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Objective The detailed characteristics and prognosis of nonsurgery-related unilateral vocal fold paralysis (NSUVFP) are currently unclear. This study evaluated the extent of laryngeal nerve lesions and the individual characteristics for patients with NSUVFP. Study Design Retrospective, case series. Methods Patients with unilateral vocal fold paralysis (UVFP) were evaluated using videolaryngostroboscopy and quantitative laryngeal electromyography. The side of nerve lesions, involvement of the external branch of the superior laryngeal nerve (eSLN), and complete vocal fold motion recovery were evaluated after ≥ 6 month follow-up. Results A total of 207 UVFP patients were recruited, including 153 surgery-related UVFP and 54 NSUVFP patients. Thirty-four (63%) and 20 (37%) NSUVFP patients were further assigned to idiopathic and nonsurgery-related–nonidiopathic (NSNI) groups, respectively. In the idiopathic group, eSLN lesions occurred in all six (100%) patients with right-side paralysis, but in only six of 28 (21%) patients with left-side paralysis (P 0.05). Conclusion Idiopathic and NSNI UVFP have different clinical presentations defined by laryngeal electromyography. NSNI UVFP had more severe denervation changes compared with idiopathic UVFP. These results may support two pathogenic mechanisms for idiopathic UVFP: 1) neuropathy specifically involving left recurrent laryngeal nerve (RLN), and 2) neuropathy affecting nerves proximal to the RLN. Level of Evidence 4. Laryngoscope, 2016

Rippling muscle disease (RMD) is a myopathy with hyperirritability, the pathophysiology for which is uncertain.We report electromyographic findings in a 30-year-old man with RMD. Clinical features included muscle rippling and percussion-induced rapid muscle contractions. Both were associated with bursts of short-duration, low-amplitude spikes, which resembled single muscle fiber discharges. Our case stands in contrast to previously reported cases, which showed either electrical silence or motor unit potential discharges associated with rippling, and may represent muscle fiber hyperexcitability.

Electrophysiologic findings in thallium intoxication are usually untimely, limited in extent, and often uninformative. This report documents serial conduction and electromyographic findings in a case of thallium poisoning, beginning 10 days after symptom onset and ending 24 months later. Initially, the plantar nerves in the foot demonstrated profound axonal loss while the sural and peroneal nerves were essentially normal. The latter two nerves subsequently underwent axonal loss. Two years were required for the sural and peroneal nerves to display recovery. At 24 months, the plantar nerves continue to remain absent. A primarily distal axonopathy, significantly worse in the lower than upper extremities and requiring more than 2 years for recovery, now documents what was previously speculated: the electrophysiologic course of thallium intoxication. Additionally, this case emphasizes the need to examine the plantar nerves of the foot to avoid missing distal axonopathies during the early course of the disease process. The clinical course and pathophysiology of thallium poisoning are also reviewed.