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Flashcards

NEUR2530 - Weeks 7-9

Mikaela Sullivan NEUR2530 Inglês 55 flashcards

Flashcards do conjunto (55)

  1. 1What are the key characteristics of voluntary movements?-Greater flexibility than reflexes or rhythmic movements
    -Goal directed
    -Begin non-specific intent to more specific signals to muscles
    -higher order (decisions making) to lower order (specific commands)
  2. 2What is the spinal cord made of?-White matter: ascending & descending tracts
    -Gray matter: cell bodies (motorneurons & interneurons)
  3. 3What are the components & features of the brain stem?-Midbrain
    -Pons
    -Medulla oblongata
    Contains groups of cell bodies: nuclei (gray matter) & relay processing centres
    -Contains fibre tracts: spinal cord (white matter)
  4. 4What are the components of the cerebrum?-Cerebral cortex
    -Diencephalon (thalamus & hypothalamus)
    -
  5. 5What are the areas of the brain?Brainstem, cerebrum, basal ganglia & cerebellum
  6. 6Name the features of the cerebrum.-Cortex has thin sheet of cell bodies (2-4mm)
    -Folded to increase area, higher processing
    -Divided into lobes: frontal, parietal, temporal, occipital
    -Primary & secondary motor cortex
  7. 7What is within the thalamus?-Group of nuclei
    -Relay and processing information
    -Basal Ganglia & cerebellum
  8. 8What is the function of the ascending pathways?-Pass info from spinal cord (sensory receptors) to brain
    -Sensory perception
    -Integrate with movement control: planning & feedback
  9. 9What are the general characteristics of ascending pathways?-Topographic organisation: based on location of receptors (maintained throughout CNS)
    -Segregation of ascending tracts
    -Relay nuclei: process & pass on info
    -Reach somatosensory cortex where somatotopic organisation maintained
  10. 10What is the function of decending pathways?-Pass info from brain to spinal cord
    -Muscle activation though direct (monosynaptic) & indirect (di-synaptic) action on mn's
    -Create info about movement commands (efference copy): intended vs. actual outcome
  11. 11How does a spinal cord injury occur?-Severity of dysfunction determined by "completeness" of lesion
    -Interupts transmission of afferent & efferent signals below lesion
  12. 12What are the different outcome of SCI?-Paresis (weakness) & paralysis (no activation)
    -Spacticity (rigidity & jerky mvm't): hyperactive velocity dependent stretch reflexes
  13. 13What are the general characteristics of decending pathways?-Tracts organised somatotopically
    -Axial muscles ventro-medial
    -Distal musces dorso-lateral
  14. 14What is the corticospinal pathway?-Decending pathway
    -1M fibres
    -Originates in Primary motor cortex, premotor areas & somatosensory cortex
    -Divides into lateral (distal) & ventral (axial) corticospinal tracts
  15. 15What is the purpose of the lateral corticospinal pathway?-Projects to alpha & gamma mn's & in's of distal muscles
    -Some direct connections w/ mn's
    - monosynaptic connection to hand > more proximal muscles
    -Greater flexibility & fine control of digits
  16. 16What is the function of ventral corticospinal tracts?-Fibres don't cross midline at pyramidal decussation
    -Fibres project bilaterally to ventro-medial spinal cord (axial muscles)
    -Innervate similar targets to ventro-medial brainstem tracts
  17. 17Explain the vestibulo-spinal pathway-Oldest decending pathway
    -Large input from vestibular apparatus and cerebellum
    -Terminate in ventro-medial grey matter (mostly interneurons)
    -Axial muscles
  18. 18What happens in the pathways between the cortical & subcortical motor areas?-Cortical motor-areas receive input directly or indirectly (via thalamic relay)
    -Send info about expected sensory outcome (cerebellum)
    -Determine how to modify commands based on movements progression etc. (sensory receptors, cerebellum etc)
    -Refine & initiate movement patterns (basal ganglia)
  19. 19What does the primary motor cortex (m1) control?-Involvement in executive control of movement in M1
  20. 20What does codes for mean?-Cells in nervous system fire based on particular characteristic of mvm't
    -E.g. cell fire fastest when elbow flexors activated and slowest when extensors activated, codes 4 activation flexor musles
    -Can find what type of info cells are responsible for in mvm't planning
  21. 21How is M1 organised?-Homonculus: loosely accurate
    -M1 cells that fire fastest for activation of different muscles overlap considerably
    -
  22. 22What exactly does M1 do?-Projects to mn's of many muscles in spinal cord
    -Makes indirect & direct connections with mn's
    -Inputs from M1 are integrated with inputs from other decending tracts & spinal circuits
  23. 23What is the relationship of motor unit firing frequency and force?-Sigmoidal
    -Slow twitch less force than fast twitch
  24. 24Results of monkey wrist extension/flexion experiment.-CTN (corticospinal tract neurons) fires prior to active wrist flexion
    -CTN fires faster when ^ Force required 4 Fl
    -CTN quiet when wrist passively moved E>F
    -M1 neurons code active movement as well as body position
  25. 25What is force coding?-M1 cells increase firing rate w/ ^ing force
    -Not linear relationship
    -4 pattern types: phasic tonic (59%), tonic (28%), phasic ramp (8%), ramp (5%)
    -Produce constant force but M1 cells switching on & off or changing frequency
  26. 26How does M1 code for direction of movement/force?-Monkey moved to 8 targets
    -Cells fire at higher rates for "preferred" movement direction
    -M1 cells directionally tuned: still fire when movement is near preferred direction
    -Movement direction can be predicted by vector sum: "population coding"
  27. 27Do M1 cells shift preferred direction with posture change?-50% cells did not shift preferred direction
    -These cells code for direction of movement in space
    -32% M1 cells shifted preferred direction in the same way as muscles
    -These cells code "muscle activation"
  28. 28What are the characteristics of the secondary motor area?-Supplementary motor area (SMA) & Premotor cortex (PMC) project to both M1 & spinal cord
    -Higher order processing & diret movement control
    -Stimulation of PMC > mvm't @ >1 joints
    -Stimulation SMA cause bilateral mvm'ts
  29. 29How do lesions interfere?-Lesions interfere with performance of complex rather than simple movements
  30. 30What was the role of SMA thought to be historically?-Primary involved in planning & control of sequential movements, that are internally initiated
    -SMA active during active & mental rehearsal
  31. 31What is the recent idea of SMA?-SMA contributes to control of "difficult" coordination tasks
    -Same area of M1 activated in synergist & non-synergist tasks
    -^ activation SMA for non-synergistic tasks
  32. 32How are cells of PMC involved in various situations?-All cells in PMC involved in control of external direction
    -Changes in PMC activity earlier than changes for M1
    -Time for corticospinal transmission and electro-mehanical delay around 60-100ms
  33. 33Is the PMC anatomically defined?-PM cortex active during both toe & finger signing
    -So organisation not strictly anatomically defined
    -Toe areas in M1 can access circuits in PMC that usually project to fingers
    -Can produce similar movement patterns in different body parts
  34. 34What invariants are evident?1) Invariant sequence of kinematic events e.g. maxima & minima in speed profile
    2) Invariant relative timin in occurence of these events (irrespective of speed or size of movement)
  35. 35Name the 5 nuclei of the basal ganglia1) caudate, 2) putamen, 3) subthalamic nucleus (STN) - input
    4) globus pallidus, 5) substantia nigra (output)
  36. 36Where do the nuclei input & output?-Input from cortex & thalamus
    -Output to cortex and brainstem
  37. 37What are the two pathways of the Basal ganglia & what is their role?Direct routh to GPi
    Indirect routh: GPe to STN to GPi
    -Modulate inhibitory output of basal ganglia
  38. 38What is the direct route?-Activating inhibits the GPi
    -Reduces normal inhibitory effect of Gpi
    -Results in LESS inhibition of thalamus & MORE excitation of cortex
    -Facilitation of movement "releasing brakes"
  39. 39What is the indirect route?-Activating (by inhibition of STN) causes excitation of GPi
