Locomotion 5 Flashcards

1
Q

Upper motor neurons what do they initiate how do they allow you to move and what mainly responsible for and where reside

A

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

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2
Q

What occurs to muscles when high intrinsic tone is gone

A

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

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3
Q

How do you continue to move

A
  • 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
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4
Q

What tracts function the following: Flexor facilitation, extensor inhibition, extensor facilitation

A

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

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5
Q

List the 6 steps in the sensory pathway from the body

A
  1. 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).
  2. Have dendrites travelling in a peripheral nerve
  3. Have a cell body in a spinal ganglion or other peripheral ganglion
  4. Have an axon passing into the spinal cord where they synapse - DORSAL HORN (sensory horn)
  5. The sensory information then passes up the spinal cord in a sensory tract and through the brainstem to the thalamus of the forebrain.
  6. All conscious sensory inputs project from the thalamus to the somatosensory cortex of the cerebrum
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6
Q

where does conscious and subconscious proprioception pathways project to and function

A

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,

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7
Q

Conscious and subconscious proprioception where do they travel and where do they travel to the forelimb and from the forelimbs

A

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

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8
Q

What occurs with defects in Conscious or subconscious proprioception and which has more effect on gait

A

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)

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9
Q

Pyramidal and extrapyramidal tracts where do they run

A

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.

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10
Q

Rubrospinal, reticulospinal and vestibulospinal where do they flow to and from and the important one

A

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

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11
Q

Clinically what are more evident, damage to LMN or UMN

A

LMN generally more evident

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12
Q

What are the 5 cells of the spinal cord and function

A

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

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13
Q

What substances make up the neuron

A

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

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14
Q

What is a mononeuropathy and polyneuropathy

A
  • PNS disease may manifest as a mononeuropathy (i.e. involving a single nerve) or a polyneuropathy (involving multiple nerves)
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15
Q

What clinical signs are involved with animals with significant disease of peripheral nerves

A

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)

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16
Q

What is denervation atrophy of skeletal muscle and is it reversible

A
  • 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
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17
Q

What is Wallerian degeneration and which parts of the damaged nerves are affected

A
  • 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
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18
Q

What is the typical sequence of events in Wallerian degeneration of the PNS

A

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

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19
Q

How do peripheral nerves regenerate in ideal circumstances

A
  • 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
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20
Q

what circumstances lead to imperfect regeneration of damaged peripheral nerves

A
  • 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
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21
Q

What is amputation neuroma

A

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

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22
Q

What domestic species are most likely to develop traumatic avulsion of the brachial plexus and prognosis for this condition

A

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
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23
Q

What circumstances are heifers likely to develop post-parturient paralysis and what complicated this

A

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)
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24
Q

what circumstances do calves develop congenital traumatic femoral nerve paralysis

A

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

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25
Q

What is caudal equina syndrome of the dogs

A

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

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26
Q

What is the cause, pathogenesis and lesions of equine laryngeal hemiphegia

A

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

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27
Q

What is the likely consequence of congenital hypoplasia or agenesis of enteric ganglia in foals

A

hypoplasia of PNS components are associated with severe anomalies of the CNS and of the musculoskeletal system -> muscle, tendons and ligaments too short

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28
Q

What clinical signs might an animal with myasthenia gravis display

A

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

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29
Q

How do congenital and acquired myasthernia gravis differ in cause and what leads to acquired

A

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

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30
Q

Which endocrinopathies may be associated with peripheral polyneuropathies in dogs and cats and the tumour associated

A

paraneoplastic peripheral neuropathies occasionally seen in dogs with insulinomas (functional malignant tumours of insulin-secreting β cells of the pancreatic islets)

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31
Q

What are potential adverse effects on the PNS of fungal or bacterial guttural pouch infections in
horses

A

ipsilateral hypoaesthesia of the pharyngeal mucosa, pharyngeal paresis, dysphagia and regurgitation
○ damage to the vagus nerve -> left laryngeal hemiplegia -> roaring
○ ± facial or vestibular nerve injury

32
Q

List infectious agents and autoimmune syndromes that can cause inflammation of multiple peripheral nerves

A
Viral infections (e.g. herpesviruses, rabies)
autoimmune disorders such as systemic lupus erythematosus
33
Q

What is idiopathic polyradiculoneuritis, why was it known as coonhound paralysis, which parts of PNS most severely affected and lesions

