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Evidence-Based Reviews

‘Meth’ recovery: 3 steps to successful chronic management

‘Moving the frontal lobe back to the front’ allows for improved executive functioning, decreased impulsivity, and increased motivation to remain drug-free

Vol. 6, No. 7 / July 2007

Clinicians could become discouraged when confronting methamphetamine-dependent patients’ wide-ranging psychiatric symptoms.

These patients often present with:

  • overlapping primary psychiatric syndromes and secondary substance abuse
  • complex histories fraught with psychological trauma, limited social supports, and court involvement.

Treatment can be successful, however, and patients can change their addictive behaviors with a chronic disease management approach that targets the drug’s cognitive sequelae and psychiatric effects. Medications show limited benefit (Box 1),1-8 but behavioral treatments—including cognitive behavioral therapy (CBT) and motivational incentives—have proven efficacy in treating methamphetamine addiction.

This article discusses how to counteract methamphetamine’s negative cognitive effects and enable patients to engage in psychosocial treatment. Our discussion is informed by an extensive literature search and clinical experience from treating patients in the Midwest—at the geographic heart of the “meth” epidemic.

CASE REPORT: Overwhelmed and suicidal

Ms. D, age 27, presents to the emergency department with anxiety, dysphoria, and a plan to commit suicide by overdose. She feels overwhelmed by her 4-hour-a-day customer service job—a prerequisite for staying at the halfway house where she has lived for 2 months. She has a 13-year history of polysubstance dependence and is under court order to complete chemical dependence treatment or go to jail.

Box 1

Medications for ‘meth’ dependence? Little empiric support

No medications are FDA-approved for treating methamphetamine dependence, and evidence supporting medication use in methamphetamine dependence is extremely limited. Research efforts are aimed at finding medications that might be neuroprotective, decrease craving, block reinforcement mechanisms, or affect other factors behind methamphetamine addiction and relapse.1 Most trials have been conducted in animal models or controlled laboratory evaluations of drug effects on methamphetamine-induced states.

Bupropion has shown slight treatment efficacy, possibly by decreasing neuronal damage and blocking reinforcement.2-4 Modafinil5 and baclofen6 may have potential, but evidence is lacking.

Some results have been unexpectedly negative. Sertraline might be contraindicated in methamphetamine dependence treatment, according to results of a randomized, placebo-controlled trial7 of sertraline and contingency management (Table 1). In a human laboratory study,8 topiramate accentuated—rather than diminished—subjective response to methamphetamine (Table 2).

Methamphetamine has been Ms. D’s primary drug of abuse for 5 years, with some intervals of treatment and sobriety. She has not used methamphetamine in 3 months, after a severe relapse when she used methamphetamine daily for 6 months.

Ms. D began using drugs at age 14 and has 3 convictions for driving under the influence of alcohol. An average student, she dropped out of high school but obtained a GED certificate. She first had psychiatric contact at age 16 and has been diagnosed at various times with attention deficit/hyperactivity disorder, bipolar disorder, and anxiety disorder. She also has been violently sexually assaulted while engaging in prostitution to support her drug habit.

Ms. D has been hospitalized multiple times—voluntarily and involuntarily—in dual diagnosis treatment centers. Her 5-year-old son no longer lives with her, and she has limited social supports beyond her parents, who live in a neighboring state.

Table 1

Antidepressant trials for treating methamphetamine dependence






Safety of bupropion with MAP


Reduced subjective effects and cue-induced craving

Clinical trial

Trend toward reduced MAP use compared with placebo


Clinical trial

Sertraline-treated subjects showed higher use of MAP compared with those receiving placebo and were less likely to complete treatment

MAP: methamphetamine

3-step approach

For patients such as Ms. D, clinical evidence supports a 3-step approach to treating methamphetamine dependence:

  • step 1: institute acute management and stabilization
  • step 2: eliminate or decrease methamphetamine use to “move the frontal lobe back to the front”
  • step 3: identify and target psychiatric and psychosocial comorbidities.

