Cardiac Amyloidosis Screening at Trigger Finger Release Surgery.

Cardiac amyloidosis is often preceded by orthopedic manifestations such as carpal tunnel syndrome, and 10% of patients who underwent idiopathic carpal tunnel release surgery will have biopsy-confirmed amyloid deposits in the tenosynovial sheath. Trigger finger is also commonly reported in patients with amyloidosis and involves the same tendon sheath as carpal tunnel syndrome, but the prevalence of amyloid deposition is unclear. This prospective cross-sectional study enrolled 100 patients aged ≥50 years at the time of surgery for idiopathic trigger finger. Patients underwent release surgery, and a sample of the tenosynovium of the affected finger was excised, stained with Congo red, and subtyped with mass spectrometry if amyloid was demonstrated. Further cardiac evaluation was performed in patients with amyloid deposition. Of the 100 patients (mean age 65.5 ± 8.1 years) enrolled, only 2 demonstrated amyloid deposits on Congo red staining. One patient with previous proteinuric kidney disease had fibrinogen A α-chain amyloidosis, and the other patient had untyped amyloidosis. Neither patient had cardiac involvement. A total of 13 of the 100 patients underwent concomitant carpal tunnel release surgery, and 2 of these patients had amyloid deposits in the carpal tunnel with "false-negative" samples from the trigger finger tenosynovium. In conclusion, biopsy during trigger finger release surgery demonstrated a 2% yield for amyloidosis, which is significantly lower than the previously published yield of 10% during carpal tunnel release surgery. This observation has important implications for the development of diagnostic algorithms to screen patients for amyloidosis during orthopedic operations.

Interleukin-6 secretion by fibroblasts in carpal tunnel syndrome patients is associated with trigger finger and inhibited by tranilast.

INTRODUCTION: In this study we aimed to clarify the association between interleukin-6 (IL-6) secretion in fibroblasts in carpal tunnel syndrome (CTS) patients and their biophysical parameters, including association with trigger finger and whether tranilast inhibits IL-6 secretion in fibroblasts. METHODS: Fibroblasts were obtained from tenosynovial tissue harvested from idiopathic CTS patients undergoing carpal tunnel release and tenosynovectomy and cultured in media containing tranilast with or without tumor necrosis-α (TNF-α) or interleukin-1ß (IL-1ß). Their proliferation was evaluated and secreted IL-6 levels and IL-6 mRNA expression were quantified. Correlations between IL-6 concentration and patient characteristics were examined. RESULTS: IL-6 secretion was significantly associated with trigger finger (P = .001). Tranilast inhibited fibroblast proliferation in a dose-dependent manner and suppressed IL-6 secretion. DISCUSSION: IL-6 overproduction in tenosynovial tissue may account for the association between CTS and trigger finger. Future studies should investigate whether tranilast can be used to treat patients with CTS.

Biochemical markers decrease and increase disproportionally in A1 pulley tissue of type 2 diabetic trigger finger patients.

OBJECTIVES: This study aims to detect the levels of some biochemical markers in A1 pulley tissue of type 2 diabetic trigger finger patients to enlighten the mechanisms leading to cellular complications. PATIENTS AND METHODS: The study included 35 trigger finger patients (5 males, 30 females; mean age 53.9±9.15 years; range, 37 to 71 years). We measured total thiol (total-SH) levels to determine the status of the non-enzymatic antioxidant defense system and advanced oxidation protein product (AOPP) levels to determine levels of oxidative protein modification in pulley tissues of trigger finger patients with or without diabetes. Extracellular matrix degradation was assessed by measuring levels of sialic acid (SA) in the pulley tissue. RESULTS: Total-SH values for the groups with and without diabetes were 22.7±1.6 vs. 38.9±5.2 nmol/mg protein, respectively, while AOPP values were 472.5±131.6 vs.175.6±9.9 mmol/g protein, respectively. The SA levels of diabetic and nondiabetic patients were 0.4±0.0 vs. 0.63±0.1 nmol/mg protein, respectively. CONCLUSION: Our results revealed that tissue SA levels and tissue SH levels decreased and AOPP levels increased disproportionally in the A1 pulley tissue of diabetic patients, which may indicate the role of oxidative protein damage and extracellular matrix changes in diabetic trigger finger etiology.

Histopathology of tenosynovium in trigger fingers.

