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OBJECTIVE: This study was designed to verify whether one or more clinical and neurophysiological parameters could predict a poor prognosis in idiopathic facial paralysis. METHODS: Seventy-three outpatients with unilateral idiopathic facial nerve paralysis who visited our hospital within 7 days of onset. All patients received treatment according to a standard therapy protocol and ocular care. Patients' baseline characteristics were assessed before initiating treatment, including demographic characteristics, facial nerve function assessment and previous medical history. House-Brackmann (H-B) grading system was performed at baseline and six months after the onset. Electroneurography (ENoG) and blink reflex tests were conducted 7-10 days after the onset of paralysis. Sunnybrook Facial Grading System (SFGS) was conducted at baseline, days 7-10 post-onset when the electrophysiological tests were performed, and one month after the onset. RESULTS: According to the H-B grade at 6 months following the onset, 58 patients (79.5 %) had a good prognosis, while 15 patients (20.5 %) had a poor prognosis. The CMAP amplitudes in three facial muscles (frontalis, orbicularis oculi, and orbicularis oris) were decreased, and ENoG values were increased in the poor prognosis group compared with the good prognosis group (all p < 0.01). The results of the blink reflex study showed that the group with a poor prognosis had a longer R1 latency compared to the group with a good prognosis. Additionally, the group with a poor prognosis exhibited a higher rate of R1 absence on the affected side (both p < 0.01). The findings of conditional logistic regression indicated that the absence of R1 on the affected side, frontalis ENoG, orbicularis oculi ENoG, and orbicularis oris ENoG were predictive factors of a poor prognosis for facial nerve palsy. The receiver operating characteristic (ROC) curves showed that the SFGS at 1 month after onset of 55 is considered a critical cutoff value for poor prognosis, with a sensitivity of 86.7 % and specificity of 91.4 %. CONCLUSION: Electroneurography (ENoG) and blink reflex tests acquired within 7-10 days after the onset of paralysis are significant and highly valuable for predicting the prognosis of idiopathic facial nerve paralysis. Higher ENoG values of the muscles innervated by the facial nerve and the absence of R1 on the affected side of the blink reflex are predictive factors for a poor prognosis. The SFGS is a clinical tool that plays an important role in evaluating the prognosis of idiopathic facial paralysis, particularly one month after onset.

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ABSTRACT: X-linked myopathy with excessive autophagy is a rare disorder caused by a mutation in the vacuolar ATPase assembly factor gene which causes slowly progressive early onset proximal weakness and loss of ambulation by the age of 50-70 years. Electrodiagnostic (EDx) testing usually shows widespread complex repetitive and myotonic discharges, even in muscles unaffected clinically. We report a 65-year-old man who presented with progressive proximal weakness since his teenage years. Extensive workup over 30 years revealed inconclusive EDx and muscle histopathology findings. The diagnosis was finally made with genetic testing. Subsequent neuromuscular ultrasound was more informative of disease severity than repeat EDx and directed a muscle biopsy that showed an autophagic vacuolar myopathy and the novel identification of vacuoles in capillary endothelial cells. Although genetic testing is required for confirmation, in milder cases of X-linked myopathy with excessive autophagy, neuromuscular ultrasound may aid in diagnosis even when EDx findings are inconclusive.

