High-grade OXA neurotoxicity can be predicted by clinical and neurophysiological information obtained at mid-treatment. Neurological assessment of acute neuropathy symptoms and radial and dorsal sural nerves NCS should be carefully monitored to predict and hopefully prevent the induction of severe OXAIPN.

We read with great interest the case report on neuralgic amyotrophy following infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). 1 Respiratory symptoms are the primary manifestations of SARS-Cov-2 infection. Reports of several neurologic manifestations have

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This prospective study sought to identify the potential reversibility of oxaliplatin-induced peripheral neuropathy (OXAIPN) by following-up its long-term course 2 years after discontinuation of oxaliplatin (OXA)-based chemotherapy. Participants were 91 colorectal cancer patients treated with OXA-based chemotherapy. Neurological assessment, clinical Total Neuropathy Score© (TNSc©) and nerve conduction studies were performed at baseline (T0), the end of chemotherapy (T1) and 2 years (T2) after discontinuation of chemotherapy. A total of 73 of 91 (80%) patients experienced OXAIPN at T1. At a median follow-up of 25 months, persistence of chronic OXAIPN was present in 61 of 73 patients (84%) and complete resolution was present in 12 patients (17%). Longitudinal comparison of TNSc© values between T1 and T2 revealed that the overall severity of OXAIPN in those 61 patients significantly decreased over time. Median TNSc© values were nine (range: 2-15) at T1 vs. four (range: 2-12) at T2 (P < 0.001). Likewise, sensory nerve conduction measures at T2 significantly improved in all sensory nerves tested, compared with T1. Severity of OXAIPN at T2 was significantly associated (P < 0.001) with high severity of OXAIPN at T1. In conclusion, persistence of OXAIPN beyond 2 years after finishing chemotherapy is common. Clinical and neurophysiological improvement is observed, although recovery is often incomplete.

ABSTRACT:Introduction: Nerve ultrasound in CharcotMarie-Tooth (CMT) disease has focused mostly on the upper limbs. We performed an evaluation of a large cohort of CMT patients in which we sonographically characterized nerve abnormalities in different disease types, ages, and nerves. Methods: Seventy patients affected by different CMT types and hereditary neuropathy with liability to pressure palsies (HNPP) were evaluated, assessing median, ulnar, fibular, tibial, and sural nerves bilaterally. Data were correlated with age. Results: Nerve dimensions were correlated with CMT type, age, and nerve site. Nerves were larger in demyelinating than in axonal neuropathies. Nerve involvement was symmetric. Discussion: CMT1 patients had larger nerves than did patients with other CMT types. Patients with HNPP showed enlargement at entrapment sites. Our study confirms the general symmetry of ultrasound nerve patterns in CMT. When compared with ultrasound studies of nerves of the upper limbs, evaluation of the lower limbs did not provide additional information. Muscle Nerve 57: E18-E23, 2018Charcot-Marie-Tooth disease (CMT) comprises a heterogeneous group of hereditary sensory-motor neuropathies with a wide spectrum of clinical and neurophysiological features. CMT is generally divided into demyelinating (CMT1) and axonal (CMT2) forms, although intermediate forms are present. CMT neuropathies are further categorized by genetic mutations. CMT1A is the most frequent form, and is associated with a duplication of the peripheral myelin protein-22 gene (PMP22). Other less common CMT1 subtypes are associated with mutations in the MPZ (CMT1B), LITAF (CMT1C), and EGR2 (CMT1D) genes. X-linked CMTX1, the second most common form, is usually considered an intermediate form, associated with mutations of the GJB1 gene, encoding connexin-32. Among CMT2 subtypes, CMT2A is caused by MFN2 mutations, CMT2E by NEFL mutations, and CMT2K by GDAP1 involvement. 1 Hereditary neuropathy with liability to pressure palsies (HNPP) is associated with deletion of the PMP22 gene and is a diffuse disease with a predisposition to focal compression neuropathies or plexopathies. It is not strictly a type of CMT, but in several studies it was considered together with CMT because of the involved gene and the neurophysiological findings. Moreover, recent preliminary results from imaging studies, either magnetic resonance imaging or ultrasound (US), showed many similarities with CMT