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1,337 results for “Neuropathy”
Data from: The genetic landscape of axonal neuropathies in the middle aged and elderly: focus on MME (supplementary information)
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Large mitochondrial DNA deletions in HIV sensory neuropathy
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Nerve ultrasound for diagnosing chronic inflammatory neuropathy: a multicenter validation study
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Nerve ultrasound improves detection of treatment-responsive chronic inflammatory neuropathies
<p><b>Objective</b></p> <p>To examine the diagnostic accuracy of nerve ultrasound in a prospective cohort of consecutive patients with a clinical suspicion of chronic inflammatory neuropathies, including chronic inflammatory demyelinating polyneuropathy, Lewis Sumner syndrome and multifocal motor neuropathy, and to determine the added value in the detection of treatment-responsive patients.</p> <p><b>Methods</b></p> <p>Between February 2015 and July 2018, we included 100 consecutive incident patients with a clinical suspicion of chronic inflammatory neuropathy. All patients underwent nerve ultrasound, extensive standardized nerve conduction studies (NCS) and other relevant diagnostic investigations. We evaluated treatment response using predefined criteria. A diagnosis of chronic inflammatory neuropathy was established when NCS were abnormal (fulfilling criteria of demyelination of the EFNS/PNS) or when the degree of nerve enlargement detected by sonography was compatible with chronic inflammatory neuropathy and there was response to treatment.</p> <p><b>Results</b></p> <p>A diagnosis of chronic inflammatory neuropathy was established in 38 patients. Sensitivity and specificity of nerve ultrasound and NCS were 97.4% and 69.4%, and 78.9% and 93.5%, respectively. The added value of nerve ultrasound in detection of treatment-responsive chronic inflammatory neuropathy patients was 21.1% compared to NCS alone.</p> <p><b>Conclusions</b></p> <p>Nerve ultrasound and NCS are complementary techniques with superior sensitivity in the former and specificity in the latter. Addition of nerve ultrasound significantly improves the detection of chronic inflammatory neuropathies. Therefore, it deserves a prominent place in the diagnostic workup of chronic inflammatory neuropathies.</p> <p><b>Classification of Evidence</b></p> <p>This study provides Class I evidence that nerve ultrasound is an accurate diagnostic tool to detect chronic inflammatory neuropathies.</p>
Data from: Impact of genetic reduction of NMNAT2 on chemotherapy-induced losses in cell viability in vitro and peripheral neuropathy in vivo
Nicotinamide mononucleotide adenylyl transferases (NMNATs) are essential neuronal maintenance factors postulated to preserve neuronal function and protect against axonal degeneration in various neurodegenerative disease states. We used in vitro and in vivo approaches to assess the impact of NMNAT2 reduction on cellular and physiological functions induced by treatment with a vinca alkaloid (vincristine) and a taxane-based (paclitaxel) chemotherapeutic agent. NMNAT2 null (NMNAT2-/-) mutant mice die at birth and cannot be used to probe functions of NMNAT2 in adult animals. Nonetheless, primary cortical cultures derived from NMNAT2-/- embryos showed reduced cell viability in response to either vincristine or paclitaxel treatment whereas those derived from NMNAT2 heterozygous (NMNAT2+/-) mice were preferentially sensitive to vincristine-induced degeneration. Adult NMNAT2+/- mice, which survive to adulthood, exhibited a 50% reduction of NMNAT2 protein levels in dorsal root ganglia relative to wildtype (WT) mice with no change in levels of other NMNAT isoforms (NMNAT1 or NMNAT3), NMNAT enzyme activity (i.e. NAD/NADH levels) or microtubule associated protein-2 (MAP2) or neurofilament protein levels. We therefore compared the impact of NMNAT2 knockdown on the development and maintenance of chemotherapy-induced peripheral neuropathy induced by vincristine and paclitaxel treatment using NMNAT2+/- and WT mice. NMNAT2+/- did not differ from WT mice in either the development or maintenance of either mechanical or cold allodynia induced by either vincristine or paclitaxel treatment. Intradermal injection of capsaicin, the pungent ingredient in hot chili peppers, produced equivalent hypersensitivity in NMNAT2+/- and WT mice receiving vehicle in lieu of paclitaxel. Capsaicin-evoked hypersensitivity was enhanced by prior paclitaxel treatment but did not differ in either NMNAT2+/- or WT mice. Thus, capsaicin failed to unmask differences in nociceptive behaviors in either paclitaxel-treated or paclitaxel-untreated NMNAT2+/- and WT mice. Moreover, no differences in motor behavior were detected between genotypes in the rotarod test. Our studies do not preclude the possibility that complete knockout of NMNAT2 in a conditional knockout animal could unmask a role for NMNAT2 in protection against detrimental effects of chemotherapeutic treatment.
