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Week 5

Dolu Falowo Foundations 4 English 77 cards

Cards in this deck (77)

  1. 1Describe some general features of the motor system-Hierarchical organisation
    -Feedback loops
    -Somatotopic organisation in the cortex and spinal cord
  2. 2What is a reflex?-Protective
    -Motor patterns are generated in the spinal cord
    -Closed loop
  3. 3What is a voluntary movement?-Goal-directed
    -Command originates from higher centres
    -Open loop (comes from the brain down the spinal cord)
  4. 4What is a rhythmic motor pattern?-Combination of reflex and voluntary movement
    -Both occur at the same time but the autonomic processes can be overridden
  5. 5How is the descending input for upper motor neurones modified?Descending input on the brain is superimposed on the intrinsic spinal circuits
  6. 6How is fine motor control maintained?-Innervated by lateral motor neurones
    -Flexors and distal muscles fall under this category
    -UMN originate from the red nucleus
  7. 7How is posture maintained?-Innervated by medial motor neurones
    -Under control of brainstem (unconscious)
    -Includes axial (trunk) and proximal muscles
    -UMN originate from the superior colliculus, reticular and vestibular nucleus
  8. 8Describe the corticospinal tract-Contralateral projection from the cortex to spinal motor neurones
    -Monosynaptic connection with alpha motor neurones which control (flexor) distal muscles
    -Axons have cell bodies in areas 4+6 in the motor cortex
  9. 9Describe the rubospinal tract-Contralateral projections from the red nucleus down the spinal cord
    -Involved in voluntary movement of distal musculature
    -Similar function to corticospinal tract (but CS tract predominates)
  10. 10What happens if there are lesions in the lateral pathways (CS and rubrospinal tract)?-Sometimes used in relief of intractable pain
    -Motor deficit can occur (slower voluntary movements)
    -Posture is unaffected
    -If CS tract is lost, rubrospinal tract can compensate
  11. 11Describe the vestibulospinal tract-Relays gravitational sensory information from the vestibular labyrinth (inner ear) and stretch receptors in axial muscles
    -Maintains head, neck and leg position
  12. 12Describe the tectospinal tract-Relays visual sensory information from the retina and visual cortex
    -Orients heads/eyes to visual and auditory stimuli (allows tracking)
  13. 13Describe the reticulo-spinal tract-Originates from the pons
    -Enhances anti-gravity reflexes of spinal cord
    -Facilitates leg extensors for maintaining standing posture
  14. 14Describe the medullary reticulospinal tract-Opposing effect of pontine reticulospinal tract
    -Frees anti-gravity muscles from reflex control (voluntary override)
  15. 15Describe the primary motor complex-Control of distal musculature
    -Fine motor control
    -Low stimulus threshold
    -Located in area 4 of the motor cortex
  16. 16Describe the premotor cortex-Control of proximal musculature and movement sequencing
    -Preparation and initiation of movement
    -Located in lateral area 6
  17. 17Describe the supplementary motor area-Role in planning and initiation of movement
    -Bi-manual coordination
    -Located in fronto/medial area 6
  18. 18Describe the primary motor cortical output neurones (ie UMNs)-Pyramidal in shape
    -Cell body in 5th cortical layer
    -Somatotopically organised
    -Activate small groups of muscles instead of single ones
    -Encodes force/direction of movement
    -Output neurone: Betz cell
  19. 19Describe the cerebellum-Closely involved with brainstem mechanism
    -Control of muscle tone
    -Coordinates sensorimotor information
    -Motor learning
    -Does not project beyond the brain
    -Split into 3 components: spino-cerebellum, vestibulo-cerebellum and cerebro-ponto-cerebellum
  20. 20Describe the connections and function of the spino-cerebellum region-Sensory input from the spinal cord
    -Output to the reticular formation and red nucleus and motor cortex
