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 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 19 children with acute infantile hemiplegia an ischemic cerebral infarct was found clinically and by serial computertomography. In 11 patients an angiography has been performed in addition. 9 of the children had chronic diseases which are known as predisposing factors for cerebrovascular disease (congenital heart disease in 7 and chronic renal failure with hypertension in 2). One child had a severe hypernatremic dehydration due to infantile diarrhea and in 1 child thrombosis of the internal carotid artery occurred 3 days after a perforating trauma of the soft palate. No obvious reason for the ischemic stroke could be evaluated in 8 children. The onset of symptoms was either acute or slowly progressive. An altered state of consciousness was present in 11 children. Hemiparesis was found in 18 patients (13 right, 5 left) accompanied by facial palsy in 12 and aphasia in 6. Seizures occurred in 6 patients. One patient with incomplete occlusion of a vertebral artery showed acute cerebellar ataxia. In children without predisposing factors the prevalence of girls was higher (2 : 6) and there was a history of a preceding acute febrile illness in 5 of 8 patients. Laboratory investigations showed polycythemia in 4 children with cyanotic heart disease and additional hypochromia in two. Blood sedimentation rate was increased in 6 out of 8 patients without a known predisposing factor. Cerebrospinal fluid (CSF) showed a slight increase of erythrocytes (36-88/cmm) in 4 children, in two others purulent CSF was obtained after the infarct had developed into a brain abscess. The etiology of ischemic stroke in childhood and the possibility of an inflammatory vascular disease are discussed.
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PMID:Acute infantile hemiplegia caused by cerebral ischemic infarction. Etiology, clinical features and investigations. 647 69

The cerebral arterial occlusion was observed from nine patients aged from 2,5 to 12 years old, between 37 children with acute acquired hemiplegia. The thrombosis had an embolic origin in three cases of cardiopathy. Six patients had primary arterial occlusion, but all these patients were febrile and the onset of hemiplegia was accompanied by seizures in five cases. The site of arterial was demonstrated by the angiography in eight cases: cervical internal carotide in one case of cardiomyopathy, intracranial portion of the internal carotide in four cases, middle and anterior cerebral artery in three cases. The regression of hemiplegia was observed in all but one case of atrial myxoma. The autopsy of this patient revealed renal and hemispheric cerebral arterial thrombosis with myxoma embolus.
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PMID:[Acute hemiplegia due to cerebral artery occlusion in children. Apropos of 9 cases]. 662 43

In the present study the pathology and treatment of occlusion of cerebral arteries in children were investigated in an attempt to find out an approach to the surgical treatment of cerebral arterial occlusive disease of childhood. We had a total of 55 children with cerebrovascular disorders seen at our Institute during the past 11 years. In this series there were 19 cases of cerebral arterial occlusive disease. The causes in 15 cases of cerebral arterial occlusive disease except for moyamoya disease were heart disease in 7 cases, trauma in 2 cases and unknown in 6 cases. The cerebral arterial occlusive disease had its onset at the age of less than 6 years in 12 of 15 cases. The disease began with hemiplegia of sudden onset. The disease onset was also attended frequently by a convulsive seizure, which distinguishes the condition from that in adults. In 10 of all 15 lesions the site of occlusion was in the distribution of the middle cerebral artery. One case in which there was occlusion of the basilar artery occurring in association with trauma was described in detail. In one instance the treatment consisted of STA-MCA anastomosis. Paroxysmal black out attacks, which had been of frequent occurrence in addition to hemiplegia were relieved postoperatively. In our opinion, STA-MCA anastomosis for cerebral arterial occlusive disease in children should be considered to be indicated only when 1) cerebral angiographic evidence of occlusion or stenosis of a trunk of cerebral artery is still present after the acute stage or 2) no extensive low density area is demonstrable on CT scan. Surgery is generally less indicated in those instances in which the occlusion is due to embolism. However since abscess may arise from such an arterial lesion, surgery should be considered, or at least its feasibility be evaluated, whenever 1) the underlying cardiac pathology well permits surgical intervention and 2) half a year has passed since an initial attack.
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PMID:[Cerebral arterial occlusive disease in children -- clinical aspects and surgical treatment (author's transl)]. 727 22

