Bagath Srinivasan Balaji1, Abhinav Mahesh1, Hemanth Kumar Arumugam1, Lakshmi Narasimhan R1, Sundar Shanmugam1, Rithvik Ramesh1, Deepa Avadhaani1, Philo Hazeena1
1Neurology, SRIHER
Objective:
To examine the association between acute insular cortex infarcts and pulmonary edema by analysing cardiovascular parameters, clinical profiles, and imaging findings in affected patients.
Background:
Insular cortex is a complex rich cortical hub involving interoception, autonomic control, social behaviour, multimodal sensory modulation and emotional control. Acute lesions like stroke and seizures result in a wide range of sensory, autonomic, cognitive, motor and emotional manifestations. Insular strokes manifest with both neurogenic and cardiogenic pulmonary edema with concurrent multi-varied cardiac manifestations.
Design/Methods:
Ten patients (4 males, 6 females) aged 45-84 years with acute ischemic strokes with insular involvement(right-6,left-4) were identified from a stroke database (January 2022- February 2025). For all cases underwent through clinical history, neurological examination, routine blood test including NT-proBNP, ECG, troponin chest radiograph, carotid and transcranial ultrasound and neuroradiology according MRI stroke protocol.
Results:
Major (more than 2/3rd insula) and minor (less than 2/3rd insula) are 5 each in number(5 anterior and posterior and 5 posterior alone). All patients developed pulmonary edema during hospitalization within first week. All 6 Right insular strokes showed tachycardia, 3 showed AF and 2 showed AF in left insular strokes. The MCA(M1,M2,M3,M4, the troponin levels were also looked into). All patients developed pulmonary edema post-stroke, reinforcing the role of the insular cortex in autonomic dysfunction. Right insular infarctions were linked to excessive sympathetic activity. Due to the small sample size, meaningful statistical analysis was not conducted.
Conclusions:
Strokes with insular involvement shows the link between insular cortex and the heart. The SYMPATHETIC overactivity results in increased heart rate and arrhythmogenicity which results in the sympathetic heart weeping for the brain. This causes flash pulmonary edema which requires watchful expectancy.
Disclaimer: Abstracts were not reviewed by Neurology® and do not reflect the views of Neurology® editors or staff.