A case of middle cerebral artery occlusion caused by dissecting aneurysm

We reported a case of middle cerebral artery occlusion caused by a dissecting aneurysm that was successfully treated by intra-arterial fibrinolysis. A 38-year-old man suddenly developed left hemiparesis and became confused. He was transferred to our hospital one hour and 27 minutes after the ictus. Right carotid angiogram (CAG) revealed aneurysmal dilatation of the horizontal portion of the middle cerebral artery and occlusion of the anterior trunk. Twelve million IU of tissue plasminogen activator was injected to fibrinolyze the thrombus of the occlusion site through a microcatheter. After this, the patient became alert and hemiparesis disappeared. It took three hours and 30 minutes to gain recanalization after the ictus. Right CAG obtained the next day demonstrated the patency of the anterior trunk and the characteristic finding of the dissecting aneurysm viz "double lumen" as a result of fibrinolysis of the thrombus in the false lumen. Right CAG obtained two weeks later demonstrated "string and pearl sign" instead of the "double lumen" as a result of partial thrombosis in the false lumen. Follow-up CAG obtained nine months after the ictus demonstrated marked reduction of the aneurysmal size as the result of progressing thrombosis of the false lumen. The characteristic angiographic findings of the dissecting aneurysm such as "double lumen" and "string and pearl sign" seemed to be mostly influenced by the status of the thrombus in the false lumen. In case of major cerebral arterial occlusion caused by the embolus or thrombus from the dissecting aneurysm, intra-arterial fibrinolysis seems to be a possible treatment modality, even though it is accompanied by the risk of giving rise to subarachnoid hemorrhage.     

Symptomatic vessel narrowing caused by spontaneous rupture of craniopharyngioma cyst--case report

A 36-year-old female presented with cerebral infarction due to severe vessel stenosis after spontaneous rupture of a craniopharyngioma, manifesting as aphasia and drowsiness. Neuroimaging showed the suprasellar cystic tumor with wall enhancement and cerebral infarction in the left temporoparietal region, and also enhancement of the left sylvian fissure and prepontine cistern. Angiography showed severe narrowing at the C1 portion of the left internal carotid artery (ICA) and the M1 portion of the left middle cerebral artery (MCA). The tumor was subtotally removed via a bifrontal craniotomy. There was accumulated milky-white debris around the left ICA and MCA. She became alert within a few days postoperatively. Repeat angiography 1 month after surgery demonstrated slight improvement of vessel narrowing. The neuroimaging and intraoperative findings suggested that the stenosis was due to vasospasm induced by chemical meningitis resulting from cyst rupture.     

A case of multiple cerebral arterial thrombosis due to congenital protein C deficiency]

We report a 49-year-old man who had right hemiparesis and motor aphasia. A computed tomography revealed hypodense areas in the left frontal subcortex. A cerebral angiography demonstrated occlusion of the left distal internal carotid artery and both anterior cerebral arteries, as well as stenosis of the left internal carotid artery at the cervical portion. The second angiogram obtained a month later showed no changes. The diagnosis of atherothrombotic cerebral infarction was established on the basis of clinical profile and angiographic findings. Protein C activity and antigen levels were reduced to approximately one half of the normal level in the patient and his brother. The patient had no other risk factors for stroke. Protein C deficiency has been considered one of the risk factors for thrombotic diseases. Venous thrombosis is the most common clinical manifestation, whereas arterial thrombosis is relatively rare. It is generally believed that arterial ischemic stroke associated with protein C deficiency occurs with embolic mechanism, and atherothrombotic infarction is extremely rare. This is the first report suggesting the possibility that protein C deficiency can cause cerebral thrombosis.     

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.     

More children are unable to get dental care than any other single health service

True congenital peripheral aneurysms of the cerebral arteries are rare and may constitute a special entity. We report a rare case of nonmycotic peripheral aneurysm of the posterior cerebral artery (PCA) found in association with aneurysms of distal middle cerebral artery (MCA), junction between basilar artery (BA) and superior cerebellar artery (SCA) and MCA trunk. Our present case was a 37-year-old man with a history of abrupt loss of consciousness. Cerebral angiography revealed a right PCA aneurysm originating at the junction between the trunk of the PCA and the posterior temporal branch, and also aneurysms of the right distal MCA, at the right BA-SCA junction and at the trunk of right MCA just distal to the anterior temporal artery. Distal PCA aneurysm causing subarachnoid hemorrhage was successfully clipped and all the other aneurysms were treated in a one-stage procedure. Pathological examination of the surgically excised distal PCA aneurysmal sac demonstrated no infectious etiology. There have not been any similar cases showing an association of vascular anomalies with distal PCA aneurysm. This is the only reported case with the association of nonmycotic peripheral aneurysms involving the MCA and PCA.     

