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At least 127 records · Page 7Linked to original sources

The surgical anatomy of the perforating branches of the basilar artery.

The perforating branches of the basilar artery were examined in 14 brain stems injected with india ink or methylmethacrylate. Three groups of the perforators were distinguished: the caudal, the middle, and the rostral. The caudal perforators varied in number from two to five and in diameter from 80 to 600 microns. In addition to their terminal branches, which entered the foramen cecum, the perforators occasionally branched off the pontomedullary artery, the pyramidal vessels, and the hypoglossal branches. The middle perforators arose either separately from the basilar artery or along with the basilar artery collateral branches. They ranged in number from five to nine and in diameter from 210 to 940 microns. The perforators gave rise to the pontomedullary artery (8.3%), the long pontine arteries (25.0%), and the anterolateral vessels (100%). The rostral perforators originated from the terminal part of the basilar artery (91.6%), as well as from the superior cerebellar artery (91.6%) and the posterolateral artery (16.6%). They varied in number from one to five and in diameter from 190 to 800 microns. The anastomoses among various perforating vessels were noted in 41.6 to 66.6% of the cases. The authors discussed the possible clinical significance of the anatomical data observed in this study.

Basilar Artery↗

[Persistent primitive first cervical intersegmental artery (proatlantal artery II) with occlusion of the basilar artery--a case report].

A rare case of persistent primitive first cervical intersegmental artery (proatlantal artery II) is reported. A 58-year-old man was admitted to our hospital with dysarthria and left hemiparesis. On admission he was stuporous with bilateral gaze palsy and left hemiparesis. CT scan on admission showed low density areas in the right cerebellar hemisphere and ventricular part of the pons. Right retrograde brachiography revealed occlusion of the basilar artery, aplasia of the right vertebral artery and an abnormal vessel connecting the right external carotid artery and the right vertebral artery. This anastomotic vessel was thought to be a persistent primitive first cervical intersegmental artery (Proatlantal artery II). Left carotid angiography revealed the left posterior cerebral artery was visualized through the posterior communicating artery, leading from the internal carotid artery. Left retrograde brachial angiography showed that the left vertebral artery terminated just distal from the branching of the left posterior inferior cerebellar artery. After admission the left hemiparesis deteriorated gradually and tracheotomy was done due to respiratory difficulties. The patient was then transferred to the rehabilitation center on his 34th day in hospital with neurological deficits.

Arterial Occlusive Diseases↗

Potassium-induced endothelium-dependent rhythmic activity in the canine basilar artery.

Rings of canine basilar arteries with and without endothelium were suspended for isometric tension recording in modified Krebs-Ringer bicarbonate solution. Increased extracellular concentrations of potassium (3-20 mM) caused rhythmic activity in rings with endothelium. This activity was reduced by the removal of the endothelium and by exposure to indomethacin, meclofenamate, diltiazem, or ouabain; it was not affected by tetrodotoxin, bretylium tosylate, phentolamine, propranolol, atropine, methiothepin, and cimetidine. Prostaglandin F2 alpha and E2 caused concentration-dependent increases in the frequency and the amplitude of this rhythmic activity and reversed the inhibitory effect of indomethacin and meclofenamate. Prostacyclin abolished the activity. These results suggest that increasing the concentration of extracellular potassium causes rhythmic activity in canine basilar arteries because of the production and/or release by the endothelium of products of cyclooxygenase such as prostaglandin F2 alpha and E2. These may initiate the contraction while prostacyclin triggers the relaxation phase of the rhythmic activity, possibly by activating Na+, K+-ATPase of the vascular smooth muscle.

Animals↗

[Arteries of the human thalamus. II. Arteries and paramedian thalamic territory of the communicating basilar artery].

The basilar communicating artery (or mesencephalic artery) gives off more often one than two paramedian thalamic arteries. The paramedian territory, infero-medial, has a variable extent. It can include the polar territory when the polar artery does not exist. The paramedian artery arises as often from the controlateral basilar communicating artery than from the ipsilateral one. One basilar communicating artery may so have a very extensive bilateral territory.

