2007
DOI: 10.1007/s11547-007-0197-9
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Transient focal lesion in the splenium of the corpus callosum: MR imaging with an attempt to clinical-physiopathological explanation and review of the literature

Abstract: 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.

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Cited by 37 publications
(26 citation statements)
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“…The differential diagnosis of splenial hyperintensity (or boomerang sign as it is sometimes described)[5] is vast including ischemia, infections – encephalitis (influenza, Escherichia coli , mumps, adenovirus, Epstein-Barr, virus and Rota virus), demyelinating lesions including multiple sclerosis, posterior reversible encephalopathy syndrome, diffuse axonal injury, Marchiafava-Bignami disease, adrenoleukodystrophy, AIDS dementia complex, lymphoma, epilepsy, antiepileptic drug usage, osmotic myelinolysis, and acute toxic encephalopathy. [6] However, mechanism of this splenial hyperintensity is incompletely understood. Various mechanisms proposed include breakdown of the blood–brain barrier,[7] reversible demyelination or transient disturbance of energy metabolism, and ionic transport causing intramyelinic edema.…”
Section: Discussionmentioning
confidence: 99%
“…The differential diagnosis of splenial hyperintensity (or boomerang sign as it is sometimes described)[5] is vast including ischemia, infections – encephalitis (influenza, Escherichia coli , mumps, adenovirus, Epstein-Barr, virus and Rota virus), demyelinating lesions including multiple sclerosis, posterior reversible encephalopathy syndrome, diffuse axonal injury, Marchiafava-Bignami disease, adrenoleukodystrophy, AIDS dementia complex, lymphoma, epilepsy, antiepileptic drug usage, osmotic myelinolysis, and acute toxic encephalopathy. [6] However, mechanism of this splenial hyperintensity is incompletely understood. Various mechanisms proposed include breakdown of the blood–brain barrier,[7] reversible demyelination or transient disturbance of energy metabolism, and ionic transport causing intramyelinic edema.…”
Section: Discussionmentioning
confidence: 99%
“…The absence of neurological symptoms has also been described, despite persistence of the focal lesion [3].…”
Section: Cerebral Vasospasm Manifesting As a Transient Lesion Of The mentioning
confidence: 97%
“…Reversible lesions have been reported in an association with epilepsy and antiepileptic drugs, alcoholism, malnutrition, vitamin B12, and folate deficiency, trauma, diffuse axonal damage, infections, hydrocephalus, posterior reversible encephalopathy, lymphoma, fluid electrolyte disorders, extrapontine myelinolysis, hypertensive encephalopathy, and systemic lupus erythematosus. [4] These lesions are totally reversible and have not been reported in association with any disconnection syndromes. [5] Changes in DWI appear earlier than T2 and FLAIR.…”
Section: Reversible Disconnection Syndrome: An Unusual Presentation Omentioning
confidence: 99%
“…Pooled data of three large series showed that 94% of patients with this sign on MRI had PANK2 mutation. [4] Typical …”
Section: Rajesh Verma Tushar Premraj Rautmentioning
confidence: 99%