Background/Objectives: Vitamin B12 deficiency is common in individuals with type 2 diabetes mellitus (T2DM) receiving long-term metformin therapy, primarily due to impaired intestinal absorption. Conventional oral B12 supplementation is often associated with delayed or inconsistent biochemical correction. A lipid-based Sucrosomial® delivery system has been shown to improve circulatory vitamin B12 levels in healthy adults with deficiency, and the present study evaluates its performance in the clinically challenging context of metformin-treated individuals with T2DM, a population characterized by pharmacologically impaired intestinal vitamin B12 absorption. Methods: This multicentre, double-blind, placebo-controlled, parallel-group randomized clinical trial evaluated the efficacy, safety, and tolerability of a Sucrosomial® vitamin B12 formulation in adults with T2DM receiving metformin and presenting with vitamin B12 deficiency. Participants were randomized (1:1) to receive oral Sucrosomial® vitamin B12 (1000 µg daily; n = 25) or placebo (n = 25) for three weeks. Serum total vitamin B12 and holotranscobalamin (HoloTC), the biologically active fraction of vitamin B12, were assessed at baseline and during follow-up, with time-to-normalization and safety analyses performed. Results: Sucrosomial® vitamin B12 supplementation resulted in rapid and sustained increases in circulating vitamin B12 levels, with early separation from placebo, and a substantially higher proportion of participants achieved normalization of serum vitamin B12 concentrations within the three-week period. Parallel improvements in HoloTC levels indicated enhanced biologically active vitamin B12 availability, and the intervention was well tolerated with no clinically relevant safety concerns. Conclusions: These findings demonstrate that an oral Sucrosomial® vitamin B12 formulation can achieve rapid and reliable biochemical repletion of both total and biologically active vitamin B12 in metformin-treated adults with T2DM, despite pharmacologically impaired intestinal absorption, while maintaining a favourable safety and tolerability profile.

Protein-energy malnutrition (PEM) remains a significant public health problem in childhood and is frequently accompanied by multiple micronutrient deficiencies and metabolic alterations. This study aimed to simultaneously evaluate micronutrient status and thyroid function in children diagnosed with PEM. A retrospective analysis was conducted of the medical records of children aged 0-17 years who were admitted to Defne State Hospital between December 2023 and May 2025 with a diagnosis of PEM. Demographic characteristics, anthropometric measurements, and laboratory parameters, including hemoglobin, serum iron, ferritin, vitamin B12, vitamin D, blood urea nitrogen, creatinine, thyroid-stimulating hormone, and free T4 were recorded. Nutritional status was assessed using World Health Organization growth standards. A total of 65 children (32 males and 33 females) were included. Mild, moderate, and severe malnutrition were identified in 38.46%, 44.62%, and 16.92% of patients, respectively. Anemia and vitamin D deficiency were the most common abnormalities observed in 23.08% and 18.46% of patients, respectively. In contrast, vitamin B12 deficiency and abnormal thyroid function test results were detected at lower rates (3.08% and 4.62%, respectively). No significant differences were observed between genders in anthropometric measurements or malnutrition severity. The relatively low prevalence of thyroid dysfunction, compared with previous studies, may be attributable to the predominance of mild-to-moderate malnutrition in the study population. These findings suggest that the impact of PEM on micronutrient metabolism and endocrine function varies according to disease severity, and highlight the importance of a comprehensive clinical approach that includes assessment of both micronutrient and hormonal status in children with PEM.

Background/Objectives: Vitamin B12 deficiency is a prevalent yet frequently underdiagnosed condition, largely due to the limited diagnostic accuracy of serum total B12 and the restricted availability of confirmatory biomarkers such as holotranscobalamin and methylmalonic acid. This study aimed to develop and validate explainable machine learning (ML) models capable of predicting vitamin B12 deficiency using only routinely available laboratory examinations, thereby supporting early detection within standard diagnostic workflows. Methods: This retrospective study included 51,630 adult patients who underwent concurrent vitamin B12 testing and routine laboratory evaluation between 2015 and 2025. An independent temporal validation cohort of 34,744 patients was used to assess generalizability. Eight supervised ML algorithms were developed within a four-stage experimental framework incorporating default modeling, probability-threshold optimization, hyperparameter tuning, and feature engineering. Model performance was evaluated using AUC-ROC, AUC-PR, sensitivity, specificity, F1 score, accuracy, Matthews correlation coefficient, and likelihood ratios. Model explainability and clinical utility were assessed using SHAP, LIME, and decision curve analysis. Results: Among all algorithms, CatBoost demonstrated the most balanced and clinically relevant performance. In the threshold-optimized configuration, the model achieved a sensitivity of 0.92, specificity of 0.67, F1 score of 0.82, AUC-ROC of 0.88, and AUC-PR of 0.86 in the test set. Temporal validation confirmed robust generalizability, with improved discrimination (AUC-ROC 0.90; AUC-PR 0.91) and stable calibration. Explainability analyses identified hematologic indices (MCV, HGB, HCT, RDW), iron-related markers, inflammatory measurands, and age as the most influential contributors, consistent with known pathophysiology. Conclusions: This study presents a large-scale, explainable, and temporally validated ML framework for predicting vitamin B12 deficiency using routine laboratory data alone. The model demonstrates strong diagnostic performance, biological plausibility, and potential for seamless integration into laboratory and clinical decision-support systems, enabling cost-effective and early identification of patients at risk.

