Coil Embolization for Ruptured Cerebral Aneurysms of 2x3 mm Diameter.

SUMMARY: Small ruptured cerebral aneurysms, such as those of 2x3 mm diameter, are considered to be difficult to embolize by detachable coils because of the risk of procedural perforation of the aneurysms. We have treated these small aneurysms and report the techniques and pitfalls of these embolizations. Twenty-four patients with ruptured cerebral aneurysms of 2x3 mm diameter were intended for treatment by coil embolization. Before coil embolization, three-dimensional digital subtraction angiography was performed, and the simulation of the volume embolization ratio (VER) was performed in all patients, except for the first basilar artery aneurysm patient. The tip of the microcatheter was steam-shaped several times and was placed on the neck of the aneurysm. A balloon neck remodeling technique was used for two aneurysms. GDC 10 softs and soft SRs were used for the first ten aneurysms, and Ultrasofts were used for the last eleven aneurysms. Out of twentyfour aneurysm embolizations, we aborted the procedure in three cases, because of a failure in catheterization; we performed clipping surgery for these cases. For the first case of a basilar tip aneurysm, the aneurysm was perforated, due to the use of too long a coil and the insertion of the tip of the microcatheter into the aneurysmal dome. Minor infarction occurred in one patient. The mean VER was 33.9%, and two aneurysms recanalized, and out of these one needed a second embolization. Six months postoperatively, 81% of patients had made in a good recovery or had a moderate disability.We recommend the following techniques to embolize aneurysms of 2x3 mm diameter: the tip of the microcatheter should be stabilized on the aneurysmal neck by steam shaping of the microcatheter, GDC 10 soft and Ultrasoft should be selected for use, and the simulation of the VER should be performed before embolization to select coils of a suitable length.

Endovascular surgery as the first-choice treatment for ruptured cerebral aneurysms: how far has it come?

SUMMARY: One hundred and seventy patients with ruptured cerebral aneurysms were treated by coil embolization from September 1997 to December 2002. After January 2000, coil embolization was selected as the first-choice treatment for ruptured aneurysms. During this period, the authors investigated the number of aborted cases, the number of complications, and how many patients could be treated by coil embolization according to the locations of ruptured cerebral aneurysms. One hundred and ninety-five sessions were performed on 170 patients, and 13 sessions (6.7%) were aborted mainly because of the difficulty of the approach and the wide necks of the aneurysms. In four patients, although procedural perforation and haemorrhage occurred, the outcome was good or excellent. Eight poorgrade patients experienced haemorrhage after coil embolization and seven patients died. The volume embolization ratios of small and large aneurysms were 27% and 21%, and the recanalization of small and large aneurysms occurred in 9% and 38% of patients, respectively. From January 2000 to December 2002, 119 (66%) of 180 ruptured cerebral aneurysms were treated by coil embolization. According to the location of aneurysms, 89% vertebrobasilar, 87% anterior cerebral, 65% internal carotid and 24% middle cerebral artery aneurysms could be treated by coil embolization. Because the tight packing of large aneurysms was difficult, the recanalization rate of large aneurysms was high. However, the results of small aneurysms were satisfactory. Almost 90% of vertebrobasilar and anterior cerebral artery aneurysms could be treated by coil embolization.

Chronological changes of perihematomal edema of human intracerebral hematoma.

Recent investigations have indicated the importance of secondary brain damage in the pathophysiology of intracerebral hemorrhage (ICH), which includes ischemic brain damage and edema formation around a hematoma. The purpose of the current study is to investigate chronological changes of perihematomal edema in patients with human ICH and also the correlation between volume of perihematomal edema and neurological status. Fourteen patients with medium-sized putaminal hemorrhage (29.4 +/- 13.2 ml) without hematoma enlargement were included in this study. To investigate chronological changes of perihematomal edema, we performed CT scans prospectively on the day of hemorrhage and repeated them on days 1, 3, 7, 14, and 28. We evaluated the patients neurologically using the NIH stroke scale on the day a CT scan was performed. The volume of perihematomal edema in human ICH increased rapidly three days after hemorrhage and the score on the NIH stroke scale showed a deterioration. The volume of perihematomal edema then increased slowly until day 14 after hemorrhage, and decreased thereafter. Despite progression of perihematomal edema, the score on the NIH stroke scale improved gradually after day 3.

Correlation between cardiac output and cerebral blood flow following subarachnoid hemorrhage.

