MR spectroscopy and MR perfusion character of cerebral sparganosis: a case report.

The authors report the case of a 46-year-old woman with cerebral sparganosis resulting from infection with a larva of Spirometra. Computed tomography and magnetic resonance imaging revealed a mass lesion with prominent perifocal oedema in the left parietal lobe. Advanced imaging pulse sequences, including MR spectroscopy and MR perfusion, were performed. During surgery for the removal of a granuloma, the parasite was discovered and excised. Following treatment, the patient's neurological deficits markedly improved.

Dermal sinus with dermoid cyst in the upper cervical spine: case note.

We describe a 5 year-old girl who had a skin dimple of the back of her upper neck. MRI showed a dermal sinus tract in the upper cervical spine, associated with an intramedullary dermoid cyst at C 2-3, and spina bifida. A laminectomy was performed, the dermoid cyst and the sinus tract were completely removed. This congenital complex is very rare.

Isovolemic hemodilution normalizes the prolonged passage of red cells and plasma through cerebral microvessels in the partially ischemic forebrain of rats.

The objective of this study was to determine whether hemodilution could normalize the mean transit times of red blood cells (Tr) and plasma (Tp) through cerebral microvessels in a partially ischemic brain. Wistar-Kyoto (WKY) rats, aged 30-40 weeks, were divided randomly into three groups. The first group was the nonocclusion, nonhemodilution (NN) normal control group. The second group was the occlusion, nonhemodilution (ON) group, in which animals were treated with bilateral carotid artery ligation. The third group was the occlusion-hemodilution (OH) group, in which animals were treated with bilateral common carotid artery ligation and, then, isovolemic hemodilution by replacing blood with the same volume of 3% modified fluid gelatin. Local cerebral blood flow (lCBF) and microvascular volumes of red blood cells (Vr) and plasma (Vp) in 14 brain structures were measured using 14C-iodoantipyrine, iron-55 labeled red blood cells, and 14C-inulin, respectively. The amount of oxygen delivered to local brain structures (OD), cerebral microvascular blood volume (Vb), mean transit time of blood (Tb), Tr, and Tp through cerebral microvessels were calculated from the data. Two hours after carotid artery ligation, lCBF decreased by approximately 38% in forebrain structures, 22% in rostral hindbrain areas, and 8% in the caudal hindbrain (29% for all 14 structures). The decreases in ODs were parallel with those of lCBFs, at 33, 17, and 2% in the three regions, respectively (24% for all structures). In contrast, Vb increased by 68, 37, and 16% in the three regions, respectively (48% for all structures). Tr and Tp were markedly prolonged (180% for Tr and 154% for Tp) in the forebrain regions, moderately (91% for Tr and 73% for Tp) in the rostral hindbrain, and mildly (60% for Tr and 13% for Tp) in the caudal hindbrain, with a mean increase of 136% for Tr and 111% for Tp in all structures. When data in the OH and NN groups were compared, lCBF values tended to be slightly higher and Vb values were significantly higher (p < 0.05) in the OH group. ODs in the eight forebrain structures were all significantly less (p < 0.05) in the OH group than the NN group. Tr and Tp values in the forebrain were similar between the OH and the NN groups. In conclusion, occlusion of the bilateral common carotid arteries in WKY rats causes partial forebrain ischemia, in which both Tr and Tp are prolonged. These prolongations of Tr and Tp can be normalized by isovolemic hemodilution. However, the ischemic forebrain remains hypoxic after hemodilution.

Hemodilution accelerates the passage of plasma (not red cells) through cerebral microvessels in rats.

