Quantitative Cervical Spinal Cord 3T Proton MR Spectroscopy in Multiple Sclerosis

Marliani, Anna Federica; Clementi, Valeria; Riccioli, L. Albini; Agati, R.; Carpenzano, M.; Salvi, Fabrizio; Leonardi, Marco

doi:10.3174/ajnr.a1738

Cited by 50 publications

(54 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A decrease in NAA levels has also been described in the spinal cord of MS patients when compared to controls; this decrease varied between 39% at the level of an acute lesion at the onset of a spinal cord relapse 24 and 21% (as ratio of NAA/total choline) in chronic spinal cord lesions. 25 Furthermore, a significant reduction in NAA concentration was found in all types of MS, 23 especially in the progressive forms 26,27 and even in patients with clinically isolated syndrome. 28 With regard to the clinical relevance of NAA, several MRS studies have described an association between reduced NAA and increased disability, as measured by the Expanded Disability Status Scale (EDSS) during an acute relapse 24,29 and in the chronic stage of the disease.…”

Section: Cns: Central Nervous Systemmentioning

confidence: 99%

The role of mitochondria in axonal degeneration and tissue repair in MS

Horssen

Witte

Ciccarelli³

2012

Mult Scler

View full text Add to dashboard Cite

Multiple sclerosis (MS) is a chronic neuroinflammatory disorder of which the aetiology and pathogenesis are still enigmatic. Most MS patients experience an episodic course of the disease, with recurrent intervals of exacerbations followed by periods of remission. The relapsing-remitting phase is characterised by massive leukocyte infiltration and extensive microglial activation in the central nervous system (CNS). Histopathological analysis of MS brain tissue reveals the presence of focal white matter lesions distributed throughout the CNS. In the initial stages (acute), MS lesions are defined by primary demyelination with abundant inflammatory infiltrates that generally consist of lymphocytes, activated microglia and macrophages, which produce vast amounts of inflammatory mediators that break down the myelin sheet, with axonal conduction block as a consequence. As a bystander effect, inflammatory mediators also mediate transection of a subset of axons. These pathological processes are thought to underlie the acute clinical symptoms that characterise an MS relapse. More advanced stages of the disease, as seen in progressive MS, are mainly characterised by widespread cortical demyelination, neuronal damage and diffuse degenerative changes throughout the CNS. Taken together, evidence is accumulating that inflammation-induced axonal damage and demyelination occur in the initial stages of the disease, and over time degenerative processes take over, eventually leading to extensive axonal loss and brain atrophy. 1 Axonal damage was already recognised by Charcot, and it is nowadays well understood that axonal damage and loss are key features of MS pathogenesis that correlate with permanent neurological deficits in MS patients. 2 Although degenerating axons are mainly observed in active demyelinating lesions and associated with the number of infiltrated macrophages, activated microglia and CD8-positive T cells, 3 axonal damage and loss are not restricted to early active lesions but also occur in more advanced stages of MS lesions. 4 The invasion of blood-borne leukocytes in the The role of mitochondria in axonal degeneration and tissue repair in MS J van Horssen 1 , ME Witte 1 and O Ciccarelli 2 Abstract Axonal injury is a key feature of multiple sclerosis (MS) pathology and is currently seen as the main correlate for permanent clinical disability. Although little is known about the pathogenetic mechanisms that drive axonal damage and loss, there is accumulating evidence highlighting the central role of mitochondrial dysfunction in axonal degeneration and associated neurodegeneration. The aim of this topical review is to provide a concise overview on the involvement of mitochondrial dysfunction in axonal damage and destruction in MS. Hereto, we will discuss putative pathological mechanisms leading to mitochondrial dysfunction and recent imaging studies performed in vivo in patients with MS. Moreover, we will focus on molecular mechanisms and novel imaging studies that address the role of mitochondrial metabolism in tiss...

show abstract

Section: Cns: Central Nervous Systemmentioning

confidence: 99%

The role of mitochondria in axonal degeneration and tissue repair in MS

Horssen

Witte

Ciccarelli³

2012

Mult Scler

View full text Add to dashboard Cite

show abstract

“…9,12,16,20,33 One of these studies published by Marliani et al 20 exhibited a proper spectral quality documented by relatively high SNR, low line width, and sample spectra. They studied 15 patients with relapsing-remitting MS with at least 1 lesion in the measurement voxel (On-line Table 2), and they compared the results with those in healthy subjects.…”

Section: Mr Spectroscopy Of the Human Spinal Cord: Clinical Studiesmentioning

confidence: 99%

“…In some investigations, the voxel dimensions are kept constant but smaller than the previously recommended size, to ensure that the voxel size fits even in subjects with a small spinal cord diameter, 9,14,19,22,29,30,33,36,37 whereas others adapt the voxel size to each individual subject. 17,18,20,21 Edden et al 26 introduced 1D…”

Section: Voxel Placementmentioning

confidence: 99%

“…1 Therefore, the water peak is usually suppressed (or reduced), for example, with chemical shift selective 43 water suppression, 3,5,9,16,[20][21][22][23]27,28 or with asymmetric variable power RF pulses with optimized relaxation delays (VAPOR). 29,30,44 In addition, Hock et al 19,30 showed that MR spectroscopy in the spinal cord is possible without water suppression by using the metabolite-cycling technique.…”

