Chronic Effects of Traumatic Brain Injury: An Image-based Review

1. Chronic Effects of Traumatic Brain Injury: An Image-based Review Chika Obele M.D., Timothy Shepherd M.D. Ph.D., Ivan Kirov Ph.D.,Sohae Chung Ph.D., Yvonne W. Lui M.D. Department of Radiology, New York University School of Medicine Control #: 2708 Title: Chronic Effects of Traumatic Brain Injury eEdE#: eEdE-107

2. No financial disclosures.

3. Background • Traumatic brain injury (TBI) is common (~1.9 million people annually in the U.S.) and can be devastating leading to hospitalization and fatalities. • With so may injury annually, aside from acute injury what are the chronic sequelae? • It is these that contribute to long-term morbidity and cost to society. • ~2% of the entire U.S. population lives with some long term disability due to TBI.

4. Educational Objective • To illustrate chronic sequelae of TBI with a focus on the role of imaging.

5. Imaging modalities CT is standard of care for assessment of acute head injury. MRI, however, is commonly used to evaluate long-term sequelae of TBI to assess: • Atrophy and gliosis • Potential epileptogenic foci • Small microhemorrhage • Brainstem and posterior fossa, typically difficult on CT. • A patient with unexplained persistent neurological deficits • And avoids ionizing radiation • research applications

6. Major secondary sequelae of TBI • Stroke / vascular • Post-traumatic epilepsy • Movement abnormality • Cognitive and behavioral difficulty • Hydrocephalus • Affective disorder

7. Vascular • There are a variety of vascular injuries that occur post-traumatically. • Can result in significant long-term morbidity. • Direct vascular injury • Ischemia (vasospasm, compression) • Hemorrhage • Venous infarct • AV Fistula • Pseudoaneurysm

8. Vascular Injury • 54yo F pedestrian with a complex skull base fracture (yellow) presented with massive epistaxis. Lateral projection from R CCA injection shows extravasation of contrast into the sphenoid sinus (red). Kelly clamp has been placed in the nasal cavity for packing. Courtesy Eytan Raz M.D. 

9. Dissection • Classic imaging findings of carotid dissection in a patient with Horner’s syndrome and neck stiffness after TBI. • Crescentic mural thrombus on T1WI with fat saturation (red) and flame-shaped tapering on MIP CTA (yellow).

10. Stroke • Stroke is #1 cause of chronic disability in the U.S. • TBI known risk factor for stroke • Greater injury severity is associated with increased risk • e.g., TBI with fracture is associated with a 20-fold increase in stroke risk over TBI without fracture

11. Stroke • 65 year old male with a history of midline shift relating to post-traumatic hemorrhage resulted in bilateral anterior cerebral artery territory infarcts (red) • Chronic classic areas of inferior temporal contusion are also seen (light blue). • Major ACA (green) branches, seen here in a different patient, are susceptible to compromise as they can be pinned along the free edge of the falx in instances of substantial midline shift.

12. Stroke / Vascular • Axial FLAIR in a patient with traumatic left vertebral artery dissection shows PICA territory gliosis (yellow). • Time-of-flight MRA shows absent flow-related signal in the left vertebral artery (red).

13. Stroke • GRE T2* image in a 88-year-old man shows susceptibility in the sulci indicative of subarachnoid hemorrhage (yellow arrow) • Time of flight MRA MIP shows asymmetrically decreased flow-related signal in the left MCA (red) secondary to vasospasm.

14. Venous infarct • Rarely venous infarcts can complicate trauma. • 33yo with subdural hematoma (yellow), 2 weeks later developed massive left frontal lobe swelling (red) felt to be disproportionate to amount of initial contusional injury. • MIP TOF MRV shows compromise of a cortical vein (blue) along edge of decompressive craniectomy

15. Carotid Cavernous Fistula • Source data from CTA after trauma shows arterial phase contrast opacification of cavernous sinuses and superior ophthalmic veins bilaterally (red) • Note lack of equivalent contrast in the dural venous sinus (blue)

16. Dural AV Fistula • Occipital fracture is present (red) • Lateral projection selective L occipital artery injection shows dural arteriovenous fistula (yellow) with early venous drainage (blue).

17. Post-traumatic Seizure Disorder • Definition: recurrent seizures due to TBI • Risk factors: • penetrating injury • injury severity (GCS <10 in first 24 hours) • multiple contusions • >5mm midline shift • >24hrs loss of consciousness • dural penetration • prolonged amnesia • early post-traumatic seizures • injuries requiring surgical intervention • MRI can detect possible epileptogenic foci, such as areas of cortical contusion (red).

