Diffuse cerebral artery vasospasm following total resection of posterior fossa meningioma: a case report]

Diffuse cerebral artery vasospasm following brain tumor resection is a rare complication. The authors reported a case of symptomatic diffuse cerebral artery vasospasm of early phase following resection of a left posterior fossa meningioma. A 50-year-old female patient was admitted to our hospital complaining of headache. No neurological deficits were detected at the time of admission. Computed tomography (CT) and magnetic resonance imaging (MRI) showed a large mass in the left posterior fossa. Cerebral angiography demonstrated mildly diffuse stenosis of the bilateral internal carotid artery. The tumor was resected totally. CT after operation showed a small amount of subarachnoid hematoma in the superior aspect of the cerebellum. Pathological specimen of the tumor showed fibrous meningioma. One day after this radical operation, the patient was found to have weakness in her left leg. Then she developed left hemiparesis, weakness in the right leg and left homonymous hemianopsia. MRI showed ischemic lesions in the bilateral parietal and the occipital lobe. Angiography demonstrated diffuse severe vasospasm throughout the whole cerebral artery. Ten days after the operation, angiographical findings were improved. This case indicates that vasospasm may occur even after resection of brain tumors which are localized outside the suprasellar area.     

Enteropathogenic E. coli: intimacy redefined

A 42 yr old male presented with left facial weakness. MRI showed lesions affecting the distal seventh nerve and third division of the trigeminal nerve. The seventh nerve was biopsied and showed a malignant epithelioid schwannoma. The patient underwent extensive resection followed by irradiation. This is one of very few examples of intracranial malignant peripheral nerve sheath tumors and the first reported example of an intracranial malignant epithelioid schwannoma. The literature is reviewed and completeness of resection appears to be the most pertinent prognostic factor.     

Occlusion of the cervical internal carotid artery due to a dog bite wound: case report

A rare case of traumatic occlusion of the carotid artery at the neck caused by a dog bite is reported. A 10-year-old boy presented delayed onset of left hemiparesis after a dog-bite wound in the right neck. CT scan revealed a cerebral infarction in the right basal ganglia, and IV-DSA disclosed complete occlusion of the right internal carotid artery at the neck. The patient was treated conservatively and his left hemiparesis improved, but impaired visual acuity remained on the right side. Repeated IV-DSA 12 days later showed recanalization of the right internal carotid artery. The mechanisms of the traumatic occlusion of the internal carotid artery were discussed with reference to the literature.     

Refusion of anterior cerebral artery after aneurysm clipping--a case report

Herein, we are describing an unusual case suffering from a left anterior cerebral artery aneurysm (A1). Both the anterior cerebral arteries were supplied by the left internal carotid artery as was found in digital substraction angiography (DSA) preoperatively. The postoperative angiograms revealed that left anterior cerebral artery was supplied from the left internal carotid artery and the right anterior cerebral artery by the right internal carotid artery respectively. This finding of cerebral angiograms is interesting and rarely mentioned in the literature. Its hemodynamic change and pathogenesis were unclear and different to that of the coronary circulation, ischemic change of gut and skeletal muscle. The causes may include: 1) vasospasm at the anterior communicating artery after manipulation at surgery; 2) desiccation or shrivelling the adjacent artery by intraoperative electrocoagulation; 3) occlusion the anterior communicating artery by the wing of clip. 4) the deprivation of the blood flow from the left internal carotid artery after totally or partially narrowing left A1 by an aneurysm clip. The redistribution of blood volume in the previously hypoplastic right anterior cerebral artery and decreased caliber of the left anterior cerebral artery (A1) are likely playing a role in this case.     

