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Browsing by Author "MAIA, L."

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  • Clinical phenotypes of Cerebral Amyloid Angiopathy
    Publication . MAIA, L.; MACKENZIE, IR.; FELDMAN, HH.
    J Neurol Sci. 2007 Jun 15;257(1-2):23-30. Epub 2007 Mar 6. Clinical phenotypes of Cerebral Amyloid Angiopathy. Maia LF, Mackenzie IR, Feldman HH. Source Department of Neurology, Hospital Geral Santo António, Porto, Portugal. Abstract The term Cerebral Amyloid Angiopathy (CAA) is used to describe the pathological changes occurring in cerebral blood vessels, both leptomeningeal and cortical that result from the deposition of amyloid proteins. This CNS vasculopathy is associated with a spectrum of clinical phenotypes that include both ischemic and hemorrhagic presentations. Dementia, cognitive impairment and transient neurological symptoms or signs are also being increasingly recognized as part of the CAA clinical spectrum. This review covers the clinical, pathological and neuroimaging aspects of CAA.
    2007-06Journal article Open access Show more
  • Hypersomnia in Whipple disease: case report.
    Publication . MAIA, L.; MARTA, M.; LOPES, V.; ROCHA, N.; LOPES, C.; MARTINS‐DA‐SILVA, A.; MONTEIRO, L.
    Arq Neuropsiquiatr. 2006 Sep;64(3B):865-8. Hypersomnia in Whipple disease: case report. Maia LF, Marta M, Lopes V, Rocha N, Lopes C, Martins-da-Silva A, Monteiro L. SourceDepartment of Neurological Disordes and Senses, Hospital Geral de Santo António, Largo Prof. Abel Salazar, 4099-001 Porto, Portugal. Abstract Whipple disease (WD) is a rare systemic infection caused by Tropheryma whippelii. Neurological involvement has been recognised in 40% of patients, either as initial manifestations or during the course of the disease. We report on a 45 years-old man with WD with initial, persistent and irresistible episodes of daytime somnolence. The patient was HLA-DQB1*0602 positive (genetic marker for narcolepsy). WD diagnosis was suspected on clinical and MRI basis and confirmed by histological and immunohistochemical study of duodenal biopsy. Forty months later all clinical features improved, narcoleptic-like episodes disappeared and cerebral MRI and CSF normalised. Longitudinal neurophysiological studies revealed persistent sleep pattern abnormalities with sleep fragmentation, paucity of slow wave and of REM sleep. The disruption of the hypocretin circuitry in the hypothalamic - diencephalic region triggered by the infection was the probable cause of the hypersomnia and narcopleptic symptoms. WD should be added to the list of causes of secondary hypersomnia.
    2006-09Journal article Open access Show more