NeuroPhys Unit 3

  1. Area 4 of motor cortex
    • Ant to cerebral sulcus on pre central gyrus
    • Primary Motor Cortex or M1
    • Movement of contralateral side of body
    • Lowest threshold for electing movement; strong connections to spinal motor neurons
  2. Area 6 of motor cortex
    • Just anterior to area 4
    • Premotor Area (PMA; lateral)
    • -Connects to reticulospinal neurons that then connect to proximal muscles = posture
    • Supplementary Motor Area (SMA; medial)
    • -Connects directly with distal muscles
    • -Influences planning and initiation of movements on basis of past experience; anticipation of movement triggers neutral transmissions in the SMA
  3. Layer V in Cortex (Input-Output of M1)
    • Input from
    • Cortex - Areas 6 (anterior) and 3, 1, 2 (posterior)
    • Project to¬†
    • SC and brain stem
  4. Coding of Movement in M1
    • M1 neurons activate immediately before and during voluntary movement
    • -Encode force and direction
    • Much of motor cortex is active for every movement
    • Cell activity is a "vote" for a particular direction of movement
  5. Posterior Parietal
    • All input to Posterior Parietal Cortex
    • Area 5: info from Somatosensory Cortical areas 3,1,2
    • Area 7: info from Visual Cortex

    • Lesion: impaired body image and perceptual-spatial
    • -Severe = neglect
  6. Prefrontal Areas jobs
    • Abstract thought
    • Decision making
    • Anticipating consequences of actions
  7. Motor Apraxia
    • Unable to carry out movements despite intact sensation, movement, and cognition
    • -Ex. cannot scratch nose to command but scratch it when itches
    • Damage to premotor or SMA
  8. Ideomotor (motor apraxia)
    • Unable to perform purposeful movement on command despite understanding concept
    • -May perform movement automatically
  9. Ideational (motor apraxia)
    • Loss of ability to conceptualize, plan, and execute sequences of motor actions involving use of tools or objects in everyday life
    • -Unable to plan movement related to an object bcs has lost perception/lost knowledge of what object represents
    • -Disturbance in sequential organization of voluntary actions
    • -Ex. comb hair with wrong side or place in mouth
  10. Posterior Parietal role in voluntary movements
    • Assesses context in which movements are being made
    • -Receives somatosensory, propriocentpive, and visual inputs and uses them to determine body positions and target in space
    • -Produces internal models of movement to be made prior to involvement of the premotor and motor cortices
    • -Works with prefrontal area to make decision about movements to be made
    • -These send info to Area 6 informing about kind of action to take
    • -Area 6 determines characteristics of appropriate movement for this purpose
  11. Posterior Parietal and Prefrontal Areas
    • Highest level of hierarchy
    • Make decisions about actions to take and likely outcome of actions
    • Send axons to Area 6
    • -Junction where signals encoding what actions are desired are converted to signals specifying how actions will be carried out = Higher-order motor planning
  12. Motor cortex areas
    • Primary (Area 4 = M1)
    • Motor homunculus
    • Area 6
    • Premotor (PMA)
    • Supplemental (SMA)
    • Regions of input
    • Post. Parietal (5&7)
    • Somatosensory
    • Prefrontal
    • Basal ganglia
    • Efferent destinations
    • Spinal cord, basal ganglia, cerebellum, retic. formation, vestibular nuclei, thalamic nuclei
  13. Basal Ganglia
    • Made up of nuclei
    • -Caudate, Putamen, Globus Pallidus (output to Thalamus), Subthalamic Nucleus, Substantia Nigra
    • Caudate and Putamen together = Striatum
    • -Target of cortical input

    • Regulates
    • M. contraction
    • M. force
    • Multijoint movements
    • Sequence of movements
  14. Basal Ganglia loop
    • Cortex to Basal Ganglia and Thalamus (VL) back to Cortex (esp. SMA)
    • Function: selection and initiation of willful movements
  15. Direct Path for Motor
    • Cortex
    • Striatum
    • Globus Pallidus
    • VL
    • SMA and PMA
    • Cortex
  16. Parkinson's Disease as a Basal Ganglia Disorder
    • Hypokinesia = decreased movement
    • -Slowness of movement = Bradykinesia
    • -Difficulty initiating movement = Akinesia
    • -Increased muscle tone = Rigidity
    • -Tremors of hands and jaw, increased at rest
    • Also cognitive deficits
    • Cause = degeneration of Substantia Nigra
  17. Substantia Nigra Role in PD
    • Degeneration =
    • -Decreased input to Striatum
    • -Uses Dopamine to activate Putamen
    • -Which releases VL from Globus Pallidus inhibition
    • -Therefore, depleted Dopamine decreases input to SMA
    • Treatment
    • -Administer Dopa
    • -BUT doesn't alter degeneration state of S.N. or progression of the disease
  18. Huntington's Disease (Basal Ganglia Disorder)
    • Hyperkinesia = excess movement
    • Also Diskinesias, dementia, and personality, mood, & memory disorders
    • Doesn't present until well into adulthood -> ppl unwittingly pass gene on to children

