to treat with a beta-blocker and angiotensin-converting enzyme inhibitor, hold out of sports for at least 3 to 6 months, perhaps implant an implantable loop recorder so that a specific diagnosis could be made if another episode of syncope occurred, and then repeat the MRI looking for resolution of delayed enhancement. Pressure to play (athlete, coach, and parent) can influence medical decision making and steer the decision away from the athlete’s best interest. Case 5: A 23-year-old male second-year medical student completed a maximal-effort Wingate test as part of a research project; prior V˙O2max testing demonstrated a maximum of 55 mLIkgj1Iminj1. Immediately after the 30-s test, the student was extremely nauseous and rapidly exited the bike to move to a trash can to vomit; after two short wobbly steps, he collapsed to the ground. He was attended to immediately by the exercise staff in attendance; he had an estimated loss of consciousness for less than 30 s and had a first set of vital signs of heart rate of 140 bpm and BP of 110/60. There was no observed seizure activity and no prior complaint of chest pain. A subsequent evaluation in the sports medicine clinic demonstrated normal clinical examination results with no history of syncope; ECG results demonstrated early repolarization variation in the precordial leads. As the syncopal event occurred immediately after exercise, a treadmill stress test and echocardiogram were performed; the student completed 17 min of Bruce protocol and had a normal echocardiogram results. The diagnosis was postexertional syncope secondary to orthostatic hypotension. Key Point: Syncope during or immediately after exercise is always concerning and warrants conscientious examination to rule out structural cardiovascular disease. Intense anaerobic exercise, which can be seen in maximal efforts like the Wingate test or weightlifting, can precipitate syncope through orthostatic hypotension and a central effect of hypocapnia leading to, or aggravating, cerebral hypoperfusion. The history of the event provides not only insight into the diagnosis but also important opportunities for prudent recommendations for prevention.
Syncope in Athletes of Neurological Origin: 2B. From Personal History and Physical Examination Sections Chad A. Asplund, MD, MPH, FACSM and Jeffrey S. Kutcher, MD Personal History: Have You Ever Nearly Lost or Actually Lost Consciousness? The History (Regarding Neurologic Causes) To determine the importance of a positive answer to this question, the following questions should be asked for each episode of loss of consciousness:
1. Was consciousness completely lost? If so, for how long? 2. Was head trauma involved? 256
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3. Was the episode witnessed? What did observers say happened? 4. Was a convulsion involved? If so, what was the duration of the convulsion and how long was the postictal period? 5. Was the episode preceded by fear, pain, prolonged standing, psychologic stress, or a medical procedure? 6. Was the episode preceded by a headache or visual symptoms? 7. Was the episode preceded by heart palpitations, lightheadedness, or tunnel vision? 8. Was the episode concurrent with the use of medications, performance enhancing substances, or illicit drugs? The first priority in the evaluation of a patient with history of loss of consciousness begins with thorough and directed history examination. It is imperative that the evaluator differentiate true syncope with transient loss of consciousness from presyncope, where consciousness is not lost. Presyncope is rarely caused by neurologic disease alone and may be a manifestation of cardiac disease, anxiety, or the side effect of a medication or supplement. If there is any concern for cardiac etiology, then at a minimum, an electrocardiogram should be performed before the neurologic evaluation continues. The second priority of the history examination is to focus on circumstances immediately before the event, the onset, the event itself, and the postevent period. Various aspects surrounding the event may help establish the diagnosis. A prodrome, postsyncopal fatigue, amnesia, or focal neurologic deficits will point the evaluator toward a neurogenic cause. Episodes of neurally mediated syncope are typically associated with postepisode fatigue and weakness, whereas the absence of a prodrome is more consistent with cardiac arrhythmia. Sensory auras, de´ja` vu or jamais vu, postictal confusion, or focal neurologic signs or symptoms all suggest a neurologic cause. Head trauma preceding loss of consciousness is highly suggestive of brain injury, such as concussion, cerebral contusion, or intracranial hemorrhage. Next, the observations of witnesses may be extremely helpful. Preevent behaviors, such as unresponsiveness or automatisms, are suggestive of seizure, as is tonic-clonic, convulsive activity. It is important to recognize that seizurelike activity that occurs prior to loss of consciousness or postural tone is more consistent with seizure while a convulsion that occurs after the patient has fallen to the ground may be the final common manifestation of cerebral hypoperfusion. Incontinence of bowel or bladder does not reliably differentiate neurologic from cardiac causes. Finally, medical history can be very helpful. History of psychologic or psychiatric disorders may point to a nonorganic cause of syncope such as a conversion disorder. History of migraine headaches should be considered as another possible cause for neurogenic syncope. In most patients, the cause of syncope can be determined with great accuracy from careful history and physical examination. However, the exact mechanism of syncope remains unexplained in approximately 35% of episodes and a neurologic cause for syncope is found in fewer than 10% of cases (1). Cardiovascular Preparticipation Evaluation
