S100b und NSE bei Migränepatienten - Eine Studie über die Durchlässigkeit der Blut-Hirn-Schranke im Migräneanfall
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Abstract
Migraines, in addition to tension headaches, are among the most frequent
primary causes of headaches (Diener, 2006). Even so, the actual causes of this
disease are as yet unknown (Soyka, 1999). Over the years, a number of theories
have been developed on the origins of migraines. As a result, we now assume
that the human migraine aura is induced by Cortical Spreading Depression
(Leão, 1944; Goadsby et al., 2002; Diener, 2006), whereas the headaches are
triggered by a second mechanism – presumably via neurovascular inflammation
(Moskowitz, 1990; Goadsby et al., 2002; Diener, 2006). The results of recent
studies reporting on plasmaextravasation and the formation of oedemas in rats
following artificially induced Cortical Spreading Depression (CSD), suggest a
causal link between the two processes (Gursoy-Ozdemir et al., 2004; Imamura
et al., 2007; Leira et al., 2007).
A breakdown in the blood-brain barrier was determined within the framework
of the inflammation triggered by CSD in rats (Gursoy-Ozdemir et al., 2004). As
early on as 1977, Harper and colleagues suspected this to also be the case in
migraine attacks. They based their theory on parallels between mediators
involved in migraine development and mediators that influence the blood-brain
barrier (Harper et al., 1977). Recent studies appear to confirm this link (e.g.,
Grant et al., 1998; Goadsby, 1997; Imamura et al., 2007; Leira et al., 2007).
There are also several case descriptions that report on CT and MRI changes
during migraine attacks that could subsequently no longer be determined
(Alvarez-Cermeno et al., 1984 and 1986; Jain and Ahuja, 1986; Müller et al.,
1987; Smith et al., 2002; Teepker et al., 2002).
The aims of this study are to find further proof for the opening of the blood-brain-barrier during migraine attacks and to thereby add a further building block to our understanding of the development of migraines. In order to accomplish this, two biochemical markers will be used: the neuron-specific enolase (NSE)and S100b.
Serum samples were taken from 21 migraine patients during migraine attacks,
as well as during intervals when they were free of complaints (a minimum of 48
h after the headache event) and NSE and S100b were determined. These
samples were compared with those of healthy patients. The Wilcoxon Signed
ranks test and the Mann-Whitney U test were used for analysis of the results.
Significantly higher S100b levels were determined in migraine patients both
during attacks as well as during intervals when they were free of complaints.
Furthermore, the S100b levels were significantly higher during the complaintfree
interval than during the migraine attack. The NSE levels were significantly
lower than those of healthy patients used for comparison, but no significant
differences were determined between levels during migraine attacks and the
complaint-free intervals.
These experimental results can be interpreted in different ways. Both
measurements constitute a snapshot in time and may correspond to varying
progression in concentrations. This is of particular importance in the case of
S100b, as different progressions permit different interpretations. In contrast, the data collected on NSE permits conclusive exclusion of the possibility of
neuronal cell damage within the framework of migraine disease.
A total of three progressions in concentrations are possible for S100b:
1. generally increased levels in migraine patients, that are reduced during
migraine attacks, e.g., through consumption or a reduction in production
2. generally increased levels in migraine patients, the serum values for which
only increase after the attack; (and are thereby determined in measurements
made during the complaint-free intervals).
3. no general increase in serum levels in migraine patients, but increases in
levels during migraine attacks that are maintained over a longer period than that
selected for the second measurement.
Different hypotheses can be formulated, depending on the progression in
concentrations:
According to the publications by Kanner, Kapural and Marchi and colleagues,
an increase in S100b serum levels associated with unchanged or reduced NSE
levels is to be regarded as a marker for a defective blood-brain barrier (Kapural et al., 2002; Kanner et al., 2003; Marchi et al., 2003, 2004 and 2007). In turn,this may occur permanently or only temporarily – if all possible progressions in concentrations are considered. Consideration of all studies conducted to date on migraines indicates that a temporary opening of the BBB during migraine attacks, the duration of which outlasts the attack for an indeterminate period, is most likely. Exactly when this occurs, how long it lasts for and whether this constitutes a possible cause or a reaction, or even a pathological mechanism, remains unclear.
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Dates
Created: 2008Issued: 2009-01-12Updated: 2011-08-10
Faculty
Medizin
Publisher
Philipps-Universität Marburg
Language
ger
Data types
DoctoralThesis
Keywords
MigraineS100Cortical spreading depression,NSEBlood-brain-barrierS100bNSES100bS100
DFG-subjects
NeuropeptideBlut-Hirn-SchrankeMigränePathophysiologie
DDC-Numbers
610
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Munk (geborene von Brocke), Karoline: S100b und NSE bei Migränepatienten - Eine Studie über die Durchlässigkeit der Blut-Hirn-Schranke im Migräneanfall. : Philipps-Universität Marburg 2009-01-12. DOI: https://doi.org/10.17192/z2008.0994.
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