Motor systems Flashcards
What are alpha motor neurones?
Axons form the ventral roots from the spinal cord
They alone directly control muscle contraction- the final common pathway of motor control
Activity controlled by sensory input- feedback from dorsal roots, spinal Interneurons- circuitry generating motor programmes, upper motor contrrol- initiation and controls
Describe the muscle spindle
Intrafusal fibres
Specialised muscle fibres in a fibrous capsule
1a afferents wrap around the central, sensory portion- fire in response to stretch
Gamma motor neurones innervate above and below the 1a afferent neurone on the intrafusal fibres- contract the fibre to maintain the 1a afferent firing
The stretch reflex- monosynaptic feedback loop ➡ reflex contraction
Describe the golgi tendon organ
In series with muscle, sensitive to tension generated by contraction
Innervated by 1b afferents
Reflex is a polysynaptic reflex arc- decreases alpha motor neurone input- protrexts against overload
Describe the flexion withdrawal reflex
A protective pathway in response to pain to withdraw limb
Sensory afferents branch in spinal cord to innervate both excitatory and inhibitory Interneurons
The crossed extension reflex- goes to both sides oif the spinal cord to effect both legs so if one limb is withdraen you don’t fall over
Describe renshaw cells
Spinal inhibitory Interneurons
Produce recurrent inhibition of motor neurones and disinhibition of antagonist muscle motor neurones
Transmission mediated by glycine
What is the significance of tetanus toxin and strychnine?
Negate the influence of renshaw cells- result in prolonged muscle spasm and death
Strychnine is a glycine receptor antagonist
Tetanus toxin targets vesicle associated membrane proteins in GABA and glkycinergic neurones preventing neural transmitter release
What are spasticity disorders and how are they treated?
Increased muscle tone and exaggerated reflexes
A CNS disorder due to damage or developmental disorders
Eg. Stroke or multiple sclerosis
Drugs- baclofen, GABA-B receptor antagonist, reduces transmitter release by presynaptic inhibition
Tizanidine- alpha 2 adrenoceptor agonist, presynaptic inhibition of descending adrenergic tone
Describe the descending signals
Visual signals
Cerebellum
MLR- mesencephalic region ➡ MRF- medial reticular formation
What are the two main types of musculature?
Posture- proximal and axial muscles
Innervated by medial neurones
Fine motor- distal
Innervated by lateral motor neurons
What are the lateral descending pathways?
The corticospinal tract- monosynaptic contact of neurones with cell bodies in the motor cortex with alpha motor neurons
The rubrospinal tract- originates in the red nucleus in the midbrai , input from the same areas as the corticospinal tract
What are the ventromedial descending motor pathways?
All originate from brain stem nuclei
Both contra- and ipsilateral descending projections
Terminate in medial neurones in the ventral horn therefore control proximal and axial muscles- posture
Pontine reticulo-spinal and medullary reticulo-spinal
Vestibular spinal and tecto-spinal
Describe the vestibular spinal ventromedial descending pathway
Relays gravitational sensory information formn the inner ear and stretch receptorsin axial muscles
Projects to circuits in the cervical spinal cord that control axial muscles for posture of head
Mono synaptic excitation of extensors
Disynaptic inhibition of flexors
Also projects to lumbar spinal cord to facilitate extensors in the leg to promote upright posture
Describe the tectospinal ventromedial descending tract
Relays visual sensory information from the retinal and visual cortex
Control head movements to allow movement of head and neck in response to visual stimulus
Involved in eye movement
Describe the pontine reticulo-spinal ventromedial descending tract
Enhances the antigravity reflexes of the cord
Facilitates extensors to legs to maintain standing posture
Describe the medullary reticulo-spinal tract
Has an opposing effect to pontine reticulo-spinal tract
Frees antigravity muscles from reflex control to allow override
Name the motor areas in the brain
Area 6- supplementary motor area (SMA) and the premotor area (PMA)
Area 4- primary motor cortex (M1)
What are the inputs and outputs of the primary motor cortex?
Inputs- SMA, PMA, primary sensory area, cerebellum, dorsal column
Outputs- corticospinal tract, extra pyramidal tract, pons➡ cerebellum
FOR CONTROL OF DISTAL MUSCULATURE AND REFLEX CONTROL
What are the inputs and outputs of the premotor cortex?
