Acute arterial hypertension caused by dissecting aneurysm of the renal artery

BACKGROUND: Aneurysm of the renal artery is an uncommon discovery at arteriography performed as part of a hypertension work-up. CASE REPORTS: We observed acute hypertension following dissection of a renal artery aneurysm which led to circulating channel stenosis. After surgical correction of the lesion, arterial pressures returned to normal. DISCUSSION: Most cases of renal artery aneurysm do not cause hypertension. In such cases, the high blood pressure is idiopathic or related to fibrodysplastic stenosis of the renal artery often associated with aneurysm formation. In rare cases with obstructive complications alone an aneurysm may lead to acute hypertension either after dissection as in our case or after thrombus formation. Surgery is generally required.     

Post-traumatic middle cerebral artery occlusion: case report and review

Occlusion of extracranial carotid and vertebral arteries following closed craniocervical trauma is well known. However occlusion of intracranial arteries following closed head injuries is infrequently reported. In fact only 25 cases of post-traumatic middle cerebral artery occlusion have been adequately documented. This entity bears re-emphasis not only because of its rarity but also because of its clinical similarity to other intracranial mass lesions.     

Giant aneurysm of the middle cerebral artery

A case of a giant aneurysm of the middle cerebral artery, (4.5 X 4.5 X 9.5 CM) presenting as a mass lesion, which was successfully excised is described. This case is compared to the few previous accounts of giant aneurysms of the middle cerebral artery larger than 3 cm in diameter.     

Prognosis of patients with middle cerebral artery occlusion

The long-term prognosis of 78 stroke patients with occlusion of the middle cerebral artery (MCA) or its branches is described. The mean age of the patients was 44 years. The mortality rate in the acute phase was 5%. The acute and total mortality rates of men were higher than those of women (p less than 0.05). Life-table analysis gave 94% probability for one year's survival, 84% for three years' survival, and 78% for five years' survival. Subsequent strokes were twice as common as cardiovascular events as the cause of death. Seventy-two percent of the survivors became fully independent in activities of daily living (ADL) , 27% required assistance, 1% was totally disabled, and 43% returned to work. Left-sided occlusion was overrepresented in those who died (p less than 0.00(1) and those who returned to work (p less than 0.05), and right-sided occlusion was overrepresented in those who required assistance in ADL (p less than 0.05).     

Development of a dissecting aneurysm on the vertebral artery immediately after occlusion of the contralateral vertebral artery: a case report

A 49 year old female presented with subarachnoid hemorrhage due to a ruptured dissecting aneurysm on the left vertebral artery (VA). Following an occlusion test, we performed proximal occlusion of the left VA with detachable balloons. However, a dissecting aneurysm on the right VA developed three weeks later. After an occlusion test had showed no change in cerebral blood flow, auditory brain stem response, or neurological status, proximal occlusion of the right VA was performed. The patient has returned to normal life without neurological deficits. Bilateral dissecting aneurysms of the VA are quite common, but de novo VA dissecting aneurysms or enlargement of such aneurysms after occlusion of contralateral VA are rare. This case suggests that hemodynamics stress may be a causal factor in the development of VA dissecting aneurysms. Careful pre- and post-operative neuroradiological examination of the contralateral VA are required in patients undergoing VA occlusion for dissecting aneurysms.     

Monofilament intraluminal middle cerebral artery occlusion in the mouse

The rat middle cerebral artery (MCA) occlusion model with an intraluminal filament is well characterized with a two hour period of occlusion in widespread use. The recent availability of transgenic animals has led to an interest in adapting the MCA model in the mouse. To date the model has not been well characterized in the mouse. We performed the present study to compare different durations of MCA occlusion and to validate new functional assessments in this model. The MCA occlusion model (5-0 filament) was used. Swiss-Webster mice, 24-44 g, were randomly assigned to four groups: one hour of occlusion; two hours of occlusion; three hours of occlusion; or permanent occlusion. At 48 hours post-ischemia, the animals were rated on three neurologic function scales, and then the brains were removed for lesion size determination. Overall, there was a significant difference in lesion volume (p < 0.001) between the groups. In the permanent group of mice, the average lesion volume was 78.41 +/- 17.47 mm (n = 12); two and three hours of ischemia produced 51.29 +/- 29.82 mm3 (n = 11) and 54.85 mm3 (n = 13), respectively, significantly different than the one hour group 14.84 +/- 31.34 mm3 (n = 11). All three functional scoring systems found significant overall differences between the four groups with our detailed General and Focal scores producing more robust between group treatment differences and showing correlation coefficients of r = 0.766 and r = 0.788, respectively to infarct volume. The MCA filament occlusion model can be successfully adapted in the mouse with either two or three hour occlusions producing reliable infarcts. New functional scoring systems unique to the mouse appear to add additional information.     

