Motor systems Flashcards
Describe the functional segregation of motor control
Functional segregation
Motor system organised in a number of different areas that control different aspects of movement
Describe the hierarchical organisation of motor control
Hierarchical organisation
high order areas of hierarchy are involved in more complex tasks (programme and decide on movements, coordinate muscle activity)
lower level areas of hierarchy perform lower level tasks (execution of movement)
Summarise motor system hierarchy
The motor cortex (both primary and association) receives information from other cortical areas and sends commands to the thalamus (via basal ganglia) and brainstem
Information from the thalamus then feeds back to the motor cortices
The motor cortex passes commands to the spinal cord ( to control muscles of the body) and brainstem to control muscles of the face, head and neck
The cerebellum and basal ganglia adjusts the commands received from other parts of the motor control system to fine-tune the movement
Cerebellum feeds to thalamus and brainstem
Basal ganglia feeds to the thalamus
Outline the hierarchy in motor control
o Level 4 (highest) – association cortex.
o Level 3 – motor cortex.
o Level 2 – brain stem and cerebellum (side loop structure (SLS)).
o Level 1 (lowest) – basal ganglia (SLS (e.g. caudate nucleus)) and spinal cord
What are the 3 main areas of the motor cortex
Has got 3 main areas:
- Primary motor cortex or M1 – Broadmann’s area 4.
- Premotor cortex – Broadmann’s area 6.
- Supplementary motor area – Broadmann’s area 6
Describe the primary motor cortex (M1)
Location: precentral gyrus, anterior to the central sulcus
Function: control fine, discrete, precise voluntary movement
Provide descending signals to execute movement
Betz cells exist in layer V of the cerebral cortex. They are the biggest cells in the cerebral cortex- pyramidal cells
They are found in the 5th layer of grey matter
The corticospinal tracts originate from here
M1 is in the frontal lobe
Describe the somatotopic organisation of the primary motor cortex
The somatotopic organisation of the primary motor cortex is known as Penfield’s motor homunculus.
Organisation: somatotopic - whereby face and lips are most lateral, moving medially to control hands > arms > legs > feet (anterior cerebral artery); more sensory receptors = larger area
The face and hands have a large area of the brain to control them because they have more fine control.
Summarise the motor homunculus
Each area of the body which is under motor control is represented in the primary motor cortex and these representations are arranged somatotopically: the foot is next to the leg which is next to the trunk which is next to the arm and the hand.
The amount of brain matter devoted to any particular body part represents the amount of control that the primary motor cortex has over that body part. A lot of cortical area is required to
control the complex movements of the hand and fingers, and these body parts have larger representations in M-I than the trunk or legs, whose muscle patterns are relatively simple
State the descending motor pathways
Corticospinal (pyramidal) and subcorticospinal tracts:
Cortico-spinal tracts (CST) Rubrospinal tracts Reticulospinal tracts Vestibulospinal tracts Organization of CST
Summarise the descending pathways
Integration of inputs from somatosensory cortex into layer IV of M1
Layer V (grey matter) contains pyramidal cells – the large Betz cells are visible
Projects to white matter below layer VI and then to internal capsule
Travels via cerebral peduncles to medulla where fibres come together as pyramids
Fibres decussate – 80% cross to form lateral corticospinal tract and 20% remain uncrossed forming anterior corticospinal tract
Tracts project to ventral horns and motoneurons
Describe the lateral and medial descending pathways
Lateral • Lateral corticospinal tract • Rubrospinal tract Medial • Anterior corticospinal tract • Reticulospinal tract • Vestibulospinal tract • Tectospinal tract
Broadly, what is the function of the lateral and medial descending pathways
Lateral • Control of proximal and distal musculature • Voluntary movements or arms and legs Medial • Control of axial muscles • Balance and posture
Describe the lateral corticospinal tract
Lateral corticospinal tract: supplies skeletal muscles in distal parts of limbs
Upper motor neurone emerges from primary motor cortex and travels through internal capsule
UMN passes through cerebral peduncle of midbrain, travelling through pons
UMN undergoes pyramidal decussation in the medulla
UMN descends down contralateral lateral corticospinal tract to the correct spinal level
UMN synapses to Lower motor neurone in ventral horn
LMN exits cord via the ventral root
Describe the anterior corticospinal tract
Anterior corticospinal tract: supplies muscles of the trunk and proximal limbs
Upper motor neurone emerges from primary motor cortex and travels through internal capsule
UMN passes through cerebral peduncle of midbrain, travelling through pons
UMN DOES NOT undergo pyramidal decussation in the medulla, remaining ipsilateral
UMN descends down ipsilateral half of anterior corticospinal tract to the correct spinal level
UMN synapses to LMN in contralateral ventral horn to Lower motor neurone
LMN exits cord via the ventral root
Describe the corticobulbar pathways
Corticobulbar pathway: supplies the muscles of the head, neck and face - carrying the motor cranial nerves (V, VII, IX and XII)
Upper motor neurone emerges from head region of motor cortex
UMN passes through corticobulbar tract to brainstem
UMN synapses to CN in contralateral brainstem motor nuclei
CN passes out of brainstem to innervate muscles
Describe the differences in synaptic transmission of the upper and Lower motor neurones
Upper to lower motor neurones NT = glutamate.
