Læknablaðið : fylgirit - 01.05.2002, Side 30

ABSTRACTS / 33RD SNC & 2ND SCNN
Both groups were comparable with regard to age, sex, degree of
diasbility, time from diagnosis. The EG was expected to train for 60
minutes three times a week for five weeks. The exercises included
warming up for 5 minutes, endurance training for 20 minutes, range
of motion for 25 min and streching/cooling down for 10 minutes.
The CG agreed to lead their normal lives during the five weeks of
the study and not to change their regular exercise pattern.
The degree of disability (EDSS), endurance (max watt/kg and
max V02 ml/kg/min), and balance (TUG) was determined at base-
line and after 5 weeks. Five patients dropped out of the EG (unre-
lated illness (2), lack of modivation (1), IV steriod treatment (1)
and MS relapse (1)). Two individuals in the CG dropped out (MS
relapse (1), unrelated illness (1)).
Results: Six individuals completed the study in the Exercise Group
and ten in the Control Group. The difference in cardirorespiratory
fitness at baseline and at 5 weeks was compared. The change in
maximum energy production (Wmax/kg) was 0.40 for the EG
group and 0,07 for the CG group (T-test; p= 0,04). The change in
maximal 02 uptake (ml/kg/min) was 4,03 for the EG group and
-0,51 for the CG group (T-test; p=0,01). No difference was detec-
ted in degree of disability (EDSS) or balance (TUG) at baseline
compared with 5 weeks later. The training was well tolerated by all.
Conclusion: Our results demonstrate that intentsive physical
exercise for five weeks markedly improves cardiorespiratory fitness
in a goup of individuals with mild MS, compared with a control
group. The participants demonstrated poor fitness at baseline
testing and the improvement observed is likely to signficantly
improve their health and quality of life. The marked improvement
seen after only five weeks of training may indicate that longer
training programs would be even more beneficial.
L38 - Changes in blood pressure, temperature, and blood
glucose within the first hours after stroke onset
Boysen G, Christensen H
Department of Neurology, Bispebjerg Hospital, University of Copenhagen,
Copenhagen 2400 NV, Denmark
Body temperature, arterial blood pressure, and plasma glucose are
almost always measured in acute stroke patients on admission to
hospital. Much has been written about these variables, however, in
most studies the measurements have been done fairly late, that is 12
to 24 hours after stroke onset. In our series patients were admitted
and the variables measured within 6 hours of stroke onset.
We then did serial measurements every two hours the first 24
hours. All patients had their neurological deficit rated on the
Scandinavian Stroke Scale (SSS), and all patients had a CT-scan.
Neurological deterioration was defined as a drop in SSS of 2 points
lasting more than 4 hours within the first 72 hours.
Temperature: The temperature was normal or subnormal in the
very early hours after stroke onset. In severe stroke patients,
defined as having SSS < 25, the temperature started to increase
after 4 to 6 hours. At 8-10 hours after stroke onset increased body
temperature was related to poor outcome at 3 months. In patients
with mild strokes there was no change in temperature. In about 5%
of the patients temperature was > 37.5°C on admission. Outcome in
these patients was not significantly different from that of patients
with normal temperature.
Blood pressure: In patients with mild ischemic stroke or with TIA,
blood pressure declined significantly within the first 6 hours after
admission. In patients with severe strokes the decrease in blood
pressure was much less pronounced. In deteriorating stroke, which
occurred in 20% of patients with ischemic stroke, blood pressure
was slightly higher than in patients without deterioration.
Glucose: In 445 stroke patients without history of diabetes mellitus
we measured blood glucose twice within 12 hours of stroke onset.
An increase in blood glucose was observed in most patients. The
increase was larger in severe stroke. In severe stroke patients blood
glucose increased from a mean of 6.2 mmol/1 to 6.7 mmol/1, p <
0.001. In patients with mild to moderate stroke patients blood
glucose increased from 5.8 mmol/1 to 6.1 mmol/1, p < 0.001. In
patients who died within 7 days (N=38) blood glucose increased
from 6.8 mmol/1 to 7.1 mmol/1, p < 0.001.
Conclusion: Stroke is a dynamic process, giving rise to alterations in
many systemic parameters. The new contributions of this study are
that temperature increases in the early hours after stroke onset in
patients with severe stroke. That blood pressure falls spontaneously
to stable values within 6-8 hours in patients with mild stroke as
contrasted to patients with severe stroke, where the adjustment of
the blood pressure takes several days. The increase in blood glucose
within 12 hours of stroke onset is more pronounced in patients with
severe stroke than in mild stroke. The increase in temperature and
blood glucose may potentially be harmful to the ischemic brain.
L39 - Stroke reduction: Impact of HMG-CoA reductase inhibitor
therapy
Þorgeirsson G
Dept. of Medicine, Landspítali University Hospital Hringbraut, Reykjavík, Iceland
Abstract not received.
L40 - Optimal Therapy for Intracranial Arterial Stenosis:
Antiplatelet agents, Anticoagulation or Angioplasty?
Chimowitz Ml
Professor of Neurology, Emory University, Atlanta, USA
Atherosclerotic stenosis of the major intracranial arteries (carotid
siphon, middle cerebral artery, vertebral artery, basilar artery) is an
important cause of ischemic stroke, especially in Blacks, Asians,
and Hispanics. In the USA, intracranial stenosis causes approxi-
mately 50,000 ischemic strokes annually. Moreover, the risk of
recurrent stroke in these patients is 7%-15% per year.
Despite the importance of intracranial stenosis as a cause of
ischemic stroke, the treatment of this disease remains empirical.
Antiplatelet agents (aspirin, ticlopidine, clopidogrel, aspirin / dipyrid-
amole combination) are frequently used in this setting based on
studies that have shown a benefit of these agents for lowering the risk
of stroke in patients with non-cardioembolic TIA or minor stroke.
However, the efficacy of antiplatelet agents has not been established
in patients with symptomatic intracranial large artery disease.
Warfarin is also frequently used for the treatment of symptomatic
intracranial large artery disease based on retrospective data that
suggests warfarin may be more effective than aspirin in this setting.
Transluminal angioplasty/stenting is another therapeutic option
for the treatment of intracranial stenosis. Early experience sugges-
ted that intracranial angioplasty was associated with an unaccep-
30 Læknablaðið/Fylgirit 43 2002/88