    -Output then leaves via the spinal cord and controls axial musculature and posture
  21. 21What happen if there is damage to the spino-cerebellum?-Hypotonia
    -Ataxia (unsteady, staggering gait)
    -Dysmetria (inaccurate termination of movement)
    -Intention tremor
  22. 22Describe the connections and function of the vestibulo-cerebellum region-Input and output to the vestibular nucleus
    -Controls posture, balance and eye movement
  23. 23What happen if there is damage to the vestibulo-cerebellum?-Slow saccades (impairment of the fast tracking movements of the eyes)
    -Nystagmus (involuntary saccades)
    -Ataxia
  24. 24Describe the connections and function of the cerebro-ponto-cerebellum region-Intracerebral motor loop (from the cortex-pons-cerebellum-dentate nucleus-ventrolateral thalamus-cortex (M1))
    -Instructs M1 regarding movement, direction, timing and force
    -Compares intended movements with actual movements and sends compensatory movements to M1
  25. 25What happen if there is damage to the cerebro-ponto-cerebellum?-Ataxia
    -Dysmetria
    -Asynergy (uncoordinated agonst/antagonist muscles)
    -Dysarthria (inarticulate speech due to poor oropharyngeal muscle control)
  26. 26Describe the 3 layers of the cerebellar cortexMolecular layer: cell bodies of stellate and basket cells, excitatory axons of granule cells and dendrites of inhibitory Purkinje cells
    Purkinje cell layer: purkinje cell bodies
    Granular layer: granule cells.
  27. 27What are the inputs of the cerebellar cortex?-Climbing fibres from the inferior olive (excite Purkinje cells)
    -Mossy fibres from brainstem nuclei (indirectly excite Purkinje cells via parallel fibres of granule cells)
  28. 28What is the output of the cerebellar cortex?Purkinje fibres which project to the deep cerebellar nuclei
  29. 29Describe the cycle of information in the cerebellumDeep cerebellar nuclei- mossy fibre/climbing fibre- Purkinje cell- deep cerebellar nuclei
  30. 30What is the function of the deep cerebellar nuclei?Compares input from mossy and climbing afferent input and checks for errors:
    -before via collaterals from axons to the purkinje cell
    -after cerebellar processing
  31. 31What is use-dependent plasticity (in relation to Purkinje cells)?-Seen in parallel fibres
    -Enables motor learning
    -Allows us to subconsciously perform complex tasks
  32. 32Describe the basal ganglia-Integration of sensory and motor information
    -Information from the cortex enters the basal ganglia and enters a cortex loop in the thalamus
  33. 33What is the function of the cortico-basal ganglia-cortical loop?-Integrates motor and sensory information from the cortex
    -Relays information back to the cortex via the thalamus
    -Motor circuit output is to the premotor cortex
    -Voluntary movement is selected and inhibited
  34. 34What are the structures of the basal ganglia?Striatum:
    -caudate nucleus
    -putamen
    -nucleus accumbens
    External and internal segment of the globus pallidus
    Reticulata and pars compacta of the substantia nigra
  35. 35Describe the effect of dopamine on the direct pathway-Promotes movement
    -Acts of excitatory D1 receptors on the striato-GPi/SNr neurone
    -Basal ganglia output to the thalamus is reduced (via GABA)
    -There is less inhibition to the thalamus so movement is promoted
  36. 36Describe the effects of dopamine on the indirect pathway-Promotes movement which would otherwise be suppressed
    -Acts on D2 receptors of striato-GPe neurones
    -This reduces GPe, STN and SNr/GPi activity
    -Increased action from the thalamus to the cortex
  37. 37Describe Parkinson's disease-Symptoms: (resting) tremor, bradykinesia, rigidity
    -Progressive disorder
    -Caused by progressive degenerative loss of the nigro-striatal dopaminergic pathway (excessive inhibition of the thalamo-cortico pathway). Lewy bodies are found in cells
  38. 38How is Parkinson's treated?-L-Dopa (dopamine replacement drugs)
    -Dopamine agonists
    -MAO-B inhibitors (prevent dopamine breakdown)