Inputs- SMA, prefrontal cortices, cortical sensory areas, cerebellum, basal ganglia
Outputs- primary motor cortex, corticospinal tract, extra pyramidal tract, pons➡ cerebellum
PREPARATION OF MOVEMENT
PROXIMAL MUSCULATURE
MOVEMENT SEQUENCE
Describe the inputs and outputs of the supplementary motor area
Inputs- prefrontal cortices, basal ganglia, contralateral SMA, anterior cingulate cortex
Outputs- premotor cortex, primary motor cortex, contralateral SMA
PLANNING AND INITIATION
BIMANUAL COORDINATION
What are primary motor cortical output neurones?
Pyramidal cells (Betz cells) fro. Cortical level 5
Activate small groups of muscles rather than single ones
Indicidulally encode the amount of force to be exerted and direction of movement
Arranged in columns
What are the pathways involved in voluntary movement of the hand?
From basal ganglia, cerebellum, other cortical areas
Activation of appropriate motor neurone pool
Muscle contraction
Feedback from corticospinal collaterals
Feedback from cutaneous and spindle afferent providing modulation at the spinal level
Somatosensory feedback involving spinothalamic and thalamocortical relays
Describe the cerbellum
Involved in brain stem mechanisms Control of muscle tone Sensorimotor coordination Motor learning Does not project outside the brain Spinal and trigeminal inputs Corticopontine inputs Visual and auditory inputs Vestibular inputs Outputs- spinocerebellum for motor execution, cerbrocellum for motor planning, vestibule cerebellum for balance and eye movement
Describe some results of damage to areas of the cerebellum
Spino-cerebellum- hypotonia, ataxia, dysmetria
Vestibulo-cerebellum - slow saccades, nystagmus, ataxia
Cerebro-cerebellum - ataxia, dysmetria, a synergy, dysarthria
Describe the circuitry of the cerebellar cortex
Inputs from the climbing fibres of the inferior olive- excitatory and act on purkinje cells
Mossy fibres from the brainstem nuc!ei- indirectly excitate purkinje cells via parallel fibres of granule cells
Outputs from cortex only purkinje fibres which project to Deep Cerebellar Nuclei (DCN) - compare input from mossy and climbing afferents before and after cerebellar processing
Describe the basal ganglia
The striatum (STR)- the caudate nucleus, putamen, nucleus accumben
Globus pallidus (GP)- internal and external
Substantial nigra- reticulata (SNr), par compacts ( SNc)
Subthalamic nucleus (STN)
Direct and indirect pathway- opposing effects on thalamocortical output
Describe the direct pathway in the basal ganglia
Promotes movement
Dopamnine acts on excitatory D1 receptors on straito-GPi/SNr neuron
Reduces basal ganglia output and facilitates movement
Describe the indirect pathway in the basal ganglia
Serves to suppress movement
Dopamine acts on inhibitory D2 receptors on striato-GPe neuron
Reduces STN activity and BG output and so facilitates voluntary movement
Describe Parkinson’s disease
Akinesia
Bradykinesia
Rigidity
Loss of nigro-striatal dopoaminergic pathway- excessive inhibition of thalamo-cortical pathway and increased activity in the STN
Treated using dopamine replacing drugs- L-DOPA
Surgery- lesion/inactivation of STN
Describe the use of L DOPA
Will also elevate NA synthesis- combine with carbidopa or benserazide to inhibit DOPA decarboxylase
Side effects- Nausea/anorexia
Postural hypotension
Psychotomimetic effects
Effectiveness diminishes over 2-5 years- improved with slow release preparations and comnbibartion with COMT inhibitors to prevent L-DOPA breakdown
What are L-DOPA alternatives?
Dopamine receptor agonists- bromocriptine, pramipexole
Apomorphine
Selegiline- MOA-B inhibitor
Amantidine- dopamine releaser
mAChR antagonist- benzhexol
Deep brain stimulation- inactivates the subthalamic nucleus
Describe Huntington’s
Hyperkinetic disorder
Loss of striatal output neuron in indirect pathway
Overactive thalamocortical pathway➡ involuntary movement
Drugs- tetrabenazine (VMAT inhibitor, decrease DA storage), chlorpromazine (DA antagonist), baclofen (GABA-B agonist, decrease spinal reflexes)
What is ballism?
Damage to subthalamic nucleus
Violent flailing contralksteral to damaged side
Drugs- DA antagonists (haloperidol, chlorpromazine)
Anticonvulsants (topiramate), spinal circuit inhibition (intrathecal baclofen)
