Hypokalemic sensory overstimulation

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Hypokalemic sensory overstimulation is a form of attention deficit hyperactivity disorder that has several similarities[1] to disorders of ion channels, in particular to the muscle disorder hypokalemic periodic paralysis.

Characterization of the disorder[edit]

The most prominent feature of hypokalemic sensory overstimulation is the feeling of sensory overstimulation that is characteristic of attention deficit disorder.[2] In hypokalemic sensory overstimulation, the sensory overstimulation goes away abruptly after taking potassium supplements; one person described the disappearance of the sensory overstimulation as being “as if a shade had been pulled down” 20 minutes after she took a dose of oral potassium.[3]

The sensory overstimulation is triggered by large carbohydrate meals, sodium chloride intake, and the period following exercise,[1] the same factors known to trigger hypokalemic periodic paralysis.[4] People with hypokalemic sensory overstimulation also have a reduced effectiveness of the local anesthetic lidocaine. This was first noted during minor surgery, in which one person was given lidocaine "in repeated injections totaling 15 mL because the patient reported continued sensation" but nevertheless he "could document the inadequacy of anesthesia by reporting accurately the location of forceps touches to the toe under conditions in which he could not see his toe".[1] Similar reduced effectiveness of lidocaine in dental work was noted in his mother[1] and subsequently in many other families.[5]

Molecular mechanism[edit]

Hypokalemic periodic paralysis results from mutations in subunits of sodium or calcium channels. Since hypokalemic sensory overstimulation and hypokalemic periodic paralysis have similar triggers and treatments, and since there is a relative ineffectiveness of the sodium-channel blocker lidocaine in hypokalemic sensory overstimulation, hypokalemic sensory overstimulation may be another disorder in the "channelopathy" group.[1] Since the lidocaine effect occurs outside the brain, this suggests that in some patients with attention deficit disorder the underlying abnormality may be overstimulation from sensory pathways rather than a defect in the brain itself.[1]

The triggering effect of carbohydrates is believed to be due to digested carbohydrates causing release of insulin, which results in uptake of potassium into cells and the resulting hypokalemia.

Treatment[edit]

Over the counter potassium supplements have been used to treat hypokalemic sensory overstimulation,[1] however potassium supplements can cause hyperkalemia if used in high doses or in very susceptible people without physician supervision. These issues and other treatment approaches are discussed in a detailed review of treatment of hypokalemic periodic paralysis [6] by Dr. Jacob O Levitt, a dermatologist who has hypokalemic periodic paralysis.

Prevention by avoiding high carbohydrate meals and excessive sodium chloride carries no risks, and there is other evidence for a subset of people with attention deficit disorder who benefit from reduction of sugar intake.[7]

To deal with the relative ineffectiveness of local anesthetics used in dental care, the more diffusible local anesthetic articaine has been used instead of lidocaine, together with potassium supplementation.[1]

Relation to other disorders[edit]

One of the original patients had symptoms of premenstrual syndrome and found that "oral potassium supplementation blunted the menstrual pain to a dramatic degree",[1] suggesting that the sensory overstimulation may be expressed more widely than just as attention deficit disorder. Occupational therapists describe a "sensory processing disorder" with findings overlapping with those of attention deficit disorder. People with hypokalemic sensory overstimulation fit criteria for both disorders, and since the genetic basis for these disorders has not been discovered, the precise relationships among these descriptions is not yet clear. Overlap with Asperger syndrome and fibromyalgia has also been suggested, with the prediction that scientists will use "mechanistic and genetic approaches to take apart this amalgamation and put it back together using biological criteria".[5]

References[edit]

  1. ^ a b c d e f g h i Segal MM, Rogers GF, Needleman HL, Chapman CA (2007). "Hypokalemic sensory overstimulation". J Child Neurol 22 (12): 1408–10. doi:10.1177/0883073807307095. PMID 18174562. 
  2. ^ PediatricNeurology.com "Sound of ADHD Simulation"
  3. ^ Health Business Blog: What causes ADHD? Some intriguing findings
  4. ^ Miller TM, Dias da Silva MR, Miller HA et al. (2004). "Correlating phenotype and genotype in the periodic paralyses". Neurology 63 (9): 1647–55. doi:10.1212/01.wnl.0000143383.91137.00. PMID 15534250. 
  5. ^ a b Segal MM (2014). "We cannot say whether attention deficit-hyperactivity disorder exists, but we can find its molecular mechanisms". Pediatr Neurol. 51 (1): 15–6. doi:10.1016/j.pediatrneurol.2014.04.014. PMID 24938135. 
  6. ^ Practical aspects in the management of hypokalemic periodic paralysis
  7. ^ National Institute of Mental Health "Attention Deficit Hyperactivity Disorder"