Lower neurone to muscle fibres NT = ACh.
What is the function of the rubrospinal tract
It is an alternative pathway that allows voluntary motor commands to be sent down the spinal cord meaning that the body can compensate for a lesion in the primary motor cortex.
It also has a role in movement velocity.
Describe the structure and function of the vestibulospinal tract
The lateral vestibulospinal tract originates at the lateral vestibular nucleus.
The medial vestibulospinal tract originates at the medial vestibular nucleus.
They mediate postural adjustments and head and eye movements
Describe the structure and function of the reticulospinal tract
It originates in the reticular formation in the brainstem then goes down the spinal cord to innervate muscle. It is involved in complex actions: • Orienting • Stretching • Maintaining a complex posture
Describe the structure and function of the tectospinal tract
It originates in the superior colliculus (brainstem)
Its function is not known but is most likely involved in reflexive turning of the head to orient to visual stimuli.
Describe the premotor cortex
Location: frontal lobe anterior to M1
Function: planning of movements and their coordination
Regulates externally cued movements
e.g. seeing an apple and reaching out for it requires moving a body part relative to another body part (intra-personal space) and movement of the body in the environment (extra-personal space)
Describe the supplementary motor cortex
Location: frontal lobe anterior to M1, medially
Function: planning complex movements; programming sequencing of movements
Regulates internally driven movements (e.g. speech)
SMA becomes active when thinking about a movement before executing that movement (rehearsing a dance)
Describe the role of the association cortices
Brain areas not strictly motor areas as their activity does not correlate with motor output/act
Posterior parietal cortex: ensures movements are targeted accurately to objects in external space
Prefrontal cortex: involved in selection of appropriate movements for a particular course of action- personality impact and influence of previous experiences
Give some important definitions relating to the motor system
Lower motor neuron Spinal cord, brainstem Upper motor neuron Corticospinal, corticobulbar Pyramidal Lateral corticospinal tract Extrapyramidal Basal ganglia, cerebellum
What are the negative signs of an upper motor neurone lesion
Loss of function (negative signs):
Paresis: graded weakness of movements
Paralysis (plegia): complete loss of muscle activity
What are the positive signs of an upper motor neurone lesion
Increased abnormal motor function (positive signs) due to loss of inhibitory descending inputs:
Spasticity: increased muscle tone
Hyper-reflexia: exaggerated reflexes
Clonus: abnormal oscillatory muscle contraction
Babinski’s sign
no muscle atrophy
What is Babinski’s sign
You stroke the plantar surface of the foot and in a normal subject you will see flexion of the toes (they curl downwards)
In the case of upper motor neurone lesions, the patient will show an EXTENSOR PLANTAR RESPONSE where their toes fan out and their big toe lifts up.
Why is atrophy not seen in upper motor neurone lesions
The lower motor neurones are still in tact and they have a role in providing nutrients to the muscle.
There will still be partial atrophy due to muscle disuse.
Describe 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)
Any disease of these areas can cause apraxia, although stroke and dementia are the most common causes
What is apraxia caused by
A disorder of skilled movement not caused by weakness, abnormal tone or posture or movement disorders (tremors or chorea).
It is caused by the loss of information on how to perform skilled tasks rather than loss of motor command to the muscles.
Describe the features of lower motor neurone lesions
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
Describe motor neurone disease
Motor Neurone Disease – A disease that affects both UPPER and LOWER motor neurones;
Motor neurone disease = Amyotrophic Lateral Sclerosis (ALS).
These are progressive neurodegenerative disorders (can affect upper and then lower or the other way around).
