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.     

Successful electroconvulsive therapy of Cotard syndrome with bitemporal hypoperfusion

A case study is presented to illustrate a rare condition described by Cotard as "délire de négation". The central symptom is a nihilistic delusion with denial of one's own existence of oneself and that of the external world. In the present case, the syndrome became manifest as an escalation of a recurrent depressive disorder late in life. After initial resistance to therapy, the syndrome was successfully treated with electroconvulsive therapy. For the first time, we report the regional cerebral blood flow measured by 99mTc-HMPAO-SPECT before and after therapy. Before treatment, significant bitemporal hypoperfusion relative to the cerebellum was found, which was no longer demonstrable on remission.     

The effect of phototherapy on cerebral blood flow velocity in preterm infants

Cerebral blood flow velocity was studied with two-dimensional/pulsed Doppler ultrasound before, during and after discontinuation of phototherapy in 22 preterm infants (gestational age < or =32 weeks), who were treated for a minimum of 12h with blue-light phototherapy for non-haemolytic hyperbilirubinaemia. Before the cerebral blood flow velocity measurements, patency of the ductus arteriosus was diagnosed by Doppler echocardiography. All infants had normal brain ultrasound scans. Mean cerebral blood flow velocity increased significantly after initiation of phototherapy in all infants. Only in "healthy" (non-ventilated) infants did cerebral blood flow velocity return to pre-phototherapy values (baseline) after discontinuation of phototherapy, whereas in "unhealthy" (ventilated) infants cerebral blood flow velocity did not return to baseline. In 10 infants the ductus arteriosus reopened during phototherapy. In those infants, mean cerebral blood flow velocity returned to pre-phototherapy values after 2 h of phototherapy prior to its discontinuation.     

Combined lytic and heart surgical therapy of in open foramen ovale incarcerated giant thrombus with pulmonary and cerebral embolization

A case of phlebothrombosis with recurrent pulmonary and cerebral embolism is presented which occurred in a 42 year old patient two weeks after treatment of a traumatic crural fracture despite of prophylaxis with low molecular heparin. By means of transthoracic echocardiography a large intracardiac thrombus was detected, entrapped in an patent foramen ovale (PFO) and prolapsing through both atrioventricular valves into both ventricles. This was found after systemic thrombolysis with rtPA had been performed because of fulminant pulmonary embolism. Subsequently the intracardiac thrombus was surgically removed and the PFO closed. The importance of an PFO for paradoxical embolism is discussed as well as the various therapeutical paths to treat an "embolus-in-transit" (cardiac surgery, thrombolytic therapy or anti-coagulation).     

Repeat angiography and magnetic resonance imaging (MRI) of dissecting aneurysms of the intracranial vertebral artery. Report of four cases

We here present 4 cases with dissecting aneurysm (DA) of the intracranial vertebral artery, who were followed up by repeat cerebral angiography and MRI. The patients consisted of 2 males and 2 females, and the mean age was 43 years. Two cases were associated with polyarteritis nodosa (PN) and hypertension, respectively. Three of the cases developed subarachnoid haemorrhage (SAH), while the other one suffered from lateral medullary syndrome. In cerebral angiography, "pearl and string" signs were revealed in all cases, while a "double lumen" indicating a true diagnostic sign of DA was demonstrated in only one case. Repeat angiography showed that a bleb formation with a bulging of the aneurysmal sac was seen in 2 cases, and an irregularity of the wall in one case. On the other hand in one case, the ectatic part shrank, while the stenotic part was restored. In magnetic resonance imaging (MRI), a hyperintensity mass on T 1-weighted image (T 1-WI) adjacent to flow void suggesting either an intramural haematoma or a linear shape hyperintensity on T 1-WI were demonstrated in 3 cases. In the follow up MRI done in 2 cases, a serial change in the intensity from iso-intensity to hyperintensity on T 1-WI was observed in one case suggesting intramural haemorrhage, while an enlargement of the ectasic flow void was seen in the other case. Three of 4 cases were operated on by trapping of the aneurysms. One, who had systemic vascular diseases due to PN, and repeat angiography showed a regression of the aneurysm, was conservatively treated.(ABSTRACT TRUNCATED AT 250 WORDS)     

Transluminal angioplasty and intra-arterial papaverine for the treatment of cerebral vasospasm after ruptured arteriovenous malformations

