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(Radiographics. 1999;19:255-258.)
© RSNA, 1999


SPECIAL EXHIBIT

Neuroradiology Case of the Day

Francis G. Greiner, MD1 and Deepak Takhtani, MD1

1 Department of Radiology, University of South Alabama Medical Center, 2451 Fillingim St, Mastin Bldg 301, Mobile, AL 36617.

Index Terms: Brain, ischemia, 153.781 • Vertebral arteries, dissection, 1751.4314


    HISTORY
 Top
 HISTORY
 FINDINGS
 DISCUSSION
 References
 
A 27-year-old black woman awakened at 5:00 a.m. with what she described as the worst headache of her life. The headache was occipital in location, nonradiating, and did not cause photophobia. The patient presented with an unsteady gait with falling to the left, vertigo, dysarthria, and anisocoria (right pupil, 4 mm; left pupil, 1–2 mm). Her family reported changes in her speech and a family history of sickle cell trait. The patient had recently been diagnosed as hypertensive and had a blood pressure of 140/102 at the time of admission. Axial magnetic resonance (MR) imaging was performed 44 hours after the onset of symptoms. Three-dimensional time-of-flight MR angiography was also performed.

In addition, catheter angiography was performed to further evaluate the vertebral artery and to evaluate for possible thrombosis and thrombolysis.


    FINDINGS
 Top
 HISTORY
 FINDINGS
 DISCUSSION
 References
 
MR imaging revealed increased signal intensity in the cerebellum and brain stem without evidence of hemorrhage (Figs 1, 2). Three-dimensional time-of-flight MR angiography revealed that the left vertebral artery had a diminished caliber (Fig 3). The source images demonstrated no signal, suggestive of methemoglobin or changes in the lumen (except stenosis).



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Figure 1a.  (a) Axial intermediate weighted MR image of the cerebellum reveals an area of increased signal intensity in the left cortical gray matter (arrow). Both vertebral arteries are visualized (the right larger than the left) with apparent flow voids (arrowheads). (b) T2-weighted MR image obtained at the same level as a again shows high signal intensity in the gray matter of the left cerebellum (arrow). Vessel flow on the left side is not as well visualized due to cerebrospinal fluid signal.

 


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Figure 1b.  (a) Axial intermediate weighted MR image of the cerebellum reveals an area of increased signal intensity in the left cortical gray matter (arrow). Both vertebral arteries are visualized (the right larger than the left) with apparent flow voids (arrowheads). (b) T2-weighted MR image obtained at the same level as a again shows high signal intensity in the gray matter of the left cerebellum (arrow). Vessel flow on the left side is not as well visualized due to cerebrospinal fluid signal.

 


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Figure 2.  Axial T2-weighted MR image through the brain stem reveals additional areas of infarct in the brain stem and cerebellum (arrow). The hypoglossal nucleus is involved.

 


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Figure 3a.  (a) Axial three-dimensional time-of-flight MR angiogram shows a normal basilar artery (arrowhead), carotid artery, and right vertebral artery (curved arrow) intracranially. The left vertebral artery has reduced flow (straight arrow). (b) Coronal three-dimensional time-of-flight MR angiogram reveals irregular contour and reduced flow in the left vertebral artery between the transverse foramen of C2 and C1 (curved arrows). The large vessels lateral to the vertebral artery (straight arrow) are jugular veins that could not be totally suppressed on the image due to the angle of acquisition.

 


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Figure 3b.  (a) Axial three-dimensional time-of-flight MR angiogram shows a normal basilar artery (arrowhead), carotid artery, and right vertebral artery (curved arrow) intracranially. The left vertebral artery has reduced flow (straight arrow). (b) Coronal three-dimensional time-of-flight MR angiogram reveals irregular contour and reduced flow in the left vertebral artery between the transverse foramen of C2 and C1 (curved arrows). The large vessels lateral to the vertebral artery (straight arrow) are jugular veins that could not be totally suppressed on the image due to the angle of acquisition.

 
DIAGNOSIS: Vertebral artery dissection and stroke.