Data from: Metabolite profile of a mouse model of Charcot-Marie-Tooth type 2D neuropathy: implications for disease mechanisms and interventions
Charcot-Marie-Tooth disease encompasses a genetically heterogeneous class of heritable polyneuropathies that result in axonal degeneration in the peripheral nervous system. Charcot-Marie-Tooth type 2D neuropathy (CMT2D) is caused by dominant mutations in glycyl tRNA synthetase (GARS). Mutations in the mouse Gars gene result in a genetically and phenotypically valid animal model of CMT2D. How mutations in GARS lead to peripheral neuropathy remains controversial. To identify putative disease mechanisms, we compared metabolites isolated from the spinal cord of Gars mutant mice and their littermate controls. A profile of altered metabolites that distinguish the affected and unaffected tissue was determined. Ascorbic acid was decreased fourfold in the spinal cord of CMT2D mice, but was not altered in serum. Carnitine and its derivatives were also significantly reduced in spinal cord tissue of mutant mice, whereas glycine was elevated. Dietary supplementation with acetyl-L-carnitine improved gross motor performance of CMT2D mice, but neither acetyl-L-carnitine nor glycine supplementation altered the parameters directly assessing neuropathy. Other metabolite changes suggestive of liver and kidney dysfunction in the CMT2D mice were validated using clinical blood chemistry. These effects were not secondary to the neuromuscular phenotype, as determined by comparison with another, genetically unrelated mouse strain with similar neuromuscular dysfunction. However, these changes do not seem to be causative or consistent metabolites of CMT2D, because they were not observed in a second mouse Gars allele or in serum samples from CMT2D patients. Therefore, the metabolite 'fingerprint' we have identified for CMT2D improves our understanding of cellular biochemical changes associated with GARS mutations, but identification of efficacious treatment strategies and elucidation of the disease mechanism will require additional studies.
COMPARATIVE EVALUATION OF COMPLICATIONS OF DIABETES MELLITUS - NEUROPATHY AND ANGIOPATHY
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Figure 1 from: Hristov M, Sabit Z, Kirilov T, Bakalov D, Tzoneva R, Apostolova S, Georgieva I, Andreeva-Gateva P (2024) Effects of riboflavin on hyperalgesia and serum glutamine-to-glutamate ratio in rats with painful diabetic neuropathy. Pharmacia 71: 1-7. https://doi.org/10.3897/pharmacia.71.e120921
Figure 1 Effects of riboflavin on changes in pain threshold were investigated using the paw pressure test. Streptozotocin administration significantly induced mechanical hyperalgesia by reducing the mechanical threshold and enhancing paw withdrawal responses, while supplementation with Vitamin B2 effectively mitigated mechanical hyperalgesia. Significant differences compared to the control group (Normal) are denoted as *P < 0.05, while significant differences compared to the diabetic group (Diabetic) are denoted as ##P < 0.01. n=8 animals per group.
Figure 3 from: Hristov M, Sabit Z, Kirilov T, Bakalov D, Tzoneva R, Apostolova S, Georgieva I, Andreeva-Gateva P (2024) Effects of riboflavin on hyperalgesia and serum glutamine-to-glutamate ratio in rats with painful diabetic neuropathy. Pharmacia 71: 1-7. https://doi.org/10.3897/pharmacia.71.e120921
Figure 3 Effects of riboflavin on changes in pain threshold were investigated using the formalin test. The ends of the boxes depict the 25th and 75th percentiles, with a line at the median, while error bars extend to the 10th and 90th percentiles. During phase 1 of the formalin test, neither the vehicle-treated diabetic group nor the introduction of riboflavin showed significant changes in nociceptive behavior compared to the control group. In phase 2, the vehicle-treated diabetic group exhibited increased nociceptive behavior, while the addition of 25 mg or 50 mg of vitamin B2 significantly alleviated formalin-induced hyperalgesia. Significant differences compared to the control group (Normal) are indicated as *P < 0.05. Significant differences compared to the diabetic group (Diabetic) are indicated as #P < 0.05. n=8 animals per group.
Figure 2 from: Hristov M, Sabit Z, Kirilov T, Bakalov D, Tzoneva R, Apostolova S, Georgieva I, Andreeva-Gateva P (2024) Effects of riboflavin on hyperalgesia and serum glutamine-to-glutamate ratio in rats with painful diabetic neuropathy. Pharmacia 71: 1-7. https://doi.org/10.3897/pharmacia.71.e120921
Figure 2 Effects of riboflavin on changes in pain threshold were investigated using the cold plate. Streptozotocin administration induced significant cold-induced hyperalgesia, alleviated notably by riboflavin in drinking water. Significant differences compared to the control group (Normal) are indicated as ***P < 0.001. Significant differences compared to the diabetic group (Diabetic) are indicated as #P < 0.05 and ###P < 0.001. n=8 animals per group.