Copyright © 2015 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
The Physical Examination A complete neurologic examination should be performed following a suspected neurogenic cause of syncope. Abnormalities of cognition and speech, visual fields, motor strength, sensation, tremor, and gait suggest an underlying neurologic disorder. The Physical Examination If an underlying neurologic disorder is suspected, further study and subspecialty consultation should be considered. If the event was preceded by head trauma with subsequent neurologic deficits, a computed tomography (CT) scan of the head to assess for gross intracranial pathology should be considered, but magnetic resonance imaging (MRI) will yield better resolution for structural or brain tissue pathology. Finally, if seizure activity is suspected, an electroencephalogram (EEG) may be warranted. If the event was preceded by fear, pain, prolonged standing, psychologic stress, or a medical procedure and the athlete has normal physical examination results, the diagnosis of vasovagal syncope or neurally mediated syncope can be made. CASE REPORTS Case 1: Cross-Country Runner with Loss of Consciousness while Running A 15-year-old male cross country runner reported loss of consciousness with exercise during his PPE. Since he was uncertain of the details, his coaches were questioned. They said he stopped running shortly after beginning the second of a two-lap course, had a contusion and laceration to the forehead, and was confused. He denies recall of what happened after he slipped, but the coaches stated that he had fallen, struck his head on a rock, and appeared to have lost consciousness for several seconds. They denied seeing any seizure-like activity. Key Point: Concussions can occur in sports other than traditional ‘‘contact/collision’’ sports and are a common cause of loss of consciousness in athletes. Case 2: Track Athlete with Loss of Consciousness during a Race A 21-year-old female track runner reported loss of consciousness during a 200-m race during her PPE. Her coaches said she was prone and unresponsive on the track, with tremulous activity in both upper and lower extremities lasting about 90 s, after which she was responsive and aware of her situation. She reported having three similar episodes while in high school. There were no other significant personal or family medical history, medication, or supplement use. Neurologic examination result was normal except for the transient inability to move her left arm. Brain imaging (CT and MRI) results were normal. When questioned about stress, she stated she had a previous injury, which occurred in the middle of a championship 200-m race, and she worried constantly about being injured again and unable to compete. Following 48 h of cognitive behavioral therapy, she improved and was able to move all extremities. She was diagnosed with conversion disorder as the cause of her ‘‘psychogenic’’ syncope. Key Point: Apparent loss of consciousness may be psychologic in origin, especially with a history of abuse, stressful www.acsm-csmr.org
incident, or anxiety/depression. Most athletes will improve with psychotherapy. Ninety seconds of ‘‘seizure-like’’ activity is much longer that the hypoxia-induced convulsions of cardiac arrhythmias. Case 3: Football Athlete with Loss of Consciousness after Practice A 19-year-old football player has a witnessed loss of consciousness at the end of practice on an extremely warm August day. He was walking to the locker room when he was noted to wander away from the team briefly before falling to the ground in a prone position. His teammates were the first on the scene, and they described him as being clearly unconscious. He then had a brief stiffening of all four extremities that lasted 15 s. He was unconscious for nearly 5 min in total, during which time, he was noted to have sparse, shallow breathing. Upon regaining consciousness, he was combative for 5 min and acutely disoriented for 25 min. He was taken to a local emergency room via emergency medical services where he was found to be fully oriented, tired, and diffusely sore upon arrival, almost 40 min after the initial loss of consciousness. A head CT in the emergency room yielded normal results, as were basic serum laboratory evaluations. He was discharged home with a normal neurologic examination result, feeling only fatigued and sore. Follow-up MRI and EEG were performed 3 d later, and both yielded normal results. Further history examination revealed no previous similar episodes and no seizure risk factors. He was diagnosed with having a provoked seizure secondary to extreme fatigue, dehydration, and possibly increased core body temperature. He was not started on antiepileptic medication. Key Point: Exertional heat stroke (EHS) should be immediately ruled out on site and immediate on-site cooling should be considered. Preevent confusion, prolonged loss of consciousness (930 s), and prolonged confusion (25 min) are all consistent with seizure and EHS. Both MRI and EEG results are frequently normal in these cases, even if epilepsy is the root cause. In this case, the diagnosis of epilepsy cannot be made, as this is his first seizure and it may have been provoked. Treatment with antiepileptic medications can be considered but is not clearly indicated. References 1. Kapoor W. Syncope. N. Engl. J. Med. 2000; 343:1856Y62. 2. Kosinski D, Grubb BP, Karas BJ, Frederick S. Exercise-induced neurocardiogenic syncope: clinical data, pathophysiological aspects, and potential role of tilt table testing. Europace. 2000; 2:77Y82.
