Motor System Flashcards
What are the DA receptors in the modulatory loops in basal ganglia doing (D1 vs D2 pathways)?
D1 (direct pathway) and D2 (indirect pathway) receptors are located in the putamin (forebrain next to the thalamus)
Both go to thalamus but D2 has layover. Has more inhibition and can be modulated more for complex movements.
D1 is like the “go” functions that initiate motor movements.
Parkinson’s has difficulty initiating
what is locked in syndrome and what causes it?
Individuals have damage to brainstem (lesions) which leads to inability to complete voluntary movements (cant speak or move but can move eyes. Ppl can communicate through eye blinks)
Cognitive and autonomic functions unaffected
Cant act on any sensations
what are the two different types of motor neurons
Lower motor neurons
Upper Motor neurons
- Pyramidal system (corticospinal tract)
- Extrapyramidal system (does not run thru spinal tract - use the basal ganglia and cerebellum)
what is the reflex arc
Reflex arc: polysynaptic (so it involves multiple synapses)
No ascending fibers to the brain, it is just within the spinal cord
Sensory neurons synapse in spinal cord and activate spinal motor neurons which send signals to activate muscles
what is a neuromuscular junction and how does it function?
is the synapse between motor neuron nerve terminal and muscle fiber that is essential for muscle contraction and movement
Converts electrical impulses in neuron into electrical activity in muscle fiber
Ach binds to nicotinic (ionotropic) or muscarinic (metabotropic) ach receptor
Improper function of these junctions can lead to the development of progressive neuromuscular diseases, some of which have no effective treatment
Injury and disease to lower motor neurons can lead to
Paralysis (flaccidity - muscles soft/tone reduced)
Loss of reflexes
Muscle atrophy (loss of trophic factors (reduction of muscle fiber itself) released by lower motor neuron)
what does a lower motor neuron (LMN) do? what can happen if it is damaged?
Lower motor neuron (LMN) consistently wants to contract to protect it self (doesnt want to over stretch)
Ex: stimulus where hammer hits patella tendon stretches the quadriceps which triggers sensory neurons. They send signal to spinal cord that synapses with lower motor neuron telling it to contract. Signal bypasses the brain; its a local system.
When damaged:
mass lowers bc LMN also releases growth factors
power also drops bc it is the neuron that tells it to contract
Hyporeflexia → reflexes are messed up
Hypotonia (flaccidity)
what does a upper motor neuron (UMN) do? what can happen if it is damaged?
cell bodies are in the cerebral cortex and connect to lower motor neuron. UMN modulates the constant desire to contract from the lower motor neuron
release glutamate
have pyramidal and extrapyramidal system
If UMN is lesioned, the LMN is not gonna be functioning appropriately either.
Mass will be reduced
Power is still present, but is reduced
Hyperreflexia (lmn is constantly contracting)
Hypertonia (spasticity)- lack of inhibition from umn means muscle is contracting when it shouldn’t
what is the pyramidal motor system? what is the corticospinal tract?
is the voluntary motor system with a descending motor tract. UMN carry signals from cerebral cortex to spinal cord
Corticospinal tract
- Cortico = cell bodies in cortex (origin)
- Spinal = axon terminal in spinal cord (target)
sends direct signals to specific muscles or muscle groups and is for conscious movement and travels through pyramids of medulla.
what are betz cells and how is ALS associated?
Betz cells are giant cells (0.1 mm) that communicate very rapidly. Can send signal directly down corticospinal tract through axons
(are in 5th layer of primary motor cortex)
Initiate and modulate voluntary movement
ALS (Amyotrophic Lateral Scelrosis) is a progressive loss of both upper & lower motor neurons
Betz cell soma are reduced
Axons in corticospinal tract degenerate
( Soma and axon sizes are reduced)
what is ALS and how do betz cells affect it?
ALS (Amyotrophic Lateral Scelrosis) is a progressive loss of both upper & lower motor neurons
Betz cell soma are reduced
Axons in corticospinal tract degenerate
( Soma and axon sizes are reduced)
what are some signs/symptoms of ALS from UMN vs LMN?