    -Increases inhibitory effect of GPi
    -MORE inhibition LESS excitation of cortex
    -Inhibits movement: "slamming brakes"
  40. 40Why are there 2 pathways for basal ganglia?1. Balance of pathways helps scale the magnitude of cortical & muscle activity. "finetuning"
    2. Direct could reinforce activation of required muscles & Indirect could ensure unwanted muscles not activated - FOCUS activation of appropriate cortical areas
  41. 41How does dopamine affect the direct & indirect pathways of the basal ganglila?-Facilitates movement
    -Excitatory to striatal neurons that project to direct route
    -Inhibitory to striatal neurons that project to indirect route
  42. 42What are the symptoms of Parkinson's disease?TRAP (tremor, rigidity, akinesea/bradykinesia, postural instability)
    Akinesea = lack of movement
    Bradykinesia = slow movement
  43. 43What causes parkinson's disease?-Degeneration of dopaminergic neurons in the substantia nigra
    -Drug induced: botched amphetamine
    -Highly toxic to dopaminergic neurons in the substanttia nigra pars compacta
  44. 44How can parkinson's be treated with drugs?-Levodopa, cable to cross blood brain barrier, dopamine receptor agonists
    -Effects decline with use (less improvement over years)
    -Can't offset the death of dopaminergic neurons on striatum
  45. 45Surgical treatments for parkinsons-Lesion of globus pallidus internal segment or subthalamic nucleus (reduced thalamic inhibition), irreversible
    -Deep brain stimulation:
    -High frequency stimulation of STN to GPi, causing interference, stops unwanted excessive inhibition
  46. 46What is huntingtons disease?-Hyperkinetic disease: inherited
    -Symptoms: abnormal movements, cognitive decline
    -Cause: specific death of indirect pathway neurons in striatum (atrophy of caudate & putamen)
    -Decrease in inhibition from indirect route, NO TREATMENT
  47. 47Describe some anatomical features of the cerebellum-Arranged in folia & 2 hemispheres
    -Cerebellar cortex - gray matter outside
    -Internal white matter: tracts & 3 pairs of deep nuclei
    -Connected to brainstem by inferior, superior & middle peduncles
  48. 48What is the role of the cerebellum?-Compares intended movement with the actual movement & helps adjust motor output accordingly
    -Removal disrupts spatial & temporal accuracy, balance, muscle tone & motor learning.
  49. 49What is the input for the cerebellum?-Massive input from cortex (intention info)
    -20M cortico-ponto-cerebellar axon
    -Input from sensory receptors provide info about execution
  50. 50What is the output of the cerebellum?-Through cerebellar nuclei to motor and premotor brain regions (via thalamus) which ontrol spinal interneurons & motoneurons
  51. 51Name and describe the functional divisions of the cerebellum-Vestibulocerebellum: most primitive, balance, eye movements
    -Spinocerebellum: ongoing control of voluntary movement, posture & locomotion
    -Cerebrocerebellum: most recent, planning & conscious assessment of mvm't
  52. 52What are the input and outputs of vestibulocerebellar?I: Vestibular apparatus, vision
    O: Vestibular nuclei, alters vestibulospinal & corticospinal tracts
    Damage: disturbances of equilibrium
    Nystagmus at same side lesion
  53. 53What are the input & outputs for the spinocerebellum?I: cortex & spinal interneurons
    O: Deep cerebellar nuclei controls proximal & distal musculature
    -Alters activity in rubrospinal & corticospinal pathways
    Damage: Unaccurate reaching, uncoordinated movement, hypotonia
  54. 54Cerebrocerebellum input & outputsI: cerebral cortex via nuclei in pons
    O: Deep cerebellar nucleus to cortico motor & premotor regions & red nucleus
    Damage: timing movements, perceptual aspects timing
  55. 55List the cerebellar movement disorders?1. Impaired balance & gait
    2. Impaired coordination (Ataxia)
    3. Decreased muscle tone (hypotonia)
    4. slow corrective movements

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NEUR2530 FlashCards sobre NEUR2530 - Weeks 7-9, criado por Mikaela Sullivan em 07-11-2017.
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