In a previous article1one of us (G. C. A.) reported a group of cases of recalcitrant pustular eruptions occurring on the palms and soles in which the causative role of focal infections was stressed. The disorder as studied in fifteen patients showed four main characteristics: 1. There are chronic recalcitrant pustular eruptions symmetrically located on the palms and soles. 2. The histologic picture shows pustules deep in the epidermis, without much acanthosis and parakeratosis, and the microscopic changes resemble those seen in cases of trichophytids. 3. The condition in our patients had a direct relationship to focal infection and was often accompanied by leukocytosis and by positive cutaneous reactions to staphylococcus and streptococcus toxins. Cultures of material from the lesions were consistently sterile. 4. Cures resulted when the focal infection was identified and removed. CLINICAL FEATURES The pustular eruptions of the hands and feet in these

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Pustular bacterids of the hands and feet

The term postherpetic isotopic response describes the occurrence of a new, unrelated disease that appears at the same location as a previously healed herpetic infection. When dealing with the pathogenetic mechanism involved in the isotopic response, several possibilities should be considered: a viral origin, an immunologic origin, a vascular origin, and a neural origin. The aim of this article is to review and discuss the different pathogenetic mechanisms with particular attention to new information related to the possible neural origin of this abnormal response of the skin.

https://www.jaad.org/article/S0190-9622(02)27064-4/pdf

Isotopic response after herpesvirus infection: An update

Background: Postherpetic neuralgia (PHN) is considered by some investigators to be predominantly a deafferentation-type central pain syndrome; others suggest that activity of remaining peripheral nociceptors plays a critical role. The authors investigated the sensory dysfunction in subjects with PHN of varying duration and at different sites to gain further insight into the mechanisms responsible for the clinical features of neuropathic pain. In addition, the relationships between ongoing pain and pain evoked by mechanical and thermal stimuli were compared in patients with trigeminal and truncal PHN, to determine if the pathophysiologic mechanisms differed among subjects. Methods : In 63 subjects with PHN, quantitative sensory testing was performed in the region of maximum allodynia or ongoing pain and the corresponding contralateral site. The intensity of ongoing pain was recorded. Sensory thresholds for warmth, coolness, heat pain, and cold pain were determined. Pain induced by various mechanical stimuli (dynamic, static, punctate) was rated using a numerical rating scale of 0-10. Results: The mean rating of ongoing PHN pain was 7.3 ± 2.0 (mean ± SD). Allodynia induced by one or more mechanical stimuli was observed in 78% of subjects. A smaller subset (40%) had hyperalgesia to heat or cold stimuli. In subjects with duration of PHN of ≤ 1 yr duration, but not in those with duration of > 1 yr, the intensity of ongoing pain correlated with intensity of allodynia induced by dynamic stimuli. Deficits in thresholds for heat and cold pain were observed in the affected region of subjects with PHN in the thoracic dermatomes (P < 0.005), but not in the trigeminal distribution. No relationship was observed between the thermal deficits and ongoing pain or mechanical allodynia in the groups of subjects with either trigeminal or thoracic PHN. conclusion: Despite a common cause, the patterns of sensory abnormalities differ between subjects. Particular differences were noted between groups with facial or truncal PHN and between groups with recent or more chronic PHN. The observations suggest that the relative contributions of peripheral and central mechanisms to the pathophysiology of pain differ among subjects and may vary over the course of PHN.

Heterogenous Patterns of Sensory Dysfunction in Postherpetic Neuralgia Suggest Multiple Pathophysiologic Mechanisms

The histopathology of striae distensae is disputed; different authorities give contradictory accounts of the microscopic changes, especially in elastic fibres. We re-evaluated the problem by taking eight elliptical biopsies across striae. Six were examined by light microscopy with appropriate stains for elastin and collagen. Two were prepared for scanning electronmicroscopy (s.e.m.), using a procedure which removes collagen, enabling the elastic network to be seen in its native form. By light microscopy, striae were sharply demarcated from normal skin, consisting mainly of fine, straight bundles of collagen arranged parallel to the surface. Fine elastic fibres were disposed similarly without fragmentation, fraying or curling. By s.e.m., the elastic network was found to be extraordinarily dense and well developed with many fine, curled fibres in random array. It was evident that the routine stains for elastin greatly underestimated the abundance of elastic fibres, probably because immature fibres contain insufficient protein matrix. The horizontal packing of collagen bundles was confirmed by s.e.m. These findings support the view that striae distensae are scars. There is no evidence that they form by stress-induced rupture of the connective tissue.

