C ase R eport

doi: 10.2176/nmc.cr.2015-0351
Online April 6, 2016

Neurol Med Chir (Tokyo) 56, 580–583, 2016

Juvenile Cerebral Infarction Caused by Bow Hunter’s
Syndrome during Sport: Two Case Reports
Hiroto Kageyama,1 Shinichi Yoshimura,1 Tomoko Iida,1 Manabu Shirakawa,1
Kazutaka Uchida,1 Yusuke Tomogane,1 and Yuki Miyaji1
1

Department of Neurosurgery, Hyogo College of Medicine, Nishinomiya, Hyogo

Abstract
We report two cases of juvenile cerebral infarction caused by bow hunter’s syndrome (BHS) during sport.
Case 1 was a 17-year-old male who developed a partial visual field defect after playing basketball. BHS
was diagnosed because cervical ultrasonography demonstrated occlusion of the vertebral artery when
the neck was rotated. After C1–2 posterior fixation was performed, his symptoms resolved. Case 2 was an
18-year-old male with recurrent visual disturbance after playing handball. Cerebral infarction occurred
repeatedly despite antiplatelet therapy. After 3 years, vertebral artery dissection was diagnosed and stenting was performed, but his symptoms did not resolve. BHS was diagnosed when he was examined at our
department. C1–2 posterior fixation was performed and his symptoms resolved. In these two cases, BHS
was caused by sporting activity. For accurate diagnosis and treatment of BHS, neuroimaging with cervical
rotation is mandatory.
Key words:

bow hunter’s syndrome, dissection, sport, cerebral infarction, surgery

Introduction

was diagnosed. Cerebral angiography showed dissection
of the right VA just distal to the transverse foramen
(Fig. 1E). Although his symptoms resolved temporarily
due to wearing a neck collar, repeat angiography after
3 months showed extension of dissection of the right
VA (Fig. 1F). Therefore, the patient underwent C1–2
posterior fixation (Fig. 1G). Postoperative angiography
showed improvement of VAD (Fig. 1H) and the patient’s
symptoms have not recurred.

Vertebral artery dissection (VAD) can be caused by various
external factors, including sporting activities, and can lead
to cerebral infarction. It is sometimes difficult to diagnose
recurrent cerebral infarction associated with VAD and
identify the cause in young patients. Here we report two
juvenile patients with symptomatic VAD caused by bow
hunter’s syndrome (BHS), leading to cerebral infarction.

Case Reports

II. Case 2: an 18-year-old male
The patient had recurrent severe headaches associated with visual disturbance. Cerebral infarction was
diagnosed by a local neurologist, but the cause was
unknown. He had repeated episodes of cerebral infarction even after starting antiplatelet therapy (Fig. 2A, B).
When he was 18 years old, disturbance of consciousness occurred suddenly in hospital and MRI showed
occlusion of the right VA. Mechanical thrombectomy
was performed and a stent was placed in the right VA
at the site of dissection. However, he still had recurrent
ischemic events. After he presented to our hospital,
BHS and VAD were diagnosed because angiography
showed occlusion of the right VA during leftward rotation of neck (Fig. 2D). There was stenosis and dilatation
of the right VA just distal to the transverse foramen
of C2 (Fig. 2C), suggesting dissection. The patient underwent C1–2 posterior fixation (Fig. 2E, F). Postoperative

I. Case 1: a 17-year-old male
The patient complained of partial visual field defects
after playing basketball. Right upper quadrantanopia was
diagnosed by a local ophthalmologist and he was referred
to our hospital. The location of the visual field defect, as
well as the side of nystagmus and hemilateral numbness,
changed each time the patient’s symptoms occurred. Head
magnetic resonance imaging (MRI) showed multiple high
intensity spots in the cerebellar hemispheres and occipital
lobes on diffusion-weighted images (DWIs) (Fig. 1A, B).
Cervical ultrasonography demonstrated occlusion of the
vertebral artery (VA) when the neck was rotated. Magnetic
resonance angiography (MRA) clearly demonstrated VA
occlusion during neck rotation (Fig. 1C, D), so BHS
Received January 6, 2016; Accepted March 1, 2016

580

Diagnosis, Therapy, and Surgery of Bow Hunter’s Syndrome

A

E

B

F

C

G

581

D

H

Fig. 1 Neuroimaging in case 1. A, B: Magnetic resonance imaging showing multiple high signal intensity spots on a diffusionweighted image. C, D: Magnetic resonance angiography demonstrated occlusion of the total course of the contralateral vertebral
artery (VA) during neck rotation (arrows). E: Angiography shows right VA dilatation just distal to the axis of the transverse
foramen, suggestion dissection (arrow). F: Repeat angiography after 3 months shows exacerbation of VA dissection (arrow).
G: Postoperative cervical X-ray film demonstrating screws inserted for C1–2 posterior fixation. H: Postoperative vertebral angiography showing improvement of dissection.

angiography showed improvement of VA dissection
(Fig. 2G, H) and the ischemic events resolved.

