Functional improvement after middle cerebral artery ischaemia seems to depend on recanalization of large-vessel occlusion as early as possible. The only approved medical treatment for
acute stroke is early IV
tissue plasminogen activator administration. However, while some patients do not benefit from quick recanalization, others recover despite persistent
middle cerebral artery occlusion. We wondered whether there are different effects of
tissue plasminogen activator treatment on large artery and small artery reopening.
METHODS: We enrolled 55
acute stroke patients who showed persisting
middle cerebral artery occlusion evidenced by transcranial colour-coded duplex ultrasonography in follow-up examination within 48 h postonset of
middle cerebral artery stroke syndromes (mean 30·8 ± 5·4 h after admission). Twenty-two of 55 had been treated with
tissue plasminogen activator and 33/55 had been treated without
tissue plasminogen activator. We compared neurological (National Institutes of Health
Stroke Scale) and functional (modified Rankin Scale) scores at baseline, after seven-days, and then after two-months. Risk factors, previous
stroke prophylaxis, as well as clinical baseline characteristics were analysed to exclude significant differences between both groups.
RESULTS: Despite later admission to hospital (
tissue plasminogen activator patients 1·6 ± 0·66 h vs. non-
tissue plasminogen activator patients 7·4 ± 5·84 h; P < 0·001), there was no significant difference between both groups concerning demographic data, severity of symptoms on admission, risk factors,
stroke prophylaxis, as well as basic laboratory values (international normalized ratio, leucocyte count,
C-reactive protein) blood pressure and body temperature on admission. Irrespective of Doppler findings demonstrating persistent
middle cerebral artery occlusion in all 55 patients, there was a significant neurological and functional improvement in
tissue plasminogen activator patients compared to non-
tissue plasminogen activator patients.
Tissue plasminogen activator patients had a mean improvement on National Institutes of Health
Stroke Scale within the first seven-days of 2·8 points, while non-
tissue plasminogen activator patients deteriorated by 2·2 points (P < 0·001). Concerning modified Rankin Scale
tissue plasminogen activator-treated patients showed a mean improvement within the first seven-days of 0·5 points, while non-
tissue plasminogen activator patients deteriorated by 0·3 points (P = 0·019). A favourable overall short-term
clinical course (i.e. improvement on National Institutes of Health
Stroke Scale >3 points and/or modified Rankin Scale >1 point) was found in 36·4% of
tissue plasminogen activator patients and in 6·1% of non-
tissue plasminogen activator patients (P = 0·0047). At two-months follow-up, patients still showed a median modified Rankin Scale of 4 points after
tissue plasminogen activator treatment and 5 points after non-
tissue plasminogen activator treatment (P = 0·023).
CONCLUSION: