How to Read an Mri Venous of the Brain
Cerebral venous thrombosis (CVT) is a rare condition which is notoriously difficult to diagnose because of its variable modes of onset and its wide spectrum of signs and symptoms.1,2 Brain imaging by itself is of little diagnostic value in CVT because it ordinarily shows nonspecific lesions, such as hemorrhage, infarct or edema, and can be normal in up to 25% of cases.three The clue to the diagnosis is the imaging of the venous arrangement, which may show either the intravascular thrombus or the occluded vessel. Although CT-scan is all the same often performed equally first line investigation on an emergency ground, information technology is now well established that the best diagnostic tool is the combination of T1-weighted spin echo (T1SE) and T2SE MRI sequences to show the hyperintense thrombosed vessel and magnetic resonance venography (MRV) to detect the nonvisualization of the same vessel.3 Still, both MRV and conventional MRI sequences are of incomplete sensitivity and specificity. MRV, as all other angiographic techniques, does not differentiate thrombosis and hypoplasia, a frequent diagnostic dilemma for the lateral sinuses. Furthermore, these techniques are usually bereft for the diagnosis of isolated cortical venous thrombosis, which all the same often requires conventional angiography. The 2 main limitations of MRI are flow artifacts (which may result in false-positives) and the absence of hyperintense indicate on T1SE-weighted images at the onset of astute thrombosis. During the first three to 5 days of CVT, the thrombus is isointense on T1SE and hypointense on T2SE,4 and thus extremely difficult to differentiate from normal veins.five Favrole et al recently suggested that the increased signal of the venous clot on diffusion-weighted imaging (DWI) images may have a predictive value for recanalization.6 The potential of echo-planar T2* susceptibility-weighted imaging (T2*SW) sequences for the diagnosis of CVT has been illustrated in 2 recent studies.7,eight Notwithstanding, little is known concerning the sensitivity of T2*SW, fluid-attenuated inversion recovery (FLAIR) or DWI images in the diagnosis of CVT. In this retrospective report of 114 MRI examinations obtained in 39 patients, the sensitivity of signal modifications equally detected on T1SE, T2SE, FLAIR, DWI or T2*SW at the site of thrombosis was analyzed co-ordinate to the time elapsed since clinical onset.
Materials and Methods
Patients
From our computerized stroke database, we selected all patients with confirmed CVT seen in our institution between April 2002 and August 2004. Simply patients who had at least 2 MRI examinations including the T2*SW sequence (first MRI obtained at time of diagnosis) were included. In all of them the diagnosis of CVT was based on the following criteria: (ane) history and clinical manifestations compatible with or suggestive of CVT; (2) presence of a fractional or complete venous apoplexy on MRV, CT-angiography or conventional angiography; and (3) typical indicate changes highly suggestive of the presence of intraluminal thrombosis in sinuses or veins on T1SE (iso- or hyperintensity) or T2SE (iso- or hyperintensity), on at least 1 MRI examination during the follow-upward.two,6–10
MRI Information
All MRI examinations were performed on a i.5-Tesla Bespeak Imager (GE Medical System) using the following parameters: T1SE (TR, 500 ms; TE, 14 ms; 20 slices, sagittal with or without axial slices; 5 mm thickness; matrix size, 256×192; field of view, 24×24 cm; conquering time, one.44 minutes; 1 excitation), T2SE (TR, 5200 ms; TE, 102 ms; xx slices; centric slices; slices thickness, five mm; matrix size, 256×320, field of view, 24×24 cm; acquisition fourth dimension, one.20 minutes; 2 excitations), FLAIR (TR, 8400 ms; TE, 145 ms; 20 slices; axial slices; v mm thickness; matrix size, 256×192; field of view, 24×24 cm; acquisition time, 3.48 minutes; 1 excitation; TI, 2100), DWI (TR, 10 000 ms; TE, 100 ms; 20 slices; axial slices; slice thickness 7 mm; matrix size, 128×128; field of view, 24×24 cm; conquering time 32 seconds, b value, 1000 s/mm2; diffusion gradient, G=22 mT/m; duration, 32 ms; separation fourth dimension, 39 ms), T2*SW (TR, 560 ms; TE, 15 ms; 20 slices; slice thickness 5 mm; matrix size, 256×192; field of view, 24×24 cm; acquisition fourth dimension ane.09 minutes;), 2-dimensional time-of-flight sequence (TR, 24 ms; TE, 4.9 ms; interleaved section, 121×1.five mm slices; matrix size, 256×128; field of view, 24×18 cm; flip angle, 20°; bandwith; 16 kHz; acquisition time, 4.54 minutes; 1 excitation).
