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      Postherpetic Neuralgia and Trigeminal Neuralgia

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          Abstract

          Postherpetic neuralgia (PHN) is an unpredictable complication of varicella zoster virus- (VZV-) induced herpes zoster (HZ) which often occurs in elderly and immunocompromised persons and which can induce psychosocial dysfunction and can negatively impact on quality of life. Preventive options for PHN include vaccination of high-risk persons against HZ, early use of antiviral agents, and robust management of pain during the early stage of acute herpes zoster. If it does occur, PHN may persist for months or even years after resolution of the HZ mucocutaneous eruptions, and treatment is often only partially effective. Classical trigeminal neuralgia is a severe orofacial neuropathic pain condition characterized by unilateral, brief but recurrent, lancinating paroxysmal pain confined to the distribution of one or more of the branches of the trigeminal nerve. It may be idiopathic or causally associated with vascular compression of the trigeminal nerve root. The anticonvulsive agents, carbamazepine or oxcarbazepine, constitute the first-line treatment. Microvascular decompression or ablative procedures should be considered when pharmacotherapy is ineffective or intolerable. The aim of this short review is briefly to discuss the etiopathogenesis, clinical features, and treatment of PHN and classical trigeminal neuralgia.

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          Most cited references35

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          Trigeminal neuralgia: pathology and pathogenesis.

          There is now persuasive evidence that trigeminal neuralgia is usually caused by demyelination of trigeminal sensory fibres within either the nerve root or, less commonly, the brainstem. In most cases, the trigeminal nerve root demyelination involves the proximal, CNS part of the root and results from compression by an overlying artery or vein. Other causes of trigeminal neuralgia in which demyelination is involved or implicated include multiple sclerosis and, probably, compressive space-occupying masses in the posterior fossa. Examination of trigeminal nerve roots from patients with compression of the nerve root by an overlying blood vessel has revealed focal demyelination in the region of compression, with close apposition of demyelinated axons and an absence of intervening glial processes. Similar foci of nerve root demyelination and juxtaposition of axons have been demonstrated in multiple sclerosis patients with trigeminal neuralgia. Experimental studies indicate that this anatomical arrangement favours the ectopic generation of spontaneous nerve impulses and their ephaptic conduction to adjacent fibres, and that spontaneous nerve activity is likely to be increased by the deformity associated with pulsatile vascular indentation. Decompression of the nerve root produces rapid relief of symptoms in most patients with vessel-associated trigeminal neuralgia, probably because the resulting separation of demyelinated axons and their release from focal distortion reduce the spontaneous generation of impulses and prevent their ephaptic spread. The role of remyelination in initial symptomatic recovery after decompression is unclear. However, remyelination may help to ensure that relief of symptoms is sustained after decompression of the nerve root and may also be responsible for the spontaneous remission of the neuralgia in some patients. In addition to causing symptomatic relief, vascular decompression leads to rapid recovery of nerve conduction across the indented root, a phenomenon that, we suggest, is likely to reflect the reversal of compression-induced conduction block in larger myelinated fibres outside the region of demyelination. Trigeminal neuralgia can occur in association with a range of other syndromes involving vascular compression and hyperactivity of cranial nerves. Clinical observations and electrophysiological studies support the concept that demyelination and ephaptic spread of excitation underlie most, if not all, of these conditions.
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            The role of microglia in the pathobiology of neuropathic pain development: what do we know?

            Neuropathic pain, a maladaptive and chronic condition that can develop after a lesion or disease affecting the somatosensory system, is characterized by allodynia, hyperalgesia and spontaneous pain, and comorbidities such as sleep deprivation, depression and anxiety. The activation of microglial cells in response to nerve injury has been implicated in the development of neuropathic pain. Mediators such as Neuregulin-1, matrix metalloproteinase (MMP)-2, MMP-9, The chemokine (C-C motif) ligand 2 (CCL2) and fractalkine are released after nerve injury and are involved in the activation of microglial cells. These activated cells in turn release factors that increase the excitation and decrease the inhibition of interneurons. Microglial cells release factors such as interleukin (IL)-6, IL-1β and tumour necrosis factor-α (TNF-α) that cause the painful symptoms. It is becoming increasingly apparent that an intricate network of cytokines and cellular signalling mechanisms underpin the complex relationship between microglia and various cell types including neurones, astrocytes, oligodendrocytes, mast cells and T-cells. Although the precise mechanism of action of microglial cells in producing neuropathic pain has not been completely elucidated, research into these different activating factors and cytokines is providing further insight into the role of microglial cells in the development and maintenance of neuropathic pain. Further studies also are required to elucidate how "pain" mediators act on neurones and how the interactions between these mediators, or between neurones and glia in the presence of these mediators occur, in order to develop effective therapies for the management of neuropathic pain.
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              Postherpetic neuralgia--pathogenesis, treatment, and prevention.

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                Author and article information

                Contributors
                Journal
                Pain Res Treat
                Pain Res Treat
                PRT
                Pain Research and Treatment
                Hindawi
                2090-1542
                2090-1550
                2017
                5 December 2017
                : 2017
                : 1681765
                Affiliations
                1Department of Periodontology and Oral Medicine, Sefako Makgatho Health Sciences University, Pretoria, South Africa
                2Department of Maxillofacial and Oral Surgery, Sefako Makgatho University, Pretoria, South Africa
                Author notes

                Academic Editor: Robert L. Barkin

                Author information
                http://orcid.org/0000-0001-8209-153X
                http://orcid.org/0000-0002-8599-8249
                Article
                10.1155/2017/1681765
                5735631
                29359044
                3920c8ce-054f-459b-8f4b-dc77935b9601
                Copyright © 2017 L. Feller et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 15 August 2017
                : 25 October 2017
                : 13 November 2017
                Categories
                Review Article

                Anesthesiology & Pain management
                Anesthesiology & Pain management

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