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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neurology 240 (1993), S. 251-253 
    ISSN: 1432-1459
    Keywords: Leber's optic neuropathy ; Magnetic resonance imaging ; Parinaud's syndrome ; Oculopalatal myoclonus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Six months after the onset of visual loss a 23-year-old male patient with Leber's optic neuropathy associated with a mitochondrial DNA mutation developed brain stem involvement with Parinaud's syndrome and oculopalatal myoclonus. Magnetic resonance imaging (MRI) revealed a high signal area in the brain stem, corresponding to a hypodense area in the CT scan that did not show contrast enhancement. Distinct diminution but not complete remission of the MRI findings was found in the 5-year follow-up, which was not accompanied by clinical improvement. Although the MRI findings were compatible with a demyelinating lesion, neither extensive evoked potential studies nor spinal fluid examination supported this.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    European archives of psychiatry and clinical neuroscience 241 (1992), S. 267-272 
    ISSN: 1433-8491
    Keywords: Human immunodeficiency virus ; Posture ; Sway path ; Neurophysiological findings ; CSF
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have recorded postural performance in 50 HIV-infected patients in different stages of the disease (Walter Reed (WR) stages I–VI) by means of a force measuring platform. The results were compared with 50 age-matched controls. A significant instability was particularly evident when standing on an unstable foot support. In patients standing with “eyes closed”, postural sway was significantly higher in every patient group (WR I–II:P〈0.02, WR III–V:P〈0.001, WR VI:P〈0.001). Patients in stage WR I–II showed no relevant neurological abnormalities. In agreement with other neurophysiological data in the literature we suggest that postural imbalance could be an early sign of central nervous system penetration of HIV. No correlation with electromyographic or cerebrospinal fluid findings could be found.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Cardiovascular drugs and therapy 8 (1994), S. 437-446 
    ISSN: 1573-7241
    Keywords: endothelium ; endocardium ; heart failure ; nitric oxide ; endothelin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of vascular endothelium, endocardium, and coronary endothelium on vascular tone and myocardial contraction-relaxation sequence in heart failure is discussed. Vascular endothelium affects underlying vascular smooth muscle through paracrine secretion of relaxing and constricting factors. In heart failure, systemic vasoconstriction results not only from neuroendocrine activation, but also from disturbed local endothelial control of vascular tone because of impaired endothelial-dependent vasodilation and because of increased plasma concentration of endothelin. Experimental evidence obtained in isolated cardiac muscle strips established the influence of endocardial endothelium on the duration of myocardial contraction and on the onset of myocardial relaxation. By analogy to vascular endothelium, both diffusible agents that abbreviate (endothelial-derived relaxation factor-like substance) and those that prolong (endocardin) myocardial contraction have been shown to be released from the endocardium. Similar agents are released from the coronary endothelium and, because of the close proximity of capillaries and myocytes, could exert a major effect on myocardial performance. Endothelial dysfunction and concomitant lack of release of myocardial relaxant factors could explain left ventricular relaxation abnormalities observed in the cardiac allograft or in arterial hypertension. Since endothelial-derived relaxation factor or nitric oxide mediates the coronary reactive hyperemic response, a negative inotropic action of nitric oxide could contribute to left ventricular failure when left ventricular wall stress is elevated, as occurs after myocardial infarction in the noninfarcted zone and during left ventricular volume or pressure overload in the absence of adequate hypertrophy.
    Type of Medium: Electronic Resource
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