psychology or neurology anyone?

dirtydingusus · Aug 5, 2010

you get board or have the time.....let me know what you think about this? just cus i could use some "outsiders" opinions.....thanks!

Complex Partial Seizures Present Diagnostic Challenge - Psychiatric Times

TLE also may be responsible for chronic rather than just acute psychoses. While any of the symptoms of schizophrenia may be encountered, paranoid traits are the most common. TLE patients can be distinguished from schizophrenic patients by the maintenance, when not acutely ill, of warm affect and good rapport. In addition to the history, the diagnosis of complex partial seizure disorder can be aided by EEG. However, since such diagnosis remains a clinical one, it should be noted that several negative EEGs do not rule out the diagnosis of TLE in a given patient.

The treatment of TLE is complicated by the fact that many times improved seizure control via anticonvulsants leads to deterioration of the neuropsychiatric status. Schizophrenia-like epileptic psychoses often emerge when anticonvulsants are normalizing or improving the seizure activity. If this antithesis isn't recognized, the psychosis will soon become more of a problem than the seizures. One expert, Dietrich Blumer, M.D., has gone so far as to claim: "It is probable that the modern schizophrenia-like epileptic psychoses are largely iatrogenic in nature, caused by modern ability to control seizures."

Brenjin · Aug 5, 2010

Interesting

dirtydingusus · Aug 5, 2010

Brenjin said:

Interesting
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you should see it from this side.....

tharedhead · Aug 5, 2010

You may find this interesting
Schizophrenia-like Psychoses of Epilepsy and Disturbances of Folate and Vitamin B12 Metabolism Induced by Anticonvulsant Drugs -- REYNOLDS 113 (501): 911 -- The British Journal of Psychiatry
Plasma folate and homocysteine levels may be relat... [J Clin Psychopharmacol. 2005] - PubMed result

Genetic and clinical data suggest that folate and homocysteine may play a role in the pathogenesis of psychiatric disorders. The total plasma homocysteine level is a sensitive measure of a functional folate deficiency. We thus investigated whether a functional folate deficiency and/or elevated levels of plasma homocysteine may be related to interictal "schizophrenia-like" psychosis (interictal psychosis ) of epilepsy. We studied the plasma folate, vitamin B12, and homocysteine levels of 32 age- and sex-matched epileptic patients with or without interictal psychosis. Each group included 25 localization-related epilepsies and 7 generalized epilepsies. The epileptic patients with interictal psychosis had significantly lower folate levels and higher homocysteine levels than those without interictal psychosis. There were no significant differences in the vitamin B12 levels between the two groups. The present study suggests that low plasma folate and high plasma homocysteine levels may be related to the pathophysiology of interictal psychosis of epilepsy. In future studies, we should investigate whether folate supplementation, in addition to antipsychotics, might play a beneficial role in the treatment of interictal psychosis in epileptic patients. Furthermore, the present findings should be confirmed by prospective longitudinal studies in a larger group of patients with epilepsy.
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dirtydingusus · Aug 5, 2010

have read several similar studies....

imagine having this shit your whole life and not knowing till 32yrs old......

dirtydingusus · Aug 7, 2010

just got out of hospital......not sure how long i was there.....status seizure again.........i have like one of the worst cases they have ever seen?

i dont even remember posting this thread?
or anything elts in the last few weeks/months?
so im reading and catching up on myself...........

dirtydingusus · Aug 10, 2010

so let me tell you - i would rather have turrets!

I have to say this "affliction" has given me a new appreciation for this place....where elts could i go and catch up on my life.....?

dirtydingusus · Aug 16, 2010

a ton of info to be found here.....Epilepsy and seizure information for patients and health professionals | epilepsy.com

if i dont write shit down i cant remember it at all.....
i am running up a stair case in an enormous void......
each step i leave falls away into nothingness.....

there is nothing behind me.....there is no past.......

only what is yet to come!

People with epilepsy commonly report having problems with their memory. Some describe having trouble remembering names that they once knew. Others forget appointments or are unable to remember to take their medications. Many others feel that they can recall things from the distant past, but cannot recollect events that happened in the past week. In fact, memory difficulties can have such a tremendous impact on people living with epilepsy that it may significantly hinder their functioning at work, in school, and at home.
In this section we will explore in-depth the relationship between epilepsy, thinking, and memory as well as diagnostic and treatment issues.