We discussed step 1 and the methamphetamine epidemic in the November 2006 Current Psychiatry.9 For Ms. D, step 1 means inpatient psychiatric care to protect her from suicidal intent and manage dysphoria and anxiety. In step 2, we aim to:

  • help her eliminate or decrease methamphetamine use to allow neuronal systems to recover
  • target maladaptive behaviors that hinder sobriety while providing motivational incentives to help her maintain a methamphetamine-free life.

Improved executive functioning, a frontal lobe task, becomes possible as the brain recovers from methamphetamine’s effects. Patients then are able to use healthier coping strategies to live drug-free. We call this step “moving the frontal lobe back to the front” because its goal is to restore the normal relationship between the frontal lobe and limbic system.

How ‘meth’ affects cognition

Methamphetamine use has been associated with cognitive dysfunction at initial abstinence and even years later in some patients.10 Ms. D’s cognitive limitations in a fast-paced customer service job—even though hours are limited—lead to anxiety, dysphoria, and loss of self-esteem when she can’t manage patrons’ requests.

Methamphetamine has profound acute and chronic effects on the sympathetic nervous system, and dopaminergic, serotonergic, and noradrenergic neuronal networks. Most evidence of chronic neuronal effects comes from animal research and reflects toxic damage to dopaminergic and serotonergic neuronal systems. Postmortem human studies of direct neurotoxicity from chronic methamphetamine exposure show:

  • decreased dopamine and tyrosine hydroxylase levels
  • reduced concentrations of dopamine transporters.11

Methamphetamine selectively affects dopamine in the nigrostriatal system, causing substantial dopamine depletion in the ventral tegmental reward system but relatively sparing motor regions. This may explain the lack of parkinsonism with methamphetamine dependence.12 In a study comparing serotonergic system damage caused by methamphetamine or 3,4-methylenedioxymethamphetamine (MDMA [“Ecstasy”]),13 methamphetamine had greater toxicity in the forebrain, including the septum, anterior cingulate, caudate nucleus, and nucleus accumbens.

In chronic methamphetamine abusers, functional magnetic resonance imaging, proton magnetic resonance spectroscopy, and positron emission tomography show:

  • changes in neurotransmitter, protein, brain metabolism, and transporter levels
  • damage in multiple brain areas including the frontal region, basal ganglia, grey matter, corpus callosum, and striatum; smaller hippocampi; and cerebral vasculature changes.14-16

Imaging studies typically have enrolled abstinent users, which emphasizes methamphetamine’s long-lasting effects. For practical purposes, the extent of brain damage is fairly dependably associated with the length and intensity of methamphetamine abuse. Because these changes may last for years and can be permanent,17 how does this play out clinically?

CASE CONTINUED: Does she understand?

After Ms. D is stabilized, her case manager expresses concern about her ability to follow through with treatment planning. He says, “I just don’t think she understands some of the things we discuss.” She then is referred for neuropsychological testing, which shows clear cognitive impairment. Specifically, she has a slowed rate of thinking, general cognitive ineficiency, deficits in learning and memory retention, and mild impulsivity.

Patients with a history of extensive methamphetamine abuse are ruled by the limbic system and may have higher cortical damage that complicates initiating, maintaining, and fully participating in treatment. Patients’ deficits in memory, executive functioning, attention, and cognitive speed may require you to simplify, repeat, and otherwise modify your treatment plan. You will need to provide clear instructions and consistent support—individually and psychosocially—and to recognize and reinforce patients’ treatment gains.

Even before using methamphetamine, patients may have had academic problems or learning disabilities that will compromise their ability to participate in treatment. Infection with HIV, syphilis, or hepatitis C can further hamper cognitive function.18

Screen methamphetamine abusers—particularly those such as Ms. D with a history of high-risk behavior—for sexually transmitted diseases. Also provide care address to common medical complications of methamphetamine abuse, including cardiac damage, dental disease, and skin lesions. Centers for Disease Control and Prevention guidelines recommend vaccinating methamphetamine-abusing patients against hepatitis A and B viruses (see Related Resources).

What treatments are effective?

