ABSTRACT
BACKGROUND: Neuropathic feet are at very high risk for infection and amputation. The slipping slipper sign (SSS) is elicited by a simple questionnaire test reported to detect the presence of severe diabetic peripheral neuropathy. This test can be administered by non-medical staff. In this study, subjects with and without the SSS were evaluated by nerve conduction studies (NCS) and ultrasound measurements of the right sural nerve diameters as well as with traditional scoring systems for peripheral and autonomic neuropathy. OBJECTIVE: To demonstrate that the Slipping Slipper Sign can be used as an index of severe diabetic peripheral neuropathyMethod:This was a prospective cross sectional study in which 74 patients with diabetes (38 positive and 36 negative for SSS) underwent ultrasonography and NCS of the right sural nerve by an examiner blinded to SSS status. Findings were evaluated against demography, clinical history, anthropometry as well as traditional clinical and autonomic neuropathic scores. RESULTS: Patients without the SSS [median (IQR)â=â10.0 years (4.0-20.3)] had a significantly shorter duration of diabetes compared with those with the SSS [median (IQR)â=â15.0 years (8.5-25.0)], pâ=â0.028. The frequencies of retinopathy (36.8% vs 2.8%, pâ< â0.05) and cerebrovascular accidents (18.4% vs 13.9 %, pâ< â0.05) were higher among those with SSS compared with those without. Differences in nerve conduction characteristics were markedly significant. The amplitude of the sural sensory nerve action potential (SNAP) was ([median (IQR)] 0 microvolts vs 4.0 microvolts (0.0-10.8) pâ< â0.002) between those with and without SSS, respectively whilst none of patients with SSS had a recordable SNAP vs 78% without a SSS. Similarly, maximal thickness of the right sural nerve at the ankle 3.0âmm (2.3-3.4) vs 3.5âmm (3.0-3.9), and leg 3.4âmm (2.7-3.8) vs 3.9âmm (3.3-4.2) was reduced, pâ< â0.01 in patients with the SSS compared with those with a negative SSS. CONCLUSION: The SSS identifies feet with objective neurophysiological and imaging characteristics of severe neuropathy.
Subject(s)
Diabetic Neuropathies/diagnostic imaging , Diabetic Neuropathies/diagnosis , Diabetic Neuropathies/physiopathology , Sural Nerve/diagnostic imaging , Sural Nerve/physiopathology , Adult , Cross-Sectional Studies , Female , Humans , Male , Middle Aged , Neural Conduction/physiology , Prospective Studies , Severity of Illness Index , Single-Blind Method , UltrasonographySubject(s)
Family , Physician-Patient Relations , Physicians, Family , Professional Role , Family Practice , Humans , SpecializationABSTRACT
Transforming growth factor-ß (TGF-ß) may play a role in the pathogenesis of primary open-angle glaucoma (POAG). Elevated levels of TGF-ß are found in the aqueous humor and in reactive optic nerve astrocytes in patients with glaucoma. In POAG, aqueous humor outflow resistance at the trabecular meshwork (TM) leads to increased intraocular pressure and retinal ganglion cell death. It is hypothesized that TGF-ß increases outflow resistance by altering extracellular matrix homeostasis and cell contractility in the TM through interactions with other proteins and signaling molecules. TGF-ß may also be involved in damage to the optic nerve head. Current available therapies for POAG focus exclusively on lowering intraocular pressure without addressing extracellular matrix homeostasis processes in the TM. The purpose of this review is to discuss possible therapeutic strategies targeting TGF-ß in the treatment of POAG. Herein, we describe the current understanding of the role of TGF-ß in POAG pathophysiology, and examine ways TGF-ß may be targeted at the levels of production, activation, downstream signaling, and homeostatic regulation.