UMN signs (manifestations of a disease visible to a physician)
- increased deep tendon reflexes, slow or rapid alternating movements,
UMN symptoms (manifestations of a disease apparent to self)
- lack of coordination with movements, poor balance, stiffness with upper and lower extremities
LMN signs (manifestations of a disease visible to a physician)
- difficulty squatting and rising from chair, waddling gait, foot drop
LMN symptoms (manifestations of a disease apparent to self)
- muscle cramps, weakness in upper and lower extremities
rundown of corticospinal tract
Precentral gyrus → cerebral peduncle → midbrain → medulla → pyramids and CROSS → lateral/anterior corticospinal tract
Internal capsule:
Midbrain:
Medulla:
Lateral corticospinal tract:
Internal capsule:
axon bundles
Vulnerable to strokes
“highway”
Midbrain: cerebral peduncle
“Stalks” of cerebrum
Medulla:
Fibers have pyramid shape
Run Length of medulla
Decussation (crossing) of pyramids
Majority of fibers cross (contralateral). Cortex controls opposite sides of the body
Lateral corticospinal tract
Majority of UMN fibers cross
Anterior
Small number of UMN fibers don’t cross
what is the clinical significance of damage to the pyramidal system? what part of the pyramidal system is the most common site for cerebrovascular accidents?
corticospinal tracts are susceptible to damage because signals use it to pass almost the whole length of the CNS
internal capsule is the most common site for cerebrovascular accidents.
- hemiplegia (half paralysis) and hemiparesis (half weakness). happen with even with a small stroke bc fibers are bundled so closely together
what is the Babinski sign?
Babinski sign: screen for UMN lesions in small children
trace the foot with a stick to see if toes fan. This should not be happening after the age of 2 yrs. Otherwise, it is a sign of UMN disorder
what is somatotopic organization and what effect does it have on the motor system?
somatotopic organization is the map of how different motor areas of the body is on the motor cortex
Parts of body requiring precision and fine control (face, hands) are disproportionately large on the cortex
Lesions to motor cortex affect the particular region of body depending on which aspect is damaged
what is the motor homunculus
Is the distorted representation of how the body is on proportion of the cortex dedicated to motor function in different parts of the body
what are the phases of voluntary movement?
- Identify and localize target
- Make plan of action
- Sequence and prepare
- Execute movement (final signal)
what parts of the brain are in charge of the different phases of voluntary movement?
Prefrontal cortex (plan movement)
When a movement was only imagined and no movement took place, brain activity was seen in the premotor area and prefrontal cortex
Posterior parietal cortex
Integrates visual information (“where” dorsal visual stream) into the motor plan
Premotor cortex (prepare and sequence movement)
Is where you see neuronal activity in anticipation of predictable environmental events
Prepares movements based on input from external or sensory cues (object derived movement)
Primary motor cortex (execute movement)
Motor cortex activity increases during movement execution
Activity changes according to direction of movement (directional tuning)
Ex: in experiment with monkeys, they found that neurons fired when monkeys moved in certain directions and not in opposite directions. This is encoded by a population of neurons not just singular cells
dopamines impact on motor movement (D1 and D2 receptors)
D1 (direct pathway) and D2 (in indirect pathway) receptor in putamin
Both go to thalamus but D2 has layover. Has more inhibition and can be modulated more for complex movements.
D1 is like the “go” functions that initiate motor movements.
Parkinson’s has difficulty initiating
Study stimulated D1 neurons (direct pathway) and found that the animal slowly tries to reach for chocolate but can’t really get to the square for it.
When D2 neurons stimulated, they can reach into the box but can’t terminate to grasp the chocolate.
D1 and D2 act together in executing movement (different temporal sequences)
Damage to extrapyramidal system: clinical significance
Parkinson’s Disease
Common in degenerative diseases
Involuntary movement: tremors and spasms
Freezing of movements; giving them a cue can help initiate movements
Parkinson’s disease:
basal ganglia contains 80% of brains dopamine (even tho its only 0.5% of brain)
Disruptions in nigrostriatal pathways and in voluntary movements
(1) Loss of striatal neurons
(2) Loss of dopaminergic neurons in Substantia Nigra
(3) disruption in dopamine metabolism → DOPAL build up → can cause neurotoxic effects
how is Parkinson’s Disease related to extrapyramidal lesions? what treatmenets are there
Parkinson’s disease:
basal ganglia contains 80% of brains dopamine (even tho its only 0.5% of brain)
Disruptions in nigrostriatal pathways and in voluntary movements
(1) Loss of striatal neurons
(2) Loss of dopaminergic neurons in Substantia Nigra
(3) disruption in dopamine metabolism → DOPAL build up → can cause neurotoxic effects
Treatments: look at DA synthesis
Tyrosine synthesis (precursor found in diet)
L-DOPA is a precursor to dopamine, and its use reduces some symptoms. Electrical stimulation within the basal ganglia can reduce symptoms, but this deep brain stimulation (DBS) requires an implanted electrode