The authors use the term "complicated migraine" to describe the onset of neurological disorder occurring during an acute attack in a patient with chronic migraine. The disturbance may last for long periods or may be permanent, and these irreversible cerebral lesions have to be differentiated from the transient neurological effects characteristic of ophthalmic on secondary migraine. Patients with migraine and retinal lesions, as well as those with ophthalmoplegic or familial hemiplegic migraine, were excluded from the study. The seven cases reported included 5 women and 2 men with an average age of 30 years (from 14 to 51 years). A more or less severe lesion in a hemisphere was present, which led to sensory-motor signs of a hemiplegia (4 cases), an aphasia (4 cases), and a homonymous lateral hemianopia (3 cases). Exploration revealed the presence of an ischemic cerebral lesion in all cases. One or more arterial occlusions were also noted in 5 out of the 6 patients who were investigated by angiography. All cases showed the presence of the criteria thought to be essential for associating the cerebral ischemic lesion with migraine. 1) the patient had true migraine, 2) there was a close chronological relationship between the migraine attack and the lasting neurological disorder, 3) no other associated vascular disease was present (atheroma, cardiopathy). The very severe and prolonged spasm, which could be the cause of neurological disturbances in secondary and ophthalmic migraine, does not appear to be sufficient for producing an irreversible ischemic lesion and, more especially, a persistent vascular obstruction. The roles played by edema of the arterial wall and parietal changes in the vessels are discussed. It could be that thrombosis formation is encouraged by the changes in blood coagulability which may be associated with a migraine attack. The fact that anomalies in platelet aggregation have been demonstrated merits closer study.
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PMID:[Cerebral ischemic accidents during migraine attacks. A report on "complicated migraine"]. 746 14

Two hundred adults who underwent surgery for congenital heart disease at our institution within a four year period were the basis for this report. Clinical data was obtained, i.e. demographic details, past medical history, physical findings, EKGs, echocardiograms, catheterization and angiography material as well as the New York Heart Association (NYHA) class. Intraoperative findings, perioperative management, complications and morbidity and mortality were assessed. After discharge the patients were followed on an outpatient basis. Again the clinical findings, laboratory results and NYHA class were recorded. Age ranged from 16 to 75 years (mean = 38). There were 114 females and 86 males. 178 patients had primary surgical correction, 18 were reoperated after prior correction and 4 underwent palliation. Eighty-three percent of the patients were symptomatic preoperatively. Seventeen percent were diagnosed per chance, for example by a preemployment physical examination, without a prior history of heart disease. The patients were grouped according to related diagnoses (Table 1). Among the 130 patients with left to right shunts, 112 had an atrial septal defect, 7 a ventricular septal defect, 5 a persistent ductus arteriosus, and 6 partial anomalous pulmonary venous return. Atrial flutter or fibrillation occurred in approximately 10% of all patients with atrial septal defects. It was terminated either by rapid overdrive pacing or DC cardioversion. Postoperatively the patients with pulmonary hypertension were monitored invasively with arterial lines and thermodilution catheters. Therapy consisted of alkalization, hyperventilation and sedation. There was only one postoperative death in this patient group due to marked pulmonary hypertension (1/130 = 0.8%). Nineteen adults had obstruction to right or left ventricular outflow. Surgery included valvotomy, infundibulectomy and valve replacement by homograft or mechanical valve. One patient with multiple previous surgeries expired due to bleeding (3%). Thirteen patients had coarctation. All of them were hypertensive, some on medication. Surgery consisted of aortic patchplasty or interposition of a graft. There was no mortality. Perioperative antihypertensive therapy was necessary in most patients and consisted of nifedipin, nitroprussid or propanolol intravenously. Upon follow up 11 patients became normotensive, 8 of these without the need for medication. Fifteen cyanotic patients underwent 11 corrective and 4 shunt procedures (3 with tricuspid atresia, 10 with Tetralogy of Fallot and 2 with complex cyanotic heart disease. Three died due to low cardiac output or dysrhythmias (20%). The survivors improved their clinical status markedly. Seven adults with Ebstein's disease had valve reconstruction and/or ASD closure. Five had recurrent supraventricular tachycardia, 2 paradoxical emboli with neurological symptoms and 4 out of 7 had decreased exercise tolerance. One patient died postoperatively because of dysrhythmias (14%). Sixteen patients had a variety of defects, i.e. status post Rastelli operation and conduit obstruction, status post Tetralogy of Fallot with pulmonary valvar disease, corrected transposition with left AV valve insufficiency, congenital mitral valve disease and double aortic arch, no deaths. The overall operative mortality was 6/200 = 3%. the late mortality was 4/200 = 2%. The morbidity included 7 reoperations due to bleeding. Five patients needed short-term hemodialysis. One patient developed hemiplegia and two patients had permanent decrease of their left ventricular function. The mean length of follow up was 21 months. The clinical status improved from a NYHA class mean of 2.1 +/- 0.9 to 1.2 +/- 0.45 (p < 0.001). In Germany significant numbers of adults with operated and unoperated congenital heart disease do exist. Detection of these patients can be difficult due to inconspicuous murmurs or stable clinical status.
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PMID:[Adults with congenital heart defects--clinical spectrum and surgical management]. 901 42

