A case report of long-latency evoked diaphragm potentials after exposure to acute intermittent hypoxia in post-West Nile virus meningoencephalitis

We present a case report of a 42-year-old female with post-West Nile virus meningoencephalitis who exhibited unique, long-latency diaphragm potentials evoked by transcranial and cervical magnetic stimulation after exposure to acute intermittent hypoxia (AIH). The subject was recruited for a study investigating AIH effects on respiratory motor function in healthy individuals. She had contracted West Nile virus infection 5 years before assessment that resulted in hospitalization and persistent allodynia but was not reported to the research team. During the study, transcranial (TMS) and cervical (CMS) magnetic stimulation were performed before and 30-60 min after a single presentation of AIH [15, 1-min hypoxic episodes (∼9% inspired O₂), with 1-min normoxic intervals]. Diaphragm EMG was recorded using chest wall surface electrodes. At baseline, evoked diaphragm potentials were within normal ranges for both TMS (onset latency = 17.0 ± 1.1 ms; peak-to-peak amplitude = 220 ± 27 µV) and CMS (onset latency = 7.8 ± 0.6 ms; peak-to-peak amplitude = 336 ± 8 µV). However, long-latency TMS- and CMS-evoked potentials were observed 30-60 min post-AIH that were not present at baseline nor in healthy subjects. The onset of long-latency potentials ranged from 50 to 808 ms. While AIH is a potentially useful therapeutic strategy to enhance motor function after neurological disease or injury, it may elicit distinct effects in individuals with a history of neuroinfectious disease. Possible explanations for these unusual responses are discussed.<b>NEW & NOTEWORTHY</b> A 42-year-old female with post-West Nile virus meningoencephalitis demonstrated long-latency diaphragmatic potentials evoked by transcranial and cervical magnetic stimulation following exposure to acute intermittent hypoxia that were not present at baseline nor in healthy subjects. Although the cause of long-latency responses is unknown, we discuss possible mechanisms whereby acute intermittent hypoxia could create unique effects on the diaphragm/phrenic motor system in individuals with a history of neuroinfectious disease.