Trigger finger at the wrist caused by an intramuscular lipoma within the carpal tunnel: A case report.

BACKGROUND: Trigger finger at the wrist, which occurs with finger movement, is an uncommon presentation. Few reports describing cases of trigger finger at the wrist have been published. Thus, we present a case of an intramuscular lipoma arising from an anomalous flexor digitorum muscle belly in a 48-year-old female patient causing painful finger triggering at the wrist and carpal tunnel syndrome (CTS). CASE SUMMARY: A 48-year-old woman with complaints of a catching sensation during wrist motion and a progressive tingling sensation on the palmar aspect of the right hand for approximately 2 years was referred to our hospital. Triggering of the index to middle finger was evident with a palpable and audible clunk over the carpal tunnel during passive motion. Tinel's sign was positive over the carpal tunnel of the right wrist with a positive Phalen's test. Nerve conduction studies of the median nerve demonstrated a right CTS. Ultrasound examination revealed a 2.5 cm × 2.0 cm subcutaneous hyperechoic mass with no obvious blood flow at the wrist of the right arm. Surgical excision of the tumor and muscle mass led to a resolution of the patient's symptoms, and any triggering or discomfort disappeared. The patient has had no evidence of recurrence at more than 1 year of follow-up. CONCLUSION: Triggering of the fingers at the wrist is rare. It must be noted that there are many possible causes and types of triggering or clicking around the wrist. Accurate diagnosis is mandatory to avoid inaccurate treatment of patients with trigger wrist. During the diagnosis and treatment of CTS, attention should be paid to the variation of tendon tissue in the carpal tunnel, to avoid only focusing on the release of transverse carpal ligament and ignoring the removal of anomalous muscle belly.

Interaction between Schwann cells and other cells during repair of peripheral nerve injury.

Peripheral nerve injury (PNI) is common and, unlike damage to the central nervous system injured nerves can effectively regenerate depending on the location and severity of injury. Peripheral myelinating glia, Schwann cells (SCs), interact with various cells in and around the injury site and are important for debris elimination, repair, and nerve regeneration. Following PNI, Wallerian degeneration of the distal stump is rapidly initiated by degeneration of damaged axons followed by morphologic changes in SCs and the recruitment of circulating macrophages. Interaction with fibroblasts from the injured nerve microenvironment also plays a role in nerve repair. The replication and migration of injury-induced dedifferentiated SCs are also important in repairing the nerve. In particular, SC migration stimulates axonal regeneration and subsequent myelination of regenerated nerve fibers. This mobility increases SC interactions with other cells in the nerve and the exogenous environment, which influence SC behavior post-injury. Following PNI, SCs directly and indirectly interact with other SCs, fibroblasts, and macrophages. In addition, the inter- and intracellular mechanisms that underlie morphological and functional changes in SCs following PNI still require further research to explain known phenomena and less understood cell-specific roles in the repair of the injured peripheral nerve. This review provides a basic assessment of SC function post-PNI, as well as a more comprehensive evaluation of the literature concerning the SC interactions with macrophages and fibroblasts that can influence SC behavior and, ultimately, repair of the injured nerve.

Role of CPEB3 protein in learning and memory: new insights from synaptic plasticity.

The cytoplasmic polyadenylation element-binding (CPEB) protein family have demonstrated a crucial role for establishing synaptic plasticity and memory in model organisms. In this review, we outline evidence for CPEB3 as a crucial regulator of learning and memory, citing evidence from behavioral, electrophysiological and morphological studies. Subsequently, the regulatory role of CPEB3 is addressed in the context of the plasticity-related proteins, including AMPA and NMDA receptor subunits, actin, and the synaptic scaffolding protein PSD95. Finally, we delve into some of the more well-studied molecular mechanisms that guide the functionality of this dynamic regulator both during synaptic stimulation and in its basal state, including a variety of upstream regulators, post-translational modifications, and important structural domains that confer the unique properties of CPEB3. Collectively, this review offers a comprehensive view of the regulatory layers that allow a pathway for CPEB3's maintenance of translational control that guides the necessary protein changes required for the establishment and maintenance of lasting synaptic plasticity and ultimately, long term learning and memory.

[Study on the clinical epidemiological features of acute cerebral stroke inducing systemic inflammatory response syndrome and multiple organ dysfunction syndrome].

OBJECTIVE: To study the risks on acute cerebral stroke (ACS) inducing systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS). METHODS: Data from 1751 patients with acute cerebral stroke were studied by prospective analysis. RESULTS: In all of the ACS patients,the incidence rate (IR) of SIRS was 36.50% with 205 patients having ACS inducing MODS, to which the IR was 11.71%, and 93 deaths. The case fatality ratio (CFR) was 45.37%. The pathogeneses condition of patients and the MR after the occurrence of MODS had positive correlation with the numbers of dysfunction organs. Study on single factor analysis revealed that the incidence of MODS had some related risk factors in the ACS inducing MODS, including age, diseased region close to the mean line, GCS, level of blood sugar, blood white cell count and the chronic disease history etc. The IR of ACS inducing SIRS and MODS was much higher in the condition of the diseased region near the mean line and the ACS of the basilar artery system. CONCLUSION: SIRS seemed the base for MODS while the probability and the development degree were not only involved ACS but also SIRS. MODS induced by ACS could be reduced through the second grade program of disease precaution. The detection of those risk factors in the early period of the ACS course could provide some prediction of the prognosis and turnover, thus some early use of intervention methods might be helpful in the treatment of the disease.