Stenosing flexor tenosynovitis, trigger finger, is a common clinical disorder causing painful locking or contracture of the involved digits, and most instances are idiopathic. This problem is generally caused by a size mismatch between the swollen flexor tendon and the thickened first annular pulley. Although hypertrophic pulleys have been histologically and ultrasonographically detected, little is known about the histopathology of the tenosynovium covering the tendons of trigger fingers. We identified chondrocytoid cells that produced hyaluronic acid in 23 (61%) fingers and hypocellular collagen matrix in 32 (84%) fingers around the tenosynovium among 38 specimens of tenosynovium from patients with trigger fingers. These chondrocytoid cells expressed the synovial B cell marker CD44, but not the chondrocyte marker S-100 protein. The incidence of these findings was much higher than that of conventional findings of synovitis, such as inflammatory infiltrate (37%), increased vascularity (37%), hyperplasia of synovial lining cells (21%), or fibrin exudation (5%). We discovered the following distinctive histopathological features of trigger finger: hyaluronic acid-producing chondrocytoid cells originated from fibroblastic synovial B cells, and a hypocellular collagen matrix surrounding the tenosynovium. Thus, an edematous extracellular matrix with active hyaluronic acid synthesis might increase pressure under the pulley and contribute to the progression of stenosis.

Estudios neurofisiológicos en los parkinsonismos / Neurophysiological studies in parkinsonism

Introducción. El estudio del sistema motor y de sus trastornos ha sido un tema importante para la neurofisiología, siendo uno de sus objetivos intentar comprender los mecanismos fisiopatológicos que subyacen a las disfunciones del mismo. Desarrollo: Se revisa lo más relevante acerca de: (1) Técnicas neurofisiológicas utilizadas en el diagnóstico de la EP y otros parkinsonismos; (2) Utilidad de la estimulación magnética transcraneal (EMT); (3) Estudios neurofisiológicos de los trastornos del sueño en la EP; (4) Aspectos neurofisiológicos de la estimulación cerebral profunda (ECP). Conclusiones: Las pruebas neurofisiológicas puede ayudar en el diagnóstico diferencial del parkinsonismo además de profundizar en la fisiopatología de los síntomas y signos parkinsonianos. Diferentes técnicas pueden emplearse en el estudio de los trastornos del sueño en la EP. La EMT resulta útil tanto desde el punto de vista diagnóstico como probablemente también terapéutico en la EP. Actualmente, los registros con microelectrodos constituyen la forma más precisa de poder identificar la diana seleccionada en la cirugía de la EP (AU)

Introduction. The study of motor system and its diseases has been an interesting topic for neurophysiology, being one of the objectives of this to know the physiopathology mechanisms. Development. We review the most relevant about: (1) Neurophysiological techniques used in the diagnosis of Parkinson's disease (PD) and other parkinsonisms; (2) Utility of transcranial magnetic stimulation (TMS); (3) Neurophysiological techniques used in the diagnosis of sleep disorders in PD patients; (4) Neurophysiological aspects of deep brain stimulation (DBS). Conclusions. Different neurophysiological techniques can be used for differential diagnosis of PD and others parkinsonisms besides to investigate in the physiopathology mechanisms. We can use different techniques for study sleep disorders in PD patients. TMS results to be utility for diagnosis and probably such as therapy in PD patients. Actually, microelectrode recording could be the best method for target identification in DBS surgery (AU)

Congenital trigger thumb in children: electron microscopy and immunohistochemical analysis of the first annular pulley.

Although numerous studies have been performed on congenital trigger thumb (CTT), the pathogenesis is still unknown. Cytocontractile proteins and myofibroblasts are present during soft-tissue contraction, and they may have a role in CTT. The aim of the study is to clarify the immunohistochemical and the electron microscopy characteristics of the first annular (A-1) pulley in CTT. The specimens from the A-1 pulleys were collected from 22 children with CTT. Electron microscopy was used to study the last five specimens. Immunohistochemistry staining demonstrated that all specimens stained positively for vimentin and for α-smooth muscle actin, and stained negatively for desmin. Electron microscopy showed fibroblasts in collagenous matrix, which contain vimentin-like material and associated at the surface with elastin-like tubular matrix filaments and elastin fibers. In two specimens, a few cells showed markers of myofibroblastic differentiation. The presence of the cytocontractile proteins and myofibroblasts suggests proliferation of fibrous tissues during either the intrauterine or extrauterine phase of development and may account for the presence of congenital stenosis at the level of the A-1 pulley. We believe that CTT may be developmental; if the process started in the intrauterine phase it might present as a fixed flexion contracture and will show mature fibroblasts. If the process started in the extrauterine phase, it might present as triggering first and will show myofibroblastic changes, then with the maturation of the fibrous tissue, result in a fixed flexion contracture.