To evaluate laboratory investigations for micronutrient deficiencies as the cause of anaemia prior to first-time red blood cell transfusions in the medical emergency department (ED) of a large academic hospital. The ED is often the first point of contact for acutely ill anaemic patients, yet patient blood management principles are underutilised. Because micronutrient deficiencies are common, treatable causes of anaemia, they should be screened for to guide targeted treatment and reduce unnecessary transfusions. We conducted a retrospective cross-sectional study of 198 adult patients receiving first-time transfusions in the medical emergency unit at Groote Schuur Hospital, South Africa, between April and October 2023. Laboratory investigations for iron, vitamin B12, and folate deficiencies were analysed and stratified by pre-transfusion mean corpuscular volume (MCV). Iron deficiency was evaluated using three locally used criteria. Data about haematinic supplementation were also collected. Only 29% of patients received a full micronutrient deficiency workup, while 39% had no testing. Iron deficiency was the most frequent abnormality, and up to 30% of these patients had normocytic indices. Iron supplementation rates were high, but many patients without iron deficiency also received iron. The ED encounter should be used as an opportunity to initiate basic micronutrient deficiency screening for anaemia, regardless of MCV.

Metformin is a key drug for the treatment of type 2 diabetes. Its efficacy and side effects depend on its chemical properties and how it is transported through transporters in the body. Research has shown that these factors influence metformin's function, individual variability, and potential safety issues. Metformin exerts its effects by inhibiting mitochondrial complex I and activating AMP-activated protein kinase (AMPK) during periods of energy deprivation. Furthermore, it alters glucose processing in the intestine and liver through the PEN2-ATP6AP1 signaling pathway. These effects also influence gut hormones and the composition of the gut microbiota. This process explains metformin's effects on blood glucose, gastrointestinal intolerance, vitamin B12 deficiency, and lactic acidosis. Understanding the underlying mechanisms of these effects opens new avenues for clinical application. Adjusting dose based on transporter differences can improve efficacy. Modifying the gut microbiota can alleviate gastric intolerance. Developing new drugs in this class could provide more effective treatment options. These results suggest that understanding metformin's function could lead to more personalized and effective treatments for type 2 diabetes.

Early detection of vitamin B12 deficiency is critical in the prevention of irreversible neurological damage caused by anemia. Therefore, a dual-mode colorimetric/electrochemical strategy was proposed for the quantification of holotranscobalamin. Urchin-like Au@Pt nanocatalysts (peroxidase-mimicking nanozymes) were synthesized and found to be catalytically superior to the traditional peroxidase enzyme. Further, the nanocatalyst-antibody conjugate was prepared and used as a signal transduction probe for delivering dual signal outputs, both electrochemical and colorimetric. In colorimetric detection, the nanozyme catalyzes the oxidation of 3,3′,5,5′-tetramethylbenzidine (TMB)-hydrogen peroxide (H2O2) system in the presence of holoTC, while in electrochemical detection, the impedance signal of the anti-holoTC/Au@Pt/FTO was enhanced and exhibited LODs of 0.036 pg mL–1 and 0.61 pg mL–1, respectively. The improved sensing performance of the sensor is attributed to the nanoscale architecture of the material, as confirmed through TEM and DLS. For real-world application, the method successfully detected holoTC in human serum samples. Hence, this study presents a strategy for clinical diagnosis of vitamin B12 deficiency, as it is the first dual-mode assay for the detection of holoTC.