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INTRODUCTION: The revised international standards for neurological classification of spinal cord injury (ISNCSCI) have facilitated the documentation of non-spinal cord injury-related impairments, such as chronic peripheral nerve injuries and muscle weakness due to immobility. This advancement addresses potential biases in muscle strength examinations. Utilizing electrically evoked contractions from paralyzed muscles, enhanced by electrodiagnosis, holds promise in identifying false-negative diagnoses of non-responsiveness to neuromuscular electrical stimulation. This concept prompts the exploration of polyneuromyopathy arising from nonuse in paralyzed muscles. CASE SERIES PRESENTATION: To substantiate our hypothesis, we recruited nine participants for a case series aimed at elucidating the potential benefits of incorporating the stimulus electrodiagnostic test (SET) to mitigate non-responsiveness during preparation for functional electrical stimulation (FES)-assisted cycling. In our convenience sample (n = 5), we conducted neurological mapping based on ISNCSCI and applied SET on the quadriceps. The SET guided optimal dosimetry for evoking contractions and revealed responses similar to those observed in peripheral neuropathies, with α coefficients equal to or lower than 2.00. This observation is likely attributable to nonuse of paralyzed muscles, indicative of an ongoing polyneuropathy in individuals with chronic spinal cord injury (SCI). DISCUSSION: Among the nine initially recruited subjects, seven exhibited responsiveness to neuromuscular electrical stimulation (78% responsiveness), with two participants excluded based on exclusion criteria. In the final five reported cases, all displayed α coefficient values indicating impaired neuromuscular accommodation, and one presented no α coefficient within the normal range. The inclusion of electrodiagnosis appears effective in averting non-responsiveness, suggesting the presence of ongoing polyneuropathies in paralyzed muscles.

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Background: Vulpian-Bernhardt syndrome is an atypical form of the motor neuron disease described since the 19th century. The importance of a timely diagnosis lies in the increased survival present in this variant. Due to the clinical rarity and complex diagnosis we report a clinical case of this disease, which is why we describe the typical clinical presentation, the diagnostic approach, and we make a bibliographic review of this neurodegenerative disorder as well. Clinical case: Latin American man whose clinical case onset was characterized by thoracic asymmetric and increasing limb weakness, showing affection from distal to proximal upper limbs area. Subsequently, symptoms worsened to the point of limiting day-to-day activities and conditioning patient's physical independence. Physical examination was consistent with motor neuron disease. Nerve conduction studies were performed and confirmed findings compatible with motor neuron involvement limited to thoracic limbs. Conclusion: Vulpian-Bernhardt syndrome is an uncommon form of motor neuron disease. Due to the rarity of its presentation, it is frequent to confuse clinical profile even for trained physicians. The importance of electrodiagnosis relies in identifying the neurogenic origin of the disease, as well as the active denervation and reinnervation data. Considering that with this syndrome patients have a longer survival than with the classic form of amyotrophic lateral sclerosis, it is important to have a clear diagnosis approach in order to provide a better quality of life and supportive treatment.

Introducción: el síndrome de Vulpian-Bernhardt es una forma atípica de la enfermedad de la motoneurona descrita desde el siglo XIX. La importancia de un diagnóstico oportuno radica en la mayor supervivencia que presenta esta variante. Debido a la rareza clínica y al diagnóstico complejo presentamos un caso clínico de esta enfermedad, por lo que describimos el cuadro clínico típico, el abordaje diagnóstico y hacemos una revisión bibliográfica de este trastorno neurodegenerativo. Caso clínico: hombre de origen latinoamericano que comenzó su padecimiento con debilidad de miembros torácicos, asimétrica y progresiva de distal a proximal. Los síntomas progresaron hasta limitar sus actividades de la vida diaria y su independencia física. La exploración física fue compatible con enfermedad de motoneurona. Se hicieron estudios de extensión y neuroconducción que confirmaron hallazgos compatibles con afectación en motoneurona limitada a miembros torácicos. Conclusión: el síndrome Vulpian-Bernhardt es una forma clínica poco común. Debido a su rareza, es fácil confundir el cuadro clínico, incluso por parte de experimentados. La importancia del electrodiagnóstico radica en identificar el origen neurogénico de la enfermedad, los datos de denervación activa y reinervación. Al ser una forma en la que se presenta una supervivencia mayor que en la forma clásica, es importante el diagnóstico claro para dar una mejor calidad de vida y tratamiento de soporte.

