Relationship between attentional bias and psychological craving in methamphetamine use disorder

Methamphetamine addiction has no FDA-approved medication. That is a sentence with real weight — opioid use disorder has buprenorphine, methadone, and naltrexone. Alcohol use disorder has naltrexone, acamprosate, and disulfiram. Stimulant use disorder has nothing with a label, after decades of trials that found promising candidates that failed to replicate or produced unacceptable side effects in high-risk populations. For the roughly 1.6 million Americans with methamphetamine use disorder, the treatment menu is behavioral therapy and hope.

A phase trial currently enrolling for dual-target Transcranial Magnetic Stimulation changes the frame in a significant way. The approach uses TMS — a non-invasive technique that applies magnetic pulses through the skull to stimulate specific brain regions — to target two circuits simultaneously: the medial prefrontal cortex (MPFC) and the dorsolateral prefrontal cortex (DPFC). These are the regions most compromised by chronic methamphetamine use and most implicated in the relapse cycle.

The MPFC is involved in self-referential processing, emotional regulation, and the valuation signals that make a drug feel worth pursuing even when the person knows the consequences. The DPFC is the executive control center — the part of the brain that, in people without addiction, says “no” when the emotional system says “yes.” In people with methamphetamine use disorder, both regions show structural and functional damage from dopamine toxicity. The dopaminergic system — the brain’s reward and motivation architecture — gets downregulated after heavy stimulant exposure, producing the anhedonia that characterizes post-acute withdrawal and the cognitive dullness that makes early recovery so difficult.

Research published in 2026 in Frontiers in Psychology and PubMed Central has added precision to the understanding of how methamphetamine withdrawal affects cognition and craving. A key finding: there are two distinct forms of craving in stimulant addiction, not one. The first is withdrawal craving — a persistent background state of anhedonia and dopamine deficit that makes the world feel grey and flat and the drug feel like the only solution. The second is cue-induced craving — the acute, impulsive response to a stimulus associated with use. These two forms of craving originate in different neural circuits and likely require different interventions.

Dual-target TMS is designed to address both. By stimulating the MPFC and DPFC in combination, the trial hypothesis is that neuroplastic changes induced by the magnetic pulses can restore some executive control function and dampen the cue-reactivity that drives impulsive relapse, while separately affecting the anhedonia that sustains withdrawal craving. It’s ambitious, and the history of addiction neuroscience is full of ambitious hypotheses that collapsed in Phase 3 trials. But TMS has an established track record for treatment-resistant depression — the FDA cleared it in 2008, and deep TMS (which reaches further into cortical tissue) received clearance for OCD in 2018 — which gives the mechanism credibility that pure pharmacological speculation lacks.

For the stimulant addiction field, which has been waiting decades for a medication, a device-based intervention with an established safety profile is at minimum worth the trial. The enrolling phase will be worth watching.