Varicella-zoster virus (VZV) infection can cause chickenpox and herpes zoster. It sometimes involves cranial nerves, and rarely, it can involve multiple cranial nerves. We aimed to study clinical presentations of cranial nerve involvement in herpes zoster infection. We included patients who had the diagnosis of herpes zoster infection and cranial nerve involvement. The diagnosis was confirmed by typical vesicles and a rash. We excluded patients who had cranial neuralgias or neuropathies but without typical skin lesions (zoster sine herpete or post-herpetic neuralgia). We included 330 patients (mean age, 55.0 ± 17.0 years) who had herpes zoster with cranial nerve involvement, including 155 men and 175 women. Most frequently involved cranial nerves were the trigeminal nerve (57.9%), facial nerve (52.1%), and vestibulocochlear nerve (20.0%). Other involved cranial nerves included the glossopharyngeal nerve (0.9%), vagus nerve (0.9%), oculomotor nerve, trochlear nerve, and abducens nerve (each 0.3%, respectively). One hundred and seventy patients (51.5%) had only sensory symptoms/signs; in contrast, 160 patients (48.5%) had both sensory and motor symptoms/signs. Of those 160 patients, sensory preceded motor symptoms/signs in 64 patients (40.0%), sensory and motor symptoms/signs occurred simultaneously in 38 patients (23.8%), and motor preceded sensory symptoms/signs in 20 patients (12.5%). At one month after herpes zoster infection, vesicles and rash disappeared in 92.6% of patients; meanwhile facial palsy showed a significant improvement in 81.4% of patients (p < 0.05). Cranial motor neuropathies are not infrequent in herpes zoster infections. Multiple cranial nerve involvement frequently occurred in Ramsay Hunt syndrome. We found a significantly increased seasonal occurrence of cranial nerve zoster in spring rather than summer. Cranial motor nerves were affected while the hosts sometimes had a compromised immune system.

Our previous studies have shown that early systemic granulocyte colony-stimulating factor (G-CSF) treatment can attenuate neuropathic pain in rats with chronic constriction injury (CCI) by modulating expression of different proinflammatory cytokines, microRNAs, and proteins. Besides the modulation of inflammatory mediators’ expression, previous studies have also reported that G-CSF can modulate autophagic and apoptotic activity. Furthermore, both autophagy and apoptosis play important roles in chronic pain modulation. In this study, we evaluated the temporal interactions of autophagy, and apoptosis in the dorsal root ganglion (DRG) and injured sciatic nerve after G-CSF treatment in CCI rats. We studied the behaviors of CCI rats with or without G-CSF treatment and the various levels of autophagic, proinflammatory, and apoptotic proteins in injured sciatic nerves and DRG neurons at different time points using Western blot analysis and immunohistochemical methods. The results showed that G-CSF treatment upregulated autophagic protein expression in the early phase and suppressed apoptotic protein expression in the late phase after nerve injury. Thus, medication such as G-CSF can modulate autophagy, apoptosis, and different proinflammatory proteins in the injured sciatic nerve and DRG neurons, which have the potential to treat neuropathic pain. However, autophagy-mediated regulation of neuropathic pain is a time-dependent process. An increase in autophagic activity in the early phase before proinflammatory cytokines reach the threshold level to induce neuropathic pain can effectively alleviate further neuropathic pain development.

Study Objectives: This retrospective study investigated prognostic factors and recovery time in patients with Bell’s palsy after different doses and durations of oral glucocorticoid treatments. Subjects and Methods: A total of 396 patients initially diagnosed with Bell’s palsy that had visited the Department of Neurology of Chang Gung Memorial Hospital, Taoyuan, a tertiary referral medical center in Taiwan, between January 2014 and December 2018 were included. Medical records, facial electroneurography (fENoG), and blink reflex (BR) tests were reviewed and analyzed. A favorable outcome was defined as patients who improved to grade ≤ II, and an unfavorable outcome was defined as patients who improved to grade ≥ III in 6 months according to the House–Brackmann (HB) grading system. Results: The rate of favorable outcomes was 89.4% (354 of 396 patients) at the 6-month follow-up. A favorable outcome (HB less than grade II) was associated with a delayed BR (odds ratio, OR, 5.38; 95% CI, 1.82 to 15.90) and fENoG values (the lesion side/the healthy side) over 33% (OR, 6.67; 95% CI, 3.02 to 14.71). The recovery time was significantly shorter for those with a delayed BR than for those with an absent BR and shorter for those with good fENoG values (>33%) than for those with poor values (≤33%). However, treatment without or with different doses and durations of oral glucocorticoid did not influence the final outcome or recovery time in this study. Conclusions: The fENoG and BR tests were significant and highly valuable examinations for predicting the final outcome. Moreover, age younger than 60 years, a delayed BR, and fENoG values > 33% were associated with shorter recovery times.