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Neuroimaging Applications in Restless Legs Syndrome.
Rizzo, G, Plazzi, G
International review of neurobiology. 2018;:31-64
Abstract
Neuroimaging studies provide information useful to understand the pathophysiology of restless legs syndrome. Molecular PET and SPECT imaging findings mainly supported dysfunction of dopaminergic pathways involving not only the nigrostriatal but also mesolimbic pathways. Magnetic resonance imaging (MRI) studies have used different techniques. Studies using iron-sensitive sequences supported the presence of a regionally variable low brain iron content, mainly at the level of substantia nigra and thalamus. The search for brain structural or microstructural abnormalities by voxel-based morphometry, diffusion tensor imaging or cortical thickness analysis has reported none or variable findings in restless legs syndrome patients, most of them in regions belonging to sensorimotor and limbic/nociceptive networks. Functional MRI studies have substantially demonstrated activation or connectivity changes in the same networks. Magnetic resonance spectroscopy studies showed metabolic changes in the thalamus, which is a hub of these networks. In summary, neuroimaging findings in restless legs syndrome support the presence of reduction of brain iron content, of dysfunction of mesolimbic and nigrostriatal dopaminergic pathways, and of abnormalities at level of limbic/nociceptive and sensorimotor networks.
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2.
A Magnetic Resonance Spectroscopy Study of Lovastatin for Treating Bipolar Mood Disorder: A 4-Week Randomized Double-Blind, Placebo- Controlled Clinical Trial.
Lotfi, M, Shafiee, S, Ghanizadeh, A, Sigaroudi, MO, Razeghian, L
Recent patents on inflammation & allergy drug discovery. 2017;(2):133-141
Abstract
BACKGROUND No trial has examined the effect of lovastatin on the brain metabolites in patients with bipolar mood disorder. OBJECTIVES Current medications for treating bipolar disorders cause metabolic syndrome. It is supposed that lovastatin not only decreases the rate of metabolic syndrome but also impacts some brain metabolites and their ratio like common treatments that are measured by Magnetic Resonance Spectroscopy. METHODS 27 Manic phase patients were randomly allocated into two groups, lovastatin and placebo as their adjuant medication. Clinical symptoms were assessed at baseline, weeks 2, 4. The brain metabolites were measured at baseline and week 4. RESULT Regarding the change of clinical symptoms, no significant difference was found between two groups. However, lovastatin significantly increased the level of NAA in cingulate gyrus in comparison to the placebo group. Moreover, lovastatin more than placebo increased creatine in the left basal ganglia. Furthermore, choline/ creatine showed a significant decrease in the left basal ganglia in lovastatin group. CONCLUSION Using MRS after treating with lovastatin showed lovastatin increases NAA in cingulate gyrus, indicating the possible effect of NAA for increasing the reduced viable neuron. Moreover, the increment of Cr by lovastatin in the left basal ganglia suggests the role of lovastatin for maintaining energy homeostasis, anti-apoptotic activity and ATP production in bipolar disorder. Some patents using lovastatin as an adjuant therapy for treating bipolar patients and depression in MDD patients are also outlined. This trial was registered in the Iranian Clinical Trials Registry (http://www.irct.ir/) (IRCT201302203930N18).
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3.
High field MR imaging and 1H-MR spectroscopy in clinically isolated syndromes suggestive of multiple sclerosis: correlation between metabolic alterations and diagnostic MR imaging criteria.
Wattjes, MP, Harzheim, M, Lutterbey, GG, Bogdanow, M, Schild, HH, Träber, F
Journal of neurology. 2008;(1):56-63
Abstract
PURPOSE To prospectively investigate metabolic changes in the normal-appearing white matter (NAWM) of patients presenting with clinically isolated syndromes (CIS) suggestive of multiple sclerosis (MS) and to correlate these changes to conventional MR imaging findings in terms of MR imaging criteria. MATERIALS AND METHODS Multisequence MR imaging of the brain and (1)H-MR spectroscopy of the parietal NAWM were performed in 31 patients presenting with CIS and in 20 controls using a 3. 0 T MR system. MR imaging criteria and International Panel criteria were assessed based on imaging, clinical and paraclinical results. Metabolite ratios and absolute concentrations of N-acetyl-aspartate (tNAA), myoinositol (Ins), choline (Cho), and total creatine (tCr) were determined. The metabolite concentrations were correlated with the fulfilled MR imaging criteria. RESULTS In comparison to the control group, the CIS group showed significantly decreased mean tNAA concentrations (-8. 1%, p = 0. 012). Significant changes could not be detected regarding Ins, tCr and Cho. No significant correlations between absolute metabolite concentrations and MR imaging criteria were observed. Patients with and without a lesion dissemination in space showed no significant differences of their metabolite concentrations. CONCLUSION As assessed by (1)H-MRS a significant axonal damage already occurs during the first demyelinating episode in patients with CIS. Conventional MR imaging in terms of diagnostic imaging criteria does not significantly reflect NAWM disease activity in terms of metabolic alterations detected by (1)H-MR spectroscopy.
