Materiały źródłowe

• #1 Postherpetic neuralgia: epidemiology, pathophysiology, and pain management pharmacology

  https://pmc.ncbi.nlm.nih.gov/articles/PMC5036669/

  Postherpetic neuralgia is a neuropathic pain syndrome characterized by pain that persists for months to years after resolution of the herpes zoster rash. […] It stems from damage to peripheral and central neurons that may be a byproduct of the immune/inflammatory response accompanying varicella zoster virus reactivation. […] PHN occurs in the same dermatomes as the HZ rash, and stems from damage to peripheral and central neurons that may be a byproduct of the immune/inflammatory response that accompanied VZV reactivation and migration. […] When damaged, peripheral and central nerve fibers may develop a lower threshold for action potentials, discharge spontaneously, and exhibit disproportionate responses to stimuli, resulting in peripheral sensitization and pain without painful stimuli (allodynia).

• #1 Postherpetic neuralgia: epidemiology, pathophysiology, and pain management pharmacology

  https://pmc.ncbi.nlm.nih.gov/articles/PMC5036669/

  Patients with PHN experience three major types of pain: 1) constant pain without a stimulus (often described as burning, aching, or throbbing), 2) intermittent pain without a stimulus (often described as stabbing, shooting, or electric shock-like), and 3) pain brought on by a stimulus but is disproportionate to the stimulus (hyperalgesia), enduring for at least 3 months after healing of the HZ-related skin rash. […] The safety and tolerability of pharmacologic therapies are important issues to consider as PHN affects primarily an older population. […] Once PHN has been diagnosed, treatment should be directed at pain control and minimizing treatment-related adverse events. […] No single best treatment has been identified. […] Current guidelines recommend treatment of PHN in a hierarchical manner, with calcium channel 2- ligands (gabapentin and pregabalin), tricyclic antidepressants (amitriptyline, nortriptyline, or desipramine), or topical lidocaine patches as first-line drugs.

• #2 Postherpetic neuralgia: epidemiology, pathophysiology, and pain manage | JMDH

  https://www.dovepress.com/postherpetic-neuralgia-epidemiology-pathophysiology-and-pain-managemen-peer-reviewed-fulltext-article-JMDH

  Postherpetic neuralgia is a neuropathic pain syndrome characterized by pain that persists for months to years after resolution of the herpes zoster rash. It stems from damage to peripheral and central neurons that may be a byproduct of the immune/inflammatory response accompanying varicella zoster virus reactivation. […] PHN occurs in the same dermatomes as the HZ rash, and stems from damage to peripheral and central neurons that may be a byproduct of the immune/inflammatory response that accompanied VZV reactivation and migration. When damaged, peripheral and central nerve fibers may develop a lower threshold for action potentials, discharge spontaneously, and exhibit disproportionate responses to stimuli, resulting in peripheral sensitization and pain without painful stimuli (allodynia).

• #2 Postherpetic neuralgia: epidemiology, pathophysiology, and pain manage | JMDH

  https://www.dovepress.com/postherpetic-neuralgia-epidemiology-pathophysiology-and-pain-managemen-peer-reviewed-fulltext-article-JMDH

  Patients with PHN experience three major types of pain: 1) constant pain without a stimulus (often described as burning, aching, or throbbing), 2) intermittent pain without a stimulus (often described as stabbing, shooting, or electric shock-like), and 3) pain brought on by a stimulus but is disproportionate to the stimulus (hyperalgesia), enduring for at least 3 months after healing of the HZ-related skin rash.

• #3 FF #272 Postherpetic Neuralgia – Palliative Care Network of Wisconsin

  https://www.mypcnow.org/fast-fact/postherpetic-neuralgia/?print=print

  Postherpetic neuralgia (PHN) is a syndrome of zoster-associated pain persisting more than 3 months after resolution of an initial herpes zoster (HZ) rash (‘shingles’). […] In acute HZ, reactivation of the virus from the dorsal root ganglia of spinal or cranial nerves causes inflammation and damage to the affected nerve tissue, resulting in acute pain. Subsequently, primary afferent neurons responding to the acute neuronal damage of zoster reactivation can cause sensitization of the nociceptive dorsal horn neurons, resulting in a prolonged exaggerated response to non-noxious stimuli. This central sensitization is thought to be a key mechanism in the development and maintenance of the pain of PHN.