A large vertebrobasilar junction aneurysm grown at the proximal end of basilar artery fenestration--usefulness of balloon occlusion test with 99mTc-HMPAO SPECT under induced hypotension and consideration in therapeutic strategies

A 48-year-old lady suffered a transient loss of consciousness. CT and MRI revealed a large vascular lesion compressing the left lower pons. Angiography revealed a large aneurysm at vertebro-basilar junction, dome of which projected anteriorly and left to midline. Her previous vertebral angiogram taken 10 years ago when she suffered a subarachnoid hemorrhage from the left MCA aneurysm, had showed a fenestration of lower basilar artery without apparent aneurysm. Bilateral super-selective vertebral angiograms revealed that the aneurysm arose at the proximal end of the fenestration, and vertebrobasilar junction was incorporated into the aneurysm indicating broad neck aneurysm. The left posterior communicating artery was well developed. Balloon test occlusion (BTO) of bilateral vertebral artery was performed under normotension and induced hypotension. 99mHM-PAO SPECT was used to examine cerebral blood flow (CBF) during hypotensive BTO. The patient tolerated the test and CBF imaging showed insignificant sight decrease in bilateral cerebellar hemispheres. Exploration of the aneurysm was carried out by the right far lateral suboccipital approach. Bilateral vertebral arteries and the right segment of the basilar artery fenestration were identified. Neck clipping of the aneurysm with reconstruction of the parent vessels were tried with fenestrate clip. However, narrow operative field and large dome of the aneurysm made it hard to identify the left segment of the fenestration. Neck clipping was given up and clipping of bilateral vertebral arteries were performed distal to posterior inferior cerebellar artery with three body clippings. The patient showed moderate postoperative left lower nerve palsy, which was gradually improved in several weeks. Follow-up angiography revealed no opacification of the aneurysm.(ABSTRACT TRUNCATED AT 250 WORDS)     

Testosterone sulphation and glucuronidation in the human liver: interindividual variability

We present a case with the traumatic extracranial internal carotid artery dissecting aneurysm. A 21-year-old man was involved in a motorcycle accident, resulting in multiple injuries but no apparent head and neck injuries. Head CT was normal on his admission. He was discharged from his local hospital 3 weeks after the accident without any neurological deficits. Five weeks after the accident, he suddenly presented with a motor aphasia and a right hemiparesis. CT and MRI showed infarctions in the left para-Sylvian and the left angular areas. Angiography showed a left extracranial carotid artery dissecting aneurysm at the level of C1 vertebral arch. The patient was initially managed by an anticoagulant agent, but he suffered from another transient ischemic attack due to distal embolism from the aneurysm. Balloon occlusion test of the left ICA was performed under monitoring EEG, SEP. Mean stump pressure (MSP) revealed 60 mmHg. and MSP/Mean systematic blood pressure revealed 67%. We judged that the left ICA ligation was a safe method to treat this patient, however, considering the patient's age and the side of the lesion, left STA-MICA bypass and ligation of the left ICA were carried out in one stage. Postoperatively, the patient did not show any cerebral ischemic complications and angiography showed disappearance of the aneurysm and patency of the bypass. The left MCA territories were filled well by cross circulation and the bypass.     

Spontaneous disappearance of arteriovenous malformation during staged treatment of multiple cerebral arteriovenous malformations--case report

A 36-year-old male presented with aphasia and right hemiparesis due to the rupture of the larger of two arteriovenous malformations (AVMs) coexisting in the left hemisphere. The two AVMs had completely separate locations and different feeding arteries and draining systems. Two months after resection of the larger AVM and evacuation of the hematoma, carotid angiography showed the residual AVM had spontaneously disappeared. He was discharged without deficits. Change of cerebral hemodynamics after removal of the larger AVM presumably caused the spontaneous regression of the smaller one. Cerebral angiograms should be carefully examined because cerebral hemodynamics may be altered after removal of an AVM.     

