Motor Cortical Control Flashcards
Broad principles of motor control
Hierarchical organisation
Functional segregation
Motor system hierarchy
Primary motor cortex Basal ganglia and cerebellum Thalamus Brainstem Spinal cord
Major descending tracts
Pyramidal tracts - pass through thepyramidsof the medulla - Motor cortex to spinal cord or cranial nerve nuclei in brainstem - Voluntary movements of body and face
Extrapyramidal tracts - Do not pass through thepyramidsof the medulla - Brainstem nuclei to spinal cord - involuntary (automatic) movements for balance, posture and locomotion
Pyramidal tracts
Corticospinal
Corticobulbar
Extrapyramidal tracts
Vestibulospinal
Tectospinal
Reticulospinal
Rubrospinal
Primary motor cortex location
Located in precentral gyrus, anterior to the central sulcus
Premotor area location
Located anterior to primary motor cortex
Supplementary motor area location
Located anterior and medial to primary motor cortex
Corticospinal tract
From upper motor neurons down cerebral peduncle to midbrain and pyramids in medulla
Decussate
85-90% crossed fibres - Limb muscles - Lateral corticospinal tract
10-15% uncrossed fibres - Trunk muscles - Anterior corticospinal tract
Homunculus and somatotopy
Motor homunculus
Somatotopic representation
Corticobulbar tract
Basal ganglia
Principal motor pathway for voluntary movements of the face (and neck)
Vestibulospinal
Stabilise head during body movements, or as head moves
Coordinate head movements with eye movements
Mediate postural adjustments
Reticulospinal
Most primitive descending tract - from medulla and pons
Changes in muscles tone associated with voluntary movement
Postural stability
Tectospinal
From superior colliculus of midbrain
Orientation of the head and neck during eye movements
Rubrospinal
From red nucleus of midbrain
In humans mainly taken over by corticospinal tract
Innervate lower motor neurons of flexors of the upper limb
Upper motor neuron lesion
Loss of voluntary motor function
Paresis: graded weakness of movements
Paralysis (plegia): complete loss of voluntary muscle activity
Increased abnormal motor function due to loss of inhibitory descending inputs
Spasticity: increased muscle tone
Hyper-reflexia: exaggerated reflexes
Clonus: abnormal oscillatory muscle contraction
Babinski’s sign
Apraxia
A disorder of skilled movement. Patients are not paretic but have lost information about how to perform skilled movements
Lesion of inferior parietal lobe, the frontal lobe (premotor cortex, supplementary motor area - SMA)
Lower motor neuron lesion
Weakness
Hypotonia (reduced muscle tone)
Hyporeflexia (reduced reflexes)
Muscle atrophy
Fasciculations: damaged motor units produce spontaneous action potentials, resulting in a visible twitch
Fibrillations: spontaneous twitching of individual muscle fibres; recorded during needle electromyography examination
Motor neuron disease (MND)
Progressive neurodegenerative disorder of the motor system
Also known as Amyotrophic Lateral Sclerosis (ALS)
Caudate nucleus
Decision to move
Lentiform nucleus (putamen + external globus pallidus) – together caudate and putamen are known as the striatum
Nucleus accumbens
Subthalamic nuclei
Elaborating associated movements (e.g. swinging arms when walking; changing facial expression to match emotions)
Substantia nigra (midbrain) Ventral pallidum, claustrum, nucleus basalis (of Meynert)
Moderating and coordinating movement (suppressing unwanted movements)
Performing movements in order
Parkinson’s disease
Degeneration of the dopaminergic neurons that originate in the substantia nigra and project to the striatum
Parkinson’s disease symptoms
Bradykinesia - slowness of (small) movements (doing up buttons, handling a knife)
Hypomimic face - expressionless, mask-like (absence of movements that normally animate the face)
Akinesia - difficulty in the initiation of movements because cannot initiate movements internally
Rigidity - muscle tone increase, causing resistance to externally imposed joint movements
Tremor at rest - 4-7 Hz, starts in one hand (“pill-rolling tremor”); with time spreads to other parts of the body
Huntington’s disease
Degeneration of GABAergic neurons in the striatum, caudate and then putamen
Huntington’s disease symptoms
Choreic movements (chorea - dance)
rapid jerky involuntary movements of the body; hands and face affected first; then legs and rest of body
Speech impairment
Difficulty swallowing
Unsteady gait
Later stages, cognitive decline and dementia
Ballism
Usually from stroke affecting the subthalamic nucleus.
