Search

A 31-year-old healthy male presented with a rare case of cerebral arteriovenous malformation (AVM) manifesting as repeated ischemic attacks and cerebral infarction causing left sensori-motor disturbance. Neuroimaging revealed cerebral infarction in the right thalamus as well as right occipital AVM without bleeding. The AVM was mainly fed by the right angular artery, and the right posterior cerebral artery (PCA) showed mild stenosis and segmental dilation at the P(2)-P(3) portion. After referral to our hospital, transient ischemic attacks causing left homonymous hemianopsia, and left arm and leg numbness were frequently recognized. Additional imaging revealed a new ischemic lesion in the occipital lobe, and repeated cerebral angiography showed right PCA occlusion at the P(2)-P(3) segment. Cerebral AVM presenting with cerebral infarction due to occlusion of feeding arteries is rare. In our case, intimal injury due to increased blood flow or spontaneous dissection of the artery were possible causes. We should monitor any changes in the architecture and rheology of the feeding vessels during the clinical course to prevent ischemic complications.

A 64-year-old man presented with subarachnoid hemorrhage from a small brainstem arteriovenous malformation (AVM). Cerebral angiography showed a small AVM in the lateral midbrain, which was fed by a basilar perforating artery, and drained into the right transverse pontine vein and superior petrous vein. Endovascular embolization in the acute stage was selected to occlude the arteriovenous shunt and provide additional intensive treatment for cerebral spasm with lower risk of rebleeding. The AVM was occluded by embolization using n-butyl cyanoacrylate. Intraparenchymal hemorrhage in the ipsilateral pons was detected 1 month after treatment. The causes of the hemorrhage remain unclear.

We compare outcomes of ruptured aneurysmal subarachnoid hemorrhage mainly treated by surgical clipping between 2000 and 2004 (early term) with outcomes of patients mainly treated by surgical clipping between 2005 and 2007 (late term) with first selection of endovascular coiling to poor-grade, posterior circulation, or elderly patients. Between January 2000 and September 2007, 287 patients were treated and 147 and 140 patients belonged to early and late terms, respectively. Poor grade patients (Hunt and Kosnik Grade IV, V) comprised 24.5% and 34.5% (NS), posterior circulation patients comprised 14.3% and 10.7% (NS), and, elderly patients (over 70 year-old) comprised 23.1% and 35.0% in early and late terms, respectively. The rate of elderly was significantly higher in late term than in early (p＜0.05). Endovascular coiling was performed on 10.9% and 29.8% of patients in early and late terms, respectively, and the rate was significantly higher in late term than in early (p＜0.01). Good outcomes were assessed with modified Rankin Scale of 0－2 at 6 months. Good outcomes were 61.2% and 62.1% in early and late terms, respectively (NS). In poor-grade patients, good outcomes were 13.9% and 27.7% (NS), in posterior circulation, 47.6% and 53.3% (NS), and in elderly, 26.5% and 53.5% in early and late terms, respectively, and the rate of good outcomes in elderly was significantly higher in late term than in early (p＜0.05). Outcomes of ruptured aneurysmal patients were significantly improved in elderly patients, but not in poor grade, nor in posterior circulation, due to first selection of endovascular coiling. Despite the significant increase of elderly patients, total outcomes of ruptured subarachnoid hemorrhage in late term were not inferior to those of early term.

The long-term outcomes of aneurysms occluded by clipping are unclear. The present study investigated 5 females aged from 45 to 72 years old (mean 63.6 years) admitted for treatment of recurrent subarachnoid hemorrhage (SAH) 7 to 19 years (mean 9.8 years) after clipping of internal carotid artery-posterior communicating artery (ICA-PCoA) aneurysms, which had caused SAH in 3 patients and were unruptured in 2 patients. Angiography delineated the well-developed PCoA in all patients. Clips had been applied to the aneurysm neck parallel to the ICA trunk at the initial surgery in 3 patients. An additional clip could be applied to the recurrent aneurysm without removal of the first clip in 2 patients, but the original clip had to be removed before reclipping in the other 3 patients. Adhesive materials and Bem-sheet used at the initial operation hindered dissection of the recurrent aneurysm from the surrounding arteries in 1 patient, resulting in infarction in the area of the PCoA perforating arteries. This study suggests that the method of clipping is very important for ICA-PCoA aneurysm, particularly the direction of clip application to the ICA trunk, and the avoidance of unnecessary or excessive wrapping of the residual neck. We recommend that neuroimaging follow-up of recurrent aneurysms in patients with a history of clipped aneurysm, especially ICA-PCoA aneurysm, be continued as long as possible.