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Neurogenic thoracic outlet syndrome (nTOS) is caused by brachial plexus compression in the thoracic outlet. It accounts for 85%-95% of thoracic outlet syndrome (TOS) cases, which may also be caused by compression of the subclavian artery and vein. Compression occurs in the interscalene triangle, costoclavicular space or subpectoralis minor space, with congenital anomalies and repetitive overhead activities as contributing factors. Diagnosis is challenging due to overlapping symptoms with other conditions. Patients commonly report pain, numbness, tingling and weakness in the neck, shoulder and arm, exacerbated by arm elevation. Symptoms related to nTOS may manifest in the distribution of the upper (C5-C6), middle (C7) and lower plexus (C8-T1). Although widely used, provocative tests have varying degrees of sensitivity and specificity and may have high false-positive rates, complicating the diagnosis. Patterns on electrodiagnostic studies provide key diagnostic clues, such as reduced sensory response in the medial antebrachial cutaneous nerve and low compound motor action potential in the median nerve. Imaging techniques like magnetic resonance imaging (MRI), alongside procedures like diagnostic and therapeutic anterior scalene blocks, assist in identifying anatomical abnormalities and predicting surgical outcomes. Management of nTOS involves lifestyle changes, physical therapy, medication and botulinum toxin injections for symptomatic relief. Surgical options may include supraclavicular, transaxillary and infraclavicular approaches, each offering specific benefits based on patient anatomy and surgeon expertise. Minimally invasive techniques, such as video-assisted thoracoscopic surgery (VATS) and robotic surgery, enhance exposure and dexterity, leading to better outcomes. Future research should focus on developing precise diagnostic tools, understanding nTOS pathophysiology, standardising diagnostic criteria and surgical approaches, comparing long-term treatment outcomes and exploring preventive measures to improve patient care and quality of life. Level of Evidence: Level V (Therapeutic).

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BACKGROUND AND PURPOSE: Various electrodiagnostic criteria have been developed in Guillain-Barré syndrome (GBS). Their performance in a broad representation of GBS patients has not been evaluated. Motor conduction data from the International GBS Outcome Study (IGOS) cohort were used to compare two widely used criterion sets and relate these to diagnostic amyotrophic lateral sclerosis criteria. METHODS: From the first 1500 patients in IGOS, nerve conduction studies from 1137 (75.8%) were available for the current study. These patients were classified according to nerve conduction studies criteria proposed by Hadden and Rajabally. RESULTS: Of the 1137 studies, 68.3% (N = 777) were classified identically according to criteria by Hadden and Rajabally: 111 (9.8%) axonal, 366 (32.2%) demyelinating, 195 (17.2%) equivocal, 35 (3.1%) inexcitable and 70 (6.2%) normal. Thus, 360 studies (31.7%) were classified differently. The areas of differences were as follows: 155 studies (13.6%) classified as demyelinating by Hadden and axonal by Rajabally; 122 studies (10.7%) classified as demyelinating by Hadden and equivocal by Rajabally; and 75 studies (6.6%) classified as equivocal by Hadden and axonal by Rajabally. Due to more strictly defined cutoffs fewer patients fulfilled demyelinating criteria by Rajabally than by Hadden, making more patients eligible for axonal or equivocal classification by Rajabally. In 234 (68.6%) axonal studies by Rajabally the revised El Escorial (amyotrophic lateral sclerosis) criteria were fulfilled; in axonal cases by Hadden this was 1.8%. CONCLUSIONS AND DISCUSSION: This study shows that electrodiagnosis in GBS is dependent on the criterion set utilized, both of which are based on expert opinion. Reappraisal of electrodiagnostic subtyping in GBS is warranted.

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Carpal tunnel syndrome (CTS) is caused by compression of the median nerve as it travels through the carpal tunnel. Patients commonly experience pain, paresthesia, and, less often, weakness in the distribution of the median nerve. Provocative maneuvers, such as the Phalen test and Tinel sign, have varying sensitivity and specificity for the diagnosis of CTS. Thenar atrophy is a late finding and highly specific for CTS. Although patients with a classic presentation of CTS do not need additional testing for diagnosis, electrodiagnostic studies can confirm the diagnosis in atypical cases, exclude other causes, and gauge severity for surgical prognosis. An abnormal nerve conduction study is useful for ruling in CTS, but a normal test does not necessarily exclude it. Over-the-counter analgesics, such as nonsteroidal anti-inflammatory drugs and acetaminophen, have not shown benefit for CTS. Patients with mild to moderate CTS initially may be offered nonsurgical treatments, such as splinting or local corticosteroid injections. Night-only splinting is as effective as continuous wear. A neutral wrist splint may be more effective than an extension splint. In patients with recent onset of CTS, corticosteroid injections provide slightly greater improvement of symptoms compared with splinting at 6 weeks, with similar outcomes at 6 months. Patients with severe CTS, including objective weakness or sensory deficits, should be offered surgical decompression. Endoscopic and open carpal tunnel release techniques are equally effective.

