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AJR 2003; 180:1476
© American Roentgen Ray Society


Trauma Cases from Harborview Medical Center

Posterior Fossa Subarachnoid Hemorrhage Due to an Atlantooccipital Dislocation

William Brinkman1, Wendy Cohen1 and Thomas Manning2

1 Department of Radiology, Harborview Medical Center, University of Washington School of Medicine, 325 Ninth Ave., Box 359728, Seattle, WA 98104-2499.
2 Department of Neurosurgery, Harborview Medical Center, University of Washington School of Medicine, Seattle, WA 98104-2499.

Received July 25, 2002; accepted after revision July 25, 2002.

 
This is another in the continuing series on radiology in trauma cases from the Harborview Medical Center. Editors: Fred A. Mann, Eric J. Stern, and Lee B. Talner.

Address correspondence to F. A. Mann.


Introduction
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Introduction
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References
 
A47-year-old man sustained multiple injuries in a high-speed motor vehicle collision. A lateral cervical spine radiograph showed a subtle increase in basion-to-dens distance (Fig. 1A). Unenhanced CT of the head showed diffuse subarachnoid hemorrhage, specifically within the basal cisterns (Fig. 1B). CT of the cervical spine confirmed bilateral atlantooccipital dislocation. CT angiography, performed to determine the source of the subarachnoid hemorrhage, showed contrast extravasation at the bifurcation of the left vertebral artery and the left posterior inferior cerebellar artery (Fig. 1C).



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Fig. 1A. 47-year-old man with bilateral atlantooccipital injury. Lateral cervical spine radiograph shows basion-to-dens distance of 13 mm (arrows) (established criteria for diagnosis of atlantooccipital dissociation include basion-to-dens distance >12 mm, posterior axis line >12 mm posterior to basion, or >4 mm anterior to basion).

 


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Fig. 1B. 47-year-old man with bilateral atlantooccipital injury. Unenhanced CT scan obtained at level of pons shows subarachnoid hemorrhage (arrowheads) in fourth ventricle and prepontine cistern.

 


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Fig. 1C. 47-year-old man with bilateral atlantooccipital injury. CT angiogram shows active extravasation in region of left vertebral artery (arrowhead), which was confirmed on cerebral angiography (not shown) as arising at origin of left posterior inferior cerebellar artery.

 


Discussion
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Introduction
Discussion
References
 
Traumatic atlantooccipital dislocation, although once considered rare, has been reported to occur in up to 31% of motor vehicle fatalities [1, 2]. Increasing numbers of survivors with satisfactory neurologic outcomes are attributed to advances in medical transport and emergency care. Up to 50% of cases are overlooked on the initial conventional radiographic evaluation [1, 2].

Atlantooccipital dislocation is caused by high-energy deceleration forces that overcome the muscular and ligamentous attachments of the craniocervical junction. Associated injuries include major facial trauma, mandibular fractures, high-energy chest trauma, and intracranial hemorrhage. Subarachnoid hemorrhage is a common finding in multitraumatized patients. However, less than 2% of subarachnoid hemorrhages in traumatic head injury are infratentorial. Subarachnoid hemorrhage at the craniocervical junction is associated with atlantooccipital dislocation, and therefore, its detection should direct the search for atlantooccipital injuries [1].

Most fatalities from atlantooccipital dislocation are attributed to mechanical damage to the brainstem and upper cervical cord. An increasing number of survivors of craniocervical junction injuries with transient or incomplete neurologic deficits may have sustained either a spinal cord contusion or ischemia from vascular injury [3]. The spectrum of vascular injury ranges from vasospasm and dissection of the carotid and vertebral arteries to complete transection with extravasation. Although transection is almost universally fatal, the treatment of dissection and vasospasm with systemic anticoagulation may be efficacious, even in the presence of an intracranial hemorrhage [4].

The diagnosis of cervical arterial injury is often delayed or overlooked in the absence of severe focal neurologic deficit. Reportedly, 20% of patients with atlantooccipital injuries have neurologically normal findings at presentation, but delayed diagnosis has been associated with severe neurologic morbidity in 56% of survivors, and mortality rates are as high as 30% [2, 4]. A low threshold for the examination of the carotid and vertebral arteries in patients with atlantooccipital dislocation and other severe cervical spine injuries would significantly increase the detection rate for these injuries and potentially reduce the associated morbidity and mortality. Although four-vessel cerebral angiography has been advocated for this purpose, CT angiography may have a role in screening patients with atlantooccipital dislocation because of its widespread availability, speed, diagnostic accuracy, and cost effectiveness.


References
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Introduction
Discussion
References
 

  1. Przybylski GJ, Clyde BL, Fitz CR. Craniocervical junction subarachnoid hemorrhage associated with atlanto-occipital dislocation. Spine 1996;21:1761 –1768[Medline]
  2. Fisher CG, Sun JCL, Dvorak M. Recognition and management of atlanto-occipital dislocation: improving survival from an often fatal condition. Can J Surg 2001;44:412 –420[Medline]
  3. Lee C, Woodring JH, Walsh JW. Carotid and vertebral artery injury in survivors of atlanto-occipital dislocation: case reports and literature review. J Trauma 1991;31:401 –407[Medline]
  4. Kerwin AJ, Bynoe RP, Murray J, et al. Liberalized screening for blunt carotid and vertebral artery injuries is justified. J Trauma 2001;51:308 –314[Medline]

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