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Movement Disorders Unit, Neurology Department, Westmead Hospital, Corner Darcy and Hawkesbury Road, Westmead, NSW 2145 AustraliaNeurology Unit, Department of Medicine, Hospital Sultanah Nur Zahirah, 20400 Kuala Terengganu, Malaysia
Movement Disorders Unit, Neurology Department, Westmead Hospital, Corner Darcy and Hawkesbury Road, Westmead, NSW 2145 AustraliaSydney Medical School, University of Sydney, Sydney, NSW, Australia
Contrast enhancing/ non-enhancing ‘sentinel lesions’ described in PCNSL can recede spontaneously or following corticosteroids.
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Histological finding can reveal lymphocyte-rich inflammation, often with demyelination and may delay diagnosis.
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‘Sentinel lesions’ of PCNSL should be considered in this spontaneously remitting clinicoradiological syndrome.
1. Answer
Sentinel lesions in Primary CNS lymphoma.
2. Discussion
These two cases are histologically-confirmed primary central nervous system, diffuse large B cell lymphoma presenting with ‘sentinel lesions’ on MRI. Both patients had multifocal T2 hyperintensities with patchy contrast enhancement on initial MRI, which regressed spontaneously (Fig. 1) or following corticosteroids (Fig. 2) on progress imaging 3 weeks later.
Fig. 1Multifocal hyperintensities on FLAIR (A1), with patchy contrast enhancement on T1-weighted sequences (A2, A3). Progress imaging after 3 weeks demonstrated regression of some lesions and reduction in enhancement (B1, B2, B3) (arrows). Progress MRI identified new lesions with contrast enhancement (C2, C3) (arrow heads).
Fig. 2Multifocal hyperintensities on FLAIR (A1), with patchy contrast enhancement on T1-weighted sequences (A2, A3). Progress imaging after 3 weeks demonstrated regression of some lesions and reduction in enhancement (B1, B2, B3) (arrows). Progress MRI identified new lesions with contrast enhancement (C2, C3) (arrow heads).
Transient, contrast enhancing or non-enhancing ‘sentinel lesions’ have been described in PCNSL that recede spontaneously or following corticosteroids [
]. ‘Sentinel lesions’ of PCNSL should be a differential diagnosis of this spontaneously remitting clinicoradiological syndrome.
Author contributions
Sophie Waller: study concept and design, first draft, literature review. Tien Lee Ong: study concept and design, first draft, literature review. Khairul Azmi Ibrahim: data acquisition, revising manuscript and critical review of manuscript. Zariah Abdul-Aziz: data acquisition, revising manuscript and critical review of manuscript. Neil Mahant: data acquisition, revising manuscript and critical review of manuscript. Victor SC Fung: study concept and design, critical review of manuscript for intellectual content, literature review.
Study funding
No targeted funding reported.
Disclosure
The authors report no disclosures relevant to the manuscript.
Declaration of Competing Interest
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
A 46-year-old female (Fig. 1) and 32-year-old man (Fig. 2) presented with progressive cognitive decline, altered behaviour and seizure. CSF was acellular, with normal biochemistry and no abnormal cells on cytology. Limbic encephalitis and antineuronal antibody panels were negative. MRI brain was performed at presentation and repeated 3 weeks later.
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