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This article describes the main visual electrodiagnostic tests relevant to neuro-ophthalmology practice, including the visual evoked potential (VEP), and the full-field, pattern and multifocal electroretinograms (ffERG; PERG; mfERG). The principles of electrophysiological interpretation are illustrated with reference to acquired and inherited optic neuropathies, and retinal disorders that may masquerade as optic neuropathy, including ffERG and PERG findings in cone and macular dystrophies, paraneoplastic and vascular retinopathies. Complementary VEP and PERG recordings are illustrated in demyelinating, ischaemic, nutritional (B12), and toxic (mercury, cobalt, and ethambutol-related) optic neuropathies and inherited disorders affecting mitochondrial function such as Leber hereditary optic neuropathy and dominant optic atrophy. The value of comprehensive electrophysiological phenotyping in syndromic diseases is highlighted in cases of SSBP1-related disease and ROSAH (Retinal dystrophy, Optic nerve oedema, Splenomegaly, Anhidrosis and Headache). The review highlights the value of different electrophysiological techniques, for the purposes of differential diagnosis and objective functional phenotyping.

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INTRODUCTION/AIMS: Using a set of process-of-care quality measures for electrodiagnostic testing in suspected carpal tunnel syndrome (CTS), the research team previously documented large variations in electrodiagnostic testing practices and adherence to quality measures. This study sought to enhance the applicability and validity of the quality measures by integrating acceptable variations in testing practices. METHODS: We recruited 13 expert electrodiagnostic medicine specialists from five specialty societies. The experts iteratively refined five quality measures, and then rated the validity of the refined quality measures (1-9 scale). During this process, the experts reviewed data on adherence to existing quality measures and variations in electrodiagnostic testing practices, and considered recently published quality measures from the American Association of Neuromuscular and Electrodiagnostic Medicine. RESULTS: Three quality measures (electrodiagnostic testing before surgery for CTS, temperature assessment during electrodiagnostic testing, and electrodiagnostic criteria for severe median neuropathy) underwent few refinements and were rated valid (medians 8-9). Two measures (essential components of electrodiagnosis, criteria for interpreting electrodiagnostic tests as median neuropathy) were judged valid (medians 8) after revisions. For these measures, experts' ratings on the recommended components of sensory or mixed nerve conduction studies varied: agreement among the experts about the use of sensory peak latency was greater than for onset latency or sensory velocity. DISCUSSION: This study produced quality measures that provide minimum standards for electrodiagnostic testing for suspected CTS that are more comprehensive and nuanced than prior versions. Future work can assess the feasibility, reliability, and validity of these refined measures in diverse physician practices.

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OBJECTIVES: Carpal tunnel syndrome (CTS) is the most common entrapment neuropathy in the body and impacts approximately 5% of the U.S. population costing nearly $5 billion/year. Electrodiagnostic (EDX) testing is considered the gold standard for CTS diagnosis. Classification systems exist that categorize CTS severity based on EDX findings. This investigation evaluated EDX findings across consecutive CTS severity categories within existing classification systems and consolidated classifications. METHODS: This retrospective study analyzed 665 hands from 468 patients undergoing EDX testing for suspected CTS. Complete classification systems and consolidated classifications were evaluated for discrimination capability across consecutive CTS severity categories based on EDX findings. Additional analysis evaluated the relationship of sex and age factors and CTS severity. RESULTS: Consolidated classifications demonstrated superior discrimination capability between consecutive CTS severity categories regardless of classification system used. Demographic factors significantly influenced EDX findings and categorization of CTS severity. CONCLUSIONS: This study underscores the value of consolidated classifications for enhancing discrimination between consecutive CTS severity categories based on EDX findings. Demographic factors should be considered when interpreting EDX findings for the purpose of categorizing CTS severity. Future research should refine existing classification systems and explore additional factors influencing CTS severity used to inform medical management.