A
  • an acute fulminating condition of dogs and rarely cats
    originally described in dogs bitten or scratched by racoons, with clinical signs of ascending paralysis developing within 7-10 days of exposure
  • most severe in the ventral spinal nerve roots
  • associated denervation atrophy of skeletal muscles can be severe
34
Q

Name 2 toxins which target the neuromuscular junction to cause lower motor neuron paralysis

A

by interfering with release of acetylcholine -> lower motor neuron paralysis

1) botulinum toxin
2) paralysis tick (Ixodes holocyclus) toxins

35
Q

What is the cause, clinical presentation and typical lesions of stringhalt

A

Cause - Australia - toxin - dandelion, flatweed
Characterised by exaggerated hindlimb flexion and delayed extension
in severe cases, there may be a bilateral bunny-hopping hindlimb gait or even forelimb involvement
- peroneal and tibial nerves and denervation atrophy of distal hindlimb muscles

36
Q

What is dysaytonomia, which species does it occur, how clinically manifest and what current cause in the horse

A
  • dysautonomia is an acquired degenerative disorder of the autonomic division of the PNS
  • clinical signs in horses largely relate to gastrointestinal stasis -> intermittent vague colic over months or peracute collapse with gastric reflux and shock
  • clinical signs in small animals are more variable,
  • inconclusive evidence implicating a Clostridium botulin type C neurotoxin in horses
37
Q

List 4 nutritional deficiencies which can lead to lesions within nerves and species affected

A

1) vitamin A def - calves and piglets
2) pantothenic acid def - pigs
3) vitamin B2 deficiency - chickens
4) vitamin E def -

38
Q

Which species are peripheral nerve sheath tumours common, what sites common and typical behaviour

A
  • most commonly in dogs and cattle
  • they may arise anywhere along peripheral nerves or from cranial or spinal nerve roots
  • peripheral nerve sheath tumours tend to be poorly circumscribed, non-encapsulated, infiltrative masses that are difficult to completely excise -> may require limb amputation -> generally benign and only locally aggressive
39
Q

what is the most common tumour involving nervous system of poultry, causes and peripheral nerves involved

A
  • lymphoma involving peripheral nerves occurs infrequently in domestic animals
    in poultry, it occurs commonly as part of Marek’s disease, a herpesvirus-induced lymphoma that may involve the CNS, PNS (especially sciatic nerves and brachial plexus) and viscera
40
Q

Which part of the spinal cord is most vulnerable to ischaemic injury

A

the border zone in the caudal cervical-cranial thoracic area is thought to be particularly vulnerable

41
Q

What is the expected consequence if the ventral spinal artery or a branch of it is occluded by a
thrombus, thromboembolus or other embolus

A

obstruction of these branches -> selective damage to spinal grey matter, especially in the ventral horns

42
Q

List 4 regions why axonal regeneration after injury usually less successful in the central nervous system than
in the peripheral nervous system

A

1) Oligodendrocytes (CNS schwann cells) often die within areas of injury, if survive limited capacity to undergo mitosis
2) no basal laminae to guide axonal sprouts
3) debris from myelin of CNS inhibit axonal sprouting
4) 1 olgiodendrocyte may be responsible for myelination of 50 neurons

43
Q

What defences does the spinal cord have to protect it from external trauma

A

well protected from external physical trauma by the vertebral column and the overlying skeletal muscles and fat
○ the cancellous nature of the vertebral bone and the presence of vertebral synovial joints, vertebral ligaments, intervertebral discs and subarachnoid cerebrospinal fluid also afford some capacity to absorb impact forces

44
Q

What is meant by a spinal concussion, causes

A

spinal concussion = immediate and (usually) temporary loss of spinal function
results from rapid acceleration and deceleration forces on the spinal cord with shearing, tensile and/or compressive forces being placed on axons, dendrites, neuronal cell bodies +/- blood vessels

45
Q

What is spinal contusion and where else might there be haemorrhage following trauma of the spinal cord

A

spinal contusion = haemorrhage within the leptomeninges and/or surrounding superficial or deep spinal blood vessels)
- epidural or subdural haemorrhage

46
Q

List 3 other injuries to the spinal cord besides concussion and contusion

A

1) compression
2) laceration - physical tearing
3) transection - complete severance

