excessive N2O-Nitrous. B12. My axonal neuropathy & reverse Lhermitte sign symptoms

[Bitstorm]

excessive N2O-Nitrous. B12. My axonal neuropathy & reverse Lhermitte sign symptoms

I have been excessive in my N2O use.
Just realized today I'm experiencing serious B12 deficiency. I fucked up and was taking a complex with a miniscule B12 (10mcg not 1000mcg)

I have electric pins and needles and have been lethargic, cognitively impaired, weak, slow all for a couple weeks without realising... i.e. I had a fever and blamed that.
Electric like body tingles were/are like having the flu, discomfort, but persistant and fuzzy... with weakness.
I have been doing some deeper reading to studies and articles I'd glanced at prior. Shit. The dangers of B12 deficiency are real and potentially permanent if untreated too long.
I did not give this the respect I should have. Looking for support.

I have got the right B12 and started taking today. I have handed my machine and chargers to a trusted friend and talked with my partner honestly.

I have read that sometime Methionine is also used to treat this situation.

If anyone else has been through serious B12 deficiency or knows of it I would love to know how big the risk is from 2 weeks of solid symptoms.
I am also worried about the breakdown of DNA expression and the damage to the spinal cord.

Sorry for this mega dump of info below is what I've collated today that seems worthwhile knowing. I hope it can help someone else in the same situation (or hopefully before!!)

btw I was doing between 50 a day up to 200 or 300 some days. with multi day breaks, but fairly consistently for the last 6 weeks. It was useful for creative work but waaay too much.
Advice appreciated (not judgement. I've stopped!)




VITAMIN B12 TABLETS 1000MCG
Also sometimes treated with Methionine
Methionine is used to prevent liver damage in acetaminophen (Tylenol) poisoning. It is also used for increasing the acidity of urine, treating liver disorders, and improving wound healing. Other uses include treating depression, alcoholism, allergies, asthma, copper poisoning, radiation side effects, schizophrenia, drug withdrawal, and Parkinson's disease.


*** Symptoms of vitamin B12 deficiency include:
cognitive impairment
gait abnormalities (abnormal walking, part of a standard neurological examination)
irritability
jaundice (yellowing of the skin or eyes, often seen in people with liver diseases)
peripheral neuropathy (nerve damage or malfunctioning nerves)
weakness

Controlled trials have shown that oral supplementation of 1000-2000 microg/day of vitamin B12 is equally effective in raising serum vitamin B12 levels as a standard parenteral dosing schedule

showing that the minimal effective oral dose is 647-1032 microg/day. It is recommended that patients with vitamin B12 deficiency be prescribed 1000 microg/day vitamin B12 orally

he response of the patient with vitamin B12 deficiency anemia to treatment is usually rapid, with reticulocytosis occurring within 2 - 5 days, and the hematocrit normalizing within weeks.10 Treatment with cobalamin effectively halts progression of the deficiency process but might not fully reverse more advanced neurologic effects.39,42


Vitamin B12 is considered safe, even at levels much higher than the recommended dose. It has not been shown to be toxic or cause cancer, birth defects, or mutations.10,75 Be aware, however, that patients who have a vitamin B12 deficiency with associated megaloblastic anemia might experience hypokalemia and fluid overload early in treatment due to increased erythropoiesis, cellular uptake of potassium, and increased blood volume. 76,77

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

SYMPTOMS OF B12 DEFICIAENCY
Lhermitte sign: Sudden transient electric-like shocks extending down the spine triggered by flexing the head forward. Due to a disorder such as compression of the cervical spine (the portion of the spinal cord within the neck).

Shocks radiating up the spine are sometimes referred to a reverse Lhermitte sign.

