MRA demonstration of "periarteritis" in Tolosa-Hunt syndrome.

BACKGROUND: Modern magnetic resonance imaging (MRI) diagnosis of Tolosa-Hunt syndrome rests upon demonstration of cavernous sinus abnormalities. We present a case of Tolosa-Hunt syndrome who has no abnormal mass lesion in the cavernous sinuses on MRI but with a diagnostic lesion on magnetic resonance angiography (MRA). CLINICAL PRESENTATION: A 48-year-old woman developed acute periorbital pain and abducens palsy of the right side at the first episode, and subacute peri-orbital pain and rapidly deteriorating visual acuity on the left side at the second episode with a four months interval. MRI showed no soft-tissue abnormality in the cavernous sinuses. FINDINGS: MRA demonstrated a narrowing of the right cavernous carotid artery at the first episode, and narrowings of the left clinoid carotid and ophthalmic arteries at the second episode. Based on these findings, the patient underwent urgent steroid therapy and the symptoms resolved dramatically in each episode. Follow-up MRA confirmed resolution of arterial narrowings. INTERPRETATION: MRA may help prompt the noninvasive diagnosis in certain cases of Tolosa-Hunt syndrome with little inflammatory reaction in the cavernous sinus but with predominant intra- and juxta-cavernous periarteritis.

Embolization of cerebral arteriovenous malformations achieved with polyvinyl alcohol particles: angiographic reappearance and complications.

BACKGROUND AND PURPOSE: The appropriate choice of embolic materials with respect to the permanency of obliterated nidi after embolization and complications related to the procedure is essential for safe and effective embolization of cerebral arteriovenous malformations (AVMs). Our purpose was to ascertain the recanalization and complication rates after AVM treatment with polyvinyl alcohol (PVA) particles. METHODS: Between 1988 and 1994, 36 AVMs were embolized with PVA particles at our institution. Follow-up angiographic findings and occurrence of complications during the embolization procedures were analyzed retrospectively. RESULTS: Complete obliteration of the nidus immediately after embolization was achieved in five patients, and 80% to 99% obliteration was attained in 12 patients. Fifty-one follow-up angiographic examinations were performed 1 week to 60 months (mean, 7 months) after embolization in 31 patients. An increase in nidal size was seen on 15 follow-up angiograms (29%) and a decrease was seen in seven (14%). In 28 of the 51 angiograms obtained more than 1 month after follow up (mean, 13 months), 12 (43%) showed AVM enlargement. In four (80%) of five cases of complete obliteration, nidi reappeared on follow-up angiograms. Hemorrhagic complications occurred in three cases and ischemic ones in seven. One patient (3%) died and five (14%) suffered persistent neurologic deficits. CONCLUSION: Embolization with PVA particles can produce significant volume reduction in AVM nidal size, but recanalization is a distinct possibility.

Radiologic and histopathologic evaluation of canine artery occlusion after collagen-coated platinum microcoil delivery.

BACKGROUND AND PURPOSE: Platinum coil embolization is one of the significant advances in interventional neuroradiologic techniques that has been introduced this decade. Our purpose was to evaluate the angiographic and histologic effects of collagen-coated platinum microcoil delivery in the canine artery. METHODS: We embolized the bilateral internal maxillary arteries of 18 dogs; one uncoated and one collagen-primed coil was used in each dog. We evaluated all coils by angiography, macroscopy, and scanning electron microscopy within 30 minutes of embolization. We then studied a proportional number of coated and collagen-primed coils at either 1 or 3 days, or 1, 2, 3, 4, 8, 12, or 16 weeks postoperatively. RESULTS: Six (33%) of 18 arteries embolized with uncoated coils were occluded 30 minutes after delivery, whereas 11 (61%) of 18 arteries treated with collagen-primed coils were occluded within 30 minutes of embolization. Late occlusion (3 weeks after embolization) occurred in 2 (25%) of 8 arteries embolized with untreated coils, and 6 (75%) of 8 arteries embolized with collagen-primed coils. We calculated differences in late occlusion rates by the chi2 (chi-square) test, and found these differences were significant (P=.04). Histologic findings of arteries embolized with unprimed coils revealed endothelial cell growth was limited to the organized thrombi 4 weeks after coil delivery. In contrast, endothelial cells grew directly on the collagen-primed coils 3 days postoperatively, and coils were completely covered by endothelial cells within 2 weeks. We found an organized thrombus in the inner space of coils in angiographically occluded arteries, a finding that was not evident in angiographically patent arteries. CONCLUSION: Collagen-coated platinum coils can produce rapid and stable occlusion of embolized vessels.