Basilar Artery↗

[MR imaging of basilar artery aneurysms].

Eight patients with basilar artery aneurysms (five fusiform, two saccular and one giant aneurysm) were studied by MRI at 1.5 tesla. Dilated lumen of basilar artery was detected in seven of eight patients on T2-weighted axial images. Deformity of pons was demonstrated in six of eight patients on T1-weighted midsagittal images. A fusiform aneurysm, 5 mm in diameter, could not be diagnosed by MRI. It was therefore concluded that MR imaging is relatively useful for diagnosing basilar artery aneurysms.

Adult↗

[Long term survival after basilar artery occlusion. 4 cases].

Four cases of basilar artery occlusion with a follow-up from 7 to 12 years are reported. The first patient, a 60 year old woman, had a proximal occlusion which was revealed by an acute brain stem ischemia. The second case was a 63 year old man with an aortic aneurysm who had a single episode of vertebro-basilar insufficiency. Cerebral angiography demonstrated a lower basilar artery occlusion. The third patient, a 60 year-old woman, had been operated from right carotid artery and left vertebral artery stenosis; 8 years later, without clinical manifestations, a left carotid artery stenosis and an occlusion of the lower part of the basilar artery were discovered. The evolution was eventless after a left carotid endarterectomy. The last case was a 60 year old man who had a lower basilar artery occlusion associated with a left internal carotid occlusion. There was a full recovery after a hemiplegic stroke. From our personal cases and the review of the literature, long term survival after basilar artery occlusion may occur in occlusions restricted to the lower or middle part of the basilar artery and with a good collateral supply from carotid and cerebellar arteries.

Arterial Occlusive Diseases↗

[A young adult case of spontaneous basilar artery dissection].

We reported a case of basilar artery dissection in a 20-year-old man suffering sudden onset of consciousness disturbance. Brain CT revealed a cerebral infarction of the whole territories of vertebro-basilar artery and his 3DCT showed the occlusion at the base of basilar artery. Autopsy revealed that the subintimal dissection was found at the base of basilar artery and the dissection was spreaded to the distal of bilateral posterior cerebral arteries. The characteristics of his vertebro-basilar artery were small in diameter, thin media and thickened intima. According to these findings, we supposed this rare case of basilar dissection occurred all at once based on a functional abnormality in his small vertebro-basilar arterial wall.

Adult↗

Inhibitory effect of recombinant iNOS gene expression on vasomotor function of canine basilar artery.

The present study was designed to determine the effect of recombinant inducible nitric oxide (NO) synthase (iNOS) gene expression on vasomotor function in cerebral arteries. Isolated canine basilar arteries were exposed ex vivo (30 min at 37 degrees C) to an adenoviral vector [10(7), 10(8), or 10(9) plaque-forming units (pfu)/ml] encoding either the iNOS gene or the beta-galactosidase reporter gene. Twenty-four hours after transduction, Western blot analysis demonstrated expression of iNOS protein only in iNOS (10(9) pfu/ml)-transduced arteries. Immunohistochemical analysis localized iNOS expression predominantly in adventitia. Vascular reactivity of isolated basilar arteries was studied by isometric force recording. Concentration-response curves to UTP (10(-9)-10(-3) M) and diethylaminodiazen-1-ium-1,2-dioate (10(-10)-10(-5) M) were significantly shifted to the right in iNOS gene (10(9) pfu/ml)-transduced rings compared with control and beta-galactosidase-transduced rings (P < 0.05, n = 5-6). Endothelium-dependent relaxation to bradykinin was significantly attenuated in iNOS-transduced rings (P < 0.001, n = 8). The basal level of cGMP and superoxide anion (O(2)(-).) production were elevated in iNOS-transduced rings (P < 0.05, n = 7 for cGMP; P < 0.01, n = 6-9 for O(2)(-). production). Our results suggest that expression of recombinant iNOS in cerebral arteries reduces vasomotor reactivity to both vasoconstrictor and vasodilator agonists. Attenuation of contractions is most likely due to functional antagonism between UTP and cGMP. Reduction of endothelium-dependent relaxation to bradykinin appears to be mediated in part by reduced reactivity of smooth muscle cells to NO.

