Lecture 5 - The Motor System Flashcards
Where does the ‘journey’ of motor action begin?
The frontal cortex
Role of prefrontal cortex
Planning
Role of premotor cortex
Sequence organization
Role of primary motor cortex (M1)
Movement production (contains homunculus)
Motor cortex vs. SS cortex
- The motor cortex lies in the frontal lobe just anterior to the central fissure
- The sensory cortex lies posterior to the central fissure and extends into the parietal lobe
Rate encoding
Firing of motor neurons before a task is proportional to the muscle force required for that task
Mental rehearsal/visualization
- Imaging movement produces a similar pattern of brain activity to planning movement (but less strong)
- Often used in training athletes in technically demanding sports, may help improve performance
2 Views of modelling movement
- Direct mapping of motor homunculus neurons to muscle fibres in the periphery
- More likely that the regions of motor homunculus represents categories of movement (a movement repertoire)
Neural mechanism for sequencing motor actions?
Lesion to the premotor cortex in animals impairs the ability to coordinate motor sequences
What are mirror neurons?
In monkeys, neurons exist which respond to both seeing action and performing action
Where are mirror neurons found in the brain?
The premotor cortex and inferior parietal lobe
Which disorder was malfunction of mirror neurons thought to play a role in?
Autism - a disorder which involves difficulty in replicating/understanding actions (not strongly supported)
What neurons are responsible for the beginning voluntary motor action?
Upper motor neurons (Betz cells)
Axons pass through the thalamus via the ________
internal capsule
Motor neurons axons form motor _______, evident in the _________ and ________
tracts, cerebral peduncles (midbrain), pyramid (medulla)
Tracts synapse with ________ in the spinal cord, which in turn affect the muscle activity
lower motor neurons
If you lesion only a part of M1 associated w/ the hand + digits, what would happen? How could you reduce this?
The whole area would shrink, could be mitigated by rehabilitation
How can the FC be damaged?
- traumatic head injury
- tumor
- neurological diseases
- stroke (most common)
What happens in a stroke?
- condition in which poor blood flow results in cell death and loss of brain function
- arises due to issues in the cerebrovascular system that supplies the brain with blood
- serious consequences for neurons, which depend upon blood for oxygen + glucose
- two types: ischemic + hemorrhagic
Ischemic Vs. Hemorrhagic Stroke
- Ischemic stroke: clot stops blood supply to an area of the brain
- Hemorrhagic stroke: hemorrhage/blood leaks into brain tissue
What are the main arteries in the brain?
Anterior cerebral artery: supplies blood to dorsal medial + frontal parietal
Middle cerebral artery: supplies blood to frontal, parietal, and occipital
Posterior cerebral artery: supplies blood to occipital (least likely to be involved in motor complications)
What would happen if there was damage to motor neurons in the frontal cortex?
This would profoundly impair movement
What is CIMT?
Constraint-induced motor therapy (CIMT): developed by Dr. Edward Taub
- involves forced use of affected limb by suppressing the unaffected limb
- based on the principle that loss of sensory function (afferent input to the spinal cord/brain) does not always result in complete loss of motor function (efferent)
What kind of restraints to they use in CIMT (to restrict the functional limb)
- braces
- mitts
- casting
CIMT and neuroplasticity
- In individuals who regain motor function, there is increased grey matter
- recovery is imperfect - but even a little bit is valuable
CIMT in practice
- Involves shaping (the reinforcement of successive approximations of the movement)
- Time-intensive (90% of waking hours) and labor-intensive (requires supervision)
- Early goal is cortical stimulation rather than task completion (which is very difficult)
- Focus on day-to-day tasks (writing, eating, doing the dishes, and so on)
How many motor nerves are there?
9 (cranial nerves) all but I, II, and VIII have motor functions
Laterality of cranial nerves
Lack of decussation means that cranial nerves mediate function on the ipsilateral side of the body (they do not crossover before entering the brainstem)
*Damage to most cranial nerves generally leads to impairment on the same side of the body
Example of cranial nerve pathology
Bell’s Palsy
The facial nerve (VII)
- responsible for motor function within the face as well as sensory functions (e.g. taste; L04)
- malfunctions in the facial nerve can cause motor impairments
Bell’s Palsy
- facial nerve travels through a ‘tight tunnel’ (bone)
- Inflammation of the nerve can lead to it being compressed against the tunnel
- compression impair motor function in the face
Treating Bell’s Palsy
- most patients recover on their own
- in severe cases, corticosteroids (to reduce inflammation) might be recommended (value of antiviral drugs is unclear)
- surgery (to improve passage of the nerve) is possible, but comes with high risks
How many segments in the spinal cord?
