Lamictal saved me for good!

Hey people. I don't know if this is even supposed to be here, but since there are atleast 1 or 2 people there who have the same symptoms I had, I think it's worth a mention.

I used to be on 100mg lamictal for depression, then I quit it a while ago. Then I came off benzos and the rollecoaster began. Now, 5 months out, I started taking 25mg lamictal daily just five days ago and bang, after two hours symptoms started to lift and now, five days after I feel like reborn. Literally. No more brainfog, got my creativity back, fatigue gone, depression gone, feelings of loneliness gone, DP/DR gone, memory improved.. I feel like every last symptom I had, lifted 97.5%. Except emotional numbness, everything is still quite blunted but I couldn't care less at the moment TBH.

Now I don't know if this was benzo related or something else, but I feel like it's past me. I will keep posting if anything changes, but at this moment I consider myself healed (don't want to start a party too early tho..).

More on lamictal:

Lamotrigine is a member of the sodium channel blocking class of antiepileptic drugs. It is a triazine derivate that inhibits voltage-sensitive sodium channels, leading to stabilization of neuronal membranes. It also blocks L-, N-, and P-type calcium channels and has weak 5-hydroxytryptamine-3 (5-HT3) receptor inhibition. These actions are thought to inhibit release of glutamate at cortical projections in the ventral striatum limbic areas, and its neuroprotective and antiglutamatergic effects have been pointed out as promising contributors to its mood stabilizing activity. Observations that lamotrigine reduced γ-aminobutyric acid (GABA) A receptor-mediated neurotransmission in rat amygdala, suggest that a GABAergic mechanism may also be involved, although this concept is controversial.

 

Lamotrigine does not have pronounced effects on any of the usual neurotransmitter receptors (adrenergic, dopamine D1 and D2, muscarinic, GABA, histaminergic H1, serotonin 5-HT2, and N-methyl-D-asparate). Inhibitory effects on 5-HT, norepinephrine, and dopamine transporters are weak. Lamotrigine is a weak inhibitor of dihydrofolate reductase, but whether this effect is sufficient to contribute to a mechanism of action or increases risk to the fetus during pregnancy is not known. Early studies of lamotrigine's mechanism of action examined its effects on the release of endogenous amino acids from rat cerebral cortex slices in vitro. As is the case for antiepileptic drugs that act on voltage-dependent sodium channels, lamotrigine inhibited the release of glutamate and aspartate evoked by the sodium-channel activator veratrine and was less effective in the inhibition of acetylcholine or GABA release. At high concentrations, it had no effect on spontaneous or potassium evoked amino acid release.

 

These studies suggested that lamotrigine acts presynaptically on voltage-gated sodium channels to decrease glutamate release. Several electrophysiological studies have investigated the effects of lamotrigine on voltage-dependent sodium channels. For example, lamotrigine blocked sustained repetitive firing in cultured mouse spinal cord neurons in a concentration-dependent manner, at concentrations that are therapeutically relevant in the treatment of human seizures. In cultured hippocampal neurons, lamotrigine reduced sodium currents in a voltage-dependent manner, and at depolarised potentials showed a small frequency-dependent inhibition. These and a variety of other results indicate that the antiepileptic effect of lamotrigine, like that of phenytoin and carbamazepine, is at least in part due to use- and voltage-dependent modulation of fast voltage-dependent sodium currents. However, lamotrigine has a broader clinical spectrum of activity than phenytoin and carbamazepine and is recognised to be protective against generalised absence epilepsy and other generalised epilepsy syndromes, including primary generalised tonic–clonic seizures, juvenile myoclonic epilepsy, and Lennox-Gastaut syndrome.

 

The basis for this broader spectrum of activity of lamotrigine is unknown, but could relate to actions of the drug on voltage-activated calcium channels. Lamotrigine blocks T-type calcium channels weakly, if at all. However, it does inhibit native and recombinant high-voltage–activated calcium channels (N- and P/Q/R-types) at therapeutic concentrations. Whether this activity on calcium channels accounts for lamotrigine's broader clinical spectrum of activity in comparison with phenytoin and carbamazepine remains to be determined.

 

It antagonises the following receptors with the following IC50 values:

 

5-HT3, IC50=18μM

σ receptors, IC50=145μM

https://en.wikipedia.org/wiki/Lamotrigine

Peace

Alesii,

          Good to hear that you've gotten some relief.

The pre-synaptic sodium-channel blockade at the glutamate terminal is allowing for these improvements. Since the action isn't at the receptor, the brain isn't as quick to notice these changes.

          Don't forget that you're only seeing symptom relief. If it doesn't backfire, I would only be on it for so long, until I started tapering. On the other hand, lamotrigine may give you the edge you need to escape the nasty parts of withdrawal. Keep us posted!