Increase of cerebral blood flow and improvement of brain motor control following spinal cord stimulation in ischemic spastic hemiparesis

A 64-year-old man had an ischemic stroke in the left parietotemporal cortical-subcortical areas. He developed a severe right spastic hemiparesis and dysphasia. An angiographic study showed left internal carotid artery occlusion and right internal carotid artery stenosis. A right internal endoarteriectomy was performed without any clinical improvement. After 1 year the patient was a candidate for cervical spinal cord stimulation (SCS) for the treatment of his spastic hemiparesis. An epidural electrode (Medtronic Sigma 3483) was positioned at the cervical level, mediodorsal to the cord. Clinical and neurophysiological studies (surface polyelectromyography, PEMG, for evaluation of brain motor control) were performed before and after 7 days of SCS (0.2 ms, 80 c/s, intensity for paresthesiae, continuous mode). A transcranial Doppler (TCD) study of both middle cerebral arteries (MCA) at rest and during SCS was performed on two occasions. SCS was followed by improvement of voluntary movement, decrease of spasticity and better endurance. The clinical findings were confirmed by the PEMG recordings. TCD examination showed an increase of flow velocities on both the right MCA (+43%) and the left MCA (+130%) during SCS. Such a TCD pattern, suggesting an increase of cerebral blood flow (CBF) during SCS, was reproducible. This case confirms efficacy of SCS in the treatment of ischemic hemiparesis and the increase of CBF following cervical SCS in man. The marked increase of CBF, particularly evident on the ischemic side, may play a role in mediating the improvement of motor control in our patient together with a possible arousal of the so-called 'sleeping neurons' of the penumbra zone.     

Paradoxical cerebral embolism during fibrinolysis therapy in deep vein thrombosis and pulmonary embolism

A 37-year-old woman with increasing dyspnoea over several months suddenly developed severe ortho- and tachypnoea as well as cyanosis of the lips and acrocyanosis. Pulmonary angiography revealed massive bilateral pulmonary emboli with a systolic pulmonary artery pressure of 75 mm Hg. Phlebography demonstrated a thrombotic occlusion of the deep veins of the left leg extending to the distal femoral vein. Thrombolysis treatment was started via an indwelling pulmonary artery catheter (500,000 IU urokinase and 10,000 IU heparin as bolus, then 1 mill. IU urokinase and 1,000 IU heparin per hour). After two hours an incomplete left-sided paresis occurred (involving ocular and facial muscles, dysarthria, left arm and left leg) and the thrombolytic infusion was stopped. But cerebral computed tomography (CT) did not demonstrate any intracerebral haemorrhage. The heparin infusion was restarted (partial thromboplastin time between 70 and 90 s). CT examinations during the next few days showed the development of an ischaemic infarction in the distribution of the right medial cerebral artery. Angiography demonstrated occlusion of the right internal carotid artery. The diagnosis of a paradoxical embolus was supported by easy cardiac catheter passage through a patent foramen ovale. Subsequent pulmonary angiography demonstrated a thrombus-free pulmonary arterial circulation with a normal pulmonary arterial pressure. There was gradual and extensive regression of the incomplete hemiparesis.     

Neurotoxicity evoked by N-methyl-D-aspartate in the organotypic static slice cultures of rat cerebral cortices: effect of GABA(A) receptor activation

BACKGROUND: von Recklinghausen's neurofibromatosis is a hereditary disease that may affect any organ or system of the body primarily or secondarily, including the vascular system. Among the rare cerebrovascular abnormalities, the most common is stenosis or occlusion of the cerebral artery. Intracranial aneurysms are uncommon. CASE DESCRIPTION: A case of an intracranial cerebral aneurysm associated with von Recklinghausen's neurofibromatosis is reported. A 55-year-old woman presented with a history of intermittent headache for 2 months and right oculomotor nerve palsy for 1 month. Widespread cutaneous neurofibromas and angiomas were found over her trunk and limbs with prominent cafe-au-lait spots. X-ray showed that her left lung was compressed by a large mass in the left chest with rib defects and lateral spinal curvature. Right internal carotid angiography revealed a saccular aneurysm between C1 and C2. Craniotomy to clip the aneurysm could not be performed because the mass in her chest made intubation for general anaesthesia almost impossible. CONCLUSION: The clinical features of this case are discussed together with a review of 15 similar cases in the literature. There are different theories about this disorder. We agree that the malformations are derived not only from ectodermal, but also from mesodermal pathology. In terms of our case, we consider the progression of this disease to be slow.     

