{'fraction_non_alphanumeric': 0.013496143958868894, 'fraction_numerical': 0.008354755784061696, 'mean_word_length': 5.5974576271186445, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
The insular cortex and cardiac response to stroke

That cerebrovascular events can endanger the heart has long been recognized. Neurologists are familiar with the fact that 10 to 20% of patients with stroke have had an antecedent myocardial infarction and that cerebral emboli may originate in the heart. They are also aware that an acute stroke commonly alters the EKG, producing repolarization abnormalities of ST segments and T waves. Following stroke there is an increased incidence of cardiac arrhythmias, which may be associated with adverse outcome.1 Only recently has research begun to clarify the basis for this neurocardiac interaction.

In the 1980s, Cechetto and Saper2 identified a viscerotopic sensory cortex in the insula, which receives convergent inputs from limbic and autonomic centers in the brain. Subsequent functional imaging studies confirmed a similar arrangement in human cortex.3 Hachinski and Cechetto4 later showed that ischemic damage to the insular cortex, particularly the right insula, can have cardiovascular consequences in experimental animals, including increased heart rate variability in the midrange frequencies, consistent with excessive sympathetic stimulation. Oppenheimer et al.5 then demonstrated functional laterality in humans such that stimulation of the left insular cortex tends to cause parasympathetic cardiac responses and of the right insular cortex sympathetic responses. Cerebral vascular lesions in areas adjacent to the right insular cortex have marked cardiac effects. The resulting augmentation …