CASE REPORT
Intracranial Arteriovenous Malformation in a College Football Player and Return-to-Play Considerations Michael S. Smith, MD, PharmD,* William A. Friedman, MD,† Kristy B. Smith, MD,‡ Anthony N. Pass, Sr, MEd, ATC, LAT, CSCS,§ and James R. Clugston, MD, MS‡
Abstract: The reported prevalence rates of arteriovenous malformations (AVMs) in the general population range from 0.001% to 0.50%. The following case describes the initial presentation of hemorrhage from an intracranial AVM in an 18-year-old college football player. It also discusses treatment of the AVM with stereotactic radiosurgery and successful return to football 17 months after radiosurgery (18.5 months after initial presentation). It is the first published description of return to contact sports after stereotactic radiosurgery for intracranial AVM. Key Words: brain arteriovenous malformation, AVM, brain hemorrhage, radiosurgery for cerebral arteriovenous malformation, intracranial vascular malformations (Clin J Sport Med 2014;24:e62–e64)
INTRODUCTION Intracranial arteriovenous malformations (AVMs) are abnormal consolidations of dilated arteries and veins, within the brain, with a loss of normal vascular architecture.1 This abnormal architecture lacks a capillary bed resulting in arteriovenous shunting from arteries directly to veins.2 This arteriovenous shunting creates altered vascular connections that are prone to rupture.1 Reported prevalence rates of AVMs in the general population range from 0.001% to 0.50%.1,3 Intracranial arteriovenous malformations typically present in patients 20 to 40 years old with intracranial hemorrhage being the most common manifestation (.50% of cases)4 followed by seizures (20%–25%) and headaches without hemorrhage (15%).5 This case report describes the sudden presentation of an AVM in a college football player, treatment with stereotactic radiosurgery, and successful return to play.
CASE REPORT An 18-year-old African American male college football player was running in an off-season, noncontact workout when he suddenly developed a throbbing headache with associated posterior neck pain. Submitted for publication February 15, 2013; accepted October 14, 2013. From the *Department of Orthopedics and Rehabilitation; †Department of Neurosurgery; ‡Department of Community Health and Family Medicine, University of Florida, Gainesville, Florida; and §Athletic Association, Texas Tech University. The authors report no conflicts of interest to disclose. Corresponding Author: Michael S. Smith, MD, PharmD, Department of Orthopedics and Rehabilitation, University of Florida, 3450 Hull Rd, Gainesville, FL 32607 ([email protected]fl.edu). Copyright © 2014 by Lippincott Williams & Wilkins
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He reported this to the athletic trainer and was removed from activity. When evaluated by the team physician, he denied weakness, fever, nausea, blurry vision, or paresthesias. He had consumed a caffeine energy drink earlier in the day but denied other drug or medication use. He denied history of recurrent headaches, but did recall having a headache several weeks before which resolved. He admitted having 2 football-related concussions 4 years before with no residual symptoms. He had no personal or family history of stroke, seizure, or other brain conditions. On physical examination, he was afebrile and vital signs were stable. He was alert, oriented, and cooperative. Cardiovascular and respiratory examinations were normal. Musculoskeletal examination revealed no head or neck tenderness with palpation, full neck range of motion, 5/5 strength in extremities, no paresthesias and negative Spurling’s maneuver. He did experience significant neck and posterior head pain with resisted neck extension. Neurologically, he had normal attention, concentration, and cranial nerve examination including visual fields. Light touch sensation and proprioception were intact in all