Sudden uncontrolled flinging of the extremities
Symptoms occur contralaterally.
Cerebellum
Located in posterior cranial fossa
Separated from cerebrum above by tentorium cerebelli
Coordinator and predictor of movement
Vestibulocerebellum
Regulation of gait, posture and equilibrium
Coordination of head movements with eye movements
Damage (tumour) causes syndrome similar to vestibular disease leading to gait ataxia and tendency to fall (even when patient sitting and eyes open)
Spinocerebellum
Coordination of speech
Adjustment of muscle tone
Coordination of limb movements
Damage (degeneration and atrophy associated with chronic alcoholism) affects mainly legs, causes abnormal gait and stance (wide-based)
Cerebrocerebellum
Coordination of skilled movements
Cognitive function, attention,
processing of language
Emotional control
Damage affects mainly arms/skilled coordinated movements (tremor) and speech
Main signs of cerebellar dysfunction
Ataxia
General impairments in movement coordination and accuracy. Disturbances of posture or gait: wide-based, staggering (“drunken”) gait
Dysmetria
Inappropriate force and distance for target-directed movements (knocking over a cup rather than grabbing it)
Intention tremor
Increasingly oscillatory trajectory of a limb in a target-directed movement (nose-finger tracking)
Dysdiadochokinesia
Inability to perform rapidly alternating movements (rapidly pronating and supinating hands and forearms)
Scanning speech
Staccato, due to impaired coordination of speech muscles
Alpha motor neuron
The lower motor neurons of the brainstem and the spinal cord
Innervate the extrafusal muscle fibres of the skeletal muscles
Motor neuron pool contains all alpha motor neurons innervating a single muscle
Motor unit
a single motor neuron together with all the muscle fibres that it innervates. It is the smallest functional unit with which to produce force.
Types of motor unit
Slow (S, type I) - slowest conduction velocity
Fast, fatigue resistant (FR, type IIA) - faster conduction velocity
Fast, fatiguable (FF, type IIB) - faster conduction velocity
Regulation of muscle force
Governed by the “size principle”. Smaller units are recruited first. As more force is required, more units are recruited. This allows fine control (e.g. when writing), under which low force levels are required.
A motor unit can fire at a range of frequencies. Slow units fire at a lower frequency.
As the firing rate increases, the force produced by the unit increases.
Summation occurs when units fire at frequency too fast to allow the muscle to relax between arriving action potentials.
Neurotrophic factors
Prevent neuronal death
Promote growth of neurons after injury
Motor unit and fibre characteristics are dependent on the nerve which innervates them.
The motor neuron has some effect on the properties of the muscle fibres it innervates.
Plasticity of motor units/muscle fibres
Type IIB to IIA most common following training
Type I to II possible in cases of severe deconditioning or spinal cord injury. Microgravity during spaceflight results in shift from slow to fast muscle fibre types
Ageing associated with loss of type I and II fibres but also preferential loss of type II fibres. This results in a larger proportion of type I fibres in aged muscle.
Reflex
An automatic response to a stimulus that involves a nerve impulse passing inward from a receptor to a nerve centre and then outward to an effector (as a muscle or gland) without reaching the level of consciousness.
An involuntary coordinated pattern of muscle contraction and relaxation elicited by peripheral stimuli.
Jendrassik manoeuvre
Try clenching the teeth, making a fist, or pulling against locked fingers when having patellar tendon tapped. The reflex becomes larger
Descending (supraspinal) control of reflexes
Higher centres of the CNS exert inhibitory and excitatory regulation upon the stretch reflex.
Rigidity and spasticity can result from brain damage giving over-active or tonic stretch reflex.
Descending (supraspinal) control of reflexes process
- Activating alpha motor neurons
- Activating inhibitory interneurons
- Activating propriospinal neurons
- Activating gamma motor neurons
- Activating terminals of afferent fibres
Hyper-reflexia
Overactive reflexes
Loss of descending inhibition
Associated with upper motor neuron lesions
Clonus
Involuntary and rhythmic muscle contractions
Loss of descending inhibition
Associated with upper motor neuron lesions
Babinski sign
When sole stimulated with blunt instrument the big toe:
Curls downwards - normal
Curls upwards – abnormal in adults. This is a positive Babinski sign.
Associated with upper motor neuron lesions
Toe curls upwards in infants – this is normal.
Hypo-reflexia
Below normal or absent reflexes
Associated with lower motor neuron diseases
