Confocal Microscopy Of Cornea Research Articles

Corneal staining patterns in vernal keratoconjunctivitis: the new VKC-CLEK scoring scale

AimTo propose a new scoring system in the assessment of ocular surface epithelial damage in vernal keratoconjunctivitis (VKC).Methods25 consecutive patients with VKC (50 eyes) were evaluated using the Quality of...

Quantification of small fiber pathology in patients with sarcoidosis and chronic pain using cornea confocal microscopy and skin biopsies.

Small fiber pathology with concomitant chronic neuropathic pain is a common complication of sarcoidosis. The gold standard of diagnosis of small fiber neuropathy (SFN) is the quantification of small nerve fibers in skin biopsies in combination with patient history and psychophysical tests; a new technique is the quantification of small nerve fibers in the cornea using cornea confocal microscopy (CCM). Here, we studied small fiber morphology in sarcoidosis patients with neuropathic pain using skin biopsies, CCM, and quantitative sensory testing (QST). Our aim was to construct specific phenotypes of neuropathic pain in sarcoidosis. Fifty-eight patients with a confirmed diagnosis of sarcoidosis and with moderate-to-severe neuropathic pain were tested. Decreased intraepidermal nerve fiber density (IENFD) from skin biopsies was found in 28% of patients, and CCM abnormalities were observed in 45% of patients. There was no correlation between CCM and IENFD abnormalities. Eighty-three percent of patients had abnormal thermal detection thresholds, a sign of small fiber dysfunction. Based on the presence or absence of abnormalities in IENFD and CCM, four distinct phenotypes were identified with a distinct homogeneous pattern of somatosensory symptoms. We argue that these distinct phenotypes have a similar mechanistic construct with specific phenotype-specific treatment options. Additionally, our data suggest the presence of patients with length- and nonlength-dependent SFN within this population of sarcoidosis patients.

Clinical presentation and diagnosis of neuropathic pain

BACKGROUND AND OBJECTIVES: Neuropathic pain is reason for distress and incapacity of several patients, being that symptoms, mechanisms and management distinguish it from nociceptive pain. This study aimed at discussing the clinical presentation and diagnosis of neuropathic pain. CONTENTS: Neuropathic pain is manifested by several symptoms, being continuous burning pain, shock sensation and mechanical alodynia the most common ones. Neurophysiologic studies and skin biopsy suggest that burning pain is reflex of spontaneous activity of afferent nociceptive fibers, while shock sensation is originated from high frequency ectopic stimuli, generated in demyelinated Aβ fibers. Clinical exam, made up of history and elementary physical neurological evaluation, is critical for the adequate diagnosis of the type of pain, as well as more detailed exams, such as quantitative sensory tests and confocal optic microscopy, may bring further subsidies to the diagnosis of the type of pain. CONCLUSION: Clinical presentation of neuropathic pain has characteristics which help the accurate diagnosis of the syndrome or disease responsible for the onset of the complaint. Adequate clinical evaluation, including directed physical neurologic exam, sensory quantitative tests and cornea confocal microscopy cooperate for a more accurate diagnosis.

Early Loss of Innervation of Cornea Epithelium in Streptozotocin-Induced Type 1 Diabetic Rats: Improvement with Ilepatril Treatment

Cornea confocal microscopy is emerging as a clinical tool to evaluate the development and progression of diabetic neuropathy. The purpose of these studies was to characterize the early changes in corneal sensitivity and innervation in a rat model of type 1 diabetes in relation to standard peripheral neuropathy endpoints and to assess the effect of Ilepatril, a vasopeptidase inhibitor which blocks angiotensin converting enzyme and neutral endopeptidase, on these endpoints. Streptozotocin-diabetic rats 8 weeks duration were treated with or without Ilepatril for the last 6 weeks of the experimental period. Afterwards, standard diabetic neuropathy endpoints, subbasal corneal nerves and innervation of the epithelium, corneal sensitivity using a Cochet-Bonnet esthesiometer, and vascular reactivity of the posterior ciliary artery were examined. Diabetes caused a decrease in nerve conduction velocity, thermal hypoalgesia, and a reduction in intraepidermal nerve fiber profiles. In the cornea there was a decrease in corneal nerve fibers innervating the epithelium and corneal sensitivity, but subbasal corneal nerve fibers was not changed. Vascular relaxation in response to acetylcholine was decreased in the posterior ciliary artery. These defects were partially to completely prevented by Ilepatril treatment. These studies suggest that in type 1 diabetic rats decreased innervation of the cornea epithelium occurs early in diabetes and prior to a detectable decrease in subbasal corneal nerves and that these and other diabetic neuropathy-related defects can be partially to completely prevented by a vasopeptidase inhibitor.