Cathepsin B and middle cerebral artery occlusion in the rat

Lysosomal proteases, although tightly regulated under physiological conditions, are known to contribute to cell injury after various forms of tissue ischemia have occurred. Because cathepsin B is a prominent lysosomal protease found in brain parenchyma, the authors hypothesized that it may contribute to neuronal cell death after focal cerebral ischemia. The authors measured the expression and spatial distribution of cathepsin B within the ischemic brain in 43 animals by means of immunohistochemical analysis in a rat model of transient middle cerebral artery (MCA) occlusion. Cathepsin B activity was also measured within specific ischemic brain regions by using an in vitro assay (22 animals). In addition, the authors tested the therapeutic effect of preischemic intraventricular administration of stefin A, a cysteine protease inhibitor, on the volume of cerebral infarction after transient MCA occlusion (15 animals). Increased cathepsin B immunoreactivity was detected exclusively within the ischemic neurons after 2 hours of reperfusion following a 2-hour MCA occlusion. Cathepsin B immunolocalization in the ischemic region decreased by 24 hours of reperfusion, but then increased by 48 hours of reperfusion because the infarct was infiltrated by inflammatory cells. Increased immunolocalization of cathepsin B in the inflammatory cells located in the necrotic infarct core continued through 7 days of reperfusion. Cathepsin B enzymatic activity was significantly increased in the ischemic tissue at 2, 8, and 48 hours, but not at 24 hours of reperfusion after 2 hours of MCA occlusion. Continuous intraventricular infusion of stefin A, before 2 hours of MCA occlusion (15 animals), significantly reduced infarct volume compared with control animals (12 animals): the percentage of hemispheric infarct volume was 20+/-3.9 compared with 33+/-3.5 (standard error of the mean; p = 0.025). These data indicate that neuronal cathepsin B undergoes increased expression and activation within 2 hours of reperfusion after a 2-hour MCA occlusion and may be a mechanism contributing to neuronal cell death. Intraventricular infusion of stefin A, an inhibitor of cathepsin B, significantly reduces cerebral infarct volume in rats.     

Endovascular treatment of acute thrombotic occlusion of the cervical internal carotid artery associated with embolic occlusion of the middle cerebral artery: case report

A 68-year-old man with acute, total thrombotic occlusion of the right cervical internal carotid artery, associated with embolic occlusion of the ipsilateral middle cerebral artery, was treated by the endovascular approach, i.e., intra-arterial fibrinolysis and balloon angioplasty. Endovascular treatment for a totally occluded internal carotid artery is indicated in the very early stage where there is no thrombus or a short thrombus that can be evacuated. Fibrinolysis of the associated embolus in the middle cerebral artery, if any, can be done in the same session, enabling an early restoration of the blood flow.     

Two cases of cerebral aneurysm detected after recanalization of the middle cerebral artery]

Two cases of aneurysm incidentally detected after recanalization of middle cerebral artery (MCA) occlusion are reported. Patient 1 was a 62-year-old male with sudden onset of left hemiparesis. We performed emergent intravascular surgery. The initial cerebral angiography revealed occlusion at the M1 portion of the right MCA. After partial recanalization with a microcatheter, carotid angiography revealed a right M1-M2 junction aneurysm. Due to the risk of aneurysmal rupture, the thrombolytic procedure was stopped. Follow up angiography after 1 month revealed complete recanalization of the right MCA and a persistent aneurysm. Patient 2 was a 65-year-old male with left hemiparesis. The initial cerebral angiography revealed occlusion at the M1 portion of the right MCA. After 1 month follow-up cerebral angiography revealed spontaneous recanalization of the right MCA and an incidental aneurysm at the M1-M2 junction. Neck clipping of the aneurysm was performed. When using a microcatheter or microballoon catheter to treat arterial occlusion, surgeons should consider the possibility of a rupture of a hidden aneurysm.     

Proximal occlusion of the dominant anterior cerebral artery for anterior communicating aneurysm

A series of six experiments examined the neural loci responsible for caerulein's suppression of eating. Caerulein is a decapeptide chemically and physiologically similar to cholecystokinin, a naturally occurring gut hormone in rats. Rats with lesions in the ventromedial hypothalamus (VMH) showed reduced sensitivity to caerulein (1 mug/kg); rats with lateral hypothalamic (LH) destruction showed heightened sensitivity. Microinjections of caerulein into the VMH, but not into the LH, limited feeding. Finally, tritiated caerulein was selectively bound to tissue in the VMH. The results are discussed in terms of the hypothesis that the VMH manages postprandial inhibition in the rat.     

