Bilateral insular compromise (chronic left, acute right) may provide a substrate for autonomic instability leading to fatal arrhythmia or Takotsubo-like cardiomyopathy.
Insular stroke may elevate sudden death risk via autonomic disruption; leaves open the role of bilateral insular injury in arrhythmia vulnerability.
To the Editor: Sudden death after ischemic stroke is most often attributed to fatal arrhythmia in older patients with limited autonomic reserve.1–3 Silent infarcts are typically small and deep.4 We report the case of a 44-year-old man with Li-Fraumeni syndrome and prior left insular injury from astrocytoma/treatment whose sudden death followed an unrecognized acute right middle cerebral artery (MCA) infarct involving the insular cortex, highlighting lethal brain–heart axis disruption. This case is notable because the large insular infarct was clinically silent in the setting of substantial baseline neurologic deficits and because bilateral insular compromise (chronic left, acute right) provides a plausible substrate for autonomic instability and not only fatal arrhythmia but a Takotsubo-like cardiomyopathy. The patient had Li-Fraumeni syndrome. A left frontotemporal astrocytoma had been treated 7 years earlier with left insular subtotal resection, radiation, and temozolomide. This was later complicated by a left internal capsule infarct and a left galeal osteosarcoma that was treated with resection followed by treatment with doxorubicin/cisplatin. He underwent repeat resections for recurrent astrocytoma/osteosarcoma 1 month before death. He had a seizure disorder treated with lacosamide and levetiracetam (last known seizure ∼1 year prior), but had no known cardiac history. Baseline deficits included nonfluent dysarthric speech/aphasia and mild right-sided weakness; his last neurologic exam 7 days before death showed no new deficits. He developed nonspecific fatigue for 1-2 days and was found unresponsive at home and could not be resuscitated.
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Idler et al. (2026) studied this question.
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