Section: Water and Fat Suppressionmentioning

confidence: 99%

See 1 more Smart Citation

¹H-MR Spectroscopy in the Human Spinal Cord

Höck

Henning

Boesiger

et al. 2012

AJNR Am J Neuroradiol

View full text Add to dashboard Cite

SUMMARY: MR spectroscopy allows insight into the chemical composition of human tissue noninvasively. Thereby it can help to better characterize pathologic processes affecting the spinal cord and may provide important clinical markers for differential diagnosis. However, due to technical challenges, it has been rarely applied to the spinal cord. The aim of this review was to summarize the technical development and clinical studies using MR spectroscopy in the spinal cord. Main challenges of applying MR spectroscopy in the spinal cord are discussed, and a description of a state-of-the-art scan protocol is given. In conclusion, MR spectroscopy is a promising tool for research and diagnosis of the spinal cord because it can provide additional information complementary to other noninvasive imaging methods. However, the application of MR spectroscopy in the spinal cord is not straightforward, and great care is required to attain optimal spectral quality.ABBREVIATIONS: CRLB ϭ Cramér-Rao lower bounds; ECG ϭ electrocardiogram; FWHM ϭ full width at half maximum; IVS ϭ inner-volume suppression; OVS ϭ

show abstract

“…Applying similar techniques to the spinal cord has been technically challenging . However, recent developments have led to applications of advanced quantitative MRI in the spinal cord in relapsing-remitting multiple sclerosis and have provided insights into underlying spinal tissue pathology Farrell et al, 2008;Marliani et al, 2010;Kearney et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Evidence for early neurodegeneration in the cervical cord of patients with primary progressive multiple sclerosis

Abdel-Aziz¹,

Schneider²,

Solanky³

et al. 2015

Brain

View full text Add to dashboard Cite

Spinal neurodegeneration is an important determinant of disability progression in patients with primary progressive multiple sclerosis. Advanced imaging techniques, such as single-voxel 1 H-magnetic resonance spectroscopy and q-space imaging, have increased pathological specificity for neurodegeneration, but are challenging to implement in the spinal cord and have yet to be applied in early primary progressive multiple sclerosis. By combining these imaging techniques with new clinical measures, which reflect spinal cord pathology more closely than conventional clinical tests, we explored the potential for spinal magnetic resonance spectroscopy and q-space imaging to detect early spinal neurodegeneration that may be responsible for clinical disability. Data from 21 patients with primary progressive multiple sclerosis within 6 years of disease onset, and 24 control subjects were analysed. Patients were clinically assessed on grip strength, vibration perception thresholds and postural stability, in addition to the Expanded Disability Status Scale, Nine Hole Peg Test, Timed 25-Foot Walk Test, Multiple Sclerosis Walking Scale-12, and Modified Ashworth Scale. All subjects underwent magnetic resonance spectroscopy and q-space imaging of the cervical cord and conventional brain and spinal magnetic resonance imaging at 3 T. Multivariate analyses and multiple regression models were used to assess the differences in imaging measures between groups and the relationship between magnetic resonance imaging measures and clinical scores, correcting for age, gender, spinal cord cross-sectional area, brain T 2 lesion volume, and brain white matter and grey matter volume fractions. Although patients did not show significant cord atrophy when compared with healthy controls, they had significantly lower total N-acetyl-aspartate (mean 4.01 versus 5.31 mmol/l, P = 0.020) and glutamate-glutamine (mean 4.65 versus 5.93 mmol/l, P = 0.043) than controls. Patients showed an increase in q-space imaging-derived indices of perpendicular diffusivity in both the whole cord and major columns compared with controls (P 5 0.05 for all indices). Lower total N-acetyl-aspartate was associated with higher disability, as assessed by the Expanded Disability Status Scale (coefficient = À 0.41, 0.01 5 P 5 0.05), Modified Ashworth Scale (coefficient = À 3.78, 0.01 5 P 5 0.05), vibration perception thresholds (coefficient = À 4.37, P = 0.021) and postural sway (P 5 0.001). Lower glutamate-glutamine predicted increased postural sway (P = 0.017). Increased perpendicular diffusivity in the whole cord and columns was associated with increased scores on the Modified Ashworth Scale, vibration perception thresholds and postural sway (P 5 0.05 in all cases). These imaging findings indicate reduced structural integrity of neurons, demyelination, and abnormalities in the glutamatergic pathways in the cervical cord of early primary progressive multiple sclerosis, in the absence of extensive spinal cord atrophy. The observed relationship between imaging measures and disa...

show abstract

Quantitative Cervical Spinal Cord 3T Proton MR Spectroscopy in Multiple Sclerosis

Cited by 50 publications

References 44 publications

The role of mitochondria in axonal degeneration and tissue repair in MS

The role of mitochondria in axonal degeneration and tissue repair in MS

¹H-MR Spectroscopy in the Human Spinal Cord

Evidence for early neurodegeneration in the cervical cord of patients with primary progressive multiple sclerosis

Contact Info

Product

Resources

About

Quantitative Cervical Spinal Cord 3T Proton MR Spectroscopy in Multiple Sclerosis

Cited by 50 publications

References 44 publications

The role of mitochondria in axonal degeneration and tissue repair in MS

The role of mitochondria in axonal degeneration and tissue repair in MS

1H-MR Spectroscopy in the Human Spinal Cord

Evidence for early neurodegeneration in the cervical cord of patients with primary progressive multiple sclerosis

Contact Info

Product

Resources

About

¹H-MR Spectroscopy in the Human Spinal Cord