Background: Vitamin B12 insufficiency, which aggravates hematological and neurological problems in diabetics, has been linked to chronic metformin therapy, the main treatment for type 2 diabetes mellitus (T2DM). This study aimed to assess the prevalence of vitamin B12 deficiency in patients with T2DM on metformin and identify associated clinical and demographic factors in an Indian tertiary care setting.Methodology: An observational cross-sectional hospital-based study was conducted among adults with T2DM. Sociodemographic data, clinical history, diabetes duration, medication use, and laboratory parameters were recorded. Serum vitamin B12 levels were measured using standard laboratory cutoffs to identify deficiency, and data were analyzed using appropriate descriptive and inferential statistical methods.Results: Among 170 participants, multivariate logistic regression analysis identified metformin use for more than five years (adjusted odds ratio (OR): 2.85; 95% confidence interval (CI): 1.32-6.12), concomitant pantoprazole use (adjusted OR: 2.41; 95% CI: 1.08-5.34), and low high-density lipoprotein cholesterol levels below 40 mg/dL (adjusted OR: 2.22; 95% CI: 1.01-4.91) as independent predictors of vitamin B12 deficiency. Low hemoglobin levels, elevated low-density lipoprotein cholesterol levels, and poor glycemic control were not significantly associated (p > 0.05).Conclusion: Patients with T2DM, especially those on long-term metformin medication, frequently lack vitamin B12. Timely supplementation and routine screening might help lower avoidable consequences.

Vitamin B12 deficiency is common in the elderly population and can cause severe complications. The use of certain medication has in previous studies been associated with vitamin B12 deficiency in the general population. To identify elderly patients at risk for vitamin B12 deficiency due to medication use, we evaluated the association between medication use and vitamin B12 deficiency in the elderly population. Hospitalized geriatric patients 65 years of age or over with a serum vitamin B12 measurement within one week of the admittance date were included. Patients were classified as either B12 normal (258–635 pmol/L) or B12 deficient (< 148 pmol/L). Upon hospital admission patients’ medication use was verified. The association between vitamin B12 deficiency and the use of antacid, antiepileptic, antidiabetic, lipid lowering and other medication was evaluated by univariate and multivariate analyses. Of the 7132 patients included in the study, 532 (7.5%) had vitamin B12 deficiency and 3433 (48.1%) patients had normal vitamin B12 concentrations. Metformin use was significantly and independently (adjusted OR 2.5; 95% CI 1.7–3.6) associated with a dose-dependent higher risk of vitamin B12 deficiency. The use of other medication evaluated in this study was not associated with vitamin B12 deficiency. Metformin use is significantly associated with vitamin B12 deficiency in the elderly, and this risk rises with higher metformin doses. Monitoring and timely start of vitamin B12 supplementation along with the lowest possible metformin dose are essential to prevent complications.

Myelodysplastic syndromes (MDS) are rare hematological malignancies often affecting the elderly. Globally, this disease accounts for 13% of cancerous blood diseases. MDS is generated by bone marrow dysfunction characteristic of ineffective hematopoiesis and the disorder of exogenous factors, including vitamin B12. The objective of this work is to study the pathophysiological characteristics of myelodysplastic syndromes in patients living in Brazzaville. The calculation of the hospital frequency of MDS, the haemogram, the myelogram, the selective grouping of blood cells by the cell profiler software, as well as the dosage of Vitamin B12, are the methods that allowed the realization of this work. Thus, the hospital frequency of MDS in Brazzaville is 4, 92%; the pathophysiological characteristics of MDS are marked by the morphological appearance of blood cells which reveals mostly the presence of metamyelocytes with banded nuclei and pleicaryocytes; The excess or deficiency of Vitamin B12 observed in MDS, is not responsible for its unexpected occurrence, it is therefore appropriate to remember that MDS contribute to the deformation of immune cells and that VIT B12 has no close relationship with the development of MDS.

The association between vitamin B12 and lipid metabolism in patients with ischemic stroke: Across-sectional study.

