Severe postherpetic neuralgia and other neuropathic pain syndromes alleviated by topical gabapentin

2015 ◽  
Vol 173 (1) ◽  
pp. 300-302 ◽  
Author(s):  
S. Hiom ◽  
G.K. Patel ◽  
R.G. Newcombe ◽  
S. Khot ◽  
C. Martin
Keyword(s):  
Neuropathic Pain ◽  
Postherpetic Neuralgia ◽  
Pain Syndromes

scholarly journals Prevalence of Neuropathic Pain and the Need for Treatment

2006 ◽  
Vol 11 (suppl a) ◽  
pp. 5A-10A ◽  
Author(s):  
Pat Morley-Forster
Keyword(s):  
Nervous System ◽  
Neuropathic Pain ◽  
Postherpetic Neuralgia ◽  
Unmet Need ◽  
The United States ◽  
Nerve Damage ◽  
Phantom Limb ◽  
Disc Disease ◽  
Pain Syndromes ◽  
Cord Injury

Recent publications have suggested that more than two million adults in the United States suffer from neuropathic pain, but this number seems to be a significant underestimate. The prevalence of neuropathic pain from diabetes and postherpetic neuralgia alone, using the most conservative estimates of incidence, would equal two million Americans. Lesions of the nervous system responsible for pain genesis can occur either in the central or the peripheral nervous system. The most common causes of peripheral neuropathic pain syndromes worldwide are diabetes, HIV infection, cancer-related neuropathy (due to tumour invasion, surgical nerve damage, radiation or chemotherapy-induced nerve damage) and lumbar degenerative disc disease. Other less common, but significant, sources of suffering are postherpetic neuralgia, complex regional pain syndrome, phantom limb pain and postsurgical nerve trauma. Central neuropathic pain can be caused by stroke (infarct or hemorrhage), multiple sclerosis, spinal cord injury and syringomyelia. Certain pain syndromes such as trigeminal neuralgia and vulvodynia, although clearly neuropathic and a source of tremendous suffering, are not discussed in the present article due to space constraints. There is an unmet need for the treatment of neuropathic pain as evidenced by reports of pain despite the use of opioids and anticonvulsants, continuing psychological difficulties, lack of access to treatments and patients seeking access to complementary therapy.

scholarly journals Sickle cell pain: a critical reappraisal

Blood ◽  
2012 ◽  
Vol 120 (18) ◽  
pp. 3647-3656 ◽  
Author(s):  
Samir K. Ballas ◽  
Kalpna Gupta ◽  
Patricia Adams-Graves
Keyword(s):  
Chronic Pain ◽  
Neuropathic Pain ◽  
Sickle Cell ◽  
Multiorgan Failure ◽  
Organ Damage ◽  
Acute Chest Syndrome ◽  
Prodromal Phase ◽  
Pain Syndromes ◽  
Painful Episode ◽  
Chronic Pain Syndromes

AbstractSickle cell pain includes 3 types: acute recurrent painful crises, chronic pain syndromes, and neuropathic pain. The acute painful crisis is the hallmark of the disease and the most common cause of hospitalization and treatment in the emergency department. It evolves through 4 phases: prodromal, initial, established, and resolving. Each acute painful episode is associated with inflammation that worsens with recurrent episodes, often culminating in serious complications and organ damage, such as acute chest syndrome, multiorgan failure, and sudden death. Three pathophysiologic events operate in unison during the prodromal phase of the crisis: vaso-occlusion, inflammation, and nociception. Aborting the acute painful episode at the prodromal phase could potentially prevent or minimize tissue damage. Our hypothesis is that managing these events with hydration, anti-inflammatory drugs, aggressive analgesia, and possibly vasodilators could abort the crisis and prevent or minimize further damage. Chronic pain syndromes are associated with or accompany avascular necrosis and leg ulcers. Neuropathic pain is not well studied in patients with sickle cell disease but has been modeled in the transgenic sickle mouse. Management of sickle cell pain should be based on its own pathophysiologic mechanisms rather than borrowing guidelines from other nonsickle pain syndromes.

