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BACKGROUND AND STUDY AIMS: Although hemorrhagic colitis due to enterohemorrhagic Escherichia coli O157:H7 (O157) infection has recently attracted increasing attention as an important enteric infection, the colonoscopic findings associated with this disease have not been sufficiently characterized. The aim of this study is to characterize the colonoscopic features of hemorrhagic colitis due to O157 infection. PATIENTS AND METHODS: The colonoscopic findings in ten patients with hemorrhagic colitis due to O157 infection were retrospectively reviewed. To assess the severity of inflammation in each part of the large intestine, colonoscopic findings were categorized into four grades: grade 1, intact mucosa; grade 2, sporadic erythema and erosion; grade 3, mostly diffuse inflammation; and grade 4, diffuse, severe inflammation. RESULTS: Eight out of ten patients had grade 4 findings in the cecum and ascending colon, grade 3 in the transverse colon and descending colon, and grade 2 in the sigmoid colon. Two of these eight patients also had grade 4 inflammation in the proximal transverse colon. Five of these eight patients revealed longitudinal ulcer-like lesions in the transverse colon and/or descending colon. The remaining two patients had grade 3 findings in the cecum to the descending colon and grade 2 findings in the sigmoid colon. All patients exhibited grade 1 finding in the terminal ileum and the rectum. Based on these colonoscopic findings, the ten patients were divided into the typical group (eight patients) and the mild-type group (two patients). CONCLUSIONS: The characteristic colonoscopic findings in most patients with hemorrhagic colitis due to O157 infection were as follows: 1) severe inflammation, including primarily marked edema and facile hemorrhage, and 2) inflammation predominating at the right-side colon; and 3) frequent appearance of longitudinal ulcer-like lesions.

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Decision making for either surgery or gamma-knife for the treatment of arteriovenous malformations (AVMs) cannot be uniform. The skill of the neurosurgeon in operating on AVMs is now being compared with that of the gamma-knife. The decision varies from case to case and is to be taken by the neurosurgeon. This report presents three cases in which such decision making was not easy. Case 1 was a non-ruptured cingulate AVM of 2.5 cm diameter in the cingulate cortex. The operative field was anticipated to be very narrow between the parietal bridging veins. Case 2 was a tiny ruptured AVM in the speech-motor area which was buried underneath the cortex. Case 3 was a large ruptured thalamo-stiriate-capsular AVM with feeders from the anterior and posterior choroidal arteries. All cases were operated without serious morbidity. A combination of pre-operative intravascular surgery (cases 1 and 3) or postoperative gamma-knife (case 3) was adopted. In conclusion, there is no unitary rule to decide on surgery or gamma-knife for the treatment of AVMs. It depends on what good or harm the responsible surgeon or the gamma-knife does.

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BACKGROUND: Jugular bulb diverticulum is a rare condition that has never been reported in association with lower cranial nerve palsy. CASE DESCRIPTION: A 54-year-old woman developed acute swallowing disturbance and hoarseness. Neuroradiological examinations demonstrated a jugular bulb diverticulum as well as unruptured internal carotid and basilar tip aneurysms on the same side. Laboratory data for both serum and cerebrospinal fluid were normal. Steroids were given, and the cranial nerve palsy disappeared within 1 month. The aneurysms were successfully clipped. During the follow-up period of more than 1 year, the patient has done well and has no neurological deficit. CONCLUSION: This is the first reported case of jugular bulb diverticulum associated with a lower cranial nerve palsy and multiple aneurysms. We recommend close observation of patients with this condition regardless of its clinical presentation.

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It has been reported that corticosteroids exert their anti-inflammatory action through de novo synthesis of phospholipase-inhibitory proteins called lipocortins (annexins). We postulated that the following may lessen the effectiveness of corticosteroids on acute ischemic brain edema: 1) lipocortins are induced several hours after administration of steroids; 2) de novo synthesis of lipocortins is suppressed in the ischemic brain; and 3) lipocortins induced systemically do not pass through the blood-brain barrier (BBB) to reach the sites of ischemic edema. To test this hypothesis, we examined whether dexamethasone, given long before ischemia or direct administration of recombinant lipocortin-1, combined with or without BBB opening, ameliorate ischemic brain edema. Three hours before occlusion of the middle cerebral artery (MCA) in the cat, 4 mg/kg of dexamethasone was injected intravenously. The animals were subjected to 4 hours of ischemia. Alternatively, 2 ug/ml (total volume 10 ml) of recombinant human lipocortin-1 (annexin-I) was perfused intermittently into the ischemic focus by catheterization into the MCA. Artificial opening of the BBB was performed by intra-arterial mannitol infusion. None of these strategies demonstrated amelioration of ischemic edema. We conclude that: Dexamethasone and recombinant lipocortin-1 seem unlikely to have robust effects on amelioration of acute ischemic edema.