47
Q

What is the progressive haemrrhagic myelomalacia and wen does it develop

A

, a potentially fatal condition
○ rapid cranial progression of the spinal damage -> ascending paralysis and ultimately paralysis of the muscles of respiration
○ this condition is seen most often in dogs following a severe intervertebral disc protrusion (see below) and may develop within 12-24 hours of the spinal injury

48
Q

What lesions would you see at the site of spinal cord compression and cranial and caudal

A

1) immediate site of injury, all parts of the spinal grey and white matter may undergo degeneration or ischaemic necrosis
2) cranial to the site of injury, Wallerian degeneration of white matter is generally limited to the ascending (sensory) tracts of the dorsal funiculi and the superficial dorsolateral parts of the lateral funiculi
3) caudal to the site of injury, Wallerian degeneration of white matter is usually limited to the descending (motor) tracts in the ventral funiculi and the more central parts of the lateral funiculi

49
Q

Where are traumatic fractures of the vertebrae most likely to develop, what potential consequence and circumstances they generally develop

A

Most likely to involve the thoracic and lumbar segments of the vertebral column

  • usually caudodorsal displacement of a sharp bone fragment into the vertebral canal -> risk of spinal cord laceration or even transection
  • arise as a consequence of pre-existing disease that has weakened the vertebral bone -> vertebral osteomyelitis (usually due to haematogenous bacterial infection) or bone lysis caused by multiple myeloma
50
Q

where are traumatic subluxations/luxation of the vertebral column most likely to develop

A
  • mainly involve the cervical vertebrae because of their longer ligaments and hence relative mobility
51
Q

What is wobbler syndrome, which species/breed most common and factors that predispose

A

Cervical vertebral stenotic myelopathy

  • a common neurological syndrome in Thoroughbred and Quarter horses and in large breeds of dogs, especially Great Danes and doberman pinschers
  • fundamental cause remains uncertain but genetic factors and a high nutritional plane that encourage rapid growth (e.g. ad libitum feeding of high protein and high energy rations) are involved in the pathogenesis -> though to be manifestation of osteochondrosis
52
Q

List the 2 main clinical presentations of wobbler syndrome

A

1) insidious onset and slow progression of ataxia of the hindlimbs (and occasionally the forelimbs) due to compression of the cervical spinal cord by the cervical vertebrae and/or their ligaments
2) vague neurological signs may be exacerbated following strenuous activity

53
Q

What is the difference between dynamic and static forms of wobbler syndrome

A

Dynamic - cervical vertebral instability
- the cord is compressed only when the neck is flexed or extended
- most common in fast growing horses
Static - cervical static stenosis
- there is continual cord compression, irrespective of the neck position especially at C5-7

54
Q

What is the difference between Hansens type I and type II inervertebral disc protrusion and which breeds are predisposed

A

1) Hansen’s type I category, with sudden and complete rupture of the annulus so that a large mass of disc material (mainly nucleus) enters the vertebral canal
2) partial rupture of the annulus and bulging of the dorsal part of the disc
common in ageing large breed dogs, especially German shepherd dogs,

55
Q

What is the most common site of intervertebral disc protusion in dogs and why

A

ince the dorsal part of the annulus is thinner than the ventral part, disc prolapse is normally in a dorsal direction

56
Q

What are some potential conseqeunces of intervertebral disc protrusion

A

1) develop progressive (ascending) haemorrhagic myelomalacia (ascending syndrome) almost always after a sudden and complete disc protrusion
2) severe epi- and subdural haemorrhage

57
Q

What is discospondylitis, cause, species most common and impact on spinal cord

A

discospondylitis = inflammation of an intervertebral disc with osteomyelitis of the adjacent vertebrae
- seen occasionally in dogs and pigs but uncommon in other species
usually caused by a haematogenous bacterial infection but can sometimes be due to a haematogenous fungal infection
- reduced IV disc space and loss of density in the vertebral epiphyses
○ grossly, see soft grey-yellow zones of discolouration and disruption of the disc with variable extension of infection into and lysis of the adjacent vertebral bone

58
Q

What is ankylosing spondylosis and spondylosis deformans

A

1) spondylosis is also known as spondylosis deformans
- a common degenerative condition of the vertebral column characterised by formation of osteophytes (new bony protrusions) usually as ventrolateral spurs from the vertebral bodies
2) Ankylosing spondylosis = bone spurs form complete bridges to unite adjacent vertebral bodies

59
Q

ankylosing spondylosis what species common in, cause and what impact on spinal cord

