Evidence of changes in brain tissue stiffness after ischemic stroke derived from ultrasound-based elastography

Authors: Xu ZS, Lee RJ, Chu SS, Yao A, Paun MK, Murphy SP, Mourad PD.

Objectives Ischemia, edema, elevated intracranial pressure, and reduced blood flow can occur in the brain as a result of ischemic stroke, including contralateral to the stroke via a process known as diaschisis. In this study, ultrasound elastography, an imaging process sensitive to the stiffness of tissue, including its relative fluid content, was used to study changes in the stiffness of individual cerebral hemispheres after transient ischemic injury. Methods Elastographic images of mouse brains were collected 24 and 72 hours after middle cerebral artery occlusion. The shear moduli of both ipsilateral and contralateral brain hemispheres for these mice were measured and compared to corresponding values of control animals. Results At 24 hours (but not 72 hours) after induction of ischemic stroke, there was a significant decrease in the shear modulus in the ipsilateral hemisphere (P < .01) and a significant increase in the shear modulus in the contralateral hemisphere compared to that of control animals (P < .01). Significant differences were also evident between ipsilateral and contralateral shear modulus values at 24 and 72 hours after infarction (P < .01 for both). Conclusions The differences between intrahemispheric averages of shear moduli of the brains of animals with stroke at 24 and 72 hours after stroke induction likely reflect the initial formation of edema and reduction of cerebral blood flow known to develop ipsilateral to ischemic infarction, the known transient increase in intracranial pressure, as well as the known initial reduction of blood flow and subsequent development of edema in the contralateral hemisphere (diaschisis). Thus, elastography offers a possible method to detect subtle changes in brain after ischemic stroke.

Blood pressure lowering in acute phase of stroke: latest evidence and clinical implications

Authors: Patarroyo SX, Anderson C.

Persistent controversy exists as to whether there are worthwhile beneficial effects of early, rapid lowering of elevated blood pressure (BP) in acute stroke. Elevated BP or 'hypertension' (i.e. systolic >140 mmHg) is common in stroke, especially in patients with pre-existing hypertension and large strokes, due to variable 'autonomic stress' and raised intracranial pressure. While positive associations between BP levels and poor outcomes are evident across a range of studies, very low BP levels and large reductions in BP have also been shown to predict death and dependence, more so for ischaemic stroke (IS) than intracerebral haemorrhage (ICH). Accumulating evidence indicates that early BP lowering can reduce haematoma expansion in ICH, but there is uncertainty over whether this translates into improved clinical outcomes, particularly since such an effect was not evident from haemostatic therapy in clinical trials. Guidelines generally recommend control of high systolic BP (>180 mmHg), but recent evidence indicates that even more modest elevation (>140 mmHg) increases risks of cerebral oedema and haemorrhagic transformation following thrombolysis in IS. Thus, any potential benefits of rapid BP lowering in acute stroke, particularly in IS, must be balanced against the potential risks of worsening cerebral ischaemia from altered autoregulation/perfusion. This paper explores current knowledge regarding the management of hypertension in acute stroke and introduces ongoing clinical trials aimed at resolving such a critical issue in the care of patients with acute stroke.

Stroke and Death Due to Spontaneous Intracranial Hypotension

Authors: Schievink WI.

BACKGROUND: Spontaneous intracranial hypotension has become a well-recognized cause of headaches and a wide variety of other manifestations have been reported. Recently, several patients with asymptomatic spontaneous intracranial hypotension were reported. I now report two patients with spontaneous intracranial hypotension who developed multiple arterial strokes associated with death in one patient, illustrating the spectrum of disease severity in spontaneous intracranial hypotension.

Factors associated with early outcome in patients with large-vessel carotid strokes

Authors: Cuadrado-Godia E, Jimena S, Ois A, Rodríguez-Campello A, Giralt-Steinhauer E, Soriano-Tarraga C, Jiménez-Conde J, Martínez-Rodríguez JE, Capellades J, Roquer J.

