The
patients
were
aged
21-60
years
who
were
76%
women
and
the
rest
=
men,
with
a
mean
age
of
34.8
years
for
women
and
37
years
for
men.
Mean
serum
level
of
Ca2+
was
3.5
mmol/L
and
4.5
mmol/L
in
women
during
the
headache
attacks
and
normal
respectively
and
Mean
serum
level
of
ionized
Ca2+
was
3.7
mmol/L
and
4.3
mmol/L
in
men
during
the
headache
attacks
and
normal
condition
(with
no
headaches)
respectively.
There
was
a
significant
difference
on
serum
Ca2+
level
during
migraine
attacks
decreased
significantly
compared
with
normal
mode
in
women
and
men
(P
values
<0.05).
Figure
1:
Decreasing
ionized
calcium
level
during
migraine
headache
Figure
2:
Mean
serum
ionized
calcium
level
reduced
significantly
during
migraine
headache
in
women
Figure
3:
Mean
serum
ionized
calcium
level
decreased
significantly
during
migraine
headaches
in
men
Migraine
seems
to
have
a
complex
pathogenesis
(2).
Several
theories
have
been
suggested
to
explain
the
mechanism
of
migraine.
A
phosphorylation
oxidative
defect,
malfunction
of
intra
neuronal
voltage
gated
calcium
channels,
intracellular
magnesium
(Mg)
deficiency
or
a
combination
of
these
may
make
the
cells
susceptible
to
spontaneous
depolarization
(17).
Many
patients
with
familial
hemiplegic
migraine
have
a
missense
mutation
in
the
P/Q
calcium
channel,
so
that
this
form
of
migraine,
at
least,
is
associated
with
a
demonstrable
calcium
channelopathy.
In
menstrual
migraine,
ionized
Mg
level
is
decreased
and
the
ratio
of
Ca/Mg
level
is
increased.
Therefore,
serum
Mg
level
may
have
a
role
in
pathogenesis
of
menstrual
migraine
(18).
The
results
of
the
present
study
showed
serum
ionized
calcium
level
decreased
substantially
in
migraine
headaches
compared
to
normal
subjects.
Also
examining
the
ionized
calcium
level
in
men
and
women
separately
showed
that
the
ion
level
in
both
genders
reduced
significantly
in
migraine
headaches
than
normal
subjects.
Findings
may
also
add
to
the
growing
evidence
for
involvement
of
magnesium
in
migraine
pathophysiology
(1).
Other
studies
show
that
Ca2+
and
other
ion
channels
are
important
in
the
mechanism
of
cortical
spreading
depression,
which
is
believed
to
initiate
migraine
attacks
(2).
Thus,
impaired
function
of
cerebral
Ca2+
channels
may
facilitate
the
initiation
of
attacks
(10).
Recent
studies
have
also
concluded
that
abnormalities
in
the
channels
within
the
cells
that
transport
calcium,
magnesium,
sodium
and
potassium
contribute
to
the
onset
of
migraines
(3).
The
calcium
channels
are
known
to
regulate
the
release
of
serotonin.
with
impaired
functioning
of
the
channels,
serotonin
may
not
effectively
be
released
or
may
be
released
in
low
quantities
(2).
As
a
consequence
of
this
dip,
a
range
of
migraine
symptoms
begin
to
occur
(19).
Previous
study
suggests
that
the
abnormality
of
glucose
level,
insulin
resistance,
and
?-cell
function
have
significant
correlation
with
alteration
of
serum
calcium
homeostasis
(20).
As
these
factors
were
not
adjusted
in
our
study,
this
is
a
limitation
for
the
present
study.
Based
on
the
results
obtained
in
the
present
study,
there
was
a
significantly
decreased
serum
ionized
calcium
level
in
patients
during
migraine
attack
in
males
and
females
compared
to
in
normal
subjects
(those
with
no
headaches).
Acknowledgement
Author
thank
the
patients
who
that
participated
in
present
study.
Also,
the
present
study
has
been
supported
by
Deputy
of
research,
Jahrom
University
of
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