Spinal Imaging Findings in Spontaneous Intracranial Hypotension

Transcription

1 Neuroradiology/Head and Neck Imaging Original Research Medina et al. MRI and CT of Intracranial Hypotension Neuroradiology/Head and Neck Imaging Original Research Jocelyn H. Medina 1 Kevin brams 2 Steven Falcone 3 Rita G. hatia 3 Medina JH, brams K, Falcone S, hatia RG Keywords: CSF leak, headache, spinal MRI, spontaneous intracranial hypotension DOI: /JR Received July 7, 2009; accepted after revision January 13, Presented in part as an Excerpta Extraordinaire at the 2006 meeting of the merican Society of Spine Radiology. 1 Mountain Empire Radiology, 1301 Sunset ve., Ste. 3, Johnson City, TN ddress correspondence to J. H. Medina (jocelynmedina@msn.com). 2 Radiology ssociates of South Florida, Department of Radiology, aptist Hospital Miami, Miami, FL. 3 Department of Radiology, University of Miami Miller School of Medicine, Jackson Memorial Hospital, Miami, FL. JR 2010; 195: X/10/ merican Roentgen Ray Society Spinal Imaging Findings in Spontaneous Intracranial Hypotension OJECTIVE. Spontaneous intracranial hypotension is a syndrome of postural headaches that arises as a result of CSF leakage and without previous lumbar puncture. The purpose of this study was to review and describe the spinal imaging findings of this entity. MTERILS ND METHODS. The spinal MRI and CT myelographic imaging findings of 13 patients with spontaneous intracranial hypotension were retrospectively reviewed. Spinal images were evaluated for spinal fluid collections, dural enhancement, dilated epidural veins, a thickened or enlarged ventral lateral epidural venous plexus, high T2 signal intensity between the spinous processes of C1 and C2 (C1 C2 sign), structural abnormalities, canal attenuation or cord compression, and active contrast extravasation. When available, brain MRI findings were reviewed. Surgical correlation was made in the cases of four patients. RESULTS. The patients were found to have spinal fluid collections (11 of 13 patients), dural enhancement (eight of 10 patients undergoing contrast administration), dilated epidural veins (10 of 13 patients), an enlarged epidural venous plexus (nine of 13 patients), C1 C2 sign (seven of 13 patients), structural abnormalities (four of 13 patients), canal attenuation or cord compression (five of 13 patients), and active contrast extravasation (four of 13 patients). CONCLUSION. Spinal imaging is likely to show one or more findings in patients with spontaneous intracranial hypotension and may be of particular value to patients with equivocal clinical or brain imaging findings and patients who need surgery. Encountering these findings on spinal images may suggest the diagnosis of spontaneous intracranial hypotension and therefore can influence patient treatment. S pontaneous intracranial hypotension is a syndrome of postural headaches that arise without previous lumbar puncture or an interventional procedure or surgery on the neural axis. It is a benign condition that is difficult to diagnose because of its highly variable and often nonspecific clinical and imaging presentation [1 3]. It is thought to be caused by development of CSF leaks, typically originating in the spinal canal [4 6]. ccording to the International Classification of Headache Disorders, second edition, spontaneous intracranial hypotension is diagnosed primarily on the basis of the presence of positional headache, resolution of headache after blood patching, low CSF pressure at lumbar puncture, the presence of CSF leak at myelography, or a combination of these findings [3, 6]. In 2008, Schievink et al. [7], proposed revised criteria that added cranial MRI findings, including diffuse pachymeningeal enhancement, downward displacement of the cerebel lar tonsils, and subdural collections. Some of these brain imaging findings, however, such as diffuse pachymeningeal enhancement, are nonspecific and can cause diagnostic confusion [8]. This diagnostic confusion may consequently lead to invasive and inappropriate workup, and the brain imaging findings are not always present [9, 10]. Neither the original International Classification of Headache Disorders criteria nor the proposed revised criteria include the full spectrum of spinal imaging findings, possibly because the role of spinal imaging in the diagnosis and management of spontaneous intracranial hypotension has not been well established in the current literature. It is being increasingly recognized, however, that a number of findings can be consistently identified in the spines of patients with spontaneous intracranial hypotension [10 15]. Furthermore, it is known that spontaneous intracranial hypotension typically develops from leaks in the spine. Consequently, imaging of the spine has JR:195, ugust