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4.
1H NMR metabonomics of plasma lipoprotein subclasses: elucidation of metabolic clustering by self-organising maps.
Suna, T, Salminen, A, Soininen, P, Laatikainen, R, Ingman, P, Mäkelä, S, Savolainen, MJ, Hannuksela, ML, Jauhiainen, M, Taskinen, MR, et al
NMR in biomedicine. 2007;(7):658-72
Abstract
(1)H NMR spectra of plasma are known to provide specific information on lipoprotein subclasses in the form of complex overlapping resonances. A combination of (1)H NMR and self-organising map (SOM) analysis was applied to investigate if automated characterisation of subclass-related metabolic interactions can be achieved. To reliably assess the intrinsic capability of (1)H NMR for resolving lipoprotein subclass profiles, sum spectra representing the pure lipoprotein subclass part of actual plasma were simulated with the aid of experimentally derived model signals for 11 distinct lipoprotein subclasses. Two biochemically characteristic categories of spectra, representing normolipidaemic and metabolic syndrome status, were generated with corresponding lipoprotein subclass profiles. A set of spectra representing a metabolic pathway between the two categories was also generated. The SOM analysis, based solely on the aliphatic resonances of these simulated spectra, clearly revealed the lipoprotein subclass profiles and their changes. Comparable SOM analysis in a group of 69 experimental (1)H NMR spectra of serum samples, which according to biochemical analyses represented a wide range of lipoprotein lipid concentrations, corroborated the findings based on the simulated data. Interestingly, the choline-N(CH(3))(3) region seems to provide more resolved clustering of lipoprotein subclasses in the SOM analyses than the methyl-CH(3) region commonly used for subclass quantification. The results illustrate the inherent suitability of (1)H NMR metabonomics for automated studies of lipoprotein subclass-related metabolism and demonstrate the power of SOM analysis in an extensive and representative case of (1)H NMR metabonomics.
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5.
Creatine has no beneficial effect on skeletal muscle energy metabolism in patients with single mitochondrial DNA deletions: a placebo-controlled, double-blind 31P-MRS crossover study.
Kornblum, C, Schröder, R, Müller, K, Vorgerd, M, Eggers, J, Bogdanow, M, Papassotiropoulos, A, Fabian, K, Klockgether, T, Zange, J
European journal of neurology. 2005;(4):300-9
Abstract
The purpose of our randomized, double-blind, placebo-controlled crossover study in 15 patients with chronic progressive external ophthalmoplegia (CPEO) or Kearns-Sayre syndrome (KSS) because of single large-scale mitochondrial (mt) DNA deletions was to determine whether oral creatine (Cr) monohydrate can improve skeletal muscle energy metabolism in vivo. Each treatment phase with Cr in a dosage of 150 mg/kg body weight/day or placebo lasted 6 weeks. The effect of Cr was estimated by phosphorus-31 magnetic resonance spectroscopy ((31)P-MRS), clinical and laboratory tests. (31)P-MRS analysis prior to treatment showed clear evidence of severe mitochondrial dysfunction. However, there were no relevant changes in (31)P-MRS parameters under Cr. In particular, phosphocreatine (PCr)/ATP at rest did not increase, and there was no facilitation of post-exercise PCr recovery. Clinical scores and laboratory tests did not alter significantly under Cr, which was tolerated without major side-effects in all patients. Cr supplementation did not improve skeletal muscle oxidative phosphorylation in our series of patients. However, one explanation for our negative findings may be the short study duration or the limited number of patients included.