We report improvements in debilitating cervicogenic dizziness (CD), as well as neck pain and upper and lower back pain, using Chiropractic BioPhysics[®] (CBP[®]) orthopedic rehabilitation with a one-year follow-up. CD is extremely debilitating and strongly impacts health outcomes. Reports of successful conservative treatments for CD combined with neck and spine pain with improved outcomes and sustained long-term results are rare, and this study adds to the literature. A 29-year-old female suffered from sudden-onset dizziness and frequent syncope elicited by cranio-cervical extension motions. The patient concomitantly reported moderate neck pain, upper mid-back pain, and low back pain, self-reported significant disability, and objectively displayed poor posture and altered spine alignment on radiography. Due to the worsening of her condition, she sought treatment at a facility in Shoreline, WA, USA. Following examination and diagnostic evaluation, she undertook an in-office treatment regimen. The multi-modal orthopedic regimen included postural exercises, postural spinal manipulation, and specific spinal structural traction. This combination Mirror Image (MI®) protocol has been shown to reduce pain and disability in musculoskeletal conditions, with improvement in CD and cervical lordosis. Following 68 in-office treatments over 5.5 months, all initial outcome assessments and physical, orthopedic, and neurological examinations were repeated and recorded. At the post-treatment assessment, the patient reported improvements in CD symptoms and neck, upper back, and lower back pain. Cervical lordosis improved from C2 to C7, measuring +9.4° (kyphotic) to -16.4° (lordotic). At the one-year follow-up, all outcome measures were stable; syncope was fully resolved, and 90% of the previously reported CD symptoms were resolved. Cervical lordosis remained stable at -17.6° (lordotic). This case documents successful treatment in a single patient using conservative spine and posture treatment protocols. This case report followed reporting guidelines. This study may contribute to the evidence aiming to fill the gap in the understanding of CD and potential conservative therapeutic interventions that are directed toward improving spine alignment.

Reactive hypoglycaemia is characterised by symptomatic hypoglycaemia occurring several hours after food intake and can significantly impair quality of life. Management is often challenging, particularly in patients who fail dietary modification or cannot tolerate conventional pharmacological therapies. We present the case of a 50-year-old woman with longstanding, debilitating reactive hypoglycaemia who experienced marked symptomatic and biochemical improvement following treatment with semaglutide, a glucagon-like peptide-1 (GLP-1) receptor agonist. The patient presented with recurrent episodes of dizziness, profound fatigue, tremulousness, and syncope despite adherence to dietary recommendations. Previous treatment with acarbose was discontinued because of gastrointestinal intolerance, and metformin failed to improve symptoms. Continuous glucose monitoring and an oral glucose tolerance test confirmed reactive hypoglycaemia. Following initiation of semaglutide, the patient experienced a substantial reduction in hypoglycaemic episodes with corresponding improvement in glucose profiles and quality of life. This case highlights the potential role of semaglutide as a novel therapeutic option in patients with refractory reactive hypoglycaemia and contributes to the emerging evidence supporting the use of GLP-1 receptor agonists in this condition.

Transthyretin cardiac amyloidosis (ATTR-CM) is an increasingly recognized infiltrative cardiomyopathy characterized by progressive myocardial amyloid deposition, leading to heart failure, arrhythmias, and conduction abnormalities. Recent studies suggest that ATTR-CM is not uncommon among older patients hospitalized with heart failure with preserved ejection fraction and left ventricular hypertrophy, highlighting that the disease remains substantially underdiagnosed. Conduction disturbances are common during the course of the disease, and advanced atrioventricular conduction disease may require permanent pacemaker implantation; however, complete heart block as the initial presentation remains uncommon. We report the case of a 70-year-old woman who presented with exertional syncope and was found to have complete atrioventricular block with a wide-QRS escape rhythm, requiring emergency temporary pacing followed by permanent dual-chamber pacemaker implantation. Transthoracic echocardiography demonstrated marked biventricular hypertrophy, biatrial enlargement, restrictive left ventricular filling pattern, and severely impaired global longitudinal strain with a characteristic apical sparing pattern, raising a strong suspicion of cardiac amyloidosis. Cardiac MRI revealed diffuse biventricular subendocardial late gadolinium enhancement and abnormal myocardial nulling, highly suggestive of amyloid infiltration. Hematological investigations excluded light-chain amyloidosis, and technetium-99m hydroxymethylene diphosphonate scintigraphy demonstrated Perugini grade 3 myocardial uptake, establishing the non-biopsy diagnosis of ATTR-CM. Tafamidis therapy was subsequently initiated. This case highlights complete heart block as an uncommon initial presentation of ATTR-CM. It underscores the pivotal role of multimodality imaging in achieving an early and accurate diagnosis, thereby enabling timely initiation of disease-modifying therapy.

Atrioventricular (AV) conduction disturbances in bicuspid aortic valve (BAV) patients are typically attributed to age-related fibrosis or post-surgical trauma. Direct mechanical impingement of the conduction system by accelerated valvular calcification causing reversible, dynamic AV block is rarely reported.