Animals↗

Functional role of charybdotoxin-sensitive K+ channels in the resting state of dog basilar artery.

To determine the possible role of Ca(2+)-activated K+ (KCa) channels in the regulation of resting tone of cerebral arteries, the effect of agents which interact with these channels on tension and 86Rb efflux was examined in endothelium-denuded strips of dog basilar artery, and data were compared with findings in the mesenteric artery. The basilar artery maintained a myogenic tone; that is, the resting tone decreased when nifedipine was added. The addition of charybdotoxin, a blocker of large conductance KCa channels, caused a concentration-dependent contraction in the basilar artery but not in the mesenteric artery. In strips preloaded with 86Rb, the basal 86Rb efflux rate constant was significantly greater in the basilar artery than in the mesenteric artery. Nifedipine decreased the basal 86Rb efflux rate constant only in the basilar artery. The basal 45Ca influx in the resting state of the basilar artery was significantly increased when compared with the mesenteric artery and this increase in the basilar artery was reduced by nifedipine. The results suggest that the charybdotoxin-sensitive KCa channels regulate the myogenic tone in the resting state of the basilar artery. The activation of KCa channels in the basilar artery appears to be secondary to the increased transmembrane Ca2+ influx probably via the activation of L-type voltage-dependent Ca2+ channels in the resting state of this artery.

Animals↗

[Intravenous thrombolytic treatment of acute basilar artery occlusion].

BACKGROUND: Acute stroke with basilar artery occlusion is a serious condition with high mortality and severe disability. MATERIAL AND METHODS: We describe three patients with acute artery basilar occlusion treated with thrombolytic agent given intravenously. RESULTS: One patient demonstrated early and considerable clinical improvement parallel to thrombolytic therapy started two and a half hour after ictus, but suffered a new occlusion and died in a "locked-in syndrome". One patient demonstrated moderate clinical improvement after less than six hours and survived with disability. One patient demonstrated no clinical improvement with thrombolytic therapy started six hours after ictus and later died of an injured brainstem. No patients had serious bleeding. INTERPRETATION: Intravenous, systemic thrombolytic treatment may have a beneficial effect in acute basilar occlusion.

Adult↗

Fatal thrombosis of the basilar artery due to a minor head injury.

A case is reported where a 20-year-old alcohol-intoxicated man was admitted to the hospital after a minor head injury. Initially there was no neurologic disturbances or complaints but after a few hours he became comatose, and he died 4 days later without regaining consciousness. The autopsy revealed no lesions of the upper cervical spine or the vertebral arteries, but the basilar artery was occluded in its entire length. No traumatic lesions could be seen by naked eye examination of the artery, and there was no accompanying subarachnoid haemorrhage. A thorough microscopic examination, however, using step-sectioning technique revealed a significant incomplete arterial rupture with an occluding luminal thrombosis superimposed, consisting predominantly of aggregated platelets. Only the very thin adventitia separated the vascular lumen from the subarachnoid space preventing the more well known fatal complication to a minor head injury: A subarachnoid haemorrhage. To the best of our knowledge, fatal thrombosis of the basilar artery due to a minor head injury has not previously been reported. The pathogenetic mechanism seems to be identical to that underlying fatal subarachnoid haemorrhage following a similar trauma apart from the resulting arterial rupture being incomplete instead of complete.

Adult↗

[A case of basilar artery occlusion caused by vertebrobasilar artery dissection presenting with mild clinical symptoms].

