The brain damage left behind after long-term cocaine use can apparently tell us quite a bit about how well a cocaine addict will do in addiction treatment – as long as we assess the right kind of damage.
Different kinds of brain matter
I’ve talked before about the fact that use of cocaine, and other drugs, can bring about long-term changes in the brain that sometimes include the actual destruction of neural pathways. What you may not know is that brain matter consists of several different components including the cell bodies of neurons (known as gray matter) and the tracts of axons that transmit messages across the brain (known as white matter). There are other parts as well, but those are the two important ones to know for this article.
Gray matter is important because brain transmission isn’t possible without a cell body, which is its operations center. But white matter is equally important because without it, the messages don’t get anywhere. It’s like having a telephone without a communication network – The phone can work perfectly and no one will ever hear you speak.
Until recently, it’s been pretty hard to measure the structure of white matter because it consists of very thin bands that twist and turn throughout the brain. But recent advancements in fMRI imaging and analysis have allowed us to look at it by measuring the direction in which water molecules flow through white matter. It’s called DTI (Diffusion Tensor Imaging) and it’s pretty complicated, but all you need to know is that it lets us know a lot about the integrity of axons in the brain.
White matter and cocaine
Use of cocaine has already been shown to cause damage to brain white matter. A recent study conducted at Yale examined whether the degree of damage can tell us anything about how well people will do in addiction treatment. Researchers took 16 participants and gave them a host of tests as well as some brain scans before sending them off to an 8 week treatment program. The addiction treatment utilized was outpatient and provided different individuals with different combinations of CBT, medication (antabuse), individual, and group therapy. At the end of treatment, the number of clean urine tests (out of 56 total tests) was used as a measure of treatment success. The more clean urines, the better, something I think we need to adopt overall instead of the all-or-nothing view that abstinence is the only form of improvement.
The bottom line: Using three different measures, the researchers found that individuals with more damaged white matter provided less clean urines throughout the addiction-treatment period. Another important fact – the damages areas that were found to be associated with treatment success were found all over the brain. Interestingly, brain damage wasn’t associated with the length of drug use, but it may have been associated with the extent of use (in terms of years and amount used), something the researchers didn’t report on.
Brain matter and addiction treatment outcomes
One day, we’ll have a battery of tests that will let us tailor treatment more effectively towards specific addicts. Genetics, brains scans, and more, will be able to tell us where an addict is especially weak so that we can focus on those areas first. Some may need specific help with impulsivity and weakened learning systems whereas others may be better off with treatment that addresses past trauma and an oversensitive stress response system.
As this research shows, brain scans can offer us a glimpse into the aspects of an addict’s brain that have been compromised. But we’re not there yet – right now, all we know is that certain genes, brain function patters, and experiences, are associated with a greater risk for addictive behavior or a lower chance of recovery. Getting better at more specifically tailoring treatment is still a little farther than we’d like.
Jiansong Xu, Elise E DeVito, Patrick D Worhunsky, Kathleen M Carroll, Bruce J Rounsaville & Marc N Potenza (2010). White Matter Integrity is Associated with Treatment Outcome Measures in Cocaine Dependence, Neuropsychopharmacology 35, 1541–1549.