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ABSTRACT: BACKGROUND: Literature has shown that work maintenance is central in order to guarantee participation to persons with disability. Knowledge about potential sources of difficulties and obstacles is then crucial in order to prevent barriers and facilitate work maintenance and career development for persons with disabilities. OBJECTIVE: Studies analyzing on-the-job barriers among employed people with multiple sclerosis (MS) have found evidence for a role of clinical determinants. The aim of this study was to describe in more detail the role of disability severity and of cognitive indices on work barriers. PARTICIPANTS: Thirty-two employed adults with a diagnosis of MS with mild to moderate disability severity were included in the study. They were involved in the descriptive study while attending their planned care in the MS unit. METHODS: Subjects completed neurocognitive tasks, a self-report measure of executive functioning and a face-to-face semi-structured interview exploring their perception of barriers at work. RESULTS: Regression analyses showed a specific role of disability severity on perception of barriers due to physical, cognitive and interpersonal relationships; while cognitive indices appeared to predict barriers ascribed to company policy (cognitive score), accessibility (planning score) or difficulties in cognitive and task related abilities (self-rated executive functioning). CONCLUSION: These findings underline the relevance of objective tasks and self-report questionnaires direct and indirect multi-dimensional assessment of functioning for early intervention planning. An ecological model of career development in adults with disabilities is also supported.
Work 03/2013; · 0.52 Impact Factor
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F Perini,
E Galloni,
I Bolgan,
G Bader,
R Ruffini,
E Arzenton,
S Alba,
C Azzini,
L Bartolomei,
G Billo, F Bortolon,
P Dudine,
P G Garofalo,
R L'Erario,
M Morra,
P Parisen,
G Stenta,
V Toso
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ABSTRACT: Homocysteine increases in the acute phase of ischaemic stroke and from the acute to the convalescent phase, suggesting that hyper-homocysteinaemia may be a consequence rather than a causal factor. Therefore we measured homocysteine plasma levels in stroke patients in order to investigate possible correlations of homocysteine with stroke severity and clinical outcome. Further we looked for eventual differences in stroke subtypes. We prospectively studied plasma homocysteine levels in acute stroke patients admitted to the stroke unit of our department. Seven hundred and seventy-five ischaemic stroke patients, 39 cerebral haemorrhages and 421 healthy control subjects have been enrolled. Stroke severity and clinical outcome were measured with the Scandinavian Stroke Scale, the Rankin Scale and the Barthel Index. Stroke severity by linear stepwise regression analysis was not an independent determinant of plasma homocysteine levels. Homocysteine was not correlated with outcome measured by the Barthel Index. Mean plasma homocysteine of both ischaemic and haemorrhagic stroke was significantly higher than controls (p<0.05). Homocysteine had an adjusted odds ratios (OR) of 4.2 (95% CI 2.77-6.54) for ischaemic stroke and of 3.69 (95% CI 1.90-7.17) for haemorrhagic stroke. Compared with the lowest quartile, the upper quartile was associated with an adjusted OR of ischaemic stroke due to small artery disease of 17.4 (95% CI 6.8-44.3). Homocysteine in the acute phase of stroke was not associated with stroke severity or outcome. Elevated plasma homocysteine in the acute phase of stroke was associated with both ischaemic and haemorrhagic stroke. Higher levels are associated with higher risk of small artery disease subtype of stroke.
Neurological Sciences 12/2005; 26(5):310-8. · 1.32 Impact Factor
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F. Perini,
E. Galloni,
I. Bolgan,
G. Bader,
R. Ruffini,
E. Arzenton,
S. Alba,
C. Azzini,
L. Bartolomei,
G. Billo, F. Bortolon,
P. Dudine,
P. G. Garofalo,
R. L’Erario,
M. Morra,
P. Parisen,
G. Stenta,
V. Toso
[show abstract]
[hide abstract]
ABSTRACT: Homocysteine increases in the acute phase of ischaemic stroke and from the acute to the convalescent phase, suggesting that
hyper-homocysteinaemia may be a consequence rather than a causal factor. Therefore we measured homocysteine plasma levels
in stroke patients in order to investigate possible correlations of homocysteine with stroke severity and clinical outcome.
Further we looked for eventual differences in stroke subtypes. We prospectively studied plasma homocysteine levels in acute
stroke patients admitted to the stroke unit of our department. Seven hundred and seventy-five ischaemic stroke patients, 39
cerebral haemorrhages and 421 healthy control subjects have been enrolled. Stroke severity and clinical outcome were measured
with the Scandinavian Stroke Scale, the Rankin Scale and the Barthel Index. Stroke severity by linear stepwise regression
analysis was not an independent determinant of plasma homocysteine levels. Homocysteine was not correlated with outcome measured
by the Barthel Index. Mean plasma homocysteine of both ischaemic and haemorrhagic stroke was significantly higher than controls
(p<0.05). Homocysteine had an adjusted odds ratios (OR) of 4.2 (95% CI 2.77–6.54) for ischaemic stroke and of 3.69 (95% CI 1.90–7.17)
for haemorrhagic stroke. Compared with the lowest quartile, the upper quartile was associated with an adjusted OR of ischaemic
stroke due to small artery disease of 17.4 (95% CI 6.8–44.3). Homocysteine in the acute phase of stroke was not associated
with stroke severity or outcome. Elevated plasma homocysteine in the acute phase of stroke was associated with both ischaemic
and haemorrhagic stroke. Higher levels are associated with higher risk of small artery disease subtype of stroke.
Neurological Sciences 11/2005; 26(5):310-318. · 1.32 Impact Factor
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ABSTRACT: In order to study the role of platelets in Multiple Sclerosis (MS) we assessed, in a group of patients during a quiescent phase of the disease, the plasma levels of beta-thromboglobulin (beta-TG) and platelet factor four (PF4) both in absence of treatment and during administration of aspirin (ASA) at the dose of 50 mg/daily. In the MS patients studied, the basal plasma levels of beta-TG and PF4 were significantly higher than in control subjects. The increase in the beta-TG plasma levels occurred independently of the age, sex and severity of the disease, whereas the modification in the PF4 plasma levels was significantly correlated with the severity of the disease. Administration to the patients of ASA, at the dose that does not affect prostacyclin production, determined a decrease of beta-TG in 77% of the patients. Mean PF4 plasma levels remained unchanged. These results suggest that PF4 in the plasma of MS patients may originate not only from the platelets but also from the mast cells following platelet aggregating factor (PAF) stimulation and immunocomplex formation.
Acta Neurologica Scandinavica 09/1987; 76(2):79-85. · 2.47 Impact Factor
