In the imaging of Traumatic Brain Injury (TBI) patients, findings such as cerebral contusions, hemorrhagic and non-hemorrhagic shearing injuries, ‘coup contrecoup’ injury, subdural hematomas, intraparenchymal hematomas, subarachnoid hemorrhage, and skull and facial fractures are sensitive and specific findings for head trauma. In most cases there is no disagreement that these findings are directly related to traumatic brain injury and the clinical history of head trauma. However, there are additional findings that can be seen in traumatic brain injury that may also be identified as normal variants, creating confusion for radiologists, clinicians, and lawyers. The understanding of these concepts is essential for attorneys managing medical legal cases relating to head trauma.
Dilated Perivascular Spaces
Dilated perivascular spaces (also called Virchow-Robin spaces) are small focal cystic areas adjacent to tiny vessels in the brain. These can be seen in asymptomatic populations as normal variants; however, these have been described as increased in size and number in patients with head trauma when compared to normal controls.1 Posttraumatic dilated perivascular spaces, can also be found adjacent to shearing injuries in a subcortical location.2, 5
An extensive literature review article on this subject concluded: “A judgment on whether dilated VRS in an individual patient is a normal variant or part of a disease process can be made by taking into account the appearance of the adjacent tissue on MRI and the clinical context”.3
Cavum Septum Pellucidum
The septum pellucidum is a thin midline structure that separates the lateral ventricles. The lateral ventricles are large central cavities which contain the cerebral spinal fluid which coats the brain. A “cavum” septum pellucidum is a fluid-filled cavity within the septum pellucidum. Although a cavum septum pellucidum is often considered a normal variant, it has also been associated with neurodevelopmental and neuropsychiatric disorders.4, 14 It has also been reported that a cavum septum pellucidum may also result from, or increase in size, following traumatic brain injury. Higher rates of a cavum septum pellucidum have been reported in TBI patients when compared to the general population.5, 14
The pituitary gland sits in the sella turcica, a bony structure in the anterior-inferior skull, and is intricately involved in endocrine/hormone production and regulation. When the pituitary gland is decreased in size, it is called a ‘partially empty sella’, or an ‘empty sella’, depending on the degree of atrophy. An empty sella may be a normal variation, but can be seen in patients with endocrine disorders and may also be acquired secondary to pituitary atrophy from TBI. Hypopituitarism may be found in up to 25% of all traumatic brain injury patients and 47% of all patients with subarachnoid hemorrhage.6 These patients may develop new endocrine dysfunction secondary to hypothalamo-pituitary dysfunction due to traumatic brain injury and this should be assessed clinically.7, 16
The cerebellar tonsils extend inferiorly from the cerebellum and posteriorly to the medulla. In most people, cerebellar tonsils terminate at or just below the foramen magnum (the boundary between the brain and spinal cord). If they extend greater than 6 mm below the foramen magnum in adults, a Chiari I malformation is present. Many Chiari I patients are asymptomatic. However, it is widely reported that symptomatic Chiari I patients may experience worsening symptoms following head trauma and asymptomatic Chiari I patients may develop new symptoms following head trauma. Therefore, clinical correlation is recommended in these patients.8, 15
Following any insult to brain tissue, whether from stroke, tumor, infection or trauma, there is often swelling in the immediate phase followed by atrophy (shrinking/decrease in size of brain tissue). Atrophy is responsible, at least in some part, for the already discussed findings of ‘empty sella’ and ‘dilated perivascular spaces’. It is common to see focal brain atrophy in the same location of previous cerebral contusions and intraparenchymal hemorrhages.
The hippocampus, a part of the inferiomedial temporal lobe, which has a variety of functions such as memory and emotions, is particularly susceptible to injury following head trauma and the resultant atrophy may be seen on MRI.9, 17
In addition, diffuse brain atrophy is also well described in TBI, particularly in patients with diffuse axonal injury (widespread damage to the brain with extensive lesions in white matter tracts).5,10 A study that followed patients over 30 years found that a reduction in hippocampal volume and lateral ventricular enlargement were significantly associated with memory function and executive functions. Specifically, the best predictor for cognitive outcome was the volume of the lateral ventricle.11 Some authors have suggested these MRI brain volumetric measures are of greater prognostic value than the initial severity of the TBI.12, 13
Interpretation of the above findings can be challenging and is often more helpful in aggregate than in isolation. Advanced neuroimaging options such as SWI, DTI, fMRI, Perfusion, NeuroQuant, LesionQuant, 3D cube FLAIR, and Spectroscopy may also assist in evaluating patients with TBI and add clarity to some the above findings. Similarly, MRIs obtained even years after the original injury can be compared to MRIs predating the injury or immediately following the injury and provide helpful diagnostic and prognostic information.
Of course, any imaging findings should be assessed in the proper clinical context and absence of supporting imaging findings does not exclude injury. Clinical corroboration is always advised.