All sequences obtained at each MRI examination were reviewed retrospectively by a neuroradiologist (M.B.) blinded to the subject'due south clinical condition. Beginning, the sites of venous apoplexy were systematically assessed by the reader on each MRI examination (based on all available information) at the following locations: superior sagittal sinus (SSS), left lateral sinus (LLS), right lateral sinus (RLS), deep venous system (DVS; vein of Galen, internal cerebral veins or straight sinus), right cortical veins (RCV) or left cortical veins (LCV). At each site of thrombosis, the presence of a normal catamenia-void, isointense signal or hyperintense point on T1SE, T2SE, DWI, and FLAIR images were recorded. In addition, the presence or absenteeism of a typical magnetic susceptibility effect on T2*SW was noted (MSE; only a strong and obvious hypointense betoken encompassing the vessel lumen was considered in this category). A second observer performed the same chore in a subset of patients (n=46 sites). The intra- and interobserver agreement was skilful or first-class (for each parameter, weighted κ coefficients were between 0.851 and 1 for the intra-observer agreement and between 0.768 and 0.939 for the inter-observer agreement).
Information Analysis
Descriptive statistics were first used for the primary clinical and MRI data. The results were presented as counts (percents) for categorical variables and as means (SD) or medians (range) for continuous variables.
Because the master objective of the present study was to investigate the signal changes occurring with time in venous clots, merely MRI results at the sites of venous occlusion were considered for statistical analysis. Given the variable delays betwixt the repeated MRI examinations and clinical onset and the different venous sites of thrombosis included in the analysis, the form of the sensitivity for the different MRI sequences was analyzed using a multilevel logistic model. This model deemed for correlations between the repeated observations during the follow-upwardly for each venous apoplexy through random furnishings.xi,12 Additionally, a 2nd level of correlation was considered using random patient effects. From the observed data, a piecewise linear model for time was first assumed, with an boosted quadratic effect of time later xxx days. In a second step, the detailed construction of both fixed and random effects best fitting the information were selected using Schwartz'due south Bayesian Information Criterion (BIC) model selection criterion.xiii Once the final model was fitted, specific hypotheses regarding fixed effects were tested.fourteen When performing 2×ii group comparisons, Hochberg'southward correction for multiple testing was used.15
The comparisons across groups outside this model were performed using the χ2 examination or the Student t examination. All tests were 2-sided, and a probability value under 0.05 was considered significant. Analyses were performed using R.2.0.one software (The R Development Core Squad).
Results
Patients
Thirty-nine patients were included (4 males, 35 females) in the study. The median historic period was 32 years (range: 14 to 62.5). Clinical onset was astute (kickoff neurological symptoms or signs since <48 hours) in half-dozen cases, subacute (48 hours to 1 month) in 31 cases, and chronic (>1 month) in 2 cases (33 days and 45 days). At the time of diagnosis, all patients complained of headache, which was the only symptom in vii cases. Seven patients had papilledema. Other clinical manifestations at onset included focal neurological deficits (n=xv), seizures (n=10) and drowsiness (north=four). All patients were treated with heparin immediately after the diagnosis. In 2 patients, mechanical endovascular treatment was likewise performed because of clinical worsening despite anticoagulation. In 26 patients, the total duration of anticoagulation (heparin, switched-over to vitamin K antagonists) varied from 6 (n=eleven) to 12 months (n=15). Two patients voluntarily stopped their treatment at 4 and 5 months. One patient was treated for eighteen months. In 9 patients, anticoagulation is still ongoing (follow- up <ane yr: vii patients; underlying coagulopathy or systemic thrombotic disease: 2 patients). Complete neurological recovery occurred in 31 patients. 4 patients had focal neurological sequelae (modified Rankin Scale score <2 in all of them), and 4 others had recurrent epileptic seizures.
