PubMed · 16418865
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J Mössner. 2006. [Disease sequelae].. https://doi.org/10.1007/s00108-005-1574-7
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Lupoid leishmaniasis is a unique form of cutaneous leishmaniasis characterized by unusual clinical features and a chronic relapsing course. Clinically and histologically it is similar to lupus vulgaris, which is thus the most important differential diagnostic consideration. All patients with granulomatous facial lesions coming from endemic areas or with a positive travel history should be suspected of having leishmaniasis. We describe a 59-year-old woman with facial lupoid leishmaniasis.
Some chronic painful conditions including e.g. fibromyalgia, whiplash associated disorders, endometriosis, and irritable bowel syndrome are associated with generalized musculoskeletal hyperalgesia. The aim of the present study was to determine whether generalized deep-tissue hyperalgesia could be demonstrated in a group of patients with chronic low-back pain with intervertebral disc herniation. Twelve patients with MRI confirmed lumbar intervertebral disc herniation and 12 age and sex matched controls were included. Subjects were exposed to quantitative nociceptive stimuli to the infraspinatus and anterior tibialis muscles. Mechanical pressure (thresholds and supra-threshold) and injection of hypertonic saline (pain intensity, duration, distribution) were used. Pain intensity to experimental stimuli was assessed on a visual analogue scale (VAS). Patients demonstrated significantly higher pain intensity (VAS), duration, and larger areas of pain referral following saline injection in both infraspinatus and tibialis anterior. The patients rated significantly higher pain intensity to supra-threshold mechanical pressure stimulation in both muscles. In patients, the pressure pain-threshold was lower in the anterior tibialis muscle compared to controls. In conclusion, generalized deep-tissue hyperalgesia was demonstrated in chronic low-back pain patients with radiating pain and MRI confirmed intervertebral disc herniation, suggesting that this central sensitization should also be addressed in the pain management regimes.
In chronic glaucoma, there is a gradual painless loss of vision, early manifestation of arcuate field defect and typical atrophy of the optic disc known as 'cupping'. Chronic glaucoma is classified into high-tension glaucoma (HTG) and normal-tension glaucoma (NTG). Although both types manifest with the same typical visual field defect and cupping of the optic disc, high-tension glaucoma has elevated intraocular pressure whereas in normal-tension glaucoma the intraocular pressure (IOP) is within the normal range (10-21 mmHg). There are several theories about the pathogenesis of chronic glaucoma ranging from high intraocular pressure directly damaging the optic disc to programmed death(apoptosis) of the ganglion cells of the retina. But none of them satisfactorily explain the manifestation of the early arcuate field defect which is a pathognomonic feature of both types of chronic glaucoma. This article focuses on two main issues. First, how and why the arcuate field defects are produced in the early stages of glaucoma and secondly to find out the common ground in the pathogenesis of both high and normal tension glaucoma. The early arcuate field defects are an important lead in discovering the pathogenesis of glaucoma, therefore if any factor or site which could not possibly produce initial sharply defined arcuate field defects was ruled out. This article presents an unconventional approach to the pathogenesis of glaucoma. Instead of looking for various factors causing glaucoma, emphasis was placed on determining the primary site of injury which could produce the initial arcuate field defects. Keeping the arcuate visual field defects in mind, the primary site of injury appears to be at the scleral edge and not the optic disc or the retina in chronic glaucoma. The border tissue which separates the sclera and choroid from the nerve fibers would atrophy due to chronic ischemia as a result of high intraocular pressure in HTG, whereas due to poor systemic circulation in NTG. In both types of chronic glaucoma, the ciliary circulation supplying the prelaminar and border tissue is compromised. As a result of atrophy of the border tissue, the optic disc sinks as a whole beginning temporally due to its tilted position and causing nerve fibers to stretch, kink, and cut at the scleral edge. This process of optic disc sinking would accelerate due to loss of nerve fibers which also provides anchorage to the optic disc. This cycle would continue until all the nerve fibers are cut at the scleral edge and the optic disc is destroyed.