India harbors the second-largest population with diabetes, with over 100 million, and type 2 diabetes mellitus (T2DM) constitutes the major share. Metformin remains the first-line pharmacotherapy for T2DM due to its safety profile, cost-effectiveness, and beneficial metabolic effects. The aim of the study was to assess the frequency of vitamin B12 deficiency in patients with T2DM on metformin therapy and compare it with their cohabiting family members who are not on metformin but share similar dietary habits. This study included 180 participants with 90 cases and controls each, and we enrolled 89 females (49.4%) and 91 males (50.6%). The mean age was 57 (± 4.88) years, and overall gender distribution and dietary pattern were nearly balanced among cases and controls. The mean duration of diabetes among cases was 7.69 ± 4.35 years, and duration of metformin use was 5.22 ± 3.77 years, ranging from 1-16 years. The mean daily dose of metformin was 1238.89 ± 586.50 mg/day, with a median dose of 1000 mg/day. The mean serum vitamin B12 level in metformin users was significantly lower than in controls (206.66 ± 59.09 pg/mL vs 301.44 ± 72.28 pg/mL, p < 0.001). Vitamin B12 deficiency was present in 40.0% of metformin users versus 11.1% of controls, yielding an odds ratio of 5.33 (95% CI: 2.44-11.65), which was a highly significant difference between the two groups (t = -9.631, p < 0.001), strongly suggesting an association between metformin use and reduced B12 levels. Neurological symptoms were observed in 14.4% of cases (OR 4.896, 95% CI: 1.345-17.827; p = 0.009). Long-term metformin use in T2DM patients is strongly associated with both biochemical vitamin B12 deficiency and an increased likelihood of neurological symptoms.

Diabetics often develop vitamin B12 deficiencies, which are crucial for blood, nerve, cognitive, and cardiovascular functions. The impact of metformin on vitamin B12 levels, leading to complications such as peripheral neuropathy and anemia, is well-known; yet no studies focus on deficiency status at diabetes diagnosis or the start of treatment. A cross-sectional study was conducted at 2 tertiary care institutions in India, Command Hospital (Western Command), Haryana, and Civil Hospital in Sirsi, Karnataka, from July 2022 to November 2023. The study included 326 newly diagnosed type II diabetes mellitus (DM) patients and prediabetes individuals attending outpatient and inpatient departments, collecting data on substance use, dietary practices, fasting blood sugar, random blood sugar, HbA1c, and vitamin B12 levels (CLIA method). The study population of 326 individuals showed significant regional differences in mean age, gender distribution, and dietary preferences. Vitamin B12 deficiency (<200 pg/mL) was prevalent in 43.4% of prediabetic and 51.9% of type II DM patients. Significant differences in fasting blood sugar, postprandial blood sugar, and HbA1c levels were observed between regions. However, no significant correlation was found between vitamin B12 levels and HbA1c, age, or fasting glucose levels. Vegetarian individuals exhibited significantly higher vitamin B12 deficiency. This study revealed a high prevalence of vitamin B12 deficiency in newly diagnosed diabetes patients, emphasizing the need for early identification and treatment to prevent complications such as neuropathy. The study recommends incorporating initial vitamin B12 assessment into the diagnosis protocol for newly detected diabetes patients to improve patient care and prevent complications in the Indian population.

Helicobacter pylori (H. pylori), a helical, flagellated Gram-negative bacterium, exhibits remarkable adaptability within the human gastric niche, enabling survival under acidic, nutrient-limited, and oxidative stress conditions. Beyond its established role in gastritis, peptic ulcer disease, and gastric adenocarcinoma, accumulating evidence implicates H. pylori in a spectrum of hematologic disorders. Iron deficiency anemia (IDA), vitamin B12 deficiency, immune thrombocytopenic purpura (ITP), and gastric mucosa-associated lymphoid tissue (MALT) lymphoma represent the most substantiated associations. Pathogenesis is multifactorial, encompassing chronic inflammation, cytokine dysregulation, molecular mimicry, impaired micronutrient absorption, and virulence factor-mediated disruption of host cellular processes, notably through CagA, VacA, SabA, and BabA components. In IDA and vitamin B12 deficiency, H. pylori-induced hypochlorhydria, altered gastric ascorbate levels, and hepcidin upregulation compromise systemic iron and cobalamin homeostasis. In contrast, in ITP, cross-reactivity between bacterial antigens and platelet epitopes triggers the production of autoantibodies and accelerates platelet clearance. Chronic antigenic stimulation and epigenetic modifications underpin lymphomagenesis in gastric MALT lymphoma, with treatment response modulated by strain-specific virulence, host genetics, and somatic translocations affecting NF-κB signaling. Clinical evidence demonstrates that targeted eradication therapy, often in combination with micronutrient supplementation, significantly restores hematologic parameters and mitigates systemic sequelae, yet patient-specific variability necessitates individualized management strategies. This review integrates current mechanistic and clinical insights into H. pylori-associated hematologic manifestations, highlighting the bacterium's systemic impact, elucidating therapeutic implications, and identifying critical gaps for future research aimed at optimizing diagnostic precision, intervention efficacy, and prognostic outcomes in affected populations.