The causes of Lhermitte sign include
and subacute combined degeneration (caused by vitamin B12 deficiency).
http://www.medicinenet.com/script/main/art.asp?articlekey=16049

***** Study ***

A 23-year-old patient developed diffuse paresthesias and sensory loss. He had mildly reduced serum vitamin B 12 concentration with unusually high levels of methylmalonic acid (MMA) and homocysteine and no evidence of B 12 malabsorption

Following parenteral B12 administration, his neurological deficit promptly resolved and B12
and MMA levels normalized, but elevated levels of homocysteine persisted. One year later,
he admitted to inhaling nitrous oxide (N2O). After
halting N2 O abuse his homocysteine level normalized

 The patient was prescribed intramuscular B 12 injec- tions with a 1000 μg dose daily for 5 days and then 1000 μg every 3 to 4 weeks. His symptoms com pletely resolved within a few weeks after initiation of B 12 sup- plementation and his neurological examination 8 weeks later was normal. His B

His B 12 and MMA levels nor- malized within 2 months, but very high homocysteine levels persisted and unexpectedly rose to 164 μmol/l (10 times upper range of normal). The patient re- mained asymptomatic with intramuscular (IM) B 12 treatment for a number of months, but subsequently he admitted inhaling, daily, large amounts of N 2 O from cartridges used as propellants for decoration of baked goods. For several months before his symptoms developed he inhaled N 2 O from between 24 to 60 car- tridges per day, and on some weekends he would ex- pend up to 240 cartridges. He complied with advice to halt N 2 O abuse and his homocysteine level was nor- mal on a follow-up visit 4 weeks later.

****Methylmalonic acid is a compound that reacts with vitamin B12 to produce coenzyme A (CoA). Coenzyme A is essential to normal cellular function. When vitamin B12 deficiencies occur, MMA levels increase. Measurement of MMA through the MMA test can provide your doctor with information about an existing vitamin B12 deficiency, especially if the B12 deficiency is mild or just beginning.****


***Elevated levels of homocysteine are associated with heart attack, stroke, andblood clots. If a person develops any of these diseases and does not have increased risk factors such as smoking, high blood pressure, high cholesterol, or diabetes, then the physician often looks for more unusual causes and risks, including checking homocysteine levels in the blood.***


****Elevated homocysteine levels in the body do not cause any symptoms.
Elevated homocysteine levels affect the interior lining of blood vessels in the body, increasing the risk ofatherosclerosis or narrowing of blood vessels. This can result in early heart attack and stroke.
There is a relationship between the levels of homocysteine in the body and the size of the carotid arteries that supply the brain with blood; the higher homocysteine level, the narrower or more stenosed the carotid artery.
The risk of deep vein thrombosis andpulmonary embolism may also be linked to elevated homocysteine levels in the body.
There may be a relationship between elevated homocysteine levels and broken bones, especially in the elderly.
Alzheimer's disease and other types ofdementia may be more frequently seen in patients with increased homocysteine in the blood.



Megaloblastic anemia (or megaloblastic anaemia) is an anemia (of macrocytic classification) that results from inhibition of DNA synthesis during red blood cell production.[1] When DNA synthesis is impaired, the cell cycle cannot progress from the G2 growth stage to the mitosis (M) stage. This leads to continuing cell growth without division, which presents as macrocytosis. Megaloblastic anemia has a rather slow onset, especially when compared to that of other anemias. The defect in red cell DNA synthesis is most often due to hypovitaminosis, specifically a deficiency of vitamin B12 and/or folic acid. Vitamin B12 deficiency alone will not cause the syndrome in the presence of sufficient folate, as the mechanism is loss of B12 dependent folate recycling, followed by folate-deficiency loss of nucleic acid synthesis (specifically thymine), leading to defects in DNA synthesis. Folic acid supplementation in the absence of vitamin B12 prevents this type of anemia (although other vitamin B12-specific pathologies may be present)

axonal lesions on peripheral nerves?

axonal
pertaining to or arising from an axon.
neuropathy
/neu·rop·a·thy/ (ndbobr-rop´ah-the) a functional disturbance or pathological change in the peripheral nervous system, sometimes limited to noninflammatory lesions as opposed to those of neuritis.