extremities. Deep tendon reflexes were 1+ and equal bilaterally. Coordination with finger-to-nose and heel-to-shin was intact. Romberg test was normal. Babinski reflex was absent, and both Brudzinski and Kernig sign were negative. The athlete was held from activity, given 650 mg of acetaminophen, and re-evaluated 30 minutes later. His headache intensified, and he was sent to the emergency department where a noncontrast computed tomography (CT) of the head showed an acute intraparenchymal hemorrhage of the right thalamus with intraventricular extension into both lateral ventricles, third ventricle, and fourth ventricle with minor ventriculomegaly. He was admitted to the neurosurgical ICU. Further imaging with CT angiography confirmed the initial findings and revealed a right thalamic AVM measuring 1.8 cm in diameter being fed by a lenticulostriate artery and drained by the right internal cerebral vein. The patient was observed and felt to be stable, thus, neurosurgical intervention was withheld. He showed clinical improvement over several days, and a magnetic resonance angiography performed before discharge on day 5 showed AVM (Figure 1) and decreased intraventricular blood. He was scheduled for outpatient follow-up with neurosurgery to discuss long-term options. Before this follow-up, he developed a headache on day 9 and presented to an out-of-town hospital where a CT revealed another hemorrhagic event in the same location. He was observed on their neurosurgical service and after 4 days was discharged with instructions to follow-up at our institution. At this follow-up, a multidisciplinary team involving neurosurgery and radiation oncology determined that the AVM’s location was not favorable for traditional neurosurgery without severe risk of neurological deficit. Stereotactic radiosurgery, which targets hundreds of small beams of radiation on the AVM nidus resulting in injury to the endothelium and eventually thickening of the vessel walls until occlusion occurs, was felt to be the best treatment option. This procedure was performed 6 weeks after his initial hemorrhage. Clin J Sport Med Volume 24, Number 6, November 2014
Clin J Sport Med Volume 24, Number 6, November 2014
FIGURE 1. Axial T2-weighted magnetic resonance angiography image of the arteriovenous malformation (arrow) in the right thalamus during initial hospitalization.
He wanted to play football again but initially was held from all physical activity for 2 months. He was then allowed to serve as a youth summer camp counselor but allowed only light physical activity. He had no headaches or other symptoms; and when he returned (5 months from radiosurgery), he was allowed to begin bodyweight exercises only—push-ups, sit-ups, pull-ups, jogging. At 6 months after radiosurgery, he was advanced to individual weight training workouts. He continued these throughout the fall; and at 9.5 months, he was allowed to rejoin the team for winter conditioning. At 11.5 months (13 months after initial presentation), he had magnetic resonance imaging (MRI) that showed 90% AVM resolution. He did not participate in spring practice. A second MRI demonstrating further resolution of the AVM was performed at 15 months after radiosurgery (Figure 2). At 17 months (18.5 months from initial presentation), he was cleared to resume all football activities. He then completed an entire season, including a post-season bowl game, successfully. He started several games and saw playing time in others.
DISCUSSION The risk of initial hemorrhage from untreated AVMs is estimated at 4%/year.6 The risk of subsequent hemorrhage is 6% during the first year and then returns to baseline.7 Ó 2014 Lippincott Williams & Wilkins
Intracranial AVM in a College Football Player
FIGURE 2. Axial T2-weighted magnetic resonance angiography image of the thalamic arteriovenous malformation (arrow) 15 months after stereotactic radiosurgery demonstrating near complete resolution.