2 Medina et al. the advantage of depicting the direct evidence of CSF leakage rather than the indirect signs seen with cranial MRI. This capability may improve diagnostic accuracy. It has been argued that identifying the site of CSF leakage with spinal imaging is not necessary because spontaneous intracranial hypotension often resolves with conservative management or lumbar blood patching. The success rates of lumbar blood patch are generally reported to be % [3, 6, 16]. The blood patch is thought to seal the leak by causing dural tamponade, preventing ongoing CSF volume loss [6]. However, spontaneous intracranial hypotension can recur or be refractory to medical management. In these cases, it may be necessary to identify the site of CSF leakage with spinal MRI, radioisotope cisternography, or CT myelography so that a surgical or invasive approach can be attempted [17, 18]. The goals of this study were to better characterize spinal findings, determine the frequency of these findings in our patients compared with those in other reported series, and to determine which findings are clinically useful. Materials and Methods etween March 2001 and February 2005, 13 patients (five men, eight women; age range, years) were treated at our institutions under the clinical diagnosis of spontaneous intracranial hypotension and were identified retrospectively. ll cranial MR images, spinal MR images, and CT myelograms were collected for each patient and reviewed retrospectively by two neuroradiologists. The images were reviewed jointly, and a consensus was reached on the presence or absence of fluid collections, intracranial and spinal dural enhancement, dilated epidural veins, fluid signal intensity between the spinous processes of C1 and C2, structural abnormalities, thickened ventral lateral epidural venous plexus, cerebellar tonsillar herniation, enlarged pituitary gland, effacement of the basal cisterns, canal attenuation or cord compression, and active contrast extravasation. These findings were selected for evaluation on the basis of a review of the literature. For each patient, a finding was considered present when there was agreement between the two reviewing neuroradiologists. If there was no consensus regarding a possible finding, the finding was not identified as present. pproval was obtained from the review boards of each institution. Imaging was performed with 1.5-T magnets. Four of the patients underwent a complete imaging workup that included cranial and spinal MRI and CT myelography of the entire spine. Five patients underwent MRI of the brain and spine but not Fig year-old man with spontaneous intracranial hypotension., xial T2-weighted fat-suppressed image shows dorsal extradural fluid collection (arrow)., Sagittal T2-weighted fat-suppressed image shows ventral displacement of cord (arrows). myelography. Four patients underwent spinal MRI only. Most of the imaging examinations included sagittal T1-weighted images, sagittal and axial T2-weighted images with fat suppression, and sagittal and axial contrast-enhanced T1-weighted images with fat suppression. Three patients did not receive gadolinium. Results Eleven of the 13 patients had postural headache. The conditions of the two patients without headache were diagnosed on the basis of clinical or surgical findings or CSF pressure measurements. However, numerous other symptoms also were seen, including tinnitus, back and neck pain, nausea and vomiting, cranial neuropathy, and myelopathy. Nine of the patients responded to bed rest and blood patching. Conservative therapy failed in four cases, and the patients needed surgery. Fluid collections were the most common imaging finding and were seen in 11 patients (85%). Nearly all of the fluid collections were nonfocal, extending over multiple spinal levels. Ten patients (77%) had dilated epidural veins. Thickened ventral epidural venous plexus was another common imaging finding, seen in nine patients (69%). Enlargement of the epidural venous plexus was most commonly seen in the cervical spine, though enlargement in the thoracic and lumbar epidural venous plexus also was seen in some cases. Patients with thickening of the plexus typically had a festooned configuration of the plexus caused by restriction of the midline by the fibrous septum. Dural enhancement was seen in eight of the 11 patients (73%) who received contrast material. Seven of the 13 patients (54%) had evidence of a focal fluid collection between the spinous processes of C1 and C2, or the false C1 C2 localizing sign. Four patients (31%) had identifiable structural defects in association with the leakage, including nerve root cysts, arachnoid diverticula, and dural rents or defects. ll four patients who underwent CT myelography had evidence of active contrast extravasation. None of the myelograms in this series showed normal findings. Three of the four patients who had surgical correlation had complete concordance of imaging and surgical findings. One of these patients had surgically confirmed leakage from a ruptured T10 nerve root cyst, one had leakage from a dorsal arachnoid diverticulum at T8 T9, and one had a large cervical dural defect with active lateral CSF leakage at C1 C2. The patient with discordant surgical and imaging findings had CT myelographic evidence of active extravasation extending from C1 C2 into the region of the right brachial 460 JR:195, ugust 2010

