Traditionally, the basic etiological concepts are considered in the views on the morphophysiological basis of hyperkinesis. Hyperkinesia is associated with hypotonia, a decrease in muscle tone, and hyperkinetic disorders are psychogenic and manifest in childhood. Hyperkinesia can be caused by a large number of various diseases, including metabolic disorders, endocrine disruption, hereditary disorders, vascular disorders or traumatic disorders. Other causes include intoxication of the nervous system, autoimmune diseases and infections. The classification of hyperkinesis is that hyperkinetic motions can be defined as any undesirable, excessive movements that can be distinguished from each other, based on the degree to which they are rhythmic, discrete, repetitive and random. When assessing a patient with suspected hyperkinesia, the doctor thoroughly records in the history of the disease a clear description of the movements, the medications prescribed in the past and present, the family history of the similar diseases, the history of the disease, including past infections, and any other influences. Treatment is aimed at reducing symptoms, restoring normal posture and improving the general condition of the patient.
2. Yassa, M.D., Ramsy (1997) [Neuroleptic-induced movement disorders] New York: Cambridge University Press. pp. 132–135.
3. Mumenthaler, Marco (2006) [Fundamentals of Neurology: An Illustrated Guide] New York, NY: Georg ThiemeVerlag. pp. 75; 132–135.
4. Sanger, Terence; et al. (2010) [Definition and Classification of Hyperkinetic Movements in Childhood"] Movement Disorders, no 25 (11), pp. 1538–1549.
5. Wishik, Jeffrey (2005). [Medical and Legal Aspects of Neurology] Tucson, AZ: Lawyers and Judges Publishing Co., Inc. pp. 306–310
6. (2011) [Hyperkinetic Movement Disorders] Movement Disorders Program. Regents of the University of Michigan.
7. Eidelberg, David. (2011) [Movement and Cerebellar Disorders"] Neurologic Disorders. Merck Sharp & Dohme Corp.
8. Eckman, Margaret (2011) [Professional Guide to Pathophysiology] Ambler, PA: Lippincott Williams & Wilkins. (3rd ed.), p. 256.
9. Fernandez-Alvarez, Emilio (2001) [Movement Disorders in Children] London WC1V 6RL, England: Mac Keith Press, pp. 232.
10. Purves, Dale (2008) [Neuroscience] Sunderland, MA: Sinaeur Associates, Inc., pp. 468–469.
11. Manju A. Kurian; et al. (2011) [Clinical and molecular characterisation of hereditary dopamine transporter deficiency syndrome: an observational cohort and experimental study] The Lancet Neurology, no. 10, pp. 54–62.
12. Dugdale, David C.; Daniel B. Hoch (2009) [Huntington's disease] PubMed Health.
13. Carlson, Neil R. (2007) [Physiology of Behavior] Boston, MA: Pearson Education, Inc. pp. 537–538.
14. Handley, Alexandra; Medcalf, Pippa; Hellier, Kate; Dutta, Dipankar (2009) [Movement disorders after stroke] Age and Ageing, no. 38 (3), pp. 260–266.
15. Tsuji, S. (1999) [Dentatorubral-pallidoluysian atrophy: Clinical features and molecular genetics] Adv Neurol. 79, pp. 399–409.
16. Hatano, T. et al. (2003) [Cervical dystonia in dentatorubral-pallidoluysian atrophy] ActaNeurol Scand., no 108 (4), pp. 287–9. Ito, D.; et al. (2002) [Corneal endothelial degeneration in dentatorubral-pallidoluysian atrophy] Arch Neurol., no 59 (2), pp. 289–91.
17. Licht D, Lynch D (2002) [Juvenile Dentatorubral-Pallidoluysian Atrophy: New Clinical Features] Pediatr Neurol., no 26 (1), pp. 51–4.
18. Jankovic, Joseph (2009) [Treatment of hyperkinetic movement disorders] The Lancet Neurology, no 8 (9), pp. 844–856.
19. Olesen, J; Hougård, K; Hertz, M (1978) [Isoproterenol and propranolol: ability to cross the blood-brain barrier and effects on cerebral circulation in man] Stroke, no 9, pp. 344–349.
20. Lanska, Douglas (2010) [History of Neurology] NewYork: Elsevier. pp. 501–502.