OBJECTIVE: To describe the severity and early neurological deterioration (END) in patients with symptomatic carotid stenosis and to analyse the influence of related factors.
METHODS: Observational cohort study of patients with ischaemic stroke, ipsilateral carotid stenosis and without evidence of cardiac sources of embolism prospectively recorded since January 2003 to January 2012. Initial severity was categorised as mild (NIH stroke scale (NIHSS) ≤7), moderate (NIHSS 8-14) or high (NIHSS >14). Logistic ordinal and regression analyses were performed for stroke severity and END risk.
RESULTS: Of 2332 ischaemic strokes attended, 338 patients were included. Stroke severity was mild in 254 (75.1%) cases, moderate in 53 (15.7%) and severe in 31 (9.2%). Adjusted ORs (95% CI) for stroke severity were: degree of carotid stenosis, 2.20 (1.55 to 3.11, p<0.001); intracranial disease, 1.93 (1.18 to 3.17, p=0.009); plasma glucose, 1.01 (1.003 to 1.02, p<0.001); and previous transient ischaemic attack (TIA), 0.37 (0.17 to 0.82, p=0.014). 78 patients (23.1%) had END. Multivariate analysis showed independent association between END and degree of carotid stenosis (OR 1.64, 1.14 to 2.34, p=0.007), previous TIA (OR 2.40, 1.25 to 4.57, p=0.008) and mean arterial pressure (OR 1.02, 1.01 to 1.04, p=0.003).
CONCLUSIONS: Strokes due to large vessel disease in the carotid artery are in general of mild severity and have a high rate of END. The degree of stenosis has a clear association with higher severity and END risk.

New approaches to bedside monitoring in stroke

Authors: Cyrous A, O'Neal B, Freeman WD.

Stroke is a common, potentially devastating disease with potential high morbidity and mortality. Recognition at the onset of acute ischemic stroke is pivotal to changing outcomes such as intravenous thrombolysis. Stroke monitoring is a burgeoning field with various methods described and newer devices that aid in detecting acute or worsening ischemia that can lead to improved bedside and intensive care unit management. This article describes various methods of bedside stroke monitoring including newer techniques of intracranial pressure monitoring using the pressure reactivity index and compensatory reserve index to detect changes in autoregulatory states, noninvasive intracranial pressure monitoring, quantitative EEG with alpha-delta ratio, transcranial Doppler, methods of arteriovenous brain oxygen monitoring such as jugular venous oxygen and near-infrared spectroscopy, invasive brain oxygen probes such as Licox™ (brain tissue O(2)), cerebral blood flow probe (CBF Hemedex™) and cerebral microdialysis.

Intracranial Pressure Pulse Waveform Correlates with Aqueductal Cerebrospinal Fluid Stroke Volume

Authors: Hamilton RB, Baldwin K, Fuller J, Vespa P, Hu X, Bergsneider M.

Introduction: This study identifies a novel relationship between cerebrospinal fluid (CSF) stroke volume through the cerebral aqueduct and the characteristic peaks of the intracranial pulse (ICP) waveform. ICP waveform analysis has become much more advanced in recent years; however, clinical practice remains restricted to mean ICP, mainly due to the lack of physiologic understanding of the ICP waveform. Therefore, the present study set out to shed some light on the physiological meaning of ICP morphological metrics derived by the Morphological Clustering and Analysis of Continuous Intracranial Pulse (MOCAIP) algorithm by investigating their relationships with a well-defined physiological variable, i.e., the stroke volume of CSF through the cerebral aqueduct. Methods: Seven patients received both overnight ICP monitoring along with a phase contrast MRI (PC-MRI) of the cerebral aqueduct to quantify aqueductal stroke volume (ASV). Waveform morphological analysis of the ICP signal was performed by the MOCAIP algorithm. Following extraction of morphological metrics from the ICP signal, nine temporal ICP metrics and two amplitude based metrics were compared to the ASV via Spearman's rank correlation. Results: Of the nine temporal metrics correlated with the ASV, only the width of the P2 region (ICP-Wi2) reached significance. Furthermore, both ICP pulse pressure amplitude (waveAmp) and mean ICP (mICP) did not reach significance. Conclusion: In this study we showed the width of the second peak (ICP-Wi2) of an ICP pulse wave is positively related to the volume of CSF movement through the cerebral aqueduct. This finding is an initial step in bridging the gap between ICP waveform morphology research and clinical practice.


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