Annals of Indian Academy of Neurology
  Users Online: 1401 Home | About the Journal | InstructionsCurrent Issue | Back IssuesLogin      Print this page Email this page  Small font size Default font size Increase font size


 
Table of Contents
CASE REPORT
Year : 2012  |  Volume : 15  |  Issue : 2  |  Page : 151-157
 

Boomerang sign: Clinical significance of transient lesion in splenium of corpus callosum


Department of Neurology, Chhatrapati Shahuji Maharaj Medical University, Uttar Pradesh, Lucknow, India

Date of Submission17-Mar-2011
Date of Decision29-Apr-2011
Date of Acceptance01-Jun-2011
Date of Web Publication13-Apr-2012

Correspondence Address:
Ravindra Kumar Garg
Department of Neurology, Chhatrapati Shahuji Maharaj Medical University, Uttar Pradesh, Lucknow - 226 003
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-2327.95005

Rights and Permissions

 

   Abstract 

Transient signal abnormality in the splenium of corpus callosum on magnetic resonance imaging (MRI) is occasionally encountered in clinical practice. It has been reported in various clinical conditions apart from patients with epilepsy. We describe 4 patients with different etiologies presenting with signal changes in the splenium of corpus callosum. They were diagnosed as having progressive myoclonic epilepsy (case 1), localization-related epilepsy (case 2), hemicrania continua (case 3), and postinfectious parkinsonism (case 4). While three patients had complete involvement of the splenium on diffusion-weighted image ("boomerang sign"), the patient having hemicrania continua showed semilunar involvement ("mini-boomerang") on T2-weighted and FLAIR image. All the cases had noncontiguous involvement of the splenium. We herein, discuss these cases with transient splenial involvement and stress that such patients do not need aggressive diagnostic and therapeutic interventions. An attempt has been made to review the literature regarding the pathophysiology, etiology, and outcome of such lesions.


Keywords: Boomerang sign, corpus callosum, diffusion-weighted imaging, epilepsy, hemicrania continua, measles, magnetic resonance imaging, splenium


How to cite this article:
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

How to cite this URL:
Malhotra HS, Garg RK, Vidhate MR, Sharma PK. Boomerang sign: Clinical significance of transient lesion in splenium of corpus callosum. Ann Indian Acad Neurol [serial online] 2012 [cited 2019 Sep 21];15:151-7. Available from: http://www.annalsofian.org/text.asp?2012/15/2/151/95005



   Introduction Top


Transient signal alteration in the splenium of corpus callosum on magnetic resonance imaging (MRI) has been reported in a variety of neurologic and nonneurologic conditions. [1],[2],[3],[4],[5],[6],[7] After the first observation in patients with epilepsy by Chason et al., [8] the involvement of the splenium has been described by many authors in neurologic conditions of varied etiologies. [1],[2],[3],[4],[5],[6],[7],[8] Splenial lesions are visualized as hyperintense lesions on T2-weighted images, fluid attenuated inversion recovery, and diffusion-weighted MR images. The images remain unaltered by gadolinium administration. Various pathophysiologic mechanisms have been put forth, but none is well proven. [2] It is a self-limiting phenomenon, which subsides over a period, once the underlying disease gets controlled. It may, sometimes, pose problems in the diagnosis and management of patients. Because of its benign nature and complete reversal without any specific treatment, aggressive diagnostic and therapeutic approaches are not needed. We describe 4 cases having different clinical scenario presenting with transient lesions of splenium on MRI.


