Case report: Diagnostic challenge: a new multiple sclerosis "relapse" leading to the diagnosis of anaplastic astrocytoma.

Cerebral tumors and multiple sclerosis (MS) can show overlapping clinical and magnetic resonance imaging (MRI) features and even occur concurrently. Due to the emergence of new symptoms, not usually MS related, an MRI was conducted in a 29-year-old woman with relapsing-remitting MS and showed a significant size progression of a parieto-occipital lesion, with mild clinical correlates, such as blurred vision, difficulty in speaking, and headache. Contrast-enhanced MRI and fluorothymidine positron-emission tomography (PET) did not point toward neoplasm, a lesion biopsy, however, showed astrocytoma, which was confirmed as grade III astrocytoma after the radical resection of the tumor. In the case of an atypical lesion, a tumor should be considered in patients with MS. A small fraction of high-grade gliomas show no enhancement on MRI and no hypermetabolism on PET. Biopsy proved to be the essential step in a successful diagnostic workup. To the best of our knowledge, this is the first case of anaplastic astrocytoma with these radiological features reported in a patient with MS.

Continuum of sensory profiles in diabetes mellitus patients with and without neuropathy and pain.

BACKGROUND: Quantitative sensory testing (QST) assesses the functional integrity of small and large nerve fibre afferents and central somatosensory pathways; QST was assumed to provide insight into the mechanisms of neuropathy. We analysed QST profiles and phenotypes in patients with diabetes mellitus to study whether these could differentiate patients with and without pain and neuropathy. METHODS: A standardized QST protocol was performed and 'loss and gain of function' abnormalities were analysed in four groups of subjects: diabetic patients with painful (pDSPN; n = 220) and non-painful distal symmetric polyneuropathy (nDSPN; n = 219), diabetic patients without neuropathy (DM; n = 23) and healthy non-diabetic subjects (n = 37). Based on the QST findings, diabetic subjects were further stratified into four predefined prototypic phenotypes: sensory loss (SL), thermal hyperalgesia (TH), mechanical hyperalgesia (MH) and healthy individuals. RESULTS: Patients in the pDSPN group showed the greatest hyposensitivity ('loss of function'), and DM patients showed the lowest, with statistically significant increases in thermal, thermal pain, mechanical and mechanical pain sensory thresholds. Accordingly, the frequency of the SL phenotype was significantly higher in the pDSPN subgroup (41.8%), than expected (p < 0.0042). The proportion of 'gain of function' abnormalities was low in both pDSPN and nDSPN patients without significant differences. CONCLUSIONS: There is a continuum in the sensory profiles of diabetic patients, with a more pronounced sensory loss in pDSPN group probably reflecting somatosensory nerve fibre degeneration. An analysis of 'gain of function' abnormalities (allodynia, hyperalgesia) did not offer a key to understanding the pathophysiology of spontaneous diabetic peripheral neuropathic pain. SIGNIFICANCE: This article, using quantitative sensory testing profiles in large cohorts of diabetic patients with and without polyneuropathy and pain, presents a continuum in the sensory profiles of diabetic patients, with more pronounced 'loss of function' abnormalities in painful polyneuropathy patients. Painful diabetic polyneuropathy probably represents a 'more progressed' type of neuropathy with more pronounced somatosensory nerve fibre degeneration. The proportion of 'gain of function' sensory abnormalities was low, and these offer limited understanding of pathophysiological mechanisms of spontaneous neuropathic pain.

Risk factors for depression and anxiety in painful and painless diabetic polyneuropathy: A multicentre observational cross-sectional study.