    -Deep brain stimulation
  39. 39Describe Huntington's disease-Autosomal dominant
    -Uncontrollable, rapid motor movements
    -Excessive 'choreiform' movements
    -Later stages: psychiatric disturbance and dementia
    -Caused by a loss of striatal ouput neurones in the indirect pathway. This suppresses the STN and decreases basal ganglia output leading to involuntary movement
    -No treaments, only symptomatic relief
  40. 40Describe hemiballismus-Damage to the subthalamic nucleus
    -Results in violent flailing movements of limbs contralateral to the damaged side
  41. 41Describe tardive dyskinesia-Increased dopamine receptor sensitivity due to long-term exposure to antipsychotic dopamine receptor antagonist drugs
    -Results in uncontrolled movements (esp facial and trunk muscles)
  42. 42What are the differences in terms of... for cerebellum vs. basal ganglia disorders? -tremor -muscle tone -prognosis-Intention tremor vs. resting tremor
    -Hypotonia vs. rigidity
    -Symptoms improve vs. get worse
  43. 43Function of the corticospinal tract?Innervation of skeletal muscles of the limbs and trunk
  44. 44Function of the corticobulbar tract?Innervates the head and neck muscles of somatic and branchial origin. Cranial nerves are the LMN
  45. 45Describe briefly spinal reflexesAfferent neurone and the motor unit it innervates are at the same segmental level in the spinal cord
  46. 46Describe briefly deep tendon reflexes-2 neurone reflex arc which provide a feedback mechanism for maintaining muscle tone
    -Afferent nerve fibres synapse directly with alpha motor neurones or indirectly via Renshaw cells (inter-neurone)
  47. 47Muscle tension is under control of the descending pathways. How does it initiate action?Via gamma motor neurones which influence specialised cells in muscle spindle increasing their sensitivity to muscle stretch.
  48. 48Where are the cell bodies of the corticobulbar/corticospinal tracts located?Pre-central gyrus (motor cortex)
  49. 49Describe the lateral corticospinal tract1) Nucleus of the UMN is in the pre-central gyrus
    2) UMN descends through internal capsule
    3) Passes through midbrain via the crus cerebri through the pons and medulla
    4) Majority of the tract decussates at the level of the medulla (at the pyramids)
    5) Synapses with LMN in the ventral horn at the appropriate spinal level
  50. 50Describe the ventral corticospinal tract1) Nucleus of the UMN is in the pre-central gyrus
    2) UMN descends through internal capsule
    3) Passes through midbrain via the crus cerebri through the pons and medulla (via pyramids)
    4) Decussates and synapses with LMN in the ventral horn at the appropriate spinal level
  51. 51Function of the corticospinal tract?Skilled voluntary control of distal (lateral tract) and proximal (ventral tract) muscle
  52. 52Describe the rubrospinal tract1) Originates from the red nucleus (midbrain tegmentum)
    2) Decussates at the level of the midbrain
    3) Passes through the pons, medulla
    4) Synapses with the LMN at the appropriate spinal level
  53. 53Function of the rubrospinal tract?Excitatory to limb flexor muscles (tone increases)
  54. 54What is the origin, function and decussation of the reticulospinal tract?-Reticular formation of pons/medulla
    Influence secondary movements and reflexes
    Various levels
  55. 55What is the origin, function and decussation of the tectospinal tract?Superior colliculus of midbrain
    Reflex postural movements on sight (startle response)
    Soon after origin: dorsal tegmental decussation
  56. 56What is the origin, function and decussation of the vestibulospinal tract?Vestibular nuclei in pons/medulla
    Mediates excitation of limb extensor muscles involved in anti-gravity tone
    None
  57. 57Define dyskinesiaInvoluntary muscle movements and diminished voluntary movements
  58. 58What type of movements is associated with lesions in the basal nuclei?-Abnormal motor control
    -Abnormal tone
    -Involuntary control (unable to suppress unwanted movements)