Discussion
VAD is a common cause of cerebral infarction in young
adults.1) It has been reported to be caused by hyperextension or hyper-rotation during sports such as yoga, golf,
American football, and Kung-fu.2–4) Sorensen initially
reported BHS, in which Wallenberg syndrome occurred
due to right VA occlusion caused by head rotation during
the bow drawing action.5) In the 1950s, it was reported
that VAD can be caused by neck rotation in cadavers,6) and
the ipsilateral, contralateral, and bilateral development of
VAD has been reported in previously healthy persons.7,8,13)
Although these findings are broadly recognized, it is still
often difficult to diagnose cerebral infarction in young
persons and identify the cause. Our two patients were

Neurol Med Chir (Tokyo) 56, September, 2016

teenagers who had recurrent cerebral infarction associated
with playing sport, which was caused by BHS associated
with VAD.
Regarding mechanisms of the cerebral infarction, we
speculated cerebral embolism due to vessel injury, rather
than hemodynamic ischemia due to vessel occlusion, was
the main cause in both cases, because collateral flow
from contralateral VA was observed on MRA in case
1, and mechanical thrombectomy of the thrombus was
performed in case 2.
The patients were young males (17 and 18 years old)
and they belonged to an age group in which cerebral
infarction is rarely observed. The sports they played were
basketball in case 1 and handball in case 2, respectively.
During ball games, players may rotate the neck extensively
and rapidly. Because the VA is fixed by fibrous tissue
around the C1–2 transverse foramen, it can be subjected
to severe traction by repeated hyper-rotation, resulting

582

H. Kageyama et al.

A

B

E

C

F

D

G

H

Fig. 2 Neuroimaging in case 2. A, B: Magnetic resonance imaging showing multiple high intensity spots in the cerebellum and
thalamus on a fluid-attenuated inversion recovery image. C: Vertebral angiography demonstrating stenosis and dilatation of the
right vertebral artery (VA) just distal to the C2 transverse foramen after stenting (arrow). D: Angiography shows right VA occlusion during leftward rotation of the neck. E, F: Postoperative cervical X-ray film showing screws inserted for C1–2 posterior
fixation and a stent in the right VA at the C2 level (arrow). G, H: Postoperative angiography showing resolution of VA dissection.

in injury to the vessel wall that can lead to embolic
cerebral infarction.
Leftward neck rotation when throwing is similar to the
mechanism of bow hunter’s stroke that occurs in archery.5)
Various symptoms have been reported due to impairment
of VA circulation.5,9–11) Yamaguchi et al. reported a case
of cerebral infarction caused by BHS associated with
VAD.12) Subsequently, Takeshima et al. suggested that the
pathological mechanism of cerebral embolism in BHS
was VA dissection, although they also mentioned that
embolism and subintimal injury have not been definitely
demonstrated.13) It is important to suspect the possibility
of BHS and perform angiography during neck rotation in
addition to diagnosis of VAD by standard angiography.14,15)
Surgical treatment of VAD is still controversial. In the
present two cases, C1–2 posterior fixation was selected
and improvement of symptoms was achieved in both
patients postoperatively. Although stenting of the VA has
been reported as minimally invasive surgery for BHS,16)
stent placement failed to stop ischemic events in our case
2. Posterior decompression at the C1 transverse foramen13,17)
and anterior decompression at the C2 transverse foramen18)

have also been reported as treatments for VAD. However,
Matsuyama et al. reported that posterior fixation achieved
a better outcome than posterior decompression.19) Jost et al.
suggested a treatment and management algorithm for
rotational vertebrobasilar insufficiency without VAD from
their review of 124 cases.11) They recommended decompression without fusion for the BHS caused by isolated
uncarthrosis or by tissue adhesion. On the other hand,
they recommended fusion with or without decompression
for BHS caused by degenerated joints such as instability
and recurrence cases. Decompression without fusion is
simple, less invasive, and physiological, so that it is more
appropriate if degenerative change is limited. Fusion
procedure decreases postoperative recurrence or patient’s
symptom, but limits neck rotation by 50%–70%.11,19)
Both our patients had VAD around the C2 transverse
foramen, and strong local fixation was considered necessary because they were young and wanted to continue
playing sports. Thus, we selected C1–2 posterior fixation,
and both patients had a good postoperative course without
recurrence. In these patients, the period from onset of
apparent ischemic symptoms to diagnosis was 4 months

Neurol Med Chir (Tokyo) 56, September, 2016

Diagnosis, Therapy, and Surgery of Bow Hunter’s Syndrome
and 3 years, respectively. Antiplatelet therapy was not
effective, which indicates that it is difficult to treat this
disease by medication alone. Based on our experience with
these two patients, surgical fixation might be a reasonable
option for VA dissection due to BHS.