Multivariate analysis of predictors of hematoma enlargement in spontaneous intracerebral hemorrhage.

BACKGROUND AND PURPOSE: We conducted this study to determine, through use of multivariate analyses, the independent predictors of hematoma enlargement occurring after hospital admission in patients with spontaneous intracerebral hemorrhage (i.c.h.). METHODS: We reviewed 627 patients with ICH admitted within 24 hours of onset. The first CT was performed at admission and the second within 24 hours of admission, and a blood sample was taken for laboratory examinations. Univariate and multivariate analyses were performed to assess the relationships between hematoma enlargement and time from onset, consciousness level, CT findings, amount of alcohol consumption, systolic blood pressure at and after admission, clinical outcome, and hematologic parameters. RESULTS: Eighty-eight patients (14.0%) showed enlarged hematomas after admission. Multivariate analyses revealed that the following five factors were independently associated with hematoma enlargement: the time from onset (odds ratio [OR], 0.26 for a 1-SD change; 4.9 hours; P < 0.001); the amount of alcohol consumption (OR, 1.50 for 1 SD; 46.3 g/d; P = 0.002); the sharp of hematoma (OR, 1.40 for 1 SD; 0.45 round; P = 0.006); the presence of consciousness disturbance (OR, 1.38 for 1 SD; 0.50 coma; P = 0.026); and the level of fibrinogen (OR, 0.74 for 1 SD; 87.1 mg/dL; P = 0.042). Hematoma enlargement was an independent factor increasing the mortality rate in the ICH patients (OR, 1.57; P < 0.001). CONCLUSIONS: A particularly high likelihood of hematoma enlargement was observed in patients who (in order of importance) were admitted shortly after onset, who were heavy drinkers; who had an irregularly shaped hematoma, whose consciousness was disturbed, and who had a low level of fibrinogen.

Intra-aneurysmal pressure changes during angiography in coil embolization.

BACKGROUND: Although elevation of blood pressure in aneurysms induced by injection of contrast medium has been postulated as a major cause of rerupture of ruptured cerebral aneurysms during angiography, no study has proved the elevation of intra-aneurysmal pressure because of difficulty in measuring the intra-aneurysmal pressure during angiography. The present study demonstrated intra-aneurysmal pressure to be raised by injection of contrast medium, using a microcatheter introduced into aneurysms. METHODS: To confirm the accuracy of pressure measurement through a microcatheter, we measured intra-aneurysmal pressure in a plastic model of an artery and an aneurysm during and after injection of contrast medium through a microcatheter and a needle inserted into the aneurysm. In a clinical study, intra-aneurysmal pressures were measured through the microcatheter in nine cerebral aneurysms of seven patients. RESULTS: In the model experiment, changes in the pressure measured through the microcatheter correlated well with those observed through the needle. In the clinical study, intra-aneurysmal systolic pressures increased by 5-23 mm Hg immediately after injection of contrast medium for 1-3 s in four basilar tip, three internal carotid-ophthalmic, and one middle cerebral artery aneurysm, whereas no pressure change was observed in a posterior cerebral artery aneurysm. Systemic blood pressure during angiography remained unchanged in all cases. CONCLUSIONS: This abruptly elevated intra-aneurysmal pressure by injection of contrast medium might cause rerupture of an aneurysm soon after rupture of the aneurysm, especially when the rupture site is fragile.

Serial changes of hemostasis in aneurysmal subarachnoid hemorrhage with special reference to delayed ischemic neurological deficits.

This study was undertaken to elucidate comprehensively the serial changes occurring in hemostatic systems after aneurysmal subarachnoid hemorrhage (SAH) and thereby to ascertain whether the examination of the integrity of these systems is helpful in predicting delayed ischemic neurological deficits (DINDs). The authors examined 117 patients admitted to the hospital within 24 hours after onset of SAH. Blood samples were collected from each patient on Days 0 (at admission), 3, 6, 14, and 30. A number of hemostatic parameters were examined in these samples, and the relationships between their changes and DINDs were assessed. Eighteen (15.4%) of the patients exhibited DINDs, and their frequency increased as the severity of subarachnoid clotting increased. Also, the frequency of DINDs was significantly higher in the patients with hydrocephalus on initial computerized tomography (CT) scans than in those without hydrocephalus. Regarding the hemostatic parameters at admission, there was no significant difference between the patients with and without DINDs. On Day 3, however, the fibrinogen and D-dimer levels were higher in the patients with than in those without DINDs. The fibrinogen and thrombin-antithrombin complex levels on Day 6 and the D-dimer level on Day 14 in the patients with DINDs were higher than the corresponding levels in those without DINDs. Multivariate analyses revealed that the following variables (in order of importance) were independent predictors of DINDs: the levels of D-dimer on Day 3, fibrinogen on Day 6, and the presence of hydrocephalus on admission. These data indicate that the levels of hemostatic parameters in concert with the CT findings may enable us to predict the appearance of DINDs.

