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VetMed Year 4- Term 1 > Neurology -Week 2 > Flashcards

Neurology -Week 2 Flashcards

1
Q

Sensory tract deficit leads to ___

Motor tract deficit leads to ____

A 
Sensory = Ataxia
Motor = paresis
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2
Q

Where in spinal cord are the sensory nuclei

A

Sensory nuceli are dorsal & lateral funiculi

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3
Q

Where in spinal cord are the motor nuclei

A

UMN = Lateral ventral funiculi

LMN: Ventral horse grey matter.

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4
Q

Why do UMN synapse with LMN?

A

UMN synapse on LMN in ventral horn grey matter.

UMN facilitates and inhibits flexor/ extensors

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5
Q

Define Paresis

A

Decreased voluntary movement

C.F. Plegaia- absence of voluntary movement

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6
Q

L4-S3 lesion would present as

A 
Normal forelimb
LMN signs (decrease tone/ reflexes)
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7
Q

T3-L3 lesion would present as

A

UMN signs-Increased tone/reflexes
Forelimb; NORMAL
Differentiate L4-S3 lesion from T3-L3 if reflex is normal therefore UMN intact = T3-L3

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8
Q

C1-C5 myopathy presentation

A

Forelimb: UMN signs
Hindlimb:
UMN signs

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9
Q

If all four limbs have LMN signs it is likely to be

A

2 lesions or more likely neuromuscular localisation

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10
Q

Forelimb: LMN signs
Hindlimb: UMN signs are likely caused by a lesion

A

Lesions C6-T2

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11
Q

Forelimb and Hindlimb UMN signs are likely caused by

A

C1-C5 myopathy
OR
Brainstem (BUT DIFFERENTIATED ON MENTATION)

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12
Q

How is the severity of myopathies assessed i.e. what is lost first?

A

First is Priorioception, then movement then nociception. (first superficial pain then deep pain)

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13
Q

How to assess Nociception

A

Conscious perception of pain.

Limb withdrawel does not equal pain (see face)

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14
Q

Example of a disease that causes C6-T2 myopathy

A

Cervical spondylomyelopathy Forelimb: LMN

Hindlimb: UMN

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15
Q

Hypervitaminosis A causes what kind of myopathy

A

IN CATS.

C1-C5 and C6-T2 myopathy.

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16
Q

Forelimb: Normal
Hindlimb: LMN signs
Appropriate reflex’ to test would be

A

Suspect L4 to S3 myopathy therefore test

  • Patella - Femoral n - L4-L6
  • Sciatic - Withdrawel- L6-S7
  • Puadendal: s1-s3 - anal sphincter
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17
Q

Example of a degenerative disease that causes L4-S3 MYOPATHY

A

Lumbosacral stenosis.
Forelimb: Normal
Hindlimb: LMN signs.

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18
Q

Signalment for Lumbosacral stensosis

A 
Older large breed dogs (GSDs)
Bladder dysfunction (affects Pudendal nerve S1-S3)
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19
Q

Difference between Hansen Type 1 disk degeneration and Type II disk degneration

A

Type I: Chondrodystrophic breeds. Dauchunds. Nucleus fibrosis mineralise and extrudes
Type II; larger dogs. More acute as protrusion of annulus fibrosis

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20
Q

Type II Hansen disk degeneration leads to _____ of the articular facets

A

Type II disk degen leads to subluxation of the articular facets which leads to a step which is an unstable join.
Leads to thickening/in-folding of the interarcuate ligament and epidural fibrosis,.
= LUMBOSACRAL STENOSIS
Can lead to Spondylosis

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21
Q

Treatment of Lumbosacral stenosis

A
  1. Conservative: Restrict exercise for 6-8 weