Skip to main content

Advertisement

Log in

Transient focal lesion in the splenium of the corpus callosum: MR imaging with an attempt to clinical-physiopathological explanation and review of the literature

Le lesioni focali transitorie dello splenio del corpo calloso: imaging RM e ipotesi eziopatogenetiche

  • Neuroradiology Neuroradiologia
  • Published:
La radiologia medica Aims and scope Submit manuscript

Abstract

Purpose

This article discusses the possible pathophysiological conditions responsible for magnetic resonance imaging (MRI) finding of transient focal lesions in the splenium of the corpus callosum on the basis of our experience and a review of the literature.

Materials and methods

In six patients undergoing computed tomography (CT) and MRI examinations, focal nonhemorrhagic lesions of the splenium of the corpus callosum were incidentally discovered. Patients had been referred for suspected encephalitis (n=2), dural sinus thrombosis (n=1) and multiple sclerosis (n=3). MRI examinations were repeated after 4, 8 and 12 weeks and in two cases also after 6 and 9 months. MRI and medical records were retrospectively reviewed with respect to patients’ clinical history, medication and laboratory findings to define lesion aetiology.

Results

In all patients, the lesions were isolated, reversible and with no contrast enhancement. In four patients, the lesion disappeared after complete remission of the underlying disease, whereas in two patients, they persisted for 6 and 9 months, respectively.

Conclusions

To our knowledge and according to previous reports, the fact that these lesions are detected in a relatively large number of conditions with heterogeneous etiopathogenetic factors leads to the hypothesis that a common underlying pathophysiological mechanism that, considering signal characteristic, reversibility and white matter location, could be represented by vasogenic oedema.

Riassunto

Obiettivi

Formulare delle ipotesi fisio-patogenetiche responsabili della comparsa all’imaging RM di lesioni focali transitorie nello splenio del corpo calloso, oltre che identificarne il significato e le eventuali correlazioni cliniche in base alla nostra esperienza e ai dati riportati finora in letteratura.

Materiali e metodi

In 6 pazienti sottoposti a indagini TC e RM sono state riscontrate incidentalmente lesioni focali non emorragiche, isolate, nel contesto dello splenio del corpo calloso. I pazienti giungevano alla nostra osservazione con sospetto clinico di patologia infettiva (2), trombotica (1), demielinizzante (3) dell’encefalo. In tutti i casi sono stati effettuati controlli RM seriati nel tempo a distanza di 4–8–12 settimane e in 2 pazienti anche dopo 6 e 9 mesi. Le immagini RM unitamente ai dati clinico-laboratoristici sono state analizzate retrospettivamente al fine di definire l’eziologia di tali lesioni.

Risultati

In tutti i pazienti le lesioni si sono rivelate focali, prive di enhancement dopo mezzo di contrasto (MdC) e reversibili. In 4 pazienti le lesioni sono scomparse dopo la remissione completa della patologia di base mentre in 2 le alterazioni sono persistite rispettivamente sino a 6 e 9 mesi.

Conclusioni

La spiegazione definitiva di tale reperto appare ancora controversa. Secondo la nostra esperienza e quella di altri autori, essendo il riscontro di tali lesioni comune a un ampio spettro di condizioni patologiche con fattori eziopatogenetici eterogenei, è ipotizzabile che attraverso un comune, complesso meccanismo fisiopatologico tali fattori possano creare squilibri responsabili della comparsa di edema vasogenico che si esprime in un’alterazione del segnale RM nello splenio del corpo calloso.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References/Bibliografia

  1. Chason DP, Fleckenstein JL, Ginsburg ML et al. (1996) Transient splenial edema in epilepsy: MR imaging evaluation. Presented at the annual meeting of the American Society of Neuroradiology; June 21–27, 1996; Seattle, WA

  2. Kim SS, Chang K-H, Kim ST et al (1999) Focal lesion in the splenium of the corpus callosum in epileptic patients: antiepileptic drug toxicity? AJNR 20:125–129

    PubMed  CAS  Google Scholar 

  3. Behrens S, Pohlmann-Eden B (2001) Reversible phenytoin-induced extrapontine myelinolysis. Nervenarzt 72:453–455

    Article  PubMed  CAS  Google Scholar 

  4. Tada H, Takanashi J, Barkovich AJ et al (2004) Clinically mild encephalitis/encephalopathy with a reversible splenial lesion. Neurology 63:1854–1858

    PubMed  CAS  Google Scholar 

  5. Kobata R, Tsukahara H, Nakai A et al (2002) Transient MR signal changes in the splenium of the corpus callosum in rotavirus encephalopathy: value of diffusion-weighted imaging. J Comput Assist Tomogr 26:825–828

    Article  PubMed  Google Scholar 

  6. Kato Z, Kozawa R, Hashimoto K, Kondo N (2003)Transient lesion in the splenium of the corpus callosum in acute cerebellitis. J Child Neurol 18:291–292

    Article  PubMed  Google Scholar 

  7. Assencio-Ferreira VJ, Lucci Mussi M, Monteiro de Paula Guirado V, Esteves Veiga JC (2005) Lesão transitória no esplênio do corpo caloso em criança epiléptica com glioma cerebral de baixo grau. Arq Neuro-Psiquiatr 63:171–172

    Google Scholar 

  8. Ogura H, Takaoka M, Kishi M et al (1998) Reversible MR findings of hemolytic uremic syndrome with mild encephalopathy. Am J Neuroradiol 19:1144–1145

    PubMed  CAS  Google Scholar 

  9. Kobuchi N, Tsukahara H, Kawamura Y, e al (2003) Reversable diffusion weighted MR findings of Salmonella enteritidis associated encefalopathy. Eur Neurol 49:182–188

    Article  PubMed  CAS  Google Scholar 

  10. Hackett PH, Yarnell PR, Hill R et al (1998) High-altitude cerebral edema evaluated with magnetic resonance imaging. JAMA 280:1920–1925

    Article  PubMed  CAS  Google Scholar 

  11. Biegon A, Eberling JL, Richardson BC et al (1994) Human corpus callosum in aging and Alzheimer’s disease: a magnetic resonance imaging study. Neurobiol Aging 15:393–397

    Article  PubMed  CAS  Google Scholar 

  12. Georgy BA, Hesselink JR, Jernigan TL (1993) MR imaging of the corpus callosum. AJR Am J Roentgenol 160:949–955

    PubMed  CAS  Google Scholar 

  13. Kieburtz KD, Ketonen L, Zettelmaier AE et al (1990) MRI findings in HIV cognitive impairment. Arch Neurol 47:643–645

    PubMed  CAS  Google Scholar 

  14. Chang KH, Cha SH, Han MH et al (1992) Marchiafava-Bignami disease: serial changes in corpus callosum on MRI. Neuroradiology 34:480–482

    Article  PubMed  CAS  Google Scholar 

  15. Tobita M, Mochizuki H, Takahashi S et al (1997) A case of Marchiafava-Bignami disease with complete recovery: sequential imaging documenting improvement of callosal lesions. Tohoku J Exp Med 182:175–179

    Article  PubMed  CAS  Google Scholar 

  16. Takanashi J, Barkovich AJ, Yamaguchi K, Kohno T. Influenza-associated encephalitis/encephalopathy with a reversible lesion in the splenium of the corpus callosum: a case report and literature review. AJNR Am J Neuroradiol 25:798–802

  17. Polster T, Hoppe M, Ebner A (2001) Transient lesion in the splenium of the corpus callosum: three further cases in epileptic patients and a pathophysiological hypothesis. J Neurol Neurosurg Psychiatry 70:459–463

    Article  PubMed  CAS  Google Scholar 

  18. Cohen-Gadol AA, Britton JW, Jack CR Jr et al (2002) Transient postictal magnetic resonance imaging abnormality of the corpus callosum in a patient with epilepsy. Case report and review of the literature. J Neurosurg 97:714–717

    PubMed  Google Scholar 

  19. Ziegler DK (1978) Toxicity to the nervous system of diphenylhydantoin: a review. Int J Neurol 11:383–400

    PubMed  CAS  Google Scholar 

  20. Ramirez JA, Mendell JR, Warmolts JR, Griggs RC (1986) Phenytoin neuropathy: structural changes in the sural nerve. Ann Neurol 19:162–167

    Article  PubMed  CAS  Google Scholar 

  21. Graham DI, Lantos PL (1997) Greenfield’s Neuropathology, 6th ed. Arnold, London

    Google Scholar 

  22. Butler WH, Ford GP, Newberne JW (1987) A study of the effects of vigabatrin on the central nervous system and retina of Sprague Dawley and Lister-Hooded rats. Toxicol Pathol 15:143–148

    PubMed  CAS  Google Scholar 

  23. Graham D (1989) Neuropathology of vigabatrin. Br J Clin Pharmacol 27(Suppl 1):43S–45S

    PubMed  CAS  Google Scholar 

  24. Gibson JP, Yarrington JT, Loudy DE et al (1990) Chronic toxicity studies with vigabatrin, a GABA-transaminase inhibitor. Toxicol Pathol 18:225–238

    Article  PubMed  CAS  Google Scholar 

  25. Shiihara T, Kato M, Hayasaka K (2005) Clinically mild encephalitis/encephalopathy with a reversible splenial lesion. Neurology 64:1487