   Case Reports Top


Case 1

A 21-year-old man with medically refractory epilepsy, constituted by partial, generalized, and myoclonic seizures for 4 years, presented to us with increase in myoclonic jerks and serial generalized seizures from 1 day. There was suggestion of cognitive impairment from the past 2 years and mild unsteadiness of gait. The patient was loaded with intravenous sodium valproate (30 mg/kg body weight) to which his seizures responded. MRI of the brain showed hyperintensity of the splenium of corpus callosum ("Boomerang sign") on diffusion-weighted image (DWI) [Figure 1]d with decreased apparent diffusion coefficient (ADC) values. T2-weighted image (T2WI), fluid attenuated inversion recovery (FLAIR), and T1-weighted image (T1WI) did not reveal any abnormal signals in splenium of corpus callosum and other areas of brain (except for an incidental cysticercus in left lentiform nucleus) [Figure 1]a-c. Currently the patient's medication regimen included valproic acid (1400 mg/day), levetiracetam (1000 mg/day), and clonazepam (1.5 mg/day). A follow-up MRI done after 6 months revealed disappearance of altered signals in the splenium on DWI images [Figure 1]e. The routine hematologic and biochemical investigations were within normal limits.
Figure 1: Magnetic resonance imaging and magnetic resonance angiography (Brain) of case 1, with refractory epilepsy, showing normal, axial, T1-weighted (a), T2-weighted (b) and fluid attenuated inversion recovery (c) images with increased signal intensity of the entire splenium of corpus callosum ("Boomerang sign") on diffusion-weighted image (d); repeat diffusion-weighted image (e), done at 6 months, showing complete resolution of abnormal signals involving the splenium. Magnetic resonance angiogram (f) did not reveal any abnormality

Click here to view


Case 2

A 38-year-old man presented with multiple episodes of left partial seizures with secondary generalization, followed by Todd's palsy. After loading the patient with intravenous sodium valproate (30 mg/kg body weight), an equivalent oral dose of sodium valproate was started. MRI of the brain done next day after admission revealed a well-defined parafalcine space occupying the lesion with perilesional edema [Figure 2]a-c. Also evident was the uniform hyperintensity of the splenium of corpus callosum ("Boomerang sign") on DWI [Figure 2]e with low ADC values. T1WI and T2WI did not reveal any abnormal signals in the splenium of corpus callosum [Figure 2]d. A follow-up MRI done after a week depicted complete disappearance of altered signals in the splenium on DWI image [Figure 2]f. The patient was transferred to the Department of Neurosurgery for further management.
Figure 2: Magnetic resonance imaging (Brain) of case 2, with localization related epilepsy, showing a right-sided well defined parafalcine extra-axial space occupying lesion, with perilesional edema, in T1-weighted axial (a), T2-weighted sagittal (b) and coronal (c) images. T2-weighted image (d), axial section, focussing on the corpus callosum appears normal while a uniform hyperintensity of the splenium of corpus callosum ("Boomerang sign") on diffusion-weighted image (e) is evident. Follow up diffusion-weighted image (f), done at 1 week, depicts complete disappearance of altered signals in the splenium

Click here to view


Case 3

A 34-year-old woman, diagnosed as a case of hemicrania continua, presented with progressively increasing headache and loss of complete responsiveness to indomethacin from a week. She was a vegetarian without any significant past history of chronic ailment or drug abuse. Apart from indomethacin (150 mg/day), she was taking 40 mg of verapamil twice daily. The clinical examination was noncontributory without any suggestion of an organic substrate. MRI of the brain was suggestive of a semilunar hyperintensity ("mini-boomerang") on T2WI and FLAIR image involving the posterior part of splenium of corpus callosum [Figure 3]a-d; there was no evidence of restriction on DWI [Figure 3]e, f. Magnetic resonance angiography was normal; however, magnetic resonance venography (MRV) showed lack of proper visualization of veins at the level of vein of Galen [Figure 3]g, h. Serum B12 was found to be low (132 pg/mL). The lady was prescribed a short course of prednisolone, starting with 60 mg/day for 3 days and reduced by 10 mg every fourth day, and the dose of verapamil was increased to 160 mg in two divided doses after checking for any rhythm disturbance. No vitamin supplementation or anticoagulants were prescribed. The lady responded well and follow-up MRI done after 3 months showed complete resolution of the splenial lesion [Figure 3]i; MRV did not reveal any change suggesting the anomaly to be a normal variant.
Figure 3: Magnetic resonance imaging, magnetic resonance angiography and magnetic resonance venography (Brain) of case 3, with hemicrania continua, showing semilunar hyperintensity ("mini-boomerang") on axial T2-weighted (a) and fluid attenuated inversion recovery (b) images with a focal hyperintensity on sagittal T2-weighted image (c); there was no evidence of restriction on diffusion-weighted image (d) and the apparant diffusion coefficient map (e) was normal. Lack of proper visualization of veins at the level of vein of Galen was evident on magnetic resonance venogram (f). Repeat T2-weighted image (g) and fluid attenuated inversion recovery image (h) at 3 months showing complete resolution of the abnormal signals in splenium. Magnetic resonance angiogram (i) did not reveal any abnormality