The number of examinations performed in each patient ranged from 2 to iv (average: 3). One hundred and fourteen examinations corresponding to 650 MR sequences (T1SE, due north=113; T2SE, n=102; FLAIR, north=113; T2*SW, due north=103; DWI, n=108; MRV, n=111) were analyzed. MRV was not obtained at follow-up in 3 MRI examinations.
Main MRI Features at Fourth dimension of Diagnosis
The presence of a thrombosed sinus or vein was detected on MRV combined with MRI at the site of SSS in 20, LLS in 21, RLS in xviii, DVS in 10, LCV in 2, and RCV in three patients. A unmarried venous site, as defined previously, was involved in 19 patients, two venous sites in 13 patients, 3 in ii patients, four in 5 patients, and 1 patient had an extensive CVT involving 5 dissimilar sites. At the time of diagnosis (first MRI examination), 75 different clots were identified at these different sites.
At the 75 sites of thrombosis (Effigy one), the jell appears on the first MRI examination as hyperintense on T1SE in 83% of sites, on T2SE in 27%, on FLAIR in 28% and on DWI in 21%. A typical MSE was detected on T2*SW at 93% of the sites of thrombosis (illustrative case shown in Figure 2).

- Download figure
- Download PowerPoint
Effigy one. Frequency of different MRI aspects of the thrombus on the first MRI examination (75 sites).

- Download effigy
- Download PowerPoint
Figure two. MRI obtained at the beginning day after clinical onset in patient 29 showing an astute thrombosis of the left LS. An isosignal was observed on parasagittal slices on T1SE MRI (a: arrow) whereas a typical MSE was detected on axial T2*SW (b: arrows). The frontal projection of 2-dimensional time-of-flight MR venography confirmed the occlusion of the respective sinus (c: arrows).
MRI was performed within three days of the onset of symptoms in seven patients. Xi sites of thrombosis were identified in these subjects with the clot appearing on T1SE as hyperintense in five/7 clots and isointense in 2/7; on T2SE as hyperintense in 1/7 clots, and isointense in 4/7 (T1SE and T2SE data were not available in 1 patient who had four sites of venous occlusion). With FLAIR and DWI, hyperintensity was detected at 1/11 sites, and on T2*SW a typical MSE was detected at x/11 sites.
Time-Related Sensitivity of Hyperintense Indicate on T1SE, T2SE, FLAIR and DWI and of the Presence of a MSE on T2*SW
All MRI data were included for this analysis respective to 166 sites of thrombosis located in the SSS (n=37), LLS (n=53), RLS (north=46), DVS (n=16), LCV (northward=5) and RCV (due north=9).
The model estimates of sensitivity for the hyperintense point of the jell as observed on T1SE, T2SE, FLAIR and DWI and for the presence of a MSE on T2*SW are presented in Figure 3. The model showed that the sensitivity of the different MRI sequences significantly differed at the starting time day of clinical onset (P<0.0001). The sensitivity of both T1SE and T2*SW were institute college than the sensitivity of the other sequences (P=0.00012 after adjustement for multiple testing). However, the difference in sensitivity between the hyperintense signal of the thrombus on T1SE (87.0%) and the presence of the MSE on T2*SW (94.three%) did non achieve statistical significance (P=0.51). Between day 1 and vii, the sensitivity of the corresponding signal modifications varied significantly between the dissimilar sequences (P<0.0001). An increase in sensitivity was observed for all sequences (significant positive slopes), except for the MSE on T2*SW whose sensitivity remained stable (gradient in the model=−0.0055; standard error (SE)=0.246; P=0.83) and differed from the other slopes (P=0.05). Between twenty-four hour period 7 and twenty-four hours thirty, no global difference was detected in the variations of sensitivity between the unlike sequences (P=0.eleven). However, the decrease in sensitivity was less rapid for the MSE on T2*SW than for the hyperintense aspect on T1SE; slopes: −0.053 (SE=0.025) versus −0.080 (SE=0.024); P=0.0076). Subsequently day 30, the variations in sensitivity too differed according to the dissimilar MRI sequences (P=0.021 on the quadratic term). A significant deviation was as well plant between the slopes of the different sensitivity curves later on day xxx, particularly between those of T1SE and T2*SW (P=0.0075). The frequent persistence of MSE on T2*SW at the very late stage of CVT is illustrated in Figure four.