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Based on evidence that corticosteroids exert their anti-inflammatory action via de novo synthesis of phospholipase A2 inhibitory proteins called lipocortins, we examined effects of high dose dexamethasone and recombinant human lipocortin-1 (annexin-I) on cold-injury brain edema in the rat. Since it takes several hours for lipocortins to be induced, dexamethasone (10 mg/kg) was injected intraperitoneally 3 hours before cold injury. Recombinant lipocortin-1 was administered intraventricularly at three different doses (0.01 mg/kg, 0.05 mg/kg, or 0.1 mg/kg: total volume 20 microliters), or via the internal carotid artery at a dose of 10(-7) M (2 ml). To induce cold injury, a liquid-nitrogen-cooled probe was placed on the exposed dura of male Wistar rats (330-370 kg) for 1 minute. Specific gravimetry and/or a wet-dry weighing method were used for measurement of brain edema at 24 or 48 hours after lesion production. In the present study, dexamethasone and recombinant lipocortin-1 failed to attenuate edema formation. The anti-inflammatory effects of dexamethasone or exogenous lipocortin-1 seemed unlikely to affect cold-injury brain edema.

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BACKGROUND: A more simplified and easier technique for the orbitozygomatic approach is sought. We have developed a new modification to fully expose the temporal base before using one-piece craniotomy. METHODS: By transposing the temporalis muscle underneath the zygomatic arch before osteotomy, the temporal base and the inferior orbital fissure can be fully exposed. Craniotomy is made in one piece with the frontotemporal and orbitozygomatic bone together by using a high-speed drill. RESULTS AND CONCLUSIONS: Osteotomy was easy and the cosmetic result was satisfactory. This technique also allows better access to the subtemporal region without removing the zygomatic arch.

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BACKGROUND: Whereas the transcranial approach has been regarded as the therapy of choice for transethmoidal encephalocele, its feasibility for transsphenoidal encephalocele has remained controversial, particularly in neonates and infants. CASE REPORT: Two cases of transsphenoidal encephalocele operated transcranially are presented. In the first case, this 6-year-old boy underwent a transpalatal operation with repair of a cleft palate in another hospital before admission. Reoperation via the transcranial route was carried out because of postoperative recurrent meningitis. With partial resection of the anterior wall, the encephalocele could be separated from the underlying tissue, and the interspace was filled with the pericranial flap. He made an uneventful recovery and has been well for the past 3 years. The second was a 3-month-old baby with a large encephalocele filling the nasopharyngeal space. As the cleft palate was absent, the transcranial approach was employed. In this case, the herniated tissue was excised at the lowest level possible. Postoperatively, panhypopituitarism became manifest. Re-evaluation of the preoperative magnetic resonance imaging (MRI) disclosed a small mass far below the dorsum sellae, which turned out to be an anomalous pituitary gland on histologic examination. CONCLUSIONS: The transcranial approach is considered a valid alternative for the therapy of transsphenoidal encephalocele, particularly when the transpalatal approach is unfeasible. While the anterior wall of the herniated sac may be safely resected, the posterior wall should under no circumstances be sacrificed. The preoperative MRI is essential, as it may provide valuable information as to the location of vital structures within the herniated tissue.

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Strain TZS-7, tentatively identified as Sphingomonas paucimobilis, was isolated from crude oil for its ability to degrade dibenzothiophene (DBT) and 4,6-dimethyldibenzothiophene (4,6-dmDBT). This strain did not utilize DBT or 4,6-dmDBT as the sole source of sulfur. However, the degradative activity was induced by various aromatic compounds, including DBT, fluorene, anthracene, naphthalene and toluene. Three products formed from 4,6-dmDBT degradation were detected and two of these were proposed to be 7-methyl-3-hydroxy-2-formylbenzothiophene and 7-methylbenzothiophene-2,3-dione by gas chromatography-mass spectrometry analysis. These findings proved that 4,6-dmDBT is degraded through a ring-destructive pathway by resting cells of strain TZS-7.

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Utilizing a specific polyclonal antibody against a peptide unique for brain-derived neurotrophic factor (BDNF), we investigated the regional and temporal profiles of immunoreactivity of the BDNF protein in the rat hippocampus after transient forebrain ischemia. The pattern of immunoreactivity for the BDNF receptor (TrkB) was also examined and compared with that for BDNF. In the early phase after ischemia, we observed a distinct regional difference in immunoreactivity between the pyramidal cell layer and the stratum radiatum of the CA1 subfield. In the pyramidal cell layer, there was a rapid and transient increase in the positive immunostaining for both BDNF and TrkB. By contrast, in the stratum radiatum there was a marked decrease in BDNF immunoreactivity, but not one in that of TrkB. One week after ischemia, high immunoreactivity for both BDNF and TrkB was observed in the reactive astrocytes in the dendritic field of the CA1 subfield. These findings suggest that a transport of BDNF from the neuronal soma to the dendrites of the stratum radiatum might be ceased after the ischemic insult. Thus, a dysfunctional autocrine mechanism of BDNF within the CA1 neuron may be involved in the pathogenesis of selective neuronal damage after ischemia.

