Progressing neurological deficit secondary to acute ischemic stroke. A study on predictability, pathogenesis, and prognosis
D. Toni, M. Fiorelli, M. Gentile, S. Bastianello, M. L. Sacchetti, C. Argentino, C. Pozzilli and C. Fieschi
I Chair of Neurology, University La Sapienza, Rome, Italy.
OBJECTIVES: To identify predictors and possible pathogenetic mechanisms of
early neurological deterioration in patients with acute ischemic strokes
and to evaluate their impact on clinical outcome. DESIGN: Case series.
SETTING: University hospital's stroke unit. PATIENTS: A continuous series
of 152 patients with first-ever ischemic hemispheric strokes were
hospitalized within 5 hours of onset, evaluated with the Canadian
Neurological Scale, and underwent a computed tomographic (CT) scan. The
initial subset of 80 patients also underwent angiography. A repeated CT
scan or autopsy was performed within 5 to 9 days of a patient's stroke.
Progressing neurological deficit was defined as a decrease of one point or
more in the global neurological scale score during hospitalization, when
compared with that at entry. RESULTS: The conditions of 39 patients (26%)
deteriorated during the initial 4 days; 20 patients (51%) had an impaired
level of consciousness, and 19 patients (49%) had impaired limb strength
and/or speech. They had been hospitalized earlier and had higher serum
glucose levels at admission; the baseline CT scans of these patients showed
an early focal hypodensity and initial mass effect more frequently. On the
repeated CT scan (144 patients) or at autopsy (eight patients), patients
with a progressing course more frequently had large infarcts, severe mass
effect, and hemorrhagic infarction. We found no differences with regard to
demographic data, medical history, and treatments that were given; only
subcutaneous heparin calcium was more frequently administered to patients
with a progressing course. Twenty-two (27%) of the 80 patients who
underwent angiography had a progressing course, of whom 20 (91%) had an
intracranial and/or extracranial arterial occlusion, with collateral blood
supply in seven patients (35%). Logistic regression analysis showed that
the independent predictors of progression were the serum glucose levels at
admission and the early focal hypodensity with cortical and
corticosubcortical locations, with the positive predictive values of the
latter being 34% (95% confidence interval [CI], 26% to 42%) and 57% (95%
CI, 47% to 67%), respectively. Among patients who underwent angiography,
logistic regression analysis showed a significant correlation between
carotid siphon occlusion and a progressing course. The 30-day case-fatality
ratio and disability (Barthel index, < 60) were higher in patients with
a progressing course (36% and 54% vs 12% and 35%, respectively).
CONCLUSIONS: Early stroke deterioration is still an event that is difficult
to predict; it is largely determined by cerebral edema following an
arterial occlusion, as indicated by an early focal hypodensity and initial
mass effect on the baseline CT scan. Since early deterioration anticipates
a bad outcome in 90% of patients, it might be used as an early surrogate
end point in therapeutic trials.