    Chorea: spontaneous, uncontrollable, purposeless movements with rapid, irregular motions of various parts of body
  19. Huntington's disease cause
    • Loss of neurons in Caudate Nucleus, Putamen, and Globus Pallidus as well as in Cerebral Cortex
    • Damage to BG structures = loss of inhibition to Thalamus = movement disorders
    • Cortical degeneration = personality changes
  20. Ballism (Basal Ganglia Disorder)
    • Type of hyperkinesia
    • Violent, flinging of extremities
    • One side of body (usually) = Hemiballism
    • Cause
    • Damage to Subthalmic Nucleus (usually CVA)
    • Role of S.Nucleus = excites neurons in Globus Pallidus that project to VL
    • So damage to S. Nucleus = loss of excitation of GP = less inhibition of VL = increased SMA activity
  21. Basal Ganglia jobs
    • Facilitates movement by focusing activity from several areas of cortex onto the SMA
    • Filter - keeps inappropriate movements from being expressed
  22. Cerebellum
    • Provides control over timing of body's movements; loop circuit connects to motor cortex and modulates signals
    • Analyzes visual signals associated with movement
    • -Calculates speed of movements and adjusts accordingly
    • Some involvement in language, attention, memory, and emotions¬†
    • Sequences muscle contractions for movement
  23. Cerebellum lesions
    • Lead to ataxia = uncoordinated movements
    • Test: touch finger to nose, then do with eye closed
    • -Cannot do with cerebellar damage
    • -Move shoulder, then elbow, then wrist = dysynergia
    • -Finger ends up short of or past nose = dysmetria
  24. Cerebellum features
    • Folia: shallow ridges
    • Deep cerebellar nuclei: white matter
    • -Relays cerebellar cortical output to brain stem
    • Vermis: bump that separates lateral Cerebellar Hemispheres
  25. Cerebellar Regions
    • Vestibulocerebellum: equilibrium and balance = postural muscles and eye movements
    • Spinocerebellum: gross limb movements
    • -Controls muscle tension at all times while releasing those muscles required to execute movements
    • Cerebrocerebellum: distal limb voluntary movements
    • -Ensures when one set of muscles initiates, the opposing set acts as a brake, so the body part arrives at its target precisely
  26. Motor Loop through Lateral Cerebellum
    • Instructs Primary Motor cortex regarding direction, timing, and force of movement
    • For very fast movements
    • -Based on predictions for outcome (too fast for feedback)
    • -Based on past experiences = motor learning
  27. Pathology of Ataxia
    • Lesions
    • Unilateral cause jerky uncoordinated movements
    • Vermal causes truncal instability
    • Paravermal causes gait and limb ataxia
    • Vistibulocerebellum causes nystagmus and difficulty maintaining balance
    • Inherited disorders - Degeneration of Purkinje cells
    • Purkinje neurons release NT GABA which inhibits the firing rate of neurons therefore inhibiting unwanted involuntary movements
  28. Primary Clinical Features of Ataxia
    • Low muscle tone
    • Asynergy - lack of coordination
    • Dysmetria - inability to judge distance or scale
    • Dysdiadochokinesia - inability to perform rapid movements

    • Primary features dependent on part of the cerebellum affected
    • -Vestibulocerebellum dysfunction
    • --Impaired balance and control of eye movements
    • --Postural instability
    • -Cerebrocerebellum dysfunction
    • --Appendicular Ataxia = impaired ability to perform smoothly coordinated voluntary movements
    • -Spinocerebellum dysfunction
    • --Wide based gait
    • --Uncertain starts and stops, lateral deviations, and unequal stops
  29. Upper Motor Neuron Lesions
    • Cerebral Palsy
    • Brain injury
    • MS
    • Brain tumors
    • CVA
    • SCI
  30. Common characteristics of UMN Lesions
    • Paresis
    • Abnormal muscle activity
    • -Cocontraciton or over/underactive m activity¬†
    • Abnormal cutaneous reflexes
    • Hyperactive stretch reflex
    • Muscle tone/spasticity = overactivity of muscles both with movement and "at rest"
Card Set
NeuroPhys Unit 3
NeuroPhys Unit 3