Changes in CSF blood-brain barrier parameters in ischaemic cerebral infarction

Hornig, C. R.; Busse, O.; Dorndorf, W.; Kaps, Manfred

doi:10.1007/bf00313492

Cited by 28 publications

(19 citation statements)

References 8 publications

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“…However, the concentration difference between plasma and extracellular fluid in the brain (Ham berger et al, 1983) is not large enough to cause the observed effects. In addition, permeability changes in the blood-brain barrier do not appear until a few hours after the ischemic insult (Hornig et al, 1983). Therefore, it is likely that the changes in extracel lular amino acids during ischemia result from an unspecific leakage from intracellular compartments.…”

Section: Discussionmentioning

confidence: 99%

Ischemia-Induced Shift of Inhibitory and Excitatory Amino Acids from Intra- to Extracellular Compartments

Hagberg

Lehmann

Sandberg³

et al. 1985

J Cereb Blood Flow Metab

660

246

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Brain ischemia was induced for 10 or 30 min by clamping the common carotid arteries in rabbits whose vertebral arteries had previously been electrocauterized. EEG and tissue content of high energy phosphates were used to verify the ischemic state and to evaluate the degree of postischemic recovery. Extracellular levels and total contents of amino acids were followed in the hippocampus during ischemia and 4 h of recirculation. At the end of a 30-min ischemic period, GABA had increased 250 times, glutamate 160 times, and aspartate and taurine 30 times in the extracellular phase. The levels returned to normal within 30 min of reflow. A delayed increase of extracellular phosphoethanolamine and ethanolamine peaked after 1–2 h of reflow. Ten minutes of ischemia elicited considerably smaller but similar effects. With respect to total amino acids in the hippocampus, glutamate and aspartate decreased to 30–50% of control while GABA appeared unaffected after 4 h of reflow. Alanine, valine, phenylalanine, leucine, and isoleucine increased severalfold. The importance of toxic extracellular levels of excitatory amino acids, as well as of high extracellular levels of inhibitory amino acids, are considered in relation to the pathophysiology of neuronal cell loss during cerebral ischemia.

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Section: Discussionmentioning

confidence: 99%

Ischemia-Induced Shift of Inhibitory and Excitatory Amino Acids from Intra- to Extracellular Compartments

Hagberg

Lehmann

Sandberg³

et al. 1985

J Cereb Blood Flow Metab

660

246

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“…Previous studies have shown that CSF protein, CSF albumin and the AR can serve as an indicator of compromised BBB function in a variety of pathological conditions, among which stroke [25,26,27,28,29]. For this indication, the AR is superior to CSF protein or CSF albumin [25,26,27,28].…”

Section: Discussionmentioning

confidence: 99%

“…Biochemical parameters for the evaluation of BBB function include analysis of serum constituents in the cerebrospinal fluid (CSF) or analysis of biomarkers in blood. Previous studies have shown that the CSF/serum albumin ratio (AR) is a reliable indicator of compromised BBB function in a variety of pathophysiological conditions, among which is stroke [25,26,27,28,29]. MMP-9 expression in peripheral blood and its temporal profile in the subacute phase appear to reflect ischemic BBB injury and are related to stroke outcome [13].…”

Section: Introductionmentioning

confidence: 99%

Biochemical Markers for Blood-Brain Barrier Dysfunction in Acute Ischemic Stroke Correlate with Evolution and Outcome

Brouns¹,

Wauters²,

Surgeloose³

et al. 2010

Eur Neurol

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Background/Aims: We evaluated the cerebrospinal fluid/serum albumin ratio (AR) and kinetics of matrix metalloproteinase-9 (MMP-9) in blood as markers for blood-brain barrier (BBB) disruption after acute ischemic stroke. Methods: The AR was determined in 88 patients with acute ischemic stroke or transient ischemic attack. MMP-9 was measured on admission, 24, 72 h and 7 days after stroke onset. Results: The AR was related to stroke severity, the occurrence of stroke progression and the modified Rankin Scale score at month 3. MMP-9 levels on admission were significantly elevated compared to controls and dropped in the first 72 h after stroke, except in patients with stroke progression and larger infarcts in the subacute phase. Conclusions:We demonstrate that the extent of BBB breakdown in hyperacute stroke relates to initial stroke severity, stroke evolution and long-term outcome. The kinetics of MMP-9 confirm its pivotal role in secondary brain damage after ischemic stroke.

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“…In VD, the presence of infarctual areas or diffuse damage of small arteries (lypohyalinosis) is considered to be the morphological basis for leakage of serum proteins into the cerebrospinal fluid compartment [1,46,82]. Several reports [29,46] have shown restoration of BBB function a few weeks after a stroke episode not evolving into dementia. This finding, confirmed also by other investigators [14,37], together with the high albumin ratio observed in MID subjects, suggests permanent alteration of barrier function, reflecting a diffuse rather than a focal vessel wall disturbance.…”

Section: Blood Brain Barriermentioning

confidence: 99%

Pathogenetic mechanisms in vascular dementia

et al. 1994

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Summary. Vascular dementia accounts for approximately20% of all cases of dementia and for about 50% in subjects over 80 years. Thromboembolism with multiple cerebral infarcts was considered to be almost the only pathogenetic pathway of vascular dementia, with multiinfarct dementia as its clinical manifestation. However, there is a great heterogeneity of vascular dementia syndromes and pathological subtypes, as documented by the number of pathogenetic mechanisms now known to underlie the clinical picture. They include thromboembolism and extracerebral and cerebral factors. Among the extracerebral factors are ischemic hypoxic dementia (i.e., dementia due to hypoperfusion), vasculitis, hyperviscosity and abnormalities of hemostasis. Among the cerebral factors are lipohyalinosis, cerebral amyloid angiopathy, disruption of the blood-brain barrier and altered regulation of cerebral blood flow. Therefore, the approach to vascular dementia should take the heterogeneity into account. In this context, the importance of non-infarct type should be considered; subcortical white matter disorder seems to be a noteworthy common pathway of vascular dementia produced by various vascular mechanisms. Finally, the heterogeneity of the vascular mechanisms involved in vascular d~mentia -namely hypoperfusion -might be a factor that can be positively influenced by targeted therapeutic intervention.

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Changes in CSF blood-brain barrier parameters in ischaemic cerebral infarction

Cited by 28 publications

References 8 publications

Ischemia-Induced Shift of Inhibitory and Excitatory Amino Acids from Intra- to Extracellular Compartments

Ischemia-Induced Shift of Inhibitory and Excitatory Amino Acids from Intra- to Extracellular Compartments

Biochemical Markers for Blood-Brain Barrier Dysfunction in Acute Ischemic Stroke Correlate with Evolution and Outcome

Pathogenetic mechanisms in vascular dementia

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