Thinking, Memory & Epilepsy

\t\t \t\t \t\t

Epilepsy.com Content

Are you concerned about changes you see in yourself? Changes in your ability to remember names, word meanings, even shopping items? Changes in how you go about making plans? Changes that affect the way you live your life, and not always for the better?
For most people—especially those who don't have very many seizures—epilepsy does not cause any serious problems with their thinking. If you have mostly primary generalized seizures, like absence, myoclonic, or tonic-clonic (grand mal) seizures, you are much less likely to have problems with your thinking than someone who has partial-onset seizures (seizures that begin in one area of the brain, often the temporal lobe). Some people with epilepsy of this kind do experience problems with their memory, language, or other kinds of thinking.
Whether you've had one or many seizures, you probably want to know how seizures affect the way you think. Does each seizure permanently change the way your brain works? Will seizures that last over 5 minutes stop you from learning new things? The answers can't be found easily, and may not be the same for every person.
How do we think?

First of all, let's talk about what goes into the way you think. To go about your daily life, many different abilities, or functions, come together. Three of these functions are memory, language, and what we call "executive function." Executive function really includes many different things, such as planning, reasoning, and stopping unwanted behavior.
The brain is organized so that one area is in charge of each task. Each area has developed over time to become very good at performing it. But because these tasks are so important, human brains developed so that different areas of the brain can work together. Communication lines formed between different areas so the brain would have a well-developed backup system.
An excellent place to find diagrams and information about the brain is at the website Neuroscience for Kids—http://faculty.washington.edu/chudler/neurok.html—good for all ages!
How do seizures change thinking?

When seizures happen, they can have two different effects on thinking:

\tA seizure can disrupt the area of the brain in charge of a particular function. So if seizures happen in the area in charge of language, you may not be able to name an object when you see it.

\tSeizures can also stop the communication between different areas. The lines are cut, so to speak. Even though you may know the name of an object, the part of the brain that knows can't tell the rest of your brain. The name is lost. One thing to remember is that where seizures start tells what function may be affected. If seizures start in several areas, or are generalized, they may affect many different functions.

Now you probably want to know what area does what, and how seizures in each area affect functioning.
Memory

Buried deep inside the temporal lobe is the hippocampus (hip-o-CAM-pus). This strange-looking thing is responsible for receiving new information and storing it. However, it only stores information for a short time. Then, if the information seems important, it ships it to a different section of the brain for long-term storage. Once the information is needed again, the hippocampus helps retrieve it. The hippocampus is the ultimate librarian.
The amygdala (a-MIG-dah-lah) is also very important to memory. This structure is responsible for basic emotions, such as fear, anger, and sexual attraction. When a person, place, or thing causes an emotional reaction, the amygdala attaches the emotion to the memory.
How do seizures affect memory?

Seizures, especially ones that start in the temporal lobe, can cause a major blow to the hippocampus. The hippocampus is very sensitive to changes in brain activity. If seizures starting here go untreated, the hippocampus starts to harden and shrink. Then it is as if the librarian has gone on strike. Information may be stored, but in a disorganized way. No one is there to find what you need. You may find what you need after a great deal of searching, or you may not find it at all. Luckily, there is one hippocampus on each side of the brain. So if one is affected by seizures, the other can help pick up the slack.
Language

Different sites are in charge of speaking, understanding, and storing words. For speaking, Broca's area takes the lead role. Broca's area is located just above the front of the temporal lobe. It is the center for outgoing words. It receives information from the many parts of the brain where words are stored. It then sends this information to the part of the brain that controls your mouth. To understand words that you hear or read, Wernicke's area steps in. Wernicke's area is on the top part of the temporal lobe, toward the back. It is the center for incoming words. When you hear and understand words, phrases, and sentences, it is because Wernicke's area has done its job. Words are stored in many different places throughout the brain. New research is finding that names and words may be stored by categories. For example, the names of animals are stored toward the front of the temporal lobe. Tools are stored farther back. Faces are stored at the bottom back section of the temporal lobe. Names of people that are close to you are stored at the very front of the temporal lobe, called the temporal pole.
How do seizures affect language?

