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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Skin biopsy is an effective test for diagnosis of peripheral nerve disorders. The most commonly reported indication of abnormality in a skin biopsy is reduction of epidermal nerve density. Morphological changes of epidermal nerves and the underlying subepidermal nerve plexus provide added evidence for the presence of neuropathy. We determined the prevalence of epidermal axon swellings, dermal axon swellings, and a unique type of epidermal nerve that we call a crawler, in a group of normal subjects, diabetic subjects, and patients with idiopathic small fiber neuropathy. Other morphologic features examined include thinning of the subepidermal nerve plexus, sprouts at nerve terminals, encapsulated endings, and immunoreactive basal cells.
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PMID:Morphological features of nerves in skin biopsies. 1644 69

Intra-articular injection of mono-iodoacetate (MIA) in the rat knee joint induces a histopathology with similarities to osteoarthritis (OA). Typically, a synovitis (days 1-3) is observed followed by thinning of articular cartilage and subsequent lesion of subchondral bone at days 8-14 onwards. Behaviourally, weight-bearing asymmetry is observed, which is sensitive to anti-inflammatory pharmacology at early but not later (days 14+) time points. As subchondral bone is densely innervated, an intriguing possibility is that focal bone pathology may cause neuropathy in this model. In male Wistar rats, activating transcription factor (ATF)-3-immunofluorescence was used as a marker of nerve injury in lumber (L)4 and L5 dorsal root ganglia of the ipsilateral knee. Significantly increased ATF-3-immunoreactivity following MIA treatment was measured in L5 on days 8 and 14 (P<0.05, Kruskal-Wallis and Mann-Whitney U-test), compared to saline controls. Furthermore, in an additional study animals were orally dosed vehicle (5 ml/kg), naproxen (0.3-10 mg/kg), celecoxib (1-10 mg/kg), amitriptyline (3-30 mg/kg) and gabapentin (10-100mg/kg) and evaluated for weight-bearing asymmetry on days 14, 21 and 28 post-MIA. Significant resolution of weight-bearing was observed at high and intermediate doses of amitriptyline and gabapentin at all time points (P<0.05, ANOVA, post-hoc Bonferroni's, vs pre-dose measurements). Transient and weak effects were observed with naproxen (10mg/kg) on days 14 and 28, whereas celecoxib showed no significant effects. Collectively, these data suggest that this putative model of OA is associated with an early phase neuropathy in the L5 innervation territory of the knee.
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PMID:Structural pathology in a rodent model of osteoarthritis is associated with neuropathic pain: increased expression of ATF-3 and pharmacological characterisation. 1727 7

The glaucomas are a group of potentially blinding optic neuropathies that are characterized by progressive pathological losses of the retinal ganglion cells (RGCs) and their axons that form the optic nerve. The causes are unknown and, therefore, the diagnosis and assessment of progression of disease depends on ophthalmic testing to identify and quantify clinical characteristics of glaucomatous neuropathy, such as the pattern of visual field defects and/or thinning of the retinal nerve fiber layer. To relate these clinical measurements to the basic pathology of glaucoma, a neuron doctrine for glaucoma has been proposed to correlate data from standard tests (standard automated perimetry and optical coherence tomography) to the loss of RGCs. The doctrine was derived through initial laboratory studies of experimental glaucoma in macaque monkeys and, then, modified and refined though patient-based clinical investigations. The final formulation of the doctrine produced concordance between subjective and objective measurements when the results were translated to their common parameter of RGCs, for both normal vision and defective vision from glaucoma. Thus, it was concluded that for individual patients, alterations in structure-function relationships usually should be in agreement for the degree and location of visual field defects caused by glaucoma.
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PMID:Charles F. Prentice Award Lecture 2006: a neuron doctrine for glaucoma. 1852 Oct 13