Describe ALS
Most common cause of MND
Lesions of both upper and lower
What are the key features of MND
Progressive neurodegenerative disorder of the motor system
Spectrum of disorders
Amyotrophic Lateral Sclerosis (ALS)
What are the upper motor neurone signs of MND
Increased muscle tone (spasticity of limbs and tongue) Brisk limbs and jaw reflexes Babinski’s sign Loss of dexterity Dysarthria Dysphagia
What are the lower motor neurone signs of MND
Weakness Muscle wasting Tongue fasciculations and wasting Nasal speech Dysphagia
Summarise the premotor area
Located laterally in front of M-I. Six-times larger than M-I PMA activity seems to facilitate multiple columns in M-I preparing them for action.
Involved in planning – particularly using external (e.g. visual) cues
Summarise the SMA
Supplementary motor area (SMA) (medial region of Brodmann area 6)
Located medially in front of leg area of M-I
Stimulation of neurons in SMA elicits complex movements involving many muscle groups rather than the highly specific movements generated by M-I stimulation. For example movements following SMA stimulation often involve the entire hand or arm or in same cases even postural movements of the whole body.
The SMA is Involved in motor planning of internally driven voluntary movements
SMA lesions result in lack of spontaneous movements and speech
Imaging studies (PET) show activity even when thinking about movement.
Summarise the structure and roles of the SMA and PMA
The principal areas of the cerebral cortex concerned with motor control beside the primary motor cortex (M-I) are the supplementary motor area (SMA) and premotor area (PMA).
SMA and PMA are also somatototpically organized.
Intracortical motor pathways. Somatotopically related areas of each of the 3 motor areas are precisely interconnected. The SMA and PMA are reciprocally interconnected and both independently provide reciprocal connection to M-I which receive afferents not only from these motor areas but also from sensory areas.
M-I Stimulation of M-I produces muscles movement at stimulus intensities far lower than those for any other part of the cerebral cortex.
Small group or populations of motor neurons are controlled by small population of cortical neurons. The control is directed at the most distal muscles of an extremity and related to the most
delicate and precise movements, as such is quite specific.
M-I neurons encode the direction of movement. They also encode (via the firing rate) the force of the muscle contraction and the velocity with which a force is applied.
Summarise upper motor lesions
Lesion to the descending motor systems cause an unique set of symptoms
This constellation of symptoms is known as UMN lesions
Clinical features:
Spastic weakness, increases muscle stretch reflexes, no signs of muscle denervation, flexion-reflex-afferent driven reflex reversed (sign of Babinski)
Summarise the components of the basal ganglia
Basal ganglia: extrapyramidal structure including:
Lentiform nucleus (putamen and external globus pallidus)
Caudate nucleus - large anterior head, and thins out to tail
Subthalamic nucleus
Substantia nigra - part of the midbrain, projects to ganglia
Ventral pallidum - DAergic neurones projecting to brain
Claustrum - layer of grey matter ?function
Nucleus accumbens - reward centre
Nucleus basalis of Meynert - ACh-ergic projections to cortex for memory
What is the basal ganglia
The basal ganglia lie deep in white matter of cerebral cortex.
Forebrain nuclei
What does the striatum consist of
Globus Pallidus
Caudate and Putamen
Describe the cross-section of the basal ganglia in the coronal plane
More anteriorly:
can see head of caudate, nucleus accumbens and putamen
as we move more posteriorly, see tail of caudate on walls of lateral ventricle
putamen and caudate seprated by internal capsule
thalamus pushes the structures out more laterally
golbus pallidus (externus and internus) medial to putamen
see diagrams!!
Describe the functions of the basal ganglia
Elaborating associated movements (e.g. swinging arms when walking; changing facial expression to match emotions)
Moderating and coordinating movement (suppressing unwanted movements)
Performing movements in order
Describe the input into the striatum
From the cerebral cortex (SMA, PMA, primary motor cortex, somatosensory and parietal cortex) projections
two pathways possible after this- direct and indirect pathways
Direct Pathway = excitatory on the motor cortex
Indirect Pathway = inhibitory on the motor cortex
Summarise the substantia nigra
The substantia nigra lies in the midbrain and is divided into a ventral pale part, the pars reticulata, which projects to the ventrolateral and ventral anterior thalamic nuclei and the superior colliculus, and a dorsal pigmented part, the pars compacta, which projects to the caudate and putamen. These use dopamine for the transmission of information.
The substantia nigra helps to facilitate the role of the direct pathway by activating cells in the putamen, which in turn releases the ventrolateral nucleus from the inhibitory influence of the globus pallidus.
