The incidences of traumatic brain injuries (TBIs) are increasing globally because of expanding population and increased dependencies on motorized vehicles and machines. This has resulted in increased socio-economic burden on the healthcare system, as TBIs are often associated with mental and physical morbidities with lifelong dependencies, and have severely limited therapeutic options. There is an emerging need to identify the molecular mechanisms orchestrating these injuries to life-long neurodegenerative disease and a therapeutic strategy to counter them. This review highlights the dynamics and role of choline-containing phospholipids during TBIs and how they can be used to evaluate the severity of injuries and later targeted to mitigate neuro-degradation, based on clinical and preclinical studies. Choline-based phospholipids are involved in maintaining the structural integrity of the neuronal/glial cell membranes and are simultaneously the essential component of various biochemical pathways, such as cholinergic neuronal transmission in the brain. Choline or its metabolite levels increase during acute and chronic phases of TBI because of excitotoxicity, ischemia and oxidative stress; this can serve as useful biomarker to predict the severity and prognosis of TBIs. Moreover, the effect of choline-replenishing agents as a post-TBI management strategy has been reviewed in clinical and preclinical studies. Overall, this review determines the theranostic potential of choline phospholipids and provides new insights in the management of TBI.

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BackgroundCoronavirus disease 2019 (COVID-19) infection is associated with troponin elevation, which is associated with increased mortality. However, it is not clear if troponin elevation is independently linked to increased mortality in COVID-19 patients. Although there is considerable literature on risk factors for mortality in COVID-19-associated myocardial injury, the Global Registry of Acute Coronary Events (GRACE), Thrombolysis in Myocardial Infarction (TIMI), and Sequential Organ Failure Assessment (SOFA) scores have not been studied in COVID-19-related myocardial injury. This data is important in risk-stratifying COVID-19 myocardial injury patients.

Hypocalcemia can manifest as a variety of presentations, ranging from neuromuscular irritability to seizures, and psychiatric manifestations such as emotional instability, anxiety, and depression. Here, we present a unique case of hypocalcemia-induced acute psychosis.A 24-year-old woman presented to the emergency department (ED) with confusion and agitation for four to five days. The patient was noted by the family to have decreased oral intake and sleep. Auditory and visual hallucinations prompted the family to bring the patient to the ED. The patient was mildly tachycardic. Initially, the patient was agitated, impulsive, and aggressive, exhibiting psychotic features including visual hallucinations, paranoid delusions, thought broadcasting, tangential and perseverative thought processes, and erotomanic delusions. She had mild leukocytosis and elevated procalcitonin on admission. A thorough workup ruled out infectious/inflammatory processes. Cerebrospinal fluid was negative for acute meningitis/encephalitis, autoimmune encephalitis antibodies, and paraneoplastic etiology. Thyroidstimulating hormone was normal and thyroid antibodies were negative. The CT brain and MRI brain were unremarkable. The patient was severely hypocalcemic (6.7) with low parathyroid hormone (<6) on admission.To note, the patient has multiple endocrine neoplasia, type 2B (MEN2B). She underwent total thyroidectomy five months prior for metastatic medullary thyroid carcinoma complicated by postsurgical hypoparathyroidism. The patient had been non-compliant with calcium and calcitriol supplementation postoperatively.The patient was started on IV calcium gluconate and transitioned to calcitriol with calcium level improvement over the next three days. She experienced marked improvement, with the resolution of her psychosis. The patient's subacute onset psychosis with no personal or family psychiatric history and a rapid response to calcium correction supports hypocalcemia etiology. This case illustrates new-onset acute psychosis in a patient with calcium regulation imbalance. The development of hypocalcemia secondary to thyroidectomy with postsurgical hypoparathyroidism and calcium supplement non-compliance precipitated psychosis. A few similar cases have been reported, and here, we note that treatment of hypocalcemia promptly resolves symptoms. As per our review, this will be the first case of neuropsychiatric symptoms without associated cortical calcifications seen on imaging. It is important to recognize hypocalcemia as a rare cause of psychosis so as to not mistakenly categorize such presentations as primary psychotic disorders and miss a medically treatable illness.