• #4 Management of Herpes Zoster (Shingles) and Postherpetic Neuralgia | AAFP

  https://www.aafp.org/pubs/afp/issues/2000/0415/p2437.html/1000

  Herpes zoster (commonly referred to as shingles) and postherpetic neuralgia result from reactivation of the varicella-zoster virus acquired during the primary varicella infection, or chickenpox. […] Reactivation of latent varicella-zoster virus from dorsal root ganglia is responsible for the classic dermatomal rash and pain that occur with herpes zoster. […] The pathophysiology of postherpetic neuralgia remains unclear. However, pathologic studies have demonstrated damage to the sensory nerves, the sensory dorsal root ganglia and the dorsal horns of the spinal cord in patients with this condition. […] The virus remains latent for decades because of varicella-zoster virus-specific cell-mediated immunity acquired during the primary infection, as well as endogenous and exogenous boosting of the immune system periodically throughout life. […] Reactivation of the virus occurs following a decrease in virus-specific cell-mediated immunity. The reactivated virus travels down the sensory nerve and is the cause for the dermatomal distribution of pain and skin lesions.

• #5

  https://link.springer.com/article/10.1007/s11916-023-01209-z

  TG-PHN, caused by the VZV reactivation, involves intricate changes in pain signaling pathways, leading to heightened pain response through nociceptors sensitization, sensitivity due to local inflammatory mediators, augmented pain pathways excitability, and diminished inhibitory control. Given structural changes found in the TG, its afferent and efferent nerve, and even the trigeminal brainstem complex, neuropathy or neuronopathy may be better terms for TG-PHN. Investigating the multifaceted pathophysiological elements and their clinical correlations may offer valuable insights into more effective treatment approaches. […] VZV replication can induce acute injury to sensory neurons, exacerbating inflammatory tissue damage. In various cell and tissue types, VZV, either directly or indirectly, triggers an increase in pro-inflammatory cytokines, such as interleukin (IL)-1, IL-2, IL-6, IL-17, IL-18, and tumor necrosis factor-alpha (TNF-). The presence of viral proteins coupled with immune responses initiates inflammation at the affected site and contributes to pain and heightened sensitivity.

• #5

  https://link.springer.com/article/10.1007/s11916-023-01209-z

  The intricate interplay between heightened inflammation and neuronal activity underscores the complexities of pain modulation. Pro-inflammatory cytokines IL-1 and TNF- play a pivotal role by sensitizing nociceptors, influencing pain signaling. […] Cellular remodeling through voltage-gated cation channels and G protein-coupled receptor modifications significantly affects pain transmission in PHN. Notably, calcium-permeable channels wield control over diverse intracellular calcium dynamics, with implications for various chronic pain disorders. […] The role of calcium channels extends to NMDA receptor antagonists, a common therapeutic target for neuropathic pain conditions, including PHN. Activation of NMDA receptors contributes to mechanical allodynia, highlighting their pivotal role in this context.

• #5

  https://link.springer.com/article/10.1007/s11916-023-01209-z

  TG-PHN often results in hyperalgesia to noxious stimuli (e.g., heat, cold, mechanical pressure, and chemical), attributed to nociceptor transduction, which plays a central role in VZV-associated pain. Transient receptor potential (TRP) channels, such as TRPV1, transient receptor potential vanilloid 1 (a nonselective cation channel, which processes heat and capsaicin sensitivity), and TRPA1, transient receptor potential ankyrin 1 (uniquely sensitive to multimodal activation, including temperature, mechanical, oxidation, and several exogenous and endogenous compounds), play a crucial role in this process. […] The cascading effects of VZV reactivation on the nervous system create the complex landscape of TG-PHN. The insights gleaned from the intertwined roles of cytokines, cation channels, TRP channels, and neuropeptides like CGRP and substance P illuminate potential avenues for more targeted interventions.