    DISCUSSION
 Top
 HISTORY
 FINDINGS
 DISCUSSION
 References
 
Although ischemic strokes most commonly occur in persons over 50 years of age, 12% of "first-ever" ischemic strokes occur in young adults (1). In our patient, areas of abnormally high signal intensity were seen within the cerebellum on T2-weighted images; these high-signal-intensity areas corresponded to the stroke deficits (Figs 1, 2). These lesions could account for the patient's symptoms of ipsilateral ataxia, contralateral loss of extremity sensation, dysphagia, dysarthria, and nystagmus accompanied by Horner syndrome. This aggregate of signs is known as lateral medullary (Wallenberg) syndrome and is frequently seen with vertebral artery dissection. Although our patient had a family history of sickle cell trait, she had no history of sickle cell disease. In addition, there was no history of substance abuse, pregnancy, or contraceptive use, which are also predisposing factors for stroke in young adults.

Patients with vertebral artery dissection most commonly present with pain. Over 50% of symptomatic patients present with occipital headache, 20% present with frontal headache, 20% present with orbital headache, and about 30% present with neck pain (1,2). Stroke may occur hours or even weeks after dissection. In general, patients with vertebral artery dissection and stroke make what is essentially a full functional recovery (88%), with some residual deficit still detectable at neurologic examination (2).

Arterial dissection may account for up to 15% of strokes in young adults (3). Fibromuscular dysplasia, Marfan syndrome, collagen vascular disease, and homocystinuria may predispose to arterial dissection (4,5). This patient was not found to have systemic lupus erythematosus or collagen vascular disease, and laboratory test results revealed a normal sedimentation rate and vitamin levels.

Trauma is the most common cause of vertebral artery dissection. Such trauma may be severe or trivial. In addition to apparently spontaneous events, activities such as chiropractic manipulation, bowling, tennis, and archery have been reported to cause vertebral artery dissection. The actual prevalence of vertebral artery dissection is difficult to estimate. Even in patients with severe trauma, unilateral vertebral artery injury may not cause stroke (6). Stroke symptoms have been reported in up to 95% of cases of vertebral artery dissection (7). In many cases, vertebral artery dissection may be clinically silent and therefore not imaged (6).

Dissection involves hemorrhage into the arterial wall of the vessel. This intramural hemorrhage may alter the morphology or signal of the vessel being imaged. On MR images, the lumen of the affected vessel may be widened and may demonstrate periarterial rim signal intensity representing hemoglobin. This rim signal intensity will change with time. Our patient was imaged acutely, and the rim sign was not evident. A diminished flow void or a decreased arterial lumen size may also indicate dissection but may also be seen with other causes of ste-nosis (Fig 3). Angiography will usually show a tapering of the artery, an intimal flap, or even complete occlusion (Fig 4) (8). Vertebral artery dissection most commonly occurs at sites of direct trauma or between C1 and C2 (9).



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Figure 4a.  (a) Lateral digital subtraction angiogram of the left vertebral artery reveals a reduction in the diameter of the artery extracranially (arrow). The intracranial vertebral and basilar arteries and the anterior inferior cerebellar artery appear normal (arrowheads). (b) Left anterior oblique digital subtraction angiogram shows an irregular narrowing of the vertebral artery between C2 and C1 (straight arrow). Curved arrow indicates a branch vessel feeding the anterior spinal artery. (c) Right anterior oblique digital subtraction angiogram again shows irregular narrowing of the dissected lumen (arrow) with a return to normal morphology intracranially.

 


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Figure 4b.  (a) Lateral digital subtraction angiogram of the left vertebral artery reveals a reduction in the diameter of the artery extracranially (arrow). The intracranial vertebral and basilar arteries and the anterior inferior cerebellar artery appear normal (arrowheads). (b) Left anterior oblique digital subtraction angiogram shows an irregular narrowing of the vertebral artery between C2 and C1 (straight arrow). Curved arrow indicates a branch vessel feeding the anterior spinal artery. (c) Right anterior oblique digital subtraction angiogram again shows irregular narrowing of the dissected lumen (arrow) with a return to normal morphology intracranially.