Anatomy of striae

Five male patients with atrophic striae in the groins are reported. All patients received Mycolog cream*topically. None received corticosteroids orally or parenterally. No corticotropin was given. Current theories of the mechanism of the production of striae are discussed. We suggest that the initial change is nonunion of groups of connective tissue fibrils. This is most clearly demonstrated for elastic tissue. The possibility is raised that local inflammation and topically applied corticosteroids may influence the production of striae. The serious consequences of striae are mentioned. Caution is advised in the use of corticosteroids in the treatment of intertrigo.

Atrophic Striae in Patients with Inguinal Intertrigo: Pathogenesis

THE MASTERLY postmortem studies of Head and Campbell, 1 nearly half a century ago, left little doubt that herpes zoster is associated with a severe inflammatory reaction in the sensory ganglion which supplies the sensory nerves to the area of the skin involved by the eruption. Subsequent work has supported these observations. However, Wohlwill 2 in 1924 showed that occasionally the inflammatory reaction might be in some other portion of the sensory tract than the ganglion. Death of a ganglion cell is followed by degeneration of its peripheral axon. Using the Marchi method of demonstrating myelin degeneration, Head and Campbell, as well as Wohlwill, found evidence of degeneration of peripheral sensory nerve fibers in the sensory nerve trunks ten to twelve days after onset of herpes zoster. In one or two instances, some degeneration was reported by them to have taken place in the nerves of the skin, but

Histologic changes in sensory nerves of the skin in herpes zoster.

From time to time during the past five years we have had the opportunity to observe an unusual type of eruption in two sisters who have been patients of Dr. Oliver S. Ormsby, through whose courtesy this study has been made possible. The disorder dates back to childhood in both cases, with periods of marked activity at irregular intervals. REPORT OF CASES Case1.— History .—Mrs. D., of American birth and German descent, was born in 1902. Her first cutaneous trouble appeared at the age of 2 months as a generalized, bright red exanthem, which suggested prickly heat. At 6 months this became exfoliative and persisted until 2 years of age. From the age of 4 years to 12 years she had four similar attacks, each lasting several months. When 15 years of age, discrete psoriasiform lesions appeared for the first time on the elbows, the trunk and

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A psoriasiform eruption with pustular exacerbations

The last decade has witnessed a revival of interest in the problem of the origin of the nevus cell in the pigmented nevus. This problem has always had an attraction, on account of the not infrequent instances of malignant degeneration of such nevi. There is a vast amount of literature on the subject. As is often the case in medicine, recent technical advances have rendered much of it obsolete. The great majority of the studies on the histogenesis of the nevus cell have been made on static material. Adequate studies of the earliest stages of rapidly evolving pigmented moles are rare. I had the opportunity to observe and study the sudden appearance, rapid evolution and maturation of an extensive eruption of pigmented nevi in a boy of 12 years. With the histologic material obtained from that source it was possible to evaluate the more recent theories of the origin of

Multiple pigmented nevi: a study of the origin of the nevus cell

Striae distensae and striae gravidarum are so common and cause so little complaint that they are more or less taken for granted and regarded as normal. Several factors have led to the belief that they are due to mechanical rupture of the elastic tissue framework of the skin or to its disorganization and thinning by increased tension: (1) their occurrence in association with rapid increase in body volume, whether due to obesity, growth, pregnancy, edema or tumor; (2) their direction, which is along the lines of cleavage of the skin and transverse to the line of greatest tension; (3) their occurrence in the areas in which the skin is delicate, and (4) their histologic structure. Certain exceptions must be explained, however, before one can accept this purely mechanical explanation for the appearance of these irregular linear areas of atrophy over the abdomen, buttocks and thighs, about the breasts and occasionally

Hypertrophic striae distensae

We have had under our observation for some time a small group of patients with a type of peribuccal pigmentation sufficiently different from the usual disorders of this area and of a sufficiently uniform character to warrant consideration as a distinct clinical entity. A review of the literature convinced us that the disorder in question is identical with that described by Brocq 1 in 1923 as erythrose peribuccale pigmentaire, so we adopted his title. Our patients were all women in the thirties or early forties. The condition absorbed a disproportionate amount of their attention on account of the cosmetic disfigurement and the extraordinary resistance to treatment. It was observed only in private patients, and we found it impossible to secure a biopsy from this region of the face. Consequently, our study is purely clinical, unsupported by histologic evidence. The disorder consists of a diffuse brownish or brownish-red pigmentation, most marked

Erythrose peribuccale pigmentaire de brocq

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