Seizures can affect language in different ways. First of all, most people have the main part of their language functions on the left side of their brain. So if your seizures start on the right side of your brain, your language may not be affected at all. But even if your seizures start on the left side of your brain, hope is not lost. Seizures, by themselves, do not stop people from speaking or understanding words. Even if seizures happen every day for most of your life, you are still able to read, speak, and understand words. The main language problem caused by seizures is with finding words. Many people cannot think of the name of something, even when it is right in front of them. This is because seizures can damage the area where the word is stored, as well as the communication lines that carry or transport the word.
Executive function

The largest part of our brain is the part that handles executive function: the frontal lobe. This goes from the front tip of the brain to about halfway back (just in front of your ears). When you make a list, plan a driving route, or organize your thoughts, it is thanks to the frontal lobe. The frontal lobe has a major role in decision making. It helps you go through the pluses and minuses logically.
The frontal lobe has the final say in your social behavior. It regulates how you interact with other people. Some people claim this is where your personality comes from. It manages how you talk to other people. The frontal lobe also helps you to stop unwanted behavior. For example, say something happens that makes you feel like laughing or yelling but you know it is not the right time or place to laugh or yell. Your frontal lobe tells you that you shouldn't do it. It also helps you to not laugh or yell.
How do seizures affect executive function?

Seizures that happen in the frontal lobe can cause your planning ability to become weaker. You may not be able to organize your thoughts or your actions in the best way. If you are making a shopping list, for instance, you may think or write the same item over and over.
It may be harder for you to interact with people. Your attention may drift much sooner than before. Some people say their personality has changed after having seizures for many years. It also may be harder for you to stop unwanted behavior. You may say what's on your mind even when it's not the right time. For example, it is probably not a good idea to say that you hate your boss when you're in the middle of your annual performance review, unless you're willing to deal with the boss's reaction.
What else I should know?

Seizures affect thinking in different ways for everyone. Even if you have seizures that start near your hippocampus, your memory may not become extremely bad. Many different things need to be considered, such as:

How long you've had seizures

\tHow long each seizure lasts

\tWhat you are naturally good and bad at

\tThe effects of your medications

Talk with your doctor if you are concerned about changes in your memory, language, or executive function.
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dirtydingusus · Nov 24, 2011

The psychoses of epilepsy -- TOONE 69 (1): 1 -- Journal of Neurology, Neurosurgery & Psychiatry

J Neurol Neurosurg Psychiatry 2000;69:1-3 doi:10.1136/jnnp.69.1.1

Editorial

The psychoses of epilepsy

B K TOONE

+ Author Affiliations

King's College Hospital, Department of Psychological Medicine, King's College Hospital, Denmark Hill, London SE5 9RS, UK

Dr B K Toone, King's College Hospital, Department of Psychological Medicine, King's College Hospital, Denmark Hill, London SE5 9RS, UK brian.toone&kcl.ac.uk

People who have epilepsy seem particularly liable to certain major psychiatric disorders: a chronic interictal psychosis that closely resembles schizophrenia; and episodic psychotic states, some of which may arise in close temporal relation with seizure activity. These disorders are conventionally referred to as the psychoses of epilepsy although some of the episodic forms would be more accurately described as acute confusional states. These conditions have for long puzzled and intrigued psychiatrists and neurologists, but in recent years this interest has quickened especially among biologically minded psychiatrists in search of a neurological model for schizophrenia. In the psychoses of epilepsy and in schizophrenia converging lines of enquiry, in neuroimaging and in neuropathology in particular, have implicated the mesial temporal structures, the more so in the dominant hemisphere, and comparable abnormalities have been reported.1 This review will seek to identify areas of progress, areas of difficulty, and persisting dilemmas.
Epilepsy and schizophrenia