FOLATE
Consequently, folate deficiency does not seem responsible for a secondary B12 malabsorption unless another etiological factor is present, such as alcohol or ileopathy.
Folic Acid, B12 and Iron[edit]
There is a complex interaction between folic acid, vitamin B12 and iron. A deficiency of one may be "masked" by excess of another so the three must always be in balance.
"Large amounts of folic acid can mask the damaging effects of vitamin B12 deficiency by correcting the megaloblastic anemia caused by vitamin B12 deficiency without correcting the neurological damage that also occurs", there are also indications that "high serum folate levels might not only mask vitamin B12 deficiency, but could also exacerbate the anemia and worsen the cognitive symptoms associated with vitamin B12 deficiency"
Limiting folic acid will not counter the irrevocable neurological damage that is caused by untreated B12 deficiency.[citation needed]



Signs and symptoms https://en.wikipedia.org/wiki/Vitamin_B12_deficiency
Vitamin B12 deficiency can lead to vitamin B12 deficiency anemia and neurologic dysfunction. A mild deficiency may not cause any discernible symptoms, but as the deficiency becomes more significant symptoms of anemia may result, such as weakness, fatigue, light-headedness, rapid heartbeat, rapid breathing and pale color to the skin. It may also cause easy bruising or bleeding, including bleeding gums. GI side effects including sore tongue, stomach upset, weight loss, and diarrhea or constipation. If the deficiency is not corrected, nerve cell damage can result. If this happens, vitamin B12 deficiency may result in tingling or numbness to the fingers and toes, difficulty walking, mood changes, depression, memory loss, disorientation and, in severe cases, dementia.
The main syndrome of vitamin B12 deficiency is pernicious anemia. It is characterized by a triad of symptoms:
Anemia with bone marrow promegaloblastosis (megaloblastic anemia). This is due to the inhibition of DNA synthesis (specifically purines and thymidine)
Gastrointestinal symptoms.[specify] These are thought to be due to defective DNA synthesis inhibiting replication in a site with a high turnover of cells. This may also be due to the autoimmune attack on the parietal cells of the stomach in pernicious anemia. There is an association with GAVE syndrome (commonly called watermelon stomach) and pernicious anemia.[8]
Neurological symptoms: Sensory or motor deficiencies (absent reflexes, diminished vibration or soft touch sensation), subacute combined degeneration of spinal cord, seizures,[9][10][11][12] or even symptoms of dementia [13] and or other psychiatric symptoms may be present. The presence of peripheral sensory-motor symptoms or subacute combined degeneration of spinal cord strongly suggests the presence of a B12 deficiency instead of folate deficiency. Methylmalonic acid, if not properly handled by B12, remains in the myelin sheath, causing fragility. Dementia and depression have been associated with this deficiency as well, possibly from the under-production of methionine because of the inability to convert homocysteine into this product. Methionine is a necessary cofactor in the production of several neurotransmitters.
Each of those symptoms can occur either alone or along with others. The neurological complex, defined as myelosis funicularis, consists of the following symptoms:
Impaired perception of deep touch, pressure and vibration, loss of sense of touch, very annoying and persistent paresthesias
Ataxia of dorsal chord type
Decrease or loss of deep muscle-tendon reflexes
Pathological reflexes — Babinski, Rossolimo and others, also severe paresis
Vitamin B12 deficiency can cause severe and irreversible damage, especially to the brain and nervous system. These symptoms of neuronal damage may not reverse after correction of hematological abnormalities, and the chance of complete reversal decreases with the length of time the neurological symptoms have been present.
Vitamin B12 deficiency symptoms also include shortness of breath and increased pallor.




http://www.cdc.gov/ncbddd/b12/patients.html



Dr Ng said Auckland Hospital treated two heavy users last year. One had been inhaling daily for 20 years, using 50 bulbs a day in the six months before seeking help.

He told doctors it was called "nanging" because of the sound distortions heard after inhaling the drug.

The man had tingling in his hands and feet, unsteadiness in walking, constipation and urinary incontinence.