Click here to view


Case 4

A 10-year-old school boy presented with a history of high-grade fever, rash, headache, and vomiting 20 days before admission. The fever subsided in 7 days but the patient developed right-sided extrapyramidal symptoms in the form of tremor, rigidity, and bradykinesia predominantly involving the upper limb. The patient did not have seizures or altered sensorium. On examination, the patient had cog-wheel rigidity and bradykinesia. MRI of brain done at the onset of extrapyramidal symptoms revealed T2WI hyperintense signals involving bilateral substantia nigra more pronounced on left side [Figure 4]a without restriction on DWI. Also noted was the uniform hyperintensity of the splenium of corpus callosum ("Boomerang sign") on DWI [Figure 4]d with low ADC values. T1WI and T2WI images denoted normal signals in the splenium of corpus callosum [Figure 4]b, c. The serology for various viruses, including Japanese Encephalitis virus in blood and cerebrospinal fluid was ordered. The serological test for measles virus was positive in blood with raised IgM antibody titers. The extrapyramidal symptoms of patient improved with pramipexole. Follow-up MRI performed 10 days after the previous one, revealed complete disappearance of altered signals in splenium [Figure 4]e. The T2 hyperintensities involving bilateral substantia nigra, however, persisted [Figure 4]f.
Figure 4: Magnetic resonance imaging (Brain) of case 4, with post-infectious  Parkinsonism More Details, showing hyperintense signals in bilateral substantia nigra on axial T2-weighted image (a), more pronounced on left side; T1-weighted (b) and T2-weighted (c) images, axial section, focussing on the corpus callosum appear normal while a uniform hyperintensity of the splenium of corpus callosum ("Boomerang sign") on diffusion-weighted image (d) is evident. Repeat diffusion-weighted image (e), done after 10 days, depicting reversibility of lesion involving the splenium of corpus callosum; the hyperintense signals involving the substantia nigra on axial T2-weighted image (f) decreased in size

Click here to view



   Discussion Top


Corpus callosum is the largest commissural white matter bundle in the brain containing 200-250 million interhemispheric fibers. [9] Major portion of the corpus callosum receives its arterial supply from the carotid system except for splenium, which is supplied by the vertebrobasilar system. [3] Several pathologic conditions, such as multiple sclerosis, Marchiafava-Bignami disease, tumors, ischemia, leukodystrophy, and HIV-related encephalopathy, may affect the corpus callosum, producing permanent changes. [2]

Various transient peri-ictal abnormalities on MRI have been documented in the literature with or without involvement of splenium of corpus callosum. [10] Transient peri-ictal signal abnormality involving solely the splenium of corpus callosum on MRI is not frequently encountered in clinical practice. So, the treating physician might be tempted to subject the patient to unnecessary diagnostic and therapeutic interventions. The occurrence of this abnormality was first described by Chason et al. as a transient post-ictal focal edema denoting transhemispheric propagation of seizure through the corpus callosum. [8] Since then, various etiologic factors have been associated with the transient hyperintensities of the splenium [Table 1].
Table 1: Clinical conditions associated with transient splenial hyperintensity

Click here to view


As mentioned earlier, several hypotheses have been put forward to explain transient changes in splenium. The association of these changes with epilepsy is complex. Breakdown of the blood-brain barrier (BBB), producing transient focal edema has been implicated by some authors in patients having seizures. [8],[11] In contrast, Kim et al. attributed it to "possible anti-epileptic drug (AED) toxicity induced reversible demyelination". [12] Mirsattari et al. and Gurtler et al. suggested the role of cytotoxic edema brought on by ischemia related to abrupt cessation of long-term AED. [13],[14] They postulated that sudden cessation of AED could lead to alteration of the arginine-vasopressin (AVP) system, resulting into hydric imbalance. Apart from carbamazepine, several antiepileptic drugs have been found to interfere with the AVP system. [15]

