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London, United Kingdom 2013 Poster Session Red Cerebrovasc Dis 2013; 35 (suppl 3)1-854 383 189 Interesting and challenging cases Two false negatives and still… endocarditis S. Varanda1, J. Rocha2, S. Rocha3, M. Ribeiro4, J. Pinho5, A. Gaspar6, A. Machado7, C. Ferreira8 Neurology Department, Hospital de Braga, Braga, PORTUGAL1, Neurology Department, Hos-pital de Braga, Braga, PORTUGAL2, Neurology Department, Hospital de Braga, Braga, PORTU-GAL3, Neuroradiology Department, Hospital de Braga, Braga, PORTUGAL4, Neurology Depart-ment, Hospital de Braga, Braga, PORTUGAL5, Cardiology Department, Hospital de Braga, Braga, PORTUGAL6, Neurology Department, Hospital de Braga, Braga, 7, Neurology Department, Hospi-tal de Braga, Braga, PORTUGAL8 Background: Infective endocarditis caused by Streptococcus agalactiae is unusual. The diagnosis is supported by echocardiogram and blood cultures, although the first may have negative results in up to 10% of the cases, and the second in five to 10%. One of the manifestations may be cerebral in-farction and, as such, it is mandatory to exclude this hypothesis, particularly in young patients. Case Report: A 34 year-old male patient was admitted for acute start of fever, headache and con-fusion. He was feverish, prostrated and disoriented, with no other deficits. The brain CT scan, per-formed at admission, was normal and he presented leucocytosis, elevated C-reactive protein and mild neutrophilic pleocytosis on CSF. The hypothesis of viral meningoencephalitis was put forward, and intravenous therapy with acyclovir was applied. The brain MRI revealed recent multiple isch-emic lesions, suggestive of embolic process. The vascular study, including transesophageal echo-cardiogram, was negative as well as the CSF bacterial and viral analyses and blood cultures. He showed clinical and analytical improvement and was discharged with anti-platelet drug. Two days later, he was re-admitted for aggravation of headache and fever. It was detected a meso-systolic murmur in mitral localization. The MRI showed new lesions with diffusion restriction. The trans-thoracic echocardiogram showed mitral valve vegetation. S. Agalactiae was isolated in all blood cul-tures. Discussion: We describe cerebral infarctions caused by bacterial endocarditis, which diagnosis was impaired by initial negative results in high sensitivity tests. Therefore, when faced with a persistent clinical suspicion of cardioembolic source, in particular of infectious nature, we underline the im-portance of repeating the complementary exams. Furthermore, we emphasize the rarity of isolating S. agalactiae in association with this condition, notably in a patient with no evident predisposing state for such. 190 Interesting and challenging cases Bilateral ptosis post right hemispheric infarction P.W. Ferdinand1, J Acharya2, S Honap3, A Salam4, A.K. Banerjee5 Russells Hall Hospital, Dudley, UNITED KINGDOM1, Russells Hall Hospital, Dudley, UNITED KINGDOM2, Russells Hall Hospital, Dudley, UNITED KINGDOM3, Russells Hall Hospital, Dud-ley, UNITED KINGDOM4, Russells Hall Hospital, Dudley, UNITED KINGDOM5 Background: We present the case of a 73 year old female who was found to have bilateral complete ptosis 48 hours post a large right middle cerebral artery territory stroke, with a reduction in con-scious level 24 hours later. Movement was exhibited on demand in other non-paralysed facial mus-cles, excluding apraxia. Thyroid, anti- acetylcholine receptor and muscle specific kinase antibodies were negative as was an endrophonium test. Resolution of the ptosis followed improvement in con-scious level more than 72 hours later. Methods: We searched PubMed, Medline and Google scholar for ‘ptosis’ and ‘stroke’. Articles in English were reviewed, particularly those relating to pathophysiology and treatment options. Results: Bilateral ptosis following stroke is a rare event, most often seen (but not exclusively) in right cerebral hemispheric strokes. Moreover, small series’ have noted that this may be followed by a reduction in conscious level or a herniation syndrome. This implies that the ptosis is either the re-sult of midbrain compression from resultant cerebral swelling or that eyelid control extends beyond midbrain nuclei and is a non-dominant hemispheric function. Conclusion: Delayed bilateral ptosis following large middle cerebral artery territory infarcts may represent an important clinical sign suggesting impending cerebral herniation and are an indication for rapid re- imaging and assessment for possible neurosurgical intervention to reduce the detri-mental effects of hemispheric swelling. The fact that not all patients with this phenomenon have resultant herniation, may well suggest hemispheric involvement in control of eyelid movement, but should also prompt exclusion of competing diagnosis and subsequent ophthalmological assessment for consideration of surgical correction of this deficit.


Karger_ESC London_2013
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