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Paper text:
bow hunter s stroke ( bhs ) is a cerebrovascular disease caused by occlusion of the vertebral artery ( va ) on head rotation.13 bhs is associated with hemodynamic changes , often leading to vertebrobasilar insufficiency symptoms , such as vertigo and faintness .
the mechanism of bhs frequently involves unilateral stenosis or hypoplasia of the va , increasing susceptibility to hemodynamic changes on temporary occlusion of the contralateral va.4,5 recently , artery - to - artery ( a - to - a ) embolism has been suggested as another cause,6 which remains controversial .
a 26-year - old man had a stroke involving the left thalamus , associated with dizziness and numbness in the right upper limb .
nine months later , dizziness and unconsciousness occurred without head rotation , and were found to be caused by an infarct in the right thalamus ( fig .
he had congenital partial aplasia of the posterior arch of the atlas , but no apparent atlantoaxial subluxation .
duplex color - coded ultrasonography showed no end - diastolic flow in the right va on head rotation to the left , unaccompanied by symptoms .
angiograms revealed rotational occlusion , associated with mild wall irregularity , and anomalous duplication of the va .
three - dimensional ct angiography , a method that clearly visualizes both vascular lesions and surrounding structures,4 showed that the lower branch of the va ran between the c1 and c2 vertebrae ( fig .
the patient declined surgical treatment , but started antiplatelet therapy ( cilostazol 200 mg / day ) and voluntary avoidance of excessive head rotation .
however , one year after the second attack mri revealed an additional , asymptomatic infarct in the left thalamus .
to our knowledge , this is the first patient who had bhs with an anomalous bypass of the va , suggesting the absence of apparently pathogenic hemodynamic changes .
in addition , an angiographic finding suggested that the adequate vertebrobasilar flow was maintained from the anomalous bypass during head rotation .
mechanisms underlying non - hemodynamic bhs remain unclear ; however , we speculate that it is associated with a - to - a embolism due to vascular damage caused by repeated va compression .
supportive evidence for this speculation has been provided by our previous study showing that a juvenile patient with repetitive vertebrobasilar infarction and va occlusion on head rotation had a mobile thrombus at the compression site.6 in our patient , the observed va wall irregularity , a finding consistent with intimal damage , might agree with the a - to - a embolism mechanism .
the sole involvement of the thalami may also support embolism in our patient.7 a large - scale ultrasonographic study ( n = 1,108 ) showed that rotational va occlusion was found in 5% of patients with possible atherosclerosis , 76% of whom had no rotation - induced symptoms.8 thus , such patients may have the potential risk of stroke , if bhs is caused by a - to - a embolism .
previous in vivo experiments showed that repeated vascular damage promotes platelet adhesion and activates various coagulation mediators.9 clinically , vascular damage ( thickness and sclerosis ) was confirmed intraoperatively at the occlusion site in a patient with bhs.10 alternatively , thrombus formation may be attributed to blood flow stasis in the va , a well - accepted mechanism underlying hemodynamic bhs.10 however , thrombi form after 1 day of stasis,9 and our patient s head was not fixed for such a long time .
in fact , the va is compressed by skeletal muscle or fascial bands at the transverse foramen of c6 , by spondylotic osteophytes within the transverse foramina from c5 to c2 , by strong membranous structures at the occipitoatlantal level , or by the atlantoaxial bones.11 among them , the last one is involved in many cases of juvenile bhs , as in our patient.10 many such patients had atlantoaxial subluxation often associated with head trauma or chiropractic manipulations , 3,6 causing excessive slide on head rotation .
the lower branch ran between the c1 and c2 vertebrae and was compressed even on moderate rotational joint movement .
a similar aberrant course of the va , but without duplication , was previously shown to cause bhs.12 interestingly , concomitant abnormalities of arteries and cervical bones are often reported,13 as in our patient .
in addition to specific factors in individual patients , greater neck mobility , generally seen in young people , may further damage the va . in conclusion
although the causal involvement of hemodynamic changes in bhs remains important , the possibility of non - hemodynamic change - related bhs should be considered in the diagnostic workup of patients with vertebrobasilar stroke , even in the absence of head - rotation - induced symptoms or abnormalities on routine mra .
bow hunter s stroke ( bhs ) is a cerebrovascular disease caused by occlusion of the vertebral artery ( va ) on head rotation . 
 bhs is generally associated with hemodynamic changes , often leading to vertebrobasilar insufficiency symptoms , such as vertigo and faintness . 
 although artery - to - artery embolism has also been proposed as an underlying mechanism , it remains controversial . 
 this report documents a case of bhs without hemodynamic changes . 
 we describe a 26-year - old male patient who had va occlusion on head rotation and repetitive infarction of thalami . 
 he had an anomalous bypass of the va and therefore no symptomatic hemodynamic changes . 
 thus , non - hemodynamic bhs should be considered in juvenile patients with vertebrobasilar stroke .