Background and purpose: Measurement of the cross‐sectional area (CSA) of peripheral nerves using ultrasound is useful in the evaluation of focal lesions like entrapment syndromes and inflammatory polyneuropathies. Here, a systematic review and meta‐analysis of published CSA reference values for upper extremity nerves was performed.Methods: Available to date nerve ultrasound studies on healthy adults were included and a meta‐analysis for CSA was provided of the following nerves: median nerve at the wrist, forearm, upper arm; ulnar nerve at the Guyon's canal, forearm, elbow, upper arm; radial nerve at the upper arm. Regression and correlation analyses for age, gender, height, weight, geographic continents and publication year are reported.Results: Seventy‐four studies with 4186 healthy volunteers (mean age 42.7 years) and 18,226 examined nerve sites were included. The calculated mean pooled CSA of the median nerve at the wrist was 8.3 mm² (95% confidence interval [95% CI] 7.9–8.7, n = 4071), at the forearm 6.4 mm² (95% CI 5.9–6.9, n = 3021), at the upper arm 8.3 mm² (95% CI 7.5–9.0, n = 1388), of the ulnar nerve at the Guyon's canal 4.1 mm² (95% CI 3.6–4.6, n = 1688), at the forearm 5.2 mm² (95% CI 4.8–5.7, n = 1983), at the elbow 5.9 mm² (95% CI 5.4–6.5, n = 2551), at the upper arm 6.6 mm² (95% CI 5.1–6.1, n = 1737) and of the radial nerve 5.1 mm² (95% CI 4.0–6.2, n = 1787). Substantial heterogeneity across studies (I² > 50%) was found only for the radial nerve. Subgroup analysis revealed a positive effect of age for the median nerve at the wrist and for height and weight for different sites of the ulnar nerve.Conclusion: The first meta‐analysis on CSA reference values for the upper extremities with no or only low heterogeneity of reported CSA values in most nerve sites is provided. Our data facilitate the goal of an international standardized evaluation protocol.

In inflammatory neuropathies, oxidative stress results in neuronal and Schwann cell (SC) death promoting early neurodegeneration and clinical disability. Treatment with the short-chain fatty acid propionate showed a significant immunoregulatory and neuroprotective effect in multiple sclerosis patients. Similar effects have been described for patients with chronic inflammatory demyelinating polyneuropathy (CIDP). Therefore, Schwann cell’s survival and dorsal root ganglia (DRG) outgrowth were evaluated in vitro after propionate treatment and application of H2O2 or S-nitroso-N-acetyl-D-L-penicillamine (SNAP) to evaluate neuroprotection. In addition, DRG resistance was evaluated by the application of oxidative stress by SNAP ex vivo after in vivo propionate treatment. Propionate treatment secondary to SNAP application on DRG served as a neuroregeneration model. Histone acetylation as well as expression of the free fatty acid receptor (FFAR) 2 and 3, histone deacetylases, neuroregeneration markers, and antioxidative mediators were investigated. β-hydroxybutyrate was used as a second FFAR3 ligand, and pertussis toxin was used as an FFAR3 antagonist. FFAR3, but not FFAR2, expression was evident on SC and DRG. Propionate-mediated activation of FFAR3 and histone 3 hyperacetylation resulted in increased catalase expression and increased resistance to oxidative stress. In addition, propionate treatment resulted in enhanced neuroregeneration with concomitant growth-associated protein 43 expression. We were able to demonstrate an antioxidative and neuroregenerative effect of propionate on SC and DRG mediated by FFAR3-induced histone acetylases expression. Our results describe a pathway to achieve neuroprotection/neuroregeneration relevant for patients with immune-mediated neuropathies.