BACKGROUND: This is the first report on the use of intra-arterial papaverine and percutaneous transluminal angioplasty in two patients with severe, symptomatic cerebral vasospasm who suffered ruptured arteriovenous malformations (AVMs). CASE DESCRIPTIONS: The source of hemorrhage was a venous aneurysm in the first case and a pedicular aneurysm of the distal posterior inferior cerebellar artery in the second case. In both cases, the AVMs were located in the superior vermis and there was minimal subarachnoid hemorrhage. The first patient underwent removal of the AVM before the period of cerebral vasospasm and the second patient underwent removal of the AVM after the cerebral vasospasm had resolved. The outcome was excellent in the first patient and poor in the second patient. CONCLUSION: Arteriovenous malformation with ruptured aneurysms may be at high risk for cerebral vasospasm even when there is minimal subarachnoid hemorrhage. We recommend early treatment of AVMs with ruptured pedicular, intranidal, or venous aneurysms to avoid rebleeding and to allow for aggressive treatment of cerebral vasospasm. The management of cerebral vasospasm after AVM rupture is discussed.     

Swyer James syndrome following Mycoplasma pneumoniae pneumonia: report of one case

Systemic vasculopathy in patients with neurofibromatosis type 1 is rare. We describe a case of unusual cerebral and renal involvement in a young, 29-year-old patient, who died of a cerebral ischemic attack one year after our observation.     

Prevalence of arterial hypertension in Cushing''s syndrome

Subacute cerebral infarcts may appear normal on T2-weighted MRI as an area isointense with surrounding normal tissue. This MRI "fogging effect" has been described in only a few cases. We present a further case of fogging observed during the evolution of a cerebellar infarct.     

Electronic documentation of images and findings in gastroenterology

Clinico-neuropathological findings recorded from one case of cerebral gliomatosis are reported in this paper. Immunocytochemical methods (GFAP, protein S-100) were used together with morphometric computer-assisted analysis for more effective investigation of certain cytopathological features such as the relationship between cerebral gliomatosis and low-graded astrocytoma. Immunohistochemically, most of the proliferating cells were positive to GFAP and/or to protein S-100, which was in fair agreement with publications elsewhere in the literature. However, varying amounts of spindle-shaped cells remained unstained. The nature of such cells is unclear. The morphometric study showed the majority of cellular parameters of cerebral gliomatosis to be comparable to cellular parameters recordable from "peripheral" regions of a series of low-grade astrocytomas.     

Progressive encephalopathy in antiphospholipid antibody syndrome

The most frequent neurological complications of antiphospholipid antibodies syndrome (APS) are cerebral infarctions. In cases with recurrent strokes this syndrome may be associated with multi infarct dementia. We report the case of a 40-year old man presenting as "primary" APS with multiple cerebral infarctions. This patient had insidiously and progressively developed a cognitive impairment predominant in memory. The progressive encephalopathy associated with APS is very different from multi infarct dementia and could be caused either by a vascular mechanism (vascular occlusion with fibrin thrombi or disseminated vasculitis) or by an immunological mechanism.     

Shortening arthrodesis of three wrist bones

We report an autopsy case of atypical presenile dementia. Shibayama, Kosaka and others had reported similar autopsy cases. These cases had the following common pathologic characteristics: circumscribed cerebral atrophy, diffuse neurofibrillary tangles (NFTs) noted in the cerebral cortex with few senile plaques (SPs), and pathological calcification. We propose the term "dementia with cerebral calcification and tangles" (DCCT) for this atypical presenile dementia. Our patient, who was female and died at the age of 65 years, also exhibited these characteristics. Her clinical diagnosis was Alzheimer's disease. She had developed apparent dementia at the age of 55. Psychological and neurological symptoms such as memory impairment, speech disturbance and abnormal behavior slowly progressed. Gradually, she had become bedridden in her own home. When she was 65 years old, she was admitted because of pneumonia, and died soon after. In the pathologic examination of our patient, the brain weight was 850 g, and severe cerebral atrophy predominant in the temporal lobe was noted. Microscopically, diffuse and numerous NFTs were also found in the cerebral cortex and brain stem. Some NFTs were observed in the dentate nucleus of the cerebellum. However, SPs were seldom noted. Calcifications were also found in the putamen, globus pallidus and cerebellar cortex. NFTs in our case had developed without the formation of SPs. The degree of the NFT formation was correlated to the extent of cerebral cortical atrophy and neuron loss. Therefore, we suspect that NFTs with neuron loss strongly contribute to clinical symptoms such as dementia. The distribution of NFTs resembles that in patients with Alzheimer's disease, they are more prominent in the temporal lobe in our case. Although there has not been any discussion about the findings of glial cells and neuropils in DCCT, our detailed examination showed argyrophilic structures in glial cells and in neuropils. Most of the glial cells appeared to be oligodendrocytes. Calcification is also a prominent characteristic of DCCT. Using analytical electron microscopy, we examined the area of calcification in the globus pallidus and cerebellum, and found an accumulation of both Fe and Ca. The role of calcification in the pathogenesis, however, remains unclear. It is very important to examine cases of atypical presenile dementia clinicopathologically, in order to study the correlation between NFTs and SPs in neurological disease, and to understand their pathogenetic significance.     

