Hi all its been a while ah, hope your all keeping well. Ive been chatting to an
italian chemist who sent me this research paper, in a nutshell what we eat can
help.

Potentiation of brain serotonin activity may inhibit
seizures, especially in drug-resistant epilepsy q
P. Mainardi *, A. Leonardi, C. Albano
Department of Neurosciences, Ophthalmology and Genetics, University of Genova,
Via de Toni 5,
16132 Genova, Italy
Received 18 June 2007; accepted 18 June 2007
Summary In spite of the large number of antiepileptic drugs (AEDs) actually
available, the problem of drug-resistant
epilepsy has not been solved. No AEDs are efficacious in patients with
pharmacoresitant epilepsy, so new hypothesises
about the mechanisms of pharmacoresistance are needed.
In the last years the ideas on the role of brain serotonin in epilepsy have been
turned upside down: increasing the
available brain serotonin is thought now to have an antiepileptic effect.
Antidepressant drugs like selective serotonin
re-uptake inhibitors, i.e., fluoxetine, have proved to be useful in seizure
control.
Tryptophan (Trp), an essential amino acid, is the only brain precursor of
serotonin, it competes with the other large
neutral amino acids (LNAAs) for the carrier of blood–brain barrier (BBB). Our
own data has shown a lowering of
plasmatic LNAA levels in epileptic patients, on the basis of these results we
could estimate a decrease of a 1/3 in the
Trp brain intake rate in epileptics in respect to controls.
Increasing plasmatic Trp levels increases brain serotonin synthesis. Trp and
5-hydroxytryptophan (5-HTP) were
tested as an add on in epilepsy, but the clinical outcome was controversial.
Free amino acids are not fully adsorbed by
the gastro-intestinal system, furthermore LNAAs, and also 5-HTP is a LNAA,
compete to cross the intestinal membrane
for the same carrier, like for the BBB. The best way to increase the plasmatic
Trp level is a protein rich in Trp and poor
in the other LNAAs. Unfortunately Trp is a limited amino acid in proteins. We
report the clinical results obtained by
adding a whey protein to the antiepileptic therapy of drug-resistant epileptic
patients: alpha-lactoalbumin, rich in Trp
and poor in the other LNAAs.
c 2007 Elsevier Ltd. All rights reserved.
Drug-resistant epileptic patients
The problem of drug-resistant epilepsy has not
been solved with the introduction of newer antiepileptic
drugs (AEDs) over the last 15 years [1]. Physicians
can now choose from over 20 different
medications, including older (`first generation')
drugs such as phenytoin, carbamazepine, phenobarbital,
and valproate, and newer (`second generation')
drugs such as lamotrigine, felbamate,
oxcarbazepine, vigabatrin, tiagabine, topiramate,
gabapentin, pregabalin, zonisamide, and levetiracetam.
However, despite the availability of these
0306-9877/$ - see front matter c 2007 Elsevier Ltd. All rights reserved.
doi:10.1016/j.mehy.2007.06.039
q No grant or funding were involved.
* Corresponding author. Tel.: +39 0103537068; fax: +39
010354180.
E-mail address: pmainardi@... (P. Mainardi).
Medical Hypotheses (2008) 70, 876–879
http://intl.elsevierhealth.com/journals/mehy
Author's personal copy
AEDs, about one third of patients with epilepsy
continue to have seizures under current pharmacotherapies.
On one side the increase in the number of drugs
available to treat epilepsy has made the management
of seizure disorders more complicated [2,3].
While in the 1980s drug selection was facilitated
by decades of clinical experience on a handful of
drugs, currently physicians have to understand the
indications and contraindications for about 20 different
AEDs, and to be familiar with their optimal
titration rates, dosing regimens, potential side effects,
and a wide range of potentially important
drug interactions.
On the other hand, the majority of currently
available AEDs fall into one of three pharmacological
classes, those that modulate neuronal voltagegated
sodium channels (carbamazepine, phenytoin,
lamotrigine, zonisamide and topiramate, even
though some of these drugs have additional actions),
those that modulate inhibitory GABAergic
neurotransmission (benzodiazepines, vigabatrin
and tiagabine) and those that their effects via an
interaction with voltage-operated calcium channels
(ethosuximide, gabapentin, pregabalin and possibly
levetiracetam).
Developing models of pharmacoresistant epilepsy
could be useful for the identification of innovative
AEDs, but, as reported by Lo¨scher [1], these
models cannot be validated because no AED is efficacious
in patients with pharmacoresitant epilepsy:
``to solve this problem, a better hypothesis
of the basic mechanisms of pharmacoresistance
are needed''.