Background Three dimensional rotational angiography (3DRA) is a powerful method for depicting intracranial vascular lesions because of its 3D imaging capability. The purpose of this study was to analyse if 3DRA had reduced the incidence of angiogram-negative subarchnoid haemorrhage (SAH) and which type of aneurysm tended to be overlooked with conventional digital subtraction angiography. Method Angiogram-negative SAH was defined as present in those patients with SAH who had no demonstrable lesion revealed by more than two adequate cerebral angiograms. From January 1, 1992, to December 31, 2004, angiography was performed on 247 patients at the Yamaguchi University Hospital. Digital subtraction angiography (DSA) alone was used for 105 patients (DSA group) from 1992 to 2000. After the technology of 3DRA was introduced to our hospital in 2000, 142 patients were evaluated by 3DRA and DSA together (3DRA group). Findings The incidence of angiogram-negative SAH was 9/105 (8.6%) in the DSA group and 6/142 (4.2%) in the 3DRA group. 3DRA revealed six aneurysms not depicted by the conventional DSA, including a basilar tip aneurysm, anterior cerebral artery aneurysm and a basilar tip aneurysm originating from a previously clipped aneurysm. Conclusion Three dimensional RA is more sensitive in detecting aneurysms, but in our study still produced a 4.2% rate of angiogram-negative SAH. Three diemensional RA has some advantages for evaluation, especially of complicated sites and previously clipped aneurysms because of its three dimensional imaging capability.

Aneurysmal subarachnoid hemorrhage (SAH) poses an immediate threat to life. The accepted paradigm of treatment generally involves surgical intervention requiring craniotomy to allow neck clipping of the ruptured cerebral aneurysm, with the alternative approach of embolization of the aneurysm sac by the deposition of detachable coils delivered through the endovascular route. The selection of the treatment method depends on the establishment of clear guidelines for the attending neurosurgeon, but unfortunately no such definitive guidelines leading to a definitive treatment policy have been developed in Japan. Controlled comparison of the alternative treatment approaches of clipping and coil embolization is rendered difficult by the lack of reported series of interventions in patients using either clipping or coil embolization, and the methodological difficulties inherent in the retrospective comparison of the specific results achieved by unrelated institutes or individual surgeons. We describe our 5 years of experience of clipping and coil embolization to promote a consensus of decision-making for acute SAH. Our therapeutic protocol emphasizes clipping, with coil embolization mainly considered for patients with poor neurological condition (Hunt & Kosnik Grades IV-V without hematoma), paraclinoid or basilar aneurysm, or serious systemic complications, and for elderly patients over 74 years old or older. We treated 198 patients, 55 males and 143 females aged from 31 to 91 years old (mean 61.3 years) with aneurysmal SAH between 2000 and 2005. Surgical clipping was performed in 164 cases, endovascular treatment in 25 cases, and conservative therapy for ruptured aneurysms in 9 cases. Overall, 95% of patients underwent radical treatment. On admission, 26% of patients were in poor neurological condition (Hunt & Kosnik Grades IV-V). Aneurysms arose from the anterior circle of Willis in 87% of cases. Eighty-seven percent of patients were treated with surgical clipping within 3 days of onset, and 84% were treated with coiling within 3 days. Favorable outcome was defined as good recovery or moderately disabled classified by Glasgow Outcome Scale at discharge, which was achieved in 71% of all patients, 76% of patients treated by clipping, and 60% of patients treated by coil embolization. Symptomatic vasospasm occurred in 21% of patients after clipping but only in 3% after coil embolization (p Recently, the Ministry of Health, Labour and Welfare has required the collection and submission of accurate and complete information about treatment options, indications, and expected results for ruptured cerebral aneurysms. The availability of such an extensive database enabling rigorous analytical correlations will provide the required foundation to establish specific indications for the selection of the optimal methodology of clipping or coil embolization treatment for patients with acute SAH.

Background The aim of this study was to compare the efficacy of surgery for spontaneous intracerebral hemorrhage with that of medical treatment, based on data from the Japan Stroke Registry Study. Methods From 1999 to 2001, 1010 patients with spontaneous intracerebral hemorrhage were registered in the Japan Standard Stroke Registry Study from 45 stroke center hospitals in Japan. The National Institutes of Health Stroke Scale (NIHSS), Japan Stroke Scale (JSS), and modified Rankin Scale scores were used to compare severity and improvement in patients given surgical and medical treatment. Conclusions Surgically treated patients, especially those with cerebellar hemorrhage, had significantly greater improvement in NIHSS or JSS score compared with medically treated patients. Our findings indicated that the patients who underwent surgery appeared to have better outcomes. But, because the study was not randomized, this observation cannot be interpreted as indicating that surgery is advantageous.

Low molecular dextran is often used in post-operative management of subarachnoid hemorrhage (SAH) to induce hypervolemia and hemodilution; however, its associated complications are not well-known. We retrospectively analyzed prothrombin time (PT%), activated partial thromboplastin time (APTT%), and fibrinogen level as coagulation markers in patients with subarachnoid hemorrhage who developed delayed intracranial hemorrhagic complications after undergoing craniotomy for clipping to examine the effect of long-term use of low molecular dextran on bleeding tendencies. Fifty-two patients with SAH who underwent craniotomy were divided into 2 groups: 26 without post-operative use of low molecular dextran (Group 1) and 26 to whom low molecular dextran was administered for more than 5 consecutive days (Group 2). Group 2 was further divided into 2 subgroups: those who developed hemorrhagic complications (Group 2A) and those without complications (Group 2B). The frequency of complications in Group 2A was 19% (5/26; 3 with subdural hematoma and epidural hematoma, 1 with epidural hematoma, and 1 with intracerebral hematoma). Complications appeared 7.6 days on average after starting low molecular dextran. Compared with Group 1, PT% and APTT% as well as pre-and post-low molecular dextran administration fibrinogen levels significantly decreased in Group 2A. Low molecular dextran is known to decrease fibrinogen levels, and patients' clinical conditions and changes in fibrinogen levels should be closely monitored to detect bleeding tendencies when low molecular dextran must be used for long periods.