We report a case of the intra-atrial vegetation removal under cardiopulmonary bypass (CPB) in a case complicated with left middle cerebral artery embolism caused by postoperative infective endocarditis. The patient was a 14-month-old boy. Two months after intracardiac repair for a complex congenital heart disease, he presented with low-grade fever and was placed on oral antibiotics. A month later an echocardiography revealed 2 vegetations on the tricuspid valve. Although the vegetations became smaller with intravenous antibiotics, right hemiplegia was noted 5 weeks later. Brain CT and MR-angiography demonstrated left middle cerebral artery embolism. For fear of another embolism caused by a remaining movable vegetation on the tricuspid valve, intra-atrial vegetation removal under CPB was performed 5 days after cerebral infarction. Intraoperative transesophageal echocardiography was utilized to locate the vegetation and confirm its removal. His postoperative course was uneventful without a recurrence of cerebral infarction or bleeding. He was weaned from the ventilator on postoperative day (POD) 1, started to move the right extremities on POD 5 and was discharged home on POD 66.
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PMID:[Intra-atrial vegetation removal in a 14-month-old boy complicated with postoperative infective endocarditis and left middle cerebral artery embolism]. 1796 24

Cardiac and vascular intervention in thrombocytopenic congenitally cyanotic patients is more dangerous. Thrombocytopenia in these patients is related to immune thrombocytopenia, polycythemia, hyperviscosity, pseudothrombocytopenia, and drugs. Herein we report on a thrombocytopenic 8-year-old girl with tricuspid valve atresia and pulmonary valve stenosis admitted for catheterization. Thrombocytopenia (21,000/mm3) and shunt occlusion was noticed. Thrombocytopenia did not recover after intravenous immunoglobulin (IVIG) and phlebotomy therapies. During preparation for surgery, she suffered cardiopulmonary arrest. A Gore-tex graft was placed in the right pulmonary artery and truncus brachiocephalicus. After surgery, her platelet count spontaneously increased to within the normal range (178,000/mm3 to 250,000/mm3). After resuscitation, she had right-sided hemiplegia sequelae, though there were no hemorrhagic findings on cranial magnetic resonance imaging (MRI) or computed tomography (CT) scans. Two months after surgery, the Blalock-Taussig (BT) shunt blood flow decreased, thrombocyte count dropped, and peripheral cyanosis reappeared. A Fontan operation was performed without hemorrhagic events, and after surgery the thrombocyte count reached 330,000/mm3. We suggest that if a patient with cyanotic heart disease has thrombocytopenia and there is no apparent cause, hypoxia-related thrombocytopenia must be considered. After reoxygenation by shunt or corrective surgeries, thrombocyte count and functions will recover.
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PMID:Shunt operations improved thrombocytopenia in a patient with congenital cyanotic heart disease. 1898 52

