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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinicopathological correlations are reported in a case with bilateral isolated infarcts in the posterior part of the parietal lobes, due to nonbacterial thrombotic endocarditis accompanying pancreatic adenocarcinoma. The initial left-sided infarct induced right visual neglect, impairment of right-beating optokinetic nystagmus (OKN), optic ataxia, Gerstmann's syndrome and apraxia. After the right-sided infarct, which occurred six weeks later, bilateral visuo-oculomotor disturbances were observed, including peripheral visual inattention, disorder of visually guided saccades, severe impairment of foveal smooth pursuit and OKN slow phase. The lesion on the left involved the upper part of the angular gyrus and a part of the adjacent superior parietal lobule (SPL). That on the right involved the supramarginal gyrus and extended posteriorly into the superoanterior extremity of the angular gyrus, into both margins of the adjacent intraparietal sulcus and into a small part of the SPL. As the oculomotor deficits and the peripheral visual inattention were bilateral after the second infarct, they probably resulted from the lesion of homologous areas in both cerebral hemispheres. The zone damaged in common included a small part of the SPL, the superoanterior extremity of the angular gyrus, and the adjacent intraparietal sulcus and a small portion of the subcortical white matter. This restricted cerebral zone could therefore, in man, be implicated both in the control of all visually guided eye movements and in visual attention. It is further suggested that two corticofugal pathways are implicated in visually guided saccades, the first arising from the frontal eye fields and projecting directly onto the premotor structures in the brainstem, the second arising from the posterior parietal cortex (probably mainly the intraparietal sulcus adjacent to the angular gyrus) and including a relay in the superior colliculus before reaching the premotor structures. Lastly, the findings support the hypothesis that optic ataxia results from interruption of direct and/or crossed occipitofrontal pathways coursing in the deep white matter of the parietal lobe.
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PMID:Infarcts of both inferior parietal lobules with impairment of visually guided eye movements, peripheral visual inattention and optic ataxia. 394 58

A 10-year-old male was referred with difficulties at school. He had particular difficulty with reading long words, following the sequence of text down a page, writing words in the correct order, writing words in line, and copying from the blackboard. He had a history of infective endocarditis complicated by intracerebral haemorrhage at the age of three years. Detailed history taking revealed symptoms typical of 'dorsal stream' pathology, namely a deficit of 'vision for action'. This included a spatial disorder of attention (simultanagnosia), defective hand and foot movements under visual control (optic ataxia), and acquired oculomotor apraxia which are consistent with Balint's syndrome. Strategies were suggested for coping with the symptoms and one year later a distinct improvement in adapting to the disability was found.
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PMID:Balint's syndrome in a 10-year-old male. 1272 50

A 74-year-old man presented with sudden onset of aphasia and apraxia. Magnetic resonance image (MRI) of the brain disclosed a left frontal hemorrhage. The concomitant low grade fever suggestive of infection was unresponsive to cefazolin 1 g q12h, and refractory to piperacillin (PIPC) 2 g q8h. Blood culture grew enterococci, establishing together with echocardiography the diagnosis of infective endocarditis. The angiography revealed cerebral hemorrhage to have resulted from the rupture of the infected intracranial aneurysm. The antimicrobial therapy was switched to ampicillin (ABPC) 2 g q4h plus gentamicin (GM) 60 mg q8h. The positive blood culture was subsequently identified Enterococcus faecium to which the minimum inhibitory concentration (MIC) of PIPC, and ABPC was 16 mcg/mL, and 4 mcg/mL, respectively. The peak concentration of serum ABPC was 83.1, median 50.8, and trough 25.8 mcg/mL. Thus, the percent time > MIC for ABPC was 100%, and the time > minimum bactericidal concentration (MBC) as well. On the other hand, time > MIC for PIPC, was found nearly 30% in retrospective analysis using population pharmacokinetics. The neurological deficit of the patient was completely restored to the normal status after 4-weeks' antimicrobial therapy with ABPC plus GM, then he underwent cardiac surgery for valvular replacement, where microbiological culture of the resected valve was negative. The constellation of the clinical, pharmacological and microbiological outcome in our case provides scientific evidence that the antibiotic therapy given to our case is the best available strategy as an antimicrobial treatment of severe enterococcal endocarditis complicated by disseminated lesion as infected intracranial aneurysm.
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PMID:Enterococcal endocarditis complicated with ruptured infected-intracranial aneurysm: with pharmacokinetic-pharmacodynamic documentation in proof of the successful antimicrobial treatment. 2515 21