DA fibres in nigro-striatal pathway
Outline the direct pathway
Direct corticostriatal loop
Cortex stimulates the striatum
Striatum inhibits the globus pallidus internus, inhibiting its ability to inhibit the thalamus (ventrolateral)
This effectively encourages the thalamus to fire, and thus stimulates the cortex- supplementary motor area
SNr also involved in direct pathway- diagramaticaly joined with GPi.
Outline the indirect pathway
Cortex stimulates the striatum
Striatum inhibits the GPe (GABA and enkephalin) reducing the inhibition of the subthalamic nucleus
The GPi is then excited and in turn inhibits output from the VL thalamus to the cortex- the SMA therefore gets less excitation.
Describe how the basal ganglia ensure that the correct motor programmes are carried out
The basal ganglia and cortex form a processing loop.
The basal ganglia enable proper motor programmes (stored in the cortex) via the direct pathway (exicitatory)
The basal ganglia inhibit the competing motor programmes via the indirect pathway
In summary, the basal ganglia and its direct and indirect pathways make sure that appropriate motor commands get transmitted down the hierarchy.
Connections with which parts of the brain allow the basal ganglia to have a role in enabling various cognitive, executive and emotional programmes?
Prefrontal association cortex
Limbic system
Describe a mathematical representation of the direct and indirect pathways
The easiest way to work through this is mathematically. The direct pathway consists of two inhibitory synapses (let us call them −1). When −1 is multiplied by itself we get +1 (−1 × −1 = +1); therefore the facilitation of movement. The indirect pathway has three inhibitory synapses therefore −1 × −1 × −1 = − 1. Thus the indirect pathway when activated inhibits movement.
Describe the pathophysiology of PD
In Parkinson’s disease the degeneration of dopaminergic cells in the substantia nigra (SNc) causes loss of dopaminergic terminals in putamen and to lesser extent in caudate. Loss of dopamine to the striatum results in less inhibition of the GPi/SNr and consequently increased inhibitory output from GPi/SNr to the thalamus.
Too much inhibition of thalamus produces decreased facilitation to the motor cortex (particularly SMA): this results in delays in the initiation of movements, slowness of movements (bradykinesia) which are the typical symptoms of Parkinson’s disease.
The lack of excitatory input interferes with the ability of the motor cortex to generate commands for voluntary movement, resulting in poverty of movement.
Describe the progressive loss of neurones in PD
It is caused by the progressive depletion of dopaminergic neurones
NOTE: symptoms only appear When 60-80% of the dopamine cells in the substantia nigra have died
What may cause the neurodegeneration in PD
Lewy bodies
alpha-synuclein deposits- can effect cognition too
lose neuromelanin- SN becomes pale- ‘locus classicus’
What was the original description of PD
“Shaking palsy (paralysis agitans) Involuntary motion, with lessened muscular power, in parts not in action even when supported, with propensity to bend the trunk forward, and to pass from a walking to a running pace: the senses and the intellect being uninjured
Describe the main motor signs of PD
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
Describe the Parkinsonian gait
Walking slowly, small steps, shuffling feet, reduced arm swing
Stooped posture with head and body bent forwards and downwards
Summarise the pathophysiology of Huntington’s disease
In Huntington’s disease the degeneration of spiny GABA neurons in the striatum (mainly caudate) results in reduced GABAergic inhibition of GPe and consequently increased
Inhibitory output from GPe to STN, the facilitatory output from STN to GPi/SNr is reduced and there is less inhibitory output from Gpi/SNr to the thalamus. The lack of inhibitory control of
the thalamus on the motor cortex results in unwanted, involuntary movements (dyskinesias and chorea) which are typical of Huntington’s disease.
What causes the pathology in Huntington’s
Genetic neurodegenerative disorder
Chromosome 4, autosomal dominant- encodes huntingtin
CAG repeat (>35)
Degeneration of GABAergic neurons in the striatum, caudate and then putamen
Describe the motor signs in Huntington’s
Choreic movements (Chorea)
rapid jerky involuntary movements of the body; hands and face affected first; then legs and rest of body (MND s distal to proximal)-
Speech impairment
Difficulty swallowing
Unsteady gait
Later stages, cognitive decline and dementia
Where is the cerebellum located and how are the cerebellar hemispheres connected
Cerebellum: posterior to fourth ventricle (posterior aspect of the pons)
Connections: transverse fibres run to pons
Summarise the anatomy of the cerebellum
Horizontally divided into 3 lobes: § Anterior. § Posterior. § Flocculonodular. Sagittally divided into 3 zones: § Vermis. § Intermediate hemisphere. § Lateral hemisphere. Connections with the cerebellum are with the SAME side of the body and OPPOSITE cerebral hemispheres. § NT: Glutamate (+), GABA (-
Describe the 3 functional units of the cerebellum
The flocculonodular lobe (vestibulocerebellum) involved in the control of posture and eye movements.