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.     

Clinical and CNS effects of oral and I.V. Thyrotropin-releasing hormone in depressed patients

Both oral and intravenous TRH produce systematic alterations in brain function of depressive patients as determined by scalp-recorded computerized cerebral biopotentials (computer EEG). The computer EEG (CEEG) profiles of both formulations are not only very similar to each other, but also resemble the CEEG profiles of psychostimulant compounds (Bio-availability). As in CEEG findings, TSH plasma levels also indicate that oral TRH is indeed an active compound. Although some "antidepressive" effects were observed after both formulations, they were not present in every patient, and it was not always the case after repetitive TRH administration, nor were the effects on depressed mood too impressive. On the other hand, in almost all patients certain behavioral effects of TRH were seen which related to "life instincts" and "life performance". The increase of interest, desire and drive for work, food and sex was one of the most striking findings, particularly after intravenous TRH. This may be responsible for the "antidepressive" effects of TRH in patients in whom depression may be the result of an inhibition of "instinctive" functions.     

Angiitis of the central nervous system in systemic diseases

PURPOSE: This review is aimed at presenting classification and diagnosis criteria of isolated central nervous system (CNS) angiitis, and at proposing guidelines for diagnosis and management of this disease. CURRENT KNOWLEDGE AND KEY POINTS: Isolated CNS angiitis are rare and most information has been provided by studies of very small series. Angiitis can be primitive or secondary to infectious, neoplastic diseases, or toxics. Clinical manifestations and radiologic abnormalities are not specific. A brain biopsy is therefore often required to confirm the diagnosis, as numerous non-inflammatory vascular diseases can mimic both clinically and radiologically isolated CNS angiitis. PERSPECTIVES AND PROJECTS: To help guide the diagnosis and therapeutical management of patients with CNS angiitis, strict classification criteria should be used: 1) rule out the various diseases that can mimic clinical and radiological CNS aspects related to isolated angiitis and differentiate "isolated CNS angiitis" from "CNS angiitis associated with systemic diseases"; 2) search for factors associated with the development of a "secondary CNS angiitis"; 3) check presumed mechanism at the origin of the cerebral vascular disease: "angiitis" versus "angiopathy"; 4) if the diagnosis of "primary CNS angiitis" is still suspected, it seems reasonable to perform cerebral and leptomeningeal biopsies. Treatment is still unknown and has to be discussed on a case by case basis according to the severity and progression of symptoms.     

Cerebral blood flow in mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes

BACKGROUND AND PURPOSE: The precise mechanism of neurological symptoms with mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS) is still controversial. We investigated the correlation between strokelike episodes and cerebral blood flow in two patients with MELAS and discuss the pathogenesis of strokelike episodes with MELAS. SUMMARY OF REPORT: Cerebral dynamic computed tomography and cerebral angiography were used to measure cerebral circulation in the first case, that of a 20-year-old woman with MELAS. The second subject was a 13-year-old female who was studied with xenon-enhanced computed tomography. The cerebral blood flow studies were performed 3-72 hours after the onset of strokelike episodes. Serial cerebral angiography, dynamic computed tomography, and xenon-enhanced computed tomography showed vasodilation localized in the affected cerebral cortexes during strokelike episodes, without any reduction in regional cerebral blood flow. CONCLUSIONS: Our study suggests that the strokelike episodes associated with MELAS are different in origin from ischemic stroke.     