The precise nature of this relation has taxed clinical observers since before the turn of the century. Over the past four decades a consensus has begun to take shape-namely, that certain forms of epilepsy may act as risk factors for the subsequent development of a chronic interictal psychosis, a syndrome sometimes referred to as the schizophrenia-like psychoses of epilepsy (SLPE). This psychosis does resemble schizophrenia in its phenomenological manifestations,2 3 pursues a similar course, is as responsive to antipsychotic medication, and is largely uninfluenced by concurrent seizure activity. Given these similarities it is reasonable to question whether this comorbidity could not have arisen as a result of a chance association between two relatively common disorders. The answer should lie in community based comparisons of unbiased samples of epileptic and non-epileptic subjects with respect to prevalence of psychosis. Attempts have been made to do this, yielding a prevalence of schizophrenia within an epileptic population that varies between 3% and 7% (prevalence in general population 1%). However, a failure to use strictly defined and internationally recognised diagnostic criteria for schizophrenia and to distinguish between SLPE and episodic psychoses may have resulted in a spurious inflation in the prevalence figures. In the past year two studies that have to some extent redressed this difficulty have been published. In Iceland a case controlled study4 found that although there was no excess of psychiatric illness in epileptic subjects, among those who were psychiatrically ill a disproportionate number were psychotic. In Denmark Bredkjaer et al 5 used two national inpatient registers for epilepsy and for psychosis respectively to compare the subsequent incidence of schizophrenia in patients who had at some point undergone admission to hospital for epilepsy with that in the general population. A standardised incidence ratio of 1.48 for all epilepsy and 2.35 for psychomotor epilepsy argues strongly for epilepsy as a risk factor for schizophrenia, but an epilepsy sample defined by need for inpatient care may be considered unrepresentative. Although vulnerable to similar criticism, the neurology clinic based study of Mendes et al 6 report convincing data. The prevalence of schizophrenia, diagnosed according to DSM3R criteria, was nine times greater among clinic attenders with epilepsy than those with migraine. Taken together these studies provide strong, though far from conclusive evidence, that the SLPE is a unique disorder and not an artefact of random association. The definitive epidemiological study is still awaited. Meanwhile other approaches could be explored: if the SLPE is indeed a secondary or symptomatic psychosis the prevalence of schizophrenia among family members should not greatly exceed the prevalence in the general population. It should certainly fall short of that found in the families of schizophrenic probands. Early studies-for example, that of Slater and Glithero,7suggest that this is the case, but as yet no family history study using state of the art methodology has been published.

Even if it is conceded that epilepsy may be a risk factor for the development of schizophrenia, it is clear that the great majority of those with epilepsy do not become psychotic. Are there epileptic characteristics that predict such a development? It has long been held that temporal lobe epilepsy, more so than idiopathic generalised epilepsy, is a risk factor for psychosis, although this has been contested8 on the grounds that the finding is based on data derived from specialist epilepsy clinics in which temporal lobe epilepsy is overrepresented. However, recent data, some of it epidemiologically derived, continue to support this conclusion.5 6 Flor-Henry9 first reported an association between left sided temporal lobe epileptic foci and SLPE. Subsequent published work has also noted, albeit inconsistently, a laterality effect, but this must be balanced against the finding that in large, relatively unselected samples, left sided foci predominate in a ratio of 60:40.10 The neuropathology of the epileptogenic lesion may be relevant, but is unlikely to be of major effect: in one large neurological series11 four out of the nine patients with gangliogliomas developed a psychosis, but this group still only accounted for 15% of the psychotic series. Andermannet al 12 reported a further six cases, but these seem to have represented but a small proportion of the denominator. An unexplained feature common to both studies is that in every case psychosis developed for the first time postoperatively. It is likely that the intrinsic neuropathological characteristics of the lesion are of less importance than the stage of cerebral maturation during which it develops. Those lesions that arise during foetal development or during the perinatal period are associated with a greater risk of psychosis.13 Most of the risk variance for SLPE still remains unexplained, but it must be remembered that even if it is accepted that epilepsy may increase the likelihood of schizophrenia, any sample of patients with SLPE will include a proportion, unfortunately unidentifiable, the presence of which is due to chance association; this group will act as a confounding factor in any search for aetiology.
The episodic psychoses

The most common by far are the postictal psychoses. Others include some drug induced psychoses and the alternating psychoses that arise during periods of improved seizure control. The salient features of postictal psychoses have been consistently reported (for example, see Logsdail and Toone14). They usually follow exacerbations, especially clusters, of complex partial seizures, sometimes without but more commonly with generalisation. Characteristically, cessation of seizure activity is followed by a brief interlude-a â€œlucid intervalâ€-of 12-72 hours before the mental state deteriorates. The psychosis, which comprises affective, schizophrenic, and confusional elements, may last for up to a week. The EEG may exhibit increased epileptic discharge activity or a slowed dominant rhythm. The episodes resolve spontaneously, but often recur, usually displaying similar phenomenology.