Stereotactic radiosurgery has been used over 20 years to treat cerebral AVMs, producing complete obliteration in 80% to 90% of patients within 2 to 3 years when AVMs are #3 cm.4 Maruyama et al8 reported that the risk of hemorrhage after radiosurgery declined by 54% during the time between treatment and obliteration, and by 88% after obliteration. The risk of hemorrhage after obliteration is low but not completely eliminated.7 Determining return to play in this case was difficult because there were no previously published reports of resumption of contact activities after hemorrhagic intracranial AVM treated with radiosurgery. Return was based on neurosurgical knowledge and imaging findings. It was felt that waiting for AVM obliteration would produce the least chance of rehemorrhage. We believed if there was uncomplicated clinical recovery from radiosurgery and obliteration of the lesion on imaging, a return to football would be reasonable. The return-to-play decision included discussions between the athlete, family, athletic trainers, and physicians. The athlete and family were aware that the rehemorrhage risk after radiosurgery would be small but not zero. As noted above, our athlete completed an entire football season without complications from his AVM. This report represents the first described case of successful return to contact sports after radiosurgery for intracranial AVM. www.cjsportmed.com |
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Smith et al
REFERENCES 1. Friedlander RM. Arteriovenous malformations of the brain. N Engl J Med. 2007;356:2704–2712. 2. Mohr JP, Pile-Spellman J, Stein BM. Arteriovenous malformations and other vascular anomalies. In: Barnett JM, Mohn JP, Stein BM, et al, eds. Stroke. Pathophysiology, Diagnosis, and Management. 3rd ed. Philadelphia, PA: Churchill Livingstone; 1998:725–750. 3. Fleetwood IG, Steinberg GK. Arteriovenous malformations. Lancet. 2002; 359:863–873. 4. Ogilvy CS, Stieg PE, Awad I, et al. AHA Scientific Statement: Recommendations for the management of intracranial arteriovenous malformations: a statement for healthcare professionals from a special writing group
e64
| www.cjsportmed.com
5. 6.
7. 8.
of the Stroke Council, American Stroke Association. Stroke. 2001;32: 1458. Brown RD, Wiebers DO, Forbes G, et al. The natural history of unruptured intracranial anteriovenous malformations. J Neurosurg. 1988;68:352–357. Ondra SL, Troupp H, George ED, et al. The natural history of symptomatic arteriovenous malformations of the brain: a 24-year follow-up assessment. J Neurosurg. 1990;73:387–391. Graf CJ, Perret GE, Torner JC. Bleeding from cerebral arteriovenous malformations as part of their natural history. J Neurosurg. 1983;58:331–337. Maruyama K, Kawahara N, Shin M, et al. The risk of hemorrhage after radiosurgery for cerebral arteriovenous malformations. N Engl J Med. 2005;352:146–153.
Ó 2014 Lippincott Williams & Wilkins
Intracranial Arteriovenous Malformation in a College Football Player and Return-to-Play Considerations Michael S. Smith, MD, PharmD,* William A. Friedman, MD,† Kristy B. Smith, MD,‡ Anthony N. Pass, Sr, MEd, ATC, LAT, CSCS,§ and James R. Clugston, MD, MS‡
Abstract: The reported prevalence rates of arteriovenous malformations (AVMs) in the general population range from 0.001% to 0.50%. The following case describes the initial presentation of hemorrhage from an intracranial AVM in an 18-year-old college football player. It also discusses treatment of the AVM with stereotactic radiosurgery and successful return to football 17 months after radiosurgery (18.5 months after initial presentation). It is the first published description of return to contact sports after stereotactic radiosurgery for intracranial AVM. Key Words: brain arteriovenous malformation, AVM, brain hemorrhage, radiosurgery for cerebral arteriovenous malformation, intracranial vascular malformations (Clin J Sport Med 2014;24:e62–e64)
INTRODUCTION Intracranial arteriovenous malformations (AVMs) are abnormal consolidations of dilated arteries and veins, within the brain, with a loss of normal vascular architecture.1 This abnormal architecture lacks a capillary bed resulting in arteriovenous shunting from arteries directly to veins.2 This arteriovenous shunting creates altered vascular connections that are prone to rupture.1 Reported prevalence rates of AVMs in the general population range from 0.001% to 0.50%.1,3 Intracranial arteriovenous malformations typically present in patients 20 to 40 years old with intracranial hemorrhage being the most common manifestation (.50% of cases)4 followed by seizures (20%–25%) and headaches without hemorrhage (15%).5 This case report describes the sudden presentation of an AVM in a college football player, treatment with stereotactic radiosurgery, and successful return to play.