Both patients recovered after treatment with vitamin B12 injections and oral supplements of folate.
http://www.bluelight.org/vb/threads...s-risk-spinal-damage?highlight=B12+deficiency


He was unaware of the vitamin B12 risk, reflecting the survey finding that 63 per cent of users thought inhaling nitrous oxide was safe.



>>Nitrous oxide deactivates vitamin B12, which is vital for making the sheath that protects the spinal cord. A shortage of the vitamin, more likely in vegetarians, can lead to cord disease. >>

chemically, is this temporary or permanent?

I believe the deactivation is permeneant for the B-12 that it deactivates, however taking vitamin supplements with B-12 in them will replace this deactivated form...so yes, the 'deactivation' is permeneant, but just till you get more (like irreversible MAO-I's.)

..
There's B12 in a plethora of foods, albeit in miniscule amounts. Your body stores enough B12 for 3-5 years and will run out if it's not replenished at all


Nitrous oxide: Nitrous oxide inactivates the cobalamin form of vitamin B12 by oxidation. Symptoms of vitamin B12 deficiency, including sensory neuropathy, myelopathy, and encephalopathy, can occur within days or weeks of exposure to nitrous oxide anesthesia in people with subclinical vitamin B12 deficiency. Symptoms are treated with high doses of vitamin B12, but recovery can be slow and incomplete. People with normal vitamin B12 levels have sufficient vitamin B12 stores to make the effects of nitrous oxide insignificant, unless exposure is repeated and prolonged (such as recreational use). Vitamin B12 levels should be checked in people with risk factors for vitamin B12 deficiency prior to using nitrous oxide anesthesia. Chronic nitrous oxide B12 poisoning (usually from use of nitrous oxide as a recreational drug), however, may result in B12 functional deficiency even with normal measured blood levels of B12.[36]

 

[endotropic]

This seems serious, have you contacted a doctor yet? Have you stopped using the N2O?

 

[Bitstorm]

I have definitely stopped the N20!

I have not seen a doctor. Everything I read on N20 induced B12 deficiency says B12 injections at 1000mcg a day for a couple weeks. Oral supplementation has also been shown to be just as effective. As this is what I could get today most quickly this is what I have done (in fact mega doses of B12 have been shown to be perfectly safe so I've taken 4000mcg today.)

example:
Myeloneuropathy from Nitrous Oxide Abuse: Unusually High Methylmalonic Acid and Homocysteine Levels
https://www.wisconsinmedicalsociety.org/_WMS/publications/wmj/pdf/102/4/43.pdf

 

[Bitstorm]

Got to a doctor this morning.
This shit is scary. your anti bodies attack the sheath in your spine.
Shown toxicity completely separate from the B12 depletion issue!
https://www.ncbi.nlm.nih.gov/pubmed/25297001

Doc doesn't know anything about it. doesn't know whether further damage will present later. will do blood tests. my reactions in extremities seem to be fine.
I feel better this morning already after taking about 5000mcg total yesterday. 1000mcg a day for a couple weeks now, then once every week or two for a few months.

Hope I haven't done permanent nervous system sheath damage. I work with my body and need my reaction times.

I've used nitrous on and off for 10 years. I had no idea there was toxicity/damage issues that are completely separate from B12 stuff. I had no idea it was this dangerous.
I calculated it and I did around 8000 bulbs over the last 19 months.
Lesson learned. That's enough NO2 for a lifetime.

scary that you can think yourself quite a knowledgeable and responsible drug user, and actually have no idea how close to the line your skating.

I hope this thread helps someone else sometime

 

[Bitstorm]

STUDY 

We describe a patient with a typical vitamin B12 deficiency syndrome after N2O abuse who recovered and then developed a severe lower motor neuron syndrome following vitamin B12 correction. This suggests N2O toxicity independent of functional vitamin B12 deficiency.