Many risk factors for subarachnoid hemorrhage (SAH), such as hypertension and recent infection, have already been established. Chlamydia pneumoniae is a common respiratory pathogen that has been implicated as a potential risk factor for hypertension and atherosclerotic diseases. The purpose of the case-control study presented here was to examine the causative relationship between C. pneumoniae infection and SAH. Serum C. pneumoniae IgG and IgA antibodies were measured using an enzyme-linked immunosorbent assay in 52 patients with SAH and in 104 healthy age-matched control subjects. Multivariate analysis revealed a significant association between SAH and both a strong seropositivity for IgG and/or IgA antibodies against C. pneumoniae (odds ratio, OR, 3.62; 95% confidence intervals, CI, 1.06–12.39; p = 0.040), which indicates the presence of acute C. pneumoniae infection, and hypertension (OR, 2.91; 95% CI, 1.42–5.96; p = 0.0035). These results provide evidence that infection with C. pneumoniae may be a risk factor for SAH from a ruptured intracranial aneurysm.

Recent experimental data have shown that levels of matrix metalloproteinase-9 (MMP-9) increase after traumatic brain injury (TBI), degrading components of the basal lamina disrupting the blood-brain barrier. However, the post-traumatic secretion patterns of MMP-9 in humans are unknown. We measured the concentration of MMP-9 in plasma after TBI at the same time as the concentration of interleukin-6 (IL-6) in serum. Levels of MMP-9 and IL-6 in systemic arterial and jugular venous blood from seven patients with TBI were measured on days 0 and 1 post-injury. All patients underwent hypothermia at 32-35 degrees C as soon as possible after admission. Before induction of hypothermia, levels of MMP-9 in arterial and internal jugular venous blood exceeded the normal range. Higher MMP-9 levels were detected in internal jugular venous blood than in arterial blood. After hypothermia had been induced, MMP-9 levels in arterial blood and internal jugular venous blood decreased significantly, to within the normal range. In addition to these changes, a significant correlation was seen between levels of MMP-9 and IL-6 in internal jugular venous blood during the investigation period. These results indicate that MMP-9 is elevated in patients with acute TBI, and may play an important role in traumatic brain damage. The elevation of MMP-9 is associated with inflammatory events following TBI. Hypothermic intervention may suppress the elevation of MMP-9 with suppression of the inflammatory response, affording neuroprotection in TBI.

Recently less invasive diagnostic tools for the brain have been developed rapidly at a time when the population of the elderly has become enormous. Likewise, the number of patients having uAN-associated ischemic complications has grown sharply. For this special category of uAN, risk-benefit analysis is extremely difficult. Higher morbidity/mortality is common but rupture rates are considered more frequent than incidental uAN. To prevent bleeding from uAN and to reduce complications triggered by precedent ischemic insult, we have performed radical surgery for such special uAN according to the following guidelines: 1) 70 years old and younger, without serious neurological deficits or general complications, capable of independent life, 2) significant interval (3-6 months) required between precedent ischemic insult and radical surgery, 3) meticulous examination for the etiology of ischemic condition and adequate treatment for the causes, 4) acceptance of prophylactic surgery such as CEA/stent (2 stage), and STA-MCA (concurrent with uAN surgery), 5) prevention of dehydration/hypotension and minimal washout of anti-platelet/thrombotic drug through perioperative period, 6) avoiding too much aspiration of CSF, long-time compression of the brain, temporarily occlusion of arteries, and sacrifice veins. We analyze the results of this series and evaluate the strategy in relation to the cause of complications. Surgical mortality was 0 and morbidity was observed in 3 patients (permanent: 1; 6.25%, transient: 1; 6.25%). Good results were obtained by our strategy. Precedent ischemic insult may not deeply influence the result. Concurrent bypass did not increase risk of ischemic complication during radical surgery for uAN. However, much attention must be paid to sclerotic perforating artery, brain atrophy, and craniocerebral disproportion in patient with uAN and precedent ischemic accident.

It has been well documented that memory difficulties in patients with anterior skull base meningioma may improve after tumour resection. However, there have been few reports on studies where precise testing of cognitive function has been conducted before and after surgery. Here we report 2 cases of anterior skull base meningioma where 2 tests of cognitive function, the Wechsler adult intelligence scale-revised (WAIS-R) and the Wechsler memory scale-revised (WMS-R), were performed by the patient before and after surgical treatment. After the operation there was a dramatic increase in the performance IQ as measured by the WAIS-R. In addition, the scores for both the “Attention/Concentration” and the “Delayed Recall” subsets of the WMS-R scale improved. There were differences between the 2 patients in the length of time required for functional recovery and this was thought to be due to the tumour size and the age of the patient. The use of these scales would enable physicians who are treating patients with anterior skull base meningioma to assess the recovery time that is likely to be needed before full return of cognitive function after surgery.