Thus, there is a clear medical need for new AEDs
with novel mechanisms of action to serve as an
alternative or adjunct therapy for the treatment
of refractory epilepsy.
Serotonin and epilepsy
Only after the 1990s has the role of serotonin in
pathogenesis of epilepsy come out. Until the
1990s selective serotonin re-uptake inhibitors
(SSRIs), largely used as antidepressant drugs, were
known as potentially pro-convulsion drugs, then an
increase in brain serotonin availability was thought
to be pro-convulsive and SSRIs were not considered
to be indicated in the treatment of depression in
epileptic patients. There was contrary evidence:
Truscott [4] in 1975 had described an anticonvulsant
effect of fluoxetine (a SSRI) in mice, earlier
work [5] had shown in animal models that 5-
hydroxytryptophan, a serotonin precursor, has an
antiepileptic effect and it was shown that reduction
of brain serotonin concentrations leads to an
increase in seizure susceptibility in animal models
of epilepsy [6,7] as well as in humans [8,9]: in
the 1990s, on the basis of this evidence, SSRIs were
tested as potential anticonvulsants as an add-on to
AEDs in drug-resistant epileptic patients [10,11]
and results suggested that potentation of the serotoninergic
system could be useful in controlling
epileptic seizures [12].
The same drugs have effect both in epilepsy and
depression.
In 2005, Jobe [13] linked epilepsy and depression,
he put forward a theory concerning the presence
in the brain of an exterior defensive shield.
Depression and epilepsy have different intrinsic
pathogenetic mechanisms, but they share common
exterior defensive shields which are made of noradrenergic
and serotoninergic neurons and protect
the brain from a deranged function of intrinsic fabricators.
If the defensive shields are impaired, the
dysfunctional neuronal circuits establish links with
other neurons and the pathology is manifested.
Depending on where the dysfunctional circuitries
are localized, the pathology may manifest as epilepsy
or depression.
According to the above hypothesis, enforcing
the serotoninergic control system could provide
an innovative approach to the control of both seizures
and depression.
Tryptophan and epilepsy
Since brain serotonin is synthesized only from tryptophan
(Trp), an essential amino acid, a decreased
brain influx of Trp is expected to affect brain serotonin
synthesis. The brain supply of Trp depends
upon several factors, including plasma Trp concentration,
its binding to proteins and the plasma concentrations
of the other large neutral amino acids
(LNAAs) tyrosine, valine, methionine, isoleucine,
leucine and phenalanine competing for the same
transport systems across the blood–brain barrier
(BBB) carrier. Therefore, the brain uptake of Trp
depends on the plasma ratio of Trp to the sum of
the other LNAAs.
In agreement with the role of serotonin in epilepsy,
Trp levels have been found to be reduced in
the cerebrospinal fluid and plasma of patients with
seizure disorders [14,15]. Furthermore, on the basis
of our results on LNAA concentrations in the blood
of patients with epilepsy, we evaluate a significant
30% reduction of Trp brain uptake rate in epileptic
patients compared with controls [16]. In agreement
with Jobe's theory, a lower Trp/LNAA ratio has also
been found in depressed patients [17,18].
Potentiation of brain serotonin activity may inhibit seizures, especially in
drug-resistant epilepsy 877
Author's personal copy
A study by PET confirmed that a decrease in
brain uptake of TRP corresponded to a decrease
in brain synthesis of serotonin and in diminished
serotonin control [19]. To potentiate the activity
of the brain serotonin control system, the plasma
Trp LNAAs ratio has to be increased.
Serplus: a food supplement with
alpha-lactoalbumin, a whey protein rich
in tryptophan
Some papers report the results obtained from a
diet rich in Trp or 5-hydroxy-1-tryptophan (5-
HTP), the precursors of serotonin: they were used
to ameliorate depression, to improve the debilitating
symptoms of fibromyalgia, to enhance weight
loss, to lower blood pressure, to prevent headaches,
and to manage insomnia. An antiepileptic
effect of 5-HTP has also been shown in experimental
animals [20].
Nevertheless, free amino acids are not freely absorbed
by the gut. In the gastro-intestinal system
LNAAs compete for the same carrier, as in BBB.