Histological interaction of cultured endothelial cells and endovascular embolic materials coated with extracellular matrix.

This study was undertaken to evaluate the histological reaction of cultured endothelial cells to endovascular embolic materials in vitro. Endothelial cells were isolated and cultured from a canine carotid artery. Embolic materials (platinum microcoils, polyvinyl alcohol particles, silicon balloons, or silk threads), either in their normal state or after having been coated with type 1 collagen, fibronectin, or laminin, were placed on endothelial cells and cocultured for 6, 12, and 24 hours and 2, 3, 7, 14, and 21 days. The cocultures were investigated histologically using a scanning electron microscope. Endothelial cells were not found on any uncoated embolic materials, even at 21 days. On the materials coated with fibronectin or laminin, endothelial cells began to proliferate in 7 days, covering the materials extensively in 14 days. On the other hand, endothelial cells began to proliferate on the collagen-coated materials in 3 days, covering them extensively in 7 days and reaching confluence with a cobblestone pattern in 21 days. The densities of endothelial cells on collagen-coated materials were much higher than those observed on the materials coated with other extracellular matrices. Future advantages of the clinical use of collagen-coated embolic materials in interventional treatment are discussed.

Ultra-early rebleeding in spontaneous subarachnoid hemorrhage.

To determine the incidence of, and risk factors for, the occurrence of rebleeding between admission and early operation (ultra-early rebleeding) in patients with spontaneous subarachnoid hemorrhage (SAH), the authors reviewed the cases of 179 patients admitted within 24 hours after their last attack of SAH. Thirty-one (17.3%) of these patients had ultra-early rebleeding despite scheduling of early operation (within 24 hours after admission). The incidence of rebleeding significantly decreased as the time interval between the last attack and admission increased. Patients with rebleeding before admission, high systolic blood pressure, intracerebral or intraventricular hematoma, those in poor neurological condition on admission, and those who underwent angiography within 6 hours of the last SAH were significantly more likely to have ultra-early rebleeding than those without these factors. The incidence of rebleeding also significantly increased as levels of enhancement of platelet sensitivity and thrombin-antithrombin complex increased. Multivariate analysis revealed that the following three factors were independently associated with ultra-early rebleeding: the level of enhancement of platelet sensitivity; the time interval between the last attack and admission; and the level of thrombin-antithrombin complex. On the basis of these findings, the authors suggest that many of the risk factors for ultra-early rebleeding are interrelated. A particularly high risk of ultra-early rebleeding was observed in those patients 1) who had platelet hypoaggregability; 2) who were admitted shortly after their last SAH; and 3) whose thrombin-antithrombin complex levels were extremely high and were thus in severe clinical condition.

Blood pressure monitoring in feeding arteries of cerebral arteriovenous malformations during embolization: a preventive role in hemodynamic complications.

To study the hemodynamics of arteriovenous malformations and to avoid hemodynamic complications during and after artificial embolization, we measured arterial blood pressures in 21 feeders in 14 patients through a microcatheter system. Before embolization, the pressures were significantly low in feeders with branches terminating in the malformation (terminal divided branches) and comparatively low in arteriovenous malformations with rapid blood flow through the malformation. The pressures in feeders with brain-nutrifying branches distal to the nidus (transient branches) were significantly high. Therefore, transient branches might be distinguishable from terminal divided branches with the use of feeder pressure monitoring. A hemorrhagic complication occurred in one patient. The feeder pressure in this patient was low before embolization and showed the maximum change among the patients after embolization. It seems that the lower the feeder pressure, the more likely complications are to occur, owing to remarkable hemodynamic alterations. Feeder pressure monitoring may be useful for preventing hemodynamic complications, especially when angiographic findings show feeding arteries giving off terminal divided or transient branches or rapid blood flow through the malformation.

Hemostasis in spontaneous subarachnoid hemorrhage.