Dear Alesii and all,

This is my next med to try.  It was suggested by my neurologist.  I am working on a few other things with other docs right now, like digestive health and nutrition, but probably in a month or so.  I sometimes feel a bit bipolar, and I can tell you some days I can just TASTE the glutamate.  So Lamitacl just makes sense for me.

As wiki said and faultandfracture reminded, it blocks glutamate pre-synaptically.  Safest way.  Well, second safest.  I just finished a good book on nutritional psychiatry called Nutrient Power by William Walsh.  It's emphasis is on healing thru nutritional balance.  That is the absolute safest way.  But.  He talks a lot about epigenetics; the idea that something in your life caused a gene to express a certain way.  I think this is true for a lot of us.  Benzo use and then withdrawal triggered an otherwise relatively quiet set of genes, that may or may not ever revert back to the way they were.

I cannot really tell from your signature how far off benzos you are as I could find "opamax."  Did you mean "Topamax?"

My point is, we are not allowed to give medical advice, so, IF I WERE YOU, I would stay on the Lamitcal as long as it helped.  I was 42 months off benzos and losing my mind when I reinstated.  I got 3 good months out of it, I am still on valium, and have only gotten sicker since.  I wish I knew about Lamitcal then.

I will keep my eye on this thread.  Keep us posted!

Be well and good luck,

Ramcon1

Dear Alesii and all,

 

This is my next med to try.  It was suggested by my neurologist.  I am working on a few other things with other docs right now, like digestive health and nutrition, but probably in a month or so.  I sometimes feel a bit bipolar, and I can tell you some days I can just TASTE the glutamate.  So Lamitacl just makes sense for me.

 

As wiki said and faultandfracture reminded, it blocks glutamate pre-synaptically.  Safest way.  Well, second safest.  I just finished a good book on nutritional psychiatry called Nutrient Power by William Walsh.  It's emphasis is on healing thru nutritional balance.  That is the absolute safest way.  But.  He talks a lot about epigenetics; the idea that something in your life caused a gene to express a certain way.  I think this is true for a lot of us.  Benzo use and then withdrawal triggered an otherwise relatively quiet set of genes, that may or may not ever revert back to the way they were.

 

I cannot really tell from your signature how far off benzos you are as I could find "opamax."  Did you mean "Topamax?"

 

My point is, we are not allowed to give medical advice, so, IF I WERE YOU, I would stay on the Lamitcal as long as it helped.  I was 42 months off benzos and losing my mind when I reinstated.  I got 3 good months out of it, I am still on valium, and have only gotten sicker since.  I wish I knew about Lamitcal then.

 

I will keep my eye on this thread.  Keep us posted!

 

Be well and good luck,

 

Ramcon1

Ram,

          My concern with lamotrigine (Lamictal) is whether or not it allows for GABA repair and withdrawal recovery while dosing.

The drug may provide symptom relief, but not allow for healing.

If someone was on Lamictal for 9 months, followed by a very slow taper, might we see an insidious return of all original signs and symptoms? Or could it leave them with 9 months of undisturbed healing and significant strides in recovery?

I'm also concerned about weaker receptor saturation and possibly GABA downstreaming.

I'm talking to a bio-chemist right now about this and will report back.

FandF

My concern with lamotrigine (Lamictal) is whether or not it allows for GABA repair and withdrawal recovery while dosing.

 

The drug may provide symptom relief, but not allow for healing.

This is what I'm concerned about also..

My gut tells me it will not effect healing, if such a thing even really happens.  I think it would have a similar effect to a VERY low glutamate/aspartate/histamne diet nearly impossible to follow. It should lower the general pool of available glutamate.  From things I have read I think that the biggest mistake is thinking a patient needs 100-200 mg when 25-50 would do the trick

But I am an engineer, not a biochemist, and I am very interested to hear what a real pro has to say.

Ramcon1

My gut tells me it will not effect healing, if such a thing even really happens.  I think it would have a similar effect to a VERY low glutamate/aspartate/histamne diet nearly impossible to follow. It should lower the general pool of available glutamate.  From things I have read I think that the biggest mistake is thinking a patient needs 100-200 mg when 25-50 would do the trick

 

But I am an engineer, not a biochemist, and I am very interested to hear what a real pro has to say.

 

Ramcon1

The problem is that you start to tolerate it pretty quickly, thats why they lift it up to 100-400mg. I'm now taking 25mg twice a day and soon start taking 50mg in the morning. I'm driving it in really slow so I can stop at when I feel good and not over do it.

