Varicella zoster encephalitis, cranial nerve neuropathies, and takotsubo syndrome: delving further into the pathogenesis

Editor – I read with great interest the communication by Bennett and Iqbal,¹ published in Clinical Medicine, about the 68-year-old woman with takotsubo syndrome (TTS) secondary to a varicella zoster encephalitis (VZE), and the arduous work of the authors in diagnosing and managing her evolving cranial nerve neuropathies (initially mononeuritis and subsequently polyneuritis), associated with rapid atrial fibrillation, and cardiac abnormalities. The rise in high sensitivity troponin was higher than expected for TTS, and making the distinction between TTS and acute coronary syndromes more difficult. The QRS voltage of the electrocardiogram (ECG) of Fig 1 is low,¹ in keeping with TTS,² and one wonders whether prior to the admission, ECGs, or ECGs from follow-up, showed higher QRS voltages. In reference to the pathophysiology of TTS, we are still far from delineating the underlying mechanism(s), but in cases like the one herein, checking for elevated blood-borne catecholamines,³ or evaluating for evidence of enhanced cardiac autonomic sympathetic nervous system (CASNS) stimulation, norepinephrine-based, exerting cardiomyocyte injury,⁴ are two promising injurious pathways, needing exploration. Indeed, current commercially available technology⁵ could provide monitoring of the CASNS function, via the chest electrodes used for ECG recordings, with analysis of filtered signals of 500 to 1,000 Hz from the skin of the thorax, reflecting activity of the stellate ganglia, and the sympathetic autonomic nerve input to the heart.