The authors examined the correlations between cerebral blood flow (CBF) during the stage of vasospasm following subarachnoid hemorrhage and four parameters, namely, cardiac output (cardiac index), mean arterial blood pressure, age, and the Glasgow coma scale score. Forty-two patients who were diagnosed to have subarachnoid hemorrhage were included in this study, and 50 measurements were performed between day 5 and 12 following the subarachnoid hemorrhage. The CBF was measured by stable xenon-enhanced CT and the mean values of four CBF maps were corrected for a PaCO2 of 34 mm Hg (CBF34). The cardiac output and cardiac index were continuously monitored during the CBF measurement. The correlation coefficients of cardiac index, mean arterial blood pressure, age, and GCS against CBF34 were, respectively, 0.436, 0.227, 0.037, and 0.225, and the p values were, respectively, 0.002, 0.074, 0.789, and 0.087. The CBF34 was positively correlated with only the cardiac index and not with any of the other three parameters. Therefore, an increase in the cardiac output is apparently associated with an increase in the CBF during the stage of vasospasm following subarachnoid hemorrhage. Furthermore, we measured the CBF and cerebral perfusion pressure before and after increasing cardiac output in three patients during the stage of vasospasm. The CBF increased by 22.5% +/- 2.9 (SD), with a 42.0% +/- 16.4 increase in the cardiac index, however, no significant change in cerebral perfusion pressure was observed. Therefore, the increase in CBF associated with the increase in cardiac output seems to be attributable to a reduction in the cerebrovascular resistance.

Isolated recurrence of granulocytic sarcoma of the brain: successful treatment with surgical resection, intrathecal injection, irradiation and prophylactic systemic chemotherapy.

We describe a 40-year-old male who developed an isolated recurrence of granulocytic sarcoma (GS) of the brain 2 years following successful treatment of acute myeloblastic leukemia (AML; M2). Computed tomography (CT) scans and magnetic resonance (MR) images demonstrated a homogeneously enhanced tumor mass in the left temporal lobe and massive peritumoral edema. There was no evidence of relapse in the bone marrow. The patient underwent an emergency surgical resection of the tumor. Five courses of injection with cytarabine and prednisolone through an Ommaya reservoir and whole brain irradiation (total 40 Gy) were performed. Furthermore, prophylactic systemic chemotherapy with cytarabine and etoposide was added. He has been in complete remission for 21 months. Our results, together with other reported cases, indicate that a favorable outcome could be obtained by intensive and combined treatment for an isolated recurrence of GS of the brain if the bone marrow remained in complete remission.

A clinical, genetic, neuropathological study in a Japanese family with SCA 6 and a review of Japanese autopsy cases of autosomal dominant cortical cerebellar atrophy.

This report concerns a Japanese family with genetically confirmed SCA 6, including an autopsy case, and a review of Japanese autopsy cases of autosomal dominant cortical cerebellar atrophy (ADCCA). The proband (Case 1) was a Japanese woman. She developed gait disturbance at age 62. The father and younger sister (Case 2) had the same disorder. She died at age 67 due to subarachnoid hemorrhage. Neuropathological examination revealed severe loss of Purkinje cells in the cerebellum, prominently in the dorsal vermis, and absence of neuronal loss in the inferior olives. Molecular genetic study showed the CAG-repeat expansion of SCA 6 gene. The younger sister (Case 2) developed gait disturbance at age 62. Neurological examination at age 66 revealed cerebellar signs without sensory disturbance. Neuroimaging at this time showed cerebellar atrophy, prominently in the vermis. She died of multiple myeloma at age 66. A neuropathological review of Japanese autopsy cases of ADCCA showed that there are two patterns in the distribution of cerebellar cortical lesions of Japanese patients with ADCCA. The distribution of cerebellar cortical lesions in genetically confirmed Japanese patients with SCA 6 is more prominent in the vermis than in the hemisphere.

Multiple spinal perimedullary arteriovenous fistulae associated with the parkes-weber syndrome. A case report.

SUMMARY: We present a rare case of multiple spinal perimedullary arteriovenous fistulae associated with the Parkes-Weber (PW) syndrome. A 31-year-old male known to have the PW syndrome involving the left leg since birth, presented with a 7-month-history of progressive myelopathy of the lower extremities and dysfunction of the bladder and bowel. Myelography demonstrated dilated intradural vessels. Angiography demonstrated two distinct single hole perimedullary arteriovenous fistulae near the conus at two different metameres. They were supplied by the left posterior spinal artery. The patient was treated by transarterial embolisation using polyvinyl alcohol particles, which resulted in venous side occlusion of the fistulae. After the treatment, the patient developed transient worsening of the spasticity of the lower extremities, and was treated by heparinization. After heparinization, the patient partially recovered from the pre-embolisation status of his myelopathy. The follow-up angiogram one year after the embolisation demonstrated persistent obliteration of both fistulae. At long-term follow-up, the patient can ambulate without assistance and work as a farmer.

