Encyclopedia of Computational Neuroscience

Living Edition
| Editors: Dieter Jaeger, Ranu Jung

Bradykinesia Models

Living reference work entry

Later version available View entry history

DOI: https://doi.org/10.1007/978-1-4614-7320-6_85-1



Bradykinesia is the cardinal symptom of Parkinson’s disease (PD). It is related to an abnormal slowness of movement. The causes of PD bradykinesia are not known largely, because there are multiple brain areas and pathways involved from the neuronal degeneration site (dopamine neurons in substantia nigra pars compacta (SNc) and ventral tegmental area (VTA)) to the muscles. Bradykinesia models are mathematical and computational constructs attempting to uncover how information is processed in the affected brain areas and what are the biophysical mechanisms giving rise to the observed slowness of movement in PD bradykinesia.

Detailed Description

Bradykinesia, the hallmark and most disabling symptom of PD, refers to an extreme slowness of movement. In early stages of the disease, PD patients have difficulties with daily activities such as walking, speaking, or getting in and out of chairs (Gibberd 1986). In the later phases...


Ventral Tegmental Area Dopamine Neuron Globus Pallidus External Output Nucleus Basal Ganglion Output 
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  1. Albin RL, Young AB, Penney JB (1989) The functional anatomy of basal ganglia disorders. TINS 12:366–375.PubMedGoogle Scholar
  2. Alexander GE, Crutcher MD (1990) Functional architecture of basal ganglia circuits: neural substrates of parallel processing. TINS 13(7):266–271PubMedGoogle Scholar
  3. Benazzouz A, Gross C, Dupont J, Bioulac B (1992) MPTP induced hemiparkinsonism in monkeys: behavioral, mechanographic, electromyographic and immunohistochemical studies. Exp Brain Res 90:116–120PubMedCrossRefGoogle Scholar
  4. Benecke R, Rothwell JC, Dick JPR (1986) Performance of simultaneous movements in patients with Parkinson’s disease. Brain 109:739–757PubMedCrossRefGoogle Scholar
  5. Berardelli A, Dick JPR, Rothwell JC, Day BL, Marsden CD (1986) Scaling of the size of the first agonist EMG burst during rapid wrist movements in patients with Parkinson’s disease. J Neurol Neurosurg Psychiatry 49:1273–1279PubMedCentralPubMedCrossRefGoogle Scholar
  6. Bevan MD, Booth PAC, Eaton SA, Bolam JP (1998) Selective innervation of neostriatal interneurons by a subclass of neuron in the globus pallidus of the rat. J Neurosci 18:9438–9452PubMedGoogle Scholar
  7. Bjorklund A, Lindvall O (1984) Dopamine containing systems in the CNS. In: Bjorklund A, Hokfelt T (eds) Handbook of chemical neuroanatomy. Classical transmitters in the CNS, Part 1, vol 2. Elsevier, Amsterdam, pp 55–121Google Scholar
  8. Camarata PJ, Parker RG, Park SK, Haines SJ, Turner DA, Chae H et al (1992) Effects of MPTP induced hemiparkinsonism on the kinematics of a two-dimensional, multi-joint arm movement in the rhesus monkey. Neuroscience 48(3):607–619PubMedCrossRefGoogle Scholar
  9. Connor NP, Abbs JH (1991) Task-dependent variations in parkinsonian motor impairments. Brain 114:321–332PubMedGoogle Scholar
  10. Contreras-Vidal JL, Stelmach G (1995) A neural model of basal ganglia-thalamocortical relations in normal and Parkinsonian movements. Biol Cybern 73:467–476PubMedCrossRefGoogle Scholar
  11. Corcos DM, Chen CM, Quinn NP, McAuley J, Rothwell JC (1996) Strength in Parkinson’s disease: relationship to rate of force generation and clinical status. Ann Neurol 39(1):79–88PubMedCrossRefGoogle Scholar
  12. Cutsuridis V (2006a) Biologically inspired neural architectures of voluntary movement in normal and disordered states of the brain. Unpublished PhD dissertationGoogle Scholar
  13. Cutsuridis V (2006b) Neural model of dopaminergic control of arm movements in Parkinson’s disease bradykinesia. In: Kolias S, StafilopatisA, Duch W (eds) ICANN 2006: artificial neural networks. LNCS, vol 4131. Springer, Berlin, pp 583–591Google Scholar
  14. Cutsuridis V (2010) Neural network modeling of voluntary single joint movement organization. II. Parkinson’s disease. In: Chaovalitwongse WA, Pardalos P, Xanthopoulos P (eds) Computational neuroscience. Springer, New York, pp 193–212CrossRefGoogle Scholar