scholarly journals Neuralgias of the Trigeminal Nerve

2000 ◽  
Vol 5 (1) ◽  
pp. 107-113 ◽  
Author(s):  
Allan S Gordon
Keyword(s):  
Neuropathic Pain ◽  
Differential Diagnosis ◽  
Trigeminal Neuralgia ◽  
Clinical Features ◽  
Trigeminal Nerve ◽  
Postherpetic Neuralgia ◽  
Facial Pain ◽  
The Other ◽  
Atypical Facial Pain ◽  
Trigeminal Neuropathic Pain

Practitioners are often presented with patients who complain bitterly of facial pain. The trigeminal nerve is involved in four conditions that are sometimes mixed up. The four conditions - trigeminal neuralgia, trigeminal neuropathic pain, postherpetic neuralgia and atypical facial pain - are discussed under the headings of clinical features, differential diagnosis, cause and treatment. This article should help practitioners to differentiate one from the other and to manage their care.

HCN2 ion channels: basic science opens up possibilities for therapeutic intervention in neuropathic pain

2016 ◽  
Vol 473 (18) ◽  
pp. 2717-2736 ◽  
Author(s):  
Christoforos Tsantoulas ◽  
Elizabeth R. Mooney ◽  
Peter A. McNaughton
Keyword(s):  
Chronic Pain ◽  
Neuropathic Pain ◽  
Ion Channels ◽  
Warning Signal ◽  
Sensory Nerves ◽  
Nociceptive Neurons ◽  
Pain Syndromes ◽  
Medical Need ◽  
Pathological Pain ◽  
Genetic Deletion

Nociception — the ability to detect painful stimuli — is an invaluable sense that warns against present or imminent damage. In patients with chronic pain, however, this warning signal persists in the absence of any genuine threat and affects all aspects of everyday life. Neuropathic pain, a form of chronic pain caused by damage to sensory nerves themselves, is dishearteningly refractory to drugs that may work in other types of pain and is a major unmet medical need begging for novel analgesics. Hyperpolarisation-activated cyclic nucleotide (HCN)-modulated ion channels are best known for their fundamental pacemaker role in the heart; here, we review data demonstrating that the HCN2 isoform acts in an analogous way as a ‘pacemaker for pain’, in that its activity in nociceptive neurons is critical for the maintenance of electrical activity and for the sensation of chronic pain in pathological pain states. Pharmacological block or genetic deletion of HCN2 in sensory neurons provides robust pain relief in a variety of animal models of inflammatory and neuropathic pain, without any effect on normal sensation of acute pain. We discuss the implications of these findings for our understanding of neuropathic pain pathogenesis, and we outline possible future opportunities for the development of efficacious and safe pharmacotherapies in a range of chronic pain syndromes.

Postherpetic Neuralgia: A Patient’s and a Physician’s Perspective

2016 ◽  
Author(s):  
James H. Diaz
Keyword(s):  
Neuropathic Pain ◽  
Herpes Zoster ◽  
Postherpetic Neuralgia ◽  
Clinical Manifestations ◽  
The United States ◽  
Evidence Based ◽  
Pain Medicine ◽  
High Prevalence ◽  
Antiviral Medications ◽  
Physician’S Perspective

Herpes zoster can plague anyone who has had varicella or has received the varicella or chickenpox vaccine. The incidence of herpes zoster increases with age and rises exponentially after 60 years of age. Postherpetic neuralgia (PHN) may occur after herpes zoster at any age but typically occurs after 50 years of age, with over 40% of persons over 60 years of age suffering from PHN after a shingles attack. Up to 1 million new cases of herpes zoster and 200,000 new cases of PHN may now be anticipated in the United States every year, with the incidence rate increasing as the population grows and ages with prolonged life expectancies. Although new antiviral medications will improve and shorten the course of herpes zoster, they do not guarantee the prevention of PHN. Given the high prevalence of PHN in an aging population and the availability of primary prevention by vaccination, the objectives of this review are to describe the epidemiology, pathophysiology, and clinical manifestations of zoster and PHN and to recommend a combination of strategies for the clinical management and prevention of PHN. This review contains 6 figures, 4 tables and 13 references Key words: evidence-based pain medicine, herpes zoster, neuropathic pain, postherpetic neuralgia

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