Background and purpose: Measurement of the cross‐sectional area (CSA) of peripheral nerves using ultrasound is useful in the evaluation of focal lesions such as entrapment syndromes and inflammatory polyneuropathies. We performed a systematic review and meta‐analysis of published CSA reference values for lower extremity nerves.Methods: We included available‐to‐date nerve ultrasound studies on healthy adults and provide meta‐analysis for CSA of the following nerves: fibular nerve at fibular head, popliteal fossa; tibial nerve at popliteal fossa, malleolus; and sural nerve at the level of the two heads of gastrocnemius muscle. We report regression and correlation analyses for age, gender distribution, height, weight, and geographic continent.Results: We included 16 studies with 1001 healthy volunteers (mean age = 47.9 years) and 4023 examined nerve sites. Calculated mean pooled CSA of fibular nerve at fibular head was 8.4 mm² (95% confidence interval [CI] = 6.8–9.9 mm², n = 1166), at popliteal fossa was 7.9 mm² (95% CI = 6.6–9.2 mm², n = 995), of tibial nerve at popliteal fossa was 25.9 mm² (95% CI = 17.5–34.4 mm², n = 771), at malleolus was 10.0 mm² (95% CI = 7.7–12.4 mm², n = 779), and of sural nerve was 2.4 mm² (95% CI = 1.7–3.1 mm², n = 312). Substantial heterogeneity across studies (I² > 50%) was found only for tibial nerve at popliteal fossa. Subgroup analysis revealed a lower CSA of tibial nerve at popliteal fossa and sural nerve in studies conducted in Europe than in North America and New Zealand.Conclusions: We provide the first meta‐analysis on CSA reference values for the lower extremities with no or low heterogeneity of reported CSA values in all nerve sites except tibial nerve at popliteal fossa. Our data facilitate the goal of an international standardized evaluation protocol.

Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is the most common chronic inflammatory neuropathy. CIDP is diagnosed according to the European Federation of Neurological Societies/Peripheral Nerve Society (EFNS/PNS) criteria, which combine clinical features with the electrophysiological evidence of demyelination. However, firstly, diagnosis is challenging, as some patients e.g. with severe early axonal damage do not fulfil the criteria. Secondly, objective and reliable tools to monitor the disease course are lacking. Thirdly, about 25% of CIDP patients do not respond to evidence-based first-line therapy. Recognition of these patients is difficult and treatment beyond first-line therapy is based on observational studies and case series only. Individualized immunomodulatory treatment does not exist due to the lack of understanding of essential aspects of the underlying pathophysiology.Novel diagnostic imaging techniques and molecular approaches can help to solve these problems but do not find enough implementation. This review gives a comprehensive overview of novel diagnostic techniques and monitoring approaches for CIDP and how these can lead to individualized treatment and better understanding of pathophysiology.

Sleep related breathing disorders (SRBD) are common in patients with ischemic stroke and are associated with poor outcome. SRBD after stroke were assumed to be a direct consequence of injury of specific central nervous system structures. However, whether specific locations of ischemic infarcts cause SRBD is yet unknown. We therefore investigated the association of ischemic lesion location with SRBD. Patients with acute ischemic stroke treated on our stroke unit were included in a prospective observational study. All patients underwent magnetic resonance imaging (MRI) and polygraphy in the acute phase after stroke. SRBD was defined by an apnea—hypopnea index (AHI) ≥10. MRI were evaluated using standardized maps to depict voxel-wise probability distribution of infarction for patients with and without SRBD. Groups were compared using logistic regression analysis. Of 142 patients included, 86 (59%) had a SRBD. Age, body mass index and prevalence of arterial hypertension were significantly higher in patients with SRBD. There was no statistically significant association between any lesion location and SRBD. We found no association of lesion location and SRBD in stroke patients, whereas established risk factors for SRBD, known from general population, were significantly associated with SRBD. Given the high prevalence of SRBD in stroke patients, these findings suggest that cerebral ischemia facilitates the occurrence of SRBD in patients with pre-existing risk factors rather than causing it by damaging specific central nervous system structures. Our findings can be used to identify stroke patients who might benefit from polygraphy screening.