Locomotion 5 Flashcards
Upper motor neurons what do they initiate how do they allow you to move and what mainly responsible for and where reside
initiate all movements that are not direct reflexes
TOO MOVE - UMN controlling extensors need to increase inhibition of extensor muscles while those controlling flexor need to decrease inhibition of flexor muscle activity
- Most important reside in the red nucleus of the midbrain
What occurs to muscles when high intrinsic tone is gone
General rule is that extensors are maintained with a higher intrinsic tone than the flexor muscles, if all higher control is lost the outcome is extensor rigidity -> captive bolt causes, not consciously aware -> brain dead
How do you continue to move
- Alteration between flexion and extension is primarily through local spinal cord reflexes
○ Activated by constant proprioceptive input from all body and limbs muscles activities - Also can occur with anatomical structures causing movement -> ligaments, tendon and muscles, movement in one thing due to movement in another
What tracts function the following: Flexor facilitation, extensor inhibition, extensor facilitation
Flexor facilitation - Lateral corticospinal tract (cats important), Rubrospinal tract (most important in other animals)
Extensor inhibition - lateral reticulospinal tract
Extensor facilitation - in order to remain upright - vestibulospinal tract (both sides) and ventral reticulospinal tract
List the 6 steps in the sensory pathway from the body
- a receptor in the periphery that responds to pressure, vibration and/or distortion of tissue (Golgi tendon organ, muscle spindle fibres, Pacinian corpuscles, Ruffini endings, free nerve endings).
- Have dendrites travelling in a peripheral nerve
- Have a cell body in a spinal ganglion or other peripheral ganglion
- Have an axon passing into the spinal cord where they synapse - DORSAL HORN (sensory horn)
- The sensory information then passes up the spinal cord in a sensory tract and through the brainstem to the thalamus of the forebrain.
- All conscious sensory inputs project from the thalamus to the somatosensory cortex of the cerebrum
where does conscious and subconscious proprioception pathways project to and function
Conscious
- Projects to the contralateral cerebral cortex
- Start off the movement
Subconscious
- Project to the ipsilateral cerebellar cortex directly so only 2 neuron system
Ensure the movement is smooth and coordinated by using patterns stored within the brain,
Conscious and subconscious proprioception where do they travel and where do they travel to the forelimb and from the forelimbs
Conscious proprioception primarily travels in the dorsal funiculus
- fasciculus gracilis from caudal to the forelimbs (ie hindlimbs etc)
- fasciculus cuneatus from the forelimbs and neck.
Subconscious proprioception primarily travels in the lateral funiculus
dorsal and ventral spinocerebellar tracts
What occurs with defects in Conscious or subconscious proprioception and which has more effect on gait
Conscious
DEFECTS - foot in normal position but abnormal weight bearing -> abnormal posture of the limb
Subconscious
DEFECTS - abnormal positions of the limb -> such as standing on themselves (may lead to tripping)
Pyramidal and extrapyramidal tracts where do they run
Pyramidal tracts are called corticospinal because they originate in the motor cortex of the cerebrum and travel through the medullary pyramids which are white matter tracts within the brain
Extrapyramidal tracts
These pathways originate, or relay/synapse in the brain stem and their axons do NOT travel in the medullary pyramids.
Rubrospinal, reticulospinal and vestibulospinal where do they flow to and from and the important one
All extrapyramidial
1) Rubrospinal from the red nucleus in the midbrain to the distal limb flexors
- considered to be the main tract controlling voluntary movement in dogs
2) Reticulospinal from the reticular formation of the medulla oblongata
3) Vestibulospinal from the vestibular nuclei of the medulla oblongata which integrate information from the inner ear.