The same question that was asked of the SLPE may also be asked of the postictal psychoses: what factors predispose the minority of epileptic patients to develop postictal psychoses? Although a far from uncommon disorder, postictal psychoses have received considerably less attention than SLPE and many of the accounts that have been published describe an iatrogenic psychosis that occurs for the first time after an increase in seizure activity due to anticonvulsant withdrawal during presurgical evaluation. Although such studies may be informative, particularly as they are prospective and accompanied by telemetric information, the cases they describe are likely to be unrepresentative of the spontaneously occurring postictal psychoses. Some centres report an association between complex partial seizures and postictal psychoses14 15; others fail to do so.16Postictal psychotic subjects report more seizure clustering17 and ictal fear (complex partial seizures containing fear as a major component).18 19 Bilateral EEG discharges are seen more often in subjects with postictal psychoses than non-psychotic controls.16-18 Compared with SLPE, both age of epilepsy onset17 and psychosis onset19 are delayed.

Other forms of episodic psychosis are distinctly uncommon. The phenomenon of forced normalisation, whereby improved seizure control, usually as a result of change of anticonvulsant medication, is associated with a â€œnormalisationâ€ of the EEG and the emergence of psychotic features, may underlie some episodes of psychotic behaviour, particularly those associated with the introduction of novel antiepileptic drugs. As first described by Landolt, forced normalisation occurred in the context of partial epilepsy, but more recent accounts implicate the succinimide group in the treatment of primary generalised epilepsy.20 The use of vigabatrin21 and zonisamide22 may also carry an increased risk of psychotic disturbance.
Psychosis and temporal lobectomy

In the early days of temporal lobe surgery for treatment of epilepsy the psychiatrically unwell made up a significant proportion, sometimes most of those who went forward for surgery. One in six was psychotic. There was then a hope, even an expectation, that surgery might benefit psychosis as it had epilepsy. This was not borne out and the proportion of epileptic patients with psychosis has gradually fallen. But as one author has pointed out, it might still be considered better to be psychotic without seizures than to be psychotic with them.23 Chronic schizophrenia need not be a contraindication and carefully selected patients may benefit from surgery.24 A history of postictal psychoses should be considered a positive indication for surgery. Psychosis may present for the first time- â€œde novo psychosisâ€-after surgery. The condition was noted in early surgical series, but has recently received greater attention. It is difficult to know whether this represents a true increase in incidence, better recognition, or a fall in the age of surgery. The de novo psychoses are a mixed bag: some are depressive in character, some schizophrenic; some pursue a chronic course, some are episodic, the de novo postictal psychoses forming a definite subgroup.25 Their aetiology may be similarly diverse. In some the development of psychosis may be predetermined by earlier events and the surgical procedure an irrelevant artefact. In a few cases seizure control may lead to forced normalisation and an alternating psychosis. Only one feature stands out clearly: preoperatively the presence of SLPE is associated with a left temporal focus; 85% of de novo psychoses follow right temporal surgery. The reasons for this are unclear. There is some indication,26hardly yet substantiated, that depression is commoner after right sided lobectomy. The amount of resected tissue is also more generous.
Aetiology of the epileptic psychosis