Apart from epilepsy, the transient signal alterations in splenium of corpus callosum have been described in patients with encephalitis/encephalopathy due to various organisms, including recent reports from tick-born and H1N1 encephalitis. [16],[17],[18] Tada et al. studied reversible splenium lesion in 15 patients with encephalitis/encephalopathy. [3] He speculated that viral antigens or receptors on the antibodies induced by the antigens had specific affinities for receptors on splenial axons, leading to raised inflammatory cytokines, such as interleukin-6, causing inflammation of splenium. Hackett et al. reported signal alterations in splenium in patients affected by high-altitudinal cerebral edema. [7] He strongly suggested the role of vasogenic edema involving predominantly the white matter. An explanation for this pathogenic mechanism may be a BBB alteration due to a cerebral capillary hydrostatic pressure increase, which is commonly observed in conditions, such as hypertensive encephalopathy, preeclampsia, posterior reversible encephalopathy syndrome, seizures, and toxic effects of cyclosporine. In contradiction, Oster et al. questioned the role of both, AEDs and vasogenic edema, in the development of transient splenial hyperintensities after seizures. [19] He demonstrated increased signal on DWI with low ADC values, which were inconsistent with vasogenic edema as the cause. The changes in splenium were attributed to transient disturbance of energy metabolism and ionic transport in reversible myelin vacuolization or intramyelinic edema. This transient disturbance of energy metabolism and ionic transport was speculated as a result of repeated excessive activity of commissural projections during seizure propagation. The similar mechanism explains the transient hyperintensity of splenium in cases 1 and 2 following serial seizures.

We would like to emphasize an important aspect that is evident from our case 2. Although the space occupying lesion (seizure focus) was also in proximity to the anterior commissural fibers, that is, genu and rostrum of corpus callosum, it was characteristically spared on MRI. We propose that the unique anatomical and physiological property of fibers of splenium of corpus callosum makes it susceptible for transient signal alterations on MRI after seizure propagation. This can be likened to reversible posterior leukoencephalopathy syndrome involving specifically the posterior parts of brain, especially if we consider the blood supply of this area.

The splenium involvement appears hyperintense on T2WI and FLAIR image and iso- or hypointense on T1WI. The changes in DWI appear earlier than the changes in T2WI and FLAIR, as reported by Oster et al., [19] as observed by us in case 1. Involvement of the splenium, based on signal changes, can be divided into two types according to its shape and extent: Oval, circumscribed, with well-defined borders usually located in the middle; or wider, with less regular borders and involving the entire splenium ("Boomerang sign"). In most of the previous case series, the focal involvement of splenium has been documented in MRI done after seizures. [5],[11],[12],[13],[14],[15] Involvement of entire splenium is occasionally reported, mainly due to hypoxic injury of corpus callosum. [20],[21] It's noteworthy to mention that cases 1 and 2 had uniform involvement of splenium of corpus callosum after serial seizures.

Disappearance of signal abnormalities in the splenium of corpus callosum has been documented by various authors and the timing of follow-up MRI performed ranges from 3 days to 1 year. [3],[5],[11] Conti et al. subjected 6 patients with isolated signal changes in splenium of corpus callosum to serial MRIs at 4, 8, and 12 weeks and demonstrated complete disappearance of lesions in 4 patients. [2]

As the changes are transient, the timing of MRI study is very crucial to pick up these abnormalities in splenium and may thus explain the rarity of occurrence in routine MRIs.

We would also like to share our experience of incidental semilunar hyperintensity ("mini-boomerang") involving predominantly the posterior part of splenium on MRI in case 3 [Figure 3]a-i. Such transient signal changes have not been reported in patients of hemicrania continua. Whether the abnormality is a sequel of the basic disease process or is attributable to subtle deviation in MRV with associated low serum B12 in case 3 cannot be said with certainty. Since the response was seen without the use of anticoagulants and vitamin supplementation, this does give a suggestion that some unknown pathophysiological mechanism might be responsible for the occurrence of transient splenial lesion in this patient.

