Touro College

Magnesium is an essential micronutrient that exerts fundamental roles at both the cellular and tissue levels, with broad therapeutic and preventive implications across a range of pathological conditions. Accumulating clinical and experimental evidence indicates that optimal magnesium homeostasis modulates key pathophysiological processes and serves as both a biological and prognostic marker in disorders such as stroke, myocardial infarction, type 2 diabetes mellitus, and renal failure. These disease states commonly originate from two major etiological determinants-hypertension and atherosclerosis-which share a unifying pro-inflammatory mediator: platelet-activating factor (PAF). PAF plays a central role in vascular inflammation by promoting platelet aggregation, macrophage infiltration, leukocyte adhesion, and vasomotor dysregulation. Importantly, magnesium demonstrates an inverse association with both platelet aggregation and PAF activity, underscoring its protective capacity in mitigating vascular inflammation and preserving endothelial function. The objective of this updated literature review is to elucidate the antagonistic interplay between magnesium and PAF, with a focus on its physiological and therapeutic significance across multiple organ systems. While emerging data support a modulatory role of magnesium in PAF-mediated inflammatory pathways, current evidence remains limited. Therefore, further mechanistic, pharmacological, and clinical investigations are warranted to clarify the multifaceted role of magnesium in attenuating PAF-driven disease processes.

Neurologic deterioration following cardiac arrest is frequently attributed to global hypoxic-ischemic brain injury. However, focal ischemic stroke may occur concurrently and represents an important diagnostic pitfall in post-resuscitation care. We report the case of a 59-year-old woman with end-stage heart failure with reduced ejection fraction who developed acute neurologic impairment following prolonged pulseless electrical activity arrest. Early non-contrast CT of the head demonstrated a focal left cerebellar infarction without diffuse cerebral edema. MRI of the brain performed four days later showed no acute intracranial abnormality, illustrating radiographic discordance between early CT and delayed MRI in posterior circulation ischemia. These complementary imaging findings informed ongoing neurologic assessment and multidisciplinary discussions. This case underscores the importance of early neuroimaging and maintaining a broad neurologic differential diagnosis in post-cardiac arrest patients.

Coronary computed tomography angiography (CCTA) is vital for diagnosing ischemic heart disease, yet its accuracy is unreliable due to varying reader expertise. Artificial Intelligence (AI)-driven automated stenosis assessment offers promise for enhancing diagnostic consistency. We aim to evaluate an AI-CCTA assessment against invasive coronary angiography, invasive FFR, and expert readings. We performed a comprehensive search in Web of Science, Scopus, PubMed, Cochrane Library, and EMBASE from inception until March 2025. Two independent reviewers screened articles and extracted data on study design, patient demographics, AI methodology, stenosis thresholds, and outcomes. For statistical analysis, we constructed summary receiver operating characteristic (SROC) curves and used a bivariate random-effects model to derive pooled sensitivity, specificity, diagnostic odds ratios (DOR), and area under the curve (AUC). Forest plots were generated to visualize these metrics. Our meta-analysis included 34 studies with 10,067 patients. AI-based CCTA demonstrated excellent diagnostic performance with an AUC of 0.932 for per-patient analysis. The pooled per-patient sensitivity was 0.89 (95% CI: 0.87-0.91) and specificity was 0.80 (95% CI: 0.74-0.86) with diagnostic OR of 37.07 (95% CI: 24.57-55.92). AI validated against expert readers achieved the highest accuracy (0.94, 95% CI: 0.87-0.98). The>70% stenosis threshold demonstrated superior performance (accuracy: 0.90, specificity: 0.96) compared to the>50% threshold (accuracy: 0.85, specificity: 0.87). Per-vessel analysis showed comparable results with an AUC of 0.905. AI-assisted coronary CT angiography delivers high diagnostic performance for coronary stenosis detection, with strong AUC values, high sensitivity and specificity, and robust diagnostic OR across both per-patient and per-vessel assessments.

Tuberculous meningitis (TBM) is the most severe form of central nervous system tuberculosis and carries high morbidity and mortality. We report a 35-year-old man from Ecuador who presented with sepsis-like systemic symptoms and rapidly progressive neurological deficits. Initial imaging revealed cavitary pulmonary lesions and hilar lymphadenopathy, suggestive of pulmonary tuberculosis. Neurological deterioration prompted magnetic resonance imaging (MRI) of the brain and cervical spine, demonstrating communicating hydrocephalus, basilar leptomeningeal enhancement, diffuse cervical cord edema, and multiple rim-enhancing subdural abscesses. Diagnosis was confirmed via bronchoalveolar lavage positive for Mycobacterium tuberculosis after multiple failed sputum induction attempts. This case illustrates a combination of sepsis-like presentation, rapid quadriparesis, and spinal cord abscesses in TBM, highlighting the importance of advanced imaging and alternative microbiologic sampling for timely diagnosis and management.