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A hypertensive 72-year-old male presented with a ruptured arteriovenous malformation (AVM) manifesting as hematoma indistinguishable from common putaminal hemorrhage on precontrast computed tomography scan. The AVM was located in the proximal sylvian region fed by branches of the anterior and middle cerebral arteries. The AVM was totally removed. Although bleeding from AVM in the elderly is uncommon, the cause of even common hypertensive hemorrhage should be identified by other imaging techniques such as magnetic resonance imaging and cerebral angiography to allow the optimum treatment.

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Using the canine chronic cerebral vasospasm model, we studied the effects of a potent new nonpeptidic endothelin-1 (ET1) receptor antagonist, bosentan (Ro 47-0203, 4-tert-butyl-N-[6-(2-hydroxy-ethoxy)-5-(2-methoxy-phenoxy)-2,2'-bipyr imidin-4 - yl]-benzenesulfonamide). Endothelin (ET) receptors are composed of the ETA receptors and the ETB receptors; ET1 acts on both of these receptors. Although it has been previously thought that the ETA receptor mediates vasoconstriction, whereas the ETB receptor mediates vasodilation, recent evidence suggests that ETB receptor also contributes to vasoconstriction. Because bosentan is a mixed antagonist that acts on both receptors, its use might indicate whether or not ET is involved in the pathogenesis of cerebral vasospasm. In this study, beagle dogs received a double injection of autologous arterial blood into the cisterna magna at 2-day intervals (i.e., on Days 0 and 2). The diameter of the basilar artery (BA) was angiographically examined up to Day 7. A total of 24 dogs were randomly allocated to either the treatment group or the no-treatment group. Eight dogs were treated with 10 mg/kg bosentan by a one-dose injection into a central venous catheter. Bosentan was given twice a day starting immediately after the first subarachnoid hemorrhage for 6 days until Day 5. Sixteen dogs served as controls, with untreated subarachnoid hemorrhage. After the injection of bosetan, blood pressure decreased by about 25 mm Hg for a few minutes and then returned to normal. In the dogs treated with bosentan, the BA spasm on Day 7 was significantly ameliorated compared with the BA spasm in the untreated dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

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In the present paper, we describe the surgical techniques of high lateral cervical approach and its feasibility for the excision of tumors located in the ventral or lateral aspect of the upper cervical vertebrae and of the craniovertebral junction. The patient is positioned laterally on the operating table, but the operator's position and the skin incision are slightly altered depending on the location of the tumor. When the lesion is situated below C1, the ipsilateral shoulder is pulled down toward the back. The operator stands rostral to the head. The attachment of the sternocleidomastoid muscle to the mastoid is detached and reflected anteriorly through a retroauricular curved skin incision. The posterior cervical muscles such as the splenius capitis, longissimus capitis, semi-spinalis capitis are detached from the occipit and retracted posteriorly. At this point, the transverse process of C1 and the articular facet of the vertebrae of C2-C4 are identified by palpation. According to the tumor location, the muscles attached to the relevant transverse processes and facets are divided and reflected posteriorly. Through careful dissection, the cervical nerve roots and the vertebral artery are exposed. The root sleeves as well as thecal sac may be exposed by resecting the posterior two-thirds of the superior and inferior articular facets and the adjacent laminae of the vertebrae. In case the whole facet was removed, an iliac bone graft is placed between the remaining transverse processes and the laminae above and below for fixation.(ABSTRACT TRUNCATED AT 250 WORDS)

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Enlargement of the foramen of Monro is an essential maneuver to obtain an appropriate surgical view when large, solid lesions in and around the third ventricle are to be removed via the anterior transcallosal approach (ATA). For this purpose, three methods, i.e., the subchoroidal, transchororidal, and transfornicial approaches have so far been reported. However, since the locations and the pathological natures of space occupying lesions in this region are widely variable, the indication as well as the feasibility of each approach has remained rather unclear. The present paper deals with our surgical experience with six patients (2 gliomas, 1 angioma, 1 AVM, 1 plexus papilloma, 1 basilar top aneurysm) operated on using the ATA in which variable methods of enlarging the foramen of Monro were employed. Aiming at complete removal or clipping of the lesion, the seemingly best among the above three approaches was determined preoperatively, considering the size, location, and pathological nature of the lesion. The shape of the choroid plexus of the roof of the IIIrd ventricle as revealed by MRI was also taken into account. The subchoroidal, transchoroidal, and the transfornicial approaches were employed in 3, 2, and 1 cases, respectively. Except for one glioma which ended up being removed extensively, all the tumors and AVM were totally removed and the aneurysm successfully clipped. From the above experience, the merits and demerits of each approach for different types of lesions are discussed in view of their suitability for achieving total removal.(ABSTRACT TRUNCATED AT 250 WORDS)

