Angelica Lupato

Universita degli studi di Ferrara, Ferrara, Emilia-Romagna, Italy

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Publications (3)1.32 Total impact

  • Article: A case of asymptomatic pontine myelinolysis.
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    ABSTRACT: Central pontine myelinolysis is an acquired, non-inflammatory demyelinating lesion usually localized in the brainstem pons basis; it usually affects patients with a history of chronic alcoholism, malnutrition or dysionemia. The exact pathogenesis of myelinolysis is still unclear. A 69-year-old Caucasian male presented intensive headache and underwent cranial MRI that showed the typical feature of central pontine myelinolysis. Neurological valuation was negative. Other examinations included extensive blood tests, electroencephalogram and multimodal evoked potentials which all gave normal results. Alcohol abuse and malabsorption syndrome were excluded. The medical history revealed a continuative use of anti-depressive drugs and exposure to glue for years. Our patient may represent one of the rare cases of asymptomatic CPM. The actual reason why he presented this lesion is not clear, but we discuss the possible role in the etiopathogenesis of his chronic use of anti-depressive drugs and the exposure to glue and chemical agents.
    Neurological Sciences 02/2010; 31(3):361-4. · 1.32 Impact Factor
  • Article: Timing of serum soluble HLA-G levels in acute and subacute phases after spontaneous intracerebral hemorrhage.
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    ABSTRACT: Serum levels of sHLA-G (sHLA-G1/HLA-G5) antigens and their soluble isoforms, sHLA-G1 and HLA-G5, were measured by ELISA in 22 patients with spontaneous intracerebral hemorrhage (SICH) at 24 h, 48 h and 7 days after bleeding. The perihematomal edema volume was calculated on non-enhanced computed tomography scans using the formula AxBxC/2 at the same time points. The mean serum concentrations of sHLA-G1/HLA-G5 and sHLA-G1 as well as the perihematomal edema volume changed significantly over time (p < 0.0001, p < 0.001 and p < 0.0001, respectively), whereas no statistical differences were found in serum HLA-G5 concentrations over the course of the experiment. In comparison to the values found at 24 h, sHLA-G1/HLA-G5 and sHLA-G1 increased at 48 h and then decreased at 7 days, whereas the perihematomal edema volume was more elevated at 48 h and, to a lesser extent, at 7 days. A positive correlation was detected between mean serum sHLA-G1/HLA-G5 and sHLA-G1 levels and perihematomal edema volume at 24 h (p < 0.02) and at 48 h (p < 0.01). Our results may indicate a role for sHLA-G in inflammatory mechanisms related to SICH, where these proteins probably act as anti-inflammatory molecules and are predominantly produced as the sHLA-G1 isoform.
    Acta neurochirurgica. Supplement 01/2010; 106:141-5.
  • Article: Timing of serum active MMP-9 and MMP-2 levels in acute and subacute phases after spontaneous intracerebral hemorrhage.
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    ABSTRACT: Serum active matrix metalloproteinase (MMP)-9 and -2 levels and their tissue inhibitors TIMP-1 and -2 were measured in 28 patients with spontaneous intracerebral hemorrhage (SICH) at 24 h, 48 h and 7 days after bleeding. Perihematomal edema volume was calculated on non-enhanced computed tomography scans by using the formula AxBxC/2 at the same time points. Mean levels of serum active MMP-9 and MMP-2, as well as perihematomal edema volume, were significantly different over time (p < 0.0001). In comparison to values observed at 24 h, serum active MMP-9 mean concentrations increased at 48 h and reached their peak at 7 days, serum active MMP-2 mean levels progressively declined at 48 h and at 7 days, whereas perihematomal edema volume increased at 48 h and at 7 days. Perihematomal edema volume was positively correlated with active MMP-9 and MMP-2 at 24 h (p < 0.02 and p < 0.05, respectively) and with active MMP-9 at 48 h (p < 0.05), but was inversely correlated with active MMP-2 at 7 days (p < 0.02). These findings suggest a different involvement of active MMP-9 and MMP-2 in perihematomal-associated inflammatory response occurring in the transition from acute to subacute phases after SICH.
    Acta neurochirurgica. Supplement 01/2010; 106:137-40.