- Download figure
- Download PowerPoint
Effigy 3. Time grade of the sensitivity estimated by the model for the hyperintense aspect of the thrombus on T1SE, T2SE, DWI and FLAIR images and for MSE on T2*SW. Note the high sensitivity of T1SE and T2*SW at the early phase of CVT and the different curves after the first week for these 2 sequences.

- Download effigy
- Download PowerPoint
Figure iv. MRI signal modifications in ii patients at the late stage of CVT. The MRI examination performed seventy days after the clinical onset in patient seven showed the thrombus every bit isointense on T1SE (a: pointer), a typical MSE on T2*SW (b: arrows) and the absence of period in the left lateral sinus and jugular vein on 2-dimensional time-of-flight MR venography (c: arrows). The MRI obtained at 106 days in patient xvi revealed no signal abnormality on midsagittal T1SE MRI (d), a MSE on axial T2*SW within the SSS (e: arrow) and the respective pause of flow on the 2-dimensional fourth dimension-of-flight MR venography (f: arrows).
Sensitivity of Different MRI Sequences to Detect Cortical Cognitive Venous Thrombosis
MR signal changes related to thrombosis in cortical veins were analyzed separately in the 89 examinations with a complete MRI data set. Xxx-eight cortical venous sites were diagnosed as thrombosed in 12 patients (cases 6, 16, 21, 23, 24, 25, 27, xxx, 34, 35, 36 and 39) amid whom ten presented with thrombosis in other venous sites and 2 as isolated cortical venous thrombosis. A typical MSE on T2*SW was found at 37 cortical venous sites, whereas hyperintensity on T1SE was detected at 30 sites (98 versus 79%; P=0.01; illustrative case shown in Figure 5). Hyperintensity corresponding to the clot was detected at only 5 sites on FLAIR images (14%), 1 site on DWI (3%) and was non detected on T2SE. Noteworthily, MRV disclosed an occluded cortical vein in but 14 sites with cortical venous thrombosis (37%).

- Download figure
- Download PowerPoint
Figure 5. MRI data obtained at mean solar day 5 and at mean solar day thirteen after the onset of symptoms in patient 23 who had isolated CVT. At day 1, parasagittal slices showed on T1SE a normal attribute of catamenia void in an isolated cortical vein (a: arrow); axial FLAIR images showed a hyperintense parenchymal lesion inside the parietal lobe without abnormal vessels (b: arrow); a typical MSE was detected on T2*SW with a tubular aspect consequent with a thombosed cortical vein (c). The images obtained at 24-hour interval 13 revealed hyperintense thrombosed cortical veins (pointer, up) and the hemorrhagic transformation of the parietal lesion (arrow, down) on T1SE (d); FLAIR images showed the hyperintense parietal lesion with hypointensity at the middle corresponding to the hemorrhagic transformation (due east). On T2*SW, a thrombosed cortical vein was detected at the surface of the brain equally a tubular MSE (f).
Discussion
This is the beginning extensive time-dependent analysis of clot-related MR signal changes in CVT. In the present series, the major female predominance, historic period of onset, frequency of subacute onset, and different clinical manifestations are those classically reported in large serial of CVT.1–3,16–19 The frequency of headache (reported by all of our patients) was higher than previously reported figure (80% to xc%).1,3 This may be related to some recruitment of patients through the emergency headache eye nowadays in our institution.
In this serial, conventional MRI sequences combined with MRV were used for diagnosis.4,9 MRV showed the presence of an occluded vein or sinus in 37/39 patients at the first MRI examination. T1SE showed a hyperintense indicate at the site of thrombosis, highly suggestive of a recent thrombosis in 84% of cases. The most important finding of this report is that a MSE was detected at 90% sites of venous thrombosis at the start MRI investigation. Interestingly, a MSE was detected at 6 sites of thrombosis when the clot was simply isointense on T1SE-weighted images. Moreover, inside the first 3 days of symptom onset, the frequency of MSE on T2*SW images was over ninety%, whereas the frequency of a hyperintense point on T1SE was &lxx%. These information suggest that T2*SW may be helpful for the diagnosis of CVT, particularly during its early stage when the point of thrombosis on T1SE is not yet hyperintense.
