Exam 3: Upper Motor System Flashcards
Anatomy—location of primary motor cortex and premotor cortex, layers of M1, location and function of Betz cells and non-Betz pyramidal neurons:
The pyramidal cells of cortical layer 5 are the upper motor neurons of the primary motor cortex.
It was originally thought that the majority of corticospinal fibers originate from the Betz cells in layer 5 of M1
Betz cells contribute less than 5% of the corticospinal fibers
Most corticospinal fibers originate from non-Betz pyramidal neurons of layer 5 in the premotor cortex and M1
Corticobulbar tract:
bilateral innervation of brainstem nuclei. Carries motor information to cranial nerve motor nuclei, Controls muscles of the face, head, and neck
Innervates cranial motor nuclei bilaterally (with a few exceptions)
Lateral corticospinal tract:
decussate in medulla. 90% of the fibers in the corticospinal tract, Decussate in the medullary pyramids = pyramidal decussation
Terminates primarily in lateral ventral horn, Controls distal movements
Ventral corticospinal tract:
10% of the fibers in the corticospinal tract, Do not decussate, Terminate bilaterally, Controls movement of trunk and proximal limb muscles
Somatotopic organization in M1
Somatotopic organization in M1 similar to the somatosensory cortex: roughly true, but somatotopic map in M1 is much more coarse–overlapping, intermingled, and fractured
M1 organized in a way that activation of particular cortical neurons activates a particular muscle?
Even small microstimulations elicit responses in several muscles
Particular movements can be elicited by stimulation of different areas
What does activity in M1 reflect? (movements vs. individual muscles)
Organized movements rather than individual muscles are represented in the map
Neurons in nearby regions linked by local cortical circuits
Microstimulation of M1 can cause activation of ⍺-motoneurons with very short latencies (down to7 ms)
When preparing a voluntary movement, activation of M1 usually starts on the order of 100 ms before motoneurons are activated.
Studies suggest that populations of neurons in M1 carry information about various movement parameters (movement direction, required force, speed, etc.)
What is spike-triggered averaging and why would you use it?
correlate the timing of a single cortical neuron’s activity with onset times of contractions in muscle
What is a muscle field?
the peripheral group of muscles which are activated by a given upper motor neuron
Describe the evidence showing that M1 contains a map of behaviorally relevant
postures. What is the argument against this?
stimulation of a single site specified a final posture rather than the direction of movement
If it were true that M1 neurons only care about final postures or final spatial locations, in recording studies one should find neurons that are maximally active for movements to a particular spatial location, regardless of the starting position. This has not been observed.
Describe the likely model of mapping between motor cortex and muscles:
Probably there is no one-to-one mapping between neurons in motor cortex and particular muscles.
Likely there is a many-to-many mapping and this mapping can still be modified by sensory feedback at both the cortical and the spinal cord level.
What type of coding is necessary for representing movement direction in M1? Why?
Upper motor neurons in M1 are broadly tuned for direction
Firing rate of individual upper motor neurons prior to each direction of movement
Population vector (red arrows) represent movement direction encoded by the simultaneous activity of the entire population of recorded units
What are the functions of the premotor cortex and supplementary motor areas?
Microstimulation in premotor cortex can elicit more complex movements than stimulation in M1, but larger currents are required
Premotor lesions–movements can still be executed, but obstacles can no longer be avoided Mental rehearsal of movements activates premotor areas, but not the primary motor cortex.
Premotor areas are more involved in motor planning.
Explain the evidence showing that responses in M1 are limb-specific while responses in
The premotor cortex is not:
Activity of a premotor cortex neuron in a monkey during an instructed-delay reaching task.
Neuron is directionally tuned with a preference for rightward movements.
The directional tuning is identical whether the left or right arm is used.
Relatively inactive during movement execution
What do neurons in SMA encode?
Some neurons in the SMA encode a specific sequence of motor acts
Mirror neurons—what do they respond to? Where are they located?
Located in the ventrolateral subdivision of the PM
Respond in preparation for a particular movement, as well as when the same action is observed
Do not respond when actions are just pantomimed•Respond during observation of behavior even when final stage of action is hidden
Anatomy of the basal ganglia:
4 nuclei: Striatum (caudate, putamen, ventral striatum) Globus pallidu Substantia nigra Subthalamic nucleus
Symptoms of damage to the basal ganglia:
Deficits in the basal ganglia do not lead to paralysis, but to involuntary movements or to immobility without paralysis. Parkinson disease (diminished movement) Huntington disease (excessive movement). Basal ganglia are also involved in cognitive/behavioral deficits.
Direct and indirect basal ganglia pathways:
Direct pathway: release thalamic neurons from tonic inhibition > activate upper motor neurons
Indirect pathway: increase tonic inhibition > inhibit upper motor neurons
Parkinson’s disease—causes, symptoms, treatment:
Dopamine deficiency resulting from degeneration of dopaminergic neurons in the substantia nigra
Relative overactivity of the indirect pathway
Consequence: output neurons of basal ganglia are more active than usual•Stronger inhibition of thalamus/cortex than usual
Consequence: hypo-or akinesia (problems with initiating or stopping movements)
Parkinson Possible Treatments
Drug therapy: administration of L-DOPA (dopamine precursor). Surgical intervention. Subthalamic nucleus: remove excitatory input to Gpi. GPi: remove inhibitory input to the thalamus/cortex. Deep brain stimulation: GP, Subthalamic nucleus, thalamus
Huntington’s disease—causes, symptoms, treatment:
Caused by a genetic defect
Leads to cell apoptosis in the striatum (primary, but not only target), affecting the indirect pathway
Consequence: indirect pathway does not provide sufficient inhibitory input to neurons in GPe
The output neurons of the basal ganglia provide less inhibition to the thalamus/ cortex. Consequence: hyperkinesia (unwanted movements)
The size of the striatum is dramatically reduced in people with advanced HD
Function of the cerebellum, what happens if it’s damage?
Involved in the adjustment of movements while in progress and during repetition
Projects mainly to premotor and motor systems of the cortex and the brain stem
Cerebellar systems are ipsilateral to the controlled muscles (in contrast to the cortex).
Damage disrupts spatial accuracy and temporal coordination of movements and impairs motor learning and certain cognitive functions.
Anatomy of the cerebellum
Spinocerebellum Cerebrocerebellum Vestbullocerebellum Vermis Nodulus Flocculus Deep cerebellar nuclei: Festigar Input mainly to the cerebellar cortex, Output mainly from the deep nuclei
