Block 3: spinal cord and descending tracts / reflexes Flashcards
What is somatotopic mapping of the motor cortex?
Describe the pattern of somatotopic mapping
How does it differ from somatosensory mapping?
What defines the proportion of cortex ratio?
- This is where specific regions of the motor cortex are devoted to the control of muscles in a particular body region.
- The proportion of motor cortex devoted to a particular body region equates to its function and the level of fine motor tuning required. Higher level of fine motor control, more motor cortex devoted to that body region, e.g. hands vs the thigh.
- The somatotopic mapping of the motor cortex begins in the longitudinal fissure with the feet and legs (note the difference to the somatosensory cortex which begins with the genitals).
- Then proceeds up the body- hips, trunk, shoulder, upper limb, hands and fingers, face, jaw/ tongue
Describe the regions of the cortex involved in motor function:
1) Primary area
- Primary cortical area = primary motor cortex, frontal lobe, located on the precentral gyrus/ Brodmann area 4, just anterior to the central sulcus.
- Involved in control of body movements on the contralateral side
- Damage leads to paralysis and paresis (weakness) of muscles on contralateral side of the body.
- is the origin of 80-90% of corticospinal neurones
- receives from the pre motor cortex and supplementary motor area (anterior to it), as well as the cerebellum and the somatosensory cortex.
Describe the regions of the cortex involved in motor function:
2) supporting areas
- Anterior to the primary motor cortex on Brodmann area 6 is the Supplemental motor area (SMA) (medial) and the pre motor cortex (lateral).
- The SMA receives from the basal ganglia and pre frontal cortex. Vital in movement planning. Prefrontal cortex sends movement intention information. SMA loss leads to unilateral akinesia (loss of voluntary muscle activity) including speech.
- The pre motor cortex is involved in motor program retrieval, receives from basal ganglia and prefrontal cortex. Output to the primary motor cortex but also fine tunes reticulospinal tract (via reticular formation). Requires external stimuli to release motor programme (visual/auditory/somatosensory). Damage to premotor cortex can lead to contralateral paresis (Weakness) of postural muscles (due to effect on reticulospinal tract).
Define a motor unit
Motor unit= lower motor neurone and the extrafusal muscle fibres it innervates
What is a myotome?
A myotome is formed by a single spinal nerve and the group of muscles it innervates.
What is the difference between the innervation of powerful, unrefined large muscles such as the knee extensors vs refined muscles of the hand?
- Large unrefined powerful muscles will have a large number of muscle fibres (1000+) innervated by a single motor neuron
- Small muscles of the hands will have a small number of muscle fibres innervated by each motor neurone (10). Multiple motor units will innervate the hand therefore allowing fine control.
What is the difference between intrafusal and extrafusal muscle fibres?
- Extrafusal muscle fibres = skeletal muscle that generates skeletal movement, innervated by alpha lower motor neurone.
- Intrafusal muscle fibre = muscle fibre housed in collagen sheath that forms the muscle spindle, detects the length of muscle and force of contraction. Innervated by gamma lower motor neurone.
What are the differences between alpha and gamma motor neurones?
- Alpha motor neurones are large diameter myelinated axons that innervate motor units of extrafusal fibres.
- Gamma motor neurones are small diameter myelinated axons that innervate the intrafusal fibres of muscle spindles. (intrafusal muscle fibres found inside the muscle spindle, housed in collagen sheath).
Name each condition shown
Define plegia
what is the fancy medical word for muscle weakness?
- Plegia= paralysis
- muscle weakness = paresis
Describe the blood supply to the spinal cord
- Spinal cord supplied by longitudinal vessels, 1 anterior spinal artery which supplies 2/3 rds of the spinal cord. If lost, issues supplying the ventral horn and lateral horns of spinal cord, therefore issues with motor function and autonomic function.
- Spinal cord supplied by two posterior vessels which supply the dorsal horns of the spinal cord. If these are lost not all sensory sensation may be lost as there may be some compensation by the anterior spinal artery.
Mutilple disorders can affect different parts of the motor system.
Valvular disease can lead to spinal cord injury and neurological signs and symptoms.
What are some causes of spinal artery infarction?