•
The vermis with the intermediate part of the hemisphere or paravermis (together known as the spinocerebellum), involved in the control of both postural and distal muscles.
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The lateral part of the hemisphere (cerebrocerebellum) involved in coordination and planning of limb movements (in conjunction with the basal ganglia)
Describe the cortical structure of the cerebellum
Cortical structure: only three layers
Outermost - molecular layer; few neurones
Middle - piriform layer; Purkinje cells - project to nuclei in white matter, huge dendritic trees (receive inputs)
Innermost - granular layer; small neurones involved in processing
Purkinje cells output to the nuclei in the white matter.
Describe the 3 sources of input to the cerebellum
mossy fibres from spinocerebellar pathways
climbing fibres from inferior olive
mossy fibres from pons bringing information from cerebral cortex (these are called corticopontine connections and cross over after synapsing in the pons).
Inferior olive projects to Purkinje cells via climbing fibres
All other input to granule cells via mossy fibres and then onwards via parallel fibres
Describe output from the cerebellum
All output from Purkinje cells via deep nuclei
fastigial nucleus (involved in balance and has connections with vestibular and reticular nuclei)
interposed
dentate nuclei are both involved with voluntary movement – they have projections to thalamus and red nucleus
Summairse the vestibulocerebellum
The vestibulocerebellum receives information from the vestibular nuclei (changes in head position relative to body position and gravity) and visual information from the lateral geniculate nuclei, superior colliculi and visual cortex. It projects to the vestibular nuclei, and thence to the oculomotor centres, and is involved in the control of axial muscles (balance) and the coordination of head and eye movements.
Describe the role of the vestibulocerebellum
Regulation of gait, posture and equilibrium
Coordination of head movements with eye movements
Describe the functions of the spinocerebellum
Coordination of speech
Adjustment of muscle tone
Coordination of limb movements
Summarise the spinocerebellum
The spinocerebellum receives its main input from the spinocerebellar tract and is concerned with the control of postural muscle tone (by setting GMN drive which affects alpha motor neuron activity through the reflex loop) and movement execution.
The vermis receives information from auditory, visual and vestibular systems, and sensory information from the proximal body. It projects to the ventromedial descending motor pathway and reticular formation.
The intermediate hemisphere receives sensory information from the distal body and projects through the red nucleus (via the superior olive) and thence to the descending rubrospinal tract. It also projects to the contralateral motor cortex (via the thalamus).
Describe the function of the cerebrocerebellum
Coordination of skilled movements
Cognitive function, attention,
processing of language
Emotional control
Where does the cerebrocerebellum receive inputs from
t receives projections from the cortex Main functions are: · Coordination of skilled movements · Cognitive function · Attention · Processing of language · Emotional control
Describe vestibulocerebellar syndrome
Vestibulocerebellar Syndrome
Damage (tumour) causes syndrome similar to vestibular disease leading to gait ataxia and tendency to fall (even when patient sitting and eyes open)
ataxic gait:- wide based stance (looks drunk)
imbalance when eyes closed (Romberg sign)
nystagmus
Describe spinocerebellar syndrome
Damage (degeneration and atrophy associated with chronic alcoholism) affects mainly legs, causes abnormal gait and stance (wide-based)
Disorder: hypotonia
Describe cerebrocerebellar or lateral cerebellar syndrome
Damage affects mainly arms/skilled coordinated movements (tremor) and speech
Tremor and clumsy movements: Movements overshoot or undershoot target (dysmetria) Coordination problems (dysdiadochokinesia).
Describe some deficits that may be apparent upon movement in 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
State an acquired and inherited form of cerebellar dysfunction
Hereditary – Friedreich’s Ataxia
Acquired – Multiple Sclerosis
Summarise neural transmission in the basal ganglia
§ The basal ganglia mediate function of the ipsilateral (same side) cortex.
§ Main NTs; Dopamine (+), Glutamate (+), ACh (+), GABA (-).