Glaucoma, an optic neuropathy, is the leading cause of world blindness. In this condition, the damage extends from the retina to the visual center in the brain, although the primary region of damage is thought to be the optic nerve head (ONH), with the lateral geniculate nucleus (LGN) being secondarily affected. We investigated time-dependent alterations in the ONH, the optic nerve (ON), and the LGN after intraocular pressure (IOP) elevation in Japanese monkeys (a species more similar to humans than other macaque species). Nine Japanese monkeys, each with an experimental glaucomatous left eye, and two naive monkeys were studied. Ocular-testing sessions (including IOP measurement and fundus photography) were held weekly. Eyes and brains were enucleated at 2-48 weeks after IOP elevation, and alterations in ONs and LGN were evaluated. The IOP of the treated eyes was monitored periodically and found to be elevated continuously throughout the observation period in each monkey. The ONH of the glaucomatous eyes exhibited time-dependent deep cupping and thinning of the rim area from 2 weeks after the IOP elevation. Loss of axons and a decrease in the area of ON were first observed at 4 and 28 weeks, respectively. Neuronal loss was first observed at 2 weeks in layers 1 and 2 of LGN [magnocellular (M)-layer] and at 12 weeks in layers 3-6 of LGN [parvocellular (P)-layer]. Neuronal shrinkage was first observed at 2 weeks in all layers in LGN. These findings indicate that in Japanese monkeys, damage to neurons in LGN can be detected in the early phase (first few weeks) after an IOP elevation, as can damage to ONH.
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PMID:Morphological changes in the visual pathway induced by experimental glaucoma in Japanese monkeys. 1934 28

A 34-year-old woman developed bilateral optic neuritis 2 weeks after the onset of acute hepatitis C. The strong temporal relationship between the initial clinical manifestations of hepatitis C and the development of optic neuritis provides a basis for thinking that the hepatitis caused the optic neuritis After corticosteroid treatment, the optic neuropathy markedly improved but left behind retinal nerve fiber thinning, as measured by optical coherence tomography, and optic disc pallor. Optic neuritis has been reported in conjunction with hepatitis A and B but not with hepatitis C.
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PMID:Bilateral optic neuritis in acute hepatitis C. 1949 36

This is the first case report of a bilateral superior segmental optic hypoplasia (SSOH) accompanied by a glaucomatous optic neuropathy (GON). A 47-year-old man incidentally diagnosed as having bilateral SSOH, simultaneously disclosed glaucomatous optic disc appearances, including enlargements of the cup of the optic nerve heads and a thinning of the infero-temporal neuroretinal rim with laminar dot sign accompanied by a retinal nerve fiber layer (RNFL) local defect of infero-temporal region in the right eye. The visual field examination revealed that the corresponding nasal step, arcuate scotoma and RNFLfield defects in the right eye.
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PMID:A case of superior segmental optic hypoplasia accompanied by a glaucomatous optic neuropathy. 1966 41

Primary open-angle glaucoma is a progressive optic neuropathy involving loss of retinal ganglion cells and their axons at the level of the optic nerve head. This change manifests as thinning and excavation of the neural tissues and nerve fiber layer. Therefore, it has long been known that the structural appearance of the optic nerve head is paramount to both glaucoma diagnosis and to the detection of progression [1-4]. Quantitative imaging methods such as Heidelberg Retinal Tomography (HRT) and Ocular Coherence Tomography (OCT) show great promise for the diagnosis and management of glaucoma and as these technologies continue to improve, they will become more important in the care of glaucoma. However, these tests cannot replace good clinical examination and indeed they depend upon clinical correlation for correct interpretation. Thus, careful and systematic clinical examination of the optic nerve remains a cornerstone of glaucoma management. In this paper, we outline a few pearls for the examination of the optic nerve and some of the pitfalls to be avoided in optic disc examination.
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PMID:Evaluating optic nerve damage: pearls and pitfalls. 1983 65

