Ageing Effects on Motor Control: Difference between revisions
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== Summary == | == Summary == | ||
<div>Motor control is the individual's abiliy to direct and regulate movement<ref>Shumway-Cook A, Woolacott MH: Motor control: translating research into clinical practice, ed 3, Philadelphia, PA, 2007, Lippincott Williams & | <div>Motor control is the individual's abiliy to direct and regulate movement<ref>Shumway-Cook A, Woolacott MH: Motor control: translating research into clinical practice, ed 3, Philadelphia, PA, 2007, Lippincott Williams & Wilkins</ref>. 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 and stroke. They can be caused by impairments of both the motor and sensory systems.</div><div></div><div><br></div><div></div><div>'''Motor system:'''</div> | ||
*Abnormal tone | *Abnormal tone | ||
*Paresis | *Paresis | ||
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=== Abnormal tone === | === Abnormal tone === | ||
Muscle tone = the resistance of | Muscle tone = the resistance of muscle to passive elongation or stretch<ref>Stolov, W.C. (1996) The Concept of Normal Muscle Tone, Hypotonia and Hypertonia. Archives of Physical Medicine and Rehabilitation. 47;156-168.</ref>.<br> | ||
==== Hypertonicity ==== | ==== Hypertonicity ==== | ||
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<ref>Porter R, Lemon RN: Corticospinal function and voluntary movement | 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<ref>Porter R, Lemon RN: Corticospinal function and voluntary movement. Vol. 45. Oxford: Oxford University Press,1993.</ref>). | ||
[[Spasticity|Spasticity]] = velocity-dependent | [[Spasticity|Spasticity]] = a velocity-dependent increase in tonic stretch reflexes (muscle tone)<ref>Lance JW. The control of muscle tone, reflexes, and movement: Robert Wartenberg Lecture. Neurol. 1980;30(12): 1303-13.</ref>, common in [[Stroke|Stroke]]. | ||
Rigidity = | Rigidity = non-velocity-dependent increase in resistance to passive movement in any direction<ref>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. | ||
</ref>, common in later stages of [[Parkinsons Clinical Presentation|Parkinson's]]. | |||
==== Hypotonicity ==== | ==== Hypotonicity ==== | ||
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Hypotonicity, ie. reduced muscle tone, is defined as a decreased resistance to passive movement, and reduced or absent stretch reflex response. | 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<ref>Fredericks CM, Saladin LK | It occurs as a result of decreased or absent neural drive to the muscles<ref>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, .</ref>, and is seen in a number of conditions affecting elderly people including degenerative [[Neuromuscular Disorders|neuromuscular diseases]] and the early stages of stroke, in addition to peripheral nerve damage. | ||
=== Paresis === | === Paresis === | ||
This is the single most common motor impairment; it is defined as the reduced ability to voluntarily activate the spinal motorneurons. It occurs primarily as a result of damage to the corticospinal system (ie. the motor cortical areas, the corticospinal tract and the spinal cord. | This is the single most common motor impairment; it is defined as the reduced ability to voluntarily activate the spinal motorneurons<ref>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. | ||
</ref>. 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. | Paresis occurs in a wide range of neurological disorders common in the older population, including stroke, multiple sclerosis and peripheral neuropathy. | ||
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=== Ataxia === | === Ataxia === | ||
This is a lack of coordination between movements and/or body parts, and occurs as a result of damage to the cerebellar inputs, outputs, and/or cerebellar structures. | 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<ref>Brunberg JA. [http://www.ajnr.org/content/ajnr/29/7/1420.full.pdf Ataxia]. Am J Neuroradiol. 2008; 29(7):1420-1422. Accessed 23 August 2018. | ||
</ref> e.g. lower limb oscillates when patellar tendon reflex is tested<ref>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 </ref>. | |||
Conditions which can cause ataxia include [[Stroke|stroke]], [[ | Conditions which can cause ataxia include [[Stroke|stroke]], [[Multiple Sclerosis (MS)|multiple sclerosis]] and spinocerebellar atrophies. | ||
=== Hypokinesia === | === Hypokinesia === | ||
This is primarily associated with [[Parkinsons Disease| | This is primarily associated with [[Parkinsons Disease|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<ref>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</ref>. | ||
=== Fractionated movement deficits === | === Fractionated movement deficits === | ||
<div> 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.</div> | <div> 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.</div> | ||
== | == Sensory Impairments == | ||
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<ref>Karnath HO, Broetz D: Understanding and treating “pusher syndrome.” Phys Ther 83(12):1119-1125, 2003</ref>. | |||
<div></div> | |||
<references /> | == References == | ||
<references /> | |||
[[Category:Neurology]] | |||
[[Category:Older People/Geriatrics]] | |||
[[Category:Older People/Geriatrics - Conditions]] | |||
Latest revision as of 17:44, 3 January 2022
Original Editor - Wendy Walker
Top Contributors - Wendy Walker, Lauren Lopez, Kim Jackson, 127.0.0.1, Admin, Tony Lowe, Garima Gedamkar, George Prudden and WikiSysop
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 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]
- ↑ Shumway-Cook A, Woolacott MH: Motor control: translating research into clinical practice, ed 3, Philadelphia, PA, 2007, Lippincott Williams & Wilkins
- ↑ Stolov, W.C. (1996) The Concept of Normal Muscle Tone, Hypotonia and Hypertonia. Archives of Physical Medicine and Rehabilitation. 47;156-168.
- ↑ Porter R, Lemon RN: Corticospinal function and voluntary movement. Vol. 45. Oxford: Oxford University Press,1993.
- ↑ Lance JW. The control of muscle tone, reflexes, and movement: Robert Wartenberg Lecture. Neurol. 1980;30(12): 1303-13.
- ↑ 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.
- ↑ 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, .
- ↑ 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.
- ↑ Brunberg JA. Ataxia. Am J Neuroradiol. 2008; 29(7):1420-1422. Accessed 23 August 2018.
- ↑ 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
- ↑ 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
- ↑ Karnath HO, Broetz D: Understanding and treating “pusher syndrome.” Phys Ther 83(12):1119-1125, 2003