18. Post-traumatic seizure disorder • 47 year old female left temporal lobe injury after MVA 13 years ago • Has medically refractory posttraumatic seizure disorder • Underwent partial temporal lobectomy (blue) to resect gliotic brain though she developed left hippocampal sclerosis in the time since injury (red) and continued to suffer from seizures

19. Chronic Movement Disorders • Movement disorders are an uncommon complication of TBI • TBI is a known risk factor for Parkinson’s disease (44% increased risk in TBI patients) • Others: Choreoathetosis, hemiballismus, hyperreflexia. • Proposed mechanism is damage to deep gray matter (basal ganglia, thalamus), or disrupted basal ganglia / thalamocortical circuits. Ribbon cutting for the Muhammed Ali Parkinson’s Center in Phoenix, AZ http://mms.businesswire.com

20. Chronic Movement Disorders • Proposed mechanism is damage to deep gray matter (basal ganglia, thalamus), or disrupted basal ganglia / thalamocortical circuits • Hemorrhagic traumatic axonal injury shown here to the left basal ganglia (red) and right temporal white matter.

21. Cognition / Behavior • Patients may have problems with attention, memory, insight, judgment, language, communication and other executive functions. • Inferior frontal and temporal lobes are specifically at risk for contusion. • Frontal lobes play key role in behavior and higher-order cognition. • Frontal injury may lead to a clinical syndrome featuring poor impulse control, impaired attention, perseveration, and diminished divergent thinking.

22. Cognition / Behavior • Temporal lobe plays a key role in long-term memory, personality and affective behavior • Also susceptible to contusion (red) as it impacts the floor of the middle cranial fossa • Chronic injury results in gliosis and volume loss (blue)

23. Cognition / Behavior • In addition to focal contusion, traumatic axonal injury can cause widespread damage, affecting complex cognitive pathways. • Microhemorrhages are best detected using GRE T2*-weighted sequence (red) • SWI has higher sensitivity than standard GRE • Even subtle microhemorrhage such as seen here are clearly depicted (blue), in this patient with memory complaints after TBI. • Though subject to phase wrap artifact, phase map can be helpful to assess small lesions. • Here phase change is opposite that of the calcified choroid, consistent with blood products

24. Axonal Injury • It is known that foci of Traumatic Axonal Injury (TAI) may be seen on FLAIR and diffusion (red) without associated susceptibility (upper right) to suggest hemorrhage.

25. Axonal Injury • Much research points to diffusion abnormalities (MD, FA, kurtosis) predominantly shown using group analyses. • Current efforts use machine learning to identify injury in individual subjects • Pictured here are disorganized Tract-based density image (TDI) streamlines in a patient 2 years after moderate TBI (top image) compared with the usual symmetry seen in an age-matched control (bottom).

26. Neurodegenerative disorders • TBI increases relative risk for later development of a host of neurodegenerative disorders including: • Parkinson’s Disease (44% increased risk) • Alzheimer’s Dementia (>100% increased risk) • Chronic Traumatic Encephalopathy (CTE) is specifically associated with repetitive head trauma, recently described in professional contact sport athletes as a distinct pathologic entity

27. 38 year old female • History of mild TBI now with persistent and progressive cognitive deficits • There is maintained overall brain volume with evidence of foci of TAI in the white matter.

28. Quantitative Volumetrics • The patient had asymmetric L hippocampal volume loss, with notably low asymmetry index compared with age-matched controls (arrow). • Hippocampal asymmetry is described in both Mild Cognitive Impairment (MCI) and Alzheimer’s dementia (AD).

29. FDG-PET • The patient demonstrated marked decrease in FDG uptake in a pattern reminiscent of Alzheimer’s Dementia (bitemporal and biparietal hypometabolism).

30. Hydrocephalus • Another factor that can contribute to cognitive decline, gait abnormalities, and shunt complications after TBI, shown here in a different patient with bifrontal cystic encephalomalacia after contusional injury.

31. Long-term brain structural changes • TBI associated not only with focal volume loss in areas of injury, but diffuse cortical atrophy. • Note the paucity of microvascular disease in this 54 year old patient with history of multiple head injuries and marked cerebral atrophy for age.

32. Conclusion • Though acute brain injury can be dramatic and life-threatening, it is the chronic sequelae of TBI that contribute to lifelong morbidity. • The main sequela span the gamut of neurological disease • vascular injuries leading to stroke, post-traumatic epilepsy, movement disorders, cognitive and behavioral changes, increased risk for neurodegenerative disorders • While CT is standard of care in assessing acute injury, MRI plays an important role in evaluating patients with TBI in the long-term especially those with persistent, unexplained symptoms.

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34. O-61 THANK YOU This work is supported in part by funding from the NIH/NINDS R01 NS039135