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Bit of an idea for possible CURE. Has some weight to it.


Fawkinchit

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Antipsychotics seem to stabilize you on an emotional level. But you got 2 main types of antipsychotics: typical and atypical. Typical is like thorazine and haldol. Atypical is like seroquel, zyrexa, ability, respirdol, etc ......Otherwise i hate these drugs. ....If you don't mind sleeping 15 hours a day, gaining 50 pounds, being complacent, mediocre, uncreative, mindless, it'll be fine for you. ....It's kind of like the theory, you use meds that make you hyperactive to treat hyperactivity. You use medicine that makes you crazy to treat craziness.

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There has been very little research medically done on the Corpus Callosum in terms of maintaining its health.

I wonder if anybody has any insight?

Isn't the corpus callosum the part of of the brain that connects the two hemispheres? In patients with severe epilepsy, sometimes the corpus callosum is surgically cut to totally cut out all weird brain activity. It's very interesting, if anybody has free time they should research the procedure and the outcome. It literally cuts the brain in half so that the two hemispheres can not communicate with eachother, however the people come out the same person as before, almost totally normal, but their brain does some weird stuff. anyways, like i said, research it, but the thing to take away from it - the procedure does cure epilepsy. I don't know which side of the brain the visual lobe (or whatever it's called) is on, or if there are different parts in both hemispheres, but what if all the weird impulses causing hppd are coming from the opposite side of the brain? it could cure hppd.

Any volunteers lol??

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Please give a brief explination in simple terms if you have time for everyone. This is great information though it shows that one thing I said earlier on in the thread is accurate, that there seems to be some sort of over activity in the brain, most likely the nuerons effeted by the 5ht2a receptors.

Has anyone tried any 5ht2a receptor antagonists? I think we should start there and see what happens, I have read that risperidone in some people makes their symptoms worse, but has anyone tried anything else? Antagonists basically make communication between neurons neutral, so somebody should give it a shot, and then post up the results, ultimately though I still think that our best bet to reverse what we have done is through inverse agonists.

Don't know how to say things simpler - how do you simplify the brain, aaauuuggghhh. Is there a part of the post in particular you are referring?

One article to refer to is http://peer.ccsd.cnr...2008.171348.pdf It is NOT easy reading but note pages 21 - 23. Connections, connections, connection !!! And a list of areas involved with some of our symptoms.

Since Klonopin slows brain activity and is effective for some with HPPD, then "disinhibition" is clear (as with Dr A's gEEGs). Dr A's drug trial results show that, for some, dopamine is a missing regulator. Since apparently articles show serotonin to be involved, we have this thread.

Because these systems are so interconnected and each person has "uniqueness", you occasionally find people responding to a med out of the blue that others don't. In short, meds alter the balance and sometimes that is all that is needed to get-the-train-back-on-the-track.

Most of us respond only partially with a med, if at all. Look at Merkan's 3 med combo as example. Finding a way to get better is like picking a combination lock. Lack of research makes us blindfolded. Lack of willingness on the part of doctors ties our hands. So we use out teeth until we are exhausted trying ... slobbering all over the tumbler.

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The Epilepsy Brain

Mutations in several genes have been linked to several types of epilepsy. Some genes that code for protein sub units of voltage-gated and ligand-gated ion channels have been associated with forms of generalized epilepsy and infantile seizure syndromes.[18]

One speculated mechanism for some forms of inherited epilepsy are mutations of the genes that code for sodium channel proteins; these defective sodium channels stay open for too long, thus making the neuron hyper-excitable. Glutamate, an excitatory neurotransmitter, may, therefore, be released from these neurons in large amounts, which — by binding with nearby glutamatergic neurons — triggers excessive calcium (Ca2+) release in these post-synaptic cells. Such excessive calcium release can be neurotoxic to the affected cell. The hippocampus, which contains a large volume of just such glutamatergic neurons (and NMDA receptors, which are permeable to Ca2+ entry after binding of both glutamate and glycine), is especially vulnerable to epileptic seizure, subsequent spread of excitation, and possible neuronal death. Another possible mechanism involves mutations leading to ineffective GABA (the brain's most common inhibitory neurotransmitter) action. Epilepsy-related mutations in some non-ion channel genes have also been identified.

Much like the channelopathies in voltage-gated ion channels, several ligand-gated ion channels have been linked to some types of frontal and generalized epilepsies.

Epileptogenesis is the process by which a normal brain develops epilepsy after trauma, such as a lesion on the brain. One interesting finding in animals is that repeated low-level electrical stimulation to some brain sites can lead to permanent increases in seizure susceptibility: in other words, a permanent decrease in seizure "threshold." This phenomenon, known as kindling (by analogy with the use of burning twigs to start a larger fire) was discovered by Dr. Graham Goddard in 1967. It is important to note that these "kindled" animals do not experience spontaneous seizures. Chemical stimulation can also induce seizures; repeated exposures to some pesticides have been shown to induce seizures in both humans and animals. One mechanism proposed for this is called excitotoxicity. The roles of kindling and excitotoxicity, if any, in human epilepsy are currently hotly debated.

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Neuromelanin

Neuromelanin is the dark pigment present in pigment-bearing neurons of mainly four deep brain nuclei. These are the substantia nigra (from the Latin black substance) - Pars Compacta part, the locus coeruleus (blue spot), the dorsal motor nucleus of the vagus nerve (cranial nerve X), and the median raphe nucleus of the pons. Both the substantia nigra and locus coeruleus can be easily identified grossly at the time of autopsy because of their dark pigmentation. In humans, these nuclei are not pigmented at the time of birth, but develop pigmentation during maturation to adulthood.

