Stroke-in-Evolution: Infarct-Inherent Mechanisms versus Systemic Causes

Abstract

Background: It is uncertain whether deterioration after acute ischemic stroke is neurological and/or systemic (somatic) in origin. Methods: 442 consecutive patients admitted with first-ever ischemic stroke (FIS) were assessed by the Unified Neurological Stroke Scale (UNSS) at admission, on hospitalization days 1, 2 and 3 and before discharge. Results: Among 71/442 (16.1%) patients deteriorated during hospitalization, the worsening from stroke onset was early (≤72 h) in 67 (94.4%) of them. The majority (57/71, 80.3%) had CT-confirmed cerebral causes and 14/71 (19.7%) had systemic causes. The causes of late deterioration were exclusively systemic. In the logistic regression analysis the initial mean UNSS score was the only significant independent predictor of stroke deterioration (p < 0.0001). Conclusions: Early clinical deterioration in FIS patients results from infarct-inherent mechanisms while late stroke deterioration is due primarily to systemic factors. An initially severe neurological deficit might predict further decline.

Steno-Occlusive Arterial Disease and Early Neurological Deterioration in Acute Ischemic Stroke

“…The rate of END in our study was 16.3%, similar to the END rates in previous studies that ranged from 13.9 to 32.2% [1,2,3,4,5,6,7,8,9], which can be explained by the diverse criteria used to evaluate the clinical worsening. Our definition of END was based on an increase in the NIHSS score of ≥4 points in the first 72 h, a restrictive criteria less influenced by subjective observations.…”

“…Neurological worsening in patients with acute ischemic stroke is a serious adverse event without current specific treatment [1,2,3,4]. Previous studies have noted the influence that several biological and clinical factors, such as blood levels of glucose and excitotoxic amino acids, blood pressure, cerebral hemodynamic reserve, and initial neurological severity may have on the development of early neurological deterioration (END) [5,6,7,8,9].…”

Hemorrhage After Thrombolytic Therapy for Stroke

“…The problem of disentangling worsening attributable to cerebral edema, infarct expansion, and other causes of ischemic stroke progression from worsening attributable to hemorrhage is difficult because the variables that independently identify patients destined for NINDS protocol-defined SICH, severe baseline NIHSS and mass effect on pretreatment CT, 21 are also variables that predict symptomatic worsening and poor final outcome even if patients are not treated with tPA. 22,23 Third, even among the subset of patients in whom hemorrhage causes early worsening, many do not have their final outcome altered as a result. On the one hand, many patients who have truly symptomatic early hemorrhages were destined for later worsening from cytotoxic edema, infarct expansion, pneumonia, or other medical complications of stroke anyway, and the occurrence of hemorrhage did not alter their final outcome.…”

The Complications of Cardioembolic Stroke: Lessons from the VISTA Database

“…While not unique to CES, stroke progression warrants special consideration. The etiology of stroke progression is likely multifactorial [12, 13] with brain edema, clot propagation, reocclusion of the parent vessel, recurrent emboli to the same territory and hemodynamic fluctuations accounting for most cases. Further research is indicated to identify additional predictors for stroke progression and test interventions (such as anticoagulation, thrombin inhibitors, platelet IIb/IIa inhibitors) to prevent it.…”