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Table of Contents    
Year : 2016  |  Volume : 64  |  Issue : 2  |  Page : 330-331

“Boomerang sign”: An ominous-looking finding in reversible maladies

Department of Neurology, Postgraduate Institute of Medical Education and Research, Dr. Ram Manohar Lohia Hospital, New Delhi, India

Date of Web Publication3-Mar-2016

Correspondence Address:
Bhupender K Bajaj
Department of Neurology, Postgraduate Institute of Medical Education and Research, Dr. Ram Manohar Lohia Hospital, New Delhi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.177623

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How to cite this article:
Bajaj BK, Wadhwa A, Pandey S. “Boomerang sign”: An ominous-looking finding in reversible maladies. Neurol India 2016;64:330-1

How to cite this URL:
Bajaj BK, Wadhwa A, Pandey S. “Boomerang sign”: An ominous-looking finding in reversible maladies. Neurol India [serial online] 2016 [cited 2021 Jun 20];64:330-1. Available from:


The radiological finding of an isolated transient focal lesion in the splenium of the corpus callosum, that appears as a hyperintense signal on T2-, fluid-attenuated inversion recovery (FLAIR), and diffusion-weighted sequences of magnetic resonance imaging (MRI), is known as the “boomerang sign.” The MRI finding is known to be associated with various central nervous system infections, myelin disorders, drug toxicity, epilepsy, lymphoma, metabolic abnormalities, and nutritional deficiencies. We report the first instance where the presence of “boomerang sign” in a patient was associated with idiopathic intracranial hypertension. The presence of the splenial lesion in our case raises pertinent pathogenetic, diagnostic, and therapeutic dilemmas.

A 26-year-old woman presented with a dull-aching, holocranial, continuous headache with superimposed episodes of early-morning aggravations and vomiting for 4 weeks, followed 2 weeks later, by gradually progressive deterioration of vision in both the eyes. She did not have any history of fever, trauma, ear discharge, prolonged drug intake, recent vaccination, migraine, epilepsy, joint pains or swelling, rash, Raynaud's phenomenon, or weight loss. She had bilateral papilledema, with visual acuity of 6/60 in both the eyes. Neurological assessment, including her mental state examination and motor–sensory examinations were normal. There were no signs of meningeal irritation. Her blood tests including the hemogram, liver function tests, renal function tests, blood sugar–fasting and postprandial, thyroid function tests, cortisol levels, ELISA (enzyme-linked immunosorbent assay) for HIV (human immunodeficiency virus), serum antinuclear antibody, chest X-ray, and electrocardiogram were normal. MRI of the brain showed the empty sella sign and a T2/FLAIR hyperintensity, with diffusion restriction in the splenium of the corpus callosum [Figure 1]. Her MR venography was normal. The lumbar puncture revealed a cerebrospinal fluid (CSF) pressure of 250 mm H2O, 15 mononuclear cells, and normal sugar (88 mg/dl) and protein (29 mg/dl) levels. Gram staining, Ziehl–Neelsen staining, India ink preparation, and culture-sensitivity examination of the CSF were normal. The diagnosis of idiopathic intracranial hypertension was made in view of bilateral papilledema, normal neurological examination except for visual impairment, normal neuroimaging of the brain, elevated CSF pressure, and normal CSF protein, glucose, and microbiological examination.[1] The patient underwent an urgent bilateral optic nerve fenestration. After the procedure, she recovered her normal visual acuity in the right eye, with only partial recovery of vision in the left eye. Her headache improved immediately after the diagnostic and therapeutic lumbar puncture. She was continued on acetazolamide and given analgesics for controlling her headache. The focal lesion in the splenium had vanished by the time a repeat MRI of the brain had been done on the follow-up visit at approximately 1 month.
Figure 1: Brain MRI (a: T2-weighted; b: FLAIR; and c and d: diffusion-weighted) images showing a hyperintense lesion in the splenium of the corpus callosum (the ′boomerang′ sign) marked with arrows