In the nowadays study, the sensitivity of different MRI sequences in the detection of clots in CVT was estimated. The results confirm betoken changes reported in T1 and T2SE in the early phase of CVT.9 Particularly, we observed that the frequency of hyperintensity at the site of venous apoplexy progressively increases during the first week and decreases after this menstruation for T1SE, FLAIR and DWI. Furthermore, nosotros plant that after 4 months, a hyperintense signal is no longer present on T1SE or DWI, in contrast to what is seen on T2SE and FLAIR images (xx% and 54% respectively). Conversely, the frequency of MSE on T2*SW is loftier early on in the class of clot formation and decreases very slowly with time. The estimated frequency of MSE on gradient repeat images remained higher than 30% four months after clinical onset. These findings suggest that T2*SW cannot be used in isolation to date the appearance of venous occlusion. Even so, the combination of different MRI sequences, particularly T1SE and T2*SW, may be helpful to determine the time elapsed since the occurrence of thrombosis.
30-eight sites of venous apoplexy involving the cortical veins were identified in 12 patients with CVT in the nowadays series. The sensitivity of T2*SW to detect these cortical venous clots was particularly high. The 98% frequency of MSE at the sites of cortical CVT was higher than the frequency of hyperintensity on T1SE and largely exceeded the diagnostic potential of MRV in these locations. T2*SW thus appears as the most sensitive MRI sequence for the diagnosis of cortical CVT, as already suggested in isolated cases.8 Therefore, this sequence should be added to conventional MRI sequences particularly when isolated cortical CVT is suspected.20
There are several limitations in the present study. First, because the assay was performed retrospectively, data were not always consummate for all MRI examinations, which could lead to imprecise estimations of sensitivity. Nonetheless, merely 4.nine% of the sequences were unavailable for assay. Second, the external validity of the present study may be contradistinct past (one) the specific MRI parameters used in our heart that may influence the results, albeit slightly, (two) the expertise of the centre in CVT, and (3) the review of films in a inquiry setting in cases with an already established diagnosis of CVT. Despite these limitations, the present data are consistent with previous analyses of betoken changes caused by clots both in vitro and in vivo.21 Finally, the time-dependent changes in sensitivity observed in the nowadays report resembles the MR signal changes reported in tissue hemorrhages.21 As reported in cognitive hemorrhages, early on MSE on T2*SW within the venous thrombus is presumably related to the appearance of deoxyhemoglobin. The persisting decrease in MR signal is attributable to secondary aggregating of methemoglobin afterwards a few days that is replaced by hemosiderin later several weeks. By contrast, the delayed increase of MR signal on T1SE is caused by the transient aggregating of methemoglobin in the clots.
In conclusion, this study shows that T2*SW is of additional diagnostic value for clot detection in CVT in conjunction with conventional MRI and MRV, specially in the acute phase of thrombosis and in cortical CVT. The results of this report should be helpful for both diagnosis and therapy in CVT.