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.     

Circulatory arrest with profound hypothermia during the surgical treatment of large internal carotid artery aneurysm--case report

A 43-year-old male presented with a cerebral aneurysm manifesting as right facial paresthesia, without neurological deficit. Angiography revealed a large aneurysm (22 mm) of the left internal carotid artery. Intravascular treatment using placement of a detachable coil was attempted, but the coil did not stay in the aneurysmal cavity and the procedure was abandoned. The patient did not tolerate the transient balloon occlusion test of the left internal carotid artery. Therefore, the aneurysm was clipped through an open craniotomy with profound hypothermia (20 degrees C) with cardiac arrest (24 minutes). The aneurysmal dome was collapsed, allowing easy dissection of the posterior communicating artery. The closed chest method was used during the extracorporeal cardiopulmonary bypass. Postoperative angiography revealed complete neck clipping with preservation of carotid blood flow. The patient recovered well and resumed his employment. Circulatory arrest with hypothermia provides several benefits for the surgical treatment of large and giant aneurysms.     

Brain lipid peroxidation and antioxidant levels in fetal lambs 72 hours after asphyxia by partial umbilical cord occlusion

Giant middle cerebral artery (MCA) trifurcation aneurysms that cannot be excluded directly can be treated by flow inversion achieved by creation of an extracranial-intracranial bypass distal to the aneurysm, followed by occlusion of the parent vessel proximal to the aneurysm. As opposed to surgical occlusion, endovascular occlusion avoids dissection of the aneurysm area, and the site of occlusion can be chosen according to the flow distribution demonstrated on angiography performed during test occlusions. Two patients with giant aneurysms of the MCA trifurcation benefited from flow inversion treatment. Forty-eight hours after an MCA-superficial temporal artery bypass had been created, the M1 segment was occluded by inserting a coil in the first patient and the internal carotid artery was occluded with balloons in the second patient (there was no communicating artery in the latter case). Both occlusions were performed immediately after a clinical test of occlusion tolerance. The patients were clinically intact during the postoperative course. Follow-up angiography performed 11 and 4 months, respectively, after vessel occlusion showed that the aneurysm occlusion was stable.     

Prognostic factors for adenocarcinoma of the gallbladder: an analysis of 162 cases

We experienced a case with sudden unexpected death caused by rupture of an intracranial aneurysm, which was confirmed by autopsy. Depending on this case, we reported the significance of the cerebellar tonsillar herniation on the cause of sudden death of ruptured cerebral aneurysm. A 58-year-old man was admitted to us for treatment of subarachnoid hemorrhage (SAH). The CT scanning showed diffuse SAH in the whole cistern. Cerebral angiography on admission revealed an aneurysm at the bifurcation of the left middle cerebral artery in association with bleb like configuration. The aneurysmal neck was clipped on the day of admission. The postoperative course was uneventful. In the early morning of postoperative 23rd day, he was found being expired. To clarify the cause of death, an autopsy was done, disclosing diffuse SAH in association with tonsillar herniation more marked on the left. Thus, the distortion of the spinomedullary junction due to asymmetrical herniation was considered to be responsible for unexpected sudden death in this case. Examination of the major cerebral artery disclosed a ruptured anterior communicating artery aneurysm.     