As observed in case 4, the T2 hyperintense signals in the splenium of corpus callosum disappeared in contrast to persistent T2 hyperintensities in substantia nigra on follow-up MRI. This interesting finding points toward different pathogenic mechanisms possible for two abnormalities after measles infection. One of the pathogenic mechanisms discussed above, especially that given by Tada et al. after encephalitis/encephalopathy, is more likely responsible for transient changes in splenium. [3] Mito et al. reported transient round signal change in the splenium of corpus callosum in 1 of 2 patients with measles encephalitis. [22]

Other possible differential diagnoses of splenial lesions include ischemia, posterior reversible encephalopathy syndrome, diffuse axonal injury, multiple sclerosis, Marchiafava-Bignami disease, lymphoma, and extrapontine myelinolysis. [9] The most important clues to differentiate transient splenium involvement from others are absence of symptoms of hemispheric disconnection (apraxias of the left hand, pseudoneglect, alien left hand, agraphia, alexia, visual apraxias, and so on) and reversibility after control of underlying disease. The importance of clinical setting cannot be overemphasized. Also most other etiologies show paramagnetic contrast enhancement, which is very rarely present with transient splenium involvement. [2]

In summary, transient signal changes in the splenium of corpus callosum appear to be the nonspecific end result of different disease processes of various etiologies with varied pathogenic mechanisms. These lesions may be encountered incidentally while looking for some organic substrate in systemic disorders or most commonly in the post-ictal phase. The predilection for only the splenial part of corpus callosum, with sparing of other parts, needs to be looked into in detail. These lesions of splenium carry a good prognosis due to their reversibility and should not be confused with serious pathologies. [26]

 
   References Top

1.Doherty MJ, Jayadev S, Konchada R, Hallam D, Watson NF. Clinical implications of splenium magnetic resonance imaging signal changes. Arch Neurol 2005;62:433-7.  Back to cited text no. 1
    
2.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
    
3.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. 3
    
4.Kato Z, Kozawa R, Hashimoto K, Kondo N. Transient lesion in the splenium of the corpus callosum in acute cerebellitis. J Child Neurol 2003;18:291-2.  Back to cited text no. 4
    
5.Polster T, Hoppe M, Ebner A. Transient lesion in the splenium of the corpus callosum: Three further cases in epileptic patients and a pathophysiological hypothesis. J Neurol Neurosurg Psychiatry 2001;70:459-63.  Back to cited text no. 5
    
6.Ogura H, Takaoka M, Kishi M, Kimoto M, Shimazu T, Yoshioka T, et al. Reversible MR findings of hemolytic uremic syndrome with mild encephalopathy. AJNR Am J Neuroradiol 1998;19:1144-5.  Back to cited text no. 6
    
7.Hackett PH, Yarnell PR, Hill R, Reynard K, Heit J, McCormick J. High-altitude cerebral edema evaluated with magnetic resonance imaging. JAMA 1998;280:1920-5.  Back to cited text no. 7
    
8.Chason DP, Fleckenstein JL, Ginsburg MI. Transient Splenial Edema in Epilepsy: MR Imaging Evaluation. Proceedings of the 34 th annual meeting of the American Society of Neuroradiology; June 21-27. 1996, Seattle, WA, USA. Chicago: Old Smith Printers, 1996.  Back to cited text no. 8
    
9.Fitsiori A, Nguyen D, Karentzos A, Delavelle J, Vargas MI. The corpus callosum: White matter or terra incognita. Br J Radiol 2011;84:5-18.  Back to cited text no. 9
    
10.Raghavendra S, Ashalatha R, Krishnamoorthy T, Kesavadas C, Thomas SV, Radhakrishnan K. Reversible periictal MRI abnormalities: Clinical correlates and long-term outcome in 12 patients. Epilepsy Res 2007;73:129-36.  Back to cited text no. 10
    
11.Cohen-Gadol AA, Britton JW, Jack CR Jr, Friedman JA, Marsh WR. Transient postictal magnetic resonance imaging abnormality of the corpus callosum in a patient with epilepsy. Case report and review of the literature. J Neurosurg 2002;97:714-7.  Back to cited text no. 11
    
12.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. 12
    
13.Mirsattari SM, Lee DH, Jones MW, Blume WT. Transient lesion in the splenium of the corpus callosum in an epileptic patient. Neurology 2003;60:1838-41.  Back to cited text no. 13
    
14.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. 14
    
15.Krause KH, Rascher W, Berlit P. Plasma arginine vasopressin concentrations in epileptics under monotherapy. J Neurol 1983;230:193-6.  Back to cited text no. 15
    
