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Year : 2019  |  Volume : 67  |  Issue : 1  |  Page : 76--77

Double inversion recovery in detection of perilesional gliosis in calcific cysticercosis

Amit Herwadkar 
 Department of Radiology, Salford Royal Foundation Trust Manchester, Greater Manchester, United Kingdom

Correspondence Address:
Dr. Amit Herwadkar
Department of Radiology, Salford Royal Foundation Trust, Manchester, Greater Manchester
United Kingdom

How to cite this article:
Herwadkar A. Double inversion recovery in detection of perilesional gliosis in calcific cysticercosis.Neurol India 2019;67:76-77

How to cite this URL:
Herwadkar A. Double inversion recovery in detection of perilesional gliosis in calcific cysticercosis. Neurol India [serial online] 2019 [cited 2019 Apr 19 ];67:76-77
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Full Text

Neurocysticercosis (NCC) is an ancient disease, described by Aristotle as a cystic form in the muscles of pigs. It is an infection of the larval form of the Taenia solium tapeworm and is the most common cause of acquired adult seizures and epilepsy in endemic regions.

Degenerating brain cysts can incite a host inflammatory response and later evolve into granulomas that frequently calcify. Degenerating cysts are a frequent cause of morbidity and seizures. There is abundant literature in NCC which concentrates on the clinical or therapeutic aspects of the degenerating cysts. Calcified lesions are a common imaging finding of NCC as they accumulate in the brain and are a measure of prior infections.

There is increasing evidence implicating calcified NCC in the genesis and maintenance of seizures in endemic populations. Calcified brain lesions are common in the computed tomographic (CT) studies of people with seizures and when symptoms appear in individuals with only calcified disease, some show perilesional brain edema around one or more of the calcifications.

The phenomenon of perilesional edema around calcified NCC lesions suggests a unique and specific underlying pathophysiology of seizures. The injury and disease due to cysticercosis are secondary to cyst inflammation; a plausible hypothesis is that edema represents an inflammatory response to calcified granulomas. Nash and others earlier speculated that an antigen is sporadically released and recognized by the host leading to episodic response.[1],[2],[3],[4]

Evidence suggests that perilesional edema/gliosis (PPG) around calcified cysticerci occurs relatively frequently and can be associated with seizures or focal neurological deficits.[4],[5],[6],[7],[8] In a previous study Nash et al., have shown that perilesional edema was present in 34.5% of patients with only calcified lesions who presented with seizures.[5]

Various magnetic resonance imaging (MRI) sequences have been used to characterise the presence of PPG. Axial T2 and inversion recovery and post-contrast T1 sequences are the mainstay of standard MR protocols in neuroimaging.[6],[7],[8] Agarwal et al.,[9] have shown that the presence of perilesional gliosis as seen on T1 weighted magnetisation transfer MRI is associated with difficult seizure control and is of value in objective prognostication of seizure outcome in these patients. Dynamic contrast enhanced MRI is also a useful tool in identifying perilesional change but needs dedicated software which is not universally available.

In inversion recovery (IR) sequences, the signal intensity of a specific tissue is suppressed by an inversion pulse. The fluid-attenuated inversion recovery (FLAIR) sequence suppresses the signal intensity of the cerebrospinal fluid (CSF), while the short-inversion time (TI) inversion recovery (STIR) sequence suppresses the signal of fat tissue. A double inversion recovery (DIR) sequence was developed by Redpath and Smith.[10] It involves the application of two different inversion pulses and a signal is obtained with the fast spin echo (FSE) method, thereby enabling the signals of two different tissues with two greatly different T1 relaxation times to be simultaneously suppressed. This sequence has found its application in the diagnoses of cortical and juxtacortical plaques in multiple sclerosis (MS), brain tumours, and in the paediatric group, with focal cortical dysplasia.[11]

The article in focus provides a retrospective analysis of 45 patients presenting with seizures with confirmed calcification on SWI imaging.[12] The control group consisted of 10 individuals with calcifications but without seizures. PPG was determined, evaluated and scored using three-dimensional (3D) volumetric imaging with DIR, FLAIR and post-contrast fat suppressed T1 imaging. There results demonstrate significant differences in the detection of PPG between 3D FLAIR and 3D DIR sequences as well as between 3D DIR and post contrast 3D T1 sequences with improved detection of PPG on DIR sequence. The authors also demonstrate good interobserver agreement on DIR as compared to the FLAIR and post contrast T1 sequence. The cohort group did not demonstrate PPG on any sequences.

This study was carried out using a 3T MRI scanner which has better signal-to-noise ratio and a higher spatial resolution. On a 1.5T MRI scanner, DIR sequences may require a relatively longer acquisition time and can be prone to cerebrospinal fluid pulsation and vascular flow artefact. This sequence has a relatively low signal-to-noise ratio, which likely reduces the sensitivity at lower, standard 1.5T, magnet strength.[13] Interpretation is partially dependent on the experience of the reader. As with many medical studies, lack of histological confirmation forms a limitation of this study. But as it is a pragmatic study, histological confirmation is often not necessary in most situations.

This study has made a strong case for adding DIR sequence into the MR sequence armament to detect PPG in calcified lesions and has paved the way to try and establish a direct relationship between DIR detected abnormalities and seizures. This would enhance the treatment paradigms in patients with recurrent seizures and provide a useful diagnostic tool to the treating physician.


1Nash TE, Patronas NJ. Edema associated with calcified lesions in neurocysticercosis. Neurology 1999;53:777-81.
2White AC Jr. Neurocysticercosis: A major cause of neurological disease worldwide. Clin Infect Dis 1997;24:101013.
3Sheth TN, Lee C, Kucharczyk W, Keystone J. Reactivation of neurocysticercosis: Case report. Am J Trop Med Hyg. 1999;60:664-7.
4Del Brutto OH. Prognostic factors for seizure recurrence after withdrawal of antiepileptic drugs in patients with neurocysticercosis. Neurology 1994;44:1706-9.
5Nash TE, Pretell J, Garcia HH. Calcified cysticerci provoke perilesional edema and seizures. Clin Infect Dis 2001;33:1649-53.
6Sheth TN, Pillon L, Keystone J, Kucharczyk W. Persistent MR contrast enhancement of calcified neurocysticercosis lesions. AJNR Am J Neuroradiol. 1998;19:79-82.
7Park SY, Barkovich AJ, Weintrub PS. Clinical implications of calcified lesions of neurocysticercosis. Pediatr Infect Dis J 2000;19:581-3.
8Antoniuk SA, Bruck I, Dos Santos LH, Pintarelli VL, Navolar FB, Brackmann PC Jr, et al. Seizures associated with calcifications and edema in neurocysticercosis. Pediatr Neurol 2001;25:309-11.
9Agarwal A, Raghav S, Husain M, Kumar R, Gupta RK. Epilepsy with focal cerebral calcification: Role of magnetization transfer imaging. Neurol India 2004;52:197-99.
10Redpath TW, Smith FW. Use of a double inversion recovery pulse sequence to image selectively grey or white brain matter. Br J Radiol 1994; 67:1258-63.
11Motegi S, Shimada T, Hayashi N, Nagase H, Taketomi-Takahashi A, Tsushima Y. Double inversion recovery imaging of the brain: deriving the most relevant sequence through real image. Radiol Phys Technol 2017;10:364-75.
12Saini 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 2019;67:136-41.
13Maura E. Utility of Double Inversion Recovery Sequences in MRI. Pediatr Neurol Briefs 2016;30:26.