Hemispheric cerebral atrophy after traumatic extra-axial hematoma in adults.

The relationship between traumatic extra-axial hematomas and cerebral atrophy was investigated in 42 adult patients aged between 15 and 50 years who required removal of extra-axial hematomas. These patients were followed up by serial computed tomography for more than 6 months after head injury. Nine of these patients developed cerebral atrophy. Their Glasgow Coma Scale score on admission was 6.4 +/- 2.8 (mean +/- SD). The score of the patients without cerebral atrophy was 9.6 +/- 3.3 (p < 0.01). These patients had three extradural and six subdural hematomas. All patients with cerebral atrophy had cerebral swelling postoperatively, more prominent in the hemisphere ipsilateral to the hematoma in seven patients. This swelling was associated with global hypodensity and persisted for 10.4 +/- 2.9 days. The severity of cerebral atrophy was more prominent in the hemisphere ipsilateral to the hematoma in five of these seven patients. Extra-axial hematoma in patients with severe head injury can induce hemispheric cerebral atrophy in the underlying cerebral hemisphere.

Correlation between cerebral blood flow values obtained by Xenon/CT and Kety-Schmidt (N2O) methods.

The means of the cerebral blood flow (CBF) values obtained by the stable xenon enhanced CT (Xe/CT) method using two different CT scanners were compared with global CBF value obtained by the Kety-Schmidt (N2O) method as a reference. Xe/CT CBF values were obtained using a GE CT9200 (31 patients, 2 flow maps, 120 kV, absorption constant of 0.040) as well as a GE ProSeed Accell (38 patients, 4 flow maps, 80 kV, absorption constant of 0.028). The protocol of inhalation in the Xe/XT method consisted of 4 min wash-in and 4-min wash-out of 35% stable xenon. In the Kety-Schmidt method, 15% N2O gas was inhaled for 10 min. The N2O content of blood samples was measured using a van Slyke-Neill blood gas analyzer. We corrected all obtained CBF values for a PaCO2 of 34 mmHG (CBF34). The global CBF34 values obtained by the Kety-Schmidt method were linearly correlated with the CBF34 values obtained using the CT9200 and with those obtained using the ProSeed Accell, and the regression line equations were, respectively, Y = 0.64X + 13.7 (X: CT9200, Y: Kety-Schmidt, r = 0.666, p < 0.01) and Y = 0.99X + 11.2 (X: ProSeed Accell, Y: Kety Schmidt, r = 0.756, p < 0.01). Since the CBF values obtained by the Xe/CT method using different CT scanners are not always the same as the global CBF values obtained by the Kety-Schmidt method, CBF values obtained by the Xe/CT method should be corrected referring to the regression line obtained by applying both methods for each patient.

Atrophy and maldevelopment of the ipsilateral cerebral hemisphere after acute subdural hematoma in infants.

Among nine infants aged less than 4 years with acute subdural hematoma admitted between 1980 and 1991, five required evacuation of a hematoma. Eight of them survived longer than 1 month and the remaining patient who had a hematoma removal died 3 days postoperatively. The four infants who required evacuation of a hematoma and survived longer than 1 month had prolonged hemispheric swelling ipsilateral to the hematoma lasting for 2 weeks postoperatively. Intracranial pressure was higher than 25 mm Hg during this period. Diffuse high density was observed in the affected hemisphere in one patient 12 days after injury, which was assumed to be hemorrhagic infarction. Subsequently, these four infants developed atrophy of the cerebral hemisphere ipsilateral to the hematoma. The pathophysiology of the atrophy of the cerebral hemisphere ipsilateral to the acute subdural hematoma is discussed.

Peritumoral edema in meningioma: a contrast enhanced CT study.

The propagation of extravasated contrast medium around 6 supratentorial meningiomas with peritumoral white matter of low density (PWL) of Lanksch II-III was investigated by repeated CT scanning at 4 h intervals, following a 1 h drip infusion of 200 ml of Iopamidol. The volume of the expanding peritumoral contrast enhancement was calculated according to a method previously described. By calculating the increase in volume from the first to the second scan, and from the second to third, we derived the rate of edema formation as well as the resolution rate of edema in the PWL. The surface area of the entire tumor (TS) and area of tumor surface facing the PWL (LS) were calculated by summating the surface areas of all CT slices, each area of which was derived from the measured length of the entire circumference of the tumor and circumference of the tumor facing the PWL, respectively, multiplied by the slice thickness of 0.5 cm. The volume of PWL, edema formation rate of entire tumor, and tumor volume x LS/TS were well correlated with each other. We concluded that the severity of peritumoral edema in meningiomas depends on the size of the tumor and the extent of tumor surface contact with the PWL.