In vivo proton magnetic resonance spectroscopy for metabolic changes in brain during chronic cerebral vasospasm in primates

OBJECTIVE: To study how neuronal cells are affected by development of chronic cerebral vasospasm after subarachnoid hemorrhage (SAH), the changes in neuronal metabolites during development of vasospasm were evaluated by in vivo localized proton magnetic resonance spectroscopy (MRS) in primates. METHODS: SAH was produced by introduction of a blood clot around the right middle cerebral artery and the right side of the circle of Willis. MRS experiments were performed before SAH and on Days 7 and 14 after SAH. Multislice magnetic resonance images were obtained to locate the volume of interest (1.0 cm3) in the bilateral parietal regions. The peak areas for choline compounds, the sum of creatine and phosphocreatine, and N-acetyl-aspartate were calculated. RESULTS: Angiograms revealed approximately 50% reduction of vessel caliber for the right main cerebral arteries on Day 7. Magnetic resonance imaging revealed no apparent cerebral infarction, even in the spasm-side hemisphere. MRS revealed a significant (P < 0.05) reduction of the N-acetyl-aspartate/creatine and phosphocreatine ratio on Days 7 and 14 and a significant increase in the choline/creatine and phosphocreatine ratio on Day 7, in the spasm-side parietal region. In the sham-operated animals, there were no significant changes in these ratios in the bilateral parietal region on Days 7 and 14 after the operation. CONCLUSION: The results suggested that the development of cerebral vasospasm after SAH caused ischemic injury in a subpopulation of neuronal cells, even when no apparent cerebral infarction was shown. Proton MRS may be useful to evaluate how neuronal cells are affected by the ischemic insult during development of vasospasm in clinical situations.     

Transverse and T fractures with fracture of the posterior wall of the acetabulum. Results of orthopedic and surgical treatment. Apropos of 52 cases

A patient developed delayed facial nerve palsy at the level of House-Brackmann grade I to grade III 10 days after vestibular schwannoma surgery by the suboccipital transmeatal approach. The palsy had completely recovered after one month. Immunological study showed reactivation of herpes simplex and magnetic resonance (MR) imaging demonstrated an abnormal enhancement pattern of the facial nerve; intense enhancement of the distal intracanalicular segment and labyrinthine segment, similar to the MR findings for Bell's palsy. A prospective control study on the enhancement pattern of the functionally preserved facial nerve after vestibular schwannoma surgery in six cases showed a similar pattern to that of the normal facial nerve. Based on these findings, we propose the hypothesis that herpes simplex reactivation is an underlying cause of delayed facial palsy after vestibular schwannoma surgery.     

Vasospasm diagnosis: theoretical and real transcranial Doppler sensitivity

In 40 patients middle cerebral artery trunk (M1) flow velocity was recorded just before 54 carotid angiography in 54 cases exhibiting vasospasm after aneurysm rupture. Angiographic vasospasm distribution was studied; cases of symptomatic vasospasm were noted and were compared with transcranial Doppler data. Angiographic vasospasm was present in M1 in 41/54 carotid angiograms. Postulating that all the cases of M1 angiographic vasospasm should be identified by transcranial Doppler, the theoretical sensitivity of TCD was 76%. In this series however the real sensitivity of TCD in vasospasm diagnosis was only 70%: besides 13 cases where vasospasm was not present in M1 (mainly after ACoA Aneurysm rupture), TCD failed to identify 3 cases of M1 angiographic vasospasm. Vasospasm may not be located in M1 even when severe and symptomatic (4 cases in this series). Transcranial Doppler remains a mediocre tool for identifying vasospasm after anterior communicating artery aneurysm rupture (sensitivity: 55%). Its reliability is better after internal carotid aneurysm rupture (sensitivity: 72%) and excellent after middle cerebral artery aneurysm rupture (sensitivity: 93%). In order to test the drugs or methods used to prevent or combat vasospasm, angiography has to be considered when during the vasospasm risk period TCD does not demonstrate vasospasm in M1, either in patients in whom clinical deterioration is occurring without other obvious explanation, or in all patients.     