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This is the first report of the “boomerang sign” appearing in a patient with idiopathic intracranial hypertension. Several hypotheses have been proposed to explain the transient changes in the splenium.[2],[3] Kim et al., proposed the occurrence of reversible demyelination due to antiepileptic drug toxicity.[4] Gurtler et al., suggested that an abrupt stoppage of chronic antiepileptic therapy could lead to ischemia, and the resultant cytotoxic edema is a consequence of the fluctuation in the arginine vasopressin system.[5] Transient splenial hyperintensities are reported in tick-borne and H1N1 encephalitis.[6],[7] Tada et al., speculated that viral antigens had a specific affinity for receptors on the splenial axons, leading to release of inflammatory cytokines that caused inflammation of the splenium.[8] Hachett et al., studied these changes in patients affected by high altitudinal cerebral edema and suggested the role of vasogenic edema and cerebral capillary hydrostatic pressure increase.[9] Oster et al., questioned the role of antiepileptic drugs and vasogenic edema in the development of transient splenial hyperintensities.[10] They demonstrated an increased signal on diffusion-weighted imaging along with low apparent diffusion coefficient values. These findings are not consistent with vasogenic edema as the cause. The changes in the splenium were attributed to transient disturbances of energy metabolism and ionic transport resulting in reversible myelin vacuolization or intramyelinic edema. The pathophysiology of the splenial sign is, therefore, not yet determined and at the present sate of knowledge, purely conjectural. Transient signal changes in the splenium of the corpus callosum may be a nonspecific end result of different disease processes due to some as-yet-obscure specific vulnerability of splenium of the corpus callosum. The finding does not always suggest a poor prognosis and is often reversible.

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  References Top

Friedman DI, Liu GT, Digre KB. Revised diagnostic criteria for the pseudotumor cerebri syndrome in adults and children. Neurology 2013;81:1159-65.  Back to cited text no. 1
Conti M, Salis A, Urigo C, Canalis L, Frau S, Canalis GC. Transient focal lesion in the splenium of the corpus callosum: MR imaging with an attempt to clinical-physiopathological explanation and review of the literature. Radiol Med 2007;112:921-35.  Back to cited text no. 2
Malhotra HS, Garg RK, Vidhate MR, Sharma PK. Boomerang sign: Clinical significance of transient lesion in splenium of corpus callosum. Ann Indian Acad Neurol 2012;15:151-7.  Back to cited text no. 3
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Kim SS, Chang KH, Kim ST, Suh DC, Cheon JE, Jeong SW, et al. Focal lesion in the splenium of the corpus callosum in epileptic patients: Antiepileptic drug toxicity? AJNR Am J Neuroradiol 1999;20:125-9.  Back to cited text no. 4
Gürtler S, Ebner A, Tuxhorn I, Ollech I, Pohlmann-Eden B, Woermann FG. Transient lesion in the splenium of the corpus callosum and antiepileptic drug withdrawal. Neurology 2005;65:1032-6  Back to cited text no. 5
Vollmann H, Hagemann G, Mentzel HJ, Witte OW, Redecker C. Isolated reversible splenial lesion in tick-borne encephalitis: A case report and literature review. Clin Neurol Neurosurg 2011;113:430-3.  Back to cited text no. 6
Ito S, Shima S, Ueda A, Kawamura N, Asakura K, Mutoh T. Transient splenial lesion of the corpus callosum in H1N1 influenza virus-associated encephalitis/encephalopathy. Intern Med 2011;50:915-8.  Back to cited text no. 7
Tada H, Takanashi J, Barkovich AJ, Oba H, Maeda M, Tsukahara H, et al. Clinically mild encephalitis/encephalopathy with a reversible splenial lesion. Neurology 2004;63:1854-8.  Back to cited text no. 8
Hackett PH, Yarnell PR, Hill R, Reynard K, Heit J, McCormick J. High-altitude cerebral edema evaluated with magnetic resonance imaging: Clinical correlation and pathophysiology. JAMA 1998;280:1920-5.  Back to cited text no. 9
Oster J, Doherty C, Grant PE, Simon M, Cole AJ. Diffusion-weighted imaging abnormalities in the splenium after seizures. Epilepsia 2003;44:852-4.  Back to cited text no. 10


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