A case of a patient with vertebrobasilar dolichoectasia complicated by hydrocephalus, impaired consciousness, and brain stem infarction due to rapid elongation of the basilar artery

In this article we present an 80 year old female patient with an unruptured giant aneurysm of the basilar artery presenting with posterior circulation ischemic symptoms. Angiography and CT revealed giant basilar aneurysmal dilatation with severe and wide intracranial arteriosclerosis. We described the uniqueness of this case. Giant basilar aneurysm is associated with various complications particularly brain stem infarction. It is emphasized that arteriosclerosis plays an important role in the formation of giant basilar aneurysms.

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Rotary Nystagmus Evoked by Lateral Eye Position in a Patient of Brain Stem Infarction.

Equilibrium Research ◽

10.3757/jser.57.491 ◽

1998 ◽

Vol 57 (5) ◽

pp. 491-496

Author(s):

Koji Yuen ◽

Hirofumi Akagi ◽

Kazunori Nishizaki ◽

Yu Masuda

Keyword(s):

Brain Stem ◽

Eye Position ◽

Brain Stem Infarction ◽

Lateral Eye

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Attenuation and Recovery of Brain Stem Autoregulation in Spontaneously Hypertensive Rats

Journal of Cerebral Blood Flow & Metabolism ◽

10.1097/00004647-199803000-00009 ◽

1998 ◽

Vol 18 (3) ◽

pp. 305-310 ◽

Cited By ~ 14

Author(s):

Kazunori Toyoda ◽

Kenichiro Fujii ◽

Setsuro Ibayashi ◽

Takanari Kitazono ◽

Tetsuhiko Nagao ◽

...

Keyword(s):

Brain Stem ◽

Basilar Artery ◽

Antihypertensive Treatment ◽

Spontaneously Hypertensive Rats ◽

Hypertensive Rats ◽

Doppler Flowmetry ◽

Spontaneously Hypertensive ◽

Large Arteries ◽

Cranial Window ◽

Severe Hypotension

Cerebral large arteries dilate actively around the lower limits of CBF autoregulation, mediated at least partly by nitric oxide, and maintain CBF during severe hypotension. We tested the hypothesis that this autoregulatory response of large arteries, as well as the response of arterioles, is altered in spontaneously hypertensive rats (SHR) and that the altered response reverts to normal during long-term antihypertensive treatment with cilazapril, an angiotensin-converting enzyme inhibitor. In anesthetized 6- to 7-month-old normotensive Wistar-Kyoto rats (WKY), 4- and 6- to 7-month-old SHR without antihypertensive treatment, and 6- to 7-month-old SHR treated with cilazapril for 10 weeks, local CBF to the brain stem was determined with laser—Doppler flowmetry and diameters of the basilar artery and its branches were measured through a cranial window during stepwise hemorrhagic hypotension. The lower limit of CBF autoregulation shifted upward in untreated SHR to 90 to 105 mm Hg from 30 to 45 mm Hg in WKY, and it reverted to 30 to 45 mm Hg in treated SHR. In response to severe hypotension, the basilar artery dilated by 21 ± 6% (mean ± SD) of the baseline internal diameter in WKY. The vasodilation was impaired in untreated SHR (10 ± 8% in 4-mo-old SHR and 4 ± 5% in 6- to 7-month-old SHR), and was restored to 22 ± 10% by treatment with cilazapril ( P < 0.005). Dilator responses of branch arterioles to hypotension showed similar attenuation and recovery as that of the basilar artery. The data indicate that chronic hypertension impairs the autoregulatory dilation of the basilar artery as well as branch arterioles and that antihypertensive treatment with cilazapril restores the diminished dilation toward normal.

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Microsurgical Endarterectomy of the Intracranial Vertebral Artery for Vertebrobasilar Transient Ischemic Attacks

Neurosurgery ◽

10.1227/00006123-198101000-00011 ◽

1981 ◽

Vol 8 (1) ◽

pp. 56-59 ◽

Cited By ~ 31

Author(s):

George S. Allen ◽

Ronald J. Cohen ◽

Thomas J. Preziosi

Keyword(s):

Vertebral Artery ◽

Brain Stem ◽

Antiplatelet Therapy ◽

Atherosclerotic Plaque ◽

Basilar Artery ◽

Neurological Deficit ◽

Operating Microscope ◽

Transient Ischemic Attacks

Abstract Two patients who had typical vertebrobasilar transient ischemic attacks (TIAs) that were refractory to anticoagulation with dicumarol and to antiplatelet therapy with aspirin and/or dipyridamole are described. Angiography revealed in both patients a stenotic atherosclerotic plaque of the intracranial vertebral artery between the posterior and anterior inferior cerebellar arteries. At operation, the first patient had an atherosclerotic plaque extending into the basilar artery, and no endarterectomy was attempted. The second patient had a 1-cm localized plaque that was removed successfully from the vertebral artery. Neither patient sustained a neurological deficit as a result of the operation. The patient whose plaque was not removed at operation continues to have vertebrobasilar TIAs and suffered a brain stem stroke 2 weeks after operation. The patient whose plaque was removed at operation continues to be free of TIAs 8 months later, and angiography performed 3 months after operation showed a widely patent vertebral artery. A portion of the intracranial vertebral artery has now been shown to be accessible to endarterectomy using the operating microscope. Angiography is helpful in determining this accessibility preoperatively.

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Role of Nitric Oxide in Regulation of Brain Stem Circulation during Hypotension

Journal of Cerebral Blood Flow & Metabolism ◽

10.1097/00004647-199710000-00011 ◽

1997 ◽

Vol 17 (10) ◽

pp. 1089-1096 ◽

Cited By ~ 23

Author(s):

Kazunori Toyoda ◽

Kenichiro Fujii ◽

Setsuro Ibayashi ◽

Tetsuhiko Nagao ◽

Takanari Kitazono ◽

...

Keyword(s):

Nitric Oxide ◽

Brain Stem ◽

Topical Application ◽

Basilar Artery ◽

Group Versus ◽

Control Group ◽

Cranial Window ◽

Severe Hypotension ◽

The Brain

We tested the hypothesis that nitric oxide (NO) plays a role in CBF autoregulation in the brain stem during hypotension. In anesthetized rats, local CBF to the brain stem was determined with laser-Doppler flowmetry, and diameters of the basilar artery and its branches were measured through an open cranial window during stepwise hemorrhagic hypotension. During topical application of 10−5 mol/L and 10−4 mol/L Nω-nitro-L-arginine (L-NNA), a nonselective inhibitor of nitric oxide synthase (NOS), CBF started to decrease at higher steps of mean arterial blood pressure in proportion to the concentration of L-NNA in stepwise hypotension (45 to 60 mm Hg in the 10−5 mol/L and 60 to 75 mm Hg in the 10−4 mol/L L-NNA group versus 30 to 45 mm Hg in the control group). Dilator response of the basilar artery to severe hypotension was significantly attenuated by topical application of L-NNA (maximum dilatation at 30 mm Hg: 16 ± 8% in the 10−5 mol/L and 12 ± 5% in the 10−4 mol/L L-NNA group versus 34 ± 4% in the control group), but that of the branches was similar between the control and L-NNA groups. Topical application of 10−5 mol/L 7-nitro indazole, a selective inhibitor of neuronal NOS, did not affect changes in CBF or vessel diameter through the entire pressure range. Thus, endothelial but not neuronal NO seems to take part in the regulation of CBF to the the brain stem during hypotension around the lower limits of CBF autoregulation. The role of NO in mediating dilatation in response to hypotension appears to be greater in large arteries than in small ones.

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