The best way to increase the TRP/LNAAs ratio is a
protein rich in Trp, but poor in other LNAAs. Unfortunately
Trp is the limiting amino acid in most sources
of protein [21]. Most proteins therefore cause a decrease
in plasma Trp–LNAAs ratio, and are therefore
unsuitable for supplementation of Trp.
Alpha-lactoalbumin (ALAC) is a whey protein,
naturally occurring in human milk, with the highest
Trp/LNAAs ratio among all quantitatively relevant,
food-derived proteins. It has been shown that ALAC
can increase the plasma Trp–LNAAs ratio of up to
48% compared to casein [22,23]. Whey protein is
fully adsorbed by the gastro-intestinal system,
mainly as short peptides. While casein proteins
form curds in the stomach, resulting in rapid hydrolysis
and slowing gastric emptying, whey proteins
do not coagulate under acidic conditions [24].
They are considered to be ``fast proteins'', as
they reach the jejunum quickly after ingestion
[25]. After reaching the small intestine, the hydrolysis
of whey is slower than that of casein, allowing
for gradual absorption over the length of the small
intestine. A randomized, single-blind study found
that whey protein produces a higher postprandial
level of plasma amino acids compared to casein
[26]. A study by Troost et al. [27] reported that
after a 50 g dose of orally administered recombinant
human lactoferrin, only 4 lg of lactoferrin
were excreted in a 24-h period and it did not reach
the colon because it was digested in the stomach
and small intestine.
Pilot trial with serotoninergic food
supplement (serplus)
Serplus (Giofarma Srl) is a food supplement containing
0.75 g ultra pure ALAC (Davisco Foods International,
Inc)/tablet. In a pilot study it has been
found to improve seizure control in drug-resistant
epileptic patients.
Fifteen drug-resistant patients, six male and
nine female, in therapy with: two pts: PB, CBZ,
VPA, four pts: PB, CBZ, one pt: PB, VPA, one
pt: PB, VPA, LTG , one pt: PB, CBZ, LTG, two
pts: PB, three pts: CBZ, one pt: VPA since, at
least from 2001. Mean age: 48 ranging from 28
to 67.
Ten patients showing partial complex seizures,
two patients myoclonic, one patient partial complex
with atonic, one patient atonic and one patient
tonic–clonic.
The add-on serplus therapy was of 1.5 g/die in
three daily administrations.
After 2 months an auto-evaluation test was carried
out (0 = no benefit, 10 = full benefit). Furthermore,
an evaluation of clinical outcome was
performed including mood, hunger and sleep
evaluation.
Before serplus treatment six pts showing from 4
to 10 seizures a month, five from 21 to 30, two
from 31 to 100, two over 100, after serplus nine
pts showing from 0 to 5 seizures at month, four
from 21 to 30, two from 31 to 100.
The average percent decrease of the number of
seizures in patients was 60%.
In 13 patients the seizures were milder than
before serplus, one pt ended the drop attach, in
five pts there was an antidepressant effect too,
one pt decreased body weight, one pt improved
sleep.
Thirteen pts showed a percent decrease in the
number of seizures from 50% to 100%.
Furthermore, an antidepressant effect has been
shown in these patients.
The clinical results after a 3 months trial were
presented at the 7th European Congress of Epileptology
[28].
Of course the clinical results have to be confirmed
in other studies on a larger number of patients,
but after one year the patients of this
pilot study persist with the clinical outcome.

Hi all its been a while ah, hope your all keeping well. Ive been chatting to an
italian chemist who sent me this research paper, in a nutshell what we eat can
help.

Potentiation of brain serotonin activity may inhibit
seizures, especially in drug-resistant epilepsy q
P. Mainardi *, A. Leonardi, C. Albano
Department of Neurosciences, Ophthalmology and Genetics, University of Genova,
Via de Toni 5,
16132 Genova, Italy
Received 18 June 2007; accepted 18 June 2007
Summary In spite of the large number of antiepileptic drugs (AEDs) actually
available, the problem of drug-resistant
epilepsy has not been solved. No AEDs are efficacious in patients with
pharmacoresitant epilepsy, so new hypothesises
about the mechanisms of pharmacoresistance are needed.
In the last years the ideas on the role of brain serotonin in epilepsy have been
turned upside down: increasing the
available brain serotonin is thought now to have an antiepileptic effect.
Antidepressant drugs like selective serotonin
re-uptake inhibitors, i.e., fluoxetine, have proved to be useful in seizure
control.