Diagnosis of middle cerebral artery stenosis by transcranial color-coded real-time sonography

BACKGROUND & PURPOSE: This study was performed to determine the usefulness of transcranial color-coded real-time sonography (TCCS) in detecting stenosis in the horizontal portion of the middle cerebral artery (MCA). METHODS: Using TCCS and the incident angle correction technique, we measured the peak-systolic flow velocity in bilateral MCAs in 45 consecutive patients in whom cerebral angiography was carried out within 1 week before or after TCCS. Three patients had a stenosis of 75% or greater and four had a unilateral occlusion of the extracranial internal carotid artery (ICA) (the ICS and ICO groups, respectively). Eight patients had a stenosis of 50% or greater (one bilateral and seven unilateral) (the M1S group). Four patients had unilateral distal occlusion of the horizontal portion of the MCA (the M1O group). Twenty-six patients had no significant extra- or intracranial stenosis on the ipsilateral or contralateral side (the control group). RESULTS: Mean peak-systolic flow velocity on the affected side was 83.0 +/- 20.8 cm/s in the ICS group, 59.8 +/- 23.2 cm/s in the ICO group, and 62.3 +/- 33.7 cm/s in the M1O group. In the control group, the mean peak-systolic flow velocity was 116.0 +/- 31.5 cm/s. In the M1S group, however, the mean peak-systolic flow velocity (334.2 +/- 35.7 cm/s) on the affected side always exceeded 180 cm/s (mean value +/- 2 SD in the control group), and was significantly higher than that in the other groups. The mean peak-systolic flow velocity in the M1S group increased with the grade of stenosis. CONCLUSION: The M1S group members could easily be distinguished from the other group members by their peak-systolic flow velocity in excess of 180 cm/s. Measurement of the peak-systolic flow velocity of the MCA by TCCS may help to identify a significant stenosis in the horizontal portion of the MCA.     

Anticarcinogenic effect of palustran on development of tumors induced by 3-(1-alpha-L-arabinopyranosyl)-1-methyl-1-nitrosourea (AMNU) in rats

Clinical manifestations of superior sagittal sinus (SSS) thrombosis are nonspecific but characterized by headache, papilledema, seizures, focal deficits, progressive coma and death. Recurrent transient focal neurologic deficit is an extremely rare manifestation in superior sagittal sinus thrombosis and the mechanism is unknown. A 45-year-old man presented with headache for two weeks and four episodes of transient (5-10 minutes) right or left hemiparesis for two days. Magnetic resonance image and transfemoral cerebral angiography revealed superior sagittal sinus thrombosis with numerous prominent collateral venous channels. There was no parenchymal lesion. After four days of heparinization, no further transient focal neurologic deficits developed. Follow-up angiography showed partial recanalization of the SSS. Possible mechanism of transient ischemic attacks in this patient is thought to be a transient functional disturbance due to a temporal reduction of tissue perfusion in the process of operating fully-enough collateral channels.     

Intracranial hemorrhage observed in the cases of cervical internal carotid artery occlusion associated with moyamoya disease-like vessels]

We report on two peculiar cases of intracranial hemorrhage due to the rupture of moyamoya disease-like vessels associated with unilateral internal carotid occlusion at its origin. The first case is 44-year-old male showing intraventricular hemorrhage associated with right internal carotid occlusion. The second case is 58-year-old female presenting sub-arachnoid hemorrhage associated with left internal carotid occlusion. Although both cases showed the unique appearance of collateral flow resembling moyamoya disease, they were not classified as moyamoya disease nor unilateral Moyamoya-like state. Vascular abnormality such as cerebral aneurysm and arteriovenous malformation were not at all detected. The etiology of hemorrhage for both cases is presumed as the rupture of moyamoya disease-like vessels, however, it is unable for us to determine why the one case showed IVH, yet the other showed SAH. The two cases showed hypoperfusion of ipsilateral cerebral hemisphere on SPECT that followed by the external-internal carotid revascularization surgery in the chronic stage. Post operative study proved the improvement of the CBF reserve. Nevertheless, whether the reconstructive vascularization prevent an occurrence of rebleeding needs the longer observation and the accumulation of the resembling cases.     

Ruptured fusiform cerebral aneurysm in a neonate

An 11-day-old male infant presented with subarachnoid and intraventricular haemorrhage caused by a ruptured intracranial aneurysm. Magnetic resonance (MR) angiogram and digital subtraction angiography (DSA) revealed a fusiform aneurysm 10 mm in diameter supplied by the proximal segment of the anterior cerebral artery (A1), with both distal segments (A2) arising from the aneurysm. The right A1 was aplastic. There have been 13 previous case reports of neonatal cerebral artery aneurysms, but only 1 of these has been fusiform. None of the earlier reports has mentioned dysplastic segments or other anomalies of the circle of Willis.