Hey Kassi

[Guest guest]

Doing some research and this hit me as something you probably already

know. Are these waves that are known as " autism-like spikes " that are

often on the EEG reports of people with autism?

10. A number of different kinds of seizure like EEG activity have been

reported in patients with lithium induced encephalopathy. These

include " runs of periodic sharp waves ... triphasic complexes ...

widespread slow activity alternating with runs of periodic sharp

waves " ( and Kocen, 1988); " increased slow waves, sharp waves and

high voltage activity ... sudden appearance of high voltage paroxysmal

groups with sharp waves and spike wave like activity " (Itil et al.,

1971); " pseudo periodic discharges " (Prima Vera et al., 1989);

" increased theta and delta especially in frontal areas with triphasic

waves and sharp waves in frontal areas " (Broussolle et al., 1989). The

possibility that lithium induced seizure activity may contribute to

the encephalopathic syndrome observed in lithium neurotoxicity is

suggested by some observations on mental status changes in a series of

patients with non convulsive status epilepsy. (Lee, 1985).

http://psycprints.ecs.soton.ac.uk/archive/00000524/

Also, this study mentions inosital as a possible anti-convulsant. Know

anything about that? I've been wondering if Allie's brain is having

some abnomormal waves that might be getting her " stuck " in thoughts.

One thing I thought about is increasing magnesium baths, now I'm

thinking about boosting the inositol as well.

Another thing, this study also mentions acetylcholine. Reminded me of

www.megson.com study with urocholine. In the Megson study she states

the urocholine stimulates post-synaptic cell membranse via receptors

for acetylcholine. The first study I referenced states:

et al. (1990) found that lithium increased both intracellular

and extracellular evoked post synaptic potentials (EPSP) as measured

in the mid portion of the stratum radiatum of region CA1 of

hippocampus. While cholinergic agonists produced opposite

(decremental) effects on these same evoked potential measures, lithium

prevented the cholinergic effects ( et al., 1990). Excitatory

effects of cholinergic agonists in brain depend primarily on

inhibition of potassium currents in postsynaptic neurons (Krnjevic,

1993). Thus, the fact that lithium potentiates the epileptogenic

effects of cholinergic agonists may be explained by its presynaptic

effects.

Does this mean that urocholine produces a decremental effects on the

same evoked potentials that lithium increases? Doesn't that mean that

this finding that cholinergic agonists do the opposite of what Megson

found?

Please explain in English. Bottom line, will lithium supps help

Allie's brain function or send her into definite epileptic issues?

TIA,

Debi