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1.
J Neuroradiol ; 45(2): 108-113, 2018 Mar.
Article in English | MEDLINE | ID: mdl-29032126

ABSTRACT

OBJECT: Pathophysiological mechanisms underlying multiple sclerosis (MS) lesion formation, including inflammation, demyelination/remyelination and axonal damage, and their temporal evolution are still not clearly understood. To this end, three acute white matter lesions were monitored using a weekly multimodal magnetic resonance (MR) protocol. MATERIALS AND METHODS: Three untreated patients with early relapsing-remitting MS and one healthy control subject were followed weekly for two months. MR protocol included conventional MR imaging (MRI), diffusion tensor imaging (DTI), and localized MR spectroscopy (MRS), performed on the largest gadolinium-enhancing lesion, selected at the first exam. RESULTS: Mean diffusivity increased and fractional anisotropy decreased in lesions compared to healthy control. Cho/Cr ratios remained elevated in lesions throughout the follow-up. In contrast, temporal profiles of mI/Cr ratios varied between patients' lesions. For patient 1, mI/Cr ratios were already elevated at the beginning of the follow-up. Patients 2 and 3 ratios increase was delayed by two and five weeks. Blood-brain barrier (BBB) recovery occurred after three weeks. CONCLUSION: This multimodal MR follow-up highlighted the complementary role of DTI and MRS in identifying temporal relationships between BBB disruption, inflammation, and demyelination. Diffusion metrics showed high sensitivity to detect inflammatory processes. The different temporal profiles of mI suggested a potential better specificity to monitor pathological mechanisms occurring after lesion formation, such as glial proliferation and remyelination.


Subject(s)
Diffusion Tensor Imaging , Magnetic Resonance Spectroscopy , Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging , Multiple Sclerosis, Relapsing-Remitting/physiopathology , Adult , Anisotropy , Brain Chemistry , Contrast Media , Female , Humans , Image Processing, Computer-Assisted , Organometallic Compounds , Signal-To-Noise Ratio
3.
Brain Behav ; 5(2): e00307, 2015 Feb.
Article in English | MEDLINE | ID: mdl-25642392

ABSTRACT

BACKGROUND AND PURPOSE: Blood-brain barrier disruption during the earliest phases of lesion formation in multiple sclerosis (MS) patients is commonly ascribed to perivenular inflammatory activity and is usually accompanied by increased diffusivity. Reduced diffusivity has also been shown in active lesions, albeit less frequently. This study aimed to characterize the development and natural history of contrast-enhanced lesions by weekly following five relapsing remitting (RR) MS patients. MATERIALS AND METHODS: Diffusion tensor imaging (DTI), perfusion imaging, FLAIR and contrast-enhanced 3D T1-weighted MR, were weekly performed on five untreated patients recently diagnosed with RR MS. RESULTS: All five patients showed significant increases of the apparent diffusion coefficient (ADC) in the lesions compared to the first time point. One of the five patients presented 98 active lesions on ADC maps among which 36 had a volume larger than 10 mm(3). In two of these lesions, a 1 week transient decrease in ADC was detected at the time of the first gadolinium enhancement. Also, the perfusion analysis showed a concomitant increase in the relative cerebral blood volume. CONCLUSIONS: The infrequency detection of such ADC decrease in a new lesion is probably due to its very short duration. This observation may be consistent with a hyper-acute inflammatory stage concomitant with an increased reactional perfusion.


Subject(s)
Multiple Sclerosis/pathology , Adult , Blood-Brain Barrier/metabolism , Blood-Brain Barrier/pathology , Brain Diseases/metabolism , Brain Diseases/pathology , Diffusion , Female , Follow-Up Studies , Humans , Longitudinal Studies , Magnetic Resonance Imaging/methods , Male , Multiple Sclerosis/metabolism , Prospective Studies
4.
Pain ; 152(10): 2357-2364, 2011 Oct.
Article in English | MEDLINE | ID: mdl-21835547

ABSTRACT

Because diffusion tensor imaging (DTI) is able to assess tissue integrity, we used diffusion to detect abnormalities in trigeminal nerves (TGN) in patients with trigeminal neuralgia (TN) caused by neurovascular compression (NVC). We also studied anatomical TGN parameters (cross-sectional area [CSA] and volume [V]). Using DTI sequencing in a 3-T magnetic resonance imaging (MRI) scanner, we measured the fraction of anisotropy (FA) and the apparent diffusion coefficient (ADC) of TGN in 10 patients selected as candidates to have microvascular decompression (MVD) for TN, and 6 normal control subjects. We compared data between the affected nerves of TN (ipsilateral TN), unaffected nerves of TN (contralateral TN), and both nerves in normal subjects (controls), and correlated these data with CSA and V. The FA of the ipsilateral TN (0.37±0.08) was significantly lower (P<.05) compared with the contralateral TN (0.48±0.08) and control values (0.52±0.04). The ADC of ipsilateral TN (5.6±0.89 mm(2)/s) was significantly higher (P<.05) compared with the contralateral TN (4.26±0.59 mm(2)/s) and control values (3.84±0.43 mm(2)/s). Ipsilateral TN had less V and CSA compared with contralateral TN and control values (P<.05). The Spearman correlation coefficient showed a strong positive correlation between loss of FA and loss of V (r=0.7576) and loss of CSA (r=0.9273) of affected nerves. The Spearman correlation coefficient showed a strong negative correlation between increase in ADC and loss of V (r=-0.7173) and loss of CSA (r=-0.7416) in affected nerves. DTI revealed alteration in the FA and ADC values of the affected TGN. These alterations were correlated with atrophic changes in patients with TN caused by NVC.


Subject(s)
Basilar Artery/pathology , Diffusion Tensor Imaging/methods , Trigeminal Nerve/pathology , Trigeminal Neuralgia/pathology , Vertebrobasilar Insufficiency/pathology , Adult , Aged , Double-Blind Method , Female , Humans , Male , Microvascular Decompression Surgery/methods , Middle Aged , Prospective Studies , Trigeminal Nerve/blood supply , Trigeminal Neuralgia/etiology , Vertebrobasilar Insufficiency/complications
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