3 MRI and CT of Intracranial Hypotension Fig year-old woman with spontaneous intracranial hypotension and surgically documented leakage at T8. Sagittal T2-weighted fat-suppressed MR image shows extensive dorsal fluid collection. plexus. t surgery, no active CSF leak was seen at C1 C2, but CSF appeared to be coming from somewhere below C1 C2. However, the site was surgically packed, the patient was treated with a blood patch, and the clinical symptoms subsequently resolved. In some patients although some of the classic intracranial findings were absent, spinal findings were present. One patient had completely normal cranial imaging findings, but active extravasation was found at spinal CT myelography. In addition, five patients lacked tonsillar displacement, but all five had the C1 C2 sign and spinal fluid collections. Four of these five patients had thickened ventral epidural venous plexuses. nother three patients lacked intracranial dural enhancement, but all three had spinal fluid collections, thickened epidural venous plexus, dilated epidural veins, and spinal dural enhancement. Discussion Fluid Collections The most frequently encountered finding was spinal fluid collections, which we saw in 85% of the patients in this series, compared with the % reported in other series [10 12, 19]. The collections tended to be nonfocal and often extended over five or more spinal segments. xial T2-weighted images were particularly useful for visualizing the dura deep to the collection, signifying an epidural location (Fig. 1). The mechanism of development of the spinal collections is not known. One explanation may be direct leakage of CSF into the epidural space with tracking of fluid through the space. nother theory is transudation of intravascular fluid from hyperemic meninges or engorged veins across a hydrostatic pressure gradient [15]. In the surgical cases in our study, the patients had extensive collections that extended to regions remote from the surgically documented site of leakage (Fig. 2). lthough some of these collections may seem to be explained by the transudation theory, at least one patient had direct extension to C1 C2 through a dural defect or fistula. Dilated Epidural Veins Dilated epidural veins (Fig. 3) were found in 77% of the patients in this series, compared with 67 88% in other series [10, 11, 15]. Enlargement of epidural veins has been described previously in association with both spontaneous intracranial hypotension [20 23] and hypotension after lumbar puncture [24]. Enlarged veins also have been reported as potential mimickers of a dural arteriovenous fistula [23]. The presence of dilated veins may be explained by the Monro-Kellie doctrine, which states that as CSF volume decreases, blood volume increases in an attempt to maintain a stable pressure, essentially leading to compensatory vasodilatation in the brain, spine, and meninges [1, 12, 15]. Epidural Venous Plexus In the assessment of the epidural venous plexus, both morphologic and size characteristics were used. The size criteria used were subjective, which is a potential weakness of this study. However, to our knowledge, no accurate measures of plexus thickening have been established in the literature. The morphologic criterion used was the festooned or light-bulb appearance of the plexus, which has been described by Chiapparini et al. [10]. The festooning results when the enlarged plexus causes collapse of the lateral aspects of the thecal sac while the sac maintains its midline attachment to the posterior longitudinal ligament (Fig. 4). Dural Enhancement ccording to the Monro-Kellie principle, dural enhancement is assumed to result from Fig year-old woman with spontaneous intracranial hypotension., xial T2-weighted fat-suppressed image shows prominent dorsal flow voids that represent dilated veins that appear to be extradural., xial T2-weighted fat-suppressed image shows veins are intradural and extradural. JR:195, ugust