• #6 Trigeminal Postherpetic Neuralgia: From Pathophysiology to Treatment | springermedizin.de

  https://www.springermedizin.de/trigeminal-postherpetic-neuralgia-from-pathophysiology-to-treatm/26653906

  Investigating the multifaceted pathophysiological elements and their clinical correlations may offer valuable insights into more effective treatment approaches. […] VZV replication can induce acute injury to sensory neurons, exacerbating inflammatory tissue damage. […] The presence of viral proteins coupled with immune responses initiates inflammation at the affected site and contributes to pain and heightened sensitivity. […] Pro-inflammatory cytokines IL-1 and TNF- play a pivotal role by sensitizing nociceptors, influencing pain signaling. […] The role of substance P (SP) and its G protein-coupled receptor NK-1R (neurokinin 1-receptor) is important in VZV-associated pain. […] While VZV infection has conventionally been associated with peripheral effects, the presence of acute or persistent inflammation and nerve damage can lead to enduring modifications in central nervous system (CNS) pain pathways. […] The cascading effects of VZV reactivation on the nervous system create the complex landscape of TG-PHN. […] Understanding the pathogenesis of TG-PHNs is imperative to overcoming the challenges of its clinical management.

• #7 Herpes Zoster and Post-Herpetic Neuralgia—Diagnosis, Treatment, and Vaccination Strategies

  https://www.mdpi.com/2076-0817/13/7/596

  There are a few mechanisms in which PHN develops: Upon damage of the nerves, roots, and ganglion, these peripheral nerves lose the ability to inhibit nociceptive pain signals. This lowers the threshold for nociceptive pain activation and produces spontaneous ectopic discharges, generating disproportionate pain with non-painful stimuli. […] With small fiber deafferentation from damage, the C fibers become sensitized and lower their threshold for action potentials. This increases their discharge rate and magnitude, resulting in peripheral nervous system-mediated spontaneous pain and allodynia. […] Lastly, there are some patients who experience constant pain in a region of profound sensory loss without allodynia, also termed anesthesia dolorosa. In these patients, there is loss of both large and small diameter fibers and the pain is likely due to intrinsic central changes with increased spontaneous activity in deafferented central neurons and/or reorganization of central connections.

• #7 Herpes Zoster and Post-Herpetic Neuralgia—Diagnosis, Treatment, and Vaccination Strategies

  https://www.mdpi.com/2076-0817/13/7/596

  The RZV is effective in reducing the incidence of herpes zoster and should be considered in patients who are at risk of herpes zoster. Procedures such as epidural blocks and subcutaneous or intracutaneous injections of local anesthetics and steroids can be considered for patients with a high risk of PHN to reduce its incidence.

• #8 Postherpetic Neuralgia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK493198/

  Postherpetic neuralgia (PHN) is the most common long-term complication of varicella-zoster virus (VZV) reactivation, also known as human herpesvirus-3 (HHV-3). […] The hallmark of PHN is a lancinating/burning pain in a unilateral dermatomal pattern that persists for three or more months after the onset of a herpes zoster (HZ) outbreak. […] The exact physiology that separates a self-limited zoster outbreak from postherpetic neuralgia is not fully understood. Histological examinations of relevant peripheral and central nervous tissue from sufferers of PHN reveal myelin and axon deficiency and atrophy of the dorsal horn in certain instances. […] Some suggest that an unchecked inflammatory response at the neuronal level is the main culprit of the eventual development of PHN, specifically via the reduction of centrally-mediated inhibition of nociceptive input and the promotion of peripheral sensitization via damaged nociceptors.