Tryptophan (Trp), an essential amino acid, is the only brain precursor of
serotonin, it competes with the other large
neutral amino acids (LNAAs) for the carrier of blood–brain barrier (BBB). Our
own data has shown a lowering of
plasmatic LNAA levels in epileptic patients, on the basis of these results we
could estimate a decrease of a 1/3 in the
Trp brain intake rate in epileptics in respect to controls.
Increasing plasmatic Trp levels increases brain serotonin synthesis. Trp and
5-hydroxytryptophan (5-HTP) were
tested as an add on in epilepsy, but the clinical outcome was controversial.
Free amino acids are not fully adsorbed by
the gastro-intestinal system, furthermore LNAAs, and also 5-HTP is a LNAA,
compete to cross the intestinal membrane
for the same carrier, like for the BBB. The best way to increase the plasmatic
Trp level is a protein rich in Trp and poor
in the other LNAAs. Unfortunately Trp is a limited amino acid in proteins. We
report the clinical results obtained by
adding a whey protein to the antiepileptic therapy of drug-resistant epileptic
patients: alpha-lactoalbumin, rich in Trp
and poor in the other LNAAs.
c 2007 Elsevier Ltd. All rights reserved.
Drug-resistant epileptic patients
The problem of drug-resistant epilepsy has not
been solved with the introduction of newer antiepileptic
drugs (AEDs) over the last 15 years [1]. Physicians
can now choose from over 20 different
medications, including older (`first generation')
drugs such as phenytoin, carbamazepine, phenobarbital,
and valproate, and newer (`second generation')
drugs such as lamotrigine, felbamate,
oxcarbazepine, vigabatrin, tiagabine, topiramate,
gabapentin, pregabalin, zonisamide, and levetiracetam.
However, despite the availability of these
0306-9877/$ - see front matter c 2007 Elsevier Ltd. All rights reserved.
doi:10.1016/j.mehy.2007.06.039
q No grant or funding were involved.
* Corresponding author. Tel.: +39 0103537068; fax: +39
010354180.
E-mail address: pmainardi@... (P. Mainardi).
Medical Hypotheses (2008) 70, 876–879
http://intl.elsevierhealth.com/journals/mehy
Author's personal copy
AEDs, about one third of patients with epilepsy
continue to have seizures under current pharmacotherapies.
On one side the increase in the number of drugs
available to treat epilepsy has made the management
of seizure disorders more complicated [2,3].
While in the 1980s drug selection was facilitated
by decades of clinical experience on a handful of
drugs, currently physicians have to understand the
indications and contraindications for about 20 different
AEDs, and to be familiar with their optimal
titration rates, dosing regimens, potential side effects,
and a wide range of potentially important
drug interactions.
On the other hand, the majority of currently
available AEDs fall into one of three pharmacological
classes, those that modulate neuronal voltagegated
sodium channels (carbamazepine, phenytoin,
lamotrigine, zonisamide and topiramate, even
though some of these drugs have additional actions),
those that modulate inhibitory GABAergic
neurotransmission (benzodiazepines, vigabatrin
and tiagabine) and those that their effects via an
interaction with voltage-operated calcium channels
(ethosuximide, gabapentin, pregabalin and possibly
levetiracetam).
Developing models of pharmacoresistant epilepsy
could be useful for the identification of innovative
AEDs, but, as reported by Lo¨scher [1], these
models cannot be validated because no AED is efficacious
in patients with pharmacoresitant epilepsy:
``to solve this problem, a better hypothesis
of the basic mechanisms of pharmacoresistance
are needed''.
Thus, there is a clear medical need for new AEDs
with novel mechanisms of action to serve as an
alternative or adjunct therapy for the treatment
of refractory epilepsy.
Serotonin and epilepsy
Only after the 1990s has the role of serotonin in
pathogenesis of epilepsy come out. Until the
1990s selective serotonin re-uptake inhibitors
(SSRIs), largely used as antidepressant drugs, were
known as potentially pro-convulsion drugs, then an
increase in brain serotonin availability was thought
to be pro-convulsive and SSRIs were not considered
to be indicated in the treatment of depression in
epileptic patients. There was contrary evidence:
Truscott [4] in 1975 had described an anticonvulsant
effect of fluoxetine (a SSRI) in mice, earlier
work [5] had shown in animal models that 5-
hydroxytryptophan, a serotonin precursor, has an
antiepileptic effect and it was shown that reduction
of brain serotonin concentrations leads to an
increase in seizure susceptibility in animal models
of epilepsy [6,7] as well as in humans [8,9]: in
the 1990s, on the basis of this evidence, SSRIs were
tested as potential anticonvulsants as an add-on to
AEDs in drug-resistant epileptic patients [10,11]
and results suggested that potentation of the serotoninergic
system could be useful in controlling
epileptic seizures [12].