- important for maintenance of posture
Clinically what are more evident, damage to LMN or UMN
LMN generally more evident
What are the 5 cells of the spinal cord and function
1) Neurons
2) Oligodendrocytes - form the myelin sheath in the CNS
3) Microglia cells - fixed macrophages in the CNS
4) Ependymal cells - Lining cells of the ventricles and spinal central canal
5) Astrocytes - star-shaped glial cells of the CNS
What substances make up the neuron
1) soma - cell body
2) nucleus - large, centrally located
3) nissl substance - basophilic substance consisting of rough ER and ribosomes
4) Axon hillock - conical part of neuronal soma from which the axon emerges
- No nissl substance - differentiate between dendrites
5) Cell processes - axon and dendrites number vary
What is a mononeuropathy and polyneuropathy
- PNS disease may manifest as a mononeuropathy (i.e. involving a single nerve) or a polyneuropathy (involving multiple nerves)
What clinical signs are involved with animals with significant disease of peripheral nerves
enervation atrophy of skeletal muscles, paresis (weakness) or flaccid paralysis of innervated structures, diminished or absent reflexes and diminished muscle tone, diminished pain responses, proprioceptive deficits and paraesthesia (abnormal or inappropriate sensation) (e.g. pins and needles)
What is denervation atrophy of skeletal muscle and is it reversible
- denervation atrophy of muscle can be reversible (if the underlying cause of denervation is reversible)
very advanced lesions (e.g. - after a year or more of denervation) may be irreversible as many of the affected fibres may contain no myofibrils or myofilaments and there may have been fibrofatty connective tissue replacement of the lost muscle mass
What is Wallerian degeneration and which parts of the damaged nerves are affected
- Wallerian degeneration is the term used to describe the degenerative events that follow either acute focal injury to a myelinated axon or death of its neuronal cell body
○ if the neuronal cell body dies, the entire axon will undergo Wallerian degeneration
○ if there is focal injury to a myelinated axon, the segment distal to the site of injury will undergo Wallerian degeneration
What is the typical sequence of events in Wallerian degeneration of the PNS
Occurring rapidly
1) swelling of the distal segment of the axon to form an axonal spheroid
2) collapse, fragmentation and disintegration of the axon - myelin sheath redundant
3) the myelin retracts and fragments to form droplets (termed ellipsoids) which surround the axonal debris -> secondary demyelination
4) axonal and myelinic debris is then removed by phagocytosis by macrophages which become filled with lipid vacuoles (gitter cells)
5) Regeneration if possible
How do peripheral nerves regenerate in ideal circumstances
- provided that the nerve cell body survives, regeneration of the axon can occur from the proximal stump
- the degree of regeneration depends on the integrity of the endoneurial tube distal to the site of axonal injury
1) Axonal and myelinic debris is cleared away
2) Schwann cells begin to proliferate and form a longitudinal column (Bungner’s bands) along the former course of the axon
3) direct the axonal migrations back to the end of the axon
what circumstances lead to imperfect regeneration of damaged peripheral nerves
- if the endoneurial tube is no longer intact (e.g. if a peripheral nerve is severed (crush, compression more likely to have endoneurial tube intact)), the Schwann cell bands persist and usually endoneurial fibrosis develops -> a tangled mass of collagen, Schwann cells and axonal sprouts -> failure of reinnervation
What is amputation neuroma
Abortive regeneration following focal axonal injury
formation of a firm, bulbous, tumour-like mass of tangled axonal sprouts, collagen (scar tissue) and Schwann cells -> no endoneurial tube to direct the axonal sprouts
Eg - debecking
What domestic species are most likely to develop traumatic avulsion of the brachial plexus and prognosis for this condition
seen most commonly in cats and dogs as a consequence of severe forelimb abduction or traction due to car accidents
- may present as radial nerve paralysis
- total avulsion of the plexus -> permanent flaccid paralysis of the affected forelimb, with denervation atrophy of forelimb muscles and sensory loss distal to the elbow
What circumstances are heifers likely to develop post-parturient paralysis and what complicated this
common in heifers with dystocia due to an oversized foetus
- characterised by recumbency, hindlimb abduction and inability to rise -> damage to the obturator nerve and sciatic nerve
- gravitational pooling of blood +/- external venous compression by the cow’s weight -> venous thrombosis -> ischaemic necrosis (especially of the semitendinosus muscle)
what circumstances do calves develop congenital traumatic femoral nerve paralysis
calves following their assisted delivery from dystocic heifers
- a large calf in cranial presentation may fail to enter the vagina if one or both stifle joints engage(s) the pelvic brim
subsequent traction on the calf’s forelimbs
What is caudal equina syndrome of the dogs
Result of chronic traumatic damage to the spinal roots of the cauda equina (i.e. roots arising from spinal segments L7, S1-S3 and C.1-.5)
- usually due to lumbosacral stenosis and/or stenosis of the intervertebral foramina -> narrows the canal at which the cauda equina runs -> pinching nerve routes in that area
What is the cause, pathogenesis and lesions of equine laryngeal hemiphegia
Cause is not identifiable but previous nerve trauma is one possibility
e.g. stretching or compression of the left recurrent laryngeal nerve
Pathogenesis
unilateral paralysis and denervation atrophy of intrinsic laryngeal muscles -> inability to abduct the left arytenoid cartilage and vocal fold -> partial airway obstruction -> inspiratory stridor (“roaring”) and decreased athletic performance
Lesions - Wallerian degeneration distal parts o the left recurrent laryngeal nerve
What is the likely consequence of congenital hypoplasia or agenesis of enteric ganglia in foals
hypoplasia of PNS components are associated with severe anomalies of the CNS and of the musculoskeletal system -> muscle, tendons and ligaments too short
What clinical signs might an animal with myasthenia gravis display
generalised myasthenia gravis, exercise -> a choppy stride followed by recumbency and refusal to move; after a few minutes, the affected animal usually gets up and walks again -> worse with exercise better after rest
How do congenital and acquired myasthernia gravis differ in cause and what leads to acquired
Congenital
reduced density of acetylcholine receptors in post-synaptic muscle membranes
Acquired
immune-mediated disorder in which antibodies are directed against acetylcholine receptors of neuromuscular junctions -> endocytosis and decreased density of receptors
Cause - underlying thymoma (in the chest) and the myasthenia gravis is regarded as a paraneoplastic syndrome
Which endocrinopathies may be associated with peripheral polyneuropathies in dogs and cats and the tumour associated
paraneoplastic peripheral neuropathies occasionally seen in dogs with insulinomas (functional malignant tumours of insulin-secreting β cells of the pancreatic islets)