A 50-year-old man presented with neuro-Behcet's disease (NBD) manifesting as a large neoplasm-like lesion affecting the brainstem, basal ganglia, and white matter of the cerebral hemisphere. He had no history of disease except for psychoneurosis. On admission, neurological examination found left hemiparesis and dysarthria. Magnetic resonance (MR) imaging showed multiple small ring-like enhancement in the basal ganglia, brainstem, and deep white matter. Biopsy of the mass was performed. Histological examination revealed invasion of inflammatory cells in the white matter, especially around the blood vessels. After the brain biopsy, the patient developed oral aphthae, genital ulcers, and skin eruptions, which are indicative of Behcet's disease. MR imaging after three courses of steroid pulse therapy revealed that the edematous lesion had become smaller with minimum midline shift. NBD should be considered in the differential diagnosis of lesions with multiple ring-like enhancement extending from the basal ganglia to the brainstem, because dermatological manifestations are sometimes obscured during periods of remission.

頭蓋内ナビゲーションは、術中に、脳神経外科医に病変部位を表示し、手術を補助する装置である。このためには、手術前に、MR画像を撮像する必要があり、頭蓋内電極留置後の皮質焦点切除には応用しにくかった。我々は、多少の工夫により、難治性てんかん患者に対し、頭蓋内電極留置によるモニタリングに引き続き行なう皮質焦点切除術の際に、ナビゲーションを併用しているので症例を提示し報告する。ナビゲーションは、頭皮上にマーカーを置き、MRを施行し、ナビゲーションのワークステーションコンピュータ上で、リファレンスを設定し、画像と術野該当構造を空間座標上に合致させる作業が必要である。頭蓋内電極留置前から、頭皮上にマーカーを置き、MR画像を撮像する。マーカー部位を、モニタリング期間中に維持し、手術操作による頭皮の腫脹などの影響を受けないように留意する必要がある。これにより、硬膜下電極によりマッピングされた皮質切除予定部位と、ナビゲーションにより表示される病変部との関係を確認しながら手術可能であった。髄液の流出と硬膜下電極による圧排による脳の偏位がナビゲーションの正確性に影響することに注意しなければならない。

We present an unusual case of a patient who was diagnosed with temporal lobe epilepsy and whose seizures were reduced markedly after excision of an angiographically occult arteriovenous malformation (AVM) located in the left medial parietal lobe. A 38-year-old man had complex partial seizures characterized by motionless staring with oroalimentary and behavioral automatisms since the age of 15 years. Magnetic resonance imaging (MRI) demonstrated a small lesion extending from the left posterior cingulate gyrus to the precuneus. There was no MRI evidence of mesial temporal sclerosis. Intracranial EEG recordings showed ictal onset from the left medial parietal lobe propagating to the medial temporal lobes. Clinical signs appeared when these discharges reached the temporal lobes. After excision of the lesion (which was histologically confirmed as an AVM), together with the marginal cortex, seizures were reduced significantly. Careful diagnostic evaluation of lesions such as the this one may reveal an epileptogenic lesion (zone) far from the region where scalp ictal discharges seem to arise. In our case, we hypothesize that false localization was due to propagation of ictal discharges from the parietal focus through the limbic system.

The urinary excretion of valproic acid (VPA) and its metabolites (3-keto VPA, 3-OH VPA, and VPA-glucuronide) in 6 epileptic patients was studied using gas chromatography-mass spectrometry. The amount of VPA and 3-OH VPA excreted in the urine was low (0.1-0.5% of the dose of VPA and 0.6-1.5% of the dose of 3-OH administered). The amount of 3-keto VPA and glucuronide (VPA-Glu) excreted was marked (5.8-26.2% and 13.1-88.7% of the dose of VPA administered, respectively). The urinary excretion of VPA and its metabolites by patients who have taken a normal amount of a VPA preparation was almost the same as that of healthy volunteers. Two epileptic patients who took a large amount of the VPA preparation showed a high excretion of VPA-Glu without an increase in their plasma VPA-Glu.

A 67-year-old man presented with multiple aneurysms arising from the caudal loop of the posterior inferior cerebellar artery (PICA), possibly as a result of blunt trauma. Computed tomography of the head revealed subarachnoid hemorrhage in the posterior fossa and sylvian fissure. Repeated angiography demonstrated an aneurysmal dilatation and an irregular wall on the caudal loop of the PICA. Under the operating microscope, two lesions were observed 10 mm distal to the apex of the caudal loop, both consisting of a tiny hole on the vessel wall with a fragile fringe of connective tissue and covered with a firm clot. The height of the lesions corresponded to the C-l lamina, so the lesions were probably traumatic rather than saccular.