• #9 A New Non-Pharmacological Approach in Treatment of Post-Herpetic Neuralgia

  https://www.gavinpublishers.com/article/view/a-new-non-pharmacological-approach-in-treatment-of-post-herpetic-neuralgia

  Post-herpetic neuralgia is chronic refractory neuropathic pain that persists more than three months after resolution of the dermatomal herpes zoster eruption. […] The pathophysiology of PHN is not well known, but recent changes suggest multiple modifications in the afferent pathways at both peripheral and central nervous system levels. […] Certainly, continuous inflammation has been suggested as one of the mechanisms that provide sustenance for the pain in PHN. […] The varicella-zoster virus affects the peripheral nerve by demyelination, Wallerian degeneration and sclerosis, but changes in the central nervous system, have also been associated with PHN. […] It is hypothesized that the frequencies might vibrate and resonate with one or more crucial bonds in the crystalline structure of the zoster virus and change the ability of the virus to interact with the cell membrane. […] These mechanisms of reducing inflammation, elongation of scar tissue and interference with viral binding to nerve tissues could explain the reduction of the spontaneous discharge of neurons and the exaggerated painful response to non-painful stimuli.

• #10 Immunological mechanism of postherpetic neuralgia and effect of pregabalin treatment on the mechanism: a prospective single-arm observational study

  https://www.epain.org/journal/view.html?doi=10.3344/kjp.2021.34.4.463

  Immunological mechanisms play an essential role in the pathogenesis of neuropathic pain, immunologically based treatment approach will be the critical point of treatment. […] Despite extensive research, the pathophysiological mechanisms which generate neuropathic pain have not been clearly revealed yet. Recent publications and increasing evidence indicate that the immune system plays an essential role in developing neuropathic pain. […] According to the present study’s results, while CD4+ T cell and Th17 cell levels increased with pregabalin treatment, Treg cell levels remained unchanged, and T cell shift improved. […] A significant decrease in ESR and CRP values after treatment, known as positive acute phase reactants, suggests that the inflammatory process that plays a role in neuropathic pain’s pathogenesis decreases after pregabalin treatment. […] The authors believe that an immunologically based treatment approach will be the critical element of future treatment, especially in treating neuropathic pain.

• #11 Unmet Need in the Treatment of Postherpetic Neuralgia

  https://www.ajmc.com/view/ad046_13jan_neuralgiasuppl_sacks

  Postherpetic neuralgia (PHN) is a chronic pain syndrome that can develop following an episode of herpes zoster. […] The pathophysiology of PHN is incompletely understood. After reactivation of the VZV, the virus replicates and spreads along a spinal or cranial nerve toward the skin, potentially causing nerve damage. In addition, reactivation of the VZV in herpes zoster may spread viral particles into the dorsal horn of the spinal cord through peripheral sensory nerves. Thus, pain may involve both the peripheral and central nervous systems. This reactivation is also accompanied by hemorrhage, immune response, and destruction of peripheral and central neurons and their fibers. […] As damaged peripheral nerves develop lowered activation threshold for pain, sensory receptors become further sensitized, producing hyperexcitability and spontaneous discharge.

• #12 Unmet Need in the Treatment of Postherpetic Neuralgia

  https://www.ajmc.com/view/ad046_13jan_neuralgiasuppl_sacks

  In response to increased peripheral nerve activity, dorsal horn neurons in the spinal cord may become altered, impairing descending inhibition of pain, and leading to central sensitization. […] With the loss of peripheral sensory fibers, central processes of surviving axons may develop aberrant connections, and the resulting anatomical and functional reorganization may lead to the allodynia and spontaneous pain frequently observed in PHN.

• #13 Postherpetic Neuralgia: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1143066-overview

  Some patients with PHN appear to have abnormal function of unmyelinated nociceptors and sensory loss (usually minimal). Pain and temperature detection systems are hypersensitive to light mechanical stimulation, leading to severe pain (allodynia). […] Other patients with PHN may have severe, spontaneous pain without allodynia, possibly secondary to increased spontaneous activity in deafferented central neurons or reorganization of central connections. An imbalance involving loss of large inhibitory fibers and an intact or increased number of small excitatory fibers has been suggested. This input on an abnormal dorsal horn containing deafferented hypersensitive neurons supports the clinical observation that both central and peripheral areas are involved in the production of pain.