16.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. 16
    
17.Singh P, Gogoi D, Vyas S, Khandelwal N. Transient splenial lesion: Further experience with two cases. Indian J Radiol Imaging 2010;20:254-7.  Back to cited text no. 17
[PUBMED]  Medknow Journal  
18.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. 18
    
19.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. 19
    
20.Pandian JD, Henderson RD. "Boomerang sign" in the splenium of the corpus callosum. Med J Aust 2005;183:628.  Back to cited text no. 20
    
21.Bianchi MT, Sims JR. Restricted diffusion in the splenium of the corpus callosum after cardiac arrest. Open Neuroimag J 2008;2:1-4.  Back to cited text no. 21
    
22.Mito Y, Yoshida K, Kikuchi S. Measles encephalitis with peculiar MRI findings: A report of two adult cases. Neurol Med 2002;56:251-6.  Back to cited text no. 22
    
23.Takanashi J, Miyamoto T, Ando N, Kubota T, Oka M, Kato Z, et al. Clinical and radiological features of rotavirus cerebellitis. AJNR Am J Neuroradiol 2010;31:1591-5.  Back to cited text no. 23
    
24.Appenzeller S, Faria A, Marini R, Costallat LT, Cendes F. Focal transient lesions of the corpus callosum in systemic lupus erythematosus. Clin Rheumatol 2006;25:568-71.  Back to cited text no. 24
    
25.Lin FY, Yang CY. Reversible splenial lesion of the corpus callosum in migraine with aura. Neurologist 2011;17:157-9.  Back to cited text no. 25
    
26.Kim E, Na DG, Kim EY, Kim JH, Son KR, Chang KH. MR imaging of metronidazole-induced encephalopathy: Lesion distribution and diffusion-weighted imaging findings. AJNR Am J Neuroradiol 2007;28:1652-8.  Back to cited text no. 26
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

  [Table 1]


This article has been cited by
1 Vanishing splenial lesion presenting as alexia with dysgraphia
Rajendra Singh Jain,Sunil Kumar,Madhuparna Paul,Rakesh Agrawal
Journal of Neurology. 2015;
[Pubmed] | [DOI]
2 Magnetic resonance imaging of a transient splenial lesion of the corpus callosum resolved within a week
R. Conforti,A.M. Porto,R. Capasso,M. Cirillo,G. Fontanella,A. Salzano,M. Fabrazzo,S. Cappabianca
Radiography. 2015;
[Pubmed] | [DOI]
3 Clinical and Radiological Profile of Children with Lesions in Corpus Callosum
Chellamani Harini,Rohit R. Das,Sanjay P. Prabhu,Kanwaljit Singh,Amit Haldar,Masanori Takeoka,Ann M. Bergin,Tobias Loddenkemper,Sanjeev V. Kothare
Journal of Neuroimaging. 2014; : n/a
[Pubmed] | [DOI]
4 Diagnosis and management of Marchiafava-Bignami disease: a review of CT/MRI confirmed cases
M. Hillbom,P. Saloheimo,S. Fujioka,Z. K. Wszolek,S. Juvela,M. A. Leone
Journal of Neurology, Neurosurgery & Psychiatry. 2014; 85(2): 168
[Pubmed] | [DOI]
5 æMini-boomerang signæ: Reversible corpus callosal signal change in neuroleptospirosis
Khanra, D., Talukdar, A.
International Journal of Infectious Diseases. 2013; 17(1): e70-e71
[Pubmed]
6 result 2 Document Commentary
Authors of Document Celis-Aguilar, E.
Journal of Neurosciences in Rural Practice. 2013;
[Pubmed]



 

Top
Print this article  Email this article

    

 
   Search
 
  
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Article in PDF (1,900 KB)
    Citation Manager
    Access Statistics
    Reader Comments
    Email Alert *
    Add to My List *
* Registration required (free)  


    Abstract
   Introduction
   Case Reports
   Discussion
    References
    Article Figures
    Article Tables

 Article Access Statistics
    Viewed7699    
    Printed131    
    Emailed3    
    PDF Downloaded253    
    Comments [Add]    
    Cited by others 6    

Recommend this journal