Bithalamic hyperintensity on T2-weighted MR: vascular causes and evaluation with MR angiography

PURPOSE: To determine whether MR angiography can be used to differentiate between the two vascular causes of bithalamic hyperintensity on T2-weighted MR images: "top of the basilar" artery occlusion and deep cerebral vein thrombosis. METHODS: A retrospective review identified six patients with bithalamic T2 hyperintensity of vascular causes. MR angiography was performed in four patients, MR angiography and conventional angiography in one patient, and conventional angiography in one patient. Data pertaining to clinical presentation and hospital course were collected. MR angiographic techniques were multislab overlapping three-dimensional time-of-flight, 2-D time-of-flight, and 2-D phase-contrast. RESULTS: Three cases of top of the basilar artery occlusion and three cases of deep cerebral vein thrombosis were recognized. In all cases, T2 hyperintensity in a vascular distribution suggested cerebral occlusive disease. Infarction involving the thalami and basal ganglia was present in two cases of deep cerebral vein thrombosis. Infarction of the thalami, mesodiencephalic region, and cerebellar hemispheres was present in two cases of basilar artery occlusion. Bithalamic infarction alone was seen in one case of deep cerebral vein thrombosis and one case of basilar artery occlusion. In the five cases in which MR angiography was used, this technique accurately distinguished the vessels involved (arterial or venous). CONCLUSION: MR angiography is a useful adjunct to MR imaging in the evaluation of bithalamic T2 hyperintensity. It does help distinguish between the two vascular causes: top of basilar artery occlusion and deep cerebral vein thrombosis.     

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.     

Evaluation of the combination of a tissue-type plasminogen activator, SUN9216, and a thromboxane A2 receptor antagonist, vapiprost, in a rat middle cerebral artery thrombosis model

BACKGROUND AND PURPOSE: We aimed to evaluate a modified tissue-type plasminogen activator, SUN9216, and the combination of SUN9216 and a thromboxane A2 receptor antagonist, vapiprost, in a rat middle cerebral artery thrombosis model. METHODS: Under anesthesia, the left middle cerebral artery was observed under an operation microscope without cutting the dura mater via a subtemporal craniotomy. Photoillumination (wave length, 540 nm) was applied to the middle cerebral artery, and then rose bengal (20 mg/kg) was administered intravenously. The reopening of the middle cerebral artery by SUN9216, injected 30 minutes after middle cerebral artery occlusion, was observed under an operation microscope for a 60-minute observation period. Twenty-four hours after the operation, sections of the cerebrum were stained with triphenyltetrazolium chloride, and the area of cerebral infarction was analyzed by a computer. RESULTS: The combination of SUN9216 and vapiprost caused reopening of the middle cerebral artery in 58.8% of the rats, which was a greater percentage than that achieved with SUN9216 alone (31.6%). In contrast, saline did not cause reopening of the middle cerebral artery during the 60-minute observation period. The area of cerebral infarction in rats reperfused with SUN9216 was significantly reduced compared with that in the control group. The infarction area in rats treated with the combination of SUN9216 and vapiprost was reduced compared with that in rats treated with SUN9216 alone; this was the case whether or not the occlusion was reperfused. There was a significant correlation between the time of reopening of the middle cerebral artery and area of cerebral infarction. CONCLUSIONS: A single injection of SUN9216 was effective in recanalizing the vessel and reducing the area of cerebral infarction.     

Anatomoclinical and angiographic study of a case of disseminated thromboangiosis with predominant cerebral manifestations

The authors describe the case of a patient of 22 with hypertension and livedo reticularis who, after presenting with a left brachial monoparesis became progressively demented over a period of five years and died at the age of 27 from a cerebro-meningeal haemorrhage. Angiographically, diffuse distal obliteration of the cerebral arteries was seen with deep networks of the moyamoya type involving the lenticulostriate arteries; similar changes were present in the upper left limb. Histopathological investigations showed obliterative thromboangiitis affecting not only the cerebrum, the brain stem and the cerebellum, but also the viscera. Analysis of this case and consideration of the theoretical possibilities leads the authors to urge that thromboangiosis together with its cerebral manifestations should be considered a nosological entity.     

Mydriatic pupil as the presenting sign of common carotid artery dissection

BACKGROUND: Ipsilateral mydriasis is known to accompany signs of cerebral ischemia in unilaterally compromised carotid blood flow. Mydriasis as the presenting sign of common carotid artery (CCA) dissection has not been reported thus far. CASE DESCRIPTION: We report the case of a patient who presented with a mydriatic pupil after intraoperative injury of the ipsilateral CCA. Mydriasis preceded complete third-nerve palsy and symptoms of cerebral ischemia for 12 hours. Cerebral angiography revealed occlusion of the CCA with slow collateral flow to the internal carotid artery and fetal origin of the posterior cerebral artery, suggesting a hemodynamic mechanism causing ischemia of the oculomotor nerve. Signs of cerebral ischemia and third-nerve palsy resolved completely after reconstructive surgery of the occluded vessel. CONCLUSIONS: A mydriatic pupil may be the unusual first sign of compromised carotid blood flow and impending cerebral ischemia.