Epilepsy and psychosis may each arise out of some form of cerebral dysfunction common to both; or psychosis may be a consequence of seizure activity. The first seems more likely. Most forms of epileptic psychoses occur more commonly in the partial epilepsies, especially complex partial seizures. Within the surgical series patients with developmental lesions may be at particular risk. Parallels have been drawn between anomalies of cerebral architecture in schizophrenia and the epileptogenic cortical dysplasias27but in clinical practice such associations have yet to be reported. Distinctive patterns of hypometabolism/hypoperfusion have been reported28 29 but with no consistency. Dominant hemispheric temporal lobe involvement may be associated with a more pure form of SLPE.30 The role of seizure activity finds its theoretical justification in the kindling hypothesis but in humans even the kindling of epileptic seizures remains debatable. There is no precedent for the kindling of behavioural change. Liability to SLPE is not related to seizure frequency or severity; indeed it often occurs at a time when seizure frequency is declining. However, the extent of mesial temporal and, particularly, extratemporal damage may be a risk factor. Recent neuroimaging data suggest that mesial temporal lesions may be associated with loss of tissue volume and with neuronal damage in areas well beyond the temporal lobes including the striatum, thalamus, and frontoparietal grey matter.31 32 Reductions in hippocampal volume, tissue damage, and neuronal loss may be progressive and may reflect the duration of epilepsy.33 34 Function may also deteriorate with chronicity.35 Extratemporal neuronal damage may also occur36 although it may be reversible. Brutonet al 37 reported ventricular enlargement, periventricular gliosis, and white matter abnormalities in epileptic patients with psychosis compared with those without. Subjects with SLPE have smaller whole brain and bilateral hippocampal volumes compared with matched non-psychotic epileptic controls (Mellerset al, personal communication). The association between degree of damage and chronicity may explain the time interval between onset of seizures and onset of psychosis in both SLPE and postictal psychoses. In conclusion, an accumulation of admittedly less than perfect evidence strongly suggests an environmental rather than a genetically determined form of psychosis. The aetiology, like that of schizophrenia itself, will in all probability prove to be multifactorial with no one factor predominating.
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BreatheUp · Nov 24, 2011

so, what do you want to know? or trying to figure out?
it seems like youre already diagnosed?

any kind of epilepsy comes with psych disorders. in fact, a lot of sever bipolar patients have similar looking EEGs compared to epileptics during a seizure/manic episode.

psycho somatics are a very slippery slope my friend.

Storm Crow · Nov 24, 2011

This may interest you -

Marijuana: an effective antiepileptic treatment in partial epilepsy? (abst - 2007)
Clinical Studies and Case Reports

And are you taking Omega 3?

The omega-3 fatty acid-derived neuroprotectin D1 limits hippocampal hyperexcitability and seizure susceptibility in kindling epileptogenesis. The omega-3 fatty acid-derived neuroprotectin D1 l... [Epilepsia. 2011] - PubMed - NCBI

So, lets put some of the stuff in my brain together- (my GDP is GOOD!)

You have PARTIAL epilepsy. To me that means you are borderline, your body halfway wants to seize. Omega 3 lessens the chance of "kindling" a seizure as seen in the study above.

Omega 3 is also necessary for the creation of working CB1 receptors (1) which "tell" cells what to do. The hippocampus is where the seizures start. Something is wrong with yours, or you wouldn't have seizures (duh!)

We need to fix your hippocampus! And guess what causes new growth in the hippocampus? (2) But if you are eating that average American diet, you are NOT getting enough Omega 3! If it doesn't have Omega 3, your body substitutes an Omega 6- which almost works. But the G i/o effector protein doesn't get attached right, so the neuron doesn't always "get the message" about what it should be doing! (1, again)

A possible "fix" would be to take large doses (3) of Omega 3 combined with a healthy diet (more veggies and fruit, less fatty meat) and smoking/vaping/eating cannabis!

The need for a healthier diet is just a "given"- the average American diet SUCKS! (4)

The Omega 3 should slow the kindling of your seizures, and help your body make healthy CB1 receptors that are necessary for normal brain function.

The cannabis will set off neurogenesis in the hippocampus, and it has quite a long history as an anti-epileptic! (5)

Will it work? But I would give it a try if I were in your shoes! Omega 3 is "heart healthy" and it lowers cholesterol. Won't hurt you at all to add it to your daily routine!

Have a Happy Thanksgiving!