Increased endothelin-1 in the rabbit model of middle cerebral artery occlusion

Human neutrophils (5 x 10(4) incubated on fibronectin precoated wells released 2.83 +/- .25 nmoles of superoxide (0(2)-) (x +/- 1 SEM, n = 15) in response to 5.9 nM (100 ng/ml) Tumor Necrosis Factor Alpha (TNF). On the contrary, the 0(2)- production induced by interleukin-8 (IL-8) (doses ranging from 0.1 nM to 1 microM) was comparable to that of "resting" cells (< .6 nmoles/5 x 10(4) cells). IL-8 (100 nM) did not affect the TNF-dependent 0(2)- production when added with TNF at the beginning of the assay, but reduced it by approximately 80% when added with TNF on neutrophils previously incubated for 1 hour on fibronectin. As compared with IL-8, N-formyl-methionyl-leucyl-phenylalanine (FMLP, 100 nM) failed to suppress the TNF-triggering of the oxidative burst in neutrophils plated on fibronectin. The data suggest that the interaction of neutrophils with fibronectin uncovers the capacity of IL-8 to limit the cell response to TNF, without affecting the response to the combination of FMLP and TNF. Thus, although the chemotactic factors IL-8 and FMLP share the capacity of triggering the oxidative burst of neutrophils incubated in suspension, only IL-8 has the potential to down-regulate the responsiveness of fibronectin-adherent cells to TNF.     

Middle cerebral artery aneurysm complicated by tuberculosis

Pentazocine, a kappa opioid receptor agonist, induced catalepsy in mice suggesting thereby that it might possess postsynaptic striatal D 2 dopamine (DA) receptor blocking activity. However, our other findings, that pentazocine pretreatment did not antagonise the cage climbing behaviour induced by the directly acting DA agonist apomorphine in mice and actually potentiated the stereotyped behaviour induced by the indirectly acting DA agonist methamphetamine in mice, indicate that pentazocine does not possess postsynaptic striatal and mesolimbic D 2 DA receptor blocking activity. Pretreatment with naloxone, an antagonist of opioid receptors, antagonised pentazocine-induced catalepsy. This suggests the possible involvement of opioid mechanisms in the induction of catalepsy by pentazocine in mice.     

Refusion of anterior cerebral artery after aneurysm clipping--a case report

Herein, we are describing an unusual case suffering from a left anterior cerebral artery aneurysm (A1). Both the anterior cerebral arteries were supplied by the left internal carotid artery as was found in digital substraction angiography (DSA) preoperatively. The postoperative angiograms revealed that left anterior cerebral artery was supplied from the left internal carotid artery and the right anterior cerebral artery by the right internal carotid artery respectively. This finding of cerebral angiograms is interesting and rarely mentioned in the literature. Its hemodynamic change and pathogenesis were unclear and different to that of the coronary circulation, ischemic change of gut and skeletal muscle. The causes may include: 1) vasospasm at the anterior communicating artery after manipulation at surgery; 2) desiccation or shrivelling the adjacent artery by intraoperative electrocoagulation; 3) occlusion the anterior communicating artery by the wing of clip. 4) the deprivation of the blood flow from the left internal carotid artery after totally or partially narrowing left A1 by an aneurysm clip. The redistribution of blood volume in the previously hypoplastic right anterior cerebral artery and decreased caliber of the left anterior cerebral artery (A1) are likely playing a role in this case.     

Large distal anterior cerebral artery aneurysm associated with azygos anterior cerebral artery: case report

