Management of an Adolescent Athlete with Sports-Related Concussion and Intraparenchymal Hemorrhage

Introduction Sports-related concussion (SRC) has been historically viewed as an injury that results in temporary impairment in neurological functioning in the absence of structural brain injury (1). However, in select cases, conventional neuroimaging studies can reveal traumatic findings that present a challenge for physicians who must decide, in the absence of evidence-based guidelines, whether the athlete is safe to return to contact and collision sports (2–4). Case Report A 16-year-old male with a history of two previous concussions and no history of prior seizures or traumatic brain injury (TBI) sustained a head injury during a soccer game. The athlete was attempting to head the ball when he fell backwards and struck his head on the goalpost. After 1 min of lost consciousness, the patient had a witnessed 30-s generalized tonic-clonic seizure that was not associated with any tongue biting or urinary incontinence. The patient regained consciousness at the scene and was transported to a hospital, where computed tomography (CT) revealed several hyperdensities located within both frontal lobes and the left parietal lobe consistent with acute intraparenchymal hemorrhages (Fig. 1A). The patient was monitored in the hospital for 4 d and discharged to a multidisciplinary pediatric concussion program.Figure: Left image (A): Axial computerized tomography imaging demonstrates a left frontal focal white matter hyperdensity suspicious for acute intraparenchymal hemorrhage (white arrow). Right image (B): Axial susceptibility-weighted MRI demonstrates multifocal acute cortical and subcortical intraparenchymal hemorrhages within bilateral frontal lobes, left temporal and occipital lobes (white arrows). Informed written consent from the patient, and his parent was obtained for use of these images.In consultation with a neurosurgeon the next day, the patient reported concussion symptoms including headache, dizziness, fatigue, light sensitivity, difficulty remembering, and difficulty falling asleep. The patient’s Post-Concussion Symptom Scale score was 17. There was no prior history of attention-deficit hyperactivity disorder or learning disorder. Neurological examination, including cranial nerve, motor, sensory, cerebellar, reflex, cervical spine, and balance testing, was normal. Vestibuloocular examination revealed a near point convergence of 12 cm and saccadic smooth pursuits. The patient was diagnosed with SRC and posttraumatic seizure and managed conservatively including recommendations to abstain from driving pending future seizure work-up and neurology consultation. Magnetic resonance imaging (MRI) of the brain demonstrated multi-focal intraparenchymal cortical and sub-cortical hemorrhages involving the bilateral frontal, temporal, and parietal lobes (Fig. 1B). One month later the patient reported a return to his neurological baseline. At three months post-injury, the patient underwent routine electroencephalography (EEG) that was normal and showed no evidence of epileptiform activity. In consultation with a neurologist, treatment with anti-epileptic medication was not recommended and the patient was allowed to resume driving. At four months post-injury, the patient underwent graded aerobic treadmill testing conducted by an exercise physiologist that revealed no symptom-limited threshold. Specifically, the patient was able to exercise to volitional exhaustion without eliciting any concussion-like symptoms at a maximum heart rate of 194 beats per minute. Initial formal neuropsychological testing performed by a clinical neuropsychologist at 4 months post-injury revealed deficits in higher order neurocognitive functioning including impairments in auditory working memory, immediate recall with prolonged interference, selective attention, verbal fluency and deductive reasoning. At 8 months post-injury the patient returned for repeat formal neuropsychological testing that revealed results that fell primarily within normal limits consistent with complete neurocognitive recovery. Neurological examination at 8 months post-injury revealed a near point convergence of 10 cm and saccadic smooth pursuits. Given the lack of visual complaints or difficulty with reading or schoolwork throughout longitudinal follow-up, it is likely that these clinical findings were longstanding and not related to the patient’s injury. Based primarily on the extent of structural brain injury on neuroimaging, the multi-disciplinary team recommended the patient avoid future contact and collision sports but acknowledged a lack of empirical evidence to support this recommendation. Discussion SRC typically manifests with physical, cognitive, sleep, and emotional symptoms reflective of temporary alterations in brain functioning; however a small proportion of patients will present with clinical features resulting from structural brain injury. Seizure-like activity in the setting of sports-related head trauma is rare but can take the form of concussive convulsions or posttraumatic seizures. Concussive convulsions are nonepileptic events that typically occur within seconds of head impact and loss of consciousness, manifest as bilateral myoclonic or tonic-clonic jerking of the extremities, and last no longer than 150 s (5). Neuroimaging and electroencephalography (EEG) studies are normal in these patients, leading some authors to propose they are caused by transient functional decerebration (5). The risk of recurrent seizures is low in these patients, therefore antiepileptic medication is not indicated, and athletes can be managed according to standard concussion return-to-play guidelines (6). In contrast, early posttraumatic seizures (occurring <7 d postinjury) are epileptic events that can manifest as focal or generalized seizures depending on the location of the associated structural brain injury (7). Management of posttraumatic seizures should only be undertaken by an experienced neurologist and include suspension of driving privileges and consideration of antiepileptic medication based on clinical, neuroimaging, and neurophysiological findings (8). Although current expert consensus opinion suggests that neuroimaging contributes little to the evaluation of SRC patients (1), the detection of traumatic abnormalities on these studies can have an impact on clinical decision making in select cases (4). The most common traumatic structural intracranial injuries reported in SRC patients are typically focal or unilateral in nature and include skull fractures, subdural and epidural hematomas (3,4,9). In contrast, neuroimaging evidence of multifocal intraparenchymal hemorrhage after adolescent sports-related head trauma is very rare. At present, there are no evidence-based guidelines to direct return-to-play and retirement decision-making in SRC patients with traumatic abnormalities detected on neuroimaging. Some authors suggest that all athletes with intracranial hemorrhage should be advised to retire from future contact and collision sports (3), whereas others suggest that in some cases return-to-play to noncollision sports can be considered for athletes at a time far removed from injury (>1 year) as long as the athlete has recovered from their clinical, neuroimaging, and cognitive baselines (2). Persistent postconcussion syndrome and persistent abnormalities on neuropsychological testing represent other indications to consider sport retirement (2–4). These reports recommend a more conservative approach in children and adolescents (2–4). The clinical decision-making process in this patient population is further complicated by the absence of a criterion standard test to confirm complete neurological recovery. Experts suggest that formal neuropsychological testing performed by a clinical neuropsychologist is helpful to document neurocognitive recovery in these patients (1). Studies also suggest that graded aerobic treadmill testing can be used to assess physiological recovery and is safe and well tolerated in pediatric SRC patients (10). In this adolescent SRC patient who presented with a posttraumatic seizure and traumatic neuroimaging findings, an EEG study was normal, and the patient did not experience any recurrent seizures over a 3-month period. As such, the neurologist decided not to recommend treatment with antiepileptic medication, and the patient was allowed to resume driving. However, despite clinical evidence of complete symptomatic, physiological, and neurocognitive recovery the findings of multifocal intraparenchymal hemorrhage on MRI led the multidisciplinary treatment team to recommend that the athlete avoid future contact and collision sports. In conclusion, the authors recommend that SRC patients with evidence of structural brain injury be managed on an individualized basis. Comprehensive multidisciplinary evaluation including formal neuropsychological testing and graded aerobic treadmill testing is recommended to provide a comprehensive assessment of neurological recovery and to help patients and parents weigh the risk of returning to contact and collision sports even in the setting of non-evidence-based sport retirement recommendations.

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