Skip to main content
Fig. 4 | Brain Imaging and Behavior

Fig. 4

From: Toward a global and reproducible science for brain imaging in neurotrauma: the ENIGMA adult moderate/severe traumatic brain injury working group

Fig. 4

The complexity of lesion characterization and behavioral phenotyping after AMS-TBI. From a structural neuroimaging perspective trauma-induced abnormalities differ by time post-injury as well as the imaging modality being used. a are all CT based showing that the size and location of the hemorrhage, parenchymal displacement and edema dynamically change over time. b demonstrates that each MRI sequence has its own unique sensitivity in assessing different aspects of neuroanatomy and neuropathology. c which presents the FLAIR, SWI and T1 signal abnormalities, demonstrates the widespread pathology differently presented by these imaging methods. By 5 months’ post-injury, widespread volume loss, cortical atrophy, ventriculomegaly and encephalomalacia have occurred. d show summary findings from a neuropsychological assessment at ~8 months post injury. This case example depicts the neuropathological heterogeneity associated with TBI along with the dynamic changes over time and their influence on neuropsychological test results. This patient sustained a severe TBI from a motorcycle collision with a vehicle. The patient was not helmeted at the time of injury and, by witness accounts, was immediately rendered unconscious. Upon emergent care at the scene of the accident, the patient was assessed to have a Glasgow Coma Scale (GCS) of 3, was life-flighted to a Level I emergency department (ED) with GCS remaining 3 throughout transport and during ED assessment and treatment. In addition to the head injuries he sustained multiple systemic injuries including leg and rib fractures, pulmonary contusion and liver laceration. An intracranial pressure monitor was inserted, the patient underwent tracheostomy for airway management and shunted. The patient remained in a coma and received neurocritical care for almost 2 months, followed by 3 months of inpatient neurorehabilitation. a Initial day-of-injury computed tomography was performed about 90 min’ post-injury. What is important to note in the initial scan is the original size of the frontal intraparenchymal hemorrhage along with the size, symmetry and configuration of the ventricular system. Within 24 h, enlargement of the intraparenchymal hemorrhage is observed along with distinct effacement of the anterior horn of the lateral ventricle and surrounding edema associated with the hemorrhage. Subsequent to this scan he was shunted, with the shunt catheter clearly visible in the 2-week follow-up scan which depicts more edema and midline shift. By 5 months’ post-injury, there is prominence of the ventricular system and cortical sulci in association with cortical atrophy and frontal encephalomalacia associated with the location of the prior hemorrhage. b At 2 weeks post-injury, MRI studies were obtained. Each sequence demonstrates a different aspect of the “Lesion.” The T1 sequence, which is the one commonly used for automated methods of image segmentation and classification for quantitative analyses, depicts coarse anatomical features of the brain, but the focal intraparenchymal hemorrhage and surrounding edema is not fully appreciated, being better distinguished by the T2 and FLAIR sequences. The SWI sequence depicts multiple, bilaterally scattered foci of hemosiderin deposition reflective of shear injury, with particularly exquisite demarcation differentiating hemorrhage, parenchymal degradation along with the surrounding edema. c Using a thresholding method for detecting white matter signal abnormality in FLAIR scans, the regions of white matter hyperintensity are depicted three dimensionally in the images on the left. Each signal abnormality likely reflects localized white matter pathology. In the middle are the regions of hemosiderin deposition detected on SWI, likewise reflecting specific foci of shear-lesion pathology constituting diffuse axonal injury. On the right are the abnormalities found on T1. d Findings from neuropsychological assessment at almost 8 months post injury are presented as z-score deviations from test manual normative data. The following tests were administered: Repeatable Battery for the Assessment of Neuropsychological Status (RBANS, https://www.pearsonassessments.com/), Rey Complex Figure Test (RCFT, https://www.parinc.com), California Verbal Learning Test-II (CVLT-II, https://www.pearsonassessments.com/), Delis-Kaplan Executive Function System (D-KFES, https://www.pearsonassessments.com/); Symptom Checklist-90 (SCL-90, https://www.pearsonassessments.com/) and the Behavioral Rating Inventory of Executive Function (BRIEF, https://www.parinc.com). Clinically, the 25-year-old presented with left side hemiparesis, emotional lability and major cognitive impairments, most notable in terms of memory and executive functioning. Family and caregivers were most concerned about the patient’s irritability and inappropriate outbursts along with impaired insight and judgment. Neuropsychological tests (lower z-scores = poorer function) demonstrated the expected left side reductions in motor control (reduced finger tapping and grip strength) consistent with the location of the large intraparenchymal right frontal hemorrhagic injury (see Fig. 4a-c). He was anosmic and unable to identify basic odors on the Smell Identification Test (https://sensonics.com/) along with diminished tactile discrimination on the left side, but no visual field defect. Constructional praxis was diminished as evident in the copy of the Rey Complex Figure Test (RCFT), with the more profound deficits most notable with impaired immediate as well as delayed memory. Memory and executive impairments were evident on the RBANS, CVLT-II and DKFES tasks. Caregiver observation, based on the BRIEF (higher z-scores = more problems) also confirmed real-world deficits in day-to-day impairments in planning, organization, decision making and problem solving. Emotionally, as also reflected in the BRIEF results, the family caregiver reported marked dysfunction in emotional regulation with poor self-monitoring and impaired insight. In contrast, on the SCL-90 (higher z-scores = more symptoms), which is a self-report measure, while somatic issues that related to mobility and pain were prominently endorsed, the Global Severity Index (GSI) was only minimally elevated, with no significant endorsement of symptoms related to depression or anxiety. This would be consistent with caregiver observations that the patient lacked insight into changes in personality and emotional control, impairments often reported to be present in TBI patients with extensive frontotemporal pathology (Krudop & Pijnenburg, 2015), as evident in this patient

Back to article page