A 35-year-old woman competing in Tricycle Class T2 (e.g. UCI Para-cycling Classification Guide) with hemiplegia of the left limb induced by transversal myelitis treated with fludrocortisone, pregabalin and codeine consulted our services because of a history of exercise-induced headache, dizziness and syncope subsequent to a concussion caused by a bicycle fall in 2012. While still symptomatic from this first concussion suffered in 2012, the patient experienced worsening of symptoms consecutive to a subsequent fall caused by a loss of consciousness at the end of a strenuous bout of exercise in a competition in August 2014. At the time of the consultation, she reported headaches, neck pain, dizziness, tonic-clonic movements post-high intensity exercise, balance problems, difficulties concentrating and memory problems for more than 1 month following mTBI, which is consistent with the World Health Organisation (ICD-10) definition of PCS. Rest and gradual return to activity was therefore recommended as proposed by major guidelines of sport-related concussion management, and was treated by an interdisciplinary team specialized in the management of patients with mTBI (Giza et al. 2013; Harmon et al. 2013; Mccrory et al. 2013; Ontario Neurotrauma Fondation, 2013, Marshall et al. 2015). Five months later, after being asymptomatic at rest and returned to normal activities and function (work/submaximal exercise training), she attempted an incremental exercise protocol at the Institut Universitaire de Cardiologie et de Pneumologie de Quebec (IUCPQ), aiming at identifying the cause of effort-related syncope.
The patient was requested to be well rested, be fasting, well hydrated, abstain from caffeinated beverages or stimulants and alcohol for 2 h prior to the assessment as well as refrained from strenuous exercise for 24 h. The patient performed a stepwise incremental upright cycling protocol carried out on a LeMond Revolution training device equipped with the WattBox system. Intensity was gradually increased every 2 min for the first 4 levels (from 30 to 56 W) and then every minute (from 65 to 220 W) up to exhaustion. Breath-by-breath pulmonary gas exchange was monitored using an automated gaz analyzer (Ultima , CardiO2  gas exchange analysis system; MGC Diagnostics , MN, USA) with the athlete breathing through a mouthpiece attached to a pneumotachometer, for determination of oxygen consumption (VO2), carbon dioxide production (VCO2), respiratory exchange ratio (RER: VCO2/VO2), ventilation and end-tidal partial pressure of carbon dioxide (PETCO2). Maximal exercise values were defined as the highest 60-s averaged values. Middle cerebral artery mean blood flow velocity (MCAvmean) was monitored by transcranial Doppler ultrasound (TCD) (Doppler Box; Compumedics DWL USA, Inc. San Juan Capistrano, CA), through the left temporal window as described by Willie et al. (2011a). Near-infrared spectroscopy (NIRS) was used to measure left frontal cerebral oxygenation (ScO2) (Oxiplex TS; ISS, Champlain, IL, USA). ScO2 was calculated by the ratio of oxygenated hemoglobin (HbO2) on total hemoglobin [HbO2 + deoxygenated hemoglobin (HHb)]: HbO2/(HbO2 + HHb) x 100. Heart rate (HR) was continuously monitored by a 12-lead electrocardiogram (ECG) and blood pressure taken manually every 2 min using a sphygmomanometer. Steady-state baseline data were monitored at rest in test position for 3 min. Data (MCAvmean and ScO2) were sampled at 1 kHz using an analog-to-digital converter (Powerlab 16/35; ADInstruments), and time-aligned with breath-by-breath measurements, for offline analyses. Data were then averaged over 60 sec up to maximal exercise.
MCAvmean increased by 20% and did not return to baseline values notwithstanding the presence of hyperventilation-induced hypocapnia at higher exercise intensities (Fig. 1). Despite this increase in cerebral perfusion, ScO2 lowered by 18% during the last 5 min of the exercise protocol (>10% decrease in the last 2 min).
The athlete reported headache during the last stages of the exercise protocol. Cardiorespiratory variables reached at maximal voluntary exercise are presented in Table 1. At test cessation, the patient lost consciousness and experienced a succession of convulsion-awakening periods with tonic-clonic movements. She was therefore transferred to the emergency room of the IUCPQ, where she was monitored on electroencephalogram, which remained normal. Thereafter, she was transferred to a specialized affiliate hospital in the field of neurology. A thorough investigation included electroencephalography, two lumbar punctures, as well as computed tomography cerebral angiography and cerebral magnetic resonance studies. At the end of the investigation, the final diagnosis was nonepileptic seizure.