My doctor prescribed gabapentin to help with sleep difficulties about a month after my concussion. After my first dose of only 300 mg, I woke up feeling worse than any time I've ever been intoxicated on alcohol. I was stumbling, I was dizzy, and my tongue was not working right. I had to stay home from work, obviously. Eventually, I felt better. I told my doctor how I reacted, and he thought it was odd, as some people take more than that dose during the day.

After a few weeks, he wanted me to try it again. I was worried about possible tardive dyskinesia, but he told me it shouldn't happen. He wanted me to pour out about 2/3 of the capsule and try it again before bedtime. Reluctantly, I did. I had nearly as strong of a reaction the 2nd time, but this time, the tongue reaction stayed. That was about a year ago. It is not noticeable to everyone else, but when I am extra tired or stressed, I have a bit of a lisp because my tongue is affected. I have to work extra hard to speak normally.

I was not someone who was med-sensitive before my concussion. But after that, and a rather strong reaction to a general anesthetic for an out-patient surgery after my concussion, I am very wary of trying new meds. What I'm finding out is that very few studies are done on how common meds affect persons with concussion or other acquired brain injury.

On top of that, a couple of months later, I saw a rather sensationalist-looking headline about neurontin (gabapentin) and Lyrica (related to neurontin) being a 'death sentence' for new synapses. Not something I want post-TBI! I followed the trail to the original study, and basically, yes, that's what it's saying. That's a good thing for preventing formation of synapses related to epilepsy (gabapentin is an anti-epileptic). Not a good thing elsewhere, IMO. I just don't want to take any chances.

I tried to post the links to the study and another article on gabapentin and presynaptic plasticity, but my post count isn't high enough. They are free on PubMed, so here are the titles:

Gabapentin receptor alpha2delta-1 is a neuronal thrombospondin receptor responsible for excitatory CNS synaptogenesis. Cell. 2009 Oct 16;139(2):380-92

Astrocyte-derived thrombospondins mediate the development of hippocampal presynaptic plasticity in vitro. J Neurosci. 2012 Sep 19;32(38)

I wish you responded earlier with this information. Im currently at 1200 mg/day. I'm looking to taper down. Can anyone help me? I'm afraid of seizures.

I've been on 600 mgs of gabapentin for 14 years. Was at 1200 mgs for the first few. I read the literature. The negatives are not at bad as they sound. First, they were only observed in rats. Second, the reduction in synapse genesis was just a reduction, not a stoppage. Third, the vast majority of synapse genesis happens in the first 5 years of life. There is very little happening in adults.

You will likely suffer much greater damage from seizures than from a reduced synapse genesis.

*administrative edit* There have been similar postings about SSRI's and just about every other med. There are negatives about Tylenol/acetaminophen, one of the most trusted meds on the planet. .