We reported a first case of basilar artery occlusion caused by vertebrobasilar artery dissection presenting with mild clinical symptoms. A 45-year-old female was admitted to our department due to the abrupt onset of pain in her posterior neck and occipital head, and numbness in the right upper and lower extremities. She had no other neurological complaints. Computerized tomography and magnetic resonance imaging (MRI) disclosed no abnormalities in parenchyma, but MRI revealed a linear high intensity structure in front of the medulla oblongata on T1 and T2 weighted images. Cerebral angiogram showed the pearl and string sign from the left vertebral artery to the proximal basilar artery, and showed the basilar artery occlusion, but the basilar artery distal to the occlusion site was perfused sufficiently by the carotid via posterior communicating arteries. We diagnosed it as basilar artery occlusion caused by vertebrobasilar artery dissection, which was confirmed during the operation to prevent a hemorrhage from the aneurysmal dilatation. In this case, collateral good circulation was thought to have contributed to her good clinical course.

Aortic Dissection↗

Evidence for functional alpha-adrenoceptors in rabbit basilar arteries.

The contractile response of rabbit basilar arteries to 1-norepinephrine was studied both in the absence and in the presence of prazosin (10 nM and 1 microM). Prazosin produced a parallel shift to the right of the norepinephrine, but not the histamine, dose-response curves indicating the presence of prazosin-sensitive alpha-adrenoceptors in this vessel. The alpha-adrenoceptor-mediated contractile responses to norepinephrine in rabbit basilar arteries were much more sensitive to the deleterious effects of storage (for 18 h at 4 degrees C) than those to histamine. It is suggested that the low number of alpha-adrenoceptors in the rabbit basilar artery combined with their low sensitivity to alpha-adrenoceptor agonists, and detrimental effects associated with tissue storage may explain some inconsistent reports in the literature regarding the presence of functional alpha-adrenoceptors in rabbit basilar arteries, particularly ligand binding studies.

Acetylcholine↗

[On the fenestration of the vertebral and basilar arteries].

The fenestration of the vertebral and basilar arteries was investigated macroscopically in 370 human cases. Altogether 43 fenestrations were found in 32 (8.6%) out of 370 cases. The fenestrations could be divided in three groups according to the position where the fenestration appeared. Group I was the fenestration observed along the vertebral artery (Fig. 1), and 7 such fenestrations were found in 6 (1.6%) out of 370 cases; 3 fenestrations among them were located on the right side, 2 were located on the left side and 1 was found on the bilateral vertebral arteries. In 4 out of 7 fenestrations in this group, the hypoglossal nerve was found passing through the fenestration. Group II was the fenestration observed along the basilar artery (Fig. 2), and 26 fenestrations of this type were found in 20 (5.4%) out of 370 cases: 23 fenestrations (88.5%) were located at the caudal half, 3 (11.5%) were located on the rostral half of the basilar artery (Fig. 5). A close relation was indicated between the side on which the fenestration appeared in the basilar artery and the largeness in caliber of the vertebral artery of either side. Group III was the fenestration observed at the lateral area of the vertebral and basilar arteries (Fig. 3), and 10 fenestrations of this type were found in 9 (2.4%) out of 370 cases; all the fenestrations were located on the right side. In this group, the hypoglossal nerve was observed passing through the fenestratin in 4 out of the 10 fenestrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

[The early hemiparesis of stroke in evolution of basilar artery--case report].

