Rowook Park

Ultrasound-guided hydrodissection and dextrose prolotherapy have evolved into anatomically explicit but mechanistically distinct strategies for musculoskeletal pain. This State-of-the-Art narrative review aimed to synthesize major recent clinical and technical developments and to interpret them within a target-based framework. PubMed and Embase via Ovid were searched for English-language publications from 1 January 2021 through 29 July 2026, supplemented by selected pre-2021 landmark studies identified through backward citation tracking. After initial deduplication, 1662 records entered Title/Abstract screening. The final narrative synthesis cited 67 publications, including selected landmark and methodological sources. One author performed screening, and a second author reviewed the final publication selection; study selection was purposive and designed for a narrative synthesis rather than exhaustive systematic inclusion. Four questions guided the review: recent refinements in hydrodissection technique and indications; increasing condition specificity of prolotherapy evidence; areas of overlap and distinction between the two procedures; and the evidentiary status of emerging applications. Hydrodissection research remains concentrated in carpal tunnel syndrome and increasingly addresses injectate, volume, tissue-plane spread, and procedural configuration, whereas evidence beyond the carpal tunnel remains incompletely replicated. Prolotherapy research has shifted from broad claims toward condition-specific studies in tendinopathy, plantar fasciopathy, knee osteoarthritis, periarticular disorders, and temporomandibular joint pathology. Across both fields, variations in concentration, volume, anatomical site, session number, comparator, rehabilitation, and procedural expertise limit generalization. Hydrodissection is defined by observable, fluid-mediated separation of a tissue interface, whereas prolotherapy involves dextrose delivery to a symptomatic connective-tissue target without requiring immediate tissue-plane separation. The proposed framework is intended to standardize terminology, organize evidence maturity, and guide future comparative research rather than prescribe a validated treatment algorithm.

Background/Objectives: Vitamin D deficiency remains common in UVB-constrained, pollution-exposed, sedentary, and ageing populations, yet recent guidelines discourage routine screening and empiric high-dose supplementation in generally healthy adults. This review clarifies the clinical distinction between untargeted population supplementation and monitored repletion of documented deficiency in high-risk individuals. Methods: We conducted a focused narrative review of PubMed/MEDLINE, Scopus, Web of Science, and the Cochrane Library. The focused evidence search supporting the narrative synthesis was completed in June 2026. References published subsequently were included during manuscript preparation only when relevant for contextual purposes and were not incorporated retrospectively into the evidence-selection process underlying the review’s clinical conclusions. Evidence was interpreted according to baseline and achieved 25-hydroxyvitamin D [25(OH)D], dosing schedule, route, body composition, endpoint, and population risk. No formal risk-of-bias assessment, certainty grading, or systematic meta-analytic synthesis was performed. Key Findings: The strongest rationale for vitamin D repletion remains musculoskeletal, particularly for osteomalacia, muscle function, osteoporosis care, and fracture-related vulnerability in deficient or high-risk patients. Management should separate generally healthy adults from patients with an indication for testing or treatment. Historical and regional expert frameworks describe time-limited higher-dose repletion for documented deficiency, but these regimens should not be interpreted as a current universal Endocrine Society treatment standard. Short-term trials using moderate cumulative oral doses suggest broadly comparable biochemical repletion with daily, weekly, or monthly schedules; equivalence has not been established for long-term clinical outcomes, frail populations, or large intermittent doses. Extra-skeletal associations remain less trial-supported. Conclusions: Vitamin D deficiency should be managed using clinically indicated assessment, explicit repletion and maintenance regimens, and selective biochemical reassessment. Targets above conventional skeletal adequacy thresholds remain investigational and should not be applied as universal treatment goals.

