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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study the effects of septic embolism on the brain, silicone rubber emboli of various types were injected into the carotid arteries of 35 dogs. Pathologic and angiographic studies were performed to assess the resultant arterial and parenchymal lesions. Pure silicone rubber emboli (14 dogs) produced occasional intra-arterial thrombosis but no arteritis. Sterile and bacterially contaminated emboli containing a lead-chromate pigment (similar to those used in previous studies of septic embolism) (11 dogs) and pure silicone rubber emboli with transversely oriented canals (10 dogs), after brief placement in a bacterial suspension, were associated with intense inflammatory arteritis. This was accompanied by focal meningitis, subarachnoid hemorrhage, thrombosis, and cerebritis of the underlying cortex. The findings resembled those found in mycotic aneurysm. Aneurysmal dilatation was observed in one postmortem angiogram. In previous models of mycotic aneurysm, the inflammation attributed to bacterial contamination was probably due to the lead-chromate pigment used.
Stroke
PMID:Cerebral arterial lesions resulting from inflammatory emboli. 10 Sep 7

A patient with bacterial endocarditis had headaches, cerebrospinal fluid pleocytosis and normal cerebral angiograms. Fifteen days later, while on appropriate antibiotic therapy, he developed an intracerebral hematoma due to a mycotic aneurysm. Mycotic aneurysm is an infrequent but serious complication of bacterial endocarditis. An aneurysm should be considered whenever a patient with bacterial endocarditis has neurologic symptoms even when the patient is receiving antibiotics.
Stroke
PMID:Cerebral hemorrhage from a mycotic aneurysm developing during appropriate antibiotic therapy. 58 May 12

In 1 year 6 patients with prosthetic heart valves (PHVs) treated with anticoagulants suffered intracranial hemorrhage. In 4, hemorrhage occurred into the site of a recent non-hemorrhagic infarction. In the others, both of whom had endocarditis, hemorrhages probably occurred as the result of rupture of a mycotic aneurysm. Five patients were treated with warfarin, 1 with heparin. In all patients the level of anticoagulant activity was greater than 1.5 times control. Five patients were in atrial fibrillation; 1 was hypertensive. The diagnosis of intracranial hemorrhage was made and its location and extent accurately determined by computed tomography (CT). Three patients underwent surgery and 2 are alive with only minor neurological deficits. Among the 3 patients who did not undergo surgery 2 died and 1 is alive with a moderate neurological deficit. The management of PHV patients with use of anticoagulants is discussed in terms of the mechanisms involved in intracranial bleeding. Emphasis is placed on prevention of emboli, discontinuation of anticoagulants once non-hemorrhagic infarction has occurred and the primacy of CT scan in diagnosis when hemorrhage is suspected. The special problems of anticoagulation in the presence of endocarditis are also discussed.
Stroke
PMID:Intracranial hemorrhage and infarction in anticoagulated patients with prosthetic heart valves. 62 39

Nine cases have been presented in detail to illustrate some of the varied causes of sudden neurological deficit in childhood: arteriovenous malformation, cryptic hamartoma, berry aneurysm, mycotic aneurysm, intraspinal arteriovenous malformation, brain tumor, migraine, arteritis, and multiple sclerosis. The Boston Children's Hospital experience with aneurysms and intracranial arteriovenous malformation has been summarized. It is noteworthy that a cutaneous hemangioma overlay one cranial and one intraspinal arteriovenous malformation. One small but deep cerebral arteriovenous malformation apparently destroyed itself after its second hemorrhage. Not only have multiple sclerosis and a brain tumor mimicked a vascular lesion, but a series of vascular accidents was misdiagnosed first as multiple sclerosis then as a thalamic tumor. The many possible causes of childhood strokes has been thoroughly cataloged in the Report of the Joint Committee for Stroke Facilities in 1973 (11). Children may be more susceptible to strokes because of congenital abnormalities such as congenital heart disease, hemophilia, and sickle cell anemia, or by diseases which more commonly occur in this age group, such as leukemia. The likelihood of brain abscess in cyanotic congenital heart disease is stressed. Arteriographic studies in our series have been safe; however, there have been reports of probable worsening of symptoms in children with multiple cerebral occlusive lesions in the presence of homocystinuria.
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PMID:Strokes in children. 98 45

Eighteen patients with neurobrucellosis are described. Eleven patients had meningitis alone or with papilledema, optic neuropathy, or radiculopathy. Four patients had meningovascular complications manifested by stroke or intracerebral hemorrhage from a presumed mycotic aneurysm. Two patients had parenchymatous dysfunction, including a child who had a cerebellar syndrome without evidence of direct infection of the central nervous system. One patient presented with polyradiculopathy. Twelve of 16 patients had pleocytosis; none had cell counts greater than 419 x 10(6)/L. Most patients had hypoglycorrhachia and elevated levels of protein in the cerebrospinal fluid (CSF). Results of an agglutination test for Brucella in serum were positive for all patients. Six of 16 patients had positive blood cultures, and four of 14 had positive CSF cultures. Antimicrobial treatment included concurrent administration of two or more of the following drugs: streptomycin, tetracycline (or doxycycline), rifampin, and trimethoprim-sulfamethoxazole. Eleven patients fully recovered. Five patients were left with residual neurological deficits. Four of these patients suffered permanent hearing loss, one of whom also had significant loss of vision in one eye. One elderly senile patient with meningovascular brucellosis remained in a vegetative state despite receiving antimicrobial therapy for 6 months. One patient died due to rupture of a mycotic aneurysm within 7 days of initiation of therapy. One other patient was treated after sustaining an intracerebral hemorrhage, but this patient's condition was diagnosed only after discharge.
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PMID:Neurobrucellosis: clinical and therapeutic features. 142 Jun 70