- Causes: atherosclerosis and plaque rupture, (atheroma), aneurysm, embolism, tumour and compression, trauma
What could also lead to spinal cord damage?
- Ventral root damage
- Spinal cord lesion
- Multiple sclerosis
- Amyotrophic lateral sclerosis
- Motor neurone disease
- Parkinson’s disease
What is amyotrophic lateral sclerosis?
How does it normally present initially?
- Amyotrophic lateral sclerosis is a neurodegenerative disease in with the corticospinal tracts and ventral horn of the spinal cord degenerate.
- Disease affects both upper motor neurones and lower motor neurones, but tends to present with lower motor neurone dysfunction first in the limbs before affecting upper motor neurones.
- Symptoms are a combination of upper and lower motor neurone symptoms:
- Spasticity/ cramps
- Fasciculations- brief contractions affecting small number of muscle fibres
- Weakness (limbs/ neck/ diaphragm)
- dysphagia
- dysponea
- dysarthria (unclear articulation of speech).
Label the image
- Pink- and lateral = lateral corticospinal tract
- Pink and anterior = ventral corticospinal tract
- Yellow and lateral = rubrospinal tract, small and unclear of function in humans, may be involved in limb flexor muscle control
- Purple and ventral= vestibulospinal tract
- Green = pontine and medullar reticulospinal tracts. Reticulospinal tracts inhibit lower motor neurons to prevent their overfiring, helps modulate their activity.
Fill in the blanks:
Corticospinal tracts control _____, _________, and _____ of movements.
Corticospinal tracts are involved in ______, _______ and ______ movement.
Corticospinal tracts control the speed, direction and agility of movements.
Corticospinal tracts are involved in rapid, skilled, fine movement.
Describe the lateral and ventral corticospinal tract pathway:
What are the differences between them?
Lateral corticospinal tract: (80- 90% of corticospinal neurons)
- Upper motor neurone from the primary motor cortex on the precentral gyrus descends from the cortex down to the brainstem.
- Does so via the internal capsule, descending down the genu and posterior limb (mainly) until it reaches the midbrain.
- At the midbrain these corticospinal tracts form the cerebral peduncles on the caudal side of the midbrain, forms the connection between the brain and midbrain.
- They descend in the cerebral peduncles until they reach the medulla where they form pyramidal tracts which decussate in the lower medulla.
- After these upper motor neurones decussate they travel down to the spinal level of appropriate exit for the target muscle.
- Here they synapse with a lower motor neurone in the ventral horn of the spinal cord.
- This lower motor neurone exits as a spinal nerve to the muscle belly it innervates.
Ventral corticospinal tract: (10-15%)
- The ventral corticospinal tract also begins in the primary motor cortex and descends via internal capsule, corticospinal tracts of the cerebral peduncles on the dorsal side of the midbrain unti lthe medulla.
- At the medulla the ventral corticospinal tracts travel down the medullary pyramids but do not decussate
- They continue down the spinal cord ipsilaterally until they reach the appropriate spinal level for their target muscle.
- Once at the target muscle level, they decussate and synapse with a lwoer motor neuron in the ventral horn.
- Spinal nerve leaves to innervate muscle.
When figuring out which motor symptoms will be observed in the case of damage what do you first need to consider?
What are sites of Upper motor neurone damage?
What are sites of lower motor neurone damage?
Whether its is an upper motor neurone or a lower motor neurone affected.
Upper motor neurone damage sites: Cortex itself, corona radiata/ internal capsule, brainstem, medulla, spinal cord
Lower motor neurone damage sites: spinal cord level of synapse, spinal nerve, cauda equina, peripheral nerve. (e.g. radial).
How do the symptoms of UMN and LMN lesions differ?
How might an UMN lesion present initially?
UMN: Lesion presents with
- No muscle wasting
- Spastic paralysis - muscles affected by persistent spasms and exaggerated tendon reflexes
- Hyperreflexia
- Extensor plantar response (Babinski’s sign) (normal response when stroking plantar sole of the foot is to curl the toes and plantarflex, with UMN damage the foot extends and toes fan out).