Obstructive sleep apnea (OSA) is a highly prevalent sleep disorder affecting a considerable proportion of the adult population. It is characterized by chronic intermittent hypoxia (CIH), resulting from recurrent partial (hypopnea) or complete obstruction (apnea) of the upper airway during sleep. Clinically, OSA produces fragmented sleep, loud snoring, excessive daytime somnolence, cognitive dysfunction, and nocturnal diaphoresis. Importantly, OSA is recognized as an independent risk factor for systemic hypertension and is associated with cardiac arrhythmias and stroke. The CIH contributes to these adverse outcomes by enhancing carotid body chemoreceptor sensitivity and promoting sympathetic overactivation, systemic inflammation, and oxidative stress. Syncope is a transient, fully reversible loss of consciousness caused by cerebral hypoperfusion. Although cardiac causes such as atrial fibrillation and brady-arrhythmias are well recognized, the vasovagal syncope (VVS) remains the most common etiology, triggered by exaggerated vagal activation. Emerging evidence suggests that OSA may contribute to VVS, as patients with unexplained syncope show a high prevalence of OSA and often improve with CPAP therapy. This minireview summarizes the potential mechanisms linking OSA to syncope, provides a brief overview of OSA pathophysiology, and discusses autonomic pathways that may underline syncope in this population, highlighting their relevance for clinical management.

Maternal cardiovascular disease is a leading cause of pregnancy-related death in the United States. Symptoms associated with cardiovascular disease include shortness of breath, palpitations, dizziness, syncope, chest pain, edema, and fatigue. Unfortunately, these symptoms are nonspecific and are common in pregnancy and postpartum. When a pregnant or postpartum person reports any of these symptoms, the provider needs a systematic approach to evaluate whether further work-up and consultation are needed or whether the patient can be reassured that the symptoms are likely "normal for pregnancy." The Society for Maternal-Fetal Medicine presents a checklist for triage of patients who report these symptoms and a checklist outlining the initial work-up of those who need further evaluation.

Cardioneuroablation (CNA), defined as endocardial catheter ablation of atrial ganglionated plexi within the intrinsic cardiac autonomic nervous system, has emerged as a mechanism-directed therapy for cardioinhibitory reflex syncope and functional bradyarrhythmias. By attenuating postganglionic parasympathetic input to the sinoatrial and atrioventricular nodes, CNA targets the autonomic substrate of cardioinhibition rather than merely treating its bradycardic consequence. Over the past two decades, the evidence base has progressed from pioneering single-center experiences to multicenter registries, systematic reviews, meta-analyses, and randomized clinical trials, with reported freedom from recurrent syncope of approximately 80-94% in carefully selected patients at medium-term follow-up. This state-of-the-art narrative review summarizes the rationale, anatomy, patient-selection principles, mapping and ablation strategies, procedural endpoints, clinical outcomes, safety profile, and emerging applications of CNA. Particular emphasis is placed on the unresolved questions that will define the future of the field: the absence, to date, of adequately powered sham-controlled efficacy data; the lack of a universally validated intraprocedural endpoint; the biological and clinical significance of vagal reinnervation; and the gap between expert-center and broader real-world outcomes. Current evidence supports CNA as a promising, anatomically grounded neuromodulatory therapy, but its transition from expert-center innovation to guideline-endorsed treatment will depend on rigorous patient selection, standardized procedural endpoints, and the results of ongoing randomized trials.

Background: Falls in older adults are a major public health and rehabilitation concern and may reflect interacting chronic disease-related mechanisms rather than diagnostic labels alone. Type 2 diabetes mellitus (T2DM), hypertension (HTN), and osteoarthritis (OA) are common in later life and may influence fall vulnerability through sensory, vascular, musculoskeletal, cognitive, medication-related, and functional pathways. This scoping review aimed to map mechanism-oriented evidence linking T2DM, HTN, and OA to falls and fall-related outcomes in older adults. Methods: A scoping review was conducted in accordance with established scoping review methodology and PRISMA-ScR guidance. PubMed, Web of Science, and Embase were searched for English-language studies published from 2016 to 2026; the final search was conducted on 15 April 2026. Evidence was charted in a structured table and synthesised descriptively and thematically across disease-specific and shared mechanism domains. Results: A total of 151 studies were included. The evidence was organised into T2DM-related sensory-neural, gait and balance, vestibular/visual-cognitive, strength-related, and glycaemic or medication-related mechanisms; HTN-related haemodynamic, cerebral perfusion, dizziness/syncope, and medication-related mechanisms; and OA-related pain, proprioceptive, strength-related, gait and balance, psychological, and compensatory-control mechanisms. Shared pathways included frailty, multimorbidity, polypharmacy, pain burden, cognitive impairment, sleep disturbance, ADL decline, dizziness, and reduced physical function. Conclusions: Falls in older adults with T2DM, HTN, OA, or multimorbidity may be better understood through interacting disease-specific and shared mechanisms than through diagnostic labels alone. Future longitudinal and multimorbidity-specific studies using standardised fall ascertainment are needed to test these pathways more directly.