This study aimed to evaluate vitamin B12 and D levels among long-term vegetarians and to assess the influence of their diet duration and diet subtypes on nutritional status in Beijing, China. A cross-sectional analysis was conducted on 104 vegetarians (84 vegans, 20 lacto-ovo vegetarians). Serum vitamin B12 and D levels were measured, and demographic, dietary, and supplement use data were collected. Statistical analyses included ANOVA, Kruskal-Wallis tests, chi-square tests, and multivariate regressions. The prevalence of vitamin B12 deficiency (<200 pg/mL) was 38.5%, with higher rates in vegans (44.1%) than lacto-ovo vegetarians (15.0%, p = 0.021). Vitamin D defi-ciency (<20 ng/mL) affected 84.6% of participants, worsening with longer diet duration (p <0.001), yet showed no significant difference between vegan and lacto-ovo subtypes (85.7% vs 80.0%, p = 0.524). Multivariate analysis revealed negative correlations between diet duration (6-10 years and >10 years) and vita-min B12 and D levels (p <0.05). Lacto-ovo vegetarians showed significantly higher vitamin B12 levels than vegans (p = 0.029), and supplement use improved both vitamins' status (p <0.05). This study reveals a dual challenge among Beijing long-term vegetarians: vitamin B12 deficiency was strongly associated with the degree of exclusion of animal products from the diet (veganism), while vitamin D deficiency was highly prevalent and worsened with longer diet duration. The near-universal vitamin D deficiency observed in this study suggests that, in the Beijing context, the risk may extend beyond dietary choice, potentially reflecting regional environmental factors; however, this requires confirmation through comparative studies with omnivores controls.

Serum gastrin levels, stratified on PPI use, improve diagnosis of pernicious anemia in the absence of intrinsic factor antibodies.

Epidemiological data from assisted reproductive technologies (ART) link vitamin B12 (VitB12) deficiency to shorter gestation, low birth weight, and reduced live birth rates. VitB12 also plays a critical role in fertility for both sexes by supporting gamete quality. Despite some contradictions, emerging evidence suggests early-life VitB12 deficiency may affect learning and cognitive development. Collectively, these findings suggest that VitB12 is a key determinant of both reproductive and developmental health. Mechanistically, VitB12 acts as a coenzyme in one-carbon metabolism, and its deficiency leads to elevated homocysteine (Hcy) and methylmalonic acid (MMA) levels, promoting oxidative stress and thereby impairing fertility. Although this remains the most established mechanism, other yet unidentified pathways may also mediate the effects of VitB12 on reproductive function. While the effects of severe VitB12 deficiency are well established, mild deficiencies may develop silently in individuals following plant-based diets or those with gastrointestinal disorders. Plant-based sources of VitB12 remain controversial, as many provide only trace amounts or biologically inactive analogs such as pseudovitamin B12, which may interfere with absorption. Further research is needed to evaluate their bioavailability and clinical effectiveness. This review synthesizes clinical evidence, mechanistic insights, and dietary considerations to highlight how VitB12 status shapes reproductive health.

A woman in her late 20s presented with a 5-year history of progressive fatigue and generalised weakness. Examination revealed signs of premature ageing, anaemia, neuropathy and hepatosplenomegaly.Investigations showed pancytopenia, dimorphic anaemia, severe vitamin B12 deficiency, hepatic fibrosis and pulmonary fibrosis. Despite correction of nutritional deficiencies, the constellation of cytopenia, premature greying, osteoporosis, hepatic and pulmonary fibrosis raised suspicion of a genetic disorder. Clinical exome sequencing identified a monoallelic PARN missense variant (c.613T>C; p.Cys205Arg), classified as a Variant of Uncertain Significance. Germline pathogenic variants in PARN have been associated with dyskeratosis congenita, autosomal recessive 6 (DKCB6) and with telomere-related pulmonary fibrosis and/or bone marrow failure 4. The clinical-genetic correlation in this case supported a diagnosis of a telomere biology disorder (TBD). This case highlights the importance of considering TBDs in young adults with unexplained multisystem disease, even when classical mucocutaneous features are absent. Early recognition is crucial for guiding genetic counselling, surveillance and consideration of bone marrow transplantation in progressive cases.