A 22-year-old man abused N2 O and presented with a dorsal column syndrome with low vitamin B12 and high homocysteine serum levels. He recovered with treatment but presented later with profound motor axonal degeneration and normal vitamin B12, homocysteine, and methlymalonic acid levels.
CONCLUSIONS:
This case illustrates that N2 O-associated severe motor neuropathy or neuronopathy can develop separately from typical vitamin B12 deficiency dorsal column myelopathy. This syndrome can present when functional measures of vitamin B12 deficiency have normalized.

http://www.ingentaconnect.com/conte...36a59386b667c4e75477e4324576b642738d1b89f86b2
http://onlinelibrary.wiley.com/doi/...ionid=2B07482F64197C4DB81CDD995528A480.f01t04


Abstract
Undifferentiated neurological presentations are not uncommon to the ED. Vitamin B (12) deficiency can lead to progressive demyelination and axonal lesions on the peripheral nerves and cervicothoracic spinal cord causing a peripheral neuropathy
http://onlinelibrary.wiley.com/doi/...ionid=2B07482F64197C4DB81CDD995528A480.f01t04

Mylenoneuropathy from nitrous oxide abuse: unusually high methylmalonic acid and homocysteine levels
https://www.wisconsinmedicalsociety.org/_WMS/publications/wmj/pdf/102/4/43.pdf


http://www.readcube.com/articles/10.1002/mus.24482#
ABSTRACT: Introduction: Nitrous oxide (N2O) toxicity cancause a sensory predominant myeloneuropathy identical to sub-acute combined degeneration caused by vitamin B12 defi-ciency. We describe a patient with a typical vitamin B12deficiency syndrome after N2O abuse who recovered and thendeveloped a severe lower motor neuron syndrome followingvitamin B12 correction. This suggests N2O toxicity independentof functional vitamin B12 deficiency. Methods: Electrophysiologi-cal, serological, and clinical evaluations were undertaken in theevaluation of this patient. Results: A 22-year-old man abusedN2O and presented with a dorsal column syndrome with lowvitamin B12 and high homocysteine serum levels. He recoveredwith treatment but presented later with profound motor axonaldegeneration and normal vitamin B12, homocysteine, andmethlymalonic acid levels. Conclusions: This case illustratesthat N2O-associated severe motor neuropathy or neuronopathycan develop separately from typical vitamin B12 deficiency dor-sal column myelopathy. This syndrome can present when func-tional measures of vitamin B12 deficiency have normalized.

ARTICLE:
The similarity of clinical manifes-tations of N2O toxicity and vitamin B12 deficiencyhas led to the generally held view that it is throughits effects on vitamin B12 that it exerts its toxicity.We present the case of young man who developeda typical vitamin B12 deficiency syndrome afterN2O abuse, but whose syndrome resolved with vita-min B12 treatment and then developed a severemotor neuropathy or neuronopathy, suggestingN2O toxicity occurred independently of functional vitamin B12 deficiency.

ASE REPORTA 22-year-old man was evaluated for 1 month ofprogressive gait instability with falls. The patientreported falling 2–3 times per day due to numb-ness in the feet, “buckling” at the knees, and thepresence of the Lhermitte symptom. He reportedinhalation of 20–30 canisters of N2O daily over thepreceding 2 months.

Hewas treated with vitamin B12, 1000 lg intramuscu-larly daily for 7 days, followed by 1,000 lg orallyweekly, thiamine, and a multivitamin daily.The patient’s sensory symptoms of numbness inthe feet and the Lhermitte symptom resolved.However, 3 weeks later (4 weeks since last N2Ouse) he developed progressive weakness in thelower extremities and a new Lhermitte symptom.

 

[Zeds(NCO2CH2CH3)2]

You don't have the manifested effects of megaloblastic anemia, but you need to stop whippet ingestion. The electric tingling parathesias are just there because you have been abusing for a while and nmda antagonists are notoriously good at partially blocking nerve impulses and neuropathic pain/feeling.

You missed that folate ingestion can make up for b12 deficiency and that your multivitamin contains much folate as well as your daily food intake. Also you aren't realizing that many of these diseases are genetically acquired and the nutritional forms of them are not present nowadays. In modern time our soft drinks, juices, Gatorade, sweet sodas and more are filled with multitudes of electrolytes and vitamins.