High colloid oncotic therapy for contusional brain edema.

We investigated whether prolonged high colloid oncotic therapy for two weeks can suppress contusional brain edema. Eighteen patients with cerebral contusion were randomly divided into two groups of patients receiving high oncotic pressure (HOP; 26-30 mmHg) treatment and those receiving normal oncotic pressure (NOP; 22-26 mmHg) treatment. Oncotic pressure was maintained for two weeks with administration of a 25% albumin solution with additional use of furosemide. Edema volume was calculated by summation of all measured low-density areas in each CT slice multiplied by 1.0 cm of slice of thickness. We expressed contusional brain edema volume as a percent increase based on each patient's initial CT. The mean percent increase of contusional brain edema in the NOP group was significantly higher than that in the HOP group at 9-15 days (208.9% and 14.0%, respectively) and 16-25 days (188.8% and 10.0%, respectively). There were no complications such as heart failure or renal failure during treatment. All the patients in the HOP group recovered with minimal or no neurological deficit. On the other hand, 30% of patients in the NOP group remained in poor condition. With frequent measurement of oncotic pressure and adjustment of fluids and electrolytes, continuous oncotic therapy for two weeks effectively and safely reduced contusional brain edema.

High colloid oncotic therapy for brain edema with cerebral hemorrhage.

We examined the effectiveness of high colloid oncotic pressure (COP) therapy to suppress and/or reduce brain edema associated with putaminal hemorrhage of patients whose clinical grades were grade 3 or 4a classified according to the Japanese neurological grading for putaminal hemorrhage. In the treated group of 11 patients, 25% albumin solution was intravenously administered (50-100 ml/day) with additional use of furosemide (20-40 mg/day) following hematoma removal. The serum COP was maintained at 25-30 mmHg for 2 weeks. In the untreated group of 11 patients, the COP therapy was not applied following hematoma removal. The serum COP was 20-25 mmHg for 2 weeks thereafter. During the 2-week observation period, serum osmolality, electrolyte, and hematocrit levels did not significantly differ between the two groups. The midline structure shift on CT of the treated group was 4.5 mm, which was significantly smaller than that of the untreated group (p < 0.05). The numbers of patients either in the vegetative state or death were 0 and 3, respectively, in the treated and the untreated groups. We concluded that high COP therapy for 2 weeks following hematoma removal was effective to suppress and/or reduce brain edema associated with putaminal hemorrhage, and that this therapy could be continued for 2 weeks without systemic complications.

[Measurement of serum colloid oncotic pressure as a parameter of hemodilution and hemoconcentration in hypervolemic-hyperdynamic therapy for symptomatic vasospasm].

Nineteen patients, who developed symptomatic vasospasm due to subarachnoid hemorrhage, were treated by hypervolemic-hyperdynamic therapy. The object of this treatment was to increase cardiac output and cerebral blood flow as a result of hypervolemia and the administration of beta-stimulants. During the treatment, if cerebral infarction occurred followed by brain edema, we applied oncotic therapy. As the parameters of therapy, we measured serum colloid oncotic pressure and cardiac functions in all of these patients. Nineteen patients were divided into two groups: group A, 9 patients, who did not develop brain edema, and group B, 10 patients, who developed brain edema. All patients underwent acute neck clipping surgery and plasma volume expansion by the infusion of albumin and/or low molecular weight dextran (LMWD). If symptomatic vasospasm occurred, a Swan-Ganz catheter was inserted and cardiac output was measured until it increased to 1.5 times the value of pretreatment. In group B, we also used oncotic therapy, raising serum oncotic pressure higher than 25 mmHg by increasing the amount of albumin and/or LMWD and administering furosemide. By this treatment, the percentage of patients who showed neurological improvement in at least one deficit was 100% in group A, and 89% in group B. In Glasgow outcome scale scores, 89% of group A and 70% of group B had disability not lower than moderate. Serum colloid oncotic pressure was maintained at around 20-25mmHg in group A, and 25-30mmHg in group B. Although pulmonary artery diastolic pressure in group B tended to be lower than that in group A, cardiac indices in both groups were high, approximately 5.0 L/min/m2.(ABSTRACT TRUNCATED AT 250 WORDS)

Regional [14C]palmitate incorporation into the hippocampus after transient cerebral ischemia in awake gerbils.