The same drugs have effect both in epilepsy and
depression.
In 2005, Jobe [13] linked epilepsy and depression,
he put forward a theory concerning the presence
in the brain of an exterior defensive shield.
Depression and epilepsy have different intrinsic
pathogenetic mechanisms, but they share common
exterior defensive shields which are made of noradrenergic
and serotoninergic neurons and protect
the brain from a deranged function of intrinsic fabricators.
If the defensive shields are impaired, the
dysfunctional neuronal circuits establish links with
other neurons and the pathology is manifested.
Depending on where the dysfunctional circuitries
are localized, the pathology may manifest as epilepsy
or depression.
According to the above hypothesis, enforcing
the serotoninergic control system could provide
an innovative approach to the control of both seizures
and depression.
Tryptophan and epilepsy
Since brain serotonin is synthesized only from tryptophan
(Trp), an essential amino acid, a decreased
brain influx of Trp is expected to affect brain serotonin
synthesis. The brain supply of Trp depends
upon several factors, including plasma Trp concentration,
its binding to proteins and the plasma concentrations
of the other large neutral amino acids
(LNAAs) tyrosine, valine, methionine, isoleucine,
leucine and phenalanine competing for the same
transport systems across the blood–brain barrier
(BBB) carrier. Therefore, the brain uptake of Trp
depends on the plasma ratio of Trp to the sum of
the other LNAAs.
In agreement with the role of serotonin in epilepsy,
Trp levels have been found to be reduced in
the cerebrospinal fluid and plasma of patients with
seizure disorders [14,15]. Furthermore, on the basis
of our results on LNAA concentrations in the blood
of patients with epilepsy, we evaluate a significant
30% reduction of Trp brain uptake rate in epileptic
patients compared with controls [16]. In agreement
with Jobe's theory, a lower Trp/LNAA ratio has also
been found in depressed patients [17,18].
Potentiation of brain serotonin activity may inhibit seizures, especially in
drug-resistant epilepsy 877
Author's personal copy
A study by PET confirmed that a decrease in
brain uptake of TRP corresponded to a decrease
in brain synthesis of serotonin and in diminished
serotonin control [19]. To potentiate the activity
of the brain serotonin control system, the plasma
Trp LNAAs ratio has to be increased.
Serplus: a food supplement with
alpha-lactoalbumin, a whey protein rich
in tryptophan
Some papers report the results obtained from a
diet rich in Trp or 5-hydroxy-1-tryptophan (5-
HTP), the precursors of serotonin: they were used
to ameliorate depression, to improve the debilitating
symptoms of fibromyalgia, to enhance weight
loss, to lower blood pressure, to prevent headaches,
and to manage insomnia. An antiepileptic
effect of 5-HTP has also been shown in experimental
animals [20].
Nevertheless, free amino acids are not freely absorbed
by the gut. In the gastro-intestinal system
LNAAs compete for the same carrier, as in BBB.
The best way to increase the TRP/LNAAs ratio is a
protein rich in Trp, but poor in other LNAAs. Unfortunately
Trp is the limiting amino acid in most sources
of protein [21]. Most proteins therefore cause a decrease
in plasma Trp–LNAAs ratio, and are therefore
unsuitable for supplementation of Trp.
Alpha-lactoalbumin (ALAC) is a whey protein,
naturally occurring in human milk, with the highest
Trp/LNAAs ratio among all quantitatively relevant,
food-derived proteins. It has been shown that ALAC
can increase the plasma Trp–LNAAs ratio of up to
48% compared to casein [22,23]. Whey protein is
fully adsorbed by the gastro-intestinal system,
mainly as short peptides. While casein proteins
form curds in the stomach, resulting in rapid hydrolysis
and slowing gastric emptying, whey proteins
do not coagulate under acidic conditions [24].
They are considered to be ``fast proteins'', as
they reach the jejunum quickly after ingestion
[25]. After reaching the small intestine, the hydrolysis
of whey is slower than that of casein, allowing
for gradual absorption over the length of the small
intestine. A randomized, single-blind study found
that whey protein produces a higher postprandial
level of plasma amino acids compared to casein
[26]. A study by Troost et al. [27] reported that
after a 50 g dose of orally administered recombinant
human lactoferrin, only 4 lg of lactoferrin
were excreted in a 24-h period and it did not reach
the colon because it was digested in the stomach
and small intestine.
