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| NI FEATURE: THE EDITORIAL DEBATE V-- PROS AND CONS |
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| Year : 2019 | Volume
: 67
| Issue : 1 | Page : 74-75 |
Three-dimensional double inversion recovery magnetic resonance sequence detects perilesional gliosis better than 3D-FLAIR and postcontrast T1 imaging in calcified neurocysticercosis
Vijay Sawlani, Markand Patel
Department of Radiology, University Hospitals, Birmingham NHS Foundation Trust; Department of Radiology, University of Birmingham, Birmingham, UK
| Date of Web Publication | 7-Mar-2019 |
Correspondence Address:
Dr. Vijay Sawlani
University Hospitals, Birmingham NHS Foundation Trust, Birmingham
UK
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0028-3886.253592
How to cite this article:
Sawlani V, Patel M. Three-dimensional double inversion recovery magnetic resonance sequence detects perilesional gliosis better than 3D-FLAIR and postcontrast T1 imaging in calcified neurocysticercosis. Neurol India 2019;67:74-5 |
How to cite this URL:
Sawlani V, Patel M. Three-dimensional double inversion recovery magnetic resonance sequence detects perilesional gliosis better than 3D-FLAIR and postcontrast T1 imaging in calcified neurocysticercosis. Neurol India [serial online] 2019 [cited 2022 May 26];67:74-5. Available from: https://www.neurologyindia.com/text.asp?2019/67/1/74/253592 |
Double inversion recovery (DIR) is a pulse sequence with suppression of cerebrospinal fluid (CSF) and white matter signal using two inversion recovery pulses, with the T1-1 of approximately 2000–3000 ms and the T1-2 of 400–450 ms, respectively. This sequence suppresses the CSF and white matter simultaneously, hence cortical and periventricular lesions are better appreciated, in contrary to the fluid attenuated inversion recovery (FLAIR) sequence, in which only CSF is suppressed, and hence, only periventricular lesions are better appreciated. The two-dimensional (FLAIR) sequence became immediately popular for the detection of periventricular lesions, particularly the multiple sclerosis (MS) plaques, and is recently being replaced by three-dimensional (3D)-FLAIR sequence. This is because smaller lesions, brain stem lesions, and posterior fossa lesions are better seen on the 3D sequences, which are instrumental in the autoquantification of the disease load. The 3D-DIR sequence has potential applications in cortical, subcortical, and periventricular lesion detection and quantification, particularly in MS and epilepsy. However, the current limitation is the long acquisition time due to the acquisition of two inversion pulse sequences.
Perilesional gliosis and inflammatory changes surrounding the calcified lesions are thought to be responsible for seizures. The authors have a vast experience in using different magnetic resonance imaging (MRI) sequences to demonstrate the presence of presumed perilesional gliosis (PPG) like T2 relaxometry, quantitative magnetization transfer MRI, dynamic contrast-enhanced imaging perfusion MRI, and FLAIR imaging.[1],[2] Based on the principles of physics of the DIR sequence, this imaging technique is well-suited to demonstrate the presence of PPG.
In the study in focus, the authors evaluated 3D-DIR with 3D-FLAIR and postcontrast 3D fat-suppressed T1 imaging for the detection of PPG in calcified cysticercal brain lesions in 45 patients with seizures.[3] They used a semi-quantitative scoring scale to grade the perilesional signal. Their results demonstrated the presence of PPG in 24 lesions only on 3D-DIR sequence, and in addition also demonstrated better visualization of PPG in 18 lesions compared with the 3D-FLAIR sequence, possibly due to inflammation and gliosis not being as visible on the FLAIR imaging. In three lesions, the 3D-FLAIR sequence was found to be superior to the 3D-DIR sequence, and postcontrast T1W images showed an enhancement in five cases where no PPG was seen on the 3D-DIR or the 3D-FLAIR sequences.
In this study, none of the patients with incidentally detected calcified granuloma showed the presence of any PPG on the 3D-DIR or 3D-FLAIR sequences. Calcified lesions with PPG show a strong association with epilepsy and may become treatment resistant.[4] The identification of PPG in patients with refractory epilepsy will help in the placement of electrodes for evaluation of seizures, in the subsequent surgical removal of the epileptogenic focus, and in achieving better outcomes.