Alesii,

Are you certain you are in "mania?" and have you ever had a manic episode before Lamitcal?

I ask this because mania is one of the things Lamitcal is SUPPOSED to prevent.  Although you would hardly be the first person to have a drug do the opposite of what it is supposed to do (I feel like CRAP on AD's) BUT, is it possible you just feel GOOD because you do not feel bad, and your brain is turning that goodness into some hypo-mania?

Just a thought.  Not only is it against BB policy to give medical advice, and even if I were a doc, which I am not, I could hardly tell over the internet, but I will give you some "safe" medical advice.  If the Lamitcal was prescribed by a psychiatrist, the psychiatrist SHOULD be able to tell you if it is giving you mania when s/he sees you.

I hope you cam see him/her soon.

Be well and good luck,

Ramcon1

Alesii,

 

Are you certain you are in "mania?" and have you ever had a manic episode before Lamitcal?

 

I ask this because mania is one of the things Lamitcal is SUPPOSED to prevent.  Although you would hardly be the first person to have a drug do the opposite of what it is supposed to do (I feel like CRAP on AD's) BUT, is it possible you just feel GOOD because you do not feel bad, and your brain is turning that goodness into some hypo-mania?

 

Just a thought.  Not only is it against BB policy to give medical advice, and even if I were a doc, which I am not, I could hardly tell over the internet, but I will give you some "safe" medical advice.  If the Lamitcal was prescribed by a psychiatrist, the psychiatrist SHOULD be able to tell you if it is giving you mania when s/he sees you.

 

I hope you cam see him/her soon.

 

Be well and good luck,

 

Ramcon1

Im 90% certain this is mania, I wwnt on spending spree and have had alots of impulses which I act on and afterwards realize what happened.

Lamictal actually is prescribed for bipolar depression, not mania. And for me it was prescribed solely on depression.

Edit. Not feeling so great either, but not half as bad as I was.

Are you trading one drug for another?  I'd rather be off of all mind altering medications of possible. .

That wasn't my intention. I used to be on lamictal and quit it due to memory related side effects. Now, as I remembered it reduces glutamate production I thought that I'd give it a spin, but just for some time. I don't know tho, I'm still unsure about how I feel and why. Are these mental fuckups in my head symptoms of benzo w/d or BPD..

Are you trading one drug for another?  I'd rather be off of all mind altering medications of possible. .

 

That wasn't my intention. I used to be on lamictal and quit it due to memory related side effects. Now, as I remembered it reduces glutamate production I thought that I'd give it a spin, but just for some time. I don't know tho, I'm still unsure about how I feel and why. Are these mental fuckups in my head symptoms of benzo w/d or BPD..

You may try asking your psychiatrist about the potential for glutamate receptor up-regulation. If they aren't being fed properly, the brain may increase receptor sensitivity.

Fault,

If you dig on Lamotrigine and LTP-Glu, recent research says it does not happen, at least in rodents,  Now after years of use in humans?  Who knows?

Ramcon1

Becks and all,

Mice off benzos, definitely glutamate receptor up tick.  Tons of studies.  Mice and rats off Lamitcal, no up tick, but remember, the studies are not that long, I cannot find) a human a long term human trial.  Just statements that withdrawal is "rare."  In other words, I am not giving anyone medical advice stating "oh you'll be fine on Lamitcal," because I research the crap out of everything and it bites me in the butt every time, so caveat emptor.

This article says it best:

https://www.verywell.com/lamictal-withdrawal-symptoms-380259

Clinical trials say withdrawal is unlikely, but remember, supposedly a properly tapered benzo w/d should be mildly unpleasant for a few months ;-)

I am still thinking about it and well get at least 3 medical professional opinions to post.

Be well and good luck,

ramcon1

Yes, but all of this - as far as we're concerned - is within the shadow of BWS.

Unless qualified, these studies do not take into consideration all factors and variables associated with the BWS stricken adult/patient. They are generic trials, performed in vivo. Our CNS is hypersensitive to all things, so nonspecific and blanket research may not necessarily apply. Plus, we're talking about lamotrigine as a possible aid with SXS; and/or to spur the healing process.

I don't have any problem with rodent studies (except for the ethical one), as they present with physiology comparable to ours.

The brain puts a very high priority on pathways responsible for neural activation, like glutamate. Chronic benzo dosing has conditioned the brain to increase glutamate levels via up-regulation, neuro-genesis, increased sensitivity...whatever  . So, I would think that even pre-synaptic blockade of glutamate transmission would further increase receptor sensitivity.

Since anecdotes and testimonials make-up the majority of my sources (since there is nothing or no one else available), I can't help but think I would have heard about lamotrigine (Lamictal) by now...