Pilot trial with serotoninergic food
supplement (serplus)
Serplus (Giofarma Srl) is a food supplement containing
0.75 g ultra pure ALAC (Davisco Foods International,
Inc)/tablet. In a pilot study it has been
found to improve seizure control in drug-resistant
epileptic patients.
Fifteen drug-resistant patients, six male and
nine female, in therapy with: two pts: PB, CBZ,
VPA, four pts: PB, CBZ, one pt: PB, VPA, one
pt: PB, VPA, LTG , one pt: PB, CBZ, LTG, two
pts: PB, three pts: CBZ, one pt: VPA since, at
least from 2001. Mean age: 48 ranging from 28
to 67.
Ten patients showing partial complex seizures,
two patients myoclonic, one patient partial complex
with atonic, one patient atonic and one patient
tonic–clonic.
The add-on serplus therapy was of 1.5 g/die in
three daily administrations.
After 2 months an auto-evaluation test was carried
out (0 = no benefit, 10 = full benefit). Furthermore,
an evaluation of clinical outcome was
performed including mood, hunger and sleep
evaluation.
Before serplus treatment six pts showing from 4
to 10 seizures a month, five from 21 to 30, two
from 31 to 100, two over 100, after serplus nine
pts showing from 0 to 5 seizures at month, four
from 21 to 30, two from 31 to 100.
The average percent decrease of the number of
seizures in patients was 60%.
In 13 patients the seizures were milder than
before serplus, one pt ended the drop attach, in
five pts there was an antidepressant effect too,
one pt decreased body weight, one pt improved
sleep.
Thirteen pts showed a percent decrease in the
number of seizures from 50% to 100%.
Furthermore, an antidepressant effect has been
shown in these patients.
The clinical results after a 3 months trial were
presented at the 7th European Congress of Epileptology
[28].
Of course the clinical results have to be confirmed
in other studies on a larger number of patients,
but after one year the patients of this
pilot study persist with the clinical outcome.

Epilepsy
So Who, What is Normal
Speaking as an epileptic to all people with or living with epileptics normal is
considered what is socially
and culturally acceptable but, social and cultural will change normal thus
altering the concerns of
cognitive social psychology. !STRANGE AH if you were born with epilepsy you are
'normal' you just have
fits, simple enough ah but, if you have had a bad hit to the head you probably
will end up having
epilepsy because of brain trauma. It is from this that (from experience and a
degree course in
psychology I speak) I can say, epilepsy is not your (there) problem it is
cognition. Because of the brain
damage the cognition (thinking processing response time) causes you/them to
appear to be not 'normal'
thus although they/you may physically be appealable a patronization comes in
between them/you and
the 'partner' and 'we' become unlovable as people. We are viewed as ohh or ahh
or poor thing not come
here i want you now? This dilemma can be further complicated if you end up on
sticks/wheelchairs.
Phenomenological psychology at face value can be a most beneficial for
understanding and/or revealing
an individuals "self" through its uninterrupted methodology through the use of
Free Association
Narrative Interviewing (FANI) to establish a subjects "self". This is where
there is a difference basically it
is all about and quite simply means, 'talk to them/us, give them/us time to
process what has been said
and to think of a reply. You will be very surprised at how clever people
actually are and--how
sexy/lovable. WHAT? Simple really, as Socrates once implied 'why should society
follow each other like
sheep. We all have an opinion and a brain to process our thoughts. Why then
should we accept
'normal/fashionable' simply because the majority says it is. Equally, Normal is
based on a majority rule
so who is right and even if normal (majority of) has an opinion why cant we
challenge it and say 'your
wrong?. I have a different life style to you. Am i wrong or are you, should the
answer be based on a
survey of 'majority rule (what's normal) or should we accept that we are both
right and then look for a
common ground that we can both agree to be normal. Why should we be alienated
because we need
sticks/wheelchairs and have fits.

Learning how to cope with epilepsy
Self consciousness, it has long been considered that this is innate it would
follow therefore that
attitudes accompany our innate self consciousness due to our automated behavior
to a situation. For
example, at maturity we look to the opposite gender! Generally speaking this
drive is both innate and an
attitude based upon the implementation of monogamous grooming from parents,
media and society.
Religion with its implications that "self' is our soul is questionable based on
our religious in doctoring
and the society we live in yet can also be used to create attitudes.