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Objective: To test the new method of iMAX (the minimum stimulus current that elicits the maximum compound muscle action potential amplitude) electrodiagnosis, verify the feasibility of this method in evaluating the excitability of peripheral motor axons, and preliminarily explore the clinical application value. Methods: This study was a cross-sectional study. A total of 50 healthy subjects were recruited from the outpatient department of Peking University Third Hospital from June 2022 to March 2023, including 25 males and 25 females, aged 25-68 (48±8) years. Eleven patients with Charcot-Marie-Pain-1A (CMT1A), 7 males and 4 females, aged 19-55 (41±13) years and 21 patients with diabetic peripheral neuropathy (DPN), 10 males and 11 females, aged 28-79 (53±16) years were enrolled in this study. iMAX of bilateral median nerves, ulnar nerves and peroneal nerves were detected in all patients. Repeatable motor responses with minimum motor threshold and amplitude of at least 0.1 mV and the minimum stimulus current intensity, at which the maximum compound muscle action potential amplitude is elicited, were measured respectively [1 mA increment is called (iUP) and, 0.1 mA adjustment is called (iMAX)].Comparison of the parameters: the parameters of threshold, iUP and iMAX were compared among different age groups, genders and sides, body mass index(BMI) values and detection time , as well as between CMT1A patients, DPN patients and healthy subjects. Results: In healthy subjects, the threshold, iUP value and iMAX value were (1.8±0.7) mA, (4.4±1.2) mA, and (4.2±1.3) mA respectively; ulnar nerve (3.1±1.6) mA, (6.8±3.2) mA, (6.4±3.2) mA; peroneal nerve (3.7±2.0) mA, (7.8±2.8) mA, (7.4±2.9) mA. There were statistically significant differences in threshold, iUP value and iMAX value among different age groups (all P<0.001).With the increase of age, there was a trend of increasing threshold, iUP, and iMAX values in different nerves, and the differences are statistically significant (all P<0.001). There were no significant differences in gender, side and detection time threshold, iUP value and iMAX value (all P>0.05). The parameters of healthy subjects with high BMI value were higher than those of healthy subjects with low BMI value(all P<0.05). Compared with the healthy subjects, the parameters of 11 CMT1A patients were significantly increased (all P<0.05), and the parameters of 21 DPN patients were slightly increased (P<0.05). Conclusion: The new iMAX method reflects the excitability of motor axons and early axonal dysfunction, which is an important supplement to the traditional nerve conduction, and can be used to monitor motor axon excitability disorders.

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INTRODUCTION/AIMS: The current diagnosis of ulnar neuropathy at the elbow (UNE) relies mainly on the clinical presentation and nerve electrodiagnostic (EDX) testing, which can be uncomfortable and yield false negatives. The aim of this study was to investigate the diagnostic value of conventional ultrasound, shear wave elastography (SWE), and superb microvascular imaging (SMI) in diagnosing UNE. METHODS: We enrolled 40 patients (48 elbows) with UNE and 48 healthy volunteers (48 elbows). The patients were categorized as having mild, moderate or severe UNE based on the findings of EDX testing. The cross-sectional area (CSA) was measured using conventional ultrasound. Ulnar nerve (UN) shear wave velocity (SWV) and SMI were performed in a longitudinal plane. RESULTS: Based on the EDX findings, UNE severity was graded as mild in 4, moderate in 10, and severe in 34. The patient group showed increased ulnar nerve CSA and stiffness at the site of maximal enlargement (CSA mean at the site of max enlargement [CSAmax] and SWV mean at the site of max enlargement [SWVmax]), ulnar nerve CSA ratio, and stiffness ratio (elbow-to-upper arm), compared with the control group (p < .001). Furthermore, the severe UNE group showed higher ulnar nerve CSAmax and SWVmax compared with the mild and moderate UNE groups (p < .001). The cutoff values for diagnosis of UNE were 9.5 mm2 for CSAmax, 3.06 m/s for SWVmax, 2.00 for CSA ratio, 1.36 for stiffness ratio, and grade 1 for SMI. DISCUSSION: Our findings suggest that SWE and SMI are valuable diagnostic tools for the diagnosis and assessment of severity of UNE.

