I think it's scripted off-label, or a newer practice
Never heard of either but found this:
The authors examined the efficacy of methylphenidate (MPH) and lithium to treat attention-deficit/ hyperactivity disorder (ADHD) in adults, usinga randomized, double-blind, crossover design. Patients received 8 weeks of MPH treatment (up to 40 mg/day) and 8 weeks of lithium treatment (up to 1,200 mg/day), by random assignment. Independent evaluators blind to group assignment assessed response every 2 weeks and at the end of each phase. The primary outcome measure was the Conners’ Adult ADHD RatingScale sum score for the clusters of hyperactivity, impulsivity, and learningproblems. Secondary outcome measures were scores of irritability, overt aggression, antisocial behavior, anxiety, and depression, and scores on tests of verbal learningand sustained attention. In this preliminary study, lithium and MPH produced similar improvements on the primary outcome measure and on measures of irritability, aggressive outbursts, antisocial behavior, anxiety, and depression.
(The Journal of Neuropsychiatry and Clinical Neurosciences 2002; 14:289–295)
Interesting that it's of similar efficacy than MPH - the norepinephrinergics for example are to my knowledge inferior and used only to avoid misuse or for some individuals which react better to it. Atomoxetine also was found to be a weak NMDA antagonist and these for sure help with the symptoms when used in low dose, for me they are superior to any stimulant.
Last time I looked for it appeared that the mechanism of lithium is still not finally elucidated but
it has some interesting properties
- Decreasing
norepinephrine release and increasing
serotonin synthesis.
[59] (<- good. While NE is required too for energy & drive, it has mostly negative mental effects like anxiety, stress, aggression, fight & flight)
- It was also reported that
NMDA receptor blockage augments antidepressant-like effects of lithium in the mouse forced swimming test,
[72] indicating the possible involvement of NMDA receptor/NO signaling in the action of lithium in this animal model of
learned helplessness. (<- yeah!)
- May interact with
nitric oxide (NO) signalling pathway in the central nervous system. (<- don't understand it yet fully but some good drugs do this)
- Lithium both directly and indirectly inhibits GSK-3β which results in the activation of
mTOR. (<- Ketamine does this and might be how the sustained AD effect comes to work.)
- Stabilizes dopamine and GABA (<- don't like the first part but as they don't say antagonize but stabilize, against both mania and depression, it still sounds good)
-
Lithium treatment has been found to inhibit the enzyme
inositol monophosphatase involved in degrading inositol monophosphate (<- Inositol is antidepressive too)
Last but not least lithium prevents suicide in a statistically relevant degree
already in very low doses as found in drinking water in some places. This made me think that maybe we don't need full therapeutic levels to provide some relief, maybe protecting against neuronal over-excitation and possible synergia with other agents like nmda antagonists but read often that even in low therapeutic doses people feel nothing at all. This doesn't have to mean it's to be inactive though, I didn't feel anything from buprenorphine either but realized in retrospection that I wasn't nearly as depressive as usual.
Always when I read about Li, I get the impression that I need to give it a try. If it just wasn't so toxic (I don't get my water and food intake controlled, forgot about it all the time).