Figure 4 from: Hristov M, Sabit Z, Kirilov T, Bakalov D, Tzoneva R, Apostolova S, Georgieva I, Andreeva-Gateva P (2024) Effects of riboflavin on hyperalgesia and serum glutamine-to-glutamate ratio in rats with painful diabetic neuropathy. Pharmacia 71: 1-7. https://doi.org/10.3897/pharmacia.71.e120921
Figure 4 Box plot illustrating the effect of riboflavin supplementation on the serum glutamine-to-glutamate ratio in diabetic rats. The ends of the boxes depict the 25th and 75th percentiles, with a line at the median, while error bars extend to the 10th and 90th percentiles. Riboflavin supplementation in the drinking water significantly altered the serum glutamine-to-glutamate ratio in diabetic rats with neuropathic pain, with a significant difference found only between the "Diabetic" and "Diabetic + Rf 50 mg" groups. Significant differences compared to the diabetic group (Diabetic) are indicated as *p < 0.05. n=8 animals per group.
COMPARATIVE EVALUATION OF COMPLICATIONS OF DIABETES MELLITUS - NEUROPATHY AND ANGIOPATHY.
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Utility of standard diffusion-weighted magnetic resonance imaging for the identification of ischemic optic neuropathy in giant cell arteritis
<p><span>Purpose: To assess diffusion abnormalities of the optic nerve (ON) in giant cell arteritis (GCA) patients with acute onset of visual impairment (VI) using diffusion-weighted magnetic resonance imaging (DWI).</span></p> <p><span>Methods: DWI scans of GCA patients with acute VI were evaluated in a case-control study. Two blinded neuroradiologists assessed randomized DWI scans of GCA and controls for ON restricted diffusion. Statistical quality criteria and inter-rater reliability (IRR) were calculated. DWI findings were compared to ophthalmological assessments.</span></p> <p><span>Results: 35 GCA patients (76.2 ± 6.4 years; 37 scans) and 35 controls (75.7±7.6 years; 38 scans) were included. ON restricted diffusion was detected in 81.1% (Reader 1) of GCA scans. Localization of ON restricted diffusion was at the optic nerve head in 80.6%, intraorbital in 11.1% and affecting both segments in 8.3%. DWI discerned affected from unaffected ON with a sensitivity, specificity, positive and negative predictive value of 87%/99%/96%/96%. IRR for ON restricted diffusion was κ<sub>inter </sub>= 0.72 (95% CI 0.59‑0.86). DWI findings challenged ophthalmologic diagnoses in 4 cases (11.4%).</span></p> <p><span>Conclusions: DWI visualizes anterior and posterior ON ischemia in GCA patients with high sensitivity and specificity, as well as substantial inter-rater reliability. DWI may complement the ophthalmological assessment in patients with acute VI.</span></p>
Extension of Phase 3 Gene Therapy for Painful Diabetic Neuropathy
ClinicalTrials.gov study NCT04055090. IPD Sharing: NO. Countries: 1. Publications: 0.
A Study to Evaluate the Efficacy, Safety, and Tolerability of Tapentadol ER Compared With Placebo in Patients With Chronic, Painful Diabetic Peripheral Neuropathy
ClinicalTrials.gov study NCT01041859. IPD Sharing: Not stated. Countries: 3. Publications: 0.
A Post Market Cohort With the Spinal Modulation Neurostimulator System in Peripheral Neuropathy
ClinicalTrials.gov study NCT02349646. IPD Sharing: Not stated. Countries: 1. Publications: 0.
The Effect of Yoga on Nerve Pain Caused by Chemotherapy (Chemotherapy-Induced Peripheral Neuropathy)
ClinicalTrials.gov study NCT05121558. IPD Sharing: YES. Countries: 1. Publications: 0.
Ricolinostat in Patients With Painful Diabetic Peripheral Neuropathy
ClinicalTrials.gov study NCT03176472. IPD Sharing: NO. Countries: 1. Publications: 0.
Diabetic Neuropathy Rapid Screening Test in Turkish Patients With Type 2 Diabetes: Sudoscan
ClinicalTrials.gov study NCT05299918. IPD Sharing: Not stated. Countries: 0. Publications: 10.
Acupuncture for Chemo-Induced Peripheral Neuropathy in Multiple Myeloma Patients
ClinicalTrials.gov study NCT04770402. IPD Sharing: NO. Countries: 1. Publications: 0.
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Allen Brain Atlas
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Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
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The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
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