Although the functional nature of neuromelanin is unknown in the brain, the pigment is made from oxyradical metabolites of monoamine neurotransmitters including dopamine and norepinephrine. Luigi Zecca and David Sulzer present evidence that neuromelanin pigment is an autophagy product that accumulates in lysosomes, which are unable to effectively degrade it.[10] In this way, the synthesis of neuromelanin is protective as its encapsulation within the autophagic organelle removes it from reacting with sites in the neuronal cytosol that could lead to neurotoxicity. Other evidence, e.g.[11][12][13]suggests a more active role. Electronic "device" functions (see below) are also possible.

While neuromelanin becomes higher throughout life in most people,[14] the loss of pigmented neurons from specific nuclei is seen in a variety of neurodegenerative diseases. In Parkinson's disease there is massive loss of dopamine-producing pigmented neurons in the substantia nigra and locus coeruleus. High levels of neuromelanin are also detected in other primates, and in carnivores such as cats and dogs.

Melanin: most common form of biological melanin is eumelanin, a brown-black polymer of dihydroxyindole carboxylic acids, and their reduced forms. Most are derived from the amino acid tyrosine.

Biosynthetic Pathways of Melanin:

The first step of the biosynthetic pathway for both eumelanins and pheomelanins is catalysed by tyrosinase:

TyrosineDOPAdopaquinone

Dopaquinone can combine with cysteine by two pathways to benzothiazines and pheomelanins

Dopaquinone + cysteine → 5-S-cysteinyldopa → benzothiazine intermediate → pheomelanin

Dopaquinone + cysteine → 2-S-cysteinyldopa → benzothiazine intermediate → pheomelanin

Alternatively, dopaquinone can be converted to leucodopachrome and follow two more pathways to the eumelanins

Dopaquinone → leucodopachrome → dopachrome → 5,6-dihydroxyindole-2-carboxylic acid → quinone → eumelanin

Dopaquinone → leucodopachrome → dopachrome → 5,6-dihydroxyindole → quinone → eumelanin

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Back to Amino Acids (such as L-Serine, L-Cysteine and Glycine):

Amino acids are made from intermediates of the citric acid cycle and other major pathways

Of the basic set of 20 amino acids (not counting selenocysteine), there are 8 that human beings cannot synthesize. In addition, the amino acids arginine, cysteine, glycine,glutamine, histidine, proline, serine, and tyrosine are considered conditionally essential, meaning they are not normally required in the diet, but must be supplied exogenously to specific populations that do not synthesize it in adequate amounts.[1][2] For example, enough arginine is synthesized by the urea cycle to meet the needs of an adult but perhaps not those of a growing child. Amino acids that must be obtained from the diet are called essential amino acids. Nonessential amino acids are produced in the body. The pathways for the synthesis of nonessential amino acids are quite simple. Glutamate dehydrogenase catalyzes the reductive amination of α-ketoglutarate to glutamate. A transamination reaction takes place in the synthesis of most amino acids. At this step, the chirality of the amino acid is established. Alanine and aspartate are synthesized by the transamination of pyruvate and oxaloacetate, respectively. Glutamine is synthesized from NH4+ and glutamate, and asparagine is synthesized similarly. Proline and arginine are derived from glutamate. Serine, formed from 3-phosphoglycerate, is the precursor of glycine and cysteine. Tyrosine is synthesized by the hydroxylation of phenylalanine, an essential amino acid. The pathways for the biosynthesis of essential amino acids are much more complex than those for the nonessential ones. activated Tetrahydrofolate, a carrier of one-carbon units, plays an important role in the metabolism of amino acids and nucleotides. This coenzyme carries one-carbon units at three oxidation states, which are interconvertible: most reduced—methyl; intermediate—methylene; and most oxidized—formyl, formimino, and methenyl. The major donor of activated methyl groups is S-adenosylmethionine, which is synthesized by the transfer of an adenosyl group from ATP to the sulfur atom of methionine. S-Adenosylhomocysteine is formed when the activated methyl group is transferred to an acceptor. It is hydrolyzed to adenosine and homocysteine, the latter of which is then methylated to methionine to complete the activated methyl cycle.

Cortisol inhibits protein synthesis.[3]

[edit]Amino acid biosynthesis is regulated by feedback inhibition

Most of the pathways of amino acid biosynthesis are regulated by feedback inhibition, in which the committed step is allosterically inhibited by the final product. Branched pathways require extensive interaction among the branches that includes both negative and positive regulation. The regulation of glutamine synthetase from E. coli is a striking demonstration of cumulative feedback inhibition and of control by a cascade of reversible covalent modifications.

[edit]

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qaiphyx-

I'm not sure. I wrote that a week ago. I'm sure it involves research i was doing w/ voltage, pH, conductance, etc.

This seems to be a unique (kind of new-class) of epilepsy drug. It may show promise with migraines and neuropathic pain.

I think that it has to do with voltage levels during resting periods that lower things well below the "triggering" threshold. This in turn tends to inhibit the whole system somewhat IMO.

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5-HT2A is expressed widely throughout the central nervous system

 (CNS). It is expressed near most of the serotoninergic terminal rich areas, includingneocortex

 (mainly prefrontal

, parietal

, andsomatosensory cortex

) and the olfactory tubercle

. Especially high concentrations of this receptor on the apical dendrites

 of pyramidal cells

 in layer V

 of the cortex may modulate cognitive processes,[8]

[9]

[10]

 by enhancing glutamate

release followed by a complex range of interactions with the 5-HT1A

,[11]

GABAA

,[12]

adenosine A1

,[13]

AMPA

,[14]

mGluR2/3

,[15]

mGlu5

,[16]

 andOX2

 receptors.[17]

[18]

 In the rat cerebellum, the protein has also been found in the Golgi cells

 of the granular layer

,[19]

 and in the Purkinje cells

.[20]

[21]

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