Evidence-Based Reviews

‘Meth’ recovery: 3 steps to successful chronic management

Current Psychiatry. 2007 July;6(7):29-40

References

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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.

Clinical Point

The extent of brain damage is fairly dependably associated with the length and intensity of ‘meth’ abuse

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

Clinical Point

CM uses vouchers, privileges, or small amounts of money linked to healthy behaviors as incentives for negative urine tests

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).