Footnotes
References
- 1 Bousser MG, Chiras J, Bories J, Castaigne P. Cerebral venous thrombosis–a review of 38 cases. Stroke . 1985; 16: 199–213.CrossrefMedlineGoogle Scholar
- two Ameri A, Bousser MG. Cerebral venous thrombosis. Neurol Clin . 1992; x: 87–111.CrossrefMedlineGoogle Scholar
- 3 Bousser MG, Russell R. Cerebral Venous Thrombosis: Major Trouble in Neurology. Philadelphia, Pa: WB Saunders, 1997.Google Scholar
- iv Connor SE, Jarosz JM. Magnetic resonance imaging of cerebral venous sinus thrombosis. Clin Radiol . 2002; 57: 449–461.CrossrefMedlineGoogle Scholar
- 5 Hinman JM, Provenzale JM. Hypointense thrombus on T2-weighted MR imaging: a potential pitfall in the diagnosis of dural sinus thrombosis. Eur J Radiol . 2002; 41: 147–152.CrossrefMedlineGoogle Scholar
- 6 Favrole P, Guichard JP, Crassard I, Bousser MG, Chabriat H. Diffusion-weighted imaging of intravascular clots in cerebral venous thrombosis. Stroke . 2004; 35: 99–103.LinkGoogle Scholar
- 7 Selim M, Fink J, Linfante I, Kumar Due south, Schlaug G, Caplan LR. Diagnosis of cerebral venous thrombosis with echo-planar T2*SW-weighted magnetic resonance imaging. Arch Neurol . 2002; 59: 1021–1026.CrossrefMedlineGoogle Scholar
- eight Cakmak S, Hermier M, Montavont A, Derex 50, Mauguiere F, Trouillas P, Nighoghossian N. T2*SW-weighted MRI in cortical venous thrombosis. Neurology . 2004; 63: 1698.CrossrefMedlineGoogle Scholar
- 9 Dormont D, Anxionnat R, Evrard South, Louaille C, Chiras J, Marsault C. MRI in cognitive venous thrombosis. J Neuroradiol . 1994; 21: 81–99.MedlineGoogle Scholar
- x Ho CL, Chen CY, Chen YC, Chao TY. Cerebral dural sinus thrombosis in astute lymphoblastic leukemia with early diagnosis by fast fluid-attenuated inversion recovery (FLAIR) MR image: a case report and review of the literature. Ann Hematol . 2000; 79: ninety–94.CrossrefMedlineGoogle Scholar
- eleven Davidian Thou, Giltinan DM. Nonlinear Models for Repeated Measurement Information. Monographs on Statistics and Applied Probability, 62, Chapman&Hall/CRC: Boca-Raton, 1995.Google Scholar
- 12 Goldstein H. Multilevel Statistical Models. Halstead Press: New York, 1995.Google Scholar
- 13 Schwartz G. Estimating the dimension of a model. The Annals of Statistics . 1978; 6: 461–464.CrossrefGoogle Scholar
- 14 Venables WN, Ripley BD. Modern Practical Statistics with Due south-PLUS, 2nd ed, Springer-Verlag: New-York, 1997.Google Scholar
- 15 Hochberg Y. A sharper Bonferroni procedure for multiple tests of significance. Biometrika . 1988; 75: 800–803.CrossrefGoogle Scholar
- 16 Einhäupl KM, Villringer A, Haberl RL, Pfister W, Deckert M, Steinhoff H, Schmeidek P. Clinical spectrum of sinus venous thrombosis. In: Einhauple KM, Kempski O, Baethmann A, eds. Cerebral Sinus Thrombosis/Experimental and Clinical Aspects. New York, 1990.Google Scholar
- 17 Cantu C, Barinagarrementeria F. Cerebral venous thrombosis associated with pregnancy and puerperium. Review of 67 cases. Stroke . 1993; 24: 1880–1884.CrossrefMedlineGoogle Scholar
- eighteen Tsai FY, Wang AM, Matovich VB, Lavin Yard, Berberian B, Simonson TM, Yuh WT. MR staging of acute dural sinus thrombosis: correlation with venous pressure level measurements and implications for treatment and prognosis. AJNR Am J Neuroradiol . 1995; 16: 1021–1029.MedlineGoogle Scholar
- nineteen Daif A, Awada A, al-Rajeh South, Abduljabbar M, al Tahan AR, Obeid T, Malibary T. Cerebral venous thrombosis in adults. A study of forty cases from Saudi arabia. Stroke . 1995; 26: 1193–1195.CrossrefMedlineGoogle Scholar
- twenty Duncan IC, Fourie PA. Imaging of cerebral isolated cortical vein thrombosis. AJR Am J Roentgenol . 2005; 184: 1317–1319.CrossrefMedlineGoogle Scholar
- 21 Alemany Ripoll G, Stenborg A, Sonninen P, Terent A, Raininko R. Detection and appearance of intraparenchymal haematomas of the brain at 1.5 T with spin-echo, FLAIR and GE sequences: poor relationship to the historic period of the haematoma. Neuroradiology . 2004; 46: 435–443.MedlineGoogle Scholar
spradlinlonty1949.blogspot.com
Source: https://www.ahajournals.org/doi/10.1161/01.str.0000206282.85610.ae
0 Response to "How to Read an Mri Venous of the Brain"
Post a Comment