Vertebral artery dissection and basilar artery thrombosis

Findings

Figure 1: Hyperdense basilar artery and edema involving the brainstem, left cerebellum with partial effacement of the fourth ventricle.
Figure 2: Hyperdense basilar artery and edema involving the brainstem, left cerebellum and left occipital lobe with near complete effacement of the fourth ventricle.
Figure 3: Edema in the left occipital lobe. Effacement of the quadrigeminal plate and right ambient cistern. Dilation of the temporal sweeps of the lateral ventricles. Normal vascular attenuation of the left posterior cerebral artery.
Figure 4 and Figure 5: DWI and ADC map shows restricted diffusion in the brainstem, bilateral superior cerebelli, and left occipital lobe.
Figure 6: 3D MIP MRA shows normal flow related signal in the normal right vertebral artery and complete lack of flow in the contralateral left vertebral artery.
Figure 7: 3D MIP MRA: Lack of normal flow signal in segment IV of the left vertebral artery and left PICA. Abrupt loss of signal in basilar artery. Normal signal in right VA and right PICA.


Diagnosis: Vertebral artery dissection and basilar artery thrombosis


Although once thought to be a rare occurrence, spontaneous dissection of the verterbral artery has become increasingly recognized as a cause of posterior circulation infarction, largely due to the advent of MR angiography. In recent literature, VAD has been shown to be the underlying etiology in up to 40 percent of posterior fossa ischemic strokes. VAD is seen 3 times more commonly in females. Predisposing factors include hypertension, and collagen vascular disease such as Ehlers-Danlos disease and Marfan syndrome, but is not uncommonly seen in completely healthy individuals, often in the setting of minor neck trauma. The most studied association is chiropractic spinal manipulation, but VAD has been described in various other minor traumas such as: yoga, ceiling painting, nose blowing, and judo.

The underlying abnormality in spontaneous VAD is thought to be an expanding hematoma within the vessel wall and, as a result, on CT angiogram an intimal flap is not always seen (unlike larger artery dissection where contrast commonly tracks into the false lumen). Patients with VAD often present with occipital headaches and nuchal pain, and when ischemia occurs, typically have vertebrobasilar symptoms. The dreaded consequence of VAD is hemodynamically significant vertebral artery stenosis/thrombosis, distal thomboembolism and subsequent ischemia. VAD carries a 10% mortality rate in the acute phase.

The vertebral artery is divided into 4 segments:
- Segment I begins at the vertebral artery origin, at the craniodorsal aspect of the subclavian artery, and extends to the transverse foramen of cervical vertebra (typically at C6 or C5)
- Segment II of this artery is defined as the segment that lies entirely within the transverse foramina from C5/C6 extending to the C2 level
- Segment III is the tortuous segment which exits the C2 transverse foramen, courses around the posterior arch of C1 and passes between the atlas and occiput
- Segment IV is the intracranial segment; it begins as the artery that pierces the dura and then continues until it joins the contralateral vertebral artery at the vertebrobasilar junction


Segment III is the most common site for spontaneous VAD.

Imaging findings in VAD include abrupt narrowing of the vessel lumen, as commonly seen on CTA. A hyperintense intramural hematoma may sometimes be seen on noncontrast axial T1 weighted imaging with fat-saturation, when blood products are in the subacute phase (methemoglobin). On occasion, it may also be termed the “crescent sign” because of its morphology. Signs of posterior fossa infarction can perhaps be seen on CT and MR even at the time of initial presentation. Mass effect from acute infarcts may lead to brain herniation, as in the patient presented herein.