There were 10 patients in this study who had focal seizures and clinicoradiological concordance was seen with the side of the calcification in eight of these patients, suggesting that there may be other causes of seizure generation that are not seen on 3D-DIR or 3D-FLAIR sequences. Although the limitations of this study are a lack of surgical confirmation of the DIR abnormality and clinical/electrophysiological correlation, the study has clearly demonstrated superiority of the 3D-DIR sequence over the existing sequences, particularly the 3D-FLAIR sequence.
To date, most of the applications of the DIR sequence have been for neuroimaging, especially for detection of MS plaques and lesions of the cerebral cortex, to estimate the lesion load, to differentiate juxta-cortical from mixed grey matter–white matter plaques, and to detect infratentorial or spinal cord lesions.[5] It is also being used to define cortical malformations which are associated with seizures.
Recently, the postcontrast DIR sequences have permitted a better detection of contrast-enhancing lesions in MS in the brain when compared with T1W imaging and may be considered an alternative to the standard MRI protocol. One study has shown that 16% more enhancing lesions were seen on postcontrast DIR sequence than on postcontrast T1W imaging.[6] The DIR sequence can also reveal hippocampal pathology and help in lateralizing hippocampal sclerosis better than FLAIR sequences in patients with mesial temporal lobe sclerosis.[7]
The authors have demonstrated the clinical application of 3D-DIR sequence as a promising technique for identifying PPG where it is less visible or not detectable on 3D-FLAIR sequence. This will expand the clinical applications of this technique in epilepsy such as in detecting the presence of mesial temporal sclerosis and cortical malformations,[8],[9] as well as in detecting any posttraumatic gliotic changes.
| » References | |  |
| 1. | Pradhan S, Kathuria MK, Gupta RK. Perilesional gliosis and seizure outcome: A study based on magnetization transfer magnetic resonance imaging in patients with neurocysticercosis. Ann Neurol 2000;48:181-7.  |
| 2. | Gupta RK, Awasthi R, Rathore RK, Verma A, Sahoo P, Paliwal VK, et al. Understanding epileptogenesis in calcified neurocysticercosis with perfusion MRI. Neurology 2012;78:618-25. |
| 3. | Saini J, Gupta PK, Gupta P, Yadav R, Yadav N, Gupta RK. Three dimensional-double inversion recovery detects perilesional gliosis better than 3D-FLAIR and post contrast T1 imaging in calcified neurocysticercosis. Neurol India 2018;67:136-41. |
| 4. | Rathore C, Thomas B, Kesavadas C, Abraham M, Radhakrishnan K. Calcified neurocysticercosis lesions and antiepileptic drug–resistant epilepsy: A surgically remediable syndrome? Epilepsia 2013;54:1815-22. |
| 5. | Riederer I, Karampinos DC, Settles M, Preibisch C, Bauer JS, Kleine JF, et al. Double inversion recovery sequence of the cervical spinal cord in multiple sclerosis and related inflammatory diseases. AJNR 2015;36:19-5. |
| 6. | Eichinger P, Kirschke JS, Hoshi MM, Zimmer C, Mühlau M, Riederer I. Pre- and postcontrast 3D double inversion recovery sequence in multiple sclerosis: A simple and effective MR imaging protocol. AJNR Am J Neuroradiol 2017;38:1941-5. |
| 7. | Li Q, Zhang Q, Sun H, Zhang Y, Bai R. Double inversion recovery magnetic resonance imaging at 3 T: Diagnostic value in hippocampal sclerosis. J Comput Assist Tomogr 2011;35:290-3. |
| 8. | Singh SP, Sankaraneni R, Antony AR. Evidence-based guidelines for the management of epilepsy. Neurol India 2017;65 (Suppl S1):6-11. |
| 9. | Coyle A, Riley J, Wu C, Sharan A. From resection to ablation: A review of resective surgical options for temporal lobe epilepsy and rationale for an ablation-based approach. Neurol India 2017;65(Suppl S1):71-7. |
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