Background: The consequences of median nerve compression at the carpal tunnel level require a precise diagnostic evaluation before a frequently applied surgical intervention. Positive Tinel or Phalen signs are not always related to abnormal results in electroneurographic examinations of sensory and motor nerve fibers, which are intended to confirm final diagnoses, thereby confusing both surgeons and neurophysiologists. In the face of contradictory data, this study aims to reinvestigate these correlations in a randomly chosen population of patients with a primary diagnosis of carpal tunnel syndrome (CTS). Methods: Seventy-five randomly chosen patients with clinically detected CTS underwent neurophysiological studies of median nerve sensory (SNAP) and motor (CMAP) fibers conduction at the wrist. Both the median and ulnar nerves were assessed to reduce the risk of misinterpretation related to anatomical variations. Results: This study provides evidence on the relatively high utility of Phalen’s test in the early clinical detection of CTS within a general population of patients, whose positive results moderately correlate (rho = −0.327) with abnormalities in amplitudes rather than the distal latency parameters of SNAP recordings. The axonal injury type is more distinct than slowing-down impulses at the wrist following compression of the sensory nerve fibers in the early course of CTS. Positive Tinel’s test results are useful in diagnosing CTS patients with advanced axonal and demyelinating changes in the motor fibers at the wrist, which weakly correlate with prolonged latency and decreased amplitude in SNAP recordings (rho = −0.214 and rho = −0.235, respectively), but not with abnormalities in recordings of both amplitudes and latencies in CMAP electroneurography. Conclusions: The correlations between clinical signs and neurophysiological findings in CTS indicate that provocative tests, such as Phalen’s and Tinel’s, have limited diagnostic value, demonstrating only weak-to-moderate associations with neural conduction parameters. A positive Tinel’s sign should be regarded mainly as a marker of severe or chronic sensory impairment, often accompanied by motor fibers involvement in advanced pathological stages, rather than as an indicator of motor damage alone. Nerve conduction studies remain essential for confirming CTS, assessing its severity, and guiding treatment decisions, including surgical qualification. The presented correlation of clinical and functional neurophysiological results in CTS diagnosis allows us not only to specify the source and severity of the pathology of the median nerve fibers but also may influence the personalization of physiotherapeutic and surgical treatments.

Background/Objectives: Psilocibin (PSY), a serotonergic hallucinogen, has attracted increasing scientific interest due to its therapeutic potential, particularly in treatment-resistant depression. In parallel with its growing clinical and research relevance, important questions have emerged regarding its safety profile, including potential effects on the liver, kidneys, cardiovascular system, and immune function. The aim of this narrative review was to systematically collect, critically appraise, and organize the dispersed evidence regarding potential multi-organ safety signals associated with PSY exposure. Methods: A narrative review was conducted including preclinical studies, pharmacological investigations, available clinical data, and published case reports, including reports of mushroom-related intoxications involving PSY-containing species. All available sources addressing potential toxicological outcomes associated with PSY were considered, regardless of exposure context, in order to reflect the current state of evidence. Results: The available evidence base is limited and heterogeneous, consisting primarily of case reports, observational data, and mechanistic preclinical studies. Reported adverse events are rare and frequently confounded by polysubstance use, uncertainty of dose, co-ingestion of other compounds, and lack of exposure standardization. Despite these limitations, biologically plausible mechanisms related to serotonergic receptor activation provide a rationale for further investigation of potential organ-specific effects. However, current controlled clinical data do not provide consistent evidence supporting intrinsic multi-organ toxicity of PSY. Conclusions: Current evidence does not confirm clinically meaningful intrinsic multi-organ toxicity of PSY under controlled conditions. Nevertheless, the available literature suggests the presence of potential safety signals that warrant further systematic evaluation. In the context of growing clinical interest in PSY, this review provides a structured synthesis of current knowledge and highlights critical gaps in understanding its organ-specific safety profile.

Introduction: Trigeminal neuralgia (TN) is a severe neuropathic pain disorder characterized by brief, electric shock – like attacks within the trigeminal distribution. Although classically linked to neurovascular compression, recent evidence indicates that its pathophysiology extends beyond peripheral mechanisms to include central sensitization and neuroinflammatory processes. Aim: The aim of this review was to analyze the neurophysiological mechanisms of TN, emphasizing the interplay between demyelination, altered ion channel expression, and central plasticity, as well as to present modern diagnostic and therapeutic approaches targeting these mechanisms. Materials and Methods: The study is a narrative review drawing on current evidence-based literature concerning the peripheral and central mechanisms of TN, including electrophysiological, neuroimaging, and experimental model data. Results: Peripheral demyelination at the root entry zone promotes ectopic discharges and ephaptic transmission between adjacent fibers, while upregulation of voltage-gated sodium channels (Nav1.6, Nav1.7) enhances neuronal hyperexcitability. Central sensitization involves activation of microglia and astrocytes releasing proinflammatory cytokines (interleukin-1β, tumor necrosis factor-α, interleukin-6) and neurotrophins (brain-derived neurotrophic factor), contributing to persistent pain. Neuroimaging demonstrates cortical and subcortical reorganization in pain-processing regions. Therapeutic advances include selective sodium and calcium channel blockers and microvascular decompression. Conclusions: TN arises from an interplay between peripheral demyelination and central neuroplasticity. Understanding these interconnected mechanisms provides a foundation for more targeted and effective therapeutic strategies that address both neuronal hyperexcitability and neuroinflammation.