`What's this to do with epilepsy'?
In modernistic terms it is argued that self consciousness, attitudes and our
innate self is dualistic, that is
to say they are one of the same. It is as important though to accept that due to
an attitude (triggers for
seizures) we all have behavioral responses, some good some bad and these can
lead us to have an
emotional deficit. To fit into our society we have to learn how to behave,
"alter your attitude"! In doing
this it can take people out of there comfort zones leaving them uncomfortable,
nervous or even
vulnerable and more prone to fits.
Attitudes and self consciousness are innate/ media and society based constraints
that are imposed upon
individuals as they grow and develop from child hood through adolescence into
adulthood where, the
link's and chains of opinions are enforced upon the next generation. This is why
it is vital that we and
our nearest and dearest understand and give us a wide birth.
A prime example of this can be seen in the modem child of today, there are few
who are aware of the
constraints of familiarity and or respect to there elders. This "mind set" is a
complete change from thirty
years ago clearly indicating that "attitudes" towards teaching respect (to
create an attitude) has
changed. It is apparent that, in this instance child rearing is not innate, it
has to be taught but, when a
child is in danger it is a self conscious innate response to protect it. So, it
is that same attitude that we all
need to adopt to ease the pressures on both the epileptic and the
family/friends.
I introduced this article by referring to attitudes/ triggers and how they
accompany our innate self
consciousness due to our automated behavior to a situation. Hence, the starting
point for this topical
research is as old as researchable recorded history, from the mass attitudinal
hysteria towards the Jews
before the Second World War to the good will drive to save the planet. These are
all attitudes which
when reaching a point of hysteria can affect self consciousness and can become
an inherent attribute
for the innate self "US" AND OUR SELF CONFIDANCE, (I wont go out just in
case---).
The concept of Social psychology of self could be summed up by Solomon Asch
(1956) where his studies
into "normal" (what is socially and culturally acceptable) groups, there social
influence and places they
are at will result in being a type of conformity. This however is a resulting
opinion of a minority (us!) not
a majority and therefore over looks the individual. It is this attitude that
affects self consciousness and is
the frustrating difficulty, helping people to help us help ourselves?
As "We" the human race come from many differences cultures a starting point for
this researchable
history into attitudes and self consciousness is through the eyes of religion-
self-soul and the inherent
parental/ cultural dis/approval of behavior. Is society to be held accountable
for these behavioral
attitudes or society for en doctoring the youth. Either way both are based on a
common ground/need,
that being cohesion based upon a fear factor. Contrary to this social influence
on behavior and to re
enforce the point raised earlier With regards to the frustrating difficulty in
researching social psychology
of self we have a strange species called the individual/non conformist. (An
example of such was
reviewed by us in the mirror) In a drive to research self and attitude
"Unfolding discourse analysis" in
post modernism has been researched by (McGuire, 1985, p. 239) raising the
concept that "attitudes are
locating objects of thought on dimensions of judgment and placing it in a
hierarchy (phenomenological
narratives). Equally Potter and Wetherell in there research are more interested
in how people talk
(cognitive processes). This turn to language research though is seen as a model
of contained, rational
and stable individual processes. For now, in short phenomenological narratives
are pictorial
descriptions, used as a method to converse with 'society', this method is used
unconsciously due to
hemispheric damage (a side of the brain). For epileptics who acquired this
disadvantage the cognitive
processes such as memory recall are not as reliable so `we' make use of
pictorial. This is partially why
'we' are all different, that and the fact that the pills we have to take change
our personality. Cognitive
and behavioral disorders often overshadow seizures and can be the greatest cause
of impaired quality of
life. People with epilepsy may have cognitive impairments, which effect
attention, memory, mental
speed, and language, as well as executive and social functions. Furthermore,
these problems often go
unrecognized and, even when identified, are often under treated or untreated. In
this section you can
see in greater detail the cognitive and behavioral disorders associated with
epilepsy. The information is
divided into two sections:
  Mood and Behavior ; gives a basic overview of mood and behavioral disorders
associated with
epilepsy. Advanced Mood & Behavior, provides a more in depth, intermediate level
of information
regarding mood & behavior disorders associated with epilepsy.
Mood and Behavior
Epilepsy and its treatment affect the way that some people with this disorder
think and behave. While a
seizure is happening, it interferes with thinking. If seizures happen over and
over again (as they
sometimes do), they can have a lasting effect on many of the brain's functions,
from memory and
language to planning and reasoning. It's possible that epilepsy may change how
you relate to others,
your mood, even your personality. But most people with epilepsy find that it has
the effect on their
behavior.
