Assessing left atrial size and pump function in ischemic stroke patients: Is cardiac MRI superior to transthoracic echocardiography?

OBJECTIVES: Current guidelines recommend transthoracic echocardiography (TTE) following an ischemic stroke as the primary technique to identify cardiac abnormalities associated with an increased risk of cerebral embolism. It is unclear whether cardiac magnetic resonance imaging (cMRI), a technique shown to provide increased imaging resolution, may also enhance the cardiac assessment of ischemic stroke patients. We compared cMRI with TTE in the evaluation of Left Atrial (LA) size and pump function in a cohort of 44 patients with ischemic stroke. MATERIALS AND METHODS: The biplane method was utilized to acquire LA diameters as well as area measurements in both TTE and cMRI. We calculated LA volume (LAV), LAV index (LAVI), LA Global Longitudinal Strain (GLS) and LA pump function. Results were compared using paired two sample for means t-test. Lin's concordance correlation coefficient (CCC) and Bland-Altman methods quantified the agreement of measurements obtained by TTE and cMRI. RESULTS: LAVI measurements by cMRI were significantly larger (34.97 v. 28.81; p = 0.001) than by TTE. The concordance correlation demonstrated only a weak agreement between LA size measured by cMRI and TTE (ρc = 0.397; p= 0.001, 95% CI 0.16 - 0.59), and the Bland-Altman plot demonstrated that LAVI measured by cMRI averaged 6.3 ml/m2 larger magnitude than those obtained by TTE. CONCLUSIONS: Using TTE alone leads to an underestimation of LA abnormalities important in the evaluation of ischemic stroke patients. Nearly one in every five ischemic stroke patients evaluated based on the current guidelines may have a missed potential source of cardiac embolism.

Cortical Spreading Depolarization and Delayed Cerebral Ischemia; Rethinking Secondary Neurological Injury in Subarachnoid Hemorrhage.

Poor outcomes in Subarachnoid Hemorrhage (SAH) are in part due to a unique form of secondary neurological injury known as Delayed Cerebral Ischemia (DCI). DCI is characterized by new neurological insults that continue to occur beyond 72 h after the onset of the hemorrhage. Historically, it was thought to be a consequence of hypoperfusion in the setting of vasospasm. However, DCI was found to occur even in the absence of radiographic evidence of vasospasm. More recent evidence indicates that catastrophic ionic disruptions known as Cortical Spreading Depolarizations (CSD) may be the culprits of DCI. CSDs occur in otherwise healthy brain tissue even without demonstrable vasospasm. Furthermore, CSDs often trigger a complex interplay of neuroinflammation, microthrombi formation, and vasoconstriction. CSDs may therefore represent measurable and modifiable prognostic factors in the prevention and treatment of DCI. Although Ketamine and Nimodipine have shown promise in the treatment and prevention of CSDs in SAH, further research is needed to determine the therapeutic potential of these as well as other agents.

COVID-19: a modern trigger for Guillain-Barre syndrome, myasthenia gravis, and small fiber neuropathy.

COVID-19 infection has had a profound impact on society. During the initial phase of the pandemic, there were several suggestions that COVID-19 may lead to acute and protracted neurologic sequelae. For example, peripheral neuropathies exhibited distinctive features as compared to those observed in critical care illness. The peripheral nervous system, lacking the protection afforded by the blood-brain barrier, has been a particular site of sequelae and complications subsequent to COVID-19 infection, including Guillain-Barre syndrome, myasthenia gravis, and small fiber neuropathy. We will discuss these disorders in terms of their clinical manifestations, diagnosis, and treatment as well as the pathophysiology in relation to COVID-19.