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INTRODUCTION: Carpal tunnel syndrome is commonly managed by hand and upper extremity surgeons. Though electrodiagnostics are considered the gold standard diagnosis, the scratch collapse test (SCT) was introduced to address uncertainty, despite remains controversial. To address this, we sought to identify if the SCT can correlate with EDS studies if the SCT can identify actual changes in measures of nerves. METHODS: We reviewed patients who underwent electrodiagnostic studies (EDX) and SCT for carpal tunnel syndrome (CTS). Demographic data as well as sensorimotor amplitudes, latencies, and velocities on nerve conduction and electromyography were collected. Analogous values based on SCT findings were analyzed for statistical significance. RESULTS: Three hundred fifty patients with CTS were included. Sensory and motor velocities and amplitudes were significantly lower in patients with a positive SCT. Motor values were independent of age, though younger patients had larger measured changes. Obese patients did not show any motor EDX changes with the scratch collapse test, though thinner patients did. All changes were seen in nerve conduction only. CONCLUSIONS: Carpal tunnel can be a difficult problem to diagnose as one study does not singularly determine the condition. The SCT was introduced to facilitate easier diagnosis. We demonstrate that the SCT correlates with changes on nerve conduction studies, especially in relation to decreased amplitudes and velocities, suggesting that it does identify changes in nerve with compression, specifically axonal, and myelin damage. These findings support the use of the SCT maneuver to evaluate and diagnose in appropriate patients.

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INTRODUCTION: Double-crush syndrome (DCS) represents a condition that involves peripheral nerve compression in combination with spinal nerve root impingement. The purpose of this study was to compare electrodiagnostic study (EDS) results in patients undergoing carpal tunnel release (CTR) for carpal tunnel syndrome with those undergoing both CTR and anterior cervical diskectomy and fusion for DCS. METHODS: Patients receiving an isolated CTR were compared with those undergoing CTR and anterior cervical diskectomy and fusion within two years of CTR. The latter group was defined as our DCS cohort. Electrodiagnostic study results were collected which included sensory and motor nerve conduction data as well as electromyogram (EMG) findings. All electrodiagnostic studies were done before CTR in both sets of patients. RESULTS: Fifty-four patients with DCS and 137 CTR-only patients were included. Patients with DCS were found to have decreased sensory onset latency (3.51 vs 4.01; P = 0.015) and peak latency (4.25 vs 5.17; P = 0.004) compared with the CTR-only patients. Patients with DCS had slower wrist motor velocity (30.5 vs 47.7; P = 0.012), decreased elbow motor latency (9.62 vs 10.6; P = 0.015), and faster elbow motor velocity (56.0 vs 49.4; P = 0.031). EMG results showed that patients with DCS were more likely to have positive findings in the biceps (31.9% vs 1.96%; P < 0.001) and triceps (24.4% vs 2.97%; P < 0.001), but not abductor pollicis brevis (APB) (45.7% vs 37.9%; P = 0.459). CONCLUSION: We identified changes on EDS between patients with and without DCS. In patients with DCS, sensory nerve studies showed shorter peak and onset latency than in CTR-only patients. Interestingly, DCS and CTR-only patients had different patterns of wrist and elbow motor nerve conduction. Providers observing positive EMG findings proximal to the APB should raise their suspicion for possible cervical radiculopathy and when present with carpal tunnel syndrome-like symptoms, should also consider DCS in their diagnostic differential.