A 55-year-old man with a mild fever and sweating developed severe headache for the days before admission. Cerebral computed tomography and selected cerebral angiography on the day of admission revealed subarachnoid hemorrhage due to rupture of an aneurysm of a distal branch of the left middle cerebral artery. Detection of vegetation on the aortic valve by two dimensional echocardiography confirmed the diagnosis of infective endocarditis with a ruptured mycotic cerebral aneurysm. Because of rapid growth of the vegetation on the aortic valve and progression of heart failure despite antibiotic therapy, emergency cardiac surgery was performed. To prevent re-rupture of the aneurysm, the aortic valve was replaced with a bioprosthetic valve, and no anticoagulant was administered postoperatively. Repeated cerebral angiography revealed that the aneurysm was becoming progressively smaller during the next 9 months. No cerebrovascular accident occurred postoperatively. We believe that it is safe to treat a ruptured mycotic cerebral aneurysm without involvement of a hematoma mass in the brain conservatively, and that use of a bioprosthetic valve, if valve replacement is mandatory, and avoidance of anticoagulant therapy during the postoperative period are advisable in the treatment of a patient with infective endocarditis and a ruptured cerebral mycotic aneurysm.
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PMID:[Valve replacement in a patient with infective endocarditis and ruptured mycotic cerebral aneurysm]. 156 43

We compared the clinical course of 68 patients with infective endocarditis and mycotic aneurysm and 147 patients with infective endocarditis but no mycotic aneurysm. Among the patients with mycotic aneurysm, 57% had subarachnoid hemorrhage without warning. Forty-three percent had a neurologic prodrome 2 days to 18 months (median 17 days) prior to discovery of the mycotic aneurysm. A focal deficit consistent with embolism was the most common prodrome (23%). However, there was no significant difference in the frequency of neurologic symptoms between patients with and without mycotic aneurysm. During an average follow-up of 40 months, there were no instances of subarachnoid hemorrhage/mycotic aneurysm among 121 patients discharged after a full course of antibiotic therapy. Therefore, the risk of rupture of an unsuspected mycotic aneurysm following a full course of antibiotics is low. When a prodrome does precede a mycotic aneurysm, it most often is a focal deficit consistent with embolism. We favor angiography in all patients with infective endocarditis who experience a focal deficit with good recovery. The timing and other indications for angiography in infective endocarditis are discussed.
Stroke
PMID:Mycotic aneurysm, subarachnoid hemorrhage, and indications for cerebral angiography in infective endocarditis. 368 77

Of 199 patients with clinico-laboratory evidence of vasculitis, 42 were submitted to cerebral angiography; 35 angiograms were abnormal, but only 21 were characteristic of the particular disease process. A pattern consistent with vasculitis diagnosed in 19 angiograms, was due to neoplasm in 4 and neurofibromatosis, DXT and amphetamines each in 1 case. Moya-Moya type collaterals shown in 20 angiograms were due to the idiopathic disease in 10 but due to non-inflammatory pathologies in 7. Fibromuscular dysplasia shown in 28 angiograms was an incidental finding in 20 of these. Of 56 cerebral angiograms for ischaemic stroke in patients under 15 years old, 17 were normal and only 8 vascular lesions were likely to have been of inflammatory origin. In routine clinical practice cerebral angiography, though essential in the management of mycotic aneurysm and in the diagnosis of Moya-Moya disease isolated vasculitis and fibromuscular dysplasia, plays only a limited role in the diagnosis of other types of vasculitis.
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PMID:Cerebral angiography in vasculitis affecting the nervous system. 615 Aug 52

Fifty-seven young stroke patients (aged 45 years and below) admitted to a rehabilitation centre were assessed for underlying risk factor/aetiology and functional outcome after rehabilitation. The mean age was 37.2 +/- 6.3 years and the mean length of stay in the rehabilitation ward 38.3 +/- 19.9 days. There were 37 (64.9%) haemorrhagic and 20 (35.1%) ischaemic strokes. Hypertension was the single most important risk factor accounting for 49.1% of all strokes. Vascular abnormalities (arteriovenous malformation, mycotic aneurysm, vasculitis and Moya-moya disease) and cardiogenic embolism secondary to rheumatic valvular heart disease were also significant causes. There was significant improvement in functional status--activities of daily living (ADL) and mobility--after rehabilitation, the mean Functional Status score improving from 9.76 +/- 2.2 on admission to 5.07 +/- 1.95 on discharge (P < 0.01). Higher ADL and mobility function and upper and lower limb motor power of grade 3 and above on admission, absence of dysphasia, left hemiplegia, age less than 40 years and rehabilitation stay of less than 28 days were associated with better functional outcome whilst sex, nature and site of stroke, and length of stay in the acute ward had no significant bearing.
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PMID:Functional outcome in young strokes. 760 88

During antibiotic therapy, a 56-year-old man with a Streptococcus bovis endocarditis developed an infarction of the right middle cerebral artery (MCA). Thirty hours after stroke onset, cranial computed tomography controls demonstrated a secondary subarachnoid hemorrhage, marked in the cistern of the right MCA. The latent period, cerebrospinal fluid analysis, angiographic and pathologic findings favor the assumption of a pyogenic arterial wall necrosis of the MCA due to a septic embolus. This pathomechanism of intracranial hemorrhage in infective endocarditis should be distinguished from a rupture of a mycotic aneurysm.
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PMID:Subarachnoid hemorrhage due to septic embolic infarction in infective endocarditis. 1020 13


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