Zoster Segmental Paralysis: Clinical and Electrodiagnostic Features in a Retrospective Case Series of 17 Patients

Background and objective Herpes zoster infection is due to reactivation of the varicella zoster virus, usually at the dorsal root ganglia, leading to classic skin lesions and neuralgic pain. Concurrent involvement of motor axons/cells may cause segmental paralysis. We sought to describe the clinical and electrodiagnostic (EDX) findings in a cohort of patients with zoster segmental paralysis (ZSP). Methods This is a retrospective study of 17 patients with historical and clinical evidence of ZSP of the upper extremities (UE) or lower extremities (LE), confirmed by EDX studies. The clinical metrics collected included (1) demographics; (2) relevant history, including herpes zoster and/or herpes zoster vaccination; and (3) clinical findings (sensory, motor, and reflexes) and localization of the motor deficit. The EDX protocol included motor and sensory nerve conduction studies and needle electromyography (EMG). Metrics collected included motor and sensory conduction velocity, alterations in compound muscle action potentials (CMAP) and sensory nerve action potentials (SNAP), and signs of denervation in muscles detected by needle EMG, as well as their topography for precise localization. Results In our study, of the 17 patients with ZSP by history, the UE were involved in 15 (88.2%) patients and the LE in two (11.8%). All patients had weakness of specific muscles of the UE or LE corresponding to the dermatomal location of the skin eruptions. Of the 15 patients who had symptoms of the UE, the most frequent clinical localization of the motor deficit was the C8 and T1 nerve roots (8 (53.3%)). Of the two patients who had symptoms of the LE, the localization of the motor deficit was the L5 and S1 nerve roots in one and the L5 nerve root in the other. Fifteen (88.2%) patients had sensory abnormalities of either the UE or LE, which consisted of either decreased pinprick sensation or allodynia. The EDX studies revealed abnormal motor conduction in 15 (88.2%) patients, displayed by diffuse slowing of motor conduction and/or low amplitude or absence of the CMAP. Sensory conduction was abnormal in 16 (94.1%) patients, with either decreased or absent SNAP. Thirteen (76.5%) patients demonstrated abnormal spontaneous activity suggestive of denervation. Of the 15 patients with UE symptoms, the EDX localization was most frequently at the C8-T1 ventral root/horn cell (V) and dorsal root ganglion (D) in 8 (53.3%) patients. In the two patients with LE symptoms, the EDX location was at the L5-S1 ventral root/horn cell and dorsal root ganglion in one, and the L5 ventral root/horn cell and dorsal root ganglion in the other. Conclusions ZSP is a rare complication of herpes zoster infection. Physicians should consider ZSP in the differential diagnosis when patients present with acute onset of muscle weakness in a radicular distribution and should look for skin lesions suggestive of herpes zoster in the corresponding dermatome. EDX studies are highly useful in confirming the radicular/segmental topography of muscle denervation. In this study of a large cohort of patients with ZSP confirmed by EDX, we describe the clinical and EDX findings to improve clinical detection of this uncommon condition.