Incorporation of plasma [14C]palmitate into the hippocampus was measured using quantitative autoradiography and a ratio method of analysis between 10 min and 7 days after 5 min of bilateral occlusion of the common carotid arteries in awake gerbils. One day after carotid occlusion, relative palmitate incorporation was elevated by 16% and 20%, respectively (p less than 0.01), in the CA4 pyramidal cell layer and dentate gyrus of the hippocampus as compared with sham-operated animals. At 3 days, significant elevations of this magnitude were found in the CA3 and CA4 cell layers, and relative incorporation was reduced by 26% in the CA1 pyramidal cell layer. At 7 days, the only significant difference from control was a 15% elevated incorporation in the CA3 pyramidal cell layer. The results suggest that the turnover of palmitate-containing lipids is retained in the CA1 pyramidal layer of the gerbil hippocampus for 1 day and then reduced at 3 days after 5-min ischemia and that lipid synthesis is stimulated in hippocampal regions affected by but recovering from an ischemic insult (CA3, CA4, dentate gyrus).

Formation and resolution of white matter oedema in various types of brain tumours.

Following infusion of 200 ml of Iopamidol for 1 hour the propagation of extravasated contrast medium around different types of 12 brain tumours was examined and imaged via CT. Increasing volume of expanding peritumoural contrast enhanced brain tissue was measured by integrating volumes of planimetrically measured enhanced area on CT slice of 0.5 cm in thickness. So far our data failed to demonstrate differences in the peritumoural contrast expansion between the different types of tumours. Formation and resolution as well as the speed of oedema propagation were determined by calculation of the increasing volume of the enhanced peritumoural brain tissue. Average formation rate of oedema fluid from 1 cm3 of tumour was 0.06 ml/hr, and was lower in larger tumours, while formation rate of oedema fluid from whole tumour was higher in larger tumours. Average resolution rate of oedema fluid during the passage through 1 cm3 of the peritumoural white matter was 0.03 ml/hr, and was not affected by tumour size. Average speed of oedema propagation was 0.59 mm/hr, and was higher in larger tumours. The main therapeutic effect of steroid in peritumoural oedema was a reduction in formation rate of oedema fluid.

Changes in cerebral hemodynamics following encephalo-duro-arterio-synangiosis (EDAS) in young patients with moyamoya disease.

To evaluate the effect of encephalo-duro-arterio-synangiosis, (EDAS), we obtained follow-up angiograms and measured regional cerebral blood flow in 21 young patients with Moyamoya disease. Carotid fork stenosis continued to progress after EDAS, although angiography demonstrated a marked increase in the number of middle cerebral artery branches via implanted arteries. Preoperative cortical blood flow was lower than normal. The post-EDAS increases in hemispheric and cortical flow were significant in patients with transient ischemic attacks, but not in patients with infarction. The increase in cortical flow at the site of EDAS was first noted 2 weeks after EDAS.

[The anatomy and pathology of the brain stem demonstrated by thin slice CT cisternography].

We demonstrated normal CT anatomy of the brain stem and adjacent structures using thin slice CT cisternography. Reducing the streak artifact caused by bony structures, thin slice CT cisternography can visualize the detailed features of the brain stem and its pathological changes. In addition, reconstructed images are also useful in diagnosis.

Regional cerebral palmitate incorporation after unilateral auditory deprivation in immature and adult Fischer-344 rats.

Regional cerebral incorporation of intravenously injected [U-14C]palmitate was measured from 1 day to 13 weeks after left cochlear destruction in 11-day- and 3 month-old, awake Fischer-344 rats. In 11-day-old animals, statistically significant left-right differences in incorporation were absent 1 day after cochlear destruction and were found only in parts of the cochlear nucleus and inferior colliculus after 1 week. After 6 to 13 weeks, consistent with functional neuroanatomy of central auditory regions, incorporation was reduced by 6 to 9% in the left cochlear nucleus and left lateral superior olivary nucleus, compared with corresponding right-side regions. The right medial superior olivary nucleus, medial nucleus of the trapezoid body, lateral lemniscus nucleus, inferior colliculus, medial geniculate body, and auditory cortex had 5 to 9% less incorporation than did corresponding left-side regions. Fewer significant differences after chronic auditory deprivation occurred in 3-month-old rats than in 11-day-old rats following cochlear destruction. Reduced incorporation corresponded to reported changes in cell morphology, which also were greater in immature than mature rats following auditory deprivation. The results suggest that the palmitate method can be used to identify long-term regional changes in the turnover of brain lipids after sensory deprivation.