Keywords
brachial plexus - gadolinium - magnetic resonance imaging - short tau inversion recovery
Recent recommendations for brachial plexus magnetic resonance imaging (MRI)[1]
[2]
[3] emphasize suppressing the signal originating from adjacent blood vessels by performing
a short tau inversion recovery (STIR) sequence after injecting intravenous gadolinium
(IV-Gd). This improves the contrast-to-noise ratio (CNR) of the plexus compared with
the background.[4] It is thus useful for visualizing the anatomical course of the plexus. Here, we
highlight a potential pitfall of this popular vessel suppression approach, particularly
relevant for clinicians used to viewing STIR images for fast screening for plexus
pathology.
The widely used STIR sequence, one of several techniques for fat saturation, helps
in detecting areas of interstitial edema. However, STIR does not specifically suppress
the signal from fat. Rather, it suppresses signal from any tissue with a short T1-value
of around 150 to 200 ms.[5] Due to the similarity of T1 in fat and contrast-avid tissues after application of
IV-Gd, there is a well-established possibility that the increased STIR signal of a
pathology would be nullified due to the concomitant uptake of IV-Gd by the same pathology.[5] This reduces the STIR signal after injecting IV-Gd in areas with increased contrast
enhancement (CE).[6] This would reduce the ability to detect pathological changes with concurrent edema
and CE, which are both generally associated with pathologies.[1]
[Fig. 1] highlights this potential pitfall in the case of examinations of the plexus with
the help of an analogy: the physiological CE (due to the lack of a blood–nerve barrier[7]) and nonenhanced STIR hyperintensity of the cervical dorsal root ganglia.[8] The ganglia thus exhibit a physiological signal behavior which is otherwise expected
in focal pathological (e.g., inflammatory) lesions of the plexus.[1] As explained earlier, a relative signal loss from the dorsal root ganglia is to
be expected in an STIR post IV-Gd even in the absence of pathological changes. The
corresponding example in the figure can help understand the potential to overlook
pathological changes due to inadvertent signal loss of contrast-enhancing lesions
in the STIR sequence.
Fig. 1 Example highlighting an interpretational pitfall following a recently popular modification
of brachial plexus MRI protocols: 3D STIR imaging (Siemens Magnetom Sola 1.5T, repetition
time: 4,000 ms, echo time: 251 ms, inversion time: 160 ms) of the brachial plexus
before (A, C) and after (B, D) injection of Gd in a patient without brachial plexus pathology. The maximum intensity
projections (A, B) highlight the improved vessel suppression and consequently improved clarity of the
anatomical course of the plexus. The detailed views (C, D) show decreased signal intensity of a dorsal root ganglion (arrows) in the image
acquired after Gd injection (D). T1 VIBE Dixon water images before (E) and after (F) Gd injection showing physiological enhancement of the ganglion (arrows).
This pitfall of a potentially reduced sensitivity for focal lesions within the plexus,
despite overall better plexus visualization has received little attention in recent
articles dealing with brachial plexus MRI.[1]
[3]
[9]
[10]
[11] In particular, there is a risk of completely missing a true pathology if either
the STIR before Gd is not acquired or STIR is used for a fast identification of plexus
disease in clinical care situations outside full radiological reporting. On the other
hand, if kept in mind, this behavior might serve as an additional marker for contrast
uptake in T1-hyperintense tissue.
It is recommended that plexus MRI sequences are interpreted in a particular order,
first looking for focal edema in STIR before Gd and then looking for a pathological
CE in the fat-saturated T1-weighted images. In this way, the likelihood of missing
out on masked pathologies could be significantly reduced. Despite these limitations,
we do, however, believe that CE 3D STIR is of high value for assessing the anatomical
course of the plexus and differentiating the plexus from adjacent vascular structures.
