Ageing Effects on Motor Control

Original Editor - Wendy Walker

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Summary[edit | edit source]

Motor control is the individual's abiliy to direct and regulate movement[1]. Neural control of movement involves coordination between large numbers of different structures within the nervous system. Motor control impairments in older adults are caused by medical conditions which primarily affect this population (i.e. not as a result of the normal ageing process), such as Parkinson's disease and stroke. They can be caused by impairments of both the motor and sensory systems.

Motor system:
  • Abnormal tone
  • Paresis
  • Ataxia
  • Hypokineisa
  • Fractionated movement deficits

Sensory system:

  • Perceptual deficits
  • Somatosensory deficits

Motor System Impairments[edit | edit source]

Abnormal tone[edit | edit source]

Muscle tone = the resistance of muscle to passive elongation or stretch[2].

Hypertonicity[edit | edit source]

Hypertonicity, increased muscle tone, occurs as a result of loss of supraspinal inhibition to the spinal cord and is usually caused by damage to either the corticospinal tract or to the parietal lobe (from where 40% of the fibres of the corticospinal tract originate[3]). 

Spasticity = a velocity-dependent increase in tonic stretch reflexes (muscle tone)[4], common in Stroke.

Rigidity =  non-velocity-dependent increase in resistance to passive movement in any direction[5], common in later stages of Parkinson's.

Hypotonicity[edit | edit source]

Hypotonicity, ie. reduced muscle tone, is defined as a decreased resistance to passive movement, and reduced or absent stretch reflex response.

It occurs as a result of decreased or absent neural drive to the muscles[6], and is seen in a number of conditions affecting elderly people including degenerative neuromuscular diseases and the early stages of stroke, in addition to peripheral nerve damage.

Paresis[edit | edit source]

This is the single most common motor impairment; it is defined as the reduced ability to voluntarily activate the spinal motorneurons[7]. It occurs primarily as a result of damage to the corticospinal system (ie. the motor cortical areas, the corticospinal tract and the spinal cord.

Paresis occurs in a wide range of neurological disorders common in the older population, including stroke, multiple sclerosis and peripheral neuropathy.

Ataxia[edit | edit source]

This is a lack of coordination between movements and/or body parts, e,g, during gait, and occurs as a result of damage to the cerebellar inputs, outputs, and/or cerebellar structures. Tone is usually reduced and reflexes may be pendular[8] e.g. lower limb oscillates when patellar tendon reflex is tested[9].

Conditions which can cause ataxia include stroke, multiple sclerosis and spinocerebellar atrophies.

Hypokinesia[edit | edit source]

This is primarily associated with Parkinson's and sometimes with dementia, and is characterised by slow movement (bradykinesia) or absence of movement (akinesia) and is usually caused by damage to the basal ganglia. Typically, people with hypokinesia struggle with the onset of movement, and can freeze during movement[10].

Fractionated  movement deficits[edit | edit source]

 This is defined as reduced ablity to isolate or fractionate movement. Many different central nervous system pathologies  which affect the corticospinal system and cause reduced ability to selectivvely activate muscles can result in  fractionate movement deficits, including stroke and multiple sclerosis.

Sensory Impairments[edit | edit source]

Conditions which cause motor impairments frequently also cause sensory impairments.

  • Somatosensory loss: this can have either a central or peripheral nervous system origin. The main effect on motor control is a reduction in the accuracy of the ongoing monitoring of movement. In many people with somatosensory loss, there is increased reliance on the visual system to plan and monitor movements.
  • Perceptual deficits: eg. "pusher syndrome" where a person who has had a stroke or brain injury pushes with the unaffected limbs toward the affected side[11].

References[edit | edit source]

  1. Shumway-Cook A, Woolacott MH: Motor control: translating research into clinical practice, ed 3, Philadelphia, PA, 2007, Lippincott Williams & Wilkins
  2. Stolov, W.C. (1996) The Concept of Normal Muscle Tone, Hypotonia and Hypertonia. Archives of Physical Medicine and Rehabilitation. 47;156-168.
  3. Porter R, Lemon RN: Corticospinal function and voluntary movement. Vol. 45. Oxford: Oxford University Press,1993.
  4. Lance JW. The control of muscle tone, reflexes, and movement: Robert Wartenberg Lecture. Neurol. 1980;30(12): 1303-13.
  5. Sanger TD, Delgado MR, Gaebler-Spira D, Hallett M, Mink JW. Classification and definition of disorders causing hypertonia in childhood. Pediatrics. 2003;111(1):e89-97.
  6. Fredericks CM, Saladin LK, Clinical Presentations in Disorders of Motor Function. In Fredericks CM, Saladin LK, editors: Pathophysiology of the motor systems: principles and clinical presentations, Philadelphia: FA Davis,1996, .
  7. Sathian K, Buxbaum LJ, Cohen LG, Krakauer JW, Lang CE, Corbetta M, Fitzpatrick SM. Neurological principles and rehabilitation of action disorders: common clinical deficits. Neurorehabil Neural Repair. 2011; 25(5 0): 21S–32S.
  8. Brunberg JA. Ataxia. Am J Neuroradiol. 2008; 29(7):1420-1422. Accessed 23 August 2018.
  9. New York University School of Medicine. The Precise Neurological Exam: Deep Tendon Reflexes [Internet]. Available Accessed 23 August 2018. Available from: https://informatics.med.nyu.edu/modules/pub/neurosurgery/reflexes.html
  10. Morris ME, Iansek R, Galna B: Gait festination and freezing in Parkinson’s disease: pathogenesis and rehabilitation. Mov Disord 23 (Suppl 2):S451-S460, 2008
  11. Karnath HO, Broetz D: Understanding and treating “pusher syndrome.” Phys Ther 83(12):1119-1125, 2003