Cerebral hyperperfusion syndrome is a rare but well-described complication following carotid endarterectomy or stenting. Clinical signs are ipsilateral, throbbing, unilateral headache with nausea or vomiting, seizures, and neurological deficits, with or without intracerebral abnormalities on CT scan, such as brain edema or intracerebral hemorrhage. Subarachnoidal hemorrhage is rarely described especially if it occurs isolated. We describe a 74-year-old man with a history of high blood pressure, hypercholesterolemia, atrioventricular block with pacemaker, and ischemic cardiopathy with coronary bypass. He underwent right carotid endarterectomy for a 90% NASCET asymptomatic stenosis. Four days after surgery, he complained of unusual headaches with right, throbbing hemicrania. Nine days after surgery, he presented with left hemiplegia and a partial motor seizure. He had fluctuant altered consciousness, left hemiplegia, and left visual and sensory neglect. Brain CT showed right frontal subarachnoidal hemorrhage without parenchymal bleeding. Cerebral angiography found no cerebral aneurysm, no vascular malformation, but a vasospasm of the left middle cerebral artery. Transcranial Doppler confirmed this vasospasm. Evolution was favorable with no recurrence of seizures but with an improvement of the neurological deficits and vasospasm. Physicians should bear in mind this very rare complication of endarterectomy and immediately perform neuroimaging in case of unusual headache following endarterectomy or angioplasty.
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PMID:Isolated Subarachnoidal Hemorrhage following Carotid Endarterectomy. 2067 62

Peripartum cardiomyopathy is a rare cardiac disorder. Although left ventricular apical thrombus formation is common in peripartum cardiomyopathy, biventricular apical thrombi formation is a very rare condition in these patients. A 21-year-old woman presented with complaints of dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and palpitations that appeared three months after labor. Transthoracic echocardiography showed severe global hypokinesis, decreased left and right ventricular ejection fraction (left 30%, right 35%), increased left ventricular end-diastolic dimension (60 mm), grade 2 mitral regurgitation, and biventricular apical thrombi. On the second day of admission, she developed global aphasia and right hemiplegia. The patient was successfully treated with recombinant tissue plasminogen activator. Transthoracic echocardiography following treatment showed disappearance of biventricular apical thrombi. She had no neurologic deficit. Treatment for heart failure was continued due to persistence of global hypokinesis and left ventricular dilatation.
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PMID:[Development of biventricular large apical thrombi and cerebral embolism in a young woman with peripartum cardiomyopathy]. 2198 72

Broad ischemic stroke is mainly due to a cardiac embolus or to an atheromatous plaque. In young subjects, one of the main causes of ischemic stroke (broad ischemic stroke in particolar) is embolic heart disease including infective endocarditis. Infective endocarditis is a contraindication against the anticoagulant therapy (which is indicated for the treatment of embolic heart disease complicated by ischemic stroke). One neurologic complications of infective endocarditis is ischemic stroke which often occurs in multiple sites. We here report the case of a 44-year old man with afebrile acute onset of severe left hemiplegia associated with a sistolic mitral murmur, who had fever in hospital on day 5 with no other obvious source of infection present. Brain CT scan showed full broad ischaemic stroke of the right middle cerebral artery territory and doppler ultrasound, performed after stroke onset, showed infective endocarditis affecting the small mitral valve. He was treated with 4 weeks of antibiotic therapy without anticoagulant therapy ; evolution was marked by the disappearance of mitral valve vegetations and by movement sequelae involving the left side of the body. In practical terms, our problem was the onset of the fever which didn't accompany or pre-exist patient's deficit, leading us to the misdiagnosis of ischemic stroke of cardioembolic origin. This case study underlines the importance of doppler ultrasound, in the diagnosis of all broad ischemic strokes, especially superficial, before starting anticoagulant therapy.
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PMID:[Broad ischemic stroke revealing infective endocarditis in a young patient: about a case]. 2815 23


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