 


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Figure 4c.  (a) Lateral digital subtraction angiogram of the left vertebral artery reveals a reduction in the diameter of the artery extracranially (arrow). The intracranial vertebral and basilar arteries and the anterior inferior cerebellar artery appear normal (arrowheads). (b) Left anterior oblique digital subtraction angiogram shows an irregular narrowing of the vertebral artery between C2 and C1 (straight arrow). Curved arrow indicates a branch vessel feeding the anterior spinal artery. (c) Right anterior oblique digital subtraction angiogram again shows irregular narrowing of the dissected lumen (arrow) with a return to normal morphology intracranially.

 
MR imaging is believed to be the modality of choice for initial evaluation of vertebral artery dissection but has some limitations (7). The smaller size of the vertebral arteries may make visualization of the intramural hematoma more difficult than with carotid artery dissection (10). Initially, the damaged artery may manifest with an eccentric signal void with an isointense to slightly hyperintense halo (8). Vertebral artery dissections have also been reported as being isointense on T1-weighted MR images, hyperintense on proton-density–weighted images, and hypointense on T2-weighted images when imaged acutely (7). In time, the intimal hemorrhage will evolve into methemoglobin and result in high signal intensity on T1- and T2-weighted images. When methemoglobin is present, three-dimensional MR angiography may not enable clear differentiation between the lumen and thrombus. Follow-up angiography of vertebral artery dissection demonstrates that 76% of arteries have either returned to normal or shown improvement (2).

In this case, contrast material–enhanced conventional angiography helped confirm a vertebral artery dissection between C1 and C2 extracranially (Fig 4). This case demonstrates a vertebral artery dissection with minimal trauma. Imaging of the neck to exclude vertebral artery injury should be considered in young patients presenting with stroke.

Our patient was immediately treated with aspirin and hospitalized shortly after presentation, and a course of coumadin therapy and stroke rehabilitation was instituted. Three months after suffering the stroke, the patient is still experiencing persistent mild residual loss of pain and sensation in the right extremities, but speech and ataxia have improved. Follow-up imaging has not been performed.


    Footnotes
 
Address reprint requests to F.G.G.

From the 1998 RSNA scientific assembly.

Received for publication August 31, 1998. Revision received September 21, 1998. October 2, 1998. Accepted for publication October 2, 1998.


    References
 Top
 HISTORY
 FINDINGS
 DISCUSSION
 References
 

  1. Bougousslavsky J, Regli F. Ischemic strokes in adults younger than 30 years of age: cause and prognosis. Arch Neurol 1987; 44:479-482.[Abstract]
  2. Mokri B, Houser OW, Sandok BA, Piepgras DG. Spontaneous dissections of the vertebral arteries. Neurology 1988; 38:880-885.[Abstract/Free Full Text]
  3. Provenzale JM, Barboriak D. Brain infarction in young adults: etiology and imaging findings. AJR 1997; 169:1161-1168.[Abstract/Free Full Text]
  4. Pavlakis SG, Gould RJ, Zito JL. Stroke in children. Adv Pediatr 1991; 38:151-179.[Medline]
  5. Kim SH, Kosnik E, Madden C, Rusin J, Wack D, Bartowski H. Cerebellar infarction from a traumatic vertebral artery dissection in a child. Pediatr Neurosurg 1997; 27:71-77.[Medline]
  6. Willis B, Greiner F, Orrison W, Benzel E. The incidence of vertebral artery injury after midcervical spine fracture or subluxation. Neurosurgery 1994; 34:435-442.[Medline]
  7. Auer A, Felber S, Schmidauer C, Waldenberger P, Aichner F. Magnetic resonance angiographic and clinical features of extracranial vertebral artery dissection. J Neurol Neurosurg Psychiatr 1998; 64:474-481.[Abstract/Free Full Text]
  8. Provenzale JM. Dissection of the internal carotid and vertebral arteries: imaging features. AJR 1995; 165:1099-1104.[Abstract/Free Full Text]
  9. Hart RG. Vertebral artery dissection. Neurology 1988; 38:987-989.[Free Full Text]
  10. Levy C, Laissy JP, Raveau V, et al. Carotid and vertebral artery dissections: three-dimensional TOF MR angiography and MR imaging versus conventional angiography. Radiology 1994; 190:97-103.[Abstract/Free Full Text]




This Article
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