Objective. Local glucocorticoid injections are used to treat carpal tunnel syndrome (CTS). However, this treatment is associated with frequent relapses. An important limitation of studies with higher relapse rates is that no attempt has been made to identify patients with mild or severe disease. We evaluated the efficacy of local glucocorticoid injection in patients with mild CTS. Method. Mild CTS was defined as intermittent symptoms without absence of sensations, muscle atrophy or weakness of the thenar muscles. Forty-eight patients with idiopathic mild CTS were evaluated before and 3 and 12 months after a single local injection of 40 mg methyl prednisolone acetate. Outcome was assessed by overall satisfaction on a 100 mm visual analogue scale, the Boston self-administered questionnaire for symptom severity and functional scores and improvement in the electrophysiological parameters. Results. At 3 months, 93.7% of the patients reported marked improvement in their symptoms, with significant improvement in the mean values of the nerve conduction parameters distal motor latency at the wrist (DML) (P = 0.00001), distal sensory latency at mid-palm (DSL MP) (P = 0.014) and distal sensory latency at the wrist (DSL W) (P = 0.0003), and symptom severity (P = 4.96 × 10⁻⁸) and the functional scores (P = 3.56 × 10⁻⁵). Significant improvement was still present for DML (P = 1.39 × 10⁻⁵) at 12 months. Almost 50% of the patients achieved normalization in the electrophysiological study. At a median follow-up of 16 months, 79% patients continued to have improvement in their symptoms. Eight patients (16.6%) relapsed following the initial response. Conclusions. Local glucocorticoid injection results in long-term improvement in nerve conduction parameters, symptom severity and functional scores in patients with mild CTS.

Ischemic stroke is one of the most disabling diseases and a leading cause of death globally. Despite advances in medical care, the global burden of stroke continues to grow, as no effective treatments to limit or reverse ischemic injury to the brain are available. However, recent preclinical findings have revealed the potential role of transient receptor potential cation 6 (TRPC6) channels as endogenous protectors of neuronal tissue. Activating TRPC6 in various cerebral ischemia models has been found to prevent neuronal death, whereas blocking TRPC6 enhances sensitivity to ischemia. Evidence has shown that Ca²⁺ influx through TRPC6 activates the cAMP (adenosine 3’,5’-cyclic monophosphate) response element-binding protein (CREB), an important transcription factor linked to neuronal survival. Additionally, TRPC6 activation may counter excitotoxic damage resulting from glutamate release by attenuating the activity of N-methyl-d-aspartate (NMDA) receptors of neurons by posttranslational means. Unresolved though, are the roles of TRPC6 channels in non-neuronal cells, such as astrocytes and endothelial cells. Moreover, TRPC6 channels may have detrimental effects on the blood–brain barrier, although their exact role in neurovascular coupling requires further investigation. This review discusses evidence-based cell-specific aspects of TRPC6 in the brain to assess the potential targets for ischemic stroke management.

Hypertension is the most common modifiable risk factor for stroke, and understanding the underlying mechanisms of hypertension and hypertension-related stroke is crucial. 20-hydroxy-5, 8, 11, 14-eicosatetraenoic acid (20-HETE), which plays an important role in vasoconstriction, autoregulation, endothelial dysfunction, angiogenesis, inflammation, and blood-brain barrier integrity, has been linked to hypertension and stroke. 20-HETE can promote hypertension by potentiating the vascular response to vasoconstrictors; it also can reduce blood pressure by inhibition of sodium transport in the kidney. The production of 20-HETE is elevated after the onset of both ischemic and hemorrhagic strokes; on the other hand, subjects with genetic variants in CYP4F2 and CYP4A11 that reduce 20-HETE production are more susceptible to stroke. This review summarizes recent genetic variants in CYP4F2, and CYP4A11 influencing 20-HETE production and discusses the role of 20-HETE in hypertension and the susceptibility to the onset, progression, and prognosis of ischemic and hemorrhagic strokes.

Transient ischemic attacks (TIAs) are brief neurological deficits ofcerebrovascular origin that are followed by complete clinical recovery. Although a

Roven beneficial for large ischemic brain infarction with massive swelling. We hypothesized that craniectomy can improve ICH outcome as well. METHODS We used the model of autologous blood injection into the basal ganglia in rats. After induction of ICH and then magnetic resonance imaging, animals were randomly allocated to groups representing no craniectomy (n = 10) or to craniectomy at 1, 6, or 24 hours. A fifth group without ICH underwent craniectomy only. Neurological and behavioral outcomes were assessed on days 1, 3, and 7 after ICH induction. Furthermore, terminal deoxynucleotidyl transferase dUTP nick-end labeling-positive cells were counted. RESULTS After 7 days, compared with the ICH + no craniectomy group, all craniectomy groups had strikingly lower mortality (P < 0.01), much better neurological outcome (P < 0.001), and more favorable behavioral outcome. A trend occurred in the ICH + no craniectomy group toward more robust apoptosis. CONCLUSION Decompressive craniectomy performed up to 24 hours improved outcome after experimental ICH, with earlier intervention of greater benefit....