Off–label uses of Memantine (Namenda)


Memantine is a NMDA (N–methyl–D–aspartate) glutamate receptor antagonist which is, as one Portland psychiatrist summarized, “…good for any distressed neuron.”

For those who discuss the roles of kynurenine and brain–derived neurotrophic factor, and the various functions of astrocytes and glia in the brain all while eating breakfast, here are several clinical tidbits for you about memantine:

  1. First clinical tidbit is about major depression. Evidence is accumulating that glutamate plays a role in major depression. Patients with major depression – both during an acute depressive episode and during remission from a depressive episode – have elevated glutamate levels in at least some brain regions. The current hypothesis is that excessive glutamate action – especially extra–synaptic glutamate – is deleterious to neuronal function (i.e., excessive glutamate action in the brain is neurotoxic) and excessive glutamate action contributes to causing major depression (at least in some folks with major depression). It is especially noteworthy that N–methyl–D–aspartate (NMDA) glutamate receptor antagonist ketamine produces a profound antidepressant effect with almost immediate onset. So, too much glutamate activity in the brain is a bad thing.
  2. Second clinical tidbit: Experimental activation of the immune system with endotoxin (a cell–wall component of gram–negative bacteria) and chronic activation of the immune system during interferon–alpha treatment causes brain inflammation which then leads to microglial activation which can then interfere with excitatory amino acid metabolism leading to inappropriate glutamate receptor activation, which can lead to brain neurotoxicity. Microglia activated by excess inflammation in the brain, astroglial loss in the brain (which can occur in some folks with major depression), and inappropriate glutamate receptor activation in the brain can disrupt the body’s delicate balance of neuroprotective versus neurotoxic effects in the brain environment, tipping this delicate balance toward neurotoxicity. Astrocytes are responsible for taking up excess glutamate to protect neurons from neurotoxicity. This occurs through excitatory amino acid transporters. If astrocytes are decreased in number or inhibited (e.g., by microglia) from doing their job, then excessive glutamate accumulates extracellularly, leading to neurotoxicity (e.g., bad things such as multiple sclerosis). Among other things, memantine decreases endotoxin–induced activation of microglia, and thus decreases brain neurotoxicity. Again, too much glutamate activity in the brain is a bad thing, and memantine decreases glutamate activity in the brain.
  3. Third clinical tidbit. It has been hypothesized that glutamate dysregulation and excitotoxicity are crucial to the development of the cognitive disturbances that underline borderline personality disorder. As such, glutamate modulators such as memantine might become a treatment of borderline personality disorder. In a randomized controlled trial (RCT), Kulkarni examined the efficacy and tolerability of memantine compared with treatment as usual in patients with borderline personality disorder. According to intention-to-treat, latent growth curve analyses, a significant change in symptom severity was observed in the memantine group at memantine 20 mg/daily across time, compared with placebo (p = 0.02). No adverse effects were significantly more frequent among participants receiving active memantine than among those receiving placebo. Kulkarni’s conclusion: memantine at a 20-mg daily dose is a well tolerated drug that can improve borderline personality disorder symptomatology.

In more germane and generic terms: memantine blocks the N–methyl–D–aspartate (NMDA) glutamate receptors (located on neuron cell membranes in the brain and spinal cord) from being excessively stimulated/overwhelmed by excitatory glutamate neurotransmitter “bullies” which might be rioting in the neighborhoods of local neurons in various parts of the brain and spinal cord.

Here is some history on memantine: developed by Merz Pharmaceuticals in 1972, memantine has been marketed in Germany since 1983. Since then, memantine has been studied in a variety of neurological and psychiatric disorders. In 2000, Forest Pharmaceuticals became licensed by Merz for the manufacture of memantine in the United States. Memantine is approved by the FDA to allow the manufacturer to advertise that memantine is effective for the treatment of dementia associated with Alzheimer’s disease. Memantine has been prescribed by physicians “off–label” with varying degrees of success in such medical/psychiatric conditions as: attention–deficit/hyperactivity disorder; Tourette’s disorder; Huntington’s disease; obsessive compulsive disorder; Parkinson’s disease, Huntington’s disease; multiple sclerosis; lupus; epilepsy; migraine headaches; chronic neuropathic back pain; complex regional pain syndrome; bipolar disorder; recurring major depression; traumatic brain injury; “chemo brain;” alcohol craving; borderline personality disorder (as above); and in the treatment of post–stroke cognitive impairment.

Memantine  generic is available in 5 and 10 mg tablets. The time–release Namenda XR capsules are available in 7mg, 14mg, 21 mg and 28 mg capsules and is branded (i.e., more expensive). The generic tablets work well enough for my patients.

While there is published literature on the use of memantine in humans up to 20 mg daily; I have a small number of patients with migraines from Hell, chronic pain from multiple sclerosis, and/or back pain from hell who report that their best response to memantine has been at higher daily doses (i.e., 30-80 mg daily).

Memantine is usually well tolerated in the non–geriatric–aged population. As of 12/9/2021, I have prescribed memantine to at about 136 patients, and I have had prompt and profoundly positive treatment results in a sizable percentage of patients from 8 to 65 years of age, with memantine being most dramatically effective in my clinical population for the treatment of migraine headaches, chronic neuropathic pain, and Tourette’s disorder.

Memantine does not have any significant food interactions.  Memantine minimally inhibits P450 enzymes, so interactions with drugs metabolized by these enzymes are unlikely.

Memantine undergoes little metabolism and is predominately excreted unchanged in the urine. The elimination half–life of memantine is 60–80 hours. Protein binding is 45%.

There is no abuse/ chemical dependence potential with memantine.

There may be drug–drug interactions between memantine and the presence of any of the following: cigarettes/nicotine; amantadine, anticholinergics, barbiturates, cimetidine, dextromethorphan (i.e., Robitussin), hydrochlorothiazide (HCTZ), ketamine, L-dopa, neuroleptics (e.g., risperidone), ranitidine, and sodium bicarbonate.


☞ Start with memantine 5 mg at bedtime nightly for at least 5  nights. Then…

☞ If no obvious benefit (or side effects), increase the dose to 5 mg twice daily (morning and bedtime) for at least the next 5 days. Then…

☞ If no obvious benefit (or side effects), then take 5 mg in the morning and 10 mg at bedtime for at least the next 5 days. Then…

☞ If no obvious benefit (or side effects), then take 10 mg twice daily.

Dr. Mortimer should then meet with his patient again within the first month of starting memantine (Namenda) so that Dr. Mortimer can carefully and thoroughly assess my patient’s response to treatment. (If there is partial improvement and no side–effects with the memantine (Namenda), they can then discuss whether to increase the memantine dose above the FDA–approved maximum daily dose of 20 mg daily.

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