A rare case of facial arteriovenous malformation (AVM) associated with consumption coagulopathy is reported. The AVM was fed solely by the external carotid arterial system with an extensive arteriovenous shunt. Laboratory testing showed prolongation of the partial thromboplastin time (PTT), and low factor VIII. The level of factor VIII became normalized after multiple embolizations concomitant with reduction of the AVM. Although embolization of facial AVM is controversial, it is one of the treatments of choice, especially when there is an associated coagulation abnormality.

A 32-year-old man presented with an arachnoid cyst of the posterior fossa manifesting as cervical syringomyelic myelopathy. Magnetic resonance (MR) imaging demonstrated edematous enlargement and T2 prolongation of the cervical spinal cord, indicating a "presyrinx" state. MR imaging showed the inferior wall of the cyst, which disturbed cerebrospinal fluid (CSF) pulsatile movement between the intraspinal and intracranial subarachnoid spaces. The cyst wall was fenestrated with a neuroendoscope. The presyrinx state and the CSF movement improved. Posterior fossa arachnoid cyst, as well as Chiari malformation, can cause CSF flow disturbance at the craniocervical junction and syringomyelia. Endoscopic fenestration is less invasive than foramen magnum decompression and should be the procedure of choice.

This study investigates the role of sphingosylphosphorylcholine (SPC) in the mechanisms underlying cerebral vasospasm after subarachnoid hemorrhage (SAH). The levels of SPC were measured in cerebrospinal fluid (CSF) of patients with SAH and also in an experimental canine model. CSF samples were collected from 11 patients with SAH, and from dogs that had received an injection of SPC into the cisterna magna to examine SPC kinetics in the CSF. SPC was assayed using solid-phase extraction and triple quadrupole mass spectrometry. The SPC concentrations in SAH patients on days 3, 8, and 14 after the onset of SAH were significantly higher than those in normal CSF. In the canine model, rapid dilution of SPC in CSF was observed. In combination with data from previous studies, these results suggest that SPC is involved in the development of cerebral vasospasm. Rapid dilution of SPC in CSF suggests that SPC is released into CSF at higher concentrations than those measured in the present study.

We report a case of intractable epilepsy caused by tuberous sclerosis with multiple tubers that was treated successfully by single resection of a tuber A 2-year-old boy developed tonic spasm-like seizures at the age of 4 months and the frequency of the seizures increased despite therapy with various anticonvulsants. He had no neurological deficits, and his intelligence was normal. MRI showed lesions in the left frontal and the right parietal lobe, and EEG (electroencephalogram) demonstrated sharp waves and spike-and-wave complex bursts over the right parietal region. Subdural electrodes were implanted over these lesions, and ictal low-voltage fast waves were demonstrated on the right parietal lesion. Therefore the right cortical lesion and the epileptogenic cortex were resected. Multiple subpial transaction was also added in the irritative cortex. Histological examination proved that the lesion was a tuberous sclerosis complex (TSC) tuber. Since surgery, the patient has remained seizure-free for 2 years. In patients with multiple TSC tubers in the cortex, we suggest that seizures can be suppressed by single resection of a tuber if the tuber can be identified as epileptogenic before surgery.

Among diseases due to cerebral parasitism, that caused by Sparganum mansoni, the larva of Spirometra mansoni, is very rare. We have encountered two such cases. A computed tomography scan in both revealed a nodular high density contrast enhanced area against an extensive low density background area. Neither calcification nor cyst formation was recognized. These computed tomography scan findings were thought to be characteristic for cerebral sparganosis mansoni and were difficult to differentiate from those of a cerebral tumor. In both cases, definitive diagnosis was achieved by identification of the worm after excision of the lesion. The best treatment for cerebral sparganosis mansoni is surgical excision of the lesion, and in the two cases presented the postoperative outcome was good.

Purpose Hematic cysts of the orbit are relatively uncommon. These cysts expand gradually, leading to progressive orbital symptoms. To clarify the cause of hematic cyst, especially the mechanisms leading to its gradual expansion, we investigated the immunohistologic expression of tissue-type plasminogen activator (tPA), a key enzyme of fibrinolysis, in cases of hematic cysts. Design Retrospective small case series. Participants Three patients with hematic cyst of the orbit were studied. Methods Three surgically removed hematic cysts were studied from a histologic perspective, including immunohistochemistry for tPA. The cyst content was also analyzed chemically. Main Outcome Measures The pathologic features of hematic cyst of the orbit, expression of tPA in the cyst wall, and coagulation-fibrinolytic factors in the content of the cyst. Results The cyst wall was composed of dense collagen fibers lacking an epithelial lining and contained many fine capillary- or venule-like vessels. Hemosiderin-laden macrophages were observed among the collagen fibers. Strong immunoreactivity for tPA was revealed in the endothelial cells of the vessels in the cyst wall. Chemical analysis of the cyst content revealed a marked delay in the activated partial thromboplastin time and prothrombin time, a low fibrinogen concentration, and high concentrations of the D-dimer and tPA-plasminogen activator inhibitor-1 complex. Conclusions Our findings indicate that blood coagulation and hemostasis occur first and that fibrinolysis occurs second in hematic cysts. Gradual expansion of the cyst may be due to hyperfibrinolysis resulting from oversecretion of tPA from the endothelial cells in the cyst wall, thus impairing normal hemostasis. Hemorrhage may then recur, resulting in enlargement of the hematic cyst. These mechanisms are similar to those occurring in chronic subdural hematomas. Financial Disclosure(s) The author(s) have no proprietary or commercial interest in any materials discussed in this article.

