, H-7623, Rét. u. 2., Pécs, Hungary. Electronic address: noemi.kovacs5@gmail.com. 3. Department of Neurosurgery, Pécs Medical School, H-7623, Rét. u. 2., Pécs, Hungary. Electronic address: tamas.viktoria@pte.hu. 4. Department of Neurosurgery, Pécs Medical School, H-7623, Rét. u. 2., Pécs, Hungary. Electronic address: kornyei.balint@windowslive.com. 5. Department of Neurosurgery, Pécs Medical School, H-7623, Rét. u. 2., Pécs, Hungary. Electronic address: nagy.mate@pte.hu. 6. Department of Neurosurgery, Pécs Medical School, H-7623, Rét. u. 2., Pécs, Hungary; Diagnostic Center of Pécs, H-7623, Rét. u. 2., Pécs, Hungary. Electronic address: andrhorvath@gmail.com. 7. Department of Radiology, Pécs Medical School, H-7624, Ifjusag str. 13., Pécs, Hungary. Electronic address: rostas.tamas@pte.hu. 8. Department of Neurosurgery, Pécs Medical School, H-7623, Rét. u. 2., Pécs, Hungary; Department of Radiology, Pécs Medical School, H-7624, Ifjusag str. 13., Pécs, Hungary. Electronic address: peter.bogner@gmail.com. 9. Department of Neurology, Pécs Medical School, H-7623, Rét. u. 2., Pécs, Hungary; MTA-PTE Clinical Neuroscience MR Research Group, Hungary. Electronic address: jozsef.janszky@gmail.com. 10. Department of Neurosurgery, Pécs Medical School, H-7623, Rét. u. 2., Pécs, Hungary; Diagnostic Center of Pécs, H-7623, Rét. u. 2., Pécs, Hungary; MTA-PTE Clinical Neuroscience MR Research Group, Hungary. Electronic address: doczi.tamas@pte.hu. 11. Department of Neurosurgery, Pécs Medical School, H-7623, Rét. u. 2., Pécs, Hungary; MTA-PTE Clinical Neuroscience MR Research Group, Hungary. Electronic address: 2saturn@pte.hu. 12. Department of Neurosurgery, Pécs Medical School, H-7623, Rét. u. 2., Pécs, Hungary; MTA-PTE Clinical Neuroscience MR Research Group, Hungary. Electronic address: schwarcz.attila@pte.hu.
Abstract
BACKGROUND AND PURPOSE: Susceptibility weighted imaging (SWI) is a very sensitive tool for the detection of microbleeds in traumatic brain injury (TBI). The number and extent of such traumatic microbleeds (TMBs) have been shown to correlate with the severity of the injury and the clinical outcome. However, the acute dynamics of TMBs have not been revealed so far. Since TBI is known to constitute dynamic pathological processes, we hypothesized that TMBs are not constant in their appearance, but may progress acutely after injury. MATERIALS AND METHODS: We present here five closed moderate/severe (Glasgow coma scale≤13) TBI patients who underwent SWI very early (average=23.4 h), and once again a week (average=185.8 h) after the injury. The TMBs were mapped at both time points by a conventional radiological approach and their numbers and volumes were measured with manual tracing tools by two observers. TMB counts and extents were compared between time points. RESULTS: TMBs were detected in four patients, three of them displaying an apparent TMB change. In these patients, TMB confluence and apparent growth were detected in the corpus callosum, coronal radiation or subcortical white matter, while unchanged TMBs were also present. These changes caused a decrease in the TMB count associated with an increase in the overall TMB volume over time. CONCLUSION: We have found a compelling evidence that diffuse axonal injury-related microbleed development is not limited strictly to the moment of injury: the TMBs might expand in the acute phase of TBI. The timing of SWI acquisition may be relevant for optimizing the prognostic utility of this imaging biomarker.
BACKGROUND AND PURPOSE: Susceptibility weighted imaging (SWI) is a very sensitive tool for the detection of microbleeds in traumatic brain injury (TBI). The number and extent of such traumatic microbleeds (TMBs) have been shown to correlate with the severity of the injury and the clinical outcome. However, the acute dynamics of TMBs have not been revealed so far. Since TBI is known to constitute dynamic pathological processes, we hypothesized that TMBs are not constant in their appearance, but may progress acutely after injury. MATERIALS AND METHODS: We present here five closed moderate/severe (Glasgow coma scale≤13) TBIpatients who underwent SWI very early (average=23.4 h), and once again a week (average=185.8 h) after the injury. The TMBs were mapped at both time points by a conventional radiological approach and their numbers and volumes were measured with manual tracing tools by two observers. TMB counts and extents were compared between time points. RESULTS: TMBs were detected in four patients, three of them displaying an apparent TMB change. In these patients, TMB confluence and apparent growth were detected in the corpus callosum, coronal radiation or subcortical white matter, while unchanged TMBs were also present. These changes caused a decrease in the TMB count associated with an increase in the overall TMB volume over time. CONCLUSION: We have found a compelling evidence that diffuse axonal injury-related microbleed development is not limited strictly to the moment of injury: the TMBs might expand in the acute phase of TBI. The timing of SWI acquisition may be relevant for optimizing the prognostic utility of this imaging biomarker.
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