Tumor lysis syndrome (TLS) is a serious medical condition in which the lysis of tumor cells results in a variety of abnormalities, including elevated uric acid, potassium, and phosphorus, decreased calcium, seizures, arrhythmias, and acute kidney injury (AKI). TLS most often occurs in hematologic cancers and after chemotherapy, whereas cases that arise without chemotherapy are termed spontaneous TLS (STLS). In our case, an 81-year-old female with a past medical history of hypertensionand chronic obstructive pulmonary disease (COPD) initially presented to the emergency department for left lower back pain that was later found to have been caused by a bony metastatic lesion secondary to a neuroendocrine tumor of the lung. Her hospital stay was complicated by a worsening AKI that was refractory to fluids and the discontinuation of nephrotoxic medications. A uric acid, urine studies, lactate dehydrogenase, and metabolic panel ruled out other causes of her kidney injury and ruled in a diagnosis of STLS. The patient's condition worsened until she required hemodialysis, which she rejected in favor of comfort care. The patient died 14 days after admission. In conclusion, despite the majority of TLS cases originating from hematologic malignancies and in response to chemotherapy, STLS should be considered in refractory AKI for cancer patients, even when secondary to solid tumors like neuroendocrine tumors of the lung.

Abnormalities in the synthesis or structure of globin chains are known as hemoglobinopathies, and they produce a wide range of clinical phenotypes. When both alleles of the same gene carry different hemoglobin variants, this results in compound heterozygosity. The condition described in this case report (hemoglobin C (HbC)/beta-zero (β⁰)-thalassemia) is one such example. On their own, neither HbC nor β⁰-thalassemia is typically associated with acute vaso-occlusive crises, and the combination of HbC/β⁰-thalassemia has not been well characterized. Limited reports indicate that this genotype is not known to cause pain episodes resembling those seen in HbSC disease. Here, we describe a 32-year-old woman with DNA-confirmed HbC/β⁰-thalassemia. She has chronic transfusion dependence, marrow expansion, and anemia, with a baseline hemoglobin of about 8 g/dL. Despite treatment with hydroxyurea and opioid therapy, she has persistent diffuse bone pain. During the current admission, she presented with worsening pain, nausea, and vomiting. Laboratory findings showed stable hemoglobin compared to her baseline, without leukocytosis or sickling, and imaging revealed no acute pathology. Her pain was managed with intravenous hydromorphone, with plans to transition to oral methadone and oxycodone as needed before discharge. This case illustrates the difficulty of managing severe pain in HbC/β⁰-thalassemia, particularly when symptoms occur with high intensity but without evidence of vaso-occlusion or acute hemolysis. While extramedullary hematopoiesis is a leading explanation for her pain, the degree of pain she experienced is unusual in the absence of acute sickling. Given the rarity of this genotype and the limited amount of published data, management remains challenging. Further research is needed to clarify the mechanisms of pain in HbC/β⁰-thalassemia and to distinguish organic causes from central sensitization in patients with chronic opioid use.

First-generation students face structural barriers and demonstrate lower self-regulated learning (SRL) than continuing-generation peers. SRL is essential for engagement and preparation for occupational therapy practice. This study examined effects of an Academic Self-Regulation (ASR) program, supported by a mobile app, on SRL among first- and continuing-generation health professions students. Mixed methods with a pretest-posttest survey and semi-structured interviews. Using the Self-Regulated Learning Perception Scale (SRLPS), first-generation students (n = 11) scored lower than continuing-generation peers (n = 6) in motivation, planning, and self-directedness at baseline. Among the eight students completing pre/post surveys, large effect sizes (Cohen's d = 1.41-1.64) indicated improvements across all domains, eliminating group differences. Satisfaction was high (M = 4.21/5). Qualitative data highlighted greater planning, strategic learning, and ownership of learning. Structured SRL instruction with digital tools may enhance academic participation, promote equity, and support professional development in occupational therapy education.

Paradoxical insomnia (sleep-state misperception) is characterized by a marked discrepancy between self-reported poor sleep and objective polysomnographic evidence of normal sleep duration and architecture. We present a case of paradoxical insomnia comorbid with mild obstructive sleep apnea (OSA), highlighting diagnostic and therapeutic challenges. A 37-year-old woman presented with severe chronic insomnia of eight years’ duration, reporting sleeping only "minutes per night," despite appearing alert and functional. A two-night home sleep test showed normal sleep latency (seven minutes), sleep efficiency (86.6%), and total sleep time (4.5 hours). Mild OSA was noted (Apnea-Hypopnea Index (AHI) = 5 events/hour) but was not considered causative of her profound subjective distress. Multiple trials of hypnotics, antidepressants, benzodiazepines, and antipsychotics yielded no subjective improvement. The patient maintained a fixed, delusional-like conviction of sleeplessness despite objective evidence to the contrary, although she lacked other psychotic features. This case underscores the importance of recognizing paradoxical insomnia, particularly when complaints are disproportionate to objective findings and mild comorbid OSA is present. Management should prioritize cognitive behavioral therapy for insomnia (CBT-I) and psychoeducation over pharmacologic escalation. Clinicians should communicate objective sleep data with empathy within a psychoeducational framework to avoid therapeutic rupture and promote engagement in behavioral interventions.

The authors declare no conflicts of interest. Data sharing not applicable to this article as no datasets were generated or analysed during the current study.