3A. Personal History: Have You Ever Had Excessive Shortness of Breath or Fatigue with Exercise beyond What Is Expected for Your Level of Fitness? Francois Haddad, MD, Gherardo Finocchiaro, MD, and Jonathan Myers, PhD The following questions can help distinguish cardiovascular from pulmonary or other causes of dyspnea. The history along with physical examination and cardiopulmonary studies Current Sports Medicine Reports
Copyright © 2015 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
257
Syncope in Athletes of Neurological Origin: 2B. From Personal History and Physical Examination Sections Chad A. Asplund, MD, MPH, FACSM and Jeffrey S. Kutcher, MD Personal History: Have You Ever Nearly Lost or Actually Lost Consciousness? The History (Regarding Neurologic Causes) To determine the importance of a positive answer to this question, the following questions should be asked for each episode of loss of consciousness:
1. Was consciousness completely lost? If so, for how long? 2. Was head trauma involved? 256
Volume 14 & Number 3 & May/June 2015
3. Was the episode witnessed? What did observers say happened? 4. Was a convulsion involved? If so, what was the duration of the convulsion and how long was the postictal period? 5. Was the episode preceded by fear, pain, prolonged standing, psychologic stress, or a medical procedure? 6. Was the episode preceded by a headache or visual symptoms? 7. Was the episode preceded by heart palpitations, lightheadedness, or tunnel vision? 8. Was the episode concurrent with the use of medications, performance enhancing substances, or illicit drugs? The first priority in the evaluation of a patient with history of loss of consciousness begins with thorough and directed history examination. It is imperative that the evaluator differentiate true syncope with transient loss of consciousness from presyncope, where consciousness is not lost. Presyncope is rarely caused by neurologic disease alone and may be a manifestation of cardiac disease, anxiety, or the side effect of a medication or supplement. If there is any concern for cardiac etiology, then at a minimum, an electrocardiogram should be performed before the neurologic evaluation continues. The second priority of the history examination is to focus on circumstances immediately before the event, the onset, the event itself, and the postevent period. Various aspects surrounding the event may help establish the diagnosis. A prodrome, postsyncopal fatigue, amnesia, or focal neurologic deficits will point the evaluator toward a neurogenic cause. Episodes of neurally mediated syncope are typically associated with postepisode fatigue and weakness, whereas the absence of a prodrome is more consistent with cardiac arrhythmia. Sensory auras, de´ja` vu or jamais vu, postictal confusion, or focal neurologic signs or symptoms all suggest a neurologic cause. Head trauma preceding loss of consciousness is highly suggestive of brain injury, such as concussion, cerebral contusion, or intracranial hemorrhage. Next, the observations of witnesses may be extremely helpful. Preevent behaviors, such as unresponsiveness or automatisms, are suggestive of seizure, as is tonic-clonic, convulsive activity. It is important to recognize that seizurelike activity that occurs prior to loss of consciousness or postural tone is more consistent with seizure while a convulsion that occurs after the patient has fallen to the ground may be the final common manifestation of cerebral hypoperfusion. Incontinence of bowel or bladder does not reliably differentiate neurologic from cardiac causes. Finally, medical history can be very helpful. History of psychologic or psychiatric disorders may point to a nonorganic cause of syncope such as a conversion disorder. History of migraine headaches should be considered as another possible cause for neurogenic syncope. In most patients, the cause of syncope can be determined with great accuracy from careful history and physical examination. However, the exact mechanism of syncope remains unexplained in approximately 35% of episodes and a neurologic cause for syncope is found in fewer than 10% of cases (1). Cardiovascular Preparticipation Evaluation
Copyright © 2015 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
The Physical Examination A complete neurologic examination should be performed following a suspected neurogenic cause of syncope. Abnormalities of cognition and speech, visual fields, motor strength, sensation, tremor, and gait suggest an underlying neurologic disorder. The Physical Examination If an underlying neurologic disorder is suspected, further study and subspecialty consultation should be considered. If the event was preceded by head trauma with subsequent neurologic deficits, a computed tomography (CT) scan of the head to assess for gross intracranial pathology should be considered, but magnetic resonance imaging (MRI) will yield better resolution for structural or brain tissue pathology. Finally, if seizure activity is suspected, an electroencephalogram (EEG) may be warranted. If the event was preceded by fear, pain, prolonged standing, psychologic stress, or