Colonization factor antigens (CFAs) of enterotoxigenic Escherichia coli can prime and boost immune responses against heterologous CFAs

Calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP) are intrinsic vasodilatory substances contained in perivascular nerve fibers innervating large intracranial arteries. Effects of these substances on delayed cerebral vasospasm were examined using a rabbit model of experimental subarachnoid hemorrhage (SAH). Sixty-one anesthetized rabbits received intrathecal fresh arterial blood on day-1 and intrathecal administration of different doses of CGRP, VIP or distilled water on day-4. Prior to the treatment, caliber of the spastic basilar artery was 73.4 +/- 0.9% of pre-SAH values. Serial angiograms after treatment demonstrated that 10(-10)mol/kg of CGRP dilated the spastic artery to 117.1% of pre-SAH levels and that dilatory effect of CGRP continued up to 6 hours after treatment. VIP injection also brought arterial dilatation up to 114.9% of pre-SAH levels, although the duration of the effect was less than 3 hours. Intrathecal administration of CGRP or VIP showed no adverse effect on the systemic and neurological state of the animals. These results indicate that intrathecal CGRP and VIP have therapeutic potential in treating delayed cerebral vasospasm after subarachnoid hemorrhage. Further investigations are expected to extend the effect of CGRP and VIP.     

Net efflux of cysteine, glutathione and related metabolites from rat hippocampal slices during oxygen/glucose deprivation: dependence on gamma-glutamyl transpeptidase

BACKGROUND: Effect of clot removal and surgical manipulation on cerebral blood flow (CBF) and delayed vasospasm was studied in early aneurysm surgery for subarachnoid hemorrhage (SAH). METHODS: Thirty-two patients in this study fulfilled the following criteria: ruptured anterior communicating aneurysms, computed tomography (CT) within 2 days and unilateral pterional approach within 3 days after the ictus, bilaterally symmetrical clots without intracerebral hematoma, no postoperative complication, and CBF studies with single photon emission computed tomography (SPECT) with 123I-IMP. RESULTS: Postoperative regional hypoperfusion due to brain retraction was frequently recognized on 123I-IMP-SPECT without infarction. The regional CBF (rCBF) showed a continuous fall during the first 4 weeks after the ictus, followed by improvement. The rCBF in the vicinity of the surgical route was significantly lower, especially in the acute stage (Day 3-7). A significant association between decrease of cisternal blood after surgery and the degree of local vasospasm and local CBF values during spasm stage was observed in the interhemispheric cisterns, A2 and medial frontal cortex, but not in the sylvian fissure or insular cisterns, M1 or M2, and frontal watershed and temporal cortex. CONCLUSIONS: The present study provides evidence for the effectiveness of direct clot removal by early surgery for SAH on local vasospasm and CBF reduction. However, a potential improvement in local CBF with clot removal could be masked by brain retraction, which was demonstrated to affect rCBF adversely. Therefore, it is critical to perform brain retraction as gently as possible.     

Differential diagnosis in dementia

The results of an autopsy of a 78-year-old female patient with an occluded of the right internal carotid artery after a traffic accident are reported. She presented with consciousness disturbance, right conjugate deviation, left hemiparesis and left pathological reflex. Evidence of right skull and clavicular fractures seemed to suggest that severe hyperextension of her neck associated with contralateral lateral flexion had stretched her carotid artery. Although she was treated with antiplatelet therapy, her cerebral swelling due to right global infarction progressed and she died due to bilateral cerebral herniation three days after injury. The autopsy disclosed right dissecting carotid artery occlusion and subadventitial dissection was revealed histologically. When a hematoma dissect the media and adventitia of the carotid artery wall, the outer wall weakens and may dilate without narrowing the lumen of the carotid artery. In this case, the vessel occlusion was considered to be due to a primary intramural hematoma which developed and subsequently ruptured through the intima into the vessel lumen. Early diagnosis and treatment are necessary for improving the prognosis of this disease entity. A patient with poor colateral flow, such as in this case, will show a rapid progression of cerebral infarction. It is best to consider surgical treatment in this case if the other traumatic lesions are able to tolerate surgery.     

