Suffering with two dissimilar diseases
Dinesh Kumar Jain in Homeopathy, 2022
“There are erythematous cutaneous eruptions of a characteristic appearance” (Pinkerton, 1971, p. 395). “Herpes zoster, commonly known as shingles, is characterized by the formation of an erythematous and vesicular eruption along the course of sensory nerves” (Pinkerton, 1971, p. 394). Similarly, smallpox and chickenpox have characteristic skin lesions. It is also known that “Antigen antibody reactions are important in causing cutaneous eruption e.g., note the absence of rashes in measles when antibodies do not form” (Pinkerton, 1971, p. 393). That's why we can say when antigen-antibody reaction is weak, then skin manifestations will be less and organs where antigen-antibody complex causes damage will also be less. In such conditions, diagnosis of disease is difficult due to the absence of characteristically specific skin lesions and less morbidity due to diminished antigen-antibody reaction or less hypersensitivity reaction.
Prognosis: Studies of disease course and outcomes
Milos Jenicek in Foundations of Evidence-Based Medicine, 2019
A survival curve is essentially a sequence of rates (proportions) of events of interest in time. Originally, a proportion of patients (usually cancer sufferers) surviving or dying at a given moment were the subject of study. Today, the terms ‘survival’ or ‘survival studies’ are rather awkward or misleading, because any event appearing during the natural or clinical course of disease may be the subject of ‘survival’ analysis. The methodology of studying survival also applies to outcomes of disease other than death: Development of complications; another spell of disease such as a migraine attack or an epilepsy ‘mal’; surgical complications after an operation; adverse effects of treatment; and others. During the last two decades, a new term, time-to-event analysis,24–27 has been applied to these studies of morbid events. In studies of treatment effectiveness, time-to-event analysis may be even more specific. For example, in such studies of migraine treatment, time-to-event analysis becomes ‘time-to-relief analysis’;28 or, elsewhere, it may become ‘time-to-effect analysis’. Both ‘survival analysis’ and ‘time-to-event analysis’ or ‘survival curves’ and ‘time-to-event curves’ are used interchangeably in this text. For example, Balfour et al.29 studied various outcomes of a herpes zoster infection. These authors established ‘survival curves’, i.e. time-to-event curves for the occurrence of new lesions, positive virus cultures from lesions, lesions not scabbed and pain occurrence, as illustrated in Figure 10.2.
Geriatric headache
Stephen D. Silberstein, Richard B. Upton, Peter J. Goadsby in Headache in Clinical Practice, 2018
Topical therapies, such as compresses of Burrow’s solution, colloidal oatmeal, or calamine lotion are used to treat acute zoster. Oral glucocorticoids may speed the resolution of acute zoster pain,69 but it is not clear if they prevent postherpetic neuralgia.67 Antiviral agents may attenuate acute herpes zoster in immunocompromised patients. A 21-day course of acyclovir (aciclovir) may ameliorate pain in the acute phase, but it has not been proven to reduce the risk of postherpetic neuralgia.67 Famcyclovir (famciclovir), an antiviral drug, may shorten the duration of postherpetic neuralgia. The most effective treatment of the pain of acute herpes zoster is neuroblockade, but it is uncertain if this will reduce postherpetic neuralgia.87
Effectiveness of pregabalin as a secondary treatment for neuropathic pain from postherpetic neuralgia
Published in Baylor University Medical Center Proceedings, 2020
Jonathan Kopel, Gregory L. Brower
Herpes zoster or shingles is a potential complication arising from the reactivation of dormant varicella zoster virus in dorsal root ganglion.1 This reactivation causes a severe painful rash that spreads along dermatomes in the face or chest wall, which leads to postherpetic neuralgia (PHN).1 In most cases, PHN occurs in older patients and persists even after the rash has cleared.1 The pain with PHN and shingles is often described as burning or stinging and sometimes includes itching, aching, and pain paroxysms.1 Currently, there is no cure for PHN, but there are many treatments to reduce pain duration and severity.2 Lidocaine patches, gabapentin, pregabalin, serotonin norepinephrine reuptake inhibitors, and tricyclic antidepressants are first-line therapies; opioid analgesics are suggested as second- or third-line options due to the addiction potential. In this case report, we describe a patient treated for PHN with pregabalin.
Dermatomal rash after Shingrix vaccination: cause or coincidence?
Published in Baylor University Medical Center Proceedings, 2022
Nitish Mittal, Nikita Dhir, Neha Mittal
Herpes zoster (Shingles) is a dermatomal rash caused by reactivation of the varicella zoster virus (VZV). VZV usually occurs in childhood, presenting as chickenpox, and remains dormant in the dorsal root ganglia.1 It is often reactivated later in life from stress, aging, or immunodeficiency. Zoster presents as a maculopapular rash that can evolve into vesicular lesions with unilateral dermatomal distribution. It can be further complicated by postherpetic neuralgia or herpes zoster encephalitis.2 The Advisory Committee on Immunization Practices currently recommends adjuvanted recombinant Shingrix vaccines in two doses for all adults over 50 to reduce the incidence of zoster and/or postherpetic neuralgia.3 While Zostavax was a live vaccine with limited efficacy in the older age group, Shingrix is an adjuvanted recombinant zoster vaccine that is widely sought due to its strong efficacy with a sustained antibody response.3
Posterior Scleritis with Choroidal Effusion Secondary to Herpes Zoster Ophthalmicus
Published in Ocular Immunology and Inflammation, 2018
Edmund Tsui, Soshian Sarrafpour, Yasha S. Modi
We report a rare case of choroidal detachment associated with posterior scleritis that occurred as an acute complication of HZO. Herpes zoster is caused by the varicella zoster virus and presents as a reactivation in individuals who have had a primary varicella infection. HZO in particular is caused by the reactivation of varicella zoster virus (VZV) in the ophthalmic division (V1) of cranial nerve V, the trigeminal nerve.2 There are numerous ocular complications associated with HZO, such as conjunctivitis, keratitis, uveitis, retinitis, and cranial nerve palsies.2 An uncommon complication associated with HZO is scleritis, which generally presents as an anterior scleritis.1 Few cases of posterior scleritis associated with HZO have been reported in the literature.3,4
Related Knowledge Centers
- Chickenpox
- Immunosuppression
- Paresthesia
- Postherpetic Neuralgia
- Rash
- Varicella Zoster Virus
- Visual Impairment
- Peripheral Neuropathy
- Viral Disease
- Virus Latency