To comprehensively examine changes in the hemostatic systems early after spontaneous subarachnoid hemorrhage (SAH) and to assess the relationships between those changes and neurological findings, computed tomographic findings, and clinical outcomes, we reviewed 167 patients who were admitted within 24 hours of the onset of SAH. Blood was taken from all of the patients at admission for detailed examinations of the hemostatic systems. The following results were obtained: 1) the levels of the thrombin-antithrombin complex (elevation indicating the activation fo the blood coagulation system), plasmin-antiplasmin complex, and D-dimer (elevation indicating the activation of the fibrinolytic system) significantly increased with the neurological severity, amount of subarachnoid clot, and severity of clinical outcome; 2) the levels of the thrombin-antithrombin complexes and plasmin-antiplasmin complexes were significantly higher in patients with intracerebral or intraventricular hematomas than in patients without those hematomas; 3) in each of almost all the neurological and computed tomographic grades, the levels of the thrombin-antithrombin complexes were significantly higher in the patients with poor outcomes than in those with good outcomes; 4) the poor outcome rate significantly increased with neurological severity and the amount of subarachnoid clot. These data suggest that the activation of the blood coagulation system as well as of the fibrinolytic system occurred early in the course of SAH and that these systems were activated to a greater extent with the severity of neurological grades, computed tomographic findings, and clinical outcome.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiogenesis in microvascular endothelial cells induced by glioma cells and inhibited by tumor necrosis factor in vitro.

Neovascularization is a prerequisite for glioma growth, so inhibition of angiogenesis may achieve control of glioma growth. We examined whether glioma cells induce angiogenesis and proliferation in microvascular endothelial cells from Fisher 344 rat brains by co-culture in a physical separation system with rat C6 glioma cells or rat T9 gliosarcoma cells. Endothelial cells cultured on type 1 collagen formed capillary-like structures. C6 glioma cells co-cultured with endothelial cells promoted the formation of these capillary-like structures. However, conditioned medium from C6 cells inhibited the proliferation of endothelial cells. T9 cells had little effect on the formation of capillary-like structures and no effect on the proliferation of endothelial cells. We also examined the effects of human tumor necrosis factor (TNF)-alpha on the formation of the capillary-like structures and on the proliferation of endothelial cells. Human TNF-alpha inhibited the formation of capillary-like structures induced by C6 glioma cells at a concentration of 100 U/ml, as well as the proliferation of endothelial cells at a concentration of 1000 U/ml. These results indicate that induction of angiogenesis varies with glioma cell lines and angiogenesis does not correspond with proliferation of endothelial cells. TNF-alpha can inhibit angiogenesis in gliomas in vitro.

Surgical experience with massive lobar haemorrhage caused by cerebral amyloid angiopathy.

Nineteen patients with massive lobar haemorrhage without angiographic lesions received direct or stereotactic surgery, and biopsy specimens were examined histologically. Ten patients (53%) were found to have vessels positive for Congo-red staining, and demonstrating amyloid angiopathy. In the patients with amyloid angiopathy, CT scan and surgical findings were investigated. Subarachnoid haemorrhage (9/10), irregularly shaped haematoma (9/10) and fluid-blood density level in the haematoma cavity (7/10) were frequently found on CT scan. The characteristic surgical findings in patients treated by direct surgery were subarachnoid haemorrhage adjacent to intracerebral haematoma (8/8) and the existence of a tangle of vessels in the haematoma cavity (4/8). Evacuation of haematomas was relatively easy, and difficulty of haemostasis was not encountered during surgery.

Effect of hypoxia on proliferation of microvascular endothelial cells derived from Mongolian gerbil brain.

This study investigated the effect of hypoxia on the proliferation of microvascular endothelial cells in the brain. Endothelial cells derived from microvessels of Mongolian gerbil brain and control cells (3T3) were incubated for 7 days under various hypoxic and normoxic conditions at 37 degrees C. The proliferation of endothelial cells was inhibited by severe hypoxia, but stimulated by moderate hypoxia. No significant effect of hypoxia on the proliferation of control cells was observed. Endothelial cell-conditioned medium cultured under moderate hypoxia did not affect the growth of endothelial cells. The stimulatory effect of moderate hypoxia on the proliferation of cultured endothelial cells is due to an inherent property of brain endothelial cells.

Liver dysfunction in spontaneous intracerebral hemorrhage.