Experimental vasospasm produced without blood cell components--hypothesis for the development of cerebral vasospasm

A canine model of cerebral vasospasm using noncellular blood material (fibrin glue) was designed to investigate the effect of cerebrospinal fluid obstruction. The arachnoid membrane covering the cerebral arteries in the basal cistern was dissected and fibrin glue was applied to the adventitial surface of the arteries in three groups of animals. In Group 1, the arachnoid membrane was extensively dissected and fibrin glue was widely applied to the cerebral arteries. In Group 2, the dissection and coating was less extensive. Group 3 was a control group in which the arachnoid membrane was dissected but fibrin glue was not applied. Cerebral angiography 1 week later clearly demonstrated vasospasm in all six dogs in Group 1 and in four of six dogs in Group 2. Vasospasm did not occur in Group 3. The dogs were sacrificed and the arteries in the basal cistern were removed. Histological investigation showed typical findings of vasospasm and inertness of fibrin glue to the tissue. Cerebral vasospasm can be induced by a noncellular material from the blood densely applied to the arterial surface suggesting that obstruction of cerebrospinal fluid circulation around the artery may be important in the development of cerebral vasospasm.     

A case of Sj?gren syndrome associated with multiple mononeuritis and dysautonomia including bilateral tonic pupils

In the present study, the feasibility of intrathecal indwelling catheters in the preparation of a repeated subarachnoid hemorrhage (SAH) model in dogs, as well as chronic intrathecal administration of therapeutic agents against the ensuing cerebral vasospasm was examined. Briefly, through a small suboccipital incision, two catheters were introduced into the subarachnoid space so that their tips were positioned in the prepontine cistern. One was used to induce SAH by infusing autologous blood, and the other to administer pharmacological agents (saline and/or saline containing a dye in this study) by means of an osmotic pump. The occurrence of cerebral vasospasm was followed by angiography via the catheter placed in the vertebral artery. The obtained results show: i) the injected blood effectively formed a subarachnoid clot in the prepontine cistern, invariably leading to the occurrence of severe cerebral vasospasm of the basilar artery; ii) the fluid injected by the osmotic pump was evenly distributed in the cisterns around the brain stem; iii) on post mortem pathological examination, no injury of the brain or the major arteries ascribable to the placement of catheters was found. Therefore, the present model is considered to be useful for both the investigation of pathophysiology and therapy of cerebral vasospasm following SAH, to be more favorable from the standpoint of animal protection, and more convenient and reliable than those used until now.     

Cord blood leptin reflects fetal fat mass

This case report describes a 15-month-old female who developed diffuse cerebral vasospasm after resection of a cerebellopontine angle primitive neuroectodermal tumor. The patient developed an acute dense left hemiparesis 16 days postoperatively with partial right ptosis. Initial magnetic resonance imaging and diffusion study were unremarkable, though a magnetic resonance angiography 1 day later demonstrated severe intracranial vasospasm of both carotid and vertebral arteries. The vasospasm was confirmed with cerebral angiography. The patient progressed to bihemispheric infarcts with laminar necrosis despite combination therapy with anticoagulation, pharmacological hypertension, hypervolemia, and nimodipine. The clinical course, radiographic, and pathological findings are presented.     

Does traumatic subarachnoid hemorrhage caused by diffuse brain injury cause delayed ischemic brain damage? Comparison with subarachnoid hemorrhage caused by ruptured intracranial aneurysms

