Introduction

Sports-related concussion (SRC) has received considerable attention over the last two decades as a significant public health issue. With improved consistency in reporting and efforts geared toward detection and prevention, the incidence of sports-related traumatic brain injuries (TBIs) has recently stabilized in the United States.¹ An understanding of the immediate clinical manifestations of SRC is critical, as early detection, recognition and protocolized action remain the pillars of on-field concussion management. One such immediate clinical manifestation is that of transient abnormal, non-volitional movements. These short-lived, stereotyped movements are known as concussive convulsions. The purpose of this chapter is to discuss the phenomenon of concussive convulsions with special attention paid to sports-related injuries. This chapter will define concussive convulsions and describe the entity’s history, pathophysiology and epidemiology. We will also discuss the diagnostic work-up, including electroencephalography (EEG) and neuroimaging. Lastly, practical recommendations for initial management and follow-up will be provided. The decision to focus within the context of sports-related injuries reflects a few important considerations: 1) SRCs are commonly isolated injuries requiring purely clinical diagnosis, therefore, specific attention is directed toward their presentation, and 2) the research surrounding concussive convulsions has relied nearly exclusively on data from sports.

Definition and History

Concussive convulsions were first described by McCrory et al. in 1997 through the observation and review of concussions suffered by Australian rules and rugby league players.² Prior to the publication of this study, it had been widely assumed that concussive convulsions were an early manifestation of post-traumatic epilepsy (PTE).² However, the authors demonstrated concussive convulsions to be a distinct entity. Retrospectively, eyewitness and video data of 22 concussive convulsions were collected from a 15-year time period. The event descriptions produced from this cohort are now considered the defining features of concussive convulsions. Typically, these convulsions involve a brief tonic phase followed by bilateral myoclonic movements, which were sometimes accompanied by abnormal head movements and/or asymmetric posturing. These episodes were observed to start within two seconds of impact, during a period of loss of consciousness, and lasted a maximum of 150 seconds. Following return of consciousness, athletes were noted to exhibit the typical neurologic and behavioral manifestations of a concussion.²

In a subsequent prospective analysis of 102 Australian footballers from McCrory et al. published in 2000, about 25% of concussed athletes showed tonic movements without clonic movements.³ These initial studies led to an understanding that the semiology of the convulsion could vary from athlete to athlete. A 2018 systematic review of 128 cases (7 studies) of sport-related concussive convulsions by Kuhl et al. provided a synopsis of observed semiologies to date. Of these 128 cases, 121 had a recorded semiology (Figure 6.1). Of note, nine of the cases included by Kuhl et al. presented with delayed epilepsy (PTE), and these are not included in Figure 6.1 or in subsequent discussion.

Figure 6.1 Convulsion semiology

Graphic adapted from Kuhl et al., 2018.⁴

The most common semiology was posturing (88/121; 72.7%), followed by generalized tonic-clonic (26/121; 21.5%), myoclonic (6/121; 5.0%) and focal motor (1/121; 0.8%).⁴ Posturing movements described include the “bear-hug” and “righting” reflexes, which most often occur immediately after head impact. Because of the relatively high prevalence of posturing in these cases, recognition of posturing is of utmost importance for quick assessment and stabilization of patients. Although the semiology may change from one concussion to another, the short duration and temporal relationship to a suspected head injury remain the defining features. Thus, we define concussive convulsions as follows:

It should be emphasized that SRC-convulsions are not believed to be a manifestation of post-traumatic epilepsy (PTE). While SRC-convulsions are an isolated, immediate manifestation of head injury, PTE represents one or more unprovoked late post-traumatic seizures occurring after at least one week post-injury.⁵ While the incidence of PTE is known to correlate with the severity of injury,⁶ a lack of evidence exists for correlation of SRC-convulsions with injury severity.

Pathophysiology

The pathophysiology of SRC convulsions remains largely unknown. The follow-up of study subjects from both investigations by McCrory et al. revealed that players did not have neuroradiologic evidence of TBI or epileptiform discharges on EEG to suggest a structural etiology or epileptogenic foci.^{2, 3} McCrory and colleagues therefore concluded that these convulsions were non-epileptic in nature and likely stem from a different pathophysiologic process than PTE.² Specifically, McCrory and colleagues drew a similarity between SRC-convulsions and convulsions seen with syncope.

During early investigations of syncopal convulsions, Dell et al. demonstrated that early cerebral hypoxia resulted in direct activation of the reticular activating formation with contemporaneous cortical suppression.⁷ This series of hypoxia-related events then results in the tonic and myoclonic movements seen with convulsive syncope.^{7, 8} An earlier study by Gastaut and Fischer-Williams had also shown that convulsive syncope did not result in epileptiform EEG changes, as similarly suspected to be the case with concussive convulsions.⁹ These elements of convulsive syncope make it appear phenotypically similar to concussive convulsions. However, in the case of concussive convulsions, this transient, functional decerebration is assumed to be initiated immediately by shear forces at the time of impact rather than by a transient period of cortical ischemia (as in syncope), leading to bulbo-pontine reticular formation disinhibition.⁸ One hypothesis suggests that strain and shear forces experienced by the ascending reticular activating formation fibers lead to transient functional decerebration.¹⁰ Therefore, while an analogy can be drawn between convulsive syncope and concussive convulsions, the exact pathophysiology remains unknown, and there remains an open investigational opportunity for better pathophysiological understanding.

Epidemiology

Demographic and epidemiologic data on concussive convulsions are lacking due to the relative dearth of studies on the topic. Moreover, published studies have inconsistently recorded important epidemiologic data. As Kuhl et al. reported, basic demographic variables are often incompletely reported. For example, gender was only recorded for 76 of 128 subjects (59.4%) across 7 included studies. Additionally, all of the study subjects were male, making it potentially difficult to generalize findings to other populations.⁴ Furthermore, age was recorded for only 27 subjects (21.1%), with an average of 22.9 years. Of note, all these male athletes were engaged in full-contact sports, as defined by the 2008 classification system from the American Academy of Pediatrics.¹¹

Regarding the incidence of concussive convulsions, an exact number is not known. In their landmark analysis of eyewitness and video footage from a combined estimated 200,000 player-games across a 15-year period, McCrory et al. identified only 22 cases of concussive convulsion.² Their subsequent prospective analysis of 102 concussion cases reported one episode of tonic-clonic movements lasting 150 seconds. However, less lengthy convulsive manifestations were more common: the righting reflex was observed in 40 of 102 subjects (39%), tonic postures in 25 of 102 subjects (25%) and clonic movement in 6 of 102 (6%).³ In a separate analysis of 35 Youtube™(Google Inc, Mountain View, CA;) videos showing concussive events, Hosseini et al. reported 23 instances (66%) of tonic posturing known as the fencing response. There were no noted tonic-clonic convulsive events.¹² Based on these studies, it can be concluded that concussive convulsion manifestations, including posturing, clonic movements and the righting reflex occur commonly in the immediate post-injury period, while tonic-clonic convulsions are a rarer consequence of head injury.