Nerve compression induces activating transcription factor 3 in neurons and Schwann cells in diabetic rats.
ABSTRACT Expression of transcription factor ATF3 in sensory neurons in dorsal root ganglion and in Schwann cells in sciatic nerve of diabetic (BB and Goto-Kakizaki rats; experimental models of types 1 and 2 diabetes, respectively) and healthy rats were examined by immunocytochemistry after nerve compression (silicone tube) for 3, 6 or 14 days. ATF3-stained sensory neurons in dorsal root ganglia and Schwann cells at compression site were more frequent in diabetic BB rats. Decompression of nerves in Goto-Kakizaki rats did not reduce number of ATF3-stained cells. Diabetes (BB; i.e. type 1) confers on the peripheral nerve an increased susceptibility to nerve compression indicated by an increased expression of stained ATF3 neurons and Schwann cells.
- SourceAvailable from: Rayaz A Malik[Show abstract] [Hide abstract]
ABSTRACT: The underlying basis of carpal tunnel syndrome (CTS) and the basis of its increased incidence in diabetes are unknown. We have quantified pathology in an uncompressed nerve (posterior interosseous nerve, PIN) in the forearm between diabetic and non-diabetic patients with CTS and control subjects. In an age- and gender-matched series, 26 diabetic patients with CTS and 20 non-diabetic patients with CTS underwent biopsy of the PIN at the time of surgical carpal tunnel release. Control subjects consisted of ten PIN biopsies taken postmortem and three biopsies taken at the time of wrist surgery. We found PIN myelinated nerve fibre density significantly reduced in diabetic (mean 5,373/mm2 [95% confidence interval, 4,835–5,911]) and non-diabetic (6,617/mm2 [5,697–7,537]) patients with CTS compared to control subjects (9,109/mm2 [7,967–10,250], P < 0.001). Furthermore, diabetic patients had a significantly lower density than non-diabetic patients (P < 0.03). Endoneurial capillary density was also reduced in diabetic (58/mm2 [50–66]) and non-diabetic (67/mm2 [55–78]) patients compared to control subjects (86/mm2 [72–101], P < 0.02) with no difference between diabetic and non-diabetic patients with CTS. Our results suggest that a reduction in myelinated nerve fibre and capillary densities may predispose patients, particularly those with diabetes, to develop CTS.Acta Neuropathologica 07/2009; 118(6):785-91. DOI:10.1007/s00401-009-0578-0 · 9.78 Impact Factor
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ABSTRACT: To determine health-related quality of life (HRQL) in diabetic and non-diabetic patients with carpal tunnel syndrome (CTS) before and after surgical treatment. In a prospective study, 35 consecutive diabetic patients with CTS were age and gender matched with 31 non-diabetic patients with idiopathic CTS. At baseline (preoperatively), 6, 12 and 52 weeks after surgical carpal tunnel release, patients completed the generic Short-Form 36 (SF-36) and the disease-specific Boston Carpal Tunnel Questionnaire (BCTQ). The SF-36 physical component scores at baseline were significantly reduced for diabetic (39+/-7.4) compared with non-diabetic patients (48+/-9.0) (P<0.05). Mixed model analysis demonstrated no differences in post-surgical improvement over time between diabetic and non-diabetic patients. The largest clinical effect was found for bodily pain (effect size 0.8). However, population norms were not reached for the diabetic patients. At baseline, no difference was found in mental component score, which deteriorated over time for diabetic patients. At baseline, BCTQ demonstrated that diabetic patients experienced more pronounced 'numbness in the hand' than non-diabetic patients. Large clinical improvements were found in both symptom severity (effect size 1.98-2.14) and functional status score (effect size 0.89-0.94) for both diabetic and non-diabetic patients, with no difference between the two patient groups. HRQL is impaired in diabetic patients with CTS compared with non-diabetic patients with CTS and population norms. However, diabetic patients experience similar symptomatic and functional benefits from carpal tunnel release as do non-diabetic patients.Diabetic Medicine 04/2010; 27(4):466-72. DOI:10.1111/j.1464-5491.2010.02970.x · 3.06 Impact Factor
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ABSTRACT: Phosphorylation of extracellular-signal-regulated kinase 1/2 (p-ERK 1/2) was investigated by immunohistochemistry at 30 min, 1 h, and 48 h after nerve transection in the sciatic nerve of healthy and diabetic [streptozotocin (STZ)-induced diabetes mellitus and BioBreeding (BB; i.e. DR.lyp/lyp or BBDP)] rats. Transection injury increased the intensity of p-ERK 1/2 in nerve stumps at all time points. Staining was confined to Schwann cells with occasional faint staining in single axons. In diabetic rats, a lower intensity of p-ERK 1/2 was found at 1 and 48 h in the distal and proximal nerve stumps compared with healthy rats. STZ-induced diabetic rats were not different from BB rats. p-ERK 1/2 is activated differentially in Schwann cells after nerve injury in diabetic rats, whereas activation in STZ-induced diabetic rats did not differ from BB rats.Neuroreport 12/2010; 22(2):73-7. DOI:10.1097/WNR.0b013e328342986c · 1.64 Impact Factor