BACKGROUND: Despite the high prevalence of depression and anxiety in chronic pain conditions, current knowledge concerning emotional distress among painful diabetic polyneuropathy (pDSPN) and other diabetes mellitus (DM) sufferers is limited. METHODS: This observational multicentre cohort study employed the Hospital Anxiety and Depression Scale, the Beck Depression Inventory II and the State-Trait Anxiety Inventory to assess symptoms of depression and anxiety in several groups with diabetes, as well as in a control group. The study cohort included 347 pDSPN patients aged 63.4 years (median), 55.9% males; 311 pain-free diabetic polyneuropathy (nDSPN) patients aged 63.7 years, 57.9% males; 50 diabetes mellitus (DM) patients without polyneuropathy aged 61.5 years, 44.0% males; and 71 healthy controls (HC) aged 63.0 years, 42.3% males. The roles played in emotional distress were explored in terms of the biological, the clinical (diabetes-, neuropathy- and pain-related), the socio-economic and the cognitive factors (catastrophizing). RESULTS: The study disclosed a significantly higher prevalence of the symptoms of depression and anxiety not only in pDSPN (46.7% and 60.7%, respectively), but also in patients with nDSPN (24.4% and 44.4%) and DM without polyneuropathy (22.0% and 30.0%) compared with HCs (7.0% and 14.1%, p < 0.001). Multiple regression analysis demonstrated the severity of pain and neuropathy, catastrophic thinking, type 2 DM, lower age and female sex as independent contributors to depression and anxiety. CONCLUSIONS: In addition to the severity of neuropathic pain and its cognitive processing, the severity of diabetic polyneuropathy and demographic factors are key independent contributors to emotional distress in diabetic individuals. SIGNIFICANCE: In large cohorts of well-defined painless and painful diabetic polyneuropathy patients and diabetic subjects without polyneuropathy, we found a high prevalence of the symptoms of depression and anxiety, mainly in painful individuals. We have confirmed neuropathic pain, its severity and cognitive processing (pain catastrophizing) as dominant risk factors for depression and anxiety. Furthermore, some demographic factors (lower age, female sex), type 2 diabetes mellitus and severity of diabetic polyneuropathy were newly identified as important contributors to emotional distress independent of pain.

Sensory and pain modulation profiles of ongoing central neuropathic extremity pain in multiple sclerosis.

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.

Anti-Müllerian hormone as an ovarian reserve marker in women with the most frequent muscular dystrophies.

Some muscular dystrophies may have a negative impact on fertility. A decreased ovarian reserve is 1 of the factors assumed to be involved in fertility impairment. AMH (anti-Müllerian hormone) is currently considered the best measure of ovarian reserve.A total of 21 females with myotonic dystrophy type 1 (MD1), 25 females with myotonic dystrophy type 2 (MD2), 12 females with facioscapulohumeral muscular dystrophy (FSHD), 12 female carriers of Duchenne muscular dystrophy mutations (cDMD) and 86 age-matched healthy controls of reproductive age (range 18 - 44 years) were included in this case control study. An enzymatically amplified 2-site immunoassay was used to measure serum AMH level.The MD1 group shows a significant decrease of AMH values (median 0.7 ng/mL; range 0 - 4.9 ng/mL) compared with age-matched healthy controls (P < .01). AMH levels were similar between patients and controls in terms of females with MD2 (P = .98), FSHD (P = .55) and cDMD (P = .60).This study suggests decreased ovarian reserve in women with MD1, but not in MD2, FSHD and cDMD.

Do lumbar magnetic resonance imaging changes predict neuropathic pain in patients with chronic non-specific low back pain?

The aim of this observational, cross-sectional study was to analyse lumbar magnetic resonance imaging (MRI) findings in patients with non-specific chronic low back pain (CLBP), and to evaluate any correlation with pain intensity and their capacity to predict neuropathic pain (NP) in these patients.Fifty-two patients with non-specific CLBP, between 21 and 62 years of age, 50% men, were investigated. Lumbar MRI was employed to assess disc degeneration, endplate changes, Modic changes, disc displacement, facet degeneration, foraminal stenosis and central lumbar spinal stenosis. The characteristics of pain were evaluated and patients were divided into 2 subgroups: with NP (24 patients) and without NP (28 patients), based on the results of a DN4-interview. Correlations between particular MRI changes and their relations to the intensity of pain were evaluated. Logistic regression was used to disclose predictors of NP.Lumbar spine degenerative features were frequent in patients with non-specific CLBP, with L4/5 the most affected level. A significant correlation emerged between the severity of degenerative changes in particular lumbar spine structures (correlation coefficient ranging between 0.325 and 0.573), while no correlation was found between severity of degenerative changes and pain. Multivariate logistic regression revealed only 2 independent predictors of NP - female sex (odds ratio [OR] = 11.9) and a mean pain intensity of ≥4.5 in the previous 4 weeks (OR = 13.1).Degenerative changes in the lumbar spine are frequent MRI findings, but do not correlate with the intensity of pain and do not predict NP. However, female sex and pain intensity do predict NP.

Evaluation of the Neuropathic Component of Chronic Low Back Pain.

