Proton MRS and quantitative MRI assessment of the short term neurological response to antiretroviral therapy in AIDS

Wilkinson, Iain D.; Lunn, Sarah; Miszkiel, Katherine; Miller, R F; Paley, Martyn N.J.; Williams, Ian; Chinn, R.J.S.; Hall-Craggs, M. A.; Newman, Stanton; Kendall, B. E.; Harrison, Michael J.

doi:10.1136/jnnp.63.4.477

Cited by 55 publications

(32 citation statements)

References 24 publications

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“…The finding of no change in Cho or Cr at short TE and yet significant change in Cho/Cr at long TE may reflect such a process. 7 No significant difference was found between the mean mI levels of the patient and control groups. However, a nonsignificant trend towards higher mI level (approximately 50%) was present in the patient group (as illustrated by the prominent resonance at 3.5 ppm in fig 1C) accompanied by a higher (20%) standard deviation.…”

Section: Discussionmentioning

confidence: 81%

“…It is thought that reduced neuronal density/death can be inferred from reduction in NAA obtained at short TE and possible reversible neuronal dysfunction can be implicated when NAA signal (and hence NAA/Cho or NAA/Cr ratios) is reduced at long TE. 7 Assuming equivalent neuronal development, the significantly lower short echo time NAA signal within the gluten ataxia group is suggestive of neuronal loss. It is possible that the results are indicative of cell dysfunction as well as neuronal loss since it has been shown that a strict gluten free diet can lead to improvement of the ataxia in these patients.…”

Section: Discussionmentioning

confidence: 99%

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Cerebellar abnormalities on proton MR spectroscopy in gluten ataxia

Wilkinson

Hadjivassiliou²,

Dickson³

et al. 2005

Journal of Neurology, Neurosurgery & Psychiatry

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Gluten sensitivity can manifest with ataxia. The metabolic status of the cerebellum was investigated in 15 patients with gluten ataxia and 10 controls using proton MR spectroscopy. Significant differences were present in mean N-acetyl aspartate levels at short echo time and N-acetyl aspartate/ choline ratios at long echo time between the patient and control groups. These data support the hypothesis that cerebellar neuronal physiology differs between patients with gluten ataxia and healthy controls. G luten sensitivity can have a diverse range of clinical manifestations including enteropathy, dermatopathy, and neurological dysfunction. It is thought to result from a heightened immunological responsiveness to ingested gluten in genetically predisposed individuals. In terms of neurological dysfunction, ataxia (gluten ataxia) is the commonest neurological manifestation.1 It has been suggested that some patients with gluten ataxia have sensory rather than cerebellar ataxia because of the absence of atrophy of the cerebellum on magnetic resonance imaging (MRI) in 40% of patients. 2In vivo proton MR spectroscopy has been applied to study the classification and pathophysiology of various neurological conditions including neoplasms, viral and retroviral infections, ischaemia, demyelination, the epilepsies and some of the dementias.3 4 Often thought of as an adjunct to standard MRI in the clinical setting, proton spectroscopy can yield information about neuronal physiology, overall energy state, membrane turnover, and glial cell status. In the present study, we investigated the cerebellar metabolic status of patients with gluten ataxia assessed by proton MR spectroscopy. PATIENTS AND METHODSThe patient group consisted of 15 patients (six men, nine women; mean age 61 years (range 37-82)) with gluten ataxia (sporadic ataxia with positive antigliadin antibodies) recruited consecutively from the gluten/neurology clinic based at the Royal Hallamshire Hospital, Sheffield. The clinical characteristics of these patients did not differ from those of 68 patients with gluten ataxia described previously. 5 An age matched control group consisted of 10 healthy volunteers (three men, seven women; mean age 60 years (range 31-75)). The protocol was approved by the South Sheffield Research Ethics Committee, and all subjects provided informed, written consent. All MR data were acquired on a 1.5 T clinical system (Eclipse, Philips Medical Systems, Cleveland, USA) that utilised a standard quadrature radiofrequency transmit/receive head coil.Two sets of images were acquired with a total imaging time of 18 minutes. A dual echo, fast spin echo technique (TE = 15 and 75 ms; TR = 8040 ms; echo train length = 4 and 4; ave = 1) was used to acquire high resolution, proton density and T2-weighted images in the transverse plane (acquisition matrix = 2566256; field of view = 230 mm; 60 contiguous 2.5 mm thick slices). A T1-weighted volume dataset with isotropic 1 mm 3 voxel resolution was acquired using a three dimensional, radiofrequency spoiled fast a...

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Section: Discussionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Cerebellar abnormalities on proton MR spectroscopy in gluten ataxia

Wilkinson

Hadjivassiliou²,

Dickson³

et al. 2005

Journal of Neurology, Neurosurgery & Psychiatry

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show abstract

“…Immunohistochemical studies have suggested that NAA, the major constituent of the N-acetyl group resonance at long echo time (TE), is localized exclusively in neurons and their processes throughout the CNS [59][60][61]. In vivo cerebral NAA determined using H-MRS has been shown to correlate with histologic neuronal density in a variety of animal models [62]. It is also used as a surrogate neuronal marker for the assessment of neuroprotective therapeutic compounds/ strategies in humans [63].…”

Section: Brain Mr Spectroscopy In Dpnmentioning

confidence: 99%

Central Nervous System Involvement in Diabetic Neuropathy

et al. 2011

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Diabetic neuropathy is a chronic and often disabling condition that affects a significant number of individuals with diabetes. Long considered a disease of the peripheral nervous system, there is now increasing evidence of central nervous system involvement. Recent advances in neuroimaging methods detailed in this review have led to a better understanding and refinement of how diabetic neuropathy affects the central nervous system. Recognition that diabetic neuropathy is, in part, a disease that affects the whole nervous system is resulting in a critical rethinking of this disorder, opening a new direction for further research.

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“…As with imaging, spectra acquired at short TE and long TR are proton density-weighted and thus reflect metabolite concentration, whereas spectra acquired at long TE are T2-weighted, influenced by both concentration and individual metabolite T2. 19 In terms of the results of this study, the former implies no change in creatine concentration, whereas the latter implies no change in molecular environment (as this influences the metabolite's T2) within the cohort's frontal lobe white matter following dietary creatine augmentation. Accordingly, the results of this study (particularly those obtained at short TE) appear to contradict the findings of Dechent et al, 20 who report regional changes in the increase of the creatine pool over several weeks using a similar short echo time spectroscopic acquisition protocol at 2.0 T. The authors detail increases in creatine within deep gray matter (thalamus), cortical gray matter, deep white matter (parieto-occipital), and central cerebellum (P , 0.05).…”

Section: Discussionmentioning

confidence: 94%