Pain
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The systemic administration of anti-nerve growth factor (NGF) antibodies can prevent local sensory hypersensitivity and block nociceptive fibers from sprouting into denervated adult rat skin. However, in the case of chronic constriction injury (CCI) in a rat, there is evidence that NGF reverses some effects of axotomy and alleviates thermal hyperalgesia. It is with this in mind that we investigated the influence of local anti-NGF and NGF on neuropathic pain and collateral sprouting caused by CCI. ⋯ The results show that the effect of anti-NGF is delayed at the onset, is short in duration, and is dependent on the dosage. However, anti-NGF but not NGF blocked collateral sprouting and decreased the severity of autotomy, suggesting that anti-NGF may be a better potential alternative analgesic for the treatment of neuropathic pain in humans. The different initiation times to abolish thermal hyperalgesia by anti-NGF (delayed onset) and NGF (early onset) suggests that alterations in neurotrophic factors contribute to the development of behavioral hyperalgesia via a complex mechanism in CCI rats.
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Trigeminal neuralgia is an example of an extreme form of neuropathic pain and continues to be a real therapeutic challenge. Although the pathophysiology of the disorder is uncertain, vascular compression of the trigeminal root resulting in damage to primary afferent neurons is thought to play a major role in the generation of pain. In the present study, we have used a recently developed rat model of trigeminal neuropathic pain, where the neuropathy is produced by a chronic constriction injury of the infraorbital branch of the trigeminal nerve (CCI-ION), and for the first time studied the effects of various pharmacological treatments on this purely sensory model of neuropathic pain. ⋯ Repeated injections of baclofen (3 mg/kg s.c.) partially alleviated the mechanical allodynia-like behaviour without effects on rotarod performance. The partial anti-allodynic effect of a single injection (5 mg/kg) of baclofen, which was already accompanied by slight motor disturbances, could be antagonized by CGP35348, a selective GABA(B)-receptor antagonist. Functional deficits in the GABAergic system may play an important role in the pathogenesis of this purely sensory rat model of trigeminal neuropathic pain.
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Clinical Trial
A blinded pilot study investigating the use of diagnostic ultrasound for detecting active myofascial trigger points.
Myofascial trigger points (MFTPs) have been cited by numerous authors as the cause of local and referred pain which arises from muscle and its surrounding fascia. At present there is no reliable objective test which is capable of determining their presence. ⋯ Eleven subjects with clinically identified, unilateral, active MFTPs were examined with diagnostic ultrasound at the site of the trigger point as well as the asymptomatic, contralateral side. The analysis of the results of this pilot study found no correlation between the clinical identification of active MFTPs and diagnostic ultrasound.
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The management of trigeminal neuralgia in older patients who do not want neurolytic block and/or surgical treatment may be problematic. This paper describes three patients who had first and/or second division trigeminal neuralgia. The analgesic effects of infraorbital nerve block using 0.5% bupivacaine or 1% mepivacaine dissipated within a few days, however, the effects of nerve blocks using 4% tetracaine dissolved in 0.5% bupivacaine continued for more than 3 months. Hypesthesia was observed in two patients within a week following the block, but sensory level returned to normal within 2 weeks and there were no further complications in any patient.
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The role of nerve growth factor (NGF) and glial-derived neurotrophic factor (GDNF) in sympathetic sprouting within the dorsal root ganglion was investigated. In nerve-intact rats, intrathecal NGF (1 mg/ml, 14 days) but not GDNF (1 mg/ml, 14 days) induced extensive sprouting of tyrosine hydroxylase immunoreactive (TH-IR) fibres and formation of pericellular TH-IR baskets within lumbar DRGs. TH-IR baskets were distributed equally to trkA-expressing and trkA-negative neuronal profiles. ⋯ Distribution of sympathetic sprouts within the DRG is independent of whether target neurons are injured or express trkA. Sequestration of NGF at the peripheral injury site does not influence basket formation within the DRG. It is likely that functional noradrenergic connections exist between sympathetic sprouts and sensory neuron cell bodies following exogenous NGF.