Motor systems Flashcards
Damage to motor neurons
Flaccid paralysis
Damage to primary motor cortex
Spastic paralysis with exaggerated spinal reflexes
Damage to brainstem pathways
Postural defects and problems with walking
Damage to higher cortical areas
Apraxia: movements aren’t ordered or appropriate to the situation
Damage to the cerebellum
Ataxia: poorly coordinated movements that may be the wrong size or shape
Damage to the basal ganglia
Hyper/hypokinesia since BG involved in action selection
Problems with negative feedback
Biological delays, so signal continues while correction starts
-> Over correction and oscillation around a set point
Slow fibre properties
Anatomical: few fibres/unit, small
Biochem: oxidative, high myoglobin
Physiological: slow twitch, low tension, fatigue resistant, slow axons
Fast fibre properties
Anatomical: large, lots of fibres/motor unit
Biochem: glycolytic, little myoglobin
Physiological: fast twitch, high tension, fast axons, fatiguable
Size principal of motoneuron recruitment
Low force units, the slow fibres, are active at low rates of stimulation
As force increases, get recruitment of higher force units
This means the increase in force is via the smallest increments possible to give smooth contraction
How does size principal of motoneuron recruitment come about
Lowest threshold motoneurons innervate few fibres and induce them to become slow, low force, fatigue resistant
Higher threshold motoneurons innervate more fibres, inducing them to become fast, fatiguable fibres
Muscle spindle afferents
Signal passive stretch
Tendon organ afferents
Signal tension, including active tension from muscle contraction
(as well as due to bones being pulled apart with passive stretch)
Bag fibres
Central region full of nuclei with no striations
Signal changes in length very well, mainly via primary spindle afferents
Chain fibres
Nuclei and striations throughout so stretch acts equally along fibre
Signal static length via secondary spindle afferents mainly
Gamma motoneurons
Innervate the ends of intrafusal fibres to make them contract to alter sensitivity of the spindles; so they have similar sensitivity despite changes in starting length of the spindle
Problems with stretch reflex proposal
Gain is measured to be less than 1 so can’t be a fully compensatory contraction for unexpected loads
Delays due to negative feedback would lead to muscle oscillation
Spasticity
Due to damage to descending pathways
- Exaggerated high gain stretch reflex
- Brisk response to tendon tapping and oscillating contraction; myoclonus
When are gamma motoneurons very active
During slow high gain reflexes such as walking on a beam
Reciprocal inhibition
reflex inhibition accompanying stretch reflex
Primary spindle afferents innervating inhibitory motoneurons off antagonistic muscles to prevent them working against the other contraction
Recurrent inhibition
reflex inhibition accompanying stretch reflex
Via Renshaw cells
Primary spindle afferents activate inhibitory interneurons of the same motoneuron pool (renshaw cells); type of negative feedback to prevent jerkiness and tremor
Tendon organ context dependent reflexes
Tendon afferents can activate alternate pathways depending on context e.g when walking compared to at rest
Infant specific reflexes
Babinski’s sign/plantar reflex
Grasp reflex
Reflex stepping
Central pattern generators
Intrinsic circuit within spinal cord to simplify a patterned movement e.g walking; just need brain input to start and stop
Most vertebrates have spinally generated locomotion but humans have lost this (except reflex stepping)
All have CPG in brainstem for breathing
Reticulospinal pathway
Ventromedial
From reticular formation
Drives spinal motor control, activating CPGs and whole body stereotypical actions