Fascicular involvement in common fibular neuropathy: Evaluation with ultrasound.

INTRODUCTION: The aim of this study was to demonstrate single fascicular involvement in common fibular (CF) neuropathy using high-resolution ultrasound (US). METHODS: We prospectively enrolled 40 adult patients with clinical and electrodiagnostic suspected CF neuropathy between April 2012 and December 2014. Two musculoskeletal radiologists used high-resolution US probes to prospectively and independently evaluate the CF nerve bilaterally in these patients. The presence of single fascicular involvement (increased cross-sectional area and loss of fascicular echotexture) was recorded. RESULTS: US revealed involvement of only 1 fascicular component of the CF nerve in 7 patients. In all these patients, US revealed involvement of the anterior fascicles corresponding to fibers for the deep fibular nerve. CONCLUSIONS: High-resolution US allowed identification of single fascicular involvement in CF neuropathy. Anterior fascicular involvement was present in up to 17% of patients with suspected CF neuropathy.

Anatomical study of the iliohypogastric, ilioinguinal, and genitofemoral nerves using high-resolution ultrasound.

INTRODUCTION: In this study we aimed to determine whether high-resolution ultrasound (US) can identify the iliohypogastric (IH), ilioinguinal (II), and genitofemoral (GF) nerves and their relations. METHODS: This investigation, initially undertaken in cadavers, was followed by a high-resolution US study in 30 healthy adult volunteers (180 nerves) by 2 musculoskeletal radiologists on separate occasions, using 2 different approaches (proximal to distal and distal to proximal). A 0-3 scale was used to assess nerve visibility. Location and course of the IH, II, and GF nerves and their relations to adjacent anatomical structures were analyzed. RESULTS: Nerves and their terminal branches were better visualized with the distal-to-proximal approach (P < 0.05). Visualization of the terminal branches was possible in up to 60% of volunteers. CONCLUSIONS: High-resolution ultrasound (US) can identify the IH, II, and GF nerves at the level of the abdominal wall and the terminal branches in the majority of volunteers.

High-resolution ultrasound of rotator cuff and biceps reflection pulley in non-elite junior tennis players: anatomical study.

BACKGROUND: Tennis is believed to be potentially harmful for the shoulder, therefore the purpose of this study is to evaluate the anatomy of the rotator cuff and the coraco-humeral ligament (CHL) in a-symptomatic non-elite junior tennis players with high-resolution ultrasound (US). METHODS: From August 2009 to September 2010 n = 90 a-symptomatic non-elite junior tennis players (mean age ± standard deviation: 15 ± 3) and a control group of age- and sex- matched subjects were included. Shoulder assessment with a customized standardized protocol was performed. Body mass index, dominant arm, years of practice, weekly hours of training, racket weight, grip (Eastern, Western and semi-Western), kind of strings were recorded. RESULTS: Abnormalities were found at ultrasound in 14/90 (15%) players. Two players had supraspinatus tendinosis, two had subacromial impingement and ten had subacromial bursitis. CHL thickness resulted comparable in the dominant and non-dominant arms (11.3 ± 4.4 mm vs. 13 ± 4.2, p > 0.05). Multivariate analysis demonstrated that no association was present among CHL thickness and the variables evaluated. In the control group, abnormalities were found at ultrasound in 6/60 (10%) subjects (sub-acromial bursitis). No statistically significant differences between players and control group were found (p = 0.71). CONCLUSION: In a-symptomatic non-elite junior tennis players only minor shoulder abnormalities were found.

Imaging of skeletal muscle in vitamin D deficiency.

Elderly people are prone to accidental falls and one of the main risk factor is considered muscle weakness. Several studies focused on muscle weakness and muscle morphology changes in the elderly that may be associated with vitamin D deficiency. The prevalence of vitamin D deficiency is higher than previously though representing an important issue for public health and prevention. There is an increased interest in vitamin D effects in skeletal muscle and imaging modalities are particularly involved in this field. In patients with vitamin D deficiency, ultrasound, computed tomography, densitometry and magnetic resonance imaging (MRI) can efficiently describe changes in muscle morphology and size. Moreover, new imaging modalities, such as MRI spectroscopy, may improve knowledge about the metabolic effects of vitamin D in skeletal muscle. In this narrative review we will discuss the role of skeletal muscle imaging in vitamin D-deficient individuals. The aim of this paper is to improve and encourage the role of radiologists in this field.

Reliability of side-to-side ultrasound cross-sectional area measurements of lower extremity nerves in healthy subjects.

INTRODUCTION: In peripheral nerve ultrasound, the healthy contralateral side may be used as internal control. Therefore, inherent side-to-side differences must be minimal. The goal of this study was to assess intrastudy, intraobserver, and interobserver reproducibility of ultrasound in comparative side-to-side evaluation of lower limb nerves. METHODS: Lower limb nerves of 60 normal subjects were evaluated by 3 radiologists. Bilateral sciatic, tibial, common fibular, sural, lateral femoral cutaneous, femoral, obturator, and saphenous nerves were evaluated. RESULTS: Overall, side-to-side differences were not statistically significant at any level. In the lower limb nerves, in a between-limb comparison, the minimum detectable difference of cross-sectional area ranged from 16.4 mm(2) (sciatic nerve at the level of piriformis muscle) to 0.4 mm(2) (saphenous nerve). CONCLUSION: In general, the healthy contralateral side can be used as an internal control.