A 67-year-old man presented with multiple aneurysms arising from the caudal loop of the posterior inferior cerebellar artery (PICA), possibly as a result of blunt trauma. Computed tomography of the head revealed subarachnoid hemorrhage in the posterior fossa and sylvian fissure. Repeated angiography demonstrated an aneurysmal dilatation and an irregular wall on the caudal loop of the PICA. Under the operating microscope, two lesions were observed 10 mm distal to the apex of the caudal loop, both consisting of a tiny hole on the vessel wall with a fragile fringe of connective tissue and covered with a firm clot. The height of the lesions corresponded to the C-l lamina, so the lesions were probably traumatic rather than saccular.

The aim of this study was to establish a treatment strategy for patients with cavernous angiomas and have seizures.We analyzed retrospectively 31 patients with cavernous angiomas presenting with seizures. Of the 31 patients, 15 (11 men, 4 women) had been treated medically (the medical group) and 16 (11 men, 5 women) had been treated surgically (the surgical group). The percentage of patients who became seizure-free and the number of anticonvulsants used were compared between these 2 groups. The mean follow-up period was 5.3 years (range, 7 months-10 years). There was no statistically significant difference between the 2 groups with regard to the number of patients, sex, age, and follow-up period.The percentage of patients who became seizure-free was higher in the surgical group than in the medical group (80% vs 19%, P.01). The number of anticonvulsants required was reduced in the surgical group after surgery (from 1.5 +/- 0.7 to 1.1 +/- 0.8, P.01) and was not reduced after in the medical group.Surgical intervention may have greater benefits than medical intervention for patients with cavernous angiomas presenting with epileptic seizures.

Many risk factors for subarachnoid hemorrhage (SAH), such as hypertension and recent infection, have already been established. Chlamydia pneumoniae is a common respiratory pathogen that has been implicated as a potential risk factor for hypertension and atherosclerotic diseases. The purpose of the case-control study presented here was to examine the causative relationship between C. pneumoniae infection and SAH. Serum C. pneumoniae IgG and IgA antibodies were measured using an enzyme-linked immunosorbent assay in 52 patients with SAH and in 104 healthy age-matched control subjects. Multivariate analysis revealed a significant association between SAH and both a strong seropositivity for IgG and/or IgA antibodies against C. pneumoniae (odds ratio, OR, 3.62; 95% confidence intervals, CI, 1.06-12.39; p = 0.040), which indicates the presence of acute C. pneumoniae infection, and hypertension (OR, 2.91; 95% CI, 1.42-5.96; p = 0.0035). These results provide evidence that infection with C. pneumoniae may be a risk factor for SAH from a ruptured intracranial aneurysm.

A 12-year-old girl had the hair on the right side of her head pulled during a quarrel, after which a subgaleal hematoma (SGH) developed over her right cranium. The subcutaneous swelling progressed to the forehead, and a marked exophthalmos then developed on the left side. The bilateral, liquefied SGH was removed surgically, and two drainage catheters connected to a vacuum-drain pump were introduced. After the surgery, the SGH disappeared. The liquefied hematoma was aspirated by puncturing the superolateral portion of the left orbit. Thereafter, the left exophthalmos rapidly disappeared. A chemical analysis of the SGH revealed that it contained extremely low levels of fibrinogen and platelets, and high levels of fibrinogen and fibrin degradation products, suggesting that secondary fibrinolysis had occurred in the subgaleal space. Subgaleal hematomas are usually treated conservatively. However, closed observation is necessary, and if increased expansion is seen, aspiration with a closed drainage system should be considered.

We present a case of intractable epilepsy presenting epileptic spasm successfully treated with anterior callosotomy in childhood. A 12-year-old boy had seizures frequently since the age of 11 months which were diagnosed as an infantile spasm. He underwent various treatments including ACTH therapy, but the seizures were intractable. Characteristics of his seizures were an abrupt axial movement leading to sustained posturing, most often truncal, and neck flexion with pronounced arm extension and abduction. He lost consciousness transiently and these seizures frequently occurred in clusters and the duration of seizure was 1 to 3 seconds. Neurologically he had no deficit, but his intelligence was below the standard level. Magnetic resonance image (MRI) showed no abnormalities in the brain. Electroencephalogram (EEG) demonstrated secondary bilateral synchrony (SBS) with left frontal dominance in amplitude. Subdural strip electrodes were implanted bilaterally over the frontal lobes to detect an epileptogenic region. However intracranial ictal-EEG demonstrated an abrupt bilateral desynchronization for 1-3 seconds. As the epileptogenic zone was not clearly identified and an abrupt bilateral desynchronization was identified, anterior callosotomy was performed. Since surgery, he has remained seizure-free for two years while taking anticonvulsants and the SBS has disappeared. This case may indicate that the corpus callosum influences the occurrence of epileptic spasm and SBS on EEG.