CASE REPORT An 18-year-old African American male college football player was running in an off-season, noncontact workout when he suddenly developed a throbbing headache with associated posterior neck pain. Submitted for publication February 15, 2013; accepted October 14, 2013. From the *Department of Orthopedics and Rehabilitation; †Department of Neurosurgery; ‡Department of Community Health and Family Medicine, University of Florida, Gainesville, Florida; and §Athletic Association, Texas Tech University. The authors report no conflicts of interest to disclose. Corresponding Author: Michael S. Smith, MD, PharmD, Department of Orthopedics and Rehabilitation, University of Florida, 3450 Hull Rd, Gainesville, FL 32607 ([email protected]fl.edu). Copyright © 2014 by Lippincott Williams & Wilkins
e62
| www.cjsportmed.com
He reported this to the athletic trainer and was removed from activity. When evaluated by the team physician, he denied weakness, fever, nausea, blurry vision, or paresthesias. He had consumed a caffeine energy drink earlier in the day but denied other drug or medication use. He denied history of recurrent headaches, but did recall having a headache several weeks before which resolved. He admitted having 2 football-related concussions 4 years before with no residual symptoms. He had no personal or family history of stroke, seizure, or other brain conditions. On physical examination, he was afebrile and vital signs were stable. He was alert, oriented, and cooperative. Cardiovascular and respiratory examinations were normal. Musculoskeletal examination revealed no head or neck tenderness with palpation, full neck range of motion, 5/5 strength in extremities, no paresthesias and negative Spurling’s maneuver. He did experience significant neck and posterior head pain with resisted neck extension. Neurologically, he had normal attention, concentration, and cranial nerve examination including visual fields. Light touch sensation and proprioception were intact in all extremities. Deep tendon reflexes were 1+ and equal bilaterally. Coordination with finger-to-nose and heel-to-shin was intact. Romberg test was normal. Babinski reflex was absent, and both Brudzinski and Kernig sign were negative. The athlete was held from activity, given 650 mg of acetaminophen, and re-evaluated 30 minutes later. His headache intensified, and he was sent to the emergency department where a noncontrast computed tomography (CT) of the head showed an acute intraparenchymal hemorrhage of the right thalamus with intraventricular extension into both lateral ventricles, third ventricle, and fourth ventricle with minor ventriculomegaly. He was admitted to the neurosurgical ICU. Further imaging with CT angiography confirmed the initial findings and revealed a right thalamic AVM measuring 1.8 cm in diameter being fed by a lenticulostriate artery and drained by the right internal cerebral vein. The patient was observed and felt to be stable, thus, neurosurgical intervention was withheld. He showed clinical improvement over several days, and a magnetic resonance angiography performed before discharge on day 5 showed AVM (Figure 1) and decreased intraventricular blood. He was scheduled for outpatient follow-up with neurosurgery to discuss long-term options. Before this follow-up, he developed a headache on day 9 and presented to an out-of-town hospital where a CT revealed another hemorrhagic event in the same location. He was observed on their neurosurgical service and after 4 days was discharged with instructions to follow-up at our institution. At this follow-up, a multidisciplinary team involving neurosurgery and radiation oncology determined that the AVM’s location was not favorable for traditional neurosurgery without severe risk of neurological deficit. Stereotactic radiosurgery, which targets hundreds of small beams of radiation on the AVM nidus resulting in injury to the endothelium and eventually thickening of the vessel walls until occlusion occurs, was felt to be the best treatment option. This procedure was performed 6 weeks after his initial hemorrhage. Clin J Sport Med Volume 24, Number 6, November 2014
Clin J Sport Med Volume 24, Number 6, November 2014
FIGURE 1. Axial T2-weighted magnetic resonance angiography image of the arteriovenous malformation (arrow) in the right thalamus during initial hospitalization.