Do any of these sound like you?
"I just don't trust my short-term memory. "
"I knew the word I wanted to say, but I couldn't get it out. Or I'd say another
word that wasn't quite
right. "
"I am more irritable now; everything is an effort."
"I'd finish watching a show, and somebody would ask me what it was about, and I
couldn't answer
them. I didn't know, and I just watched it!"
Not only can seizures and epilepsy affect how you react to the world, but they
also can affect how the
world reacts to you. Many people don't know what to do when they see a seizure.
Some can't
understand that a person who looks pretty normal may not understand a single
word being said. The
workplace can bring new challenges, and some people with epilepsy have to find
other jobs because of
their seizures.
Advanced Mood and Behavior
Neurobehavioral disorders including fatigue, depression, anxiety, and psychosis
commonly affect
patients with epilepsy. In addition to neurobehavioral disorders, patients with
epilepsy may present
with cognitive impairments, which effect attention, memory, mental speed, and
language, as well as
executive and social functions. Cognitive and behavioral disorders often
overshadow the seizures
themselves and can be the greatest cause of impaired quality of life.
Furthermore, these problems often
go unrecognized and, even when identified, are often under treated or untreated.
Patients with epilepsy
frequently suffer from cognitive and behavioral disorders that range from subtle
to severe. Behavior
changes occur during and immediately after most seizures. However, in some
cases, cognition and
behavior also change for prolonged periods after individual seizures or
throughout the long interacted
gaps. Aggressive control of seizures, and possibly reduction of interacted
epilepsy activity's may help
prevent interacted cognitive and behavioral disorders. The late 19th century
view of epilepsy as a
progressive disorder-in terms of both seizures and cognitive-behavioral
disorders-is finding support from
modern studies (1). While the best therapy for cognitive and behavioral
disorders may be prevention,
there is little systematic study of the phenomenon either retrospectively or
prospectively .
A less pleasant but equally as informative fact with epilepsy is;
Epilepsy has long been recognized and invoked as a significant ingredient in the
mechanism of sudden
unexpected death, particularly in the setting of status seizures, trauma,
drowning's and aspiration of
gastric content However, a wider appreciation that epilepsy per se may be a
major cause of, rather than
contributory factor to death, is a relatively recent concept which may not be
widely comprehended or
accepted by the community at large, epileptic patients and their physicians, and
perhaps some
pathologists. Since these cases present as sudden, unexpected and often
unexplained death, they will
fall under the jurisdiction of the coroner, and in most circumstances require
specialist forensic
pathological investigation.
Like that other acronym SIDS (sudden infant death syndrome), the term SUDEP
(sudden unexpected
death-) hints at a relatively stereotypical series of circumstances allied to an
unascertained cause of
death; but unlike SIDS (or perhaps the more controversial SADS (sudden adult
death syndrome)), the
field of potential causative mechanisms appears narrower and is arguably better
delineated, holding the
promise of effective intervention strategies.
Much research over the past few years has pointed to complex cerebral and cardio
respiratory factors,
which individually or in concert may result in death during or shortly after a
seizure. If the task of
clinicians is to predict and intervene, the role of the forensic pathologist and
coroner might best be seen
as recognition and comprehensive investigation so that the true incidence (at
various points in time) is
documented, and effective multidisciplinary remedies implemented. A vital first
step along this path is
uniformity of approach, but many factors need to be addressed before this
pathological nirvana is
attained, some of which may be subject to considerable regional and situational
constraints.
This last section of course is by no means a Chrystal ball view of our future
just an awareness of possible
events which, we and our attitudes can alter (a bit like should we stop
smoking?).

To close the article on a positive note;
Society in general is not an alien species as they may appear? The main driving
force of there `attitudes'
towards epileptics is (believe it or not, fear and ignorance) the `not knowing
what to do or how to
behave. `IF' like most things in life people are given the tools to deal with a
given situation then `normal'
for one would be the same for the other thus all would be treated the same.
Sadly though we don't live
in Utopia where equality and normal are –well-normal everyday situations so, is
it not down to each of
us to pass on the tools, I hope in some small way I have at least given you the
reader a `starter kit'. Just
remember that `we' the chosen few, the selected above others, the elite of
society have the
edge over them, we know what its like and can rise above them and there
attitudes. How,
simple because we have the knowledge there frightened of so stand proud??