SUMMARY Though the syndrome of carotid artery dissection is well known, "spontaneous" vertebral artery dissection is rarely recognized. We now report clinical and radiologic findings in five patients with presumed vertebral dissection, one pathologically confirmed.Mean age was 35.2 years (range 27-41). Two were men; three women. None had hypertension, vascular disease, or trauma. Headache and neck or occipital pain was prominent in all, often preceding other symptoms. Four of five patients had unilateral partial alteral medullary syndromes, in one accompanied by medial medullary signs. One patient had a cerebellar infarct. Angiography in four patients showed severe irregular stenosis of the distal extracranial vertebral artery (three bilaterally and subsequently has been widely reported.3 " 5 Migraine 6 ' 7 and fibromuscular dysplasia 8 have been associated with arterial dissection. Intramural clot separates the media often compromising the lumen; clot can dissect into the lumen through the torn intima. Because of intimal and endothelial disruption platelet nidi can form in the lumen and reduced flow potentiates the development of intraluminal clot. Distal ischemia is caused by emoblization of luminal clot or reduced distal flow. Dissections and intimal tears are usually traumatic and are termed "spontaneous" when no definite trauma is recalled by the patient. Though "spontaneous" dissection of the vertebral artery has been reported, 19 " 14 the clinical and radiologic features are less well known than the findings in carotid dissection. We now report clinical and radiologic findings in 4 patients with presumed vertebral artery dissection and radiographic and pathologic findings in 1 patient with surgically proven vertebral dissection. The clinical and radiologic signs of spontaneous vertebral dissection closely resemble those described in vertebral artery trauma and chiropractic manipulation. She recalled no unusual recent neck motion or trauma. Two hours after awakening, she suddenly noted tingling at the corner of her left mouth and tongue, dizziness, vomiting, and a sensation that her body was being pulled to the left. Later her right hand felt cold. On examination, blood pressure and general examination were normal. Neurological abnormalities included: coarse horizontal nystagmus to the left, left facial hypalgesia, diminished left corneal response, and left limb dysmetria. She veered to the left when she walked. CT was normal. Bilateral vertebral angiography showed moderately severe narrowing and irregular stenosis of the third segment of the right vertebral artery and severe stenosis of a short segment of the third portion of the left vertebral artery ( fig. la, b). Warfarin anticoagulation was begun. Neurologic examination returned to normal and she had no symptoms. A left vertebral angiogram 5 months after onset was normal with no residual stenosis ( fig. lc). Warfarin was stopped. Two years after the original episode, the patient had no neurologic signs or symptoms. Patient 2fJ.R., a 39 year old man ha...

We performed transluminal balloon angioplasty In 24 cadaver and nine amputated limb superficial femoral arteries under controlled experimental conditions. The cadaver arteries were excised, restored to in situ length, redistended, and maintained at 100 mm Hg Intraluminal pressure at 37° C throughout the anglographlc and dilation procedure and during fixation. The amputated limb arteries were dilated and pressure perfusion-flxed after dilation. Quantitative analysis of cadaver vessels revealed that arteries with prominent atherosclerotic lesions had the same internal elastic lamina (IEL) circumference (15.6 ± 1.0 mm) as those with little or no stenosis (16.8 ± 0.5 mm) but lumen area (8.8 ± 1 . 7 mm 2 ) was markedly reduced compared to nonstenotlc sites (20.0 ± 1.9 mm 2 , p < 0.01). Lesions occupied 49 ± 6% of the area circumscribed by the IEL In cadaver arteries with prominent plaques. After dilatation, lumen areas at stenotic sites were enlarged 43% on hlstologic sections (12.6 ± 1.8 mm 2 vs 8.8 ± 1 . 7 mm 2 , p < 0.

To assess the extent to which endothellal cell (EC) structure Is modified by hyperllpldemla and by the formation of Irrtlmal plaques, we undertook a quantitative ultrastructural study of aortic EC of cynomolgus monkeys after 3 or 6 months on an atherogenic diet We compared EC In lesion-free areas ( I n an earlier study of diet-induced atherogenesis in the cynomolgus monkey, 1 we reported that endothelial cells were markedly attenuated over early intimaJ foam cell accumulations, but we could find no evidence of endothelial cell (EC) degeneration, disruption, or desquamation either over lesions or in lesion-free areas. Interruptions of lumen surface continuity occurred only over Received September 20, 1988; revision accepted June 27, 1989. some multilayered confluent lesions where foam cells penetrated between adjacent endothelial cells or through pores or gaps in endothelial cell bodies. Subsequent investigations in rabbits and in stump-tail monkeys 2 -3 also revealed that diet-induced lesions were not associated initially with EC disruption. Platelet deposition over more advanced plaques has been considered a consequence of endotheliaJ discontinuities, which develop with continued plaque deposition. It has been proposed 4 that such changes are a basis for the transition from fatty streaks to complex plaques. Whether or not EC disruption actually occurs as a complication of plaque enlargement, the attenuation and reshaping of EC over earty intimal lesions suggests a plasticity that would tend to preserve the integrity of the endotheliaJ lining.In an attempt to characterize this presumably adaptive process, we undertook a quantitative investigation of EC

No abstract

No abstract