Kiyoshi Nagata

Dural arteriovenous fistula of the posterior fossa developing after surgical occlusion of the sigmoid sinus

✓ In this article, the authors present five cases of dural arteriovenous fistula (AVF) that developed in the transverse—sigmoid sinus 2 to 6 years after sacrifice of the sigmoid sinus because of tumor involvement. The original tumor was meningioma in two patients and neurinoma, glomus jugulare tumor, and ameloblastoma in one patient each. The involved sigmoid sinus was resected along with the tumor and ligated at the normal edge; all that remained of the sigmoid sinus was a small stump on the retrosigmoid portion. Serial angiography performed before and after tumor surgery revealed no abnormal arteriovenous communications or dural AVF in any of the cases. Although many reports have suggested that sinus thrombosis is a precipitating factor in the pathogenesis of dural AVFs, this has been difficult to verify because of the small number of cases in which serial angiography was performed before the development of a dural AVF. In all of the cases presented in this article, surgical resection of a dural AVF and...

Observation of arterial and venous thrombus formation by scanning and transmission electron microscopy

SummaryBackground. In order to examine the process of thrombosis formation in artery and vein, the reactions of the arterial and venous endothelial surfaces were examined by scanning electron microscopy (SEM) and transmission electron microscopy (TEM) in the photothrombosis model. Materials and methods. Thirty-nine rats were divided into the following 4 groups: 1) Sham group (n=5) without illumination, 2) group A (n=10) irradiated for 1 min, 3) group B (n=10) irradiated for 5 min, 4) group C (n=14) irradiated for 10 min at the level of the left common carotid artery and internal jugular vein. Results. SEM provided no evidence of damage or adhesion of blood platelets to the endothelium of either the artery or vein in shams or group A animals. In group B, evidence of damage to endothelial cell membrane (e.g., plasmalemmal pits, crater-like structures associated with tears between endothelial cells, and decreased number of microvilli) was obtaind in the arterial wall but not in the vein. In group C, there was extensive or widespread adhesion of blood platelets and other cells, tears between arterial endothelial cells, and a decrease in the number of microvilli in the artery but not in the vein (p<0.05). Conclusions. Cell membrane injuries, tears between the endothelial cells, and endothelial detachment occur before adhesion of blood platelets and thrombus formation in the blood vessel occlusion model by photochemical reaction. These changes occur significantly earlier in the artery than in the vein.

The effect of brain compression under venous circulatory impairment.

Abstract It is well known that surgical obliteration of the cerebral veins with additional brain compression by retractors is dangerous. To evaluate the mechanism, we, studied the change in cerebral microcirculation and parenchymal damage following brain compression with venous circulatory impairment using a rat model. The animals were divided into the following four groups (each n = 5) (1) a sham-operated control; (2) group A, one cortical vein occlusion; (3) group B, a 30 mmHg compression pressure; and (4) group C, one cortical vein occlusion with 30 mmHg compression. The cortical vein was occluded photochemically. Local cerebral blood flow (I-CBF) in the compressed area was measured by stationary laser-Doppler (LO) flowmetry and regional CBF (r-CBF) in the surrounding area was also measured by LO scanning technique for 120 min. I-CBF in the compressed area decreased significantly in groups Band C. A gradual and significant increase in group B and decrease in group C in r-CBF of the surrounding area were observed. Histologically, more extensive damage was observed in group C than in group A and B. The degree of hypoperfusion of the affected brain correlated well with the subsequent brain damage in the experiments. We demonstrated that, compared with vein occlusion or brain compression alone, the accumulated episode caused severe ischemia, then increased the vulnerability of the rat brain to tissue damage. [Neural Res 2000; 22: 713-720]

Intermittent isometric exposure prevents brain retraction injury under venous circulatory impairment