Nutritional peripheral neuropathy is a clinically important condition associated with inadequate intake, malabsorption, bariatric surgery, aging, metabolic disease, and chronic medication exposure. B vitamins serve as essential coenzymes in mitochondrial energy metabolism, one-carbon metabolism, neurotransmitter synthesis, redox regulation, and myelin maintenance. This narrative review synthesizes mechanistic and clinical evidence linking B vitamin-dependent coenzyme systems to nutritional neuropathy and selected neuropsychiatric manifestations. Particular emphasis is placed on the tricarboxylic acid cycle, electron transport chain, urea cycle, folate–methionine cycle, and MTHFR-dependent one-carbon metabolism. The proposed “dynamic coenzyme network” is intended as an integrative mechanistic framework rather than a stand-alone therapeutic recommendation. Although biochemical interdependence among B vitamins supports evaluation for combined or functional deficiencies in selected patients, mechanistic plausibility should not be equated with clinical efficacy. Clinical consideration of B vitamin repletion should be guided by documented deficiency, dietary and gastrointestinal risk factors, medication exposure, neurological phenotype, and functional biomarkers such as homocysteine and methylmalonic acid. Adjunctive nutrients, including alpha-lipoic acid and acetyl-L-carnitine, may have context-specific relevance, particularly in metabolic neuropathies, but evidence for fixed multi-nutrient combinations remains heterogeneous. Further well-designed clinical studies are needed to determine whether this mechanistic framework translates into meaningful neurological or neuropsychiatric benefit beyond established deficiency states.

Magnesium (Mg) is an essential divalent cation involved in more than 600 enzymatic reactions and plays a fundamental role in vascular, metabolic, and neural homeostasis. Although Mg is frequently discussed as an analgesic supplement, emerging evidence suggests that it acts as a neurovascular–metabolic modulator. Low magnesium status has been associated with endothelial dysfunction, atherosclerotic burden, impaired microcirculatory function, and overlapping ischemic and neuropathic pain phenotypes, although direct causal clinical evidence remains limited. This narrative review integrates mechanistic and clinical evidence across three intersecting domains: (1) the role of Mg in endothelial dysfunction, vascular calcification, and atherogenesis; (2) the contribution of Mg deficiency to ischemic pain through peripheral arterial disease and microcirculatory failure; and (3) the modulation of neuropathic pain through NMDA receptor antagonism, neuroinflammatory suppression, and maintenance of blood–brain barrier integrity. In populations with atherosclerosis, diabetes mellitus, or nutritional insufficiency, hypomagnesemia may serve as a unifying pathophysiological link connecting vascular injury to pain sensitization. The recognition of Mg not merely as an analgesic agent, but as a neurovascular interface regulator, may inform more comprehensive therapeutic strategies in chronic vascular and neuropathic pain syndromes. This review emphasizes nutritional magnesium status and biologically plausible mechanisms rather than presenting magnesium supplementation as an established treatment for vascular or neuropathic pain. The evidence is strongest for mechanistic vascular and neuropathic pathways, whereas direct clinical evidence for magnesium supplementation in PAD-related ischemic limb pain remains limited.

Background: The traditional A1-centric paradigm for trigger finger (TF) management does not fully capture heterogeneous pathology spanning isolated pulley stenosis, tendon degeneration, and impaired tendon–sheath gliding. Methods: A comprehensive literature synthesis (2010–2025) integrating anatomy, biomechanics, and ultrasound-guided interventions was performed to develop a testable, phenotype-driven framework. Results: A continuum model is proposed emphasizing (i) origin-to-insertion assessment of the flexor apparatus, (ii) pragmatic ultrasound phenotyping into pulley-dominant, tendon-dominant, and mixed patterns, and (iii) a stepwise, phenotype-matched management pathway incorporating conservative care, ultrasound-guided injection, selected adjuncts (e.g., hydrodissection, prolotherapy, ESWT) for tendon-dominant or mixed presentations, and percutaneous or open release when an A1 bottleneck is confirmed. Conclusions: This framework is presented as a hypothesis to guide standardized reporting, reliability testing, and phenotype-stratified comparative trials, rather than as a validated clinical guideline. This article proposes a novel, phenotype-driven clinical framework to address this limitation. Contemporary evidence is integrated to construct a model emphasizing (i) a whole-length, origin-to-insertion assessment of the flexor apparatus, (ii) sonographic phenotyping into pulley-dominant, tendon-dominant, and mixed patterns, and (iii) a stepwise treatment algorithm integrating conservative care, ultrasound-guided injections, ultrasound-guided percutaneous release, and selected adjunctive approaches such as hydrodissection (HD), prolotherapy (Prolo), and extracorporeal shockwave therapy (ESWT). While evidence supports individual modalities, the framework’s primary innovation lies in matching interventions to phenotype. This sonographic phenotyping system is presented not as a validated tool, but as a testable hypothesis designed to guide future validation studies. The proposed framework establishes research priorities, including standardized criteria, reliability testing, and comparative effectiveness research for phenotype-stratified management.