• #14 Post-herpetic neuralgia – Pathos

  https://www.pathos-journal.com/2024_1_246.html

  A wide variety of factors have been implicated in the pathogenesis of PHN, which explains the diversity of treatments proposed and the lack of a clear correlation between them and the pathogenetic mechanism. The only universally accepted finding is that in individuals who have contracted chickenpox in childhood, the varicella-zoster virus remains nested in the sensory ganglia throughout life and its reactivation is prevented by the cellular immunity induced by the primitive infection. It is a reduction in immune defences that allows it to reactivate and resume replication. Over a lifetime, the risk of reactivation of virus with HZ production would be around 30%. […] Historically, there have been numerous hypotheses to explain the pathogenesis of PHN and it is worth briefly reviewing the most significant ones because, although they are not individually exhaustive, each provide a piece to its understanding.

• #14 Post-herpetic neuralgia – Pathos

  https://www.pathos-journal.com/2024_1_246.html

  The input imbalance hypothesis is the best known of those proposed to explain the pathogenesis of PHN. […] Upon infecting the rat dorsal root ganglia with HZ virus, Schon et al observed that ganglioradiculitis, possibly due to the establishment of ephaptic contacts, results in a repetitive, hypersynchronous discharge of ganglion cells that may be responsible for chronic abnormal input to the medulla and thus the persistence of pain. […] PHN would be sustained by the persistence of inflammation caused by virus reactivation. […] In support of the inflammation thesis, Kim et al evaluated the importance of investigating markers of inflammation (ESR, C-reactive protein and white blood cell count) as a predictor of the evolution of HZ into PHN, reporting that ESR is the most significant marker.

• #14 Post-herpetic neuralgia – Pathos

  https://www.pathos-journal.com/2024_1_246.html

  According to Colding, ganglioradiculitis causes abnormal input on the dorsal horn of the spinal cord and the resulting sympathetic hypertone produces isosegmental vasoconstriction responsible for ischaemia, hypoxia and cell lysis. […] A more recent pathogenetic hypothesis is that of ectopic pacemakers which would be found in the axon and DRG. […] In addition to ectopic electrogenesis at the distal axonal level, ectopic pacemaker thesis also considers possible ectopic electrogenesis in the DRG. […] In the ectopic pacemaker hypothesis, the role of central sensitisation induced and maintained by afferents from foci of ectopic electrogenesis in microneuromas in nerve fibre terminals and ganglion cells is emphasised. […] Ultimately, according to the pathogenetic hypothesis of ectopic pacemakers, focus should be shifted from CNS to PNS: it would no longer be a question of deafferentation or central pain, but of peripheral neuropathic pain from activation of an ectopic electrogenesis in the axon or DRG where central hyperexcitability would function as an aggravating factor.

• #14 Post-herpetic neuralgia – Pathos

  https://www.pathos-journal.com/2024_1_246.html

  Although none of the previous hypotheses explains the complex pathogenesis of PHN on its own, by taking up a few concepts and placing them in a certain sequence, one may think that ganglion phlogosis induces sympathetic hypertone and that this, in turn, causes vasoconstriction and consequently ischaemic nerve tissue damage. […] From this it is clear that PHN is not a single pathogenetic entity but a clinical reality where all the pathogenetic types of neuropathic pain are possible, singularly or variously represented, causing the different severity of the clinical picture and conditioning the prognosis, which may be that of a disease destined to heal or to last forever.

• #15

  https://journals.lww.com/painrpts/fulltext/2018/12000/rethinking_the_causes_of_pain_in_herpes_zoster_and.1.aspx

  Pain in herpes zoster (HZ) and postherpetic neuralgia (PHN) is traditionally explained in terms of 2 processes: irritable nociceptors in the rash-inflamed skin and, later, deafferentation due to destruction of sensory neurons in one virally infected dorsal root ganglion. […] This model, the ectopic pacemaker hypothesis of HZ and PHN, proposes that pain in both conditions is driven by hyperexcitable ectopic pacemaker sites at various locations in primary sensory neurons affected by the causative varicella zoster virus infection. This peripheral input is exacerbated by central sensitization induced and maintained by the ectopic activity. […] The shift in perspective regarding the pain mechanism in HZ/PHN has specific implications for clinical management. […] The ectopic pacemaker hypothesis of pain in HZ and PHN attempts to interpret the clinical facts surrounding HZ/PHN in light of recent advances in our understanding on the biology of neuropathic pain. In a nutshell, the hypothesis has 2 elements: (1) spontaneous pain in both HZ and PHN is proposed to be due to spontaneous impulse discharge arising at ectopic pacemaker sites in the PNS, sites associated with the dying-back of axons ends and pathology in sensory somata in the VZV-infected DRG.

