NeuroPhys Unit 3

• 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

• 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

• Input from
• Cortex - Areas 6 (anterior) and 3, 1, 2 (posterior)
• Project to 
• SC and brain stem

• 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

• 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

• Abstract thought
• Decision making
• Anticipating consequences of actions

• 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

• Unable to perform purposeful movement on command despite understanding concept
• -May perform movement automatically

• 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

• 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

• 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

• 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

• 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

• Cortex to Basal Ganglia and Thalamus (VL) back to Cortex (esp. SMA)
• Function: selection and initiation of willful movements

• Cortex
• Striatum
• Globus Pallidus
• VL
• SMA and PMA
• Cortex

• 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

• 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

• 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

• 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

• 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

• Facilitates movement by focusing activity from several areas of cortex onto the SMA
• Filter - keeps inappropriate movements from being expressed

• 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

• 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

• Folia: shallow ridges
• Deep cerebellar nuclei: white matter
• -Relays cerebellar cortical output to brain stem
• Vermis: bump that separates lateral Cerebellar Hemispheres

• 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

• 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

• 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

• 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

• Cerebral Palsy
• Brain injury
• MS
• Brain tumors
• CVA
• SCI

• 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"