In basilar artery thrombosis, hemiparesis without obvious brainstem signs may precede the tetraplegia with coma or a locked-in state. This premonitory hemiparesis was called as "herald hemiparesis" by Fisher (1988). Its early detection is important because immediate anticoagulant therapy may prevent its evolution. We reported two patients with such hemiparesis. The first case was a 71-year-old diabetic and hypertensive man who was admitted because of right hemiparesis, dysarthria and decreased spontaneous speech. Initially, his symptoms looked like those of a left cerebral lesion. CT scans revealed no fresh cerebrovascular lesion. A few hours later, a myoclonic movement appeared in his left lower limb, and right MLF syndrome developed. We thought he had basilar artery thrombosis and we started intravenous administration of heparin. But he developed tetraplegia with locked-in state. The second case was a 76-year-old diabetic and hypertensive man with a confusional state, right hemiparesis, dysarthria and conjugate gaze deviation to left. After admission, he rapidly became comatose and developed respiratory arrest. CT scans revealed low density areas in the brainstem, cerebellum and the occipital lobe. He died ten days later. Early detection of herald hemiparesis is by no means easy. However, severe dysarthria and myoclonic jerks in a patient with hemiparesis should be considered as warning signs to indicate the herald hemiparesis with subsequent severe brainstem infarction.

Aged↗

Increased Ca2+ influx in the resting state maintains the myogenic tone and activates charybdotoxin-sensitive K+ channels in dog basilar artery.

We examined whether Ca2+ channel function in the resting state alters the resting tone and Ca(2+)-activated K+ (KCa) channel function in dog basilar artery: data were compared with findings in the mesenteric artery. Isolated dog basilar artery maintained a myogenic tone; that is, the resting tone decreased when either the Krebs solution was replaced with a Ca(2+)-free solution or nifedipine was added. The basal 45Ca influx in the resting state of the basilar artery was significantly increased compared with that in the mesenteric artery, and this increase in the basilar artery was reduced by nifedipine. The addition of charybdotoxin (ChTX), a blocker of large-conductance KCa channels, to the resting strips caused a concentration-dependent contraction in the basilar artery but not in the mesenteric artery. The ChTX-induced contraction in the basilar artery was abolished by nifedipine. In resting strips preloaded with 86Rb, the basal 86Rb efflux rate constant was significantly greater in the basilar artery than in the mesenteric artery. The addition of nifedipine to the resting strips decreased the basal 86Rb efflux rate constant only in the basilar artery. These results suggest that the transmembrane Ca2+ influx via L-type voltage-dependent Ca2+ channels was significantly increased in the resting state of the basilar artery and that the myogenic tone was therefore maintained and the ChTX-sensitive KCa channels were highly activated.

Animals↗

Responses of rat basilar artery to acetylcholine and platelet products in vivo.

Studies in vitro suggest that the basilar artery has distinctive responses to endothelium-dependent stimuli. Our first goal was to examine the effects of acetylcholine on diameter of the basilar artery in vivo. Because aggregating platelets may have important effects on cerebral arteries, our second goal was to examine the effects on the basilar artery of products that are released by platelets (thromboxane, serotonin, and adenosine 5'-diphosphate). Diameter of the basilar artery was measured through a cranial window in anesthetized rats (n = 25). Baseline diameter of the basilar artery was 247 +/- 10 microns mean +/- SEM. Topical application of acetylcholine at 10(-6) and 10(-5) M dilated the basilar artery by 13 +/- 2% and 19 +/- 2%, respectively. The thromboxane analogue U46619 at 10(-8) and 10(-7) M reduced the diameter of the basilar artery by 18 +/- 5% and 29 +/- 4%, respectively. At 10(-8) and 10(-7) M, serotonin had little effect on pial arterioles on the cerebrum but constricted the basilar artery by 18 +/- 2% and 29 +/- 4%, respectively. At 10(-6) and 10(-5) M, adenosine 5'-diphosphate produced marked dilatation of pial arterioles on the cerebrum (9 +/- 2% and 20 +/- 3%, respectively) but had little effect on the basilar artery (increased diameter by 4 +/- 2% and 6 +/- 2%, respectively). Thus, in contrast to some studies of the basilar artery in vitro, acetylcholine produces dilatation of the basilar artery in vivo. Potent constrictor responses to thromboxane and serotonin, in combination with the minimal dilator effect of adenosine 5'-diphosphate, suggest that release of these products during platelet aggregation would favor constriction of the basilar artery.

Acetylcholine↗