A 51-year-old woman presented with a distal anterior cerebral artery aneurysm (DACAA) manifesting as severe headache and monoparesis of the left lower limb. Computed tomography revealed subarachnoid hemorrhage in the interhemispheric fissure, bilateral sylvian fissures, and basal cistern, and a hematoma in the supracallosal region. Angiography showed a large aneurysm (23 x 18 mm) located on the distal end of the azygos anterior cerebral artery (azygos ACA) at the supracallosal portion. T2-weighted magnetic resonance imaging demonstrated the hematoma as a mixed intensity mass, compressing the corpus callosum downward, and the aneurysm as a flow void anterior to the hematoma. Unilateral frontoparietal parasagittal craniotomy was performed with a horse-shoe shaped incision. The aneurysm was clipped via the interhemispheric approach, and the hematoma was aspirated. Postoperative angiography showed disappearance of the aneurysm and intact azygos ACA. The patient was discharged with mild monoparesis, paresthesia of the left lower limb and diagnostic dyspraxia. DACAA almost always arises at or near the genu of the corpus callosum and is often associated with vascular anomaly. In the literature, 22 of 26 cases of large and giant DACAA were located at or near the genu, but only 3 cases, including ours, in the supracallosal area. 11 cases were associated with azygos ACA. Therefore, hemodynamic stress caused by vascular anomaly may be involved in the formation of large or giant DACAA in contrast with cases of normal DACAA.     

Fenestrated oculomotor nerve caused by internal carotid-posterior communicating artery aneurysm: case report

OBJECTIVE AND IMPORTANCE: The fenestrated oculomotor nerve associated with the internal carotid-posterior communicating artery aneurysm is very rare. CLINICAL PRESENTATION: A 48-year-old woman had a history of subarachnoid hemorrhage caused by a ruptured right middle cerebral artery aneurysm, which was wrapped with good postoperative course. Twenty years later, the patient suffered frontal headache with a mild oculomotor nerve paresis in the right side. Follow-up neuroimaging studies demonstrated a de novo right internal carotid-posterior communicating artery aneurysm. INTERVENTION: The aneurysm was exposed and clipped via a right pterional route. The fenestrated oculomotor nerve associated with the aneurysm was confirmed at surgery. CONCLUSION: We speculated that the fenestration was most likely caused, by the growth of the aneurysm.     

Ruptured distal accessory anterior cerebral artery aneurysm: case report

OBJECTIVE AND IMPORTANCE: Accessory anterior cerebral artery (ACA), which is a type of median artery of anomalous triplicate ACA, is not rare, but aneurysmal formation is extremely rare. We report a rare case with ruptured aneurysm arising from a distal accessory ACA. We discuss the characteristics and causes of this type of aneurysm and classification of this anomaly. CLINICAL PRESENTATION: A 63-year-old man suddenly developed severe headache and then loss of consciousness and paraplegia. Computed tomography disclosed thick and diffuse subarachnoid hemorrhage and interhemispheric hematoma. Subsequent bleeding occurred 2 hours after the first hemorrhage. Cerebral angiography disclosed a saccular aneurysm arising from the distal accessory ACA. INTERVENTION: Neck clipping of the aneurysm was performed 22 hours after the second episode, using an interhemispheric approach. CONCLUSION: Although transient paraplegia occurred 8 days after onset, the patient recovered well after surgery without neurological deficit. The characteristics of the aneurysm arising from distal accessory ACA are considered similar to those of distal ACA aneurysm. There is, however, some confusion regarding the terminology of the anterior communicating artery complex anomalies, which we discuss.     

Collateral hemodynamics after middle cerebral artery occlusion in Wistar and Fischer-344 rats

We investigated whether the difference in infarction volume after occlusion of a long proximal segment of the middle cerebral artery between Wistar and Fischer-344 rats, is caused by differences in collateral blood flow rate through leptomeningeal anastomoses. In view of the retrograde direction of collateral blood flow into the middle cerebral artery territory, we developed parasagittal laser-Doppler flowmetry. Using this method two laser-Doppler probes are placed on the cerebral cortex: probe 1 is placed near the anastomoses between the middle- and anterior cerebral artery, probe 2 is placed 2 mm further away from these anastomoses than probe 1. We found in both rat strains a comparable relation between the areas under the curve of the signal measured by both laser-Doppler probes for 2 h after middle cerebral artery occlusion. This relation is considered to be a measurement of the collateral blood flow rate into the middle cerebral artery territory through leptomeningeal anastomoses after middle cerebral artery occlusion. We conclude that collateral blood flow for the two strains were essentially similar for the initial 2 h after MCA occlusion. Although these collateral blood flows could have been different at a later time, it is unlikely that the interstrain difference in cerebral infarction volume between Wistar and Fischer-344 rats after proximal middle cerebral artery occlusion is caused by an apparent interstrain difference in the magnitude of collateral blood flow rate through leptomeningeal anastomoses. The parasagittal laser-Doppler flowmetry technique we developed for these experiments is currently successfully used in our laboratory to evaluate the efficacy of hemodynamically active pharmacotherapeutical agents in raising the collateral blood flow rate into the middle cerebral artery territory after middle cerebral artery occlusion.