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LETTER TO EDITOR
Year : 2012  |  Volume : 60  |  Issue : 5  |  Page : 520-521

Bow hunter's stroke - A rare presentation of CV junction anomaly: Case report


Department of Neurosciences, Narayana Hrudayalaya Institute of Neurosciences, Bangalore, India

Date of Web Publication3-Nov-2012

Correspondence Address:
Sathwik Raviraj Shetty
Department of Neurosciences, Narayana Hrudayalaya Institute of Neurosciences, Bangalore
India
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DOI: 10.4103/0028-3886.103204

PMID: 23135032

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How to cite this article:
Shetty SR, Shankaraiah BA, Hegde T, Nagarajaiah RK. Bow hunter's stroke - A rare presentation of CV junction anomaly: Case report. Neurol India 2012;60:520-1

How to cite this URL:
Shetty SR, Shankaraiah BA, Hegde T, Nagarajaiah RK. Bow hunter's stroke - A rare presentation of CV junction anomaly: Case report. Neurol India [serial online] 2012 [cited 2014 Dec 20];60:520-1. Available from: http://www.neurologyindia.com/text.asp?2012/60/5/520/103204


Sir,

Bow Hunter's stroke (BHS) is defined as hemodynamic vertebrobasilar insufficiency (VBI) secondary to intermittent vertebral artery (VA) occlusion resulting from head rotation. [1] The presentation can be in the form of transient ischemic attacks or stroke. Patients with cranio-vertebral junction (CVJ) anomalies presenting with posterior fossa stroke are extremely rare.

An 18-year-old student presented with symptoms of vertigo, diplopia, recurrent vomiting, gait unsteadiness and lapsed into altered sensorium. She had history of two prior surgeries for an occipital encephalocoele 4 years and 8 years back. On examination, she had Glasgow coma scale score of E3V3M6 with slurred speech, bilateral sixth nerve paresis, bilateral cerebellar signs and gait ataxia. Computed tomogram (CT) of the head showed an acute/subacute infarct involving the entire left cerebellum with no mass effect or hydrocephalus [Figure 1]. In view of her prior history of occipital encephalocoele, a thorough evaluation of the CVJ was done which showed rotary atlantoaxial dislocation with displacement of the odontoid process to the left [Figure 2]. CT-angiogram showed a short segment complete occlusion of left vertebral artery (VA) at C1-C2 level [Figure 3]a. Multiple tandem filling defects of VA and basilar arteries were seen [Figure 3]b. She was managed conservatively. Neck immobilization was done with Philadelphia collar, 24 h later she worsened in sensorium. A repeat CT scan showed an increase in the mass effect with obstructive hydrocephalus [Figure 4].
Figure 1: Left cerebellar infarct

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Figure 2: Rotary atlantoaxial dislocation

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Figure 3: (a) CT Angiogram - short segment complete occlusion of the left vertebral artery at C1-C2 level (b) Multiple tandem filling defects of the left vertebral and basilar arteries seen

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Figure 4: Cerebellar infarct with increase in mass effect with midline shift and obstructive hydrocephalus

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She underwent an emergent limited left unilateral sub-occipital craniectomy and infarct was decompressed till fourth ventricle opened up ensuring good cerebrospinal fluid egress [Figure 5]. Care was taken to preserve the muscular and ligament attachments at the posterior CV junction. Post operatively, she recovered well and returned to normal consciousness and improvement in cerebellar signs. Surgical options for realignment and stabilization of the CV junction along with left VA decompression were discussed. As the patient was recovering from stroke, it was decided to continue conservative treatment in the form of restricted neck movement and close monitoring. At the last follow-up, she was ambulating independently and her lower cranial nerve paresis had also recovered.
Figure 5: Left unilateral sub occipital craniectomy and decompression of infarct

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CVJ anomalies very rarely can present with BHS [2] and occur as a result of mechanical occlusion of either the dominant or non-dominant VA. [3] BHS should be suspected in patients with symptoms of vertebro-basilar artery insufficiency (VBI) precipitated by head movement. In BHS, occlusion usually involves the VA contralateral to the direction of rotation and usually occurs at the C1-2 junction due to immobility of the VA at this location. [4] The segment of VA between C1 and C2 gets stretched, and sometimes gets narrowed or occluded. Diagnosis of BHS is by cerebral angiogram. Dynamic cerebral angiography (DCA) has been suggested by some authors [3] to verify the patency of VA during head turning but significant consequences can be precipitated by DCA in patients with BHS. [2] The stroke per se is managed with anticoagulation and decompressive surgery where required. The treatment options for rotational compression of the C1-C2 portion of the VA include restriction of head and neck rotation either with braces or by surgical fusion and VA decompression at C1-2 level. [5] Studies have also shown that in young patients with VBI or posterior fossa stroke a high index of suspicion should be kept for CVJ anomalies. [2] In conclusion, this patient highlights the importance of being aware of the atypical presentation of CVJ anomalies. It is also imperative that a detailed assessment of the VAs is done in patients with CVJ anomalies which would help in taking appropriate steps to prevent strokes in these patients.

 
  References Top

1.Sorenson BF. Bow Hunter's stroke. Neurosurgery 1978;2:259-61.  Back to cited text no. 1
    
2.Panda S, Ravishankar S, Nagaraja D. Bilateral Vertebral Artery Dissection Caused by Atlantoaxial Dislocation. J Assoc Physicians India 2010;58:186-8.  Back to cited text no. 2
    
3.MatsuyamaT, MorimotoT, SakakiT. Bow Hunter's Stroke caused by non dominant vertebral artery occlusion - Case report. Neurosurgery 1997;41:1393-5.  Back to cited text no. 3
    
4.Lemole GM, Henn JS, SpetzlerRF, Joseph M. Zabramski. Bow Hunter's stroke.BNI Q2001;17:4-10.  Back to cited text no. 4
    
5.Shimizu T, Waga S, Kojima T, Niwa S. Decompression of the vertebral artery for Bow Hunter's stroke. Case report. J Neurosurg1988;69:127-31.  Back to cited text no. 5
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]



 

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