31 segments + nerve pairs
Cervical section of SC
C1-C8
Thoracic section of SC
T1-T12
Lumbar section of SC
L1-L5
Sacral section of SC
S1-S5
Coccygeal
1 segment
Two types of motor impairment with SC injury
Tetraplegia (most severe), paraplegia (less severe)
Sensory pathways are in the ________ region
dorsal (posterior)
Motor pathways are in the ________ region
ventral (anterior)
Dorsolateral column of the SC
- lateral corticospinal pathway
- rubrospinal pathway (contacts red nucleus)
Ventromedial column of the SC
- anterior corticospinal pathway
- vestibulospinal (vestibular nuclei) - balance + head-turning
- reticulospinal (reticular formation) - locomotion and posture
- tectospinal pathway (superior colliculus) - orientation to stimuli, head/neck/eye movements
Tracts are typically named for their starting location and terminal destination
corticospinal = cortex to spinal cord
Two divisions of the corticospinal tract
Lateral corticospinal tract: carries commands for movement of limbs + digits (distal muscles)
Anterior corticospinal tract: carries commands for movement of the body’s midline (proximal muscles, e.g., trunk)
Decussation of CS tracts
- lateral corticospinal tracts decussates at the medulla, before the SC (~90% of fibres)
- anterior corticospinal tract decussates at the level of the lower motor neurons in the SC (~10% of fibres)
Rubrospinal tract
- extrapyramidal (outside pyramidal) tract
- involves red nucleus at the level of the midbrain
- important for large muscle movement and coordinating fine movements
- may be more functionally significant in other animals
Anteromedial pathway system
Vestibulospinal pathway: (connected with vestibular nuclei for CN8) is important for balance and head-turning
Reticulospinal pathway: (connected with the reticular formation) important for locomotion and posture
Tectispinal pathway: (connected with superior colliculus) important for orientation to stimuli, head/neck/eye movements
The problem with SC lesions
No sensory info coming in, no motor instructions going out
What is potentially a neurorehabilitation method for paralysis of SC lesions?
If we could measure signals we could perhaps transfer them directly to muscles or another apparatus (i.e. bypass the injury too SC)
*Many researchers are experimenting with implants to measure neural activity (e.g., Neuralink)
Robot-guided movements
- once you have the correct signal, you can direct it to a machine that can complete movements
- the individual can learn to control their movements better through the machine (feedback is vital)
- much research into this possibility
What is the Basal Ganglia?
Network of structures involved in coordinating movement
- caudate and putamen (together referred to as the striatum)
- globus pallidus (internal and external)
- subthalamic nucleus
- substantia nigra
The _________ through the BG is thought to play an important role in initiating movements
direct pathway
The _________ is through the BG is thought to play a role in inhibiting unwanted movements
indirect pathway
Which receptors inhibit/excite which pathways?
Inhibitory actions of the DA are mediated by D2 receptors (left, indirect) whereas excitatory actions are mediated by D1 receptors (right, direct)
What is the defining feature of Parkinson’s Disease?
Loss of DA-projecting neurons (>60%)
What is Parkinson’s Disease (PD)?
- progressive disorder of the nervous system that affects movement
- develops gradually, advancing over time
- though primarily considered a motor disorder, involves non-motor symptoms
PD motor symptoms
- resting tremor
- cogwheel rigidity: stiffness and jerky motions, decreased range of motion
- bradykinesia/akinesia: slow to start/finish movements, less spontaneous movement, difficulty w/ repeated movements, decreased facial expressivity, short, shuffling steps
- postural instability: loss of balance when standing or when pressure is applied
PD non-motor symptoms
- may occur before motor symptoms (predictor of later PD diagnosis)
- many examples: loss of smell, constipation, sleep disorders (REM), mood disorders, orthostatic hypotension, cognitive deficits (dementia)
- pathological gambling occurs more frequently (3.4-6.1%) than in the general population (0.25-2%)
- other impulse control disorders are also more common, including binge eating, compulsive shopping, and ‘hypersexuality’
- risk for impulse control disorders may be linked to medications for the disorder, though this is still controversial
Etiology of PD
- Environmental factors: pesticide exposure, agricultural occupation, prior head injury, rural living, beta-blocker use, well-water drinking
- Genetic factors (family history): alpha-synuclein gene (x1.5 risk), ~18 genes linked to PD, heritability ~ 0.40 (out of 1.00)
Increasing DA in PD
- we cannot administer DA directly (won’t cross the blood-brain barrier) so we need another solution
- L-DOPA, the immediate precursor for DA, can cross the blood barrier
- If we administer L-DOPA (levodopa; in drug form), it will be converted to DA inside the brain, correcting the DA deficiency
Increasing DA through other targets (target metabolism of DA instead)
Monoamine Oxidase B (MAOB) Inhibitors: delays breakdown of DA by MAO-B, used as monotherapy or in conjunction with L-DOPA, it can reduce the dosage of L-DOPA by 15%
Catechol O-Methyl Transferase (COMT) Inhibitors: delays breakdown of DA by COMT, mainly used in combination with L-DOPA, increases the half-life of L-DOPA, delays “wearing-off” effect of L-DOPA and other motor complications such as dyskinesia
Concerns of increasing DA
- L-DOPA non-selectively increases DA levels in the entire brain, not just in the substantia nigra (other systems are affected - e.g., cognitive)
- Increased DA elicited by L-DOPA is not as precise as endogenous DA neurotransmission (sometimes effects are too strong or too weak)
- L-DOPA has unpleasant side effects (nausea, dyskinesia, psychosis, and delusion)
Deep Brain Stimulation (DBS) in PD
- Electrodes can be planted in the subthalamic nucleus (more effective, preferred) or globlus pallidus internus to modulate the activity of these structures
What is the role of the cerebellum in movement?
- role in posture, balance, coordination, and adapting movements
- contains a topographic representation of the body