PURPOSE. To describe the association of retinal vascular tortuosity, measured quantitatively, with the neuroretinal rim. METHODS. A population-based, cross-sectional study was conducted in Malay persons aged 40 to 80 years residing in Singapore. Retinal vascular tortuosity was quantified by using a semiautomated, computer-assisted program assessing retinal fundus photographs, according to a standardized protocol. Optic disc measurements including disc area, rim area, and rim-to-disc area (RDA) ratio were obtained with a confocal scanning laser ophthalmoscope. RESULTS. In analyses adjusting for age, sex, spherical equivalent, and retinal vascular caliber, reduced arteriolar and venular tortuosity were associated with a decrease in global RDA ratio (P = 0.006 and P = 0.001, respectively). When compared with the arterioles, retinal venular tortuosity demonstrated a stronger association with RDA ratio. The temporal-inferior region of the neuroretinal rim was most strongly associated with retinal vascular tortuosity. CONCLUSIONS. Straighter retinal vessels were significantly associated with a thinning neuroretinal rim. These findings may provide additional insights into the geometric retinal vascular changes seen in early glaucomatous optic neuropathy.
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PMID:Relationship of retinal vascular tortuosity with the neuroretinal rim: the singapore malay eye study. 2020 64

Optical coherence tomography studies in multiple sclerosis have primarily focused on evaluation of the retinal nerve fibre layer. The aetiology of retinal changes in multiple sclerosis is thought to be secondary to optic nerve demyelination. The objective of this study was to use optical coherence tomography to determine if a subset of patients with multiple sclerosis exhibit primary retinal neuronopathy, in the absence of retrograde degeneration of the retinal nerve fibre layer and to ascertain if such patients may have any distinguishing clinical characteristics. We identified 50 patients with multiple sclerosis with predominantly macular thinning (normal retinal nerve fibre-layer thickness with average macular thickness < 5th percentile), a previously undescribed optical coherence tomography defined phenotype in multiple sclerosis, and compared them with 48 patients with multiple sclerosis with normal optical coherence tomography findings, 48 patients with multiple sclerosis with abnormal optical coherence tomography findings (typical for multiple sclerosis) and 86 healthy controls. Utilizing a novel retinal segmentation protocol, we found that those with predominant macular thinning had significant thinning of both the inner and outer nuclear layers, when compared with other patients with multiple sclerosis (P < 0.001 for both), with relative sparing of the ganglion cell layer. Inner and outer nuclear layer thicknesses in patients with non-macular thinning predominant multiple sclerosis were not different from healthy controls. Segmentation analyses thereby demonstrated extensive deeper disruption of retinal architecture in this subtype than may be expected due to retrograde degeneration from either typical clinical or sub-clinical optic neuropathy. Functional corroboration of retinal dysfunction was provided through multi-focal electroretinography in a subset of such patients. These findings support the possibility of primary retinal pathology in a subset of patients with multiple sclerosis. Multiple sclerosis-severity scores were also significantly increased in patients with the macular thinning predominant phenotype, compared with those without this phenotype (n = 96, P=0.006). We have identified a unique subset of patients with multiple sclerosis in whom there appears to be disproportionate thinning of the inner and outer nuclear layers, which may be occurring as a primary process independent of optic nerve pathology. In vivo analyses of retinal layers in multiple sclerosis have not been previously performed, and structural demonstration of pathology in the deeper retinal layers, such as the outer nuclear layer, has not been previously described in multiple sclerosis. Patients with inner and outer nuclear layer pathology have more rapid disability progression and thus retinal neuronal pathology may be a harbinger of a more aggressive form of multiple sclerosis.
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PMID:Primary retinal pathology in multiple sclerosis as detected by optical coherence tomography. 2159 63

The diabetic ulceration is not uncommon, and becomes refractory, as the skin in a diabetic patient is relatively thin as well as hypoesthetic and less sensitive to temperature. As there are already preexisting histological and cellular derangement in the skin, healing of the skin injury is difficult, thus resulting in an intractable ulceration. When diabetes is not controlled, the skin contents of sugar and advanced glycation end product accumulate, invoking cellular deformation and accumulation of matrix metalloproteinases (MMP), resulting in an imbalance between MMP and its inhibitors, malfunction of growth factors, and inflammatory reaction. These processes lead to obvious skin thinning, denaturation of connective tissues, thickening of vascular basal membrane, and neuropathy, etc. These pathological alterations could be recognized as "covert disorder" of skin in diabetic patients and may be underlying disorders in producing indolent diabetic ulcers.
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PMID:[Advances in research of the mechanism of "covert disorder" in diabetic skin]. 2249 May 41


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