Medications. Evidence is extremely limited, and no medications are approved to treat methamphetamine-addicted patients. Bupropion has shown some efficacy (Table 1),2-4,7 but other drugs such as sertraline and topiramate may aggravate rather than diminish methamphetamine dependence (Table 2).5,6,8,19

Behavioral treatments supply the evidence basis for methamphetamine dependence treatment. Cognitive behavioral therapy (CBT),20 contingency management (CM),21,22 and a manualized structured treatment—the Matrix Model23—all have proven efficacy.

CBT involves functional analysis and skills training. Patients are guided through analyzing their drug use and associated cognitions, emotions, and expectations and in identifying situations that trigger methamphetamine use or relapse. Skills training involves identifying, reinforcing, and practicing coping skills to help the patient avoid drug use and reinforce the ability to refuse use.

CM is based on operant conditioning—the use of consequences to modify behavior. It involves establishing a “contingent” relationship between a desired behavior/outcome (such as methamphetamine-free urinalysis) and delivering a positive reinforcing event to promote abstinence:

  • Vouchers, privileges, or small amounts of money linked to healthy behaviors serve as incentives for negative urine testing.
  • Rewards increase as periods of confirmed abstinence lengthen and are reset to smaller rewards if relapse occurs.

The precise reward structure that provides optimal treatment value is under study.24

CM does not require extensive staff training and has been described as relatively simple to implement. CM also has been used successfully in urban gay and bisexual men with methamphetamine dependence (Box 2).18,25-29

Although CM’s efficacy is well-supported by clinical trials, we have encountered some resistance to the idea of “paying individuals to not use drugs” when training medical students, allied health staff, and residents. The National Institute on Drug Abuse (NIDA) supports the use of motivational incentives in treating substance abuse and offers support materials, resources, and training on this approach (see Related Resources).

Multiple studies show that CBT and CM are equally effective for treating chronic methamphetamine abuse at a 1-year follow-up, although CM may be more effective than CBT for acute treatment.

The Matrix model is a 4-month intensive, manualized treatment program that uses CBT, education on drug effects, positive reinforcement for intended behavioral change, and a 12-step approach.

Methamphetamine dependence outcomes based on the Matrix treatment model were compared with community treatment as usual in a project sponsored by The Center for Substance Abuse Treatment of the Substance Abuse and Mental Health Services Administration, U.S. Department of Health and Human Services.30 End-point outcomes were similar, but the Matrix treatment was more effective in early treatment, including decreased urinalyses positive for methamphetamine and increased abstinence.

Box 2

Methamphetamine abuse increases risk of HIV infection

Methamphetamine use is estimated to be 5 to 10 times more prevalent in U.S. urban gay and bisexual groups than in the general population25 and likely is contributing to rising human immunodeficiency virus (HIV) infection rates in men having sex with men (MSM).

Used to enhance sexual performance, libido, and mood, methamphetamine is associated with increased rates of unprotected anal sex and multiple partners in MSM.26 An HIV infection rate of 61% was reported in methamphetamine-dependent MSM seeking treatment in a Los Angeles clinical trial.27 Methamphetamine also results in high-risk sexual practices and multiple partners among heterosexual men and women.28

Although seroconverted men report using methamphetamine to alleviate HIV-associated depression, the combination of HIV infection and methamphetamine use may have powerful negative effects. Methamphetamine use is associated with HIV treatment nonadherence and also may suppress immune function.29 Cognitive impairments associated with HIV and methamphetamine use are additive and are further exacerbated by hepatitis C infection.18

Recommendation. Screen for methamphetamine use in MSM populations, and educate these patients about risks associated with methamphetamine use. In all patient groups who report using methamphetamine, provide counseling on high-risk sexual behavior, screen for sexually transmitted diseases, and ensure that patients are vaccinated against hepatitis A and B infection (see Related Resources). Most important, refer for medical treatment when indicated.

Recommendations. Select a psychosocial treatment approach with your patient’s strengths, social setting, and community resources in mind. Twelve-step approaches may play an important role.

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