Background and purpose Non‐myelopathic degenerative cervical spinal cord compression (NMDC) frequently occurs throughout aging and may progress to potentially irreversible degenerative cervical myelopathy (DCM). Whereas standard clinical magnetic resonance imaging (MRI) and electrophysiological measures assess compression severity and neurological dysfunction, respectively, underlying microstructural deficits still have to be established in NMDC and DCM patients. The study aims to establish tract‐specific diffusion MRI markers of electrophysiological deficits to predict the progression of asymptomatic NMDC to symptomatic DCM. Methods High‐resolution 3 T diffusion MRI was acquired for 103 NMDC and 21 DCM patients compared to 60 healthy controls to reveal diffusion alterations and relationships between tract‐specific diffusion metrics and corresponding electrophysiological measures and compression severity. Relationship between the degree of DCM disability, assessed by the modified Japanese Orthopaedic Association scale, and tract‐specific microstructural changes in DCM patients was also explored. Results The study identified diffusion‐derived abnormalities in the gray matter, dorsal and lateral tracts congruent with trans‐synaptic degeneration and demyelination in chronic degenerative spinal cord compression with more profound alterations in DCM than NMDC. Diffusion metrics were affected in the C3‐6 area as well as above the compression level at C3 with more profound rostral deficits in DCM than NMDC. Alterations in lateral motor and dorsal sensory tracts correlated with motor and sensory evoked potentials, respectively, whereas electromyography outcomes corresponded with gray matter microstructure. DCM disability corresponded with microstructure alteration in lateral columns. Conclusions Outcomes imply the necessity of high‐resolution tract‐specific diffusion MRI for monitoring degenerative spinal pathology in longitudinal studies.
Background Central neuropathic extremity pain (CNEP) is the most frequent type of pain in multiple sclerosis (MS). The aim of the present study was to evaluate sensory and pain modulation profiles in MS patients with CNEP. Methods In a single‐centre observational study, a group of 56 CNEP MS patients was compared with 63 pain‐free MS patients and with a sex‐ and age‐adjusted control group. Standardized quantitative sensory testing (QST) and dynamic QST (dQST) protocols comprising temporal summation and conditioned pain modulation tests were used to compare sensory profiles. Results Loss‐type QST abnormalities in both thermal and mechanical QST modalities prevailed in both MS subgroups and correlated significantly with higher degree of disability expressed as Expanded Disability Status Scale (EDSS). Comparison of sensory phenotypes disclosed a higher frequency of the ‘sensory loss’ prototypic sensory phenotype in the CNEP subgroup (30%) compared with pain‐free MS patients (6%; p = .003). Conclusion The role of aging process and higher lesion load in the spinothalamocortical pathway might be possible explanation for pain development in this particular ‘deafferentation’ subtype of central neuropathic pain in MS. We were unable to support the role of central sensitization or endogenous facilitatory and inhibitory mechanisms in the development of CNEP in MS. Significance This article presents higher prevalence of the ‘sensory loss’ prototypic sensory phenotype in multiple sclerosis patients with central extremity neuropathic pain compared to pain‐free patients. Higher degree of disability underlines the possible role of higher lesion load in the somatosensory pathways in this particular ‘deafferentation’ type of central neuropathic pain.
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