Laughlin, Ruple S.

BACKGROUND: Retrospective and prospective studies 2 decades ago from the authors’ institution reported the incidence of perioperative ulnar neuropathy persisting for at least several months in a noncardiac adult surgical population to be between 30 and 40 per 100,000 cases. The aim of this project was to assess the incidence and explore risk factors for perioperative ulnar neuropathy in a recent cohort of patients from the same institution using a similar definition for ulnar neuropathy. METHODS: We performed a retrospective incidence and case-control study of all adults (≥18 years) undergoing noncardiac procedures with anesthesia services between 2011 and 2015. Each incident case of persistent ulnar neuropathy within 6 months of surgery was matched by age, sex, procedure date, and procedure type to 5 surgical patient controls. For the case-control study, separate conditional logistic regression analyses were performed to assess specific risk factors including the patient’s body position and arm position, as well as body mass index (BMI), surgical duration, and selected patient comorbidities. RESULTS: Persistent ulnar neuropathy of at least 2 months duration was found in 22 of 324,124 anesthetics for patients who underwent these procedures during the study period for an incidence rate of 6.8 (95% confidence interval [CI], 4.3-10.3) per 100,000 anesthetics. The incidence of ulnar neuropathy was higher in men compared to women (10.7 vs 3.0 per 100,000; P = .016). From the matched case-control study, the odds of ulnar neuropathy increased with higher BMI (odds ratio [OR] = 1.67 [1.16-2.42] per 5 kg/m 2 increase in BMI; P = .006), history of cancer (OR = 6.46 [1.64-25.49]; P = .008), longer procedures (OR = 1.53 [1.18-1.99] per hour; P = .001), and when 1 or both arms were tucked during surgery (OR = 6.16 [1.85-20.59]; P = .003). CONCLUSIONS: The incidence of persistent perioperative ulnar neuropathy observed in this study was lower than the incidence reported 2 decades ago from the same institution and using a similar definition for ulnar neuropathy. Several of the previously reported risk factors continue to be associated with the development of persistent perioperative ulnar neuropathy, providing ongoing targets for practice changes that might further decrease the incidence of this problem.

Background: Image guided intercostal blocks are commonly performed and considered relatively safe. Chemical denervation is commonly used in clinical practice for treatment of chronic noncancer associated pain. Objective: To report a case of spinal cord injury resulting from fluoroscopically guided intercostal blocks with phenol. Study Design: Case report. Setting: Inpatient hospital service. Results/Case Report: A 53 year-old women was transferred from her local facility for acute onset of lower extremity paresis beginning shortly after right intercostal nerve injections of 2 mL of preservative-free phenol at the T7, 8, 9 levels. She had previous intercostal blocks for chronic rightsided mid thoracic/abdominal pain every 3 months for at least one year without sequelae. Within 20 minutes of the injection, she developed a sensation of right leg weakness and heaviness. Over several hours she developed worsening right leg weakness, and then left leg weakness, followed by urinary retention. Admission examination revealed severe right greater than left leg weakness, right lower extremity hyperesthesia to T10, absent lower extremity reflexes, and bilateral extensor plantar responses. Magnetic resonance imaging (MRI) of the entire spine demonstrated extensive T2/DWI hyperintensity in the central spinal cord from T1 to L1 with mild cord enlargement and enhancement at T7-9 (sites of injection). Extensive serum and cerebrospinal fluid (CSF) evaluation did not show any evidence of an infectious, inflammatory, or metabolic cause to her myelopathy. Repeat MRI of the entire spine demonstrated near complete resolution of the T2 signal abnormality. One month after presentation, despite radiographic improvement, the patient showed some clinical improvement, but remained walker dependent and with neurogenic bowel and bladder. Limitations: This report describes a single case report. Conclusion: This case offers several lessons for a pain specialist including 1) the potential for a neurologic catastrophe (spinal cord injury) from aqueous neurolytic intercostal blocks despite “safe” contrast spread; 2) potential mechanisms of neurogenic injury with intercostal blocks; 3) review of modifiable factors to decrease the risk of neurogenic injury; and 4) review of potential interventions (steroids, lumbar drain) to improve outcome in the setting of iatrogenic procedural related spinal cord injury. Key words: Phenol, myelopathy, paraparesis, chemical denervation, neurolysis, intercostal block, epidural spread, chronic pain, complication, transverse myelitis