a medical procedure and the athlete has normal physical examination results, the diagnosis of vasovagal syncope or neurally mediated syncope can be made. CASE REPORTS Case 1: Cross-Country Runner with Loss of Consciousness while Running A 15-year-old male cross country runner reported loss of consciousness with exercise during his PPE. Since he was uncertain of the details, his coaches were questioned. They said he stopped running shortly after beginning the second of a two-lap course, had a contusion and laceration to the forehead, and was confused. He denies recall of what happened after he slipped, but the coaches stated that he had fallen, struck his head on a rock, and appeared to have lost consciousness for several seconds. They denied seeing any seizure-like activity. Key Point: Concussions can occur in sports other than traditional ‘‘contact/collision’’ sports and are a common cause of loss of consciousness in athletes. Case 2: Track Athlete with Loss of Consciousness during a Race A 21-year-old female track runner reported loss of consciousness during a 200-m race during her PPE. Her coaches said she was prone and unresponsive on the track, with tremulous activity in both upper and lower extremities lasting about 90 s, after which she was responsive and aware of her situation. She reported having three similar episodes while in high school. There were no other significant personal or family medical history, medication, or supplement use. Neurologic examination result was normal except for the transient inability to move her left arm. Brain imaging (CT and MRI) results were normal. When questioned about stress, she stated she had a previous injury, which occurred in the middle of a championship 200-m race, and she worried constantly about being injured again and unable to compete. Following 48 h of cognitive behavioral therapy, she improved and was able to move all extremities. She was diagnosed with conversion disorder as the cause of her ‘‘psychogenic’’ syncope. Key Point: Apparent loss of consciousness may be psychologic in origin, especially with a history of abuse, stressful www.acsm-csmr.org
incident, or anxiety/depression. Most athletes will improve with psychotherapy. Ninety seconds of ‘‘seizure-like’’ activity is much longer that the hypoxia-induced convulsions of cardiac arrhythmias. Case 3: Football Athlete with Loss of Consciousness after Practice A 19-year-old football player has a witnessed loss of consciousness at the end of practice on an extremely warm August day. He was walking to the locker room when he was noted to wander away from the team briefly before falling to the ground in a prone position. His teammates were the first on the scene, and they described him as being clearly unconscious. He then had a brief stiffening of all four extremities that lasted 15 s. He was unconscious for nearly 5 min in total, during which time, he was noted to have sparse, shallow breathing. Upon regaining consciousness, he was combative for 5 min and acutely disoriented for 25 min. He was taken to a local emergency room via emergency medical services where he was found to be fully oriented, tired, and diffusely sore upon arrival, almost 40 min after the initial loss of consciousness. A head CT in the emergency room yielded normal results, as were basic serum laboratory evaluations. He was discharged home with a normal neurologic examination result, feeling only fatigued and sore. Follow-up MRI and EEG were performed 3 d later, and both yielded normal results. Further history examination revealed no previous similar episodes and no seizure risk factors. He was diagnosed with having a provoked seizure secondary to extreme fatigue, dehydration, and possibly increased core body temperature. He was not started on antiepileptic medication. Key Point: Exertional heat stroke (EHS) should be immediately ruled out on site and immediate on-site cooling should be considered. Preevent confusion, prolonged loss of consciousness (930 s), and prolonged confusion (25 min) are all consistent with seizure and EHS. Both MRI and EEG results are frequently normal in these cases, even if epilepsy is the root cause. In this case, the diagnosis of epilepsy cannot be made, as this is his first seizure and it may have been provoked. Treatment with antiepileptic medications can be considered but is not clearly indicated. References 1. Kapoor W. Syncope. N. Engl. J. Med. 2000; 343:1856Y62. 2. Kosinski D, Grubb BP, Karas BJ, Frederick S. Exercise-induced neurocardiogenic syncope: clinical data, pathophysiological aspects, and potential role of tilt table testing. Europace. 2000; 2:77Y82.
3A. Personal History: Have You Ever Had Excessive Shortness of Breath or Fatigue with Exercise beyond What Is Expected for Your Level of Fitness? Francois Haddad, MD, Gherardo Finocchiaro, MD, and Jonathan Myers, PhD The following questions can help distinguish cardiovascular from pulmonary or other causes of dyspnea. The history along with physical examination and cardiopulmonary studies Current Sports Medicine Reports
Copyright © 2015 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
257