He wanted to play football again but initially was held from all physical activity for 2 months. He was then allowed to serve as a youth summer camp counselor but allowed only light physical activity. He had no headaches or other symptoms; and when he returned (5 months from radiosurgery), he was allowed to begin bodyweight exercises only—push-ups, sit-ups, pull-ups, jogging. At 6 months after radiosurgery, he was advanced to individual weight training workouts. He continued these throughout the fall; and at 9.5 months, he was allowed to rejoin the team for winter conditioning. At 11.5 months (13 months after initial presentation), he had magnetic resonance imaging (MRI) that showed 90% AVM resolution. He did not participate in spring practice. A second MRI demonstrating further resolution of the AVM was performed at 15 months after radiosurgery (Figure 2). At 17 months (18.5 months from initial presentation), he was cleared to resume all football activities. He then completed an entire season, including a post-season bowl game, successfully. He started several games and saw playing time in others.
DISCUSSION The risk of initial hemorrhage from untreated AVMs is estimated at 4%/year.6 The risk of subsequent hemorrhage is 6% during the first year and then returns to baseline.7 Ó 2014 Lippincott Williams & Wilkins
Intracranial AVM in a College Football Player
FIGURE 2. Axial T2-weighted magnetic resonance angiography image of the thalamic arteriovenous malformation (arrow) 15 months after stereotactic radiosurgery demonstrating near complete resolution.
Stereotactic radiosurgery has been used over 20 years to treat cerebral AVMs, producing complete obliteration in 80% to 90% of patients within 2 to 3 years when AVMs are #3 cm.4 Maruyama et al8 reported that the risk of hemorrhage after radiosurgery declined by 54% during the time between treatment and obliteration, and by 88% after obliteration. The risk of hemorrhage after obliteration is low but not completely eliminated.7 Determining return to play in this case was difficult because there were no previously published reports of resumption of contact activities after hemorrhagic intracranial AVM treated with radiosurgery. Return was based on neurosurgical knowledge and imaging findings. It was felt that waiting for AVM obliteration would produce the least chance of rehemorrhage. We believed if there was uncomplicated clinical recovery from radiosurgery and obliteration of the lesion on imaging, a return to football would be reasonable. The return-to-play decision included discussions between the athlete, family, athletic trainers, and physicians. The athlete and family were aware that the rehemorrhage risk after radiosurgery would be small but not zero. As noted above, our athlete completed an entire football season without complications from his AVM. This report represents the first described case of successful return to contact sports after radiosurgery for intracranial AVM. www.cjsportmed.com |
e63
Clin J Sport Med Volume 24, Number 6, November 2014
Smith et al
REFERENCES 1. Friedlander RM. Arteriovenous malformations of the brain. N Engl J Med. 2007;356:2704–2712. 2. Mohr JP, Pile-Spellman J, Stein BM. Arteriovenous malformations and other vascular anomalies. In: Barnett JM, Mohn JP, Stein BM, et al, eds. Stroke. Pathophysiology, Diagnosis, and Management. 3rd ed. Philadelphia, PA: Churchill Livingstone; 1998:725–750. 3. Fleetwood IG, Steinberg GK. Arteriovenous malformations. Lancet. 2002; 359:863–873. 4. Ogilvy CS, Stieg PE, Awad I, et al. AHA Scientific Statement: Recommendations for the management of intracranial arteriovenous malformations: a statement for healthcare professionals from a special writing group
e64
| www.cjsportmed.com
5. 6.
7. 8.
of the Stroke Council, American Stroke Association. Stroke. 2001;32: 1458. Brown RD, Wiebers DO, Forbes G, et al. The natural history of unruptured intracranial anteriovenous malformations. J Neurosurg. 1988;68:352–357. Ondra SL, Troupp H, George ED, et al. The natural history of symptomatic arteriovenous malformations of the brain: a 24-year follow-up assessment. J Neurosurg. 1990;73:387–391. Graf CJ, Perret GE, Torner JC. Bleeding from cerebral arteriovenous malformations as part of their natural history. J Neurosurg. 1983;58:331–337. Maruyama K, Kawahara N, Shin M, et al. The risk of hemorrhage after radiosurgery for cerebral arteriovenous malformations. N Engl J Med. 2005;352:146–153.
Ó 2014 Lippincott Williams & Wilkins
