Hyperkinesia Project Proposal
Hyperkinesia is a state of excessive restlessness which incorporates a large variety of different attention disorders, such as ADHD, and disorders that affect the ability to control motor movement such as Huntington’s disease. Hyperkinesia occurs when dopamine receptors, and norepinephrine receptors to a lesser extent, within the cortex and the brainstem are more sensitive to dopamine or when the dopaminergic receptors/neurons are hyperactive. Hyperkinesia can be caused by a large number of different diseases including metabolic disorders, endocrine disorders, heritable disorders, vascular disorders, or traumatic disorders. Other causes include toxins to the brain, autoimmune diseases, and infections like meningitis.
Hyperkinesia is the hallmark symptom of Huntington’s Disease, which is characterized further by the gradual onset of defects in behavior and cognition beginning in the fourth or fifth decades of life. It is a progressive disorder, leading to death within 10-20 years. It is caused by the Huntingtin gene, which is a mutation that causes unstable triple repeats. This mutation eventually contributes to selective atrophy of the caudate and putamen, with some additional degeneration of the frontal and temporal cortices of the brain. The extent of the hyperkinesia exhibited in the disease can vary from solely the little finger to the entire body. There is no known cure for Huntington’s Disease, yet there is treatment available for the symptoms.
In Wistar rats, hyperkinesia developing in the pattern caused by Huntingdon’s chorea was induced by injections of picrotoxin into the striatum. The striate nuclei in the gray matter of the cerebral hemispheres contribute to autonomic motor functions in mammals. Impairment of such functions could lead to the involuntary excessive head and extremity movement evident in hyperkinesia. These nuclei are receptive to the convergence of neurons releasing GABAA which is an inhibitory neurotransmitter. When received in the striate nuclei, this neurotransmitter will cause inhibition of elementary motor automatisms; hence, in clinical hyperkinesia, GABAA cannot execute its chemical function. Picrotoxin is a GABAA receptor blocker, found to mimick the cause of hyperkinesia found in Huntingdon's chorea by preventing GABAA from being received in the striate nuclei.
In our edited Wiki page of hyperkinesia, we plan to elaborate on the above highlighted topics, discussing the mechanisms behind the scientific evidence in more detail using primary and secondary scientific literature. We also intend to expand the currently featured topics on the existing hyperkinesia stub, such as the various psychological and social disorders associated with it. Ian will focus on causes of the phenomenon and its associated motor disorders, Lauren will focus on associated cognitive disorders, and Jessica will focus on treatment for the phenomenon.
O'Connell, John, M.D. Personal Interview. 19 January 2011.
Purves, Dale, George J. Augustine, David Fitzpatrick, William C. Hall, Anthony-Samuel LaMantia, James O. McNamara, and Leonard E. White, eds. Neuroscience, 7th ed. Sunderland, MA: Sinauer Associates, Inc., 2008.
Yakimovskii, A.F. and Varshavskaya, V.M. "Magnesium Ions Prevent the Development of Hyperkinesia Evoked by Administration of Picrotoxin into the Rat Neostriatum." Neuroscience and Behavioral Physiology (2007): 821-826.