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OBJECTIVE: To establish a simple electrophysiological scale for patients with distal symmetric axonal polyneuropathy, in order to promote standardized and informative electrodiagnostic reporting, and understand the complex relationship between electrophysiological and clinical polyneuropathy severity. METHODS: We included 76 patients with distal symmetric axonal polyneuropathy, from a cohort of 151 patients with polyneuropathy prospectively recruited from November 2016 to May 2017. Patients underwent nerve conduction studies (NCS), were evaluated by the Toronto Clinical Neuropathy Score (TCNS), and additional tests. The number of abnormal NCS parameters was determined, within the range of 0-4, considering low amplitude or conduction velocity in the sural and peroneal nerve. RESULTS: Higher number of NCS abnormalities was associated with higher TCNS, indicating more severe polyneuropathy. Polyneuropathy severity per the TCNS was most frequently (63%-70%) mild in patients with a low (0-1) number of NCS abnormalities, and most frequently (57%-67%) severe in patients with a high number (3-4) of NCS abnormalities, while patients with an intermediate (2) number of NCS abnormalities showed mainly mild and moderate severity with equal distribution (40%). CONCLUSIONS: A simple NCS classification system can objectively grade polyneuropathy severity, although significant overlap exists especially at the intermediate range, underscoring the importance of clinical based scoring.

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Peripheral neuropathy is a commonly encountered diagnosis in both neurology and primary care office settings. It is important for primary care providers to identify, characterize, and diagnose patients with neuropathy. This study aims to describe the clinical presentation, diagnostic work up, and treatment options for this entity, as well as the identification of atypical features that should prompt specialized laboratory testing, electrodiagnostic testing, and neurologic consultation.

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This chapter covers axillary and musculocutaneous neuropathies, with a focus on clinically relevant anatomy, electrodiagnostic approaches, etiologic considerations, and management principles. Disorders of the lateral antebrachial cutaneous nerve, a derivative of the musculocutaneous nerve, are also reviewed. We emphasize the importance of objective findings, including the physical examination and electrodiagnostic evaluation in confirming the isolated involvement of each nerve which, along with the clinical history, informs etiologic considerations. Axillary and musculocutaneous neuropathies are both rare in isolation and most frequently occur in the setting of trauma. Less commonly encountered etiologies include external compression or entrapment, neoplastic involvement, or immune-mediated disorders including neuralgic amyotrophy, postsurgical inflammatory neuropathy, multifocal motor neuropathy, vasculitic neuropathy, and multifocal chronic inflammatory demyelinating polyradiculoneuropathy.

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Electrodiagnostic testing (EDX) has been the diagnostic tool of choice in peripheral nerve disease for many years, but in recent years, peripheral nerve imaging has been used ever more frequently in daily clinical practice. Nerve ultrasound and magnetic resonance (MR) neurography are able to visualize nerve structures reliably. These techniques can aid in localizing nerve pathology and can reveal significant anatomical abnormalities underlying nerve pathology that may have been otherwise undetected by EDX. As such, nerve ultrasound and MR neurography can significantly improve diagnostic accuracy and can have a significant effect on treatment strategy. In this chapter, the basic principles and recent developments of these techniques will be discussed, as well as their potential application in several types of peripheral nerve disease, such as carpal tunnel syndrome (CTS), ulnar neuropathy at the elbow (UNE), radial neuropathy, brachial and lumbosacral plexopathy, neuralgic amyotrophy (NA), fibular, tibial, sciatic, femoral neuropathy, meralgia paresthetica, peripheral nerve trauma, tumors, and inflammatory neuropathies.

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The sciatic nerve is the body's largest peripheral nerve. Along with their two terminal divisions (tibial and fibular), their anatomic location makes them particularly vulnerable to trauma and iatrogenic injuries. A thorough understanding of the functional anatomy is required to adequately localize lesions in this lengthy neural pathway. Proximal disorders of the nerve can be challenging to precisely localize among a range of possibilities including lumbosacral pathology, radiculopathy, or piriformis syndrome. A correct diagnosis is based upon a thorough history and physical examination, which will then appropriately direct adjunctive investigations such as imaging and electrodiagnostic testing. Disorders of the sciatic nerve and its terminal branches are disabling for patients, and expert assessment by rehabilitation professionals is important in limiting their impact. Applying techniques established in the upper extremity, surgical reconstruction of lower extremity nerve dysfunction is rapidly improving and evolving. These new techniques, such as nerve transfers, require electrodiagnostic assessment of both the injured nerve(s) as well as healthy, potential donor nerves as part of a complete neurophysiological examination.

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