I came of age in the Ritalin generation, which meant that plenty of my classmates in elementary school went to the nurse’s office for their little dose of drug. At the time, I remember being jealous of these kids, who not only got to miss 10 minutes of instruction but got to have a real, genuine medical affliction. (I was one of those confused children who, for a brief period, thought it would be awesome to have braces and/or a big cast on my arm.)
In retrospect, I can appreciate the complexities of the ADHD debate. On the one hand, ADHD is a real syndrome, with identifiable neural correlates. For instance, in November 2007, a team of researchers from the National Institute of Mental Health and McGill University uncovered the specific deficits of the ADHD brain. The disorder turns out to be a developmental problem: the brains of kids with ADHD develop at a significantly slower pace than normal. This lag was most obvious in the prefrontal cortex, which is a brain area that’s crucial for things like directed attention and impulse control. (On average, their frontal lobes were three and a half years behind schedule.)
And yet, I often wonder about the medical treatments we’ve come to rely on for the treatment of ADHD. Ritalin (aka methylphenidate) is a potent, psychoactive drug. We prescribed it to millions of kids with little knowledge of the long-term consequences. While I know Ritalin can be effective – I’ve seen it perform wonders on my elementary school friends, not to mention all the undergraduates who juiced their attention with crushed pills – there are many uncertainties concerning its long-term application. A new PNAS paper by scientists at the National Institute for Drug Abuse (NIDA) makes this clear. I’m forced to clip from the press release, as the paper itself isn’t out yet:
Investigators funded by the National Institute on Drug Abuse (NIDA) have shown that the medication methylphenidate (Ritalin), which is commonly prescribed to treat attention-deficit hyperactivity disorder (ADHD), can cause physical changes in neurons in reward regions of mouse brains; in some cases, these effects overlapped with those of cocaine. Both methylphenidate and cocaine are in the class of drugs known as psychostimulants. While methylphenidate is widely prescribed, this study highlights the need for more research into its long-term effects on the brain. These research findings will be published February3 in Proceedings of the National Academy of Sciences.
“Studies to date suggest that prescribed use of methylphenidate in patients with ADHD does not increase their risk for subsequent addiction. However, nonmedical use of methylphenidate and other stimulant medications can lead to addiction as well as a variety of other health consequences,” said NIDA Director Dr. Nora Volkow. “This study highlights the fact that we know very little about how methylphenidate affects the structure of and communication between brain cells.”
The researchers exposed mice to 2 weeks of daily injections ofcocaine or methylphenidate, after which reward areas of the brain were examined for changes in dendritic spine formation, which is related to the formation of synapses and the communication between nerve cells; and the expression of a protein, delta Fos B, which has been implicated in the long-term actions of addictive drugs. Both drugs increased dendritic spine formation and the expression of delta Fos B; however, the precise pattern of their effects was distinct. It differed in the types of spine saffected, the cells that were affected, and the brain regions. In some cases, there was overlap between the two drugs; further, in some cases, methylphenidate produced greater effects than cocaine–for example, on protein expression in certain regions.
It’s worth noting, though, that previous studies found no link between stimulant treatment for ADHD and drug abuse. The takeaway from this latest study is NOT that Ritalin is just a fancy brand of cocaine, or that delta Fos B is a gene uniquely turned on by amphetamines or illicit drugs. (It seems to be part of the BDNF pathway, which is why its expression leads to the growth of dendritic spines.) Rather, it’s that we really don’t know how stimulants like Ritalin influence fundamental pathways in the brain.
Thanks for the tip, Dave!