Abstract It is recognized that surgical obliteration of the cerebral veins by additional brain compression using retractors is dangerous. However, there is a lack of satisfactory management of this problem. We investigated whether intermittent brain compression can reduce brain injury from cerebral venous circulation disturbances (CVCDs). In Wistar rats (n = 25), a solitary cortical vein was occluded photochemically. The brain surface was compressed by a spring balance and constant compression at 30 mmHg was carried out for 60 min. Intermittent procedure compression protocols included four 15 min compressions at 5 min intervals, intermittent isometric exposure (IM), and intermittent isotonic exposure (IT). Local cerebral blood flow (lCBF) in the compressed area was measured together by laser-Doppler (LD) with the degree of brain compression. After 24 h, the brains were examined histologically. The animals were divided into the following five groups (each n = 5): 1, a sham operated control; 2, cortical vein occlusion (VO); 3, VO + continuous brain compression (CC); 4, VO + IM; and 5, VO + IT. The lCBF decreased significantly during the compression; however, recovery after the series of compressions was observed only in the VO + IM group, not in the VO + CC and the VO + IT groups (p < 0.05). The depth of the brain surface increased stepwise in the VO + IT group compared with the VO + IM group (p < 0.01). The resulting tissue damage was significantly larger in the VO + CC and VO + IT groups than in the vein occlusion group (p < 0.05), but not in the VO + IM group. The results of the present study suggest that intermittent isometric exposure under CVCDs could decrease brain retraction injury during neurosurgical operations and be more beneficial than continuous compression, providing that the compression pressure declines as the process advances. [Neurol Res 2001; 23: 739-744]

Extensive Parasellar Chondroma with Ollier's Disease

A 37-year-old woman with known Olliers disease presented with visual ®eld disturbance. Computed tomography and magnetic resonance imaging (Fig. 1 a) revealed a partially calci®ed or ossi®ed intracranial mass in the right parasellar region arising from the right upper clivus and cerebellopontine angle region. Three-dimensional axial reconstruction from axial CT data with contrast media demonstrated that the right internal carotid and anterior cerebral arteries were buried under the tumour (Fig. 1 b). Selective right internal and external carotid angiography revealed the large hypovascular mass to be displacing the carotid canal part of the right internal carotid artery antero-laterally and the anterior cerebral artery rostrally. Partial removal was performed through Le Fort I maxillotomy, revealing a soft, extradural, gelatinous tumour with a calci®ed component extending cranially. Histologically, the tumour cells, including double nucleated cells, demonstrated relatively high cellularity with mild atypia. The postoperative course was uneventful, and she returned to her job one month after the operation.

Delayed intracerebral haemorrhage after intracranial surgery

Intracerebral haemorrhage may occur several hours after intracranial surgery. The exact mechanism by which this occurs is still unclear, although prolonged brain retraction is considered to be the most responsible factor. In these delayed postoperative haematoma cases, serial angiography has never been performed. We performed angiographic evaluation in such 12 cases and, in 5 of them, surgical evacuation of the haematoma was performed because of life-threatening mass effect and the cortical veins and the surrounding cerebral tissues were examined histologically. In all cases, angiographically thrombotic difufse occlusion of the cortical vein(s) without collateral circulation was observed, and histologically there was marked damage to the intima of the vein, remarkable macrophage infiltration into the subadventitial spaces, and extensive red cell extravasation into the subarachnoid space and brain parenchyma from the maximally dilated venules and capillaries. These findings suggest that diffuse intravenous thrombosis induced by cortical vein injury and prolonged brain retraction may be important causes of unexpected delayed postoperative intracerebral haematoma in surgery using the interhemispheric or subtemporal approach.

A Case of Recurrent Hemorrhages due to a Chronic Expanding Encapsulated Intracranial Hematoma

Few case reports of encapsulated intracranial hematoma (EIH) exist, and the mechanisms underlying the onset and enlargement of EIH remain unclear. Here, we report on a 39-year-old woman with an EIH that repeatedly hemorrhaged and swelled and was ultimately surgically removed. In June 2012, the patient visited her local doctor, complaining of headaches. A magnetic resonance imaging (MRI) scan identified a small hemorrhage of approximately 7 mm in her right basal ganglia, and a wait-and-see approach was adopted. Six months later, her headaches recurred. She was admitted to our department after MRI showed tumor lesions accompanying the intermittent hemorrhaging in the right basal ganglia. After admission, hemorrhaging was again observed, with symptoms progressing to left-sided hemiplegia and fluctuating consciousness; thus, a craniotomy was performed. No obvious abnormal blood vessels were observed on the preoperative cerebral angiography. We accessed the lesion using a transcortical approach via a right frontotemporal craniotomy and removed the subacute hematoma by extracting the encapsulated tumor as a single mass. Subsequent pathological examinations showed that the hematoma exhibited abnormal internal vascularization and was covered with a capsule formed from growing capillaries and accumulating collagen fibers, suggesting that it was an EIH. No lingering neurological symptoms were noted upon postoperative follow-up. This type of hematoma expands slowly and is asymptomatic, with reported cases consisting of patients that already have neurological deficits due to progressive hematoma growth. Our report is one of a few to provide a clinical picture of the initial stages that occur prior to hematoma encapsulation.