Chronic pain is a critical clinical problem with an increasing prevalence. However, there are limited effective prevention measures and treatments for chronic pain. Astrocytes are the most abundant glial cells in the central nervous system and play important roles in both physiological and pathological conditions. Over the past few decades, a growing body of evidence indicates that astrocytes are involved in the regulation of chronic pain. Recently, reactive astrocytes were further classified into A1 astrocytes and A2 astrocytes according to their functions. After nerve injury, A1 astrocytes can secrete neurotoxins that induce rapid death of neurons and oligodendrocytes, whereas A2 astrocytes promote neuronal survival and tissue repair. These findings can well explain the dual effects of reactive astrocytes in central nervous injury and diseases. In this review, we will summarise the (1) changes in the morphology and function of astrocytes after noxious stimulation and nerve injury, (2) molecular regulators and signalling mechanisms involved in the activation of astrocytes and chronic pain, (3) the role of spinal and cortical astrocyte activation in chronic pain, and (4) the roles of different subtypes of reactive astrocytes (A1 and A2 phenotypes) in nerve injury that is associated with chronic pain. This review provides updated information on the role of astrocytes in the regulation of chronic pain. In particular, we discuss recent findings about A1 and A2 subtypes of reactive astrocytes and make several suggestions for potential therapeutic targets for chronic pain.

Morphine tolerance is a classic, challenging clinical issue. However, the mechanism underlying this phenomenon remains poorly understood. Recently, studies have shown that ferroptosis correlates with drug resistance. Therefore, this study investigated whether spinal cord ferroptosis contributes to morphine tolerance. C57BL/6 mice were continuously subcutaneously injected with morphine, with or without the ferroptosis inhibitor liproxstatin-1. We found that chronic morphine exposure led to morphine antinociception tolerance, accompanied by loss of spinal cord neurons, increase in the levels of iron, malondialdehyde, and reactive oxygen species, and decreases in the levels of superoxide dismutase. Additionally, inflammatory response and mitochondrial shrinkage, processes that are involved in ferroptosis, were observed. Simultaneously, we found that 10 mg/kg of liproxstatin-1 could alleviate iron overload by balancing transferrin receptor protein 1/ferroportin expression and attenuate morphine tolerance by increasing glutathione peroxidase 4 levels, while reducing the levels of malondialdehyde and reactive oxygen species. It also downregulated the expression of extracellularly regulated protein kinases that had been induced by chronic morphine exposure. Our results indicate that spinal cord ferroptosis contributes to morphine tolerance, while liproxstatin-1 attenuates the development of morphine tolerance. These findings suggest that ferroptosis may be a potential therapeutic target for morphine tolerance.

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The aim of the study was to describe and evaluate the efficacy of the keyhole microsurgery to manage patients with trigeminal neuralgia (TN), hemifacial spasm (HFS) and glossopharyngeal neuralgia (GPN). Two hundred and seven patients underwent microvascular decompression (MVD) and neurotomy via retrosigmoid keyhole approach in our department clinic: MVD for trigeminal neuralgia 169 cases, hemifacial spasm 31 cases, glossopharyngeal neuralgia 4 cases and neurotomy for glossopharyngeal neuralgia 3 cases. There was no serious complication such as deaths or infarction in the cerebellum or the brainstem. Complete and partial symptoms relief was obtained in 160 (94.7%) cases and failure 9 (5.3%) cases with MVD for trigeminal neuralgia, postoperatively. Meanwhile, complications occurred in one case with cerebellar hematoma only. The postoperative results of MVD for hemifacial spasm with symptoms relief was noted in 29 (93.5%) cases and failure 2 (6.5%) cases. Postoperative complications occurred in one case with moderate hearing loss, another three cases complained of transient facial paralysis. Symptoms relief achieved in all 7 (100%) cases undergone MVD or neurotomy for glosspharyngeal neuralgia. Postoperative complications occurred in one case with moderate vocal paralysis. We think that microsurgery via retrosigmoid keyhole approach is safe and effective for CPA hyperactive cranial nerve dysfunction syndromes.

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Background During medical imaging, cystic radiation encephalopathy and brain metastasis are difficult to differentiate, and hence they are easily misdiagnosed. To our knowledge, a nasopharyngeal carcinoma recurrence after more than seven years with cerebral metastasis that mimicked cystic radiation encephalopathy has not been reported. Case presentation A 52-year-old man was admitted to the hospital owing to weakness of the right limb for one month, which increased in intensity for three days. He had been diagnosed with nasopharyngeal carcinoma in 2011, which was treated by radiotherapy. The patient successively developed cystic radiation encephalopathy and brain metastasis from the nasopharyngeal carcinoma, which mimicked cystic radiation encephalopathy relapse. Left frontotemporal craniotomy, surgical resection of brain metastasis, and repair of the skull base and dura were performed. Postoperative computed tomography showed that midline deviation recovered, and brain edema was reduced. Conclusions This report is significant because brain metastasis from nasopharyngeal carcinoma can masquerade as a benign entity and cause fatal consequences. In patients presenting with cystic radiation encephalopathy, brain metastasis should be considered as a differential diagnosis.

Disruption of neural connections among regions regulating mood and cognition rather than cerebrovascular lesions may contribute to post-stroke depression (PSD). In this paper, we hypothesized that structural abnormalities in white matter structure like cingulate cortex induced by focal infarcts would play a role in mood regulation or depression after stroke onset. Various DTI coefficients including FA, RD and ADC with multiple signal distribution measurements were collected and statistically analyzed. The results identify significant differences in volume and multiple diffusion indices of DTI intensity distribution in cingulate cortex between PSD patients and the normal control. It indicates the neuronal loss secondary to demyelination in cingulate cortex due to stroke. Additionally, the volume loss of cingulate cortex in PSD patients observed in the results may further demonstrate the reduction of glial cells in cingulate cortex, as the axonal number/size changed little.