Background: Deep gluteal syndrome (DGS) is an underdiagnosed cause of sciatica-like pain, involving the entrapment of the sciatic nerve by various structures within the subgluteal space. While cases of ossification or calcification in the context of severe pelvic imbalance have been rarely reported, isolated SSL calcification as a primary cause of DGS remains largely unexplored and undocumented. This case report presents the first documented instance of sacrospinous ligament (SSL) calcification identified as the primary cause of DGS and its successful management with ultrasound-guided prolotherapy. Case Presentation: A 51-year-old female presented with severe, worsening left-sided sciatica of several months’ duration. Physical examination revealed an antalgic gait, positive sacroiliac joint tests, and multiple positive DGS-specific provocative tests (FAIR, Pace sign, Seated Piriformis Stretch). Radiographs and musculoskeletal ultrasound (MSK-US) confirmed calcification within the left sacrospinous ligament, with associated sciatic nerve swelling. The patient underwent three sessions of ultrasound-guided prolotherapy (dextrose 10% with lidocaine) targeting the calcification site, followed by a structured rehabilitation program. Results: The patient reported a significant reduction in pain, from a Visual Analog Scale (VAS) score of 10/10 to 1/10 within one month. All previously positive provocative tests converted to negative, indicating a resolution of the nerve entrapment. Functional mobility was fully restored. Conclusions: This case highlights isolated sacrospinous ligament calcification as a potential and previously overlooked pathological entity responsible for deep gluteal syndrome. To our knowledge, this is the first report to implicate ligamentous calcification as a primary etiological factor in DGS. Musculoskeletal ultrasound proved indispensable for both diagnosis and treatment guidance. Furthermore, ultrasound-guided prolotherapy emerged as a successful and minimally invasive therapeutic option in this case, potentially by stabilizing the ligament and reducing neurogenic inflammation. This case expands the differential diagnosis of sciatica, introduces a new target for intervention in refractory cases, and underscores the need for future studies in larger patient cohorts to validate these findings.

Background: Deep gluteal syndrome (DGS) is an underdiagnosed cause of sciatica-like pain, involving the entrapment of the sciatic nerve by various structures within the subgluteal space. While muscular and fibrovascular causes are well-documented, ligamentous pathologies, particularly calcification, remain an unexplored etiology. This case report presents the first documented instance of sacrospinous ligament (SSL) calcification identified as the primary cause of DGS and its successful management with ultrasound-guided prolotherapy. Case Presentation: A 51-year-old female presented with severe, worsening left-sided sciatica of several months' duration. Physical examination revealed an antalgic gait, positive sacroiliac joint tests, and multiple positive DGS-specific provocative tests (FAIR, Pace sign, Seated Piriformis Stretch). Radiographs and musculoskeletal ultrasound (MSK-US) confirmed calcification within the left sacrospinous ligament, with associated sciatic nerve swelling. The patient underwent three sessions of ultrasound-guided prolotherapy (dextrose 10% with lidocaine) targeting the calcification site, followed by a structured rehabilitation program. Results: The patient reported a significant reduction in pain, from a Visual Analog Scale (VAS) score of 10/10 to 1/10 within one month. All previously positive provocative tests converted to negative, indicating a resolution of the nerve entrapment. Functional mobility was fully restored. Conclusions: This case highlights sacrospinous ligament calcification as a novel and previously unreported pathological entity responsible for deep gluteal syndrome. To our knowledge, this is the first report to implicate ligamentous calcification as a primary etiological factor in DGS. Musculoskeletal ultrasound proved indispensable for both diagnosis and treatment guidance. Furthermore, ultrasound-guided prolotherapy emerged as a successful and minimally invasive therapeutic option in this case, potentially by stabilizing the ligament and reducing neurogenic inflammation. This case expands the differential diagnosis of sciatica, introduces a new target for intervention in refractory cases, and underscores the need for future studies in larger patient cohorts to validate these findings.