LMN: Lesion presents with
- Muscle wasting/ atrophy
- Hyporeflexia
- Flaccid paralysis
- Fasciculations - flickering muscle contraction
An upper motor neurone lesion may initially present with flaccid paralysis (a LMN sign) then after a few days/ weeks become spastic and UMN signs take over.
What would occur if there was a hemilesion of the spinal cord at this site? (referring to UMN and LMN damage)
- Lesion at that level would affect LMN exiting the spinal cord at A
- It would then induce UMN effects below the lesion, as now no UMN’s can descend any further than that point.
- Would present with LMN signs at the site of the lesion and UMN signs below it.
- Also need to consider that sensory tracts will be affected in a hemilesion of the spinal cord (Dorsal column, spinothalamic tract, spinocerebellar tracts).
Consider the lesion shown:
what tracts are affected?
What sensations/ motor fibres do they carry?
Where do they decussate and therefore what side is affected?
What symptoms will the individual present with?
- Sensory: dorsal columns, spino cerebellar (lateral portion) and spinothalamic (anterior)
- Motor: lateral and ventral corticospinal tract
- Dorsal column carries concious proprioception, vibration and discriminitive touch, decussates at lower medulla therefore ipsilateral side will lose these sensations.
- Spinocerebellar carries proprioception from muscles to the cerebellum, and travels ipsilaterally (mostly some cross over then cross over again) therefore loss on same side, cerebellar symptoms on the ipsilateral side.
- Spinothalamic tract carries pain, temperature and simple touch. Enters spinal cord and ascends 1-2 levels in tract of lissauer before synapsing in dorsal horn with 2nd order neurone, 2nd order neurone decussates in anterior white commisure before ascending to VPL of thalamus which sends 3rd order to cortex. Mostly spinothalamic 2nd order neurones travel contralaterally, therefore loss on the contralateral side.
- Lateral Corticospinal tract- Voluntary and skilled motor movement. Carries motor innervation from cortex, descends to medulla where it decussates, continues to ventral horn of spinal cord where it synapses with a lower motor neurone. Majority (80-90%) is lateral, therefore most of the deficit will be on the contralateral side.
Lesion shown in the image below:
Describe the signs the patient would show
- Dorsal column pathway: carries concious proprioception, vibration and discriminitive touch. Fibres need to ascend to medulla to decussate but aren’t able to reach medulla. Therefore loss of sensation ipsilateral side.
- Spinocerebellar pathway: mostly, proprioceptive fibres enter the spinal cord and ascend ipsilaterally, therefore will see cerebellar symptoms ipsilaterally.
- Spinothalamic pathway: Carries pain/ temp/simple touch. Fibres enter spinal cord, travel 1-2 levels in tract of lissaeur before synapsing in dorsal horn. 2nd order neurone then decussates and ascends. Mostly these fibres travel contralaterally, therefore loss of sensation slightly below lesion (as fibres ascend).
- Corticospinal tracts: decussation occurs at the level of the medullary pyramids, lesion will not allow UMN impulse to progress, therefore loss on ipsilateral side of lesion. Get LMN symptoms (flaccid paralysis) at the level of the lesion.
What is the major motor innervation pathway to the face?
How does this differ from the lateral corticospinal tract?
- Major motor innervation to the face is via the corticobulbar tract
- Upper motor neurones from the left cortex descend and decussate at the level of the pons before continuing as LMN’s that innervate the face.
- Motor neurones from the cortex (UMN) descend to the contralateral trigeminal (CN V) and facial nuclei (CN VII- muscle of facial expression) of the pons (decussate higher up).
- These then send lower motor neurones to innervate the face.
- Differs from the lateral corticospinal tract which decussates lower at the pyramidal tracts of the medulla.
What would happen to motor innervation to the face and the rest of the body with a brainstem lesion at this site?
- Left brainstem lesion would lead to ipsilateral facial paralysis due to loss of function of the lower motor neurones leaving the pons at that level. (left sided facial paralysis).
- The effect on the motor innervation to the rest of the body would be on the contralateral side- as the left hemisphere needs to send its upper motor neurone through the brainstem, down the spinal cord to synapse with a LMN that innervates the right side of the body. The signal cannot pass, therefore UMN signs on the right side.