    PubMed  Google Scholar 

  26. Mirsattari SM, Lee DH, Jones MW, Blume WT (2003)Transient lesion in the splenium of the corpus callosum in an epileptic patient. Neurology 60:1838–1841

    PubMed  Google Scholar 

  27. Tsugane S, Suzuki Y, Takayasu M et al (1994) Effects of vasopressin on regional cerebral blood flow in dogs. J Auton Nerv Sys 49:S133–S136

    Article  CAS  Google Scholar 

  28. Doczi T, Szerdahelyi P, Gulya K et al (1982) Brain water accumulation after central administration of vasopressin. Neurosurgery 11:402–407

    Article  PubMed  CAS  Google Scholar 

  29. Raichle ME, Grubb RL (1978) Regulation of brain water permeability by centrally-released vasopressin. Brain Res 143:191–194

    Article  PubMed  CAS  Google Scholar 

  30. Krause KH, Rascher W, Berlit P (1983) Plasma arginine vasopressin concentrations in epileptics under monotherapy. J Neurol 230:193–196

    Article  PubMed  CAS  Google Scholar 

  31. Stephens WP, Coe JY, Baylis PH (1978) Plasma arginine vasopressin concentrations and antidiuretic action of carbamazepine. BMJ i:1445–1447

    Article  Google Scholar 

  32. Soelberg Sørensen P, Hammer M (1984) Effects of long-term carbamazepine treatment on water metabolism and plasma vasopressin concentration. Eur J Clin Pharmacol 26:719–722

    Article  PubMed  Google Scholar 

  33. Bradley WB (1987) Pathophysiologic correlates of signal alteration. In: Brant-Zawadzki M, Norman D (eds) Magnetic Resonance Imaging of the central nervous system. Raven Press, New York, NY pp 29–33

    Google Scholar 

  34. Simmonson TM, Yuh WTC (1996) Stroke and cerebral ischemia. In: Edelman RR, Zlatkin MB, Hesselink JR (eds) Clinical Magnetic Resonance Imaging, 2nd ed. WB Saunders, Philadelphia, PA, pp 767–773

    Google Scholar 

  35. Fishman RA (1975) Brain edema. N Engl J Med 293:706–711

    Article  PubMed  CAS  Google Scholar 

  36. Hauser RA, Lacey DM, Knight MR (1988) Ipertensive encefalopathy: magnetic resonance imaging demonstration of reversible cortical and white matter lesions. Arch Neurol 45:1078–1083

    PubMed  CAS  Google Scholar 

  37. Raroque HG, Orrison WW, Rosemberg GA (1990) Neurologic involvement in toxiemia of pregnancy: reversible MRI lesions. Neurology 40:167–169

    PubMed  Google Scholar 

  38. Yaffe K, Ferriero D, Barkovich J, Rowley H (1995) Reversible MRI abnormalities following seizures. Neurology 45:104–108

    PubMed  CAS  Google Scholar 

  39. Krasney J (1997) Cerebral hemodynamics and high altitude cerebral edema. In: Houston C, Coates G (eds) Hypoxia: women at altitude. Queen City Press, Burlington, WT, pp 254–268

    Google Scholar 

  40. Joo F, Klatzo I (1989) Role of cerebral endothelium in brain oedema. Neurol Res 11:67–75

    PubMed  CAS  Google Scholar 

  41. Schilling L, Wahl M (1997) Brain edema: pathogenesys and therapy. Kidney Int 51(suppl 59):s69–s75

    Google Scholar 

  42. Plateel M, Dehouck M-P, Torpier G, Cecchelli R, Tessier E (1995) Hipoxia increases the susceptibility to oxidant stress and the permeability of the bloodbrain-barrier endothelial cell monolyer. J Neuro-Chem. 65:2138–2145

    CAS  Google Scholar 

  43. Bartsch P, Shaw S, Francioli M, Gnadinger MP, Weidmann P (1988) Atrial natriuretic peptide in acute mountain sickness. J Appl Phisiol. 65:1929–1937

    CAS  Google Scholar 

  44. Richalet JP, Hormych A, Rathat C, Aumont J, Larmignant P, Remy P (1991) Plasma prostaglandins leukotrienes and thromboxane in acute high altitude hypoxia. Respir Physion 85:205–215

    Article  CAS  Google Scholar 

  45. Neeraj B. Chepuri, Yi-Fen Yen, Jonathan H. Burdette, Hong Li, Dixon M. Moody, and Joseph A. Maldjian (2002) Diffusion Anisotropy in the Corpus Callosum AJNR Am J Neuroradiol 23:803–808

    PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to M. Conti.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Conti, M., Salis, A., Urigo, C. et al. 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 112, 921–935 (2007). https://doi.org/10.1007/s11547-007-0197-9

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s11547-007-0197-9

Key words

Parole chiave

Navigation