The ability to diagnose moderate to severe intracranial trauma accurately has traditionally been the domain of CT in the emergent setting (1). MR imaging has enhanced diagnosing shearing injuries (gradient echo imaging), subtle extraaxial hemorrhages (secondary to its multiplanar capabilities and superb soft tissue contrast), and subarachnoid hemorrhage (fluid-attenuated inversion recovery [FLAIR] pulse sequence). Even so, the ability to detect mild and subtle trauma continues to be an enigma. In this issue of the AJNR, Inglese et al have elegantly described that dilated perivascular spaces (PVSs, also known as Virchow-Robin spaces) in the deep white matter on T2-weighted images are often seen in patients with mild traumatic brain injury (TBI), a finding not previously reported. Enlarged PVS was defined as greater than 2 mm. The authors also proposed that an inflammatory component is a contributing etiology to the dilated PVS.
This study compared MR findings in 24 patients, 18–50 years of age, with mild TBI, along with a control group. The TBI group was further subdivided into early MR imaging (15 patients imaged 1–9 days from the date of the initial trauma) and late MR imaging (nine patients imaged 0.6–13.4 years from the date of initial trauma), with the control group similarly subdivided. The number of dilated PVSs was analyzed as were cerebral and CSF volumes. Thin-section MR imaging (3-mm contiguous cuts) with a high matrix was obtained on a 1.5T unit using T1-weighted, T2-weighted, and FLAIR pulse sequences with volumetric image analysis performed on a Sun workstation with in-house–developed Multimodal Image Data Analysis System (MIDAS) software. The average number of PVSs in TBI patients was significantly higher (7.1) than in the control group (2.4). The number of PVSs did not correlate with brain or CSF volumes, the age of the patients, or the elapsed time from injury in the TBI group, reflecting early and permanent brain changes.
The etiology for dilated PVS is nonspecific and has been described in the normal population. It has been associated with aging, neurosarcoidosis, cryptococcus, mucopolysaccharidosis, and recently, in early MS (2). Dilated PVS as a marker for early and permanent findings in patients with mild TBI is novel and may add to the radiologic imaging armamentarium; however before this becomes dogma, more-detailed analysis is needed. The authors examined only 24 patients and lacked baseline MR imaging studies before the trauma and neuropsychological testing, factors they have acknowledged. Serial studies with larger numbers are needed to validate the authors’ findings. Retrospective studies analyzing for dilated PVS in both mild and severe trauma will also be helpful. The study is further limited because contiguous 3-mm sections without interleaving were obtained; the potential for cross-talk artifact was not addressed.
The etiology of dilated PVS with TBI is speculative. The authors provide references to experimental and human studies to support the theory of the inflammatory cascade being at least a contributing factor for enlarged PVS in patients with mild TBI, superimposed on shear strain as the etiology (3, 4). The authors state that histologic data are missing and that further work is necessary. Imagine the possibility of limiting or negating the traumatic brain response with early antiinflammatory treatment. Inglese et al predict that the use of higher-field-strength magnets with a higher matrix or resolution will lead to better visualization and quantification of high convexity VRS. This manuscript “stirs the pot,” both from an imaging point of view and in terms of potential therapeutic treatment of mild posttraumatic findings depicted by MR imaging.
References
- American Society of Neuroradiology