What is the primary function of the lateral Vestibulospinal tract?
- Primary function of the lateral vestibulospinal tract is ANTIGRAVITY, POSTURE AND BALANCE.
- Vestibulospinal tract innervates extensor muscles that work against gravity- keep you upright.
- Signal sent from the vestibular nuclei in the pons and medulla, down the spinal cord
- Synapses directly with lower motor neurones on the ipsilateral side.
- Excites LMN that innervates extensor muscles
- Inhibits LMN that innervates flexor muscles.
Where do reticulospinal tracts originate?
How do Reticulospinal tracts modulate LMN output?
What would occur if reticulospinal tract function was lost?
- Reticulospinal tracts originate in nuclei within the pons and medulla and act on LMN.
- Reticulospinal tracts activate Renshaw cells which are inhibitory interneurons that inhibit LMN’s.
- If reticulospinal tract function was lost, you will lose the ability to inhibit hyper excitable LMN’s, leading to muscle spasticity.
Lower motor neurone disease:
Often see muscle wasting/ atrophy. What are the other signs of lower motor neurone disease?
Why does muscle atrophy occur?
- Other signs of lower motor neurone disease are flaccid paralysis, muscle weakness, hyporeflexia/areflexia (do not respond at all) and fasciculations.
- Muscle atrophy occurs both due to loss of innervation of the muscle by the lower motor neurone but also due to neurogenic degeneration of the UMN by loss of the LMN.
- The LMN and UMN are mutally dependent.
What is the myotactic (stretch reflex)?
Describe the mechanism
What is its function?
- Myotactic reflex is a reflex arc mediated by muscle spindles within the extrafusal muscle fibre.
- Remember muscle spindles are intrafusal muscle fibres, separated from the muscle body by collagen sheath, and are noncontractile fibres that monitor the length of a muscle, innervated by gamma motor neurones.
- Muscle spindles send sensory impulses via primary 1a afferent neurones which synapse directly with an alpha motor neurone that innervates that muscle belly.
- When the muscle is stretched (e.g. paterllar tendon hit by hammer), this sends afferent signals from muscle spindles to the alpha motor neurone within the spinal cord which splits to 1) activate contraction in the stretched muscle 2) inhibit contraction/ relax the antagonistic muscle.
- (i.e contract the quadriceps and relax the hamstrings).
- Forms a reflex arc
- We also have concious (dorsal column) and unconcious proprioception (spinocerebellar- muscle spindle and golgi tendon organs) of this reflex contraction sent back to the cortex.
- Function: protect muscle fibres from overstretching, postural maitenance
What is the inverse myotactic reflex (Golgi tendon reflex)?
- Golgi tendon organs detect the amount of tension within a muscle by measuring the stretch in tendons and initiate a tendon- protective reflex.
- When a muscle is contracting under force this activates golgi tendon organs which send afferent signals back to the spinal cord to protect the muscle from rupturing.
- Synapses with a motor neurone that leads to contraction of the antagonist muscle and relaxation of the muscle under tension - agonist muscle.
- Protects the muscle from rupturing under strain, if tension is great enough the inverse myotactic reflex will override the myotactic reflex.
- E.g. pick up large heavy boulder, tension detected in biceps muscle, sends afferent signal to motor neurone within spinal cord, leads to contraction of the antagonist muscle (triceps) and relaxation of the agonist muscle (biceps)- drop boulder.
What is the flexor withdraw reflex?
- Flexor withdraw reflex= quick withdraw of a limb from painful/ noxious stimuli.
- Noxious stimuli detected by sensory receptor within the skin (temp R)/ free nerve ending which sends afferent signal to dorsal horn of the spinal cord
- Synapses with interneurone within the spinal cord that excites an alpha motor neurone to the flexor muscles of affected body part
- at same time interneurone inhibits extensory muscles of affected body part
- Overall get withdrawal of the limb from noxious stimuli
- Noxious afferent stimulus also synapses with motor neurones that contract postural muscles on the contralateral side, moving the centre of gravity and preventing falling.
- Contralateral stabilisation = crossed extension reflex.