Granny

1-“Nutritional omega-3 deficiency abolishes endocannabinoid-mediated neuronal functions.”
Unbound MEDLINE | Nutritional omega-3 deficiency abolishes endocannabinoid-mediated neuronal functions. PubMed Journal article abstract

Granny’s translation – “The US diet sucks big time and we are fat, undernourished, and crazy because of it. We get WAY too much Omega 6 and not enough Omega 3. Not getting enough Omega 3 can make you crazy because without it, the CB1 cannabinoid receptors in your brain aren’t made right- a chunk that is supposed to be attached, isn’t! Broken receptors give you “impaired emotional behavior”. So we think it’s the low Omega 3 diet is making the US totally nuts!”

2- Cannabinoids promote hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects
(full - 2005) \tJCI - Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects

High-dose cannabis stimulates growth of brain cells in rats (news – 2005)
High-dose cannabis stimulates growth of brain cells in rats - Health News - Health & Families - The Independent

Good News For The Medical Marijuana Movement: Pot Proliferates Brain Cells And Boosts Mood
(news - 2005) Good News For The Medical Marijuana Movement: Pot Proliferates Brain Cells And Boosts Mood

3- Up to 4 grams a day has been safely used in heart/cholesterol studies with fishy burps, easier bruising and softer bowel movement being the side effects. I could dig up the studies if you want....

4- O-6 vs. O-3 ratio
Omega-6 to Omega-3 Ratio - Discover the Shocking Reality That Ruins Your Health More than You Think! - Free Online Library

5- Anti-epileptic Action of Marijuana-Active Substances (full - 1949) http://www.mikuriya.com/s3_6.pdf

Anticonvulsant nature of marihuana smoking. (abst - 1975)
Clinical Studies and Case Reports

dirtydingusus · Nov 25, 2011

BreatheUp said:

so, what do you want to know? or trying to figure out?
it seems like youre already diagnosed?

any kind of epilepsy comes with psych disorders. in fact, a lot of sever bipolar patients have similar looking EEGs compared to epileptics during a seizure/manic episode.

psycho somatics are a very slippery slope my friend.
Click to expand...

im way passed diagnosed.....

what do i want to know...or am i trying to figure out.....
everything i can find out!

i have of coarse read much already...over some time.....

but who knows what one of my fellow blades may be able to let me in on?
you may..or may not as the case may be....be surprised how much information the people on this site have led me to....

just look at a cupple of the contributions to this thread alone.....

Granny and tharedhead always have excellent contributions.....all over the board....(thank you both!)and they are not alone

what do i expect ......?idk?
but so far i have already gotten more then i had found on my own
more in a bit

BreatheUp · Nov 25, 2011

i see. your initial posts were in the form of a question and since youre already way beyond diagnosis i was a bit confused about what you actually wanted to know.
if youre just looking for general info theres a ton on this site so search around but if you cant even remember than i for sure feel ignorant for even saying anything haha. a thread no doubt helps. im a complete dumbass really and dont know what im talking about half the time but i try :/

i used to date a girl who had grand mals.
granny and thareadhead (my old girl was a red head that had seizures i fuckin love red heads) did give a lot of info but i mean, this thread could be pages and pages long if you wanted to post everything out there on psych disorders related to epilepsy and vice versa.

its like trying to mind dump with no starting point. i dont really read studies from the internet cause after a while staring at a display screen just hurts and literally starts to destroy your brain. reading a screen doesnt stimulate like a book. in fact, it throws it into atrophy so i stay away.

seizures (and most psych disorders as well) dont really have anything to do with neurons themselves. its a shame, but most cells in your brain arent even grey matter. theyre white (about 80% of brain cells are white matter glia). no one really has been studying them. astrocytes, microglia, schwann, and oligodendrocytes are the main types of glia. theyre not electrically conducive like neurons so most of the studies havent focused on them.
theyre the reason for cancer and most brain disorders in general. the only problem is theyre also the cure - its a fine line. white matter research is in its infancy but most of the studies and info granny posted as far as omega 3 and even thareadheads folate and b12 info has to do with glia and not neurons. the hippocampus does produce neurons but it produces more glia than anything. the G proteins and fatty acids dont stick to neurons at all, they stick to glia since theyre made of fat. neurons communicate like hard wired phone calls, glia communicate like cell phones. so yea, partial complexes may start in the hippocampus but spread to other parts very rapidly which is why they start to effect other functions like those broca examples she posted. temporal lobes and PFC as well.

