Articles: neuropathic-pain.
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The present study investigated the role of the amygdala N-methyl-d-aspartate (NMDA) receptors/nitric oxide synthase pathway in morphine-induced anti-allodynia. Concurrently with the bilateral cannulation of the central amygdala, chronic constriction of the sciatic nerve was performed on male Wistar rats. Morphine (3-5 mg/kg) was administered intraperitoneally to induce anti-allodynia. ⋯ PERSPECTIVE: Neuropathic pain is difficult to treat and the exact mechanisms remain unknown. This article suggests the importance of the amygdala glutamatergic and nitric oxide systems in morphine-induced anti-allodynia. These findings might be used in clinical studies to reach a better understanding of neuropathic pain mechanisms and treatment.
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Case Reports
Spinal Cord Stimulator Explant and Revision Complicated by Syrinx Formation: A Case Report and Literature Review.
Spinal cord stimulation (SCS) has been shown to be a safe, effective, and drug-free treatment option for many chronic pain conditions including refractory low back pain. The most commonly reported complication of SCS is equipment failure. We report a case of spinal cord injury (SCI) during SCS explant and revision. This 61-year-old female veteran complained of intermittent shock-like sensations 3-4 times a week for three months prior to her clinic visit. The device was initially implanted in 2009 secondary to neurogenic claudication with appropriate relief. The battery was replaced in 2015. Pain Management Service referred the patient to neurosurgery for replacement of the original SCS unit. Immediately following surgery she complained of severe left lower extremity pain concentrated in the medial thigh radiating into the groin and buttock. She also complained of pain, weakness and numbness in both legs (left more than right). Magnetic resonance imaging (MRI) revealed an edematous area in the left spinal cord between T11-T12. The patient was placed on steroids, ketamine infusion for pain control, and MRI the next day showed slight improvement of the edema and she was discharged home. Follow-up MRI two months later revealed mild diminution in the size of the cord edema. Her pre-operative shock-like sensations had not returned. While rare, spinal cord injury can occur and should be identified and managed expeditiously. Our case here reports for the first time an association between SCS explant/revision and syrinx formation.
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Herpes zoster (HZ) is caused by the reactivation of varicella zoster virus. The incidence of herpes zoster and associated problems increases with age. With a life-long prevalence of 30%, every second 85-year-old person experiences HZ once in his lifetime. ⋯ HZ vaccination represents a substantial improvement in terms of prevention of herpes zoster and reduction of long-term complications, such as PHN. The permanent vaccination commission of the Robert Koch Institute recommends vaccination with dead virus for all persons over the age of 60 years. Risk groups like immunosuppressed patients are advised to be vaccinated starting at the age of 50 years.
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Spinal cord injury (SCI) results in not only motor dysfunction but also chronic neuropathic pain. Allodynia, an abnormal sensation that evokes pain against non-noxious stimuli, is a major symptom of post-SCI neuropathic pain. Astrocytic activation is a cause of post-SCI neuropathic pain and is considered a key treatment target. However, no effective treatment for these problems is available to date. ONO-2506 is a novel agent that suppresses astrocytic activation by inhibition of S100B production from astrocytes. Recently, it has been demonstrated that ONO-2506 inhibits secondary injury and improves motor function after SCI. ⋯ Administration of ONO-2506 attenuated post-SCI neuropathic pain in a rat model of incomplete SCI. Histologic results support that the inhibition of S100B production and subsequent suppression of astrocytic activation contributed to the reduction in neuropathic pain.
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Hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels are activated during hyperpolarization, and there is an inward flow of current, which is termed as hyperpolarization-activated current, Ih. Initially, these channels were identified on the pacemaker cells of the heart. Nowadays, these are identified on different regions of the nervous system, including peripheral nerves, dorsal root ganglia, dorsal horns, and different parts of the brain. ⋯ There have been few studies documenting the relationship of HCN channels with other mediators of pain. Nevertheless, it may be proposed that the HCN channel activity is modulated by endogenous opioids and cyclo-oxygenase-2, whereas the activation of these channels may modulate the actions of substance P and the expression of spinal N-methyl-D-aspartate receptor subunit 2B to modulate pain. The present review describes the role and mechanisms of HCN ion channels in the development of neuropathic pain.