Please relax, you don't have cord atrophy you might have parathesias but unless you have marked loss of deep tendon reflexes then there Is no way you can treated for this. Just relax you are sober now, eat right and get a job.. Whippets are death to your functional life a dissociative regularly repeatable is enough to turn many into addicts but you must stop forever..
Zedz

 

[Bitstorm]

Nice one Zedz. Thanks for the reassurance. Much appreciated.
Don't worry I get it, I'm done with N2O.

 

[Bitchniggaz]

Someone very close to me has become very ill from long term nitrous abuse.
The person has quit all drug use since then.

We suspect that the gas has damaged the bodys ability to take upp b12.
Since super high doses of methyl cobalamin barely improves the symptoms.
Patches combined with sublingual tabs seems to improve it slightly.

The symptoms are mostly extreme lethargy and dizziness.
Gets worse with movement, which has led to alot of bedtime.
Also alot of issues with oxygen absorption.
Or a huge heavyness of breath.

This has absolutely destroyed the life of this person.

The doctors here are clueless, they have done some lung tests and other things that doesnt show anything wrong like serum b12.

We are going to a private lab to take tests for homocystein levels aswell as methylmalonate.
As high levels of these could be a marker of b12 absorption issues.

 

[Pomzazed]

B12 FORM is important

The active form of B12 in your body is hydroxycobalamin, but this form is quite unstable so it is not sold in vitamin supplement
Most commonly sold B12 is cyanocobalamin, this is actually only a precursor for body to turn it to active one by decyanation et al. This will take some time till you "get B12" that works, and the process has saturation too.
This is actually because in the B12 synth last step, it was purified by activated charcoal, where the Co center picks up CN from it and become stable form for selling.

There is also an active form of B12 sold, the Methylcobalamin; the body can use it directly but the price is more expensive; but i suggest it.

 

[Bitchniggaz]

Yes i know about various forms of b12.
I stated clearly that we used the methyl version.

Ive also ordered adenosylcobalamin which is another natural form that the body needs.
If there is a conversion issue then this may be a bog factor.

 

[sekio]

b12 has pretty high bioavailibility & conversion is usually mostly by gut bacteria iirc.

if all else fails you can get the dr's to try cyanokit, it's some absurd amount of hydroxycobalamin (5 grams?) administered IV... but this doesn't sound like b12 issues, more possibly some sort of physical lung damage from inhaling high pressure/cold gases.. even then that should show on cxr or a ct/mri scan of chest...

 

[Bitchniggaz]

I forgot to mention that there has been periods of the classic tingles and numbness in various parts.
We will do the tests this week and hopefully find something or at least be able to eliminate an alternative.

My personal guess is that its a combination of health issues including some b12 relaterad issue.
I work with health and finess so im trying to see every issue from a holistic point of view.

Also Im aware that these kind of issues can take time to improve if at all.
But this is a generally healthy person who just got into a bad whippet addition for awhile.
So hopefully it can be treated by supplements or injections of b12.

 

[elixir1]

Okay. So I admit I didn't read it all, but I too used to have an issue with doing LOTS of nitrous which did cause me to have extremely low B12...
A doctor should run a lab to get your level, you may need intramuscular injections of B12 (cyanocobalamin)... Usually RXd 1mL (1000mcg/mL solution) every two weeks.
BE is VERY poorly absorbed by the GI tract. Most primary docs can quickly test your level, and if it is extremely low (Yes, nitrous rapidly depletes B12) they may want to start you on injections.
I haven't done nitrous in over a decade, but I still give myself b12 injections as they hello with chronic fatigue, plus you're right in you can't take to much... You just pee it out.

I scanned down your post at the other stuff... I.e. long-term Neuro effects.
I believe it was thought at one time they caused Olney's lesions ("holes"in the brain) but this has since been unsupported. I THINK, NOT 100% POSITIVE...
But (both long-term nitrous use and B12 deficiency) does make you feel just really bad and VERY tired all the time...
But again, oral b12 may not be the best option to replenish it. I'd see a doc if at all possible.