Nerves of the hand beyond the carpal tunnel.

Imaging studies including ultrasound (US) and magnetic resonance imaging may be required to evaluate the median nerve in patients with suspected carpal tunnel syndrome. However, the radial and ulnar nerves contribute to sensory and motor innervations to the hand as well. Compressive, traumatic, and iatrogenic events may damage the small terminal branches of these nerves. In the hand, US is able to identify injuries of the median, ulnar, radial nerve, and terminal branches. This article presents the role of imaging to evaluate the nerves of the hand with an emphasis on US. Due to its high-resolution capabilities, US is useful to determine the location, extent, and type of nerve lesion. Moreover, US is useful for a postsurgical assessment. The anterior interosseous nerve, Guyon's tunnel syndrome, and Wartenberg's syndrome are also described.

Effects of cholinergic enhancing drugs on cholinergic transporters in the brain and peripheral blood lymphocytes of spontaneously hypertensive rats.

Cholinergic hypofunction is a trait of Alzheimer's disease and vascular dementia and countering it is one of the main therapeutic strategies available for these disorders. Cholinergic transporters control cellular mechanisms of acetylcholine (ACh) synthesis and release at presynaptic terminals. This study has assessed the influence of 4 week treatment with two different cholinergic enhancing drugs, the cholinergic precursor choline alphoscerate (alpha-glyceryl-phosphorylcholine) or the acetylcholinesterase (AChE) inhibitor galantamine on high affinity choline uptake transporter (CHT) and vesicular ACh transporter (VAChT) expression in the brain of spontaneously hypertensive rats (SHR). SHR represent an animal model of cerebrovascular injury characterized by cholinergic hypofunction. Analysis was performed by immunochemistry, ELISA and immunohistochemistry on frontal cortex, striatum and hippocampus. Immunochemical and ELISA analysis was extended to peripheral blood lymphocytes (PBL), used as a peripheral reference of changes of brain cholinergic markers. An increased expression of VAChT and CHT was observed in brain areas investigated and in PBL of SHR. The similar trend for cholinergic transporters observed in brain and PBL suggests these cells may represent a marker of brain cholinergic transporters. Treatment with choline alphoscerate increased CHT and to a greater extent VAChT expression. Treatment with galantamine countered the increase of CHT and VAChT. The different activity of the cholinergic precursor and of the AChE inhibitor on parameters investigated is likely related to their mechanism of action. Choline alphoscerate increases ACh synthesis and release. This requires an augmentation of systems regulating neurotransmitter uptake and storage. The effect of choline alphoscerate on CHT and VAChT observed in this study suggests an improved synaptic efficiency elicited by the compound. The AChE inhibitor slows-down ACh degradation in the synaptic cleft. A greater availability of neurotransmitter elicited by galantamine counters the enhanced activity of cholinergic transporters compensating cholinergic deficits. Differences in the activity of the cholinergic precursor and AChE inhibitor investigated on CHT and VAChT suggests that association between choline alphoscerate and AChE/cholinesterase inhibitors may represent a strategy for potentiating deficient cholinergic neurotransmission worthwhile of being investigated in clinical trials.

Different cellular and molecular mechanisms for early and late-onset myelin protein zero mutations.

Mutations in the gene MPZ, encoding myelin protein zero (MPZ), cause inherited neuropathies collectively called Charcot-Marie-Tooth type 1B (CMT1B). Based on the age of onset, clinical and pathological features, most MPZ mutations are separable into two groups: one causing a severe, early-onset, demyelinating neuropathy and a second, causing a late-onset neuropathy with prominent axonal loss. To investigate potential pathomechanisms underlying the two phenotypes, we transiently transfected HeLa cells with two late-onset (T95M, H10P) and two early-onset (H52R, S22_W28 deletion) mutations and analyzed their effects on intracellular protein trafficking, glycosylation, cell viability and intercellular adhesion. We found that the two late-onset mutations were both transported to the cell membrane and moderately reduced MPZ-mediated intercellular adhesion. The two early-onset mutations caused two distinct abnormalities. H52R was correctly glycosylated and trafficked to the plasma membrane, but strongly affected intercellular adhesion. When co-expressed with wild-type MPZ (wtMPZ), a functional dominant negative effect was observed. Alternatively, S22_W28 deletion was retained within the cytoplasm and reduced both adhesion caused by wtMPZ and cellular viability. Since the same trafficking patterns were observed in transfected murine Schwann cells, they are not an artifact of heterologous cell expression. Our results suggest that at least some late-onset mutations cause a partial loss of function in the transfected cells, whereas multiple abnormal gain of function pathways can result in early-onset neuropathy. Further characterization of these pathways will lead to a better understanding of the pathogenesis of CMT1B and a rational basis for treating these debilitating inherited neuropathies.