Conclusion
We reported two cases of juvenile cerebral infarction
caused by BHS and associated with sporting activity. For
accurate diagnosis and treatment of BHS, neuroimaging
with cervical rotation is mandatory.

Conflicts of Interest Disclosure
The authors declare no conflicts of interest. This report
did not receive any funding from the public or from any
commercial agencies.

References
1)	Gottesman RF, Sharma P, Robinson KA, Arnan M, Tsui
M, Ladha K, Newman-Toker DE: Clinical characteristics
of symptomatic vertebral artery dissection: a systematic
review. Neurologist 18: 245–254, 2012
2)	McCrory P: Vertebral artery dissection causing stroke in sport.
J Clin Neurosci 7: 298–300, 2000
3)	Maroon JC, Gardner P, Abla AA, El-Kadi H, Bost J: “Golfer’s
stroke”: golf-induced stroke from vertebral artery dissection. Surg Neurol 67: 163–168; discussion 168, 2007
4) Pacei F, Valvassori L, Bet L: Vertebral artery dissection during
Kung-Fu training. Neurol Sci 35: 331–332, 2014
5) Sorensen BF: Bow hunter’s stroke. Neurosurgery 2: 259–261,
1978
6) Tissington Tatlow WF, Bammer HG: Syndrome of vertebral
artery compression. Neurology 7: 331–340, 1957
7) Faris AA, Poser CM, Wilmore DW, Agnew CH: Radiologic
visualization of neck vessels in healthy men. Neurology
13: 386–396, 1963
8) Toole JF, Tucker SH: Influence of head position upon cerebral
circulation. Studies on blood flow in cadavers. Arch Neurol
2: 616–623, 1960

Neurol Med Chir (Tokyo) 56, September, 2016

583

9)	Rastogi V, Rawls A, Moore O, Victorica B, Khan S, Saravanapavan P, Midivelli S, Raviraj P, Khanna A, Bidari S, Hedna
VS: Rare etiology of bow hunter’s syndrome and systematic
review of literature. J Vasc Interv Neurol 8: 7–16, 2015
10)	Anene-Maidoh TI, Vega RA, Fautheree GL, Reavey-Cantwell
JF: An unusual case of pediatric bow hunter’s stroke. Surg
Neurol Int 4: 148, 2013
11)	Jost GF, Dailey AT: Bow hunter’s syndrome revisited: 2 new
cases and literature review of 124 cases. Neurosurg Focus
38: E7, 2015
12)	Yamaguchi Y, Nagasawa H, Yamakawa T, Kato T: Bow hunter’s
syndrome after contralateral vertebral artery dissection.
J Stroke Cerebrovasc Dis 21: 916.e7–e9, 2012
13) Takeshima Y, Nishimura F, Park YS, Nakase H: Fusion surgery
for recurrent cerebellar infarctions due to bilateral atlantoaxial rotational vertebral artery occlusion. Spine (Phila
Pa 1976) 39: E860–E863, 2014
14) Hanakita J, Miyake H, Nagayasu S, Nishi S, Suzuki T:
Angiographic examination and surgical treatment of bow
hunter’s stroke. Neurosurgery 23: 228–232, 1988
15) Zaidi HA, Albuquerque FC, Chowdhry SA, Zabramski JM,
Ducruet AF, Spetzler RF: Diagnosis and management of
bow hunter’s syndrome: 15-year experience at barrow
neurological institute. World Neurosurg 82: 733–738, 2014
16) Sugiu K, Agari T, Tokunaga K, Nishida A, Date I: Endovascular treatment for bow hunter’s syndrome: case report.
Minim Invasive Neurosurg 52: 193–195, 2009
17) Shimizu T, Waga S, Kojima T, Niwa S: Decompression of
the vertebral artery for bow-hunter’s stroke. Case report.
J Neurosurg 69: 127–131, 1988
18) Seki T, Hida K, Akino M, Iwasaki Y: Anterior decompression
of the atlantoaxial vertebral artery to treat bow hunter’s stroke:
technical case report. Neurosurgery 49: 1474–1476, 2001
19)	Matsuyama T, Morimoto T, Sakaki T: Comparison of C1-2
posterior fusion and decompression of the vertebral artery
in the treatment of bow hunter’s stroke. J Neurosurg 86:
619–623, 1997

Address reprint requests to: Shinichi Yoshimura, MD, PhD,
Department of Neurosurgery, Hyogo College of Medicine,
Mukogawa, Nishinomiya, Hyogo 663-8501, Japan.
		e-mail: s-yoshi@hyo-med.ac.jp