OBJECTIVES: Assessment of neuropathic pain in chronic low back syndromes is important. However, there is currently no gold standard for its diagnosis. The aim of this observational cross-sectional study was to assess the neuropathic component of pain in various chronic low back pain syndromes using a range of diagnostic tests. MATERIALS AND METHODS: Included in this study were 63 patients with chronic axial low back pain (ALBP), 48 patients with chronic radicular syndromes (CRS) comprising 23 with discogenic compression (CDRS) and 25 with lumbar spinal stenosis (LSS), and 74 controls. PainDETECT questionnaire (PDQ), quantitative sensory testing (QST), and skin biopsy with evaluation of intraepidermal nerve fiber density (IENFD) were used to assess the neuropathic pain component. RESULTS: Positive PDQ (≥19) was obtained more frequently in patients with CDRS and LSS (26.1% and 12.0%, respectively) compared with patients with ALBP (1.6%, P<0.001). The proportion of patients with sensory loss confirmed by QST was lowest in the ALBP subgroup (23.8%) compared with CDRS (47.8%), and LSS (68.0%) subgroups (P<0.001). A reduction in IENFD was disclosed in a proportion of up to 52.0% of affected roots in patients with CRS. DISCUSSION: Neuropathic pain is quite frequent in CRS, and QST reveals sensory loss as a frequent abnormality in patients with CRS. Using a cut-off value of 19, PDQ identified a neuropathic component in a relatively low proportion of patients with CRS. CRS may be associated with a reduction in IENFD.

Sensory phenotype and risk factors for painful diabetic neuropathy: a cross-sectional observational study.

Different sensory profiles in diabetic distal symmetrical sensory-motor polyneuropathy (DSPN) may be associated with pain and the responsiveness to analgesia. We aimed to characterize sensory phenotypes of patients with painful and painless diabetic neuropathy and to assess demographic, clinical, metabolic, and electrophysiological parameters related to the presence of neuropathic pain in a large cohort of well-defined DSPN subjects. This observational cross-sectional multi-center cohort study (performed as part of the ncRNAPain EU consortium) of 232 subjects with nonpainful (n = 74) and painful (n = 158) DSPN associated with diabetes mellitus of type 1 and 2 (median age 63 years, range 21-87 years; 92 women) comprised detailed history taking, laboratory tests, neurological examination, quantitative sensory testing, nerve conduction studies, and neuropathy severity scores. All parameters were analyzed with regard to the presence and severity of neuropathic pain. Neuropathic pain was positively correlated with the severity of neuropathy and thermal hyposensitivity (P < 0.001). A minority of patients with painful DSPN (14.6%) had a sensory profile, indicating thermal hypersensitivity that was associated with less severe neuropathy. Neuropathic pain was further linked to female sex and higher cognitive appraisal of pain as assessed by the pain catastrophizing scale (P < 0.001), while parameters related to diabetes showed no influence on neuropathic pain with the exception of laboratory signs of nephropathy. This study confirms the value of comprehensive DSPN phenotyping and underlines the importance of the severity of neuropathy for the presence of pain. Different sensory phenotypes might be useful for stratification of patients with painful DSPN for analgesic treatment and drug trials.

A-waves increase the risk of developing neuropathy.

INTRODUCTION: A-waves, which are observed following the M-wave during motor nerve conduction studies (NCS), are late responses that are frequently found in many types of neurogenic disorders. However, A-waves are also common in healthy individuals, where their significance remains unclear. The aim of this study was to examine whether the occurrence of A-waves does in fact represent an increased risk for the future development of changes upon NCS or needle electromyography (EMG) in the corresponding nerve. METHODS: Nerve conduction studies/needle electromyography findings at control examination were evaluated in relation to the occurrence of initial A-waves in 327 individuals who had undergone repeated NCS/EMG examination and exhibited normal initial findings, with or without the occurrence of A-waves as the only acceptable abnormality. RESULTS: The odds ratio, which reflects the predictive power of the occurrence of A-waves at the initial testing for the development of an abnormality (neuropathy or radiculopathy) at the follow-up examination, ranged from 2.7 (p = .041) in the tibial nerve and 3.9 (p = .034) in peroneal one, to 30.0 (p = .002) in the ulnar nerve. CONCLUSIONS: A-waves constitute an initial abnormality in all nerves, and they may be predictive for the future development of broader NCS/EMG abnormalities in the corresponding nerve.