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Although almost all infants suffering chronic subdural hematomas (CSDH) are successfully treated by established methods such as a subdural puncture, burr holes and shunting procedures, infantile CSDH with progressive craniocerebral disproportion requires a special therapeutical regimen. Clinical efforts such as reduction cranioplasty have been made as a treatment for these cases. This is a case report of a 9-month-old male infant with an intractable CSDH, bilateral and large, and subsequent brain atrophy caused by traumatic head injury. Excellent results were obtained by a modified reduction cranioplasty. In brief, the patient was supine-positioned with a 20-degree flexion of the head in an attempt to obtain a large operative field. Bicoronal skin incision was combined with an additional linear one on the midline (T-shaped incision). Bilateral frontoparietal craniotomy with periosteum was made to keep the midline bony bridge overlying the superior sagittal sinus (SSS). The resulting extensive dural opening allowed complete evacuation of the subdural hematoma. Thereafter, the anterior part, ca. 4cm in width, of the bony bridge was removed in order to make the remaining bone able to be manipulated and connected to the frontal bone. Prior to this stage, SSS close to the crista galli was ligated and cut with the falx to avoid postoperative kinking. The dura mater was sutured so as not to leave an excessive subdural space. The bone flaps were trimmed to complete a good-shaped reconstruction. Finally, the excessive scalp was removed because the original scalp was too large for the reconstructed skull.(ABSTRACT TRUNCATED AT 250 WORDS)

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Involvement of nerve growth factor (NGF) in the pathogenesis of delayed neuronal death (DND) of CA1 neurons in the hippocampus has been suggested. We measured regional changes in the content of tissue NGF of the hippocampus in the Mongolian gerbil after 5 min forebrain ischemia. The NGF content was found to decrease significantly in the CA3 and dentate regions by 32% two days after ischemia. By contrast in the CA1 region, the level of NGF became significantly elevated by 50% two weeks after ischemia or later. The early reduction of NGF content in the afferent area projecting to the CA1 sector might be primarily linked to the pathogenesis of DND, whereas the delayed increase within the CA1 sector might be a secondary local response mainly of reactive astroglia.

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A rare case of delayed traumatic intracerebellar hematoma (DTIC1H) in a 54-year-old male achieved an excellent outcome without surgery. Analysis of this case and other reported cases suggests that DTIC1H occurs in two types: Group I with hematoma developing in previously contused areas, and Group II with hematoma developing in areas appearing normal on the initial computed tomographic scan. Group I hematomas occurred in the cerebellar cortex, but Group II hematomas occurred in the subcortical region or vermis where direct impact is less likely to have an effect. This suggests different mechanisms of development for DTIC1H.

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Selective neuronal death in the CA1 sector of the hippocampus [delayed neuronal death (DND)] develops several days after transient global cerebral ischemia in rodents. Because NGF plays a potential role in neuronal survival, it was decided to study its effect in DND. We report here that intraventricular injection of NGF either before or after 5 min forebrain ischemia in the Mongolian gerbil significantly reduced the occurrence of DND. The tissue content of NGF in the hippocampus was decreased 2 d after ischemia and recovered to the preischemic level by 1 week. By the Golgi staining technique, changes first began in the dendrites of affected neurons as early as 3 hr. Such changes could be ameliorated by NGF treatment. Although previous knowledge of NGF is limited to the survival of cholinergic neurons in the CNS, it is assumed that other mechanisms must be operating in the hippocampus, for example, postsynaptic modification at dendrites or aberrant expression of NGF receptors possibly at the initial excitation period by glutamate. Furthermore, because previous work has shown that inhibition of protein synthesis reduces the occurrence of DND, a program leading to cell death might also be operating via de novo synthesis of certain protein(s), collectively termed "killer protein," because of a lack of NGF.

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The role of endothelin, a newly found vasoconstrictor peptide, is examined in the pathogenesis of cerebral vasospasm after experimental subarachnoid hemorrhage (SAH) in the dog. Endothelin immunoreactivity was overexpressed in the endothelium of the vasospastic basilar artery. Because endothelin synthesis is regulated at the messenger ribonucleic acid transcription level, the effect of actinomycin D, a ribonucleic acid synthesis inhibitor, was studied as a means of preventing vasospasm. It was found that treatment with intravenous actinomycin D for 5 days beginning on the day of SAH completely inhibited the development of vasospasm. This novel experimental therapy may lead not only to the elucidation of the pathogenesis of cerebral vasospasm but also to the availability of a prophylactic adjuvant therapy for patients with SAH.

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