• #16

  https://journals.lww.com/painrpts/fulltext/2018/12000/rethinking_the_causes_of_pain_in_herpes_zoster_and.1.aspx

  Tactile allodynia is proposed to result from intensification of the sensory effects of normal cutaneous A touch afferents by central sensitization. The central sensitization, in turn, is maintained by the spontaneous ectopic discharge. […] The ectopic pacemaker hypothesis adopts a very different explanation. Rather than reflecting neuronal degeneration, the loss of epidermal endings is supposed to represent dying-back of the distal end of the axon because of metabolic stress in infected DRG neurons. […] The process of dying-back is well established in peripheral polyneuropathies (eg, diabetic polyneuropathy or CMT-2) and usually manifests with sensory loss, sometimes accompanied by ongoing pain in a stocking-glove pattern. […] The explanation of tactile allodynia according to the ectopic pacemaker hypothesis is like other neuropathies and not much different from inflammatory pain as laid out above. Both attribute the allodynia to touch-evoked activity in low-threshold A afferents rendered painful by central sensitization. The major difference is that, under the ectopic pacemaker hypothesis, central sensitization is presumed to be maintained by afferent discharge arising at ectopic pacemaker sites in dying-back nerve fibers and/or the VZV-infected DRG.

• #17 Investigational Drugs for the Treatment of Postherpetic Neuralgia: Systematic Review of Randomized Controlled Trials

  https://www.mdpi.com/1422-0067/24/16/12987

  The pharmacological treatment of postherpetic neuralgia (PHN) is unsatisfactory, and there is a clinical need for new approaches. […] The development of PHN involves mechanisms at both the central and peripheral nervous system levels. […] On the one hand, there is peripheral nociceptor sensitization with a reduction in the excitation threshold, the appearance of spontaneous ectopic discharges in peripheral and central axons, and a loss of descending pain inhibitory controls. On the other hand, central sensitization occurs through neuronal sensitization, along with spinal hyperexcitability. […] The aim of this systematic review is to summarize the results of drugs evaluated in Phase II/III/IV clinical trials between 2016 and 2023 in order to provide an overview and make predictions for the molecules and pharmacological targets that may be available in the future therapeutic arsenal.

• #17 Investigational Drugs for the Treatment of Postherpetic Neuralgia: Systematic Review of Randomized Controlled Trials

  https://www.mdpi.com/1422-0067/24/16/12987

  There is increasing evidence implicating the Renin–Angiotensin System (RAS) in multiple facets of NP. […] The involvement of this target in NP has been known for years. […] The importance of Voltage-Gated Sodium Channel (VGSC) blockade in pain transduction is well known. […] Cyclooxygenase inhibitors are effective and widely used for inflammatory pain treatment, but efficacy in NP is controversial. […] Preclinical studies have shown that the genetic depletion of AAK1 reduces pain in models of persistent pain but not acute pain without showing side effects or motor deficiencies. […] NMDA receptor antagonists have been suggested for the treatment of NP for years, as they participate in the transmission of pain signals. […] It is well established, based on animal and human studies, that NGF is fundamental for nociception modulation. […] Since 2016, 15 different molecules have been evaluated in Phase II, III and IV clinical trials for PHN. […] Among them, we found four first-in-class targets for the treatment of PHN: AT2R antagonism, AAK1 inhibition, LANCL activation and NGF inhibition.