The purpose of this study was to investigate the relationship between mild degrees of liver dysfunction and spontaneous intracerebral hemorrhage (ICH) from the hemostatic standpoint. A detailed study of hemostatic systems was made in 462 patients with ICH. To compare ICH with the other cerebrovascular diseases, data from 120 patients with subarachnoid hemorrhage and 114 others with cerebral infarction were reviewed. At admission, the medical histories of the patients, including information about previous alcohol consumption, was taken, and blood samples were collected to perform the following studies: platelet count, fibrinogen level, prothrombin time, activated partial thromboplastin time, antithrombin III, plasminogen and alpha 2-antiplasmin activity, platelet aggregability, and liver function tests. The incidence of liver dysfunction and alcohol consumption in patients with ICH was significantly (P < 0.05) higher than in patients with subarachnoid hemorrhage and in those with cerebral infarction. Hematoma volume, mortality rate, and past alcohol consumption in patients with ICH significantly increased with worsening severity of liver dysfunction. Although almost all hemostatic parameters became worse with increasing severity of liver dysfunction, they changed within the normal limits. Platelet aggregability and alpha 2-antiplasmin activity in patients with liver dysfunction were remarkably deteriorated beyond normal limits. In conclusion, liver dysfunction associated with alcohol consumption appears to be an important factor in the deterioration of the clinical status of patients with ICH and may be one of the causative factors in the development of ICH. Although mildly impaired hemostatic systems may be partially responsible for these adverse effects of liver dysfunction on ICH, it seems probable that nonhemostatic mechanisms are attributed to the effects.

Serial changes in hemostasis after intracranial surgery.

We performed hemostatic studies on eight patients undergoing clipping of unruptured cerebral aneurysms to assess the influence of intracranial surgery itself on hemostasis. Blood samples were collected from each patient 10 times: before and after the induction of anesthesia and 6, 12, and 24 hours and 2, 3, 5, and 7 days immediately after surgery. The changes and our interpretation of them include the following: 1) the elevation of thrombin antithrombin III complex levels (activation of blood coagulation) was transient and monophasic; 2) the elevation of plasmin alpha 2-antiplasmin complex and D-dimer levels (activation of fibrinolysis) was biphasic, despite the monophasic elevation of tissue plasminogen activator or plasminogen activator inhibitor-1 levels; 3) the elevation of beta-thromboglobulin and platelet-factor-4 levels (activation of platelet) was also biphasic; 4) fibrinogen level and alpha 2-antiplasmin activity increased in the acute phase of the postoperative course (acute phase reaction); 5) the changes in hematocrit appeared to parallel those in various other parameters, especially platelet count, antithrombin III, and plasminogen levels for 1 or 2 days after surgery; 6) fibronectin appeared to be consumed in the acute phase of postoperative course; and 7) general anesthesia did not significantly affect hemostasis. These serial changes seem to be related to the activation of hemostatic systems after intracranial surgery and the subsequent acute phase reaction.

Arteriovenous malformation associated with moyamoya disease: case report.

A rare case of arteriovenous malformation associated with moyamoya disease is reported. In this case, an interesting angiographic change was obtained during the follow-up period. The feeding artery from the internal carotid artery gradually disappeared as the moyamoya disease progressed, and a new feeding artery appeared from the external carotid artery.

Cerebral haemodynamic changes after endovascular treatment of arteriovenous malformations: evaluation by single-photon emission CT.

Cerebral haemodynamic changes in 17 patients with cerebral arteriovenous malformations (AVMs), who showed hypoperfusion on single-photon emission computed tomography (SPECT) before endovascular treatment, were studied after embolization. Nine of them had non-haemorrhagic clinical manifestations and the other eight had a history of intracranial haemorrhage. Obliteration of AVMs was nearly total in six patients and partial in eleven. New low density lesions on X-ray computed tomography (CT) developed in 3 of 6 patients after nearly total obliteration and one of 11 patients after partial obliteration. The first SPECT after embolization showed diminished hypoperfusion in 11 of 13 patients without new low density lesions and one of 4 patients with new low density lesions. Diminution of hypoperfusion was seen even in two patients who underwent SPECT study immediately after the embolization. Cerebral circulation was improved in five of eight patients with low density lesions before embolization and in nine of eleven patients after partial obliteration. Hypoperfused state in the haemorrhagic group tended to remain unchanged compared with that in the non-haemorrhagic group. The hypoperfused area was expanded after embolization in three patients with new cerebral infarction. It is important for improvement of cerebral circulation to reduce the shunt flow without causing new infarction due to the embolization itself. In one of two patients who had a hyperperfused area surrounding the AVM after embolization, an unexpected and abnormal degree of brain swelling and haemorrhage occurred at the end of the surgery 20 days after the embolization. In the other patient, total extirpation was successfully performed after confirming disappearance of hyperperfusion in the follow-up SPECT.(ABSTRACT TRUNCATED AT 250 WORDS)