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Background and Purpose-There is no consensus concerning the number of patients developing spasticity or the relationship between spasticity and disabilities after acute stroke. The aim of the present study was to describe the extent to which spasticity occurs and is associated with disabilities (motor impairments and activity limitations). Methods-Ninety-five patients with first-ever stroke were examined initially (mean, 5.4 days) and 3 months after stroke with the Modified Ashworth Scale for spasticity; self-reported muscle stiffness; tendon reflexes; Birgitta Lindmark motor performance; Nine Hole Peg Test for manual dexterity; Rivermead Mobility Index; Get-Up and Go test; and Barthel Index. Results-Of the 95 patients studied, 64 were hemiparetic, 18 were spastic, 6 reported muscle stiffness, and 18 had increased tendon reflexes 3 months after stroke. Patients who were nonspastic (nϭ77) had statistically significantly better motor and activity scores than spastic patients (nϭ18). However, the correlations between muscle tone and disability scores were low, and severe disabilities were seen in almost the same number of nonspastic as spastic patients. Conclusions-Although spasticity seems to contribute to disabilities after stroke, spasticity was present in only 19% of the patients investigated 3 months after stroke. Severe disabilities were seen in almost the same number of nonspastic as spastic patients. These findings indicate that the focus on spasticity in stroke rehabilitation is out of step with its clinical importance. Careful and continual evaluation to establish the cause of the patient's disabilities is essential before a decision is made on the most proper rehabilitation approach.

INTRODUCTION Large elevations of high sensitive Troponin T (hsTnT) in ischemic stroke patients is associated with a poor outcome. In a pilot study we found a high prevalence of malignancies among these patients. Since neutrophil extracellular traps (NETs) have been linked to cancer-associated thrombosis, we hypothesized that the concomitant cerebral and myocardial ischemia could be the result of a NET-induced hypercoagulable state. MATERIALS AND METHODS Clinical assessments, plasma analyses and autopsies with histopathology (in cases of in-hospital mortality) were performed on ischemic stroke patients with high elevations of hsTnT (n=12) and normal hsTnT (n=19). RESULTS Patients with hsTnT elevation had an unexpectedly higher prevalence of cancer (p=0.002), half of which were diagnosed post-mortem. Autopsies of these patients revealed widespread myocardial, cerebral and pulmonary microthrombosis with H3Cit in thrombi. A pro-coagulant state and an increase of the NET specific marker citrullinated histone H3 (H3Cit) was found in plasma of patients with elevated hsTnT compared to patients with normal levels (p<0.001). Plasma analyses in cancer patients showed even higher H3Cit levels (p<0.001), and an increase in granulocyte colony-stimulating factor, known to prime neutrophils towards NETosis. H3Cit correlated positively with thrombin-antithrombin complex (p=0.004) and soluble P-selectin (p<0.001), further linking NETosis to the prothrombotic state. CONCLUSIONS The high prevalence of known or occult cancer in our study suggests that cancer-associated arterial microthrombosis may be underestimated. By linking the thrombosis to NETs, we suggest markers of NETosis that could aid in revealing cancer in arterial microthrombosis as well as arterial microthrombosis in cancer.