OBJECTIVE: To examine whether traumatic subarachnoid hemorrhage (TSAH) caused by severe diffuse brain injury leads to delayed ischemic brain damage and secondary deterioration of outcome, as does aneurysmal subarachnoid hemorrhage (ASAH). METHODS: We examined 99 patients with diffuse brain injury with TSAH and 114 patients with ASAH. Computed tomographic (CT) findings, cerebral blood flow, and neurological outcomes were assessed during the acute and subacute phases and were compared between the two groups. RESULTS: The distribution of subarachnoid hemorrhage on the CT scans differed between the two groups. Unlike ASAH, TSAH was not limited to cisterns surrounding the circle of Willis but extended to supratentorial regions and interhemispheric fissures. Computed tomography-detected subarachnoid hemorrhage disappeared very early with TSAH and gradually with ASAH. In the ASAH group, mean cerebral blood flow decreased to 75% of normal during the acute phase and decreased a further 10% during the subacute phase. In the TSAH group, mean cerebral blood flow decreased to 85% of normal during the acute phase and increased slightly during the subacute phase. Neurological deterioration and in-hospital death peaked on Day 0 in association with TSAH and showed twin peaks in association with ASAH. The incidence of low-density areas on the CT scans was significantly higher with ASAH than with TSAH. All low-density areas on the CT scans of patients with ASAH corresponded to vascular territories, but low-density areas on the CT scans of patients with TSAH were rarely associated with vascular territories and contained deep-seated or gliding contusion types. CONCLUSION: The findings suggest that the incidence of vasospasm is low in association with TSAH and that the cause is different compared with ASAH. There is no evidence that the presence of TSAH in cases of diffuse brain injury leads to delayed ischemic brain damage and secondary deterioration of outcome.     

Prevention of cerebrovasospasm following subarachnoid hemorrhage in rabbits by the platelet-activating factor antagonist, E5880

Recently, an important role of platelet-activating factor (PAF), an inflammation mediator, has been demonstrated in the genesis of cerebral vasospasm following subarachnoid hemorrhage (SAH). In the current study, the authors examined whether intravenous administration of the novel PAF antagonist, E5880, can prevent vasospasm following SAH in rabbits. A vasospasm model was produced in three groups of rabbits using two subarachnoid injections of autologous arterial blood, followed by intravenous administration of distilled water (control), a low dose of E5880 (0.1 mg/kg in distilled water), or a high dose of E5880 (0.5 mg/kg in distilled water). Neurological deterioration was largely prevented in the rabbits that received E5880. Basilar artery constriction was also reduced by both doses of E5880. Histological examination at autopsy predominantly showed ischemic changes in the brain. Animals in each E5880-treated group exhibited ischemic changes less frequently than those in the control group. Plasma thromboxane B2 concentrations were reduced in rabbits treated with E5880. Platelet-activating factor was immunolocalized in the intima and media of the basilar artery in the control group. The PAF immunoreactivity demonstrated in the basilar artery was decreased in the E5880 groups in a dose-dependent manner. Thus, this study provides evidence that PAF may play a role in the pathogenesis of vasospasm after SAH and that intravenous administration of E5880 is a promising approach in preventing vasospasm.     

Schwannoma of the superficial peroneal nerve presenting as web space pain

A 55-year-old male presented complaining of pain at his right fourth toe and dorsal fourth web space. Physical examination findings pointed to a lesion affecting the superficial peroneal nerve. A schwannoma of the superficial peroneal nerve was subsequently excised, relieving the patient's symptoms. In the differential diagnosis of nontraumatic and/or nonarthritic toe and foot pain, benign tumors, including schwannomas of the tibial and peroneal nerves, should be considered.     

Gastric schwannoma

A rare case of gastric schwannoma is reported. A 36-year-old woman whose endoscopy showed a mucosa tumor, biopsy findings were suggestive for leiomyoma. Diagnosis was made only with postoperative histology that revealed the benign schwannoma. Immunohistochemical staining showed positivity for S-100 protein and the neuron specific enolase, schwannoma is often associated with Von Recklinghausen's disease. Surgical resection is recommended as their malignant potentiality. Gastric and small intestine localizations are often with bleeding. They also represent almost the 24% of all gastrointestinal stromal tumors (GIST) and the 4% of all primary retroperitoneal tumors.     

Identification and characterization of two thrombin-activatable fibrinolysis inhibitor isoforms

OBJECT: The indications, operative findings, and outcomes of vestibular schwannoma microsurgery are controversial when it is performed after stereotactic radiosurgery. To address these issues, the authors reviewed the experience at two academic medical centers. METHODS: During a 10-year interval, 452 patients with unilateral vestibular schwannomas underwent gamma knife radiosurgery. Thirteen patients (2.9%) underwent delayed microsurgery at a median of 27 months (range 7-72 months) after they had undergone radiosurgery. Six of the 13 patients had undergone one or more microsurgical procedures before they underwent radiosurgery. The indications for surgery were tumor enlargement with stable symptoms in five patients, tumor enlargement with new or increased symptoms in five patients, and increased symptoms without evidence of tumor growth in three patients. Gross-total resection was achieved in seven patients and near-gross-total resection in four patients. The surgery was described as more difficult than that typically performed for schwannoma in eight patients, no different in four patients, and easier in one patient. At the last follow-up evaluation, three patients had normal or near-normal facial function, three patients had moderate facial dysfunction, and seven had facial palsies. Three patients were incapable of caring for themselves, and one patient died of progression of a malignant triton tumor. CONCLUSIONS: Failed radiosurgery in cases of vestibular schwannoma was rare. No clear relationship was demonstrated between the use of radiosurgery and the subsequent ease or difficulty of delayed microsurgery. Because some patients have temporary enlargement of their tumor after radiosurgery, the need for surgical resection after radiosurgery should be reviewed with the neurosurgeon who performed the radiosurgery and should be delayed until sustained tumor growth is confirmed. A subtotal tumor resection should be considered for patients who require surgical resection of their tumor after vestibular schwannoma radiosurgery.     

A 23-year-old patient with neurofibromatosis associated with acute myocardial infarction, vasospasm and a coronary artery ectasis

We treated a 23-year-old male with neurofibromatosis with acute myocardial infarction. Cardiac catheterization revealed severe organic stenosis in the left anterior descending artery, an ectasic left circumflex artery and a small right coronary artery. Percutaneous transluminal coronary angioplasty (PTCA) was performed on the stenosis. In follow-up catheterizations, intracoronary administration of ergometrine induced vasospasm of the left coronary artery including at the PTCA site. An I 123 metaiodobenzylguanidine (MIBG) scintigram showed defects in the septum, inferior wall and apex. These findings suggest abnormality of the cardiac sympathetic nerve in neurofibromatosis.     

Internal carotid artery occlusion related to seat belt shoulder strap: report of two cases

Two cases of traumatic internal carotid artery occlusion probably related to the seat belt shoulder strap are reported. Case 1. A 20-year-old woman was driving and was struck on the right front side of her car by another car. There were neither bruises, abrasions on her neck, nor weakness in her extremities. About 4 hours later, she developed left hemiplegia, and CT scan taken on the following day revealed low density areas in the capsulostriatal area on the right. The right carotid angiography revealed occlusion of the internal carotid artery about 3 cm distal to the bifurcation. Case 2. A 43-year-old man was driving and was struck on the front of his car by a hard iron railing. He sustained a sternum fracture, but there was no disturbance of consciousness or paresis of the extremities. His neck was unremarkable externally. About 50 days later, he developed left hemiplegia. CT scan and MRI revealed a massive infarction in the distribution of the right middle cerebral artery territories. The carotid angiography revealed occlusion of the right internal carotid artery about 3 cm distal to the bifurcation. In each cases, the driver was wearing a three-point shoulder seatbelt when the car was struck on the front or on the right front. Previous experimental studies have revealed in these situations the neck is flexed right anteriorly, and then quickly overextended left posteriorly. The overextension of the neck probably injured the intima of the internal carotid artery ipsilateral to the shoulder fixed in the seatbelt, resulting in the subsequent occlusion by a thrombus.