  15. Cutsuridis V (2013) Bradykinesia models of Parkinson’s disease. Scholarpedia, under reviewGoogle Scholar
  16. Cutsuridis V, Perantonis S (2006) A neural model of Parkinson’s disease bradykinesia. Neural Netw 19(4):354–374PubMedCrossRefGoogle Scholar
  17. Doudet DJ, Gross C, Lebrun-Grandie P, Bioulac B (1985) MPTP primate model of Parkinson’s disease: a mechanographic and electromyographic study. Brain Res 335:194–199PubMedCrossRefGoogle Scholar
  18. Doudet DJ, Gross C, Arluison M, Bioulac B (1990) Modifications of precentral cortex discharge and EMG activity in monkeys with MPTP induced lesions of DA nigral lesions. Exp Brain Res 80:177–188PubMedCrossRefGoogle Scholar
  19. Gerfen CR, Engber TM, Mahan LC, Susel Z, Chase TN, Monsma FJ Jr, Sibley DR (1990) D1 and D2 dopamine receptor-regulated gene expression of striatonigral and striatopallidal neurons. Science 250:1429–1432PubMedCrossRefGoogle Scholar
  20. Gibberd FB (1986) The management of Parkinson’s disease. Practitioner 230:139–146PubMedGoogle Scholar
  21. Godaux E, Koulischer D, Jacquy J (1992) Parkinsonian bradykinesia is due to depression in the rate of rise of muscle activity. Ann Neurol 31(1):93–100PubMedCrossRefGoogle Scholar
  22. Gross C, Feger J, Seal J, Haramburu P, Bioulac B (1983) Neuronal activity of area 4 and movement parameters recorded in trained monkeys after unilateral lesion of the substantia nigra. Exp Brain Res 7:181–193CrossRefGoogle Scholar
  23. Hallett M, Khoshbin S (1980) A physiological mechanism of bradykinesia. Brain 103:301–314PubMedCrossRefGoogle Scholar
  24. Lazarus JC, Stelmach GE (1992) Inter-limb coordination in Parkinson’s disease. Mov Disord 7:159–170PubMedCrossRefGoogle Scholar
  25. Mink JW (1996) The basal ganglia: focused selection and inhibition of competing motor programs. Prog Neurobiol 50:381–425PubMedCrossRefGoogle Scholar
  26. Moroney R, Heida C, Geelen J (2008) Increased bradykinesia in Parkinson’s disease with increased movement complexity: elbow flexion-extension movements. J Comput Neurosci 25:501–519PubMedCrossRefGoogle Scholar
  27. Nambu A, Tokuno H, Takada M (2002) Functional significance of the cortico-subthalamo-pallidal ‘hyperdirect’ pathway. Neurosci Res 43:111–117PubMedCrossRefGoogle Scholar
  28. Parent A et al (2000) Organization of the basal ganglia: the importance of axonal collateralization. Trends Neurosci 23:S20–S27PubMedCrossRefGoogle Scholar
  29. Rand MK, Stelmach GE, Bloedel JR (2000) Movement accuracy constraints in Parkinson’s disease patients. Neuropsychologia 38:203–212PubMedCrossRefGoogle Scholar
  30. Smith Y, Bevan MD, Shink E, Bolam JP (1998) Microcircuitry of the direct and indirect pathways of the basal ganglia. Neuroscience 86:353–387PubMedCrossRefGoogle Scholar
  31. Tremblay L, Filion M, Bedard PJ (1989) Responses of pallidal neurons to striatal stimulation in monkeys with MPTP-induced parkinsonism. Brain Res 498(1):17–33PubMedCrossRefGoogle Scholar
  32. Watts RL, Mandir AS (1992) The role of motor cortex in the pathophysiology of voluntary movement deficits associated with parkinsonism. Neurol Clin 10(2):451–469PubMedGoogle Scholar
  33. Weiss P, Stelmach GE, Adler CH, Waterman C (1996) Parkinsonian arm movements as altered by task difficulty. Parkinsonism and Related Disorders 2(4):215–223PubMedCrossRefGoogle Scholar
  34. Williams SM, Goldman-Rakic PS (1998) Widespread origin of the primate mesofrontal dopamine system. Cereb Cortex 8:321–345PubMedCrossRefGoogle Scholar

Further Reading: Scholarpedia

  1. Basal GangliaGoogle Scholar
  2. Dopamine AnatomyGoogle Scholar
  3. Models of Basal GangliaGoogle Scholar
  4. Models of Parkinson’s Disease BradykinesiaGoogle Scholar
  5. Models of Spinal CordGoogle Scholar
  6. Models of Thalamocortical SystemGoogle Scholar

Further Reading: Wikipedia

  1. HypokinesiaGoogle Scholar
  2. Motor ControlGoogle Scholar
  3. Motor SystemGoogle Scholar
  4. Parkinson’s DiseaseGoogle Scholar

Authors and Affiliations

  1. 1.Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology - HellasHeraklion, CreteGreece