theres been a pretty good amount of research on the b 12 effect. no joke, those 5 hour energy things are crazy medically for seizures. its 3000% b 12. even shizo disorders can benefit from 5 hour energy.
another big one is gluten. its been shown to worsen shizo/epileptic symptoms.
if you smoke cigs, stop. they worsen symptoms. nicotine is an antagonist and kills glia which again, is the cause of cancer.
theres a lot that can be done to improve your life but really it just comes down to balance which im sure you know all about. besides different meds i mean.
vitamins, minerals, amino acids etc etc.
your brain is a plant and it needs to be nurtured just like anything else. its a balance of ingredients.

as far as the psychology or neurology question...
the answer is both really. although neurology has more to do with spines than anything. not many neurologists deal with brains specifically.
stress obviously is psychiatric but has physical effects. im sure you can feel auras easier when your stressed.

idk im just gonna stop trippin out in this thread now. i dont know anything. in hindsight there is probably nothing of relevance in this post

good luck.

dirtydingusus · Nov 30, 2011

Storm Crow said:

You have PARTIAL epilepsy. To me that means you are borderline, your body halfway wants to seize. .
Click to expand...

i wish it was that simple!!!!!!!
by partial...they mean that it is "confined" to certain parts of my brain...it starts in my temporal lobe...and travels to my frontal lobe....rather then "generalized" where the whole brain is involved....(i have those too just not as often and never had one before they fed me anti-epileptic drugs)

so we took out the temporal lobe they came from.....and the frontal lobe missed it so much...it figured out how to get it from the left side......
this is likely in part because i spent all my life before that trying to hold on to that feeling everytime it came....and looking for it when it wasnt there....

Storm Crow said:

Omega 3 is also necessary for the creation of working CB1 receptors (1) which "tell" cells what to do. The hippocampus is where the seizures start. Something is wrong with yours, or you wouldn't have seizures (duh!)

We need to fix your hippocampus! And guess what causes new growth in the hippocampus?
Click to expand...

physically....there is nothing wrong with my brain at all....even before surgery...all my MRIs were always perfect......
my old neurologist took copies of my MRIs to a conference he was speaking at to show around because he had never seen or heard of anyone having as many seizures as i do...and having such a perfect MRI.....
the problem i have with my hippocampus is when it goes on vacation!!!!!!!!and doesnt bother "laying down" any new memories for awhile....
i have been trying some things with my diet.....will see how it goes?

Storm Crow said:

Will it work? But I would give it a try if I were in your shoes! Omega 3 is "heart healthy" and it lowers cholesterol. Won't hurt you at all to add it to your daily routine!
Click to expand...

i have been trying some things with my diet.....will see how it goes?

@tharedhead
what i am finding...in my reading and in my experience.....is that the psychosis is without a doubt compounded by the meds.....or by stopping or reducing the seizures in anyway......
i am much better off without them....

now even without the meds....and having little simple partials all the time... and the occasional complex partials as well as who knows how often im having generalized(at least 3 in the last month that i know about-and only know cus i bit part of my tongue off each of those times)
the psychosis is still quite apparent...it is at its peek in the postictal state....
and it is different now....post surgery...
and i am reading that often when it is the left lobe(the one i have left) that the seizures come from that the psychosis is more prevalent....

tharedhead · Nov 30, 2011

Did you try L-methylfolate supplementation?

Deplin Oral : Uses, Side Effects, Interactions, Pictures, Warnings & Dosing - WebMD

dirtydingusus · Nov 30, 2011

tharedhead said:

Did you try L-methylfolate supplementation?

Deplin Oral : Uses, Side Effects, Interactions, Pictures, Warnings & Dosing - WebMD
Click to expand...

not yet i havent....
some days are ruff.....
just trying to keep myself together has been a bitch these last few months....
i been staying with my sister the last cupple years...since surgery.....and it has come to a point where i need to be finding someplace elts to go.....
she has a man now that she didnt have before and they have become serious enough to want to be moving in together...and they probably would have done so already if not for me.....and she wont say so...but i see it....so now it is time to figure out which way to wonder.....

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