Recent progress in diagnostic imaging techniques, such as MRI and CT, has shown that Rathke's cleft cyst is more common than once thought. However, few cases have been reported in which a cerebral arterial aneurysm was merged with a symptomatic Rathke's cleft cyst. We present a case of bilateral internal carotid aneurysms associated with a symptomatic giant Rathke's cleft cyst. A 66-year-old-woman with a visual disturbance was admitted to our hospital. CT and MRI showed a large mass in the frontal base to the suprasellar region. The mass showed isosignal intensity in T1-weighted images (WI), a ringed enhancement with Gd-DTPA, and hyperintensity in T2WI. An angiography showed bilateral A1 elevation but no tumor stain. In addition, unruptured aneurysms appeared in the inside back C2 portion of the bilateral internal carotid arteries. For these lesions, a bifrontal craniotomy was performed. In a single operative approach, the mass lesion was removed and the aneurysms were successfully clipped. The aneurysms adhered strongly to the wall of the mass. The histological diagnosis of the mass was Rathke's cleft cyst. A precise pre-operative understanding of the anatomical structure and a careful operative procedure are important for the treatment of these complex lesions.

The characteristics of seizures associated with parietal lobe epilepsy were investigated in six consecutive patients with medically intractable epilepsy due to parietal lobe lesions. Intracranial electrode recordings were retrospectively reviewed to investigate the seizure onset symptoms and spreading patterns associated with the disorder. All six patients underwent implantation of subdural or depth electrodes and subsequent video/electroencephalography monitoring. Common symptoms included motionless stare, contralateral eye deviation, and head turn. Tonic posturing, contralateral sensory disturbance, and motor weakness were also seen. Asymmetrical generalized tonic and clonic seizures were seen in all six patients. All seizure activities began in the parietal lobe harboring the lesions, and then spread immediately to the adjacent lobes in most seizures, where the clinical symptoms were produced. The parietal lobe is a pure generator of seizures, whereas most clinical symptoms originate from adjacent lobes following seizure onset. No apparent specific symptoms other than sensory disturbance arising from the parietal lobe proper were recognized. Regardless of clinical symptoms, the seizure onset occurred in the parietal lobe harboring the lesion.

In this study, we investigated the pattern of increased matrix metalloproteinase-9 (MMP-9), which causes disruption of the blood-brain barrier, in plasma of patients with traumatic brain injury (TBI) in hypothermic therapy, and we also investigated the pattern of interleukin (IL)-6 levels of serum, because both of them will be activated during inflammatory states. Using an enzyme immunoassay (EIA), MMP-9 and IL-6 levels in blood from the systemic artery and internal jugular vein in eight patients with TBI were measured on 0, 1, and 3 days postinjury. All patients underwent hypothermia in the range of 32-35°C. Before inducing hypothermia, MMP-9 levels in the blood exceeded the normal range. Specifically, MMP-9 levels in the internal jugular vein greater than arterial levels were detected in most of the patients (6 out of 8). After inducing hypothermia, MMP-9 levels in the blood decreased significantly to within the normal range, while IL-6 levels in the blood before induction of hypothermia exceeded the normal range, with the levels in the internal jugular vein being greater than arterial levels in all patients. Consistent with previous reports, after induction of hypothermia, levels of IL-6 decreased significantly by 3 days postinjury. In addition to these changes, a significant correlation between levels of MMP-9 and IL-6 in internal jugular venous blood was seen during the period of investigation. These results indicate that MMP-9 is elevated in patients with acute TBI. This elevation of MMP-9 is associated with inflammatory events following TBI. Furthermore, hypothermic intervention may suppress this elevation of MMP-9 with suppression of the inflammatory response followed by neuroprotection to TBI.

The use of brain hypothermia therapy was initiated at our institution in 1994. At the same time, we also began a policy of managing the body temperature of patients. Recently, our protocol for management of patients with severe traumatic brain injuries (TBI) has become standardized. Intracranial hematomas are evacuated and external decompression is performed. In patients for whom hypothermia therapy is appropriate, brain and body temperatures are maintained at 32°–33°C for 3–8 days. Mild hypothermia (34°–35°C) is induced according to the patient’s condition. Even if hypothermia is not induced, the brain temperature is kept below 37°C. Many parameters such as intracranial pressure, cerebral perfusion pressure, blood gas are monitored, and systemic circulation are monitored using a Swan-Ganz catheter. Compared with the first 5 years (1989–1993), the number of favorable outcomes (good recovery and moderate disability on the Glasgow Outcome Scale) increased during the second 6-year period (1994–1999) and in the most recent 4 years (2000–2003). The number of favorable outcomes was greatly increased for patients under 50 years of age. We believe that patient selection for hypothermia therapy and temperature management for patients in whom hypothermia is not applied is important for effective management of severe TBI.