  59. 59What anomalies of movement is associated with Parkinson's disease? Cause?-Tremor
    -Muscular rigidity
    -Slow imprecise movement
    Degeneration of substantia Nigra (loss of dopamine)
  60. 60What anomalies of movement is associated with Huntington's chorea?-Lack of coordination
    -Unsteady gait
    -Uncontrolled rapid jerky movements
  61. 61What anomalies of movement is associated with Athetosis? Cause?-Abnormal muscle contraction
    -Involuntary writhing movements
    Lesion to corpus sriatum
  62. 62What anomalies of movement is associated with Hemiballism? Cause?-Involuntary flinging motions (usually restricted to 1 arm)
    -Jerky, involuntary movement
    Basal ganglia disease (subthalamic nuclei)
  63. 63What are some disorders of the extrapyramidal system that influence LMN activity?-Diseases of the basal ganglia
    -Abnormal involuntary movement
    -Occur at rest, disappear in sleep
    -No paralysis/sensory loss
  64. 64What are features of a UMN lesion?-No muscle wasting
    -Spasticity
    -Hyperreflexia
    -Positive babinski reflex
    -Muscle weakness
    -Paralysis
    -Contralateral side is affected
  65. 65What are features of a LMN lesion?-Muscle wasting
    -Fasciculations/fibrillations
    -Hyporeflexia (/absent)
    -Normal babinski reflex
    -Flaccid paralysis
    -Decreased muscle tone
    -Muscle weakness
  66. 66What is hemiparesis?-Weakness affecting 1 side of the body
    -Indicates UMN lesion of contralateral side
    -Due to infarction, haemorrhage or cerebral lesion
  67. 67What is paraparesis?-Partial paralysis of lower limbs
    -Indicates multiple sclerosis or damage in the spinal cord
  68. 68Reduced/absent muscle tone is associated with LMN lesions. Why does it occur? How do you assess?-Due to damage to gamma motor neurones (innervate intrafusal fibres)
    -Patient relaxes, each limb is passively moved at several joints assessing resistance/rigidity
  69. 69What is spasticity? Why does it occur?-Tight/stiff muscles and an inability to control them. Reflexes may persist for too long/be too strong
    -UMN lesion: loss of excitatory input leading to passive stretching of muscles
  70. 70What are the major causes of UMN lesions?-Vascular: stroke
    -Trauma: space occupying lesion
    -Cerebral palsy
    -Degenerative disease (MS)
    -Infection
  71. 71What are the major causes of LMN lesions?-Ischaemia: stroke
    -Trauma (direct: impact to head, indirect: brain damaged inside skull)
    -Disease: polio
    -AI: Guillain Barre
  72. 72What is atrophy? Why does it occur?Progressive loss of muscle bulk
    -Occurs due to muscle disease + absent innervation of extrafusal fibres
  73. 73The motor supply of the tongue is the hypoglossal nerve (CNXII). What are the signs of UMN and LMN lesions?UMN: contralateral deviation of the tongue
    LMN: ipsilateral deviation of the tongue (unopposed action from genioglossus muscle)
  74. 74How does motor supply to the frontalis differ from the orbicularis oris muscle?Frontalis: temporal branch of facial n. Bilateral innervation
    Orbicularis oris: buccal branch of facial n. Unilateral innervation
  75. 75How would you differentiate between UMN and LMN lesions of the facial nerve?LMN: ipsilateral paralysis of whole face
    UMN: ipsilateral paralysis of lower 2/3 of the face but forehead is intact (bilateral innervation so 1 tract is still intact)
  76. 76What is bulbar and pseudobulbar palsy?Bulbar: impairment of CN IX-XII due to LMN lesion
    Pseudobulbar: impairment of CN IX-XII due to (bilateral) UMN lesion
  77. 77Where is the site of damage for: -motor neurone disease -syringomyelia -multiple sclerosis-Degeneration of ventral horn cells
    -Selective damage of spinothalamic tract (central canal is enlarged, second order neurones are damaged)
    -Damage to fasiculus cuneatus

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Motor control Topography of the major motor systems
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Dolu Falowo
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