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sodium valproate and lamotrigine may have bad effects autism be lethal epilepsy

Kayla55

Well-Known Member
VPA is well tolerated, and the most commonly occurring adverse reactions are gastrointestinal disturbances, this may be a bad cocktail mix for autism and epilepsy. May also aggrivate poor muscle tone in autism.

sodium valproate and lamotrigine (epilepsy drug)​

 
It could be with epilepsy connection to autism and poor muscle tone, could be gut microbes reacted to electrical impulses. Maybe more research required on epilepsy and how drugs work before able to say exactly what kind of effect autism has on this underlying medical condition.

I am Thumb guessing here but autism
The muscles are not as firm or tight as developmentally expected. Children with low muscle tone normally have delayed motor skills, difficulty with motor coordination and weakness in the muscles to name a few.
muscle tone is often seen in children
autism

My mom's old and has osteoporosis already so that was my initial outrage over her using epilum....it's aggravated medical condition not just side effect, maybe nothing to do with diabetes

Epilum is most favoured drug for epilepsy....how or why corrects electrical impulses in brain uunknown.just considered to eliminate symptoms

Consideringm utilization of VPA and LTG, healthcare providers should be aware of them as a possible cause of tremor. When necessary, an attempt of discontinuing the suspected drugs should be made to confirm the diagnosis, instead of symptomatic treatment, especially when the adverse event was severe and fatal.


VPA is well tolerated, and the most commonly occurring adverse reactions are gastrointestinal disturbances,

Although many patients will remain seizure free on the first or second drug, combinations are usually prescribed in those unresponsive to monotherapy.[2] Sodium valproate (VPA) is the most widely used antiepileptic drug worldwide, and lamotrigine (LTG) is a novel antiepileptic agent. A study shows that VPA-LTG comedication exhibits a favorable pharmacodynamic interaction in patients with refractory partial epilepsy.[3]
Disabling tremor induced by drugs was initially diagnosed based on the chronic worsening process, an exposure history of many drugs acting on the central nervous system, and the exclusion of known causes of secondary tremor by above clinical and laboratory evaluation. In treatment, LTG (100 mg qd) and amantadine (100 mg bid) were discontinued immediately; dosage of VPA was gradually reduced (sodium valproate sustained-release tablet: 1000 mg bid for 4 days, subsequently, 500 mg bid for 5 days) and was ceased after 9 days. In other words, within 9 days all of LTG, amantadine, and VPA were withdrawn. The degree of upper limbs tremor was not increased, but somewhat reduced. With that, remaining therapy was benzhexol for 2 mg tid, flupentixol, and melitracen (flupentixol 0.5 mg and melitracen 10 mg) for 1 piece, bid (8 am and noon). At follow-up examination 2.5 months after stopping above 3 drugs, his upper limbs tremor had apparently improved, and twitch of eyelids and facial region also improved except mouth. In addition, his mental state improved compared to 2.5 months ago, and he could work as a security guard according to his wife. There was no recurrence of the upper limbs tremor at 6 months follow-up.

3. Discussion​

In this case, we have reported an unusual patient with upper limbs resting-type tremor induced by VPA and LTG, which improved after discontinuation of the culprit drugs. This confirms the initial diagnosis of drug-induced tremor. This case is unusual in 2 regards: firstly, his tremor is disabling and not mild; secondly, this case is the first documented case of resting-type tremor which is different from postural and action tremor caused by LTG with VPA reported in 1993.[5]
Indeed, the patient had been treated initially with VPA and LTG due to epilepsy, approximately 1.5 years later, the patient developed restin
 

Ask people to share errata on their medication experience so that we can draw conclusions to better decide and do proper research into making this better. Even if you just input small but it can be vital​

I would need more than two hands to count the psych meds I’ve been given.​

There are enough that I don’t remember all of them; it started in the first grade. Some were just regular ADHD meds—which I needed—not psychotropic. As years passed, others were anti-anxiety SSRIs, and then antipsychotics; many well before I’d hit the end of middle school (these include Risperdal, Paxil, and Wellbutrin).

While I was not diagnosed autistic until I was 14 or 15, the logic under which these drugs were prescribed to me was the same as for those diagnosed autistic: The psychiatrists likely said the medications would manage my anxiety and my outbursts. (I now know the outbursts occurred from a trauma history, and having a hard time communicating.)

But the medications were like a merry-go-round. Some effectively sedated me, others made me uncontrollably irritable. Abilify is proving difficult to get off of, even though I’m experiencing the side effect moderate akathisia, which is “a movement disorder
 
The only medications known to increase the risk of ASD are used for epilepsy or as a muscle relaxer in anesthesia. For example, the anti-seizure drug valproate increases the risk of autism from 1.9% to 4.4%.
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