4 Medina et al. dural vasodilation and engorgement. Dural enhancement was assessed in the 11 patients who underwent contrast-enhanced spinal examinations and was seen in 73% of the patients, compared with 66 86% in other series [10, 12]. The enhancement tended to be smooth and circumferential (Fig. 5) and was often but not always accompanied by intracranial dural enhancement. Three patients in the study lacked intracranial dural enhancement but did have spinal dural enhancement. Mokri et al. [9] reported lack of intracranial pachymeningeal enhancement in several patients with symptomatic spontaneous intracranial hypotension and suggested that the quantitative volume losses and pressure changes might not have been sufficient to induce the intracranial dural engorgement and enhancement. Structural bnormalities There have been several reports [25 28] of an association between spontaneous intracranial hypotension and structural abnormalities. ssociation of spontaneous intracranial hypotension with nerve root cysts, pseudomeningocele, disk herniation, and transdural osteophytes has been reported. The abnormalities seen in our study included dural defects, dorsal arachnoid diverticula (Fig. 6), and nerve root cysts. minority (31%) of patients in this series had imaging findings of identifiable structural abnormalities in association with the site of leakage, compared with 6 35% in other series, in which conventional noninvasive spinal MRI was used [10, 11, 19]. Fig year-old woman with spontaneous intracranial hypotension. xial contrast-enhanced fat-suppressed T1-weighted image of cervical spine shows smooth dural enhancement that extends into neural foramina. In two studies [18, 29] in which mainly invasive imaging such as MRI, CT myelography, or nuclear cisternography was performed, higher rates of association (58 69%) between structural abnormalities (meningeal diverticula) and spontaneous intracranial hypotension were found. In those studies, conservative therapy such as bed rest, caffeine intake, and blood patching had already failed, a factor that might have skewed the results. Fig year-old man with spontaneous intracranial hypotension., xial contrast-enhanced fat-suppressed T1-weighted MR image shows festooned appearance of cervical epidural venous plexus at level of C3. Mass effect on thecal sac is evident., xial T2-weighted fat-suppressed MR image at level of L3 shows festooned appearance elsewhere in spine. The data from the two studies [18, 29] suggest that conservative therapy is more likely to fail in the care of patients with spontaneous intracranial hypotension with structural defects than it is in the care of patients without these defects. Likewise, we found that two of our three patients with imaging findings of structural abnormalities underwent unsuccessful conservative treatment, and they needed reparative surgery for cure. Fig. 6 Spontaneous intracranial hypotension., xial image from CT myelogram in 29-year-old woman shows active extravasation from perineural cyst on left side at T10 T11. Conservative therapy failed, and surgical ligation of leaking cyst was performed., xial T2-weighted fat-suppressed image in 25-year-old woman shows dorsal arachnoid diverticulum protruding through dural defect confirmed at surgery to be actively leaking CSF. 462 JR:195, ugust 2010

5 MRI and CT of Intracranial Hypotension nalysis of a larger number of patients certainly is required for statistical proof of this finding. Hyun et al. [17] also found a significantly increased likelihood of failure of conservative treatment of patients with direct signs of leakage at nuclear cisternography. It is important to note that if a patient does not have symptoms, the presence of a structural abnormality alone has not been proved to indicate any increased risk of development of a leak. Fig. 8 lgorithm for imaging of spontaneous intracranial hypotension. C1 C2 Sign One finding that deserves special mention is the C1 C2 sign. This sign, which has also been called the C1 C2 false localizing sign [30, 31], is seen on MR images as a focal area of fluidlike signal intensity and on CT myelograms as a CSF collection between the spinous processes of C1 and C2 (Fig. 7). More than one half of the patients in this series had this sign, suggesting a clear association. In other series, this sign has been found 33 67% of the time [15, 19]. It should be noted that this fluid collection does not necessarily denote the site of CSF leakage. Two of our four surgical patients also had the C1 C2 sign. The first was found to also have leakage in the thoracic spine at myelography that was confirmed at surgery. The other patient had contrast leakage at C1 C2 extending into the area of the right brachial plexus at myelography, but at surgery the leakage was not found at C1 C2 and instead appeared to originate from below that level. These two cases exemplify how the C1 C2 sign can incorrectly localize the site of leakage, sometimes even when contrast leakage is perceived at C1 C2 at myelography. This sign also has been reported in association with intracranial hypotension after lumbar puncture [15], which further supports the assertion that retrospinal fluid at C1 C2 does not represent direct CSF leakage. If the fluid at C1 C2 is not from direct leakage, it may be from indirect leakage. Schievink et al. [30] postulated that these collections are true CSF collections that occur when fluid from a spinal epidural collection travels rostrally and escapes from the epidural