A
  • common in bulls, dogs and pigs and occasionally affects horses and cats
  • spondylosis can be caused by any process that causes abnormal mobility of vertebrae and hence abnormal forces being placed on the annulus fibrosus of the IV discs
    ○ e.g. discospondylitis, IV disc protrusion, congenital vertebral malformations
  • may cause narrowing of intervertebral foramina -> compression of nerves
60
Q

What are 4 important things to remember with spinal radiography

A

1) anaesthetise the patient - safety, and image quality
2) use padding - nose, neck and waist -> straight spine so even disc spaces and how they align
3) beware parallax error - diverging X-ray bean arising from a source results in uneven vertebral spaces in the periphery
4) Take orthogonal view

61
Q

Myelography what is it and what used for

A
  • Inject contrast agent into subarachnoid space around the spinal cord -> highlights the shape of the spinal cord
    ○ Use on-ionic (if bathe nerves in ionic tissue could induce seizures) iodinated (high atomic number appear weight)
    ○ contrast agent Shows the margins of the spinal cord
62
Q

List 4 times you would do a myelogram

A

1) Clinical myelopathy
2) Normal radiographs but know the animal has some clinical myelopathy
3) Better define a lesion confirm presence evaluate extent
4) Information can give prognosis and surgical planning

63
Q

What are the 3 location of lesions within the spinal cord and list some differentials

A

1) Extradural - outside meninges
- intervertebral disc extrusion
2) Intradural - extramedullary
- neiplasia, tumor
3) Intramedullary (within the spinal cord)
- cord oedema, neoplasia, haemorrhage

64
Q

Spinal CT list 5 advantages

A

1) rapid
2) bone
3) Soft tissue
4) cross-sectional - important with fractures
5) MPRs & 3D - severity of pathology

65
Q

Spinal MRI what best to look at

A

1) spinal cord & nerves
2) soft tissue
3) Bone
4) cross-sectional
5) MPRs

66
Q

What are the 6 indications ofr spinal CT and the one difference with spinal MRI

A

1) spinal trauma
2) acute onset painful myelopathy -> IVDD? neoplasia?
3) slow onset, progressive myelopathy -> neoplasia? degenerative?
4) back pain but normal radiographs -> occult discospondylitis? IVDD? neoplasia?
5) cauda equina signs -> lumbosacral stenosis?
6) cervical myelopathy in large breed dog -> CSM? IVDD?
MRI
Instead of 1) change to - Acute onset non-painful myelopathy -> FCE? (fibrocartilaginous embolism) ANNPE? (acute non-progressive nucleu pulposus extrusion)

67
Q

Intervetebral disease what are the 3 radiographic findings

A

1) May see reduced size of disc space, intervertebral foramen, articular facet joint space
2) May see ‘in-situ’ mineralised disc, or mineralised material within vertebral canal
3) May see nothing

68
Q

Discospondylitis and vertebral neiplasia radiographic findings

A

Discospondylitis
- shows vertebral end plate lysis, sclerosis and narrowing of the disc space
- May look normal in early stages of disease
Vertebral neoplasia
- Shows aggressive pattern of lysis +/- interrupted PNB (periosteum new bone formation)
- Subtle lesions are more clearly seen with advances imaging

69
Q

List 6 interesting radiopgraphic findings that may not be associated with clinical signs

A

1) Transitional vertebrae
2) Hemivertebrae
3) Butterfly vertebrae
4) spina bifida
5) block vertebrae
6) vertebral spondylosis

70
Q

Transitional vertebrae what is it

A
  • Possess characteristics of two spinal segments

Malformed short transitional processes

71
Q

Hemivertebrae what is it and what breeds common

A
  • commonly seen in ‘screw-tail’ breeds and can be incidental
  • result in severe cord compression
  • Twisted spinal column
72
Q

Butterfly vertebrae what is it

A
  • failure of fusion of lateral halves of vertebral body

- May be associated with spina bifida or incidental

73
Q

Block vertebrae what is it and cause

A
  • Result from fusion of multiple spinal segments

- Always congenital malformation

74
Q

Vertebral spondylosis what is it, what species common finding

A
  • New bone that is formed on the ventral aspect of the vertebral bodies and bridges the intervertebral space
  • Common finding in old dogs
75
Q

DISH (Disseminated idiopathic skeletal hyperostosis) what is it

A
  • Rare but spectacular disease
  • Causes spinal fusion
    Often not associated with clinical signs