Abstract Delayed diagnosis of immune-mediated necrotizing myopathy leads to increased morbidity. Patients with the chronic course without 3-hydroxy-3-methylglutaryl-coenzyme-A reductase-IgG or signal recognition particle-IgG are often challenging to diagnose. Immunotherapy response can also be difficult to assess. We created a statistical model to assist immune-mediated necrotizing myopathy diagnosis. Electrical myotonia versus fibrillations were reviewed as biomarkers for immunotherapy treatment response. Identified were 119 immune-mediated necrotizing myopathy cases and 938 other myopathy patients. Inclusion criteria included all having electrophysiological evaluations, muscle biopsies showing inflammatory/necrotizing myopathies, comprehensively recorded neurological examinations, and creatine kinase values. Electrical myotonia was recorded in 56% (67/119) of retrospective and 67% (20/30) of our validation immune-mediated necrotizing myopathy cohorts, and significantly (P < 0.001) favoured immune-mediated necrotizing myopathy over other myopathies: sporadic inclusion body myositis (odds ratio = 4.78); dermatomyositis (odds ratio = 10.61); non-specific inflammatory myopathies (odds ratio = 8.46); limb-girdle muscular dystrophies (odds ratio = 5.34) or mitochondrial myopathies (odds ratio = 14.17). Electrical myotonia occurred in immune-mediated necrotizing myopathy seropositive (3-hydroxy-3-methylglutaryl-coenzyme-A reductase-IgG 70%, 37/53; signal recognition particle-IgG 29%, 5/17) and seronegative (51%, 25/49). Multivariate regression analysis of 20 variables identified 8 (including electrical myotonia) in combination accurately predicted immune-mediated necrotizing myopathy (97.1% area-under-curve). The model was validated in a separate cohort of 30 immune-mediated necrotizing myopathy cases. Delayed diagnosis of cases with electrical myotonia occurred in 24% (16/67, mean 8 months; range 0–194). Half (8/19) had a chronic course and were seronegative, with high model prediction (>86%) at the first visit. Inherited myopathies were commonly first suspected in them. Follow-up evaluation in patients with electrical myotonia on immunotherapy was available in 19 (median 21 months, range 2–124) which reduced from 36% (58/162) of muscles to 7% (8/121; P < 0.001). Reduced myotonia correlated with immunotherapy response in 64% (9/14) as well as with median creatine kinase reduction of 1779 U/l (range 401–9238, P < 0.001). Modelling clinical features with electrical myotonia is especially helpful in immune-mediated necrotizing myopathy diagnostic suspicion among chronic indolent and seronegative cases. Electrical myotonia favours immune-mediated necrotizing myopathy diagnosis and can serve as an adjuvant immunotherapy biomarker.

Summary: A 55-year-old woman presented with an 18-month history of intermittent left-hand paresthesias affecting her first, second, and third digits. A small, immobile, nontender midline mass on the volar aspect of the left wrist was also present. Evaluation included normal routine nerve conduction studies and needle electromyography. An ultrasound was performed in the electromyography laboratory, verifying median nerve involvement of the mass within the proximal carpal tunnel. This finding guided the electromyographer to perform the unconventional technique of sensory nerve short segmental stimulation across the carpal tunnel, which confirmed focal slowing across the lesion, achieving electrodiagnostic confirmation of median nerve impairment. This case of atypical carpal tunnel syndrome due to a median nerve schwannoma demonstrates both the utility and specificity of short segmental sensory stimulation in some cases of median neuropathy at the wrist and the value of sonography in the electromyography laboratory.

Purpose: We present a unique technique applying F-wave latencies to assist in the diagnosis of peripheral neuropathy within the pediatric age group. Methods: We calculated an F-wave estimated deviance adjusted for limb length measurements, distal motor conduction velocity, and distal motor latencies. We compared the F-wave estimated deviance from the normal subjects with those with peripheral neuropathy (both axonal and demyelinating) to establish diagnostic accuracy in pediatric patients. Results: The normal range for the F-wave estimated deviance in the upper limb was −1 to +6 ms and in the lower limb was −8 to +5 ms. When compared with 82 subjects with peripheral neuropathy, there was a significant difference between the normal subjects and those with neuropathy (P values between 0.002 and 0.0005 for each of the individual nerves tested). Conclusions: The F-wave estimated deviance is independent of age and can be accurately applied to the electrodiagnostic testing of pediatric patients with suspected neuropathy.