Surgical reconstruction of the carotid artery using a synthetic graft is rarely performed. A 71-year-old woman developed hoarseness and was diagnosed as having thyroid cancer. Computed tomography (CT) and angiography revealed an irregular thyroid tumor invading the left common carotid artery, and encasement of the artery by the tumor. Left common carotid angiography showed an irregularity of the common carotid artery wall and a dense tumor stain fed by the superior thyroid artery. Dissection of the thyroid cancer from the common carotid artery was judged to be impossible during surgery, so resection of the whole tumor together with the common carotid artery was carried out. The left common carotid artery was reconstructed using an expanded polytetrafluoroethylene (ePTFE) graft. No cerebral ischemia was evident after surgery. Postoperative CT and magnetic resonance angiography demonstrated patency of the carotid artery, and no tumor recurrence was confirmed at a 27-month follow up. The ePTFE graft appears to be a suitable synthetic graft for reconstruction of the carotid artery.

A 22-year-old woman was admitted to our department after developing a headache. The neurological findings were unremarkable on her first visit, but CT demonstrated a lot of low-density masses in the subarachnoid space. The largest mass was in the right sylvian fissure. These lesions appeared hyper-intense in T1, T2 and diffusion-weighted MR images. A right frontotemporal craniotomy was performed to remove the main mass lesion in the right sylvian fissure. During surgery, thickening of the arachnoid membrane and floating oily globules were seen in the subarachnoid space. The histopathological examination revealed that the tumor was a dermoid cyst. Follow-up MRI revealed that some of the small lesions had moved since the operation. These findings suggested that the tumor was a ruptured dermoid cyst. The patient's postoperative course was uneventful and her headache disappeared completely.

A 50-year-old man presented with neuro-Behçet's disease (NBD) manifesting as a large neoplasm-like lesion affecting the brainstem, basal ganglia, and white matter of the cerebral hemisphere. He had no history of disease except for psychoneurosis. On admission, neurological examination found left hemiparesis and dysarthria. Magnetic resonance (MR) imaging showed multiple small ring-like enhancement in the basal ganglia, brainstem, and deep white matter. Biopsy of the mass was performed. Histological examination revealed invasion of inflammatory cells in the white matter, especially around the blood vessels. After the brain biopsy, the patient developed oral aphthae, genital ulcers, and skin eruptions, which are indicative of Behçet's disease. MR imaging after three courses of steroid pulse therapy revealed that the edematous lesion had become smaller with minimum midline shift. NBD should be considered in the differential diagnosis of lesions with multiple ring-like enhancement extending from the basal ganglia to the brainstem, because dermatological manifestations are sometimes obscured during periods of remission.

Objective and importance Epilepsy associated with cavernous malformations is often effectively controlled by lesionectomy alone. Detailed preoperative evaluation is necessary if the lesions are multiple and the seizures are medically intractable. We report on a patient with multiple cavernous malformations associated with medically intractable seizures who became seizure-free after a single gyrus resection. The importance of electroencephalography with video monitoring is emphasized. Clinical presentation The patient was a 25-year-old man with a 10-year history of complex partial and generalized convulsions. Magnetic resonance imaging revealed more than 10 cavernous malformations. Video-electroencephalographic monitoring indicated that seizures originated from either the frontal or temporal lobe of the right hemisphere. Intervention Subdural electrodes were implanted, covering both frontal and both temporal lobes. The seizures originated in the right frontal lobe. The gyrus, including a calcified cavernous malformation, was removed, and multiple subpial transections of the surrounding cortices were performed. The patient has been free of seizures for 22 months after surgery. Conclusion Medically intractable seizures associated with multiple cavernous angiomas can be controlled by a single resective procedure.

Recent studies have demonstrated the presence of transferrin receptors (Tf-R) in the central nervous system. The present study of Wistar rats with experimentally induced brain injuries, using immunohistochemistry at the light microscopy level, demonstrated the presence of Tf-R in regenerated endothelial cells, reactive astrocytes and in other cells, probably macrophages. Although Tf-R were seen in proliferating cells, Tf-R were also observed in non-proliferating cells, many of them macrophages. The receptors perhaps bind transferrin in edema fluid and play an important role in lesion repair.

Dural arteries are potential donor arteries for cortical revascularization. In this report, a technique of indirect anastomosis using a split dura is presented. At surgery, the dura near the branches of the middle meningeal artery was split into outer and inner layers, and the split surface of the outer layer was attached to the cortical surface (split duro-encephalo-synangiosis; split DES). This procedure, combined with standard encephalo-duro-arterio-synangiosis, was applied to 25 hemispheres in 18 patients with pediatric Moyamoya disease (mean age, 6 years). Postoperative superselective angiograms demonstrated effective cortical revascularization through the dural arteries in addition to the supply from the scalp arteries. All the patients were symptom free by 1.5 years after surgery. Postoperative reversible ischemic neurological deficit and infarction were seen in three (12%) and one (4%), respectively. The follow-up period ranged from 1 to 12 years (mean, 6.5 years). Thirteen of 16 (81%) patients led normal lives and three were mildly handicapped due to mental retardation that existed preoperatively. The split DES is a useful technique to extend the area of revascularization of ischemic hemispheres in Moyamoya disease.