BACKGROUND AND PURPOSE: Hemodilution lowers the total circulatory red cell mass and blood viscosity and thereby may alter the time of passage of red cells and plasma through cerebral microvessels. This study was designed to clarify this question. METHODS: Adult Wistar-Kyoto rats, aged approximately 32 weeks, were divided into hemodilution and control groups. Local cerebral blood flow and microvascular red cell and plasma volumes in 14 brain structures were measured with the use of [14C]iodoantipyrine, 55Fe-labeled red cells, and [14C]inulin, respectively. RESULTS: In the control group, the hematocrit in cerebral microvessels ranged from 0.29 to 0.45 with a mean of 0.36, which was 71% of the systemic hematocrit (0.51). The mean transit times of blood, red cells, and plasma through microvessels were 0.62 to 1.77 seconds (mean, 0.92 second), 0.44 to 1.15 seconds (mean, 0.65 second), and 0.78 to 2.5 seconds (mean, 1.25 seconds), respectively. In the hemodilution group, the mean hematocrit in microvessels was 0.28, which was 89% of the systemic hematocrit (0.32). Local cerebral blood flow was approximately 59% higher (P < .01) than that of the control animals. The rate of oxygen delivered to the brain was slightly increased (9%) after hemodilution. Blood volume in cerebral microvessels was similar to that of the control group. Mean transit time of blood was 0.62 second (68% of the control), transit time of red cells was 0.53 second (85% of the control), and transit time of plasma was 0.67 second (54% of the control). CONCLUSIONS: These findings indicate that isovolemic hemodilution accelerates the plasma (not red cell) flow velocity in cerebral microvessels.

Transdural cortical stabbing facilitates the drainage of edema fluid out of cold-injured brain.

Recent experimental results indicate that cerebral glia lining and glia limitans may be barriers for plasma protein extravasated from injured cerebral microvessels flowing into the adjacent subarachnoid space. Therefore, it has been hypothesized that a transdural cortical stabbing which opens both the pia lining and glia limitans may facilitate drainage of edema fluid into the subarachnoid space and minimize brain edema. This hypothesis was tested in Sprague-Dawley rats with a transdural cold-injury on the right parietal cortex. The animals were sacrificed 24 hours later. One hour before being sacrificed 0.6 ml of 2% Evans blue was intravenously injected to determining the Evans blue distribution area. For measuring the inulin retention volume in the brain, 14C-inulin (10 microCi) in 1 ml of saline was injected intravenously at 10 min before sacrifice. The extent of brain edema was assessed by measuring the water content, the inulin retention volume, and the distribution area of Evans blue in the brain. Our results showed that the transdural cortical stabbing did not alter the water content of the cerebral hemisphere with cold lesion. However, it did effectively diminish the inulin retention volume by 26% as well as the distribution area of Evans blue by 22% in the cerebral hemisphere with cold lesion. In conclusion, a transdural cortical stabbing on the injured cortex may be beneficial for vasogenic brain edema.

Combined treatment with nicardipine, phenobarbital, and methylprednisolone ameliorates vasogenic brain edema.

Free radicals formed around the edematous areas of the brain can cause lipoperoxidation of the cellular membrane, followed by calcium influx into the cell through calcium channels. These secondary insults may aggravate vasogenic brain edema. Since phenobarbital is a free radical scavenger, methylprednisolone has an antilipoperoxidation effect; and nicardipine is a calcium channel blocker, we hypothesized that combined treatment with phenobarbital, methylprednisolone, and nicardipine would be beneficial in vasogenic brain edema. This hypothesis was tested in Sprague-Dawley rats with a transdural cold-injury on the right parietal cortex. The animals were randomly divided into two groups. Animals in the treatment group were injected intraperitoneally with phenobarbital (4 mg/kg), methylprednisolone (50 mg/kg), and nicardipine (10 micrograms/kg) at 5 min and 8 hours after the cold-injury. The control animals were injected with saline. These animals were sacrificed 24 hours after the injury. The extent of brain edema was assessed by measuring the water content, the inulin distribution volume, and the distribution area of Evans blue in the brain. Our results showed that the water content of the edematous hemisphere was similar in the control and the treatment groups. However, Evans blue distribution area and inulin distribution volume of the treatment group were less than those of the control group by 12% and 31%, respectively. In conclusion, the combined treatment with phenobarbital, methylprednisolone and nicardipine is beneficial in vasogenic brain edema.