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277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuropathic pain is a debilitating form of chronic pain resulting from nerve injury, disease states, or toxic insults. Neuropathic pain is often refractory to conventional pharmacotherapies, necessitating validation of novel analgesics. Cannabinoids, drugs that share the same target as Delta(9)-tetrahydrocannabinol (Delta(9)-THC), the psychoactive ingredient in cannabis, have the potential to address this unmet need. Here, we review studies evaluating cannabinoids for neuropathic pain management in the clinical and preclinical literature. Neuropathic pain associated with nerve injury, diabetes, chemotherapeutic treatment, human immunodeficiency virus, multiple sclerosis, and herpes zoster infection is considered. In animals, cannabinoids attenuate neuropathic nociception produced by traumatic nerve injury, disease, and toxic insults. Effects of mixed cannabinoid CB(1)/CB(2) agonists, CB(2) selective agonists, and modulators of the endocannabinoid system (i.e., inhibitors of transport or degradation) are compared. Effects of genetic disruption of cannabinoid receptors or enzymes controlling endocannabinoid degradation on neuropathic nociception are described. Specific forms of allodynia and hyperalgesia modulated by cannabinoids are also considered. In humans, effects of smoked marijuana, synthetic Delta(9)-THC analogs (e.g., Marinol, Cesamet) and medicinal cannabis preparations containing both Delta(9)-THC and cannabidiol (e.g., Sativex, Cannador) in neuropathic pain states are reviewed. Clinical studies largely affirm that neuropathic pain patients derive benefits from cannabinoid treatment. Subjective (i.e., rating scales) and objective (i.e., stimulus-evoked) measures of pain and quality of life are considered. Finally, limitations of cannabinoid pharmacotherapies are discussed together with directions for future research.
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PMID:Cannabinoids as pharmacotherapies for neuropathic pain: from the bench to the bedside. 1978 75

Cell-mediated immunity (CMI) has been shown to be critical for the prevention and control of varicella-zoster virus (VZV)-related diseases. Because a large population-based study has revealed that diabetes mellitus is a risk factor for herpes zoster, we studied VZV-specific immune responses of patients with diabetes mellitus and compared them with those of healthy individuals. In this study, we found that patients with diabetes mellitus had significantly lower CMI to VZV than did healthy individuals. These results suggest that the increased risk for herpes zoster among patients with diabetes mellitus may be related to decreased VZV-specific CMI.
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PMID:Comparison of varicella-zoster virus-specific immunity of patients with diabetes mellitus and healthy individuals. 1982 19

Neuropathic pain refers to pain that originates from pathology of the nervous system. Diabetes, infection (herpes zoster), nerve compression, nerve trauma, and autoimmune diseases are examples of diseases that may cause neuropathic pain. Unfortunately no satisfactory treatment is yet available for this type of pain. This consideration has led to an explosion of interest for the underlying mechanisms, accompanied by a growing number of animal models. In recent years, most of the neuropathic pain models initially developed in the rat have been translated to mice in order to exploit the resource represented by genetically modified mice. Obviously the most useful animal models of pain would be ones in which the etiology of the pain would be endogenous and not induced by the experimenters: together with the classic models based on peripheral nerve ligation, in the last years other techniques are being developed that mimic more closely clinical pain syndromes, often by attempting to induce the disease associated to neuropathic pain. Although several variables must be taken into account when using animal models for mimicking clinical neuropathic pain, the huge number of models that are now reproducible and well characterized should help to reach important goals in the comprehension of mechanisms and to discover novel therapeutic target for this disease.
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PMID:Murine models of human neuropathic pain. 1987 43

To analyse the epidemiological characteristics and related costs of herpes zoster in Taiwan, a nationally representative cohort of 1,000,000 individuals from the National Health Insurance register was followed up from 2000 to 2006 and their claims data analysed. Overall, 34,280 patients were diagnosed with zoster (incidence 4.89/1000 person-years) and 2944 patients (8.6%) developed post-herpetic neuralgia 3 months after the start of the zoster rash (incidence 0.42/1000 person-years). People with older age, diabetes, and immunocompromising conditions were at higher risk of developing zoster and post-herpetic neuralgia. The overall hospitalization rate for zoster was 16.1 cases per 100,000 person-years. The cost for each home care case and per hospitalized case were approximately 53.30 euro and 1224.70 euro, respectively. Further research into the cost-effectiveness of zoster vaccine is needed.
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PMID:Epidemiological features and costs of herpes zoster in Taiwan: a national study 2000 to 2006. 1999 93