Dr. Snyder is a 2009 Touro University of Nevada Osteopathic Medical School graduate and a current assistant adjunct professor of Radiology and Neuroradiology at Touro. He completed his radiology residency at McLaren Macomb (Michigan State) in Michigan and his neuroradiology fellowship at the University of Miami and returned to Las Vegas to practice at SimonMed Imaging in Las Vegas. He has special interests in teaching rotating medical students, lecturing, and research on advanced imaging techniques for traumatic brain injury and carbon monoxide poisoning.
1 Inglese,M., Bomsztyka, E., et al. (2005). “Dilated Perivascular Spaces: Hallmarks of Mild Traumatic Brain Injury”. AJNR 26: 719-724.
2 Inglese M, Grossman RI, Diller L, Babb JS, Gonen O, Silver JM, Rusinek H. (2006). “Clinical significance of dilated Virchow-Robin spaces in mild traumatic brain injury”. Brain Inj. 20(1):15-21.
3 Groeschel S1, Chong WK, Surtees R, Hanefeld F. (2006). “Virchow-Robin spaces on magnetic resonance images: normative data, their dilatation, and a review of the literature”. Neuroradiology. 48(10):745-54.
4 Raine A, Lee L, Yang Y, and Colletti P. (2010). “Neurodevelopmental marker for limbic maldevelopment in antisocial personality disorder and psychopathy”. Br J Psychiatry. 197(3):186-92;
5 Orrison WW, Hanson EH, Alamo T, Watson D, Sharma M, Perkins TG, Tandy RD. (2009). “Traumatic brain injury: a review and high-field MRI findings in 100 unarmed combatants using a literature-based checklist approach”. J Neurotrauma. 26(5):689-701; Silk T, Beare R, Crossley L, Rogers K, Emsell L, Catroppa C, Beauchamp M, Anderson V. (2013). “Cavum septum pellucidum in pediatric traumatic brain injury”. Psychiatry Res. 213(3):186-92.
6 Schneider HJ, Kreitschmann-Andermahr I, Ghigo E, Stalla GK, and Agha A. (2007). “Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a systematic review”. JAMA. 298(12): 1429-38.
7 Krahulik D, Zapletalova J, Frysak Z, and Vaverka M. (2010). “Dysfunction of hypothalamic-hypophysial axis after traumatic brain injury in adults”. J Neurosurg. 113(3):581-4; Benvenga S, CampennÍ A, Ruggeri RM, and Trimarchi F. (2000). “Hypopituitarism Secondary to Head Trauma”. J Clin Endocrinol Metab. 85 (4): 1353-1361.
8 Wan MJ, Nomura H, and Tator CH. (2008). “Conversion to symptomatic Chiari I malformation after minor head or neck trauma.” Neurosurgery. 63(4):748-53
9 Tate DF and Bigler ED. (2000). “Fornix and Hippocampal Atrophy in Traumatic Brain Injury”. Learn. Mem. 7: 442-446;
10 MacKenzie JD, Siddiqi F, Babb JS, Bagley LJ, Mannon LJ, Sinson GP, and Grossman RI. (2002). “Brain Atrophy in Mild or Moderate Traumatic Brain Injury: A Longitudinal Quantitative Analysis”. American Journal of Neuroradiology. 23 (9) 1509-1515;
11 Himanen, Leena & Portin, Raija & Isoniemi, Heli & Helenius, Hans & Kurki, Timo & Tenovuo, Olli. (2005). Cognitive functions in relation to MRI findings 30 years after traumatic brain injury. Brain injury : [BI]. 19. 93-100. 10.1080/02699050410001720031.
12 Himanen, Leena & Portin, Raija & Isoniemi, Heli & Helenius, Hans & Kurki, Timo & Tenovuo, Olli. (2005). Cognitive functions in relation to MRI findings 30 years after traumatic brain injury. Brain injury : [BI]. 19. 93-100. 10.1080/02699050410001720031;
13 Timming R, Orrison WW, Mikula JA. (1982). “Computerized tomography and rehabilitation outcome after severe head trauma”. Arch Phys Med Rehabil. 63(4):154-9.
14 Silk T, Beare R, Crossley L, Rogers K, Emsell L, Catroppa C, Beauchamp M, Anderson V. (2013). “Cavum septum pellucidum in pediatric traumatic brain injury”. Psychiatry Res. 213(3):186-92.
15 Mehta, A. I., Grant, G. A., Gray, L., & Sampson, J. H. (2011). “Radiographic progression of a Chiari I malformation after minor head trauma: Final increment of obstruction to create pathophysiology”. Journal of Surgical Radiology. 2(3), 290-293.
16 Benvenga S, CampennÍ A, Ruggeri RM, and Trimarchi F. (2000). “Hypopituitarism Secondary to Head Trauma”. J Clin Endocrinol Metab. 85 (4): 1353-1361.
17 Ross DE, Ochs AL, DeSmit ME, Seabaugh JM, Havranek MD. (2015). “Alzheimer’s Disease Neuroimaging Initiative. Man Versus Machine Part 2: Comparison of Radiologists’ Interpretations and NeuroQuant Measures of Brain Asymmetry and Progressive Atrophy in Patients With Traumatic Brain Injury”. J Neuropsychiatry Clin Neurosci. 27(2):147-52.
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