Thalamic Lesions: A Radiological Review

Renard, Dimitri; Castelnovo, Giovanni; Campello, Chantal; Bouly, S.; Floch, Anne Le; Thouvenot, Éric; Waconge, Anne; Taïeb, Guillaume

doi:10.1155/2014/154631

Cited by 40 publications

(51 citation statements)

References 21 publications

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“…However, blood brain barrier disruption in cortex and deep GM is uncommonly observed in MS using contrast-enhanced MRI 10,11 , and all patients were stable in terms of clinical relapses and MS-related treatments, suggesting that microglia/macrophages activation likely, largely reflected chronic inflammation, especially in SPMS.…”

Section: Discussionmentioning

confidence: 95%

Neuroinflammatory component of gray matter pathology in multiple sclerosis

Herranz

Giannì

Louapre

et al. 2016

Annals of Neurology

167

182

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Objective In multiple sclerosis (MS), using simultaneous magnetic resonance-positron emission tomography (MR-PET) imaging with 11C-PBR28, we quantified expression of the 18kDa translocator protein (TSPO), a marker of activated microglia/macrophages, in cortex, cortical lesions, deep gray matter (GM), white matter (WM) lesions and normal-appearing WM (NAWM) to investigate the in vivo pathological and clinical relevance of neuroinflammation. Methods Fifteen secondary-progressive MS (SPMS) and 12 relapsing-remitting MS (RRMS) cases, and 14 matched healthy controls underwent 11C-PBR28 MR-PET. MS subjects underwent 7 Tesla T2*-weighted imaging for cortical lesions segmentation; neurological and cognitive evaluation. 11C-PBR28 binding was measured using normalized 60-90-minutes standardized uptake values and volume of distribution ratios. Results Relative to controls, MS subjects exhibited abnormally high 11C-PBR28 binding across the brain, the greatest increases being in cortex and cortical lesions, thalamus, hippocampus, and NAWM. MS WM lesions showed relatively modest TSPO increases. With the exception of cortical lesions, where TSPO expression was similar, 11C-PBR28 uptake across the brain was greater in SPMS than in RRMS. In MS, increased 11C-PBR28 binding in cortex, deep GM, and NAWM correlated with neurological disability and impaired cognitive performance; cortical thinning correlated with increased thalamic TSPO levels. Interpretation In MS, neuroinflammation is present in the cortex, cortical lesions, deep GM, and NAWM, and closely linked to poor clinical outcome and, at least partly, to neurodegeneration. Distinct inflammatory-mediated factors may underlie accumulation of cortical and WM lesions. Quantification of TSPO levels in MS could prove a sensitive tool for evaluating in vivo the inflammatory component of GM pathology, particularly in cortical lesions.

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Section: Discussionmentioning

confidence: 95%

Neuroinflammatory component of gray matter pathology in multiple sclerosis

Herranz

Giannì

Louapre

et al. 2016

Annals of Neurology

167

182

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“…17 In particular, T1WI hyperintensity in the pulvinar has also been described in patients who received chemotherapy/radiation therapy, in patients with neurofibromatosis type 1, and in subjects with Fahr disease or disturbances of the calcium-phosphorus metabolism or even laminar necrosis. [36][37][38] To date, the real pathogenesis of the PS in FD is still unclear. The most reliable hypothesis is the development of subtle dystrophic calcification, confirmed by CT brain scans, probably related to chronic hypoperfusion secondary to microvascular alterations.…”

Section: Discussionmentioning

confidence: 99%

Redefining the Pulvinar Sign in Fabry Disease

Cocozza

Russo

Pisani

et al. 2017

AJNR Am J Neuroradiol

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“…Ischemic stroke is cited as a complication of antiangiogenic therapy (3). Basal ganglia and, rarely, thalamic calcifications have been described after both radio-and chemotherapy (4).…”

Section: Central Nervous System Lesions After Cancer Treatmentmentioning

confidence: 99%

Migrainous Headache and Gliotic Thalamic Lesion after Treated Neuroblastoma in Childhood

Nita¹,

Teleanu²,

Epure³

et al. 2019

Ro J Neurol.

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Objective. This article aims to bring into attention the challenges of diagnosing a case of migraine in a child with a history of neuroblastoma and an associated finding of gliotic thalamic lesion on the cerebral MRI. Materials and methods. The patient underwent a thorough neurological examination, followed by paraclinical tests: blood workup, cerebral MRI with TOF (time-of-flight) angiography, electroencephalogram (EEG), carotid and vertebral arterial Doppler examination, trancranial Doppler examination, cardiac and abdominal ultrasounds, psychological evaluation. results. The neurological examination was normal, except for right sided post-surgical Claude Bernard-Horner's syndrome. His blood workup, ultrasounds, EEG, as well as vascular and transcranial Doppler examinations were within normal limits. His cerebral MRI showed a right anterior thalamic ischemic gliotic lesion. Discussions. Neuroblastoma is a common tumor in childhood and its treatment involves surgery, chemotherapy and radiotherapy. A patient with a history of neuroblastoma who has new onset headache has to be evaluated for a possible connection to his pathological background and to the treatment associated with it. A new malignancy and long term side effects of radiotherapy or chemotherapy must be taken into consideration. conclusions. The headache episodes were considered as migraine without aura. The article aims to bring into attention the difficulties of diagnosing migraine in children, especially in patients with a neurological history.

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Thalamic Lesions: A Radiological Review

Cited by 40 publications

References 21 publications

Neuroinflammatory component of gray matter pathology in multiple sclerosis

Neuroinflammatory component of gray matter pathology in multiple sclerosis

Redefining the Pulvinar Sign in Fabry Disease

Migrainous Headache and Gliotic Thalamic Lesion after Treated Neuroblastoma in Childhood

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