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Background/Aims. Despite the wide use of acupuncture for the management of visceral pain and the growing interest in the pathophysiology of visceral pain, there is no conclusive elucidation of the mechanisms behind the effects of acupuncture on visceral pain. This systematic review aims to provide an integrative understanding of the treatment mechanism of acupuncture for visceral pain. Methods. Electronic and hand searches were conducted to identify studies that involved visceral pain and acupuncture. Results. We retrieved 192 articles, out of which 46 studies were included in our review. The results of our review demonstrated that visceral pain behaviors were significantly alleviated in response to acupuncture treatment in groups treated with this intervention compared to in sham acupuncture or no-treatment groups. Changes in the concentrations of β-endorphin, epinephrine, cortisol, and prostaglandin E2 in plasma, the levels of c-Fos, substance P, corticotropin-releasing hormone, P2X3, acetylcholinesterase (AchE), N-methyl-D-aspartate (NMDA) receptors, and serotonin in the gut/spinal cord, and the neuronal activity of the thalamus were associated with acupuncture treatment in visceral pain. Conclusions. Acupuncture reduced visceral pain behavior and induced significant changes in neuronal activity as well as in the levels of pain/inflammation-related cytokines and neurotransmitters in the brain-gut axis. Further researches on the thalamus and on a standard animal model are warranted to improve our knowledge on the mechanism of acupuncture that facilitates visceral pain modulation. [ABSTRACT FROM AUTHOR]

Pain can trigger central amplification called central sensitization, which ultimately results in hyperalgesia and/or allodynia. Many reports have showed acupuncture has an analgesic effect. We searched the related article on PubMed database and Cochrane database to discover central sensitization pathway in acupuncture analgesia. We summarized that acupuncture enhances the descending inhibitory effect and modulates the feeling of pain, thus modifying central sensitization. The possible mechanisms underlying the analgesic effects of acupuncture include segmental inhibition and the activation of the endogenous opioid, adrenergic, 5-hydroxytryptamine, and N-methyl-D-aspartic acid, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/kainate pathways. Moreover, acupuncture can locally reduce the levels of inflammatory mediators. In clinical settings, acupuncture can be used to treat headache, neuropathic pain, low back pain, osteoarthritis, and irritable bowel syndrome. These mechanisms of acupuncture analgesia may be involved in the alleviation of central sensitization. [ABSTRACT FROM AUTHOR]

Neuronal signaling together with synapse activity in the central nervous system requires a precisely regulated microenvironment. Recently, the blood-brain barrier is considered as a “neuro-glia-vascular unit,” a structural and functional compound composed of capillary endothelial cells, glial cells, pericytes, and neurons, which plays a pivotal role in maintaining the balance of the microenvironment in and out of the brain. Tight junctions and adherens junctions, which function as barriers of the blood-brain barrier, are two well-known kinds in the endothelial cell junctions. In this review, we focus on the less-concerned contribution of gap junction proteins, connexins in blood-brain barrier integrity under physio-/pathology conditions. In the neuro-glia-vascular unit, connexins are expressed in the capillary endothelial cells and prominent in astrocyte endfeet around and associated with maturation and function of the blood-brain barrier through a unique signaling pathway and an interaction with tight junction proteins. Connexin hemichannels and connexin gap junction channels contribute to the physiological or pathological progress of the blood-brain barrier; in addition, the interaction with other cell-cell-adhesive proteins is also associated with the maintenance of the blood-brain barrier. Lastly, we explore the connexins and connexin channels involved in the blood-brain barrier in neurological diseases and any programme for drug discovery or delivery to target or avoid the blood-brain barrier. [ABSTRACT FROM AUTHOR]

Nowadays, mantle cell lymphoma is considered to have one of the worst prognostic profiles among lymphoid malignancies. Mantle cell lymphoma rarely affects the central nervous system (CNS) as it represents about 0.9% of diagnosis and 4% among recurrent cases. Here, we present the case of a 69-year-old male patient who was diagnosed with mantle cell lymphoma in 2006. The patient relapsed three times, without affecting the CNS, then was treated accordingly, and achieved complete remission three times. Four years after his last complete remission, upon receiving his last dose of treatment, the medical team noted a rapid worsening of the patient’s neurological status followed by a deep coma state causing MCL neurological recurrence by exclusion diagnosis. The patient then received ibrutinib via a nasogastric tube at a dose of 560 mg daily. Two days after receiving his last dose of ibrutinib, the patient regained full consciousness, and 10 days later, he was discharged from the hospital. The patient achieved complete remission and showed no signs of neurological damages for 24 months following his ibrutinib treatment. We believe that the administration of ibrutinib through the nasogastric tube was a determinant factor in this patient’s remission and survival. [ABSTRACT FROM AUTHOR]

Peripheral nerve regeneration is a unique process in which cellular rather than tissue response is involved. Depending on the extent and proximity of the lesion and the age and type of the neuronal soma, the cell body may either initiate a reparative response or may die. Microsurgical intervention may alter the prognosis after a peripheral nerve injury but to a certain extent. By altering the biochemical microenvironment of the neuron, we can increase the proportion of neurons that survive the injury and initiate the reparative response. Thyroid hormone critically regulates tissue growth and differentiation and plays a crucial role during organ development. Furthermore, recent research has provided new insight into thyroid hormone cellular action. Thyroid hormone regulates stress response intracellular signaling and targets molecules important for cytoskeletal stability and cell integrity. Changes in thyroid hormone signaling occur in nerve and other tissues, with important physiological consequences. The interest in thyroid hormone in the context of nerve regeneration has recently been revived. [ABSTRACT FROM AUTHOR]