Background and Clinical Significance: Radial nerve palsy typically presents as wrist drop due to nerve compression, with conventional management often yielding prolonged recovery. We report a case where ultrasound-guided hydrodissection (HD) with 5% dextrose in water (D5W) achieved immediate functional restoration, suggesting neurapraxia as the underlying pathology. Case Presentation: A 54-year-old diabetic female presented with acute left wrist drop without trauma. Examination confirmed radial nerve palsy (MRC grade 0 wrist extension), while radiographs ruled out structural causes. Ultrasound revealed fascicular swelling at the spiral groove. Under real-time guidance, 50 mL D5W (no local anesthetic) was injected to hydrodissect the radial nerve. Immediate post-procedure assessment showed restored wrist extension (medical research council (MRC) grade 4+). At one- and three-month follow-ups, the patient maintained complete resolution of symptoms and normal function. Conclusions: This case highlights two key findings: (1) HD with D5W can serve as both a diagnostic tool (confirming reversible neurapraxia through immediate response) and therapeutic intervention, and (2) early HD may circumvent prolonged disability associated with conservative management. The absence of electrodiagnostic studies limits objective severity assessment, though ultrasound localized the lesion. While promising, these observations require validation through controlled trials comparing HD to standard care, particularly in diabetic patients with heightened compression susceptibility. Technical considerations—including optimal injectate volume and the role of adjuvant therapies—warrant further investigation. US-guided HD with D5W emerges as a minimally invasive, surgery-sparing option for acute compressive radial neuropathies, with potential to redefine treatment paradigms when applied at symptom onset.

Introduction: Radial nerve palsy, often manifesting as wrist drop, is a peripheral neuropathy typically resulting from compression. While conservative management is often employed, recovery can be prolonged. It has been commonly taught that cases like this involve a conduction block, which significantly limits diagnostic physical examination or electrodiagnosis. However, if hydrodissection (HD) can immediately restore function, it may indicate that the injury is merely neurapraxia, and highlight its degree of reversibility, profoundly influencing the course of recovery. We present a case of acute radial nerve palsy successfully treated with ultrasound-guided (US-guided) HD. Case Presentation: A 54-year-old woman with diabetes presented with sudden onset of left wrist drop with no apparent trauma. Physical examination revealed an inability to actively extend her wrist, and plain radiographs were unremarkable. Given the clinical presentation suggestive of radial nerve palsy, US-guided HD was performed at the proximal spiral groove using 50 mL of 5% dextrose in water (D5W) with no local anesthetic (LA). Immediate post-procedural assessment showed marked improvement in wrist extension. At one-month follow-up, the patient reported complete resolution of wrist drop and restoration of normal daily activities, with no loss of work, which was maintained at a three-month telephone review. Electrodiagnostic studies were not performed due to the retrospective nature of this case report. Discussion: This case demonstrates the potential for rapid and nearly complete clinical recovery from acute compressive radial nerve palsy following a single US-guided HD injection using D5W without LA, confirming the presence of neuropraxia and its nearly complete reversibility. However, an electromyogram (EMG) showing the pattern of motor fiber recruitment post injection was not available. Conclusion: US-guided HD with D5W with no LA may be a promising therapeutic option for selected patients with acute compressive radial nerve palsy. However, further research - including controlled trials and electrodiagnostic confirmation - is needed to determine the frequency in which immediate diagnostic and therapeutic HD with D5W is expected to be therapeutically valuable in altering function and optimizing rehabilitation