Correlation between tissue depolarizations and damage in focal ischemic rat brain1Published on the World Wide Web on 12 July 1999.1

Dijkhuizen, Rick M.; Beekwilder, J.P.; Worp, H.Bernardus van der; Sprenkel, Jan Willem Berkelbach van der; Tulleken, K A; Nicolay, Klaas

doi:10.1016/s0006-8993(99)01769-2

Cited by 153 publications

(140 citation statements)

References 33 publications

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“…PIDs have quite similar features compared to artificially elicited CSDs, including cortical DC shifts of around À20 mV, massive disturbances of membrane ion homeostasis, and propagation velocities of typically 3 to 5 mm/min. Expansion of infarct size has been shown to correlate with the number of PIDs (Mies et al, 1993) or with their cumulative duration (Dijkhuizen et al, 1999). In a study combining focal ischemia with CSDs evoked in normal brain outside the penumbra, Busch et al (1996) were able to show directly that acceleration of infarct growth is related to the number of induced events spreading into the penumbra and there believed to take on the characteristics and pathogenicity of PIDs.…”

Section: Malignant Hemispheric Strokementioning

confidence: 99%

Clinical Relevance of Cortical Spreading Depression in Neurological Disorders: Migraine, Malignant Stroke, Subarachnoid and Intracranial Hemorrhage, and Traumatic Brain Injury

Lauritzen

Dreier

Fabricius

et al. 2010

J Cereb Blood Flow Metab

675

582

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Cortical spreading depression (CSD) and depolarization waves are associated with dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells, increased energy metabolism and changes in cerebral blood flow (CBF). There is strong clinical and experimental evidence to suggest that CSD is involved in the mechanism of migraine, stroke, subarachnoid hemorrhage and traumatic brain injury. The implications of these findings are widespread and suggest that intrinsic brain mechanisms have the potential to worsen the outcome of cerebrovascular episodes or brain trauma. The consequences of these intrinsic mechanisms are intimately linked to the composition of the brain extracellular microenvironment and to the level of brain perfusion and in consequence brain energy supply. This paper summarizes the evidence provided by novel invasive techniques, which implicates CSD as a pathophysiological mechanism for this group of acute neurological disorders. The findings have implications for monitoring and treatment of patients with acute brain disorders in the intensive care unit. Drawing on the large body of experimental findings from animal studies of CSD obtained during decades we suggest treatment strategies, which may be used to prevent or attenuate secondary neuronal damage in acutely injured human brain cortex caused by depolarization waves.

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Section: Malignant Hemispheric Strokementioning

confidence: 99%

Clinical Relevance of Cortical Spreading Depression in Neurological Disorders: Migraine, Malignant Stroke, Subarachnoid and Intracranial Hemorrhage, and Traumatic Brain Injury

Lauritzen

Dreier

Fabricius

et al. 2010

J Cereb Blood Flow Metab

675

582

View full text Add to dashboard Cite

show abstract

“…Spreading depression may exacerbate pathological mechanisms by propagating ionic imbalances, and releasing glutamate at increasingly distal cortical locations. Spreading cellular depolarizations can last 1 to 5 minutes and the incidence of spreading depression has previously been correlated with infarct size (Dijkhuizen et al, 1999). Hartings and colleagues (2003) have described two waves of spreading depression after MCA occlusion stroke in the rat.…”

Section: Electrophysiological Changesmentioning

confidence: 99%

Thinning, movement, and volume loss of residual cortical tissue occurs after stroke in the adult rat as identified by histological and magnetic resonance imaging analysis

et al. 2010

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“…Our findings that dramatic recovery occurs more often with faster and complete clot lysis are in agreement with experimental data that a shorter depolarization time after reperfusion leads to a smaller extent of ischemic damage. 13 Also, positron-emission tomography studies in humans suggest that early postischemic tissue hyperperfusion may not be detrimental by itself. 14 The utility of transcranial 2-MHz ultrasound should be considered in future studies of thrombolytic therapies, particularly if a new-generation tPA, a new dose, or experimental external devices to enhance the effect of tPA are subjected to clinical trials.…”

Section: Alexandrov Et Al Duration Of Arterial Recanalizationmentioning

confidence: 99%

Speed of Intracranial Clot Lysis With Intravenous Tissue Plasminogen Activator Therapy

et al. 2001

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Background —Arterial recanalization precedes clinical improvement or may lead to hemorrhage or reperfusion injury. Speed of clot lysis was not previously measured in human stroke. Methods and Results —Transcranial Doppler (TCD) and the National Institutes of Health Stroke Scale (NIHSS) were used to monitor consecutive patients receiving intravenous tissue plasminogen activator (tPA), before tPA bolus and at 24 hours. Patients with complete or partial recanalization of the middle cerebral or basilar artery on TCD were studied. Recanalization was classified a priori as sudden (abrupt appearance of a normal or stenotic low-resistance signal), stepwise (flow improvement over 1 to 29 minutes), or slow (≥30 minutes). Recanalization was documented in 43 tPA-treated patients (age 68±17 years; NIHSS score 16.8±6, median 15 points). tPA bolus was given at a mean of 135±61 minutes after symptom onset. Recanalization began at a median of 17 minutes and was completed at 35 minutes after tPA bolus, with mean duration of recanalization of 23±16 minutes. Recanalization was sudden in 5, stepwise in 23, and slow in 15 patients. Faster recanalization predicted better short-term improvement ( P =0.03). At 24 hours, 80%, 30%, and 13% of patients in these respective recanalization groups had NIHSS scores of 0 to 3. Symptomatic hemorrhage occurred in only 1 patient, who had stepwise recanalization 5.5 hours after stroke onset. Slow or partial recanalization with dampened flow signal was found in 53% of patients with total NIHSS scores >10 points at 24 hours ( P =0.01). Complete recanalization (n=25) occurred faster (median 10 minutes) than partial recanalization (n=18; median 30 minutes; P =0.0001). Conclusions —Rapid arterial recanalization is associated with better short-term improvement, mostly likely because of faster and more complete clot breakup with low resistance of the distal circulatory bed. Slow (≥30 minutes) flow improvement and dampened flow signal are less favorable prognostic signs. These findings may be evaluated to assist with selection of patients for additional pharmacological or interventional treatment.

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Correlation between tissue depolarizations and damage in focal ischemic rat brain1Published on the World Wide Web on 12 July 1999.1

Cited by 153 publications

References 33 publications

Clinical Relevance of Cortical Spreading Depression in Neurological Disorders: Migraine, Malignant Stroke, Subarachnoid and Intracranial Hemorrhage, and Traumatic Brain Injury

Clinical Relevance of Cortical Spreading Depression in Neurological Disorders: Migraine, Malignant Stroke, Subarachnoid and Intracranial Hemorrhage, and Traumatic Brain Injury

Thinning, movement, and volume loss of residual cortical tissue occurs after stroke in the adult rat as identified by histological and magnetic resonance imaging analysis

Speed of Intracranial Clot Lysis With Intravenous Tissue Plasminogen Activator Therapy

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