space into the retrospinal soft tissues. The C1 C2 level may be prone to the escape of fluid because of lack of osseous support, mobility of the segment, lack of epidural fat, and laxity of the connective tissues at this level. In our series, six of the seven patients with the C1 C2 sign also had epidural collections. Lack of Intracranial Findings number of patients in this series lacked some of the typical intracranial findings. One patient had completely normal cranial and spinal MRI findings but had abnormal CT myelographic findings. Five patients lacked Fig year-old man with spontaneous intracranial hypotension., Sagittal T2-weighted fat-suppressed image shows fluid signal intensity collection between spinous processes of C1 and C2. Patient responded to conservative therapy with lumbar blood patch., xial CT myelogram shows contrast collection dorsal to C1 C2. cerebellar tonsillar depression, and these patients did have multiple spinal findings, including the C1 C2 sign and fluid collections. Three patients lacked intracranial dural enhancement but had dural enhancement in the spine, fluid collections, dilated epidural venous plexus, and dilated veins. This finding suggests that spinal imaging may have a role in cases in which intracranial findings are Clinical signs and symptoms of spontaneous intracranial hypotension (SIH) Trial of noninvasive conservative therapy (bed rest, hydration) If no response, then cranial and spinal MRI with and without contrast administration. (CT myelography with opening pressure may be performed if MRI is contraindicated.) Yes MRI signs of intracranial hypotension present (including extrathecal CSF, epidural collection, dual enhancement, tonsillar depression, dilated epidural veins with C1 C2 sign, enlarged venous plexus) Nonsurgical therapy for SIH (including indirect lumbar blood patch and fibrin patch). Repeated blood patch may also be performed. Response to therapy in 72 hours CT myelography with opening Yes No No pressure (if not already performed) SIH diagnosis is confirmed. No further imaging required. Surgical consultation. Consider surgical therapy or directed site-specific blood patch. Yes No CT myelography with opening pressure Visualization of extrathecal CSF Consider alternative diagnosis. If clinical suspicion remains high, consider nuclear cisternography. JR:195, ugust

6 Medina et al. absent or equivocal. Results of other studies also have shown the absence of intracranial findings in 10 28% of cases [7, 11, 29]. nial hypotension. J Neurosurg 1996; 84: Schaltenbrand G. Neuere nschauungen zur Pathophysiologie der Liquorzirkulation. Zentralbl management planning of spontaneous intracranial hypotension. Clin Neurol Neurosurg 2008; 110: Utility of MRI Sequences and Imaging lgorithm xial T2-weighted fat-suppressed images were useful for detection of fluid collections, vein enlargement, and venous plexus enlargement. We found sagittal T2-weighted fat-suppressed images helpful for evaluation of the overall extent of epidural fluid collections and epidural vein enlargement. The C1 C2 sign is often subtle and is best visualized on sagittal fat-suppressed T2-weighted images. If some form of fat-suppressed T2-weighted sagittal image is not obtained, this sign is likely to be underrecognized. xial and sagittal contrastenhanced T1-weighted images were of great value for visualizing dural enhancement venous plexus enlargement. n imaging algorithm based on our experience and findings in the literature is shown in Figure 8. We identified an array of spinal findings of spontaneous intracranial hypotension. These findings were identified in all 13 patients in this series, compared with 88 94% in other series [10, 11, 19]. Specifically, fluid collections, thickened epidural venous plexus, dilated veins, and dural enhancement were present in most of our patients and have been consistently encountered in other series. Though analysis of a larger number of cases is required to determine whether these findings are truly characteristic of the syndrome, it appears that spinal imaging will likely show one or more findings in patients with spontaneous intracranial hypotension. We therefore advocate imaging of the spine with contrastenhanced sagittal T1-weighted, sagittal and axial T2-weighted fat-suppressed, and unenhanced sagittal and axial T1-weighted fat-suppressed sequences in the care of patients with suspected spontaneous intracranial hypotension, particularly when the intracranial findings are absent or equivocal and when surgery is planned. The C1 C2 false localizing sign is another important finding. Visualization of this finding can lead to the radiologic diagnosis of spontaneous intracranial hypotension. It is also important to realize that this finding is not necessarily indicative of the leakage site. References 1. Schievink WI, Meyer F, tkinson JLD, et al. 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