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Concussive convulsions: A YouTube video analysis
Author(s) -
Tényi Dalma,
Gyimesi Csilla,
Horváth Réka,
Kovács Norbert,
Ábrahám Hajnalka,
Darnai Gergely,
Fogarasi András,
Büki András,
Janszky József
Publication year - 2016
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/epi.13432
Subject(s) - clonus , concussion , psychology , anesthesia , medicine , reflex , neuroscience , poison control , physical medicine and rehabilitation , audiology , epilepsy , injury prevention , environmental health
Summary Objective To analyze seizure‐like motor phenomena immediately occurring after concussion (concussive convulsions). Methods Twenty‐five videos of concussive convulsions were obtained from YouTube as a result of numerous sports‐related search terms. The videos were analyzed by four independent observers, documenting observations of the casualty, the head injury, motor symptoms of the concussive convulsions, the postictal period, and the outcome. Results Immediate responses included the fencing response, bear hug position, and bilateral leg extension. Fencing response was the most common. The side of the hit (p = 0.039) and the head turning (p = 0.0002) was ipsilateral to the extended arm. There was a tendency that if the blow had only a vertical component, the bear hug position appeared more frequently (p = 0.12). The motor symptom that appeared with latency of 6 ± 3 s was clonus, sometimes superimposed with tonic motor phenomena. Clonus was focal, focally evolving bilateral or bilateral, with a duration of 27 ± 19 s (5–72 s). Where lateralization of clonus could be determined, the side of clonus and the side of hit were contralateral (p = 0.039). Significance Concussive convulsions consist of two phases. The short‐latency first phase encompasses motor phenomena resembling neonatal reflexes and may be of brainstem origin. The long‐latency second phase consists of clonus. We hypothesize that the motor symptoms of the long‐latency phase are attributed to cortical structures; however, they are probably not epileptic in origin but rather a result of a transient cortical neuronal disturbance induced by mechanical forces.