Disorders affecting the spinal cord (myelopathies) can cause severe disability. Despite diagnostic advances, approximately 12-18% of myelopathy cases continue to elude an etiological diagnosis, hampering effective treatment. This retrospective, multicenter, tertiary care cohort study conducted from 2014 to 2025 evaluated archived biofluids from patients with IM, known autoimmune myelitis, or other neurological diseases (ONDs). Proteome-wide phage display was used to discover novel autoantibodies. Targeted immunoassays were used to screen for a candidate autoantibody. Downstream metabolites were measured in the cerebrospinal fluid (CSF). Autoantibodies targeting the transcobalamin receptor (CD320) responsible for cellular transport of vitamin B12 were identified in 18 out of 32 IM patients (56%) in a discovery cohort. Bioactive B12 concentration was decreased in the CSF of anti-CD320 positive patients compared to OND controls ( P = 0.0273), indicative of autoimmune B12 central deficiency (ABCD). Compared to anti-CD320 negative IM cases, anti-CD320 positive IM cases demonstrated a higher frequency of subacute time course (56% vs 7%, P = 0.008), normal CSF profile (83% vs 50%, P = 0.044), and dorsolateral spinal cord abnormalities on magnetic resonance imaging (MRI) (61% vs 7%, P = 0.003). In two independent validation cohorts comprising 94 and 25 patients with IM, anti-CD320 was detected in 43 (46%) and 12 (48%) patients, respectively. Comorbid anti-CD320 was detected in a smaller proportion of patients with other known autoimmune etiologies of myelopathy. Five anti-CD320 positive IM patients received B12 supplementation with or without concurrent immunosuppression, and four out of five clinically improved. ABCD is associated with a substantial proportion of IM. Screening for anti-CD320 followed by metabolic confirmation of a CNS-restricted B12 deficiency may be considered in the diagnostic evaluation of myelopathy.

This review examines both historical and recent evidence to clarify the current understanding of the relationship between B vitamin deficiencies and neuropathies. Vitamin B1 (thiamine) deficiency can lead to neurological disorders such as beriberi and Wernicke's encephalopathy, conditions with significant prevalence and mortality rates. Vitamin B12 (Cobalamin) is crucial for DNA synthesis, fatty acid metabolism, and myelin production, with its deficiency leading to neuropathies and cognitive disorders. Excess vitamin B6 (pyridoxine), rather than deficiency, appears to be associated with neuropathy. Vitamin B1 and B12 deficiencies are linked to classic neuropathies, while the connection between vitamin B6 deficiency and neuropathy is less clear, though excess B6 is associated with neurotoxicity. Nutritional deficiencies are less common in developed countries but remain significant in developing nations. In developed countries, factors like alcohol consumption, bariatric surgery, and metformin use are increasing these deficiencies in clinical practice.

Background: Burning Vertex Syndrome (BVS) is a dysesthetic condition, a new headache type, characterized by persistent or episodic burning sensation over the vertex of the scalp with or without associated symtpoms like photophobia or phonophobia or nausea or any other autonomic symptoms. Due to unclear etiology and limited clinical data, patients often undergo extensive investigations with delayed diagnosis. Understanding clinical, radiological, and biochemical associations is essential for accurate evaluation and management.Aim and Objective: To study the clinical profile, MRI brain findings, and serum biochemical parameters in patients presenting with Burning Vertex Syndrome.Materials and Methods: A cross-sectional observational study was conducted on 100 consecutive patients presenting with vertex scalp burning for more than four weeks. Detailed demographic data, sleep status, psychological stressors, and local scalp examination findings were recorded. All patients underwent MRI brain imaging and serum investigations including hemoglobin, serum iron, thyroid-stimulating hormone, and vitamin B12 levels. Data were analyzed using descriptive statistics.Results: Females constituted 80% of the study population, with maximum patients in the 30–50-year age group (70%). MRI brain was normal in 65% of cases. Chronic small vessel ischemic disease was observed in 21%, and CSVID with generalized cortical atrophy in 12%. Cerebral venous sinus thrombosis and meningioma were detected in 1% each. Anemia and low serum iron were found in 10% of patients, while vitamin B12 deficiency and hypothyroidism were present in 5% each. Sleep disturbance and psychological stress were reported by 80% and 75% of patients respectively. Local scalp pathology was noted in only 5%.Conclusion: Burning Vertex Syndrome predominantly affects middle-aged females and is strongly associated with sleep disturbance and psychological stress. Although MRI is normal in most cases, microvascular ischemic changes are common radiological findings. Routine neuroimaging and metabolic screening are recommended to exclude secondary causes and guide multidisciplinary management.