Neuropathic pain refers to pain that originates from pathology of the nervous system. Common causes of neuropathic pain are diabetes mellitus, reactivation of herpes zoster, nerve compression or radiculopathy, alcohol, chemotherapy or abuse of some drugs, and trigeminal neuralgia. Specific symptoms of neuropathic pain are mechanical allodynia and cold hyperalgesia. Drugs to treat neuropathic pain can be divided into adjuvant analgesics (antidepressants and anticonvulsants), opioids and topical agents. The use of multiple drug therapies is common in practice. Despite considerable increase in the number of randomized placebo-controlled trials in neuropathic pain in the last few years, the medical treatment of neuropathic pain is still far from being satisfactory, with less than half of patients achieving significant benefit with any pharmacological drug.
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PMID:Neuropathic pain. 2005 64

Ramsay Hunt syndrome is a lower motor neurone weakness of the seventh (facial) cranial nerve caused by reactivation of the herpes zoster virus. The virus infects the geniculate ganglion of the nerve causing facial weakness. The onset of a motor neuropathy makes it inherently different from the more typical presentation of shingles, which predominantly causes a sensory neuropathy. Around 20-30% of individuals will be affected by herpes zoster during their lives. Ramsay Hunt syndrome is a rare disease, affecting fewer than 1 in 1500 people in the United States. The syndrome can present with vague and non-specific symptoms, especially during early onset of the disease. A high index of suspicion and frequent follow up are imperative for early diagnosis. A vesicular erythematous rash on, or around, the pinna (zoster oticus) may be present. Advanced age, diabetes mellitus and hypertension appear to be significant poor prognostic features with patients more likely to suffer complications. There is clear evidence to support the use of early antiviral therapy along with oral corticosteroid use. Early and appropriate intervention has resulted in significant improvement in treatment and complication outcomes.
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PMID:Ramsay Hunt syndrome presenting in primary care. 2040 31

Eleven case of disseminated herpes zoster (DHZ) who were hospitalised in the Dermatovenereology ward from January 1992 to April 1995 were selected for this study. All had classical herpes zoster (HZ) but within another 2 to 15 days had developed aberrant vesicles on the trunk, limbs and face. None of them had serious associated immunosuppressive disorder or malignancy. However, 3 cases had diabetes mellitus, 2 were receiving prednisolone 15 mg daily for the last few days, 2 had anaemia and deficiencies and 1 had a urinary tract infection. Only one patient needed oral acyclovir therapy. All were cured without any sequelae.
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PMID:Disseminated herpes zoster. 2095 30

Reactive perforating collagenosis is a disease whose pathogenesis is still not fully understood. Histological findings are degenerated collagen bundles which are arranged in vertical direction penetrating the epidermis into a dome-shaped crater. Usually diabetes mellitus and renal failure can be found among patients with reactive perforating collagenosis. To date, there have been five cases described where the eruption of reactive perforating collagenosis followed herpes zoster infection. This could be a form of Wolf's isotopic response, a term that is used for dermatoses which arise after the healing of a preexisting dermatosis. We report the sixth case of a herpes zoster-associated reactive perforating collagenosis and discuss the current literature.
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PMID:[Acquired reactive perforating collagenosis following herpes zoster as isotopic response?]. 2173 60

Herpes zoster is caused by the reactivation of the varicella-zoster virus (VZV) and usually appears many years after primary infection (varicella), induced by immunosuppression due to underlying diseases. Few epidemiological data in Italy are available concerning Herpes zoster, mainly because disease notification is not mandatory. An observational perspective trial was conducted for 12 months by 41 Italian general practitioners belonging to the Netaudit network to determine herpes zoster incidence and its correlation to patients' characteristics (age, gender, educational qualification, co-morbidities), the delay from correct diagnosis to the start of treatment and different drug prescription. In all, the study involved 193 patients with herpes zoster: this population included mostly female (60.6%) and elderly subjects (59.6%) with a mean age of 60.4 years. 46.1% of patients presented underlying diseases (diabetes 13%, solid tumours 5.7%). Correct diagnosis was achieved after a mean delay of 49 hours while therapy was started within 48 hours in most cases (75.1%). Aciclovir (51%) and valaciclovir (24%) were the most commonly used drugs. A significant correlation between educational level and prompt treatment suggests the major role of education in primary health prevention campaigns.
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PMID:[Herpes zoster in general medicine: experience of the Italian group Netaudit]. 2175 50

A 36-year-old woman with neuromyelitis optica had been treated with steroids for the prevention of relapse. However, her treatment was not effective and she showed adverse effects such as diabetes mellitus, osteoporosis, compression fractures, and Pneumocystis carinii pneumonia. Therefore, we started her on mitoxantrone treatment. After five courses of mitoxantrone injection, she developed a herpes zoster infection in her thigh followed by aseptic meningitis. PCR for varicella zoster virus (VZV)-DNA was positive in the cerebrospinal fluid. The mechanisms that caused VZV reactivation by mitoxantrone are not known. Opportunistic herpes virus reactivation may occur easily with increasing use of immunosuppressive drugs for both neuromyelitis optica and multiple sclerosis. These drugs must be used under careful supervision.
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PMID:[A case of neuromyelitis optica with varicella zoster virus meningitis during mitoxantrone treatment]. 2194 29


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