Rerun: What causes ADHD? Some intriguing findings

The Health Business Blog is on summer vacation until Labor Day, and will be re-running some classic posts from now till then.

This item originally ran on January 11, 2008 and has had perhaps more profound impact on certain individuals than any other post I’ve run. Read the comments section of the original post and you’ll see what I mean.

A short paper in the current issue of the Journal of Child Neurology (Hypokalemic Sensory Overstimulation) raises some tantalizing possibilities:

  • In some patients, ADHD may be caused by an excess of sensory stimulation arriving at the brain, rather than being a disorder of the brain itself
  • For such patients, potassium supplements may be an effective treatment
  • ADHD symptoms may indeed be triggered by sugar in some people
  • ADHD and PMS may be related in some women –and their PMS may also be treatable with potassium
  • Dentists may be well-positioned to identify possible ADHD patients

Conventional wisdom is that attention deficit disorder results from a problem in the brain. This seems reasonable since the stimulants used to treat ADHD work on particular pathways in the brain. But conventional wisdom is not getting much traction: researchers have studied the genes in these dopamine pathways and found only weak effects on ADHD.

Now, a group of Harvard-associated doctors –including Health Business Blog contributor Michael Segal MD PhD– has suggested a different model for ADHD based on an excess of sensory stimulation arriving at the brain. They came up with this model by stumbling across a family with some peculiar issues, and by having the background to understand the importance of what the patients were describing. Interestingly, they were able to treat the ADHD with a simple over the counter medication – potassium supplements.

The authors were not originally focused on ADHD. They were drawn into the area when a woman described to a neurologist that one of the core features of ADHD, a sense of being bombarded by sensory input, suddenly went away, –as if a shade had been pulled down.” This occurred 20 minutes after she took an oral potassium supplement for muscle cramps.

The neurologist was intrigued. It reminded him of the muscle disease hypokalemic periodic paralysis, in which ion channels in muscle become over-active when potassium levels in the blood are low. The woman described the factors that triggered her symptoms, and they were the same as those noted in the muscle disease: meals high in carbohydrates, food high in salt, and resting after exercise. Her son, who was having attention problems in school, also found the same triggers and got the same benefit from taking potassium.

Hypokalemic periodic paralysis is part of a family of “channelopathies.” Other variants were known in the heart (producing arrhythmias), in the brain (producing seizures), and in sensory nerves (producing pain). No variants producing ADHD had been described, and it would be difficult to suggest a channelopathy producing ADHD since the evidence in this family seemed “soft” –based as it was on subjective patient reports.

That all changed one day. The boy got a shot of the local anesthetic lidocaine for minor toe surgery, but he insisted that the numbing medicine wasn’t taking effect, even after repeated shots. The surgeon was skeptical but touched the boy’s toe lightly with his instruments and was surprised when the boy could describe exactly where he touched. The doctors knew that lidocaine works on sodium channels, and realized that an insensitivity to lidocaine would fit very well with a channelopathy causing sensory overstimulation. When the mother heard the details later that day she recounted that lidocaine hardly worked for her in dental procedures. Now the doctors had some objective evidence suggesting a channelopathy accounting for the core symptom in ADHD.

The way to confirm such a hypothesis is to find the gene for the mutant ion channel, which is hard to do using a small family. The doctors knew that it would take more families to do “positional cloning” to find the gene, and wrote up their paper, hoping to find other families. The paper appeared in early January and within days of publication another family sent an email to the contact address on the paper to describe a similar story in their family. If you have a story like that you may also want to make contact using the email address listed here.

Until the gene is found it is hard to say whether this sensory overstimulation form of ADHD is common or rare. Some factors suggest this clinical picture may be common – some people with ADHD think their symptoms are worse after consuming sugar, and occupational therapists describe a “sensory integration disorder” in many people with ADHD. One intriguing line in the paper even suggests that the sensory overstimulation may show up in ways that might not have seemed connected at all to ADHD: the mother “suffered for many years from strong menstrual pelvic cramping and noticed in her mid-40s that oral potassium supplementation blunted the menstrual pain to a dramatic degree.”

As people become familiar with the sensory overstimulation model of ADHD and researchers do the genetics we may soon have an understanding of ADHD at the molecular level and have new forms of treatment and prevention.

If you’d like to leave a comment please do so on the original post.

August 24, 2010