Comparison of Prognostic Scoring Systems to Predict Durable Pain Relief After Microvascular Decompression for Trigeminal Neuralgia.

BACKGROUND: Microvascular decompression (MVD) is an effective treatment for trigeminal neuralgia, but pain recurs in a substantial minority of patients. Two recently published scoring systems by Hardaway et al. and Panczykowski et al. use simple preoperative clinical and imaging features to predict durable pain relief following MVD, but their predictive performance has not been independently validated. This study aimed to compare predictive performance of the Hardaway et al. score (HS) and Panczykowski et al. score (PS) for 1-year, 3-year, and long-term pain-free outcomes after MVD for trigeminal neuralgia. METHODS: HS and PS were computed for a retrospective, single-institution cohort of 68 patients with trigeminal neuralgia who underwent MVD. Primary outcome was pain recurrence after MVD. Predictive performance of HSs and PSs was evaluated with area under the curve sensitivity analysis and regression models for survival analyses at 1 year, 3 years, and last follow-up. RESULTS: Area under the curve for predicting pain-free outcome was higher for PS versus HS at 1 year (0.873 vs. 0.775) and 3 years (0.793 vs. 0.704). Cox proportional hazard models showed that PS better predicted long-term pain-free outcomes compared with HS (P < 0.05). One-year pain-free outcome was best predicted by pain type; longer-term outcomes were better predicted by presence and degree of neurovascular compression on preoperative imaging. CONCLUSIONS: PS is superior to HS in predicting pain-free outcomes after MVD, which may aid in patient selection and counseling. Overall, more significant neurovascular compression of the trigeminal nerve root, and to a lesser extent classical paroxysmal pain, are good predictors of durable pain relief after MVD.

Human endogenous retrovirus-K(II) envelope induction protects neurons during HIV/AIDS.

Human endogenous retroviruses (HERVs) are differentially expressed depending on the cell type and physiological circumstances. HERV-K has been implicated in the pathogenesis of several diseases although the functional consequences of its expression remain unknown. Human immunodeficiency virus (HIV) infection causes neuroinflammation with neuronal damage and death. Herein, we investigated HERV-K(II)/(HML-2) envelope (Env) expression and its actions in the brain during HIV/AIDS. HERV-K(II) Env expression was assessed in healthy brain tissues, autopsied HIV HIV- infected (HIV+) and uninfected (HIV-) brains and in neural cell cultures by real time RT-PCR, massively parallel (deep) sequencing, immunoblotting and immunohistochemistry. Neuronal and neural stem cells expressing HERV-K(II) Env were analyzed in assays of host responses including cellular viability, immune responses and neurobehavioral outcomes. Deep sequencing of human brain transcriptomes disclosed that RNA sequences encoded by HERV-K were among the most abundant HERV sequences detected in human brain. Comparison of different cell types revealed that HERV-K(II) env RNA abundance was highest in cultured human neurons but was suppressed by epidermal growth factor exposure. HERV-K(II) Env immunoreactivity was increased in the cerebral cortex from persons with HIV/AIDS, principally localized in neurons. Human neuronal cells transfected with HERV-K(II) Env exhibited increased NGF and BDNF expression. Expression of HERV-K(II) Env in neuronal cells increased cellular viability and prevented neurotoxicity mediated by HIV-1 Vpr. Intracerebral delivery of HERV-K(II) Env expressed by neural stem cells suppressed TNF-α expression and microglial activation while also improving neurobehavioral deficits in vpr/RAG1-/- mice. HERV-K(II) Env was highly expressed in human neurons, especially during HIV/AIDS, but in addition exerted neuroprotective effects. These findings imply that HERV gene products might exert adaptive effects in circumstances of pathophysiological stress, perhaps underlying the conservation of HERVs within the human genome.