• #18 Post-herpetic Neuralgia:

  https://www.patientcareonline.com/view/post-herpetic-neuralgia

  Post-herpetic neuralgia is a common complication of herpes zoster (shingles). Nearly 1 million cases occur each year in the United States, and the incidence is expected to rise as baby boomers age. […] Until the early 1990s, tricyclic antidepressants (TCAs) were the only effective treatment available. Since then, evidence supporting the use of gabapentin, opioids, and lidocaine patches has emerged. Still, management of the condition can be frustrating for both patient and physician because no single modality produces excellent pain control and the majority of patients do not respond to medical treatment. […] The main risk factors for the development of post-herpetic neuralgia after a shingles attack are presented in Table 1. Of these, the most notable are advanced age and a severe shingles attack.

• #18 Post-herpetic Neuralgia:

  https://www.patientcareonline.com/view/post-herpetic-neuralgia

  Prompt treatment of shingles with acyclovir-ideally within 72 hours-does not prevent post-herpetic neuralgia, but it does reduce the pain and duration of the disorder, especially in patients older than 60 years. […] Acyclovir and similar agents have no role in the treatment of post-herpetic neuralgia; they are useful only in acute shingles. Treatment of shingles with corticosteroids has no effect on post-herpetic neuralgia. […] Treatment of shingles with amitriptyline helps ameliorate post-herpetic neuralgia (NNT, 5.1), and a low dose is usually well tolerated. […] Gabapentin effectively treats pain and sleep disturbance caused by post-herpetic neuralgia. […] The FDA has approved gabapentin for the treatment of post-herpetic neuralgia, and in 2003 the members of the Fourth Annual Conference on the Mechanism and Treatment of Neuropathic Pain designated gabapentin as a first-line medication for the treatment of post-herpetic neuralgia.

• #19 Acute Herpes Zoster and Postherpetic Neuralgia | PM&R KnowledgeNow

  https://now.aapmr.org/acute-herpes-zoster-and-post-herpetic-neuralgia/

  The reactivation of VZV in the sensory ganglia causes inflammation and neuronal destruction. The virus travels along the sensory nerve to the skin, resulting in vesicular lesions, primary afferent nerve damage, and generalized cell necrosis. Nerve damage starts early in the acute phase of HZ prior to rash onset and may correlate with the severity of painful neuropathy. Histopathology reveals intraepidermal blisters with surrounding inflammatory infiltrate. On biopsy multinucleated giant cells with intranuclear inclusions are characteristic. […] The incidence of developing PHN is 10-25%, and increases with age, more severe rash and acute HZ pain, ophthalmic involvement, and presence of prodromal symptoms (pain, dysesthesia, and allodynia). Other risk factors include immunosuppression, diabetes, sensory abnormalities in the affected dermatomes, polyneuropathy, and trauma.

• #20 Postherpetic neuralgia – Medical Services – Yuwa Clinic

  https://yuwa-clinic.com/en/medical_treatment/content04.html

  This persistence of postherpetic neuralgia pain is due to pain memory from long-term excitation of the nerve junction (called long-term potentiation), combined with proliferation of painful nerve circuits following inflammation of the spinal cord dorsal horn by the virus. […] After 3-4 weeks of shingles, when the pain does not subside, the acute phase of shingles shifts to post-herpetic neuralgia. The mechanism of the transition is that the pain is stored in the dorsal horn of the spinal cord. Once the pain is stored, it becomes resistant to treatment and becomes more intractable the longer it has been present. […] The „ease/difficulty of healing” of shingles is strongly influenced by the time since onset of shingles. […] Thus, if left untreated, the memory of pain becomes stronger and more intractable, so early treatment is necessary.

• #21 Prevention and Treatment of Postherpetic Neuralgia | AAFP

  https://www.aafp.org/pubs/afp/issues/1999/0301/p1295.html

  Approximately 10 percent of cases of herpes zoster infection result in significant postherpetic neuralgia. The incidence of postherpetic neuralgia rises dramatically with age, with over one half of all cases of herpes zoster in patients older than 60 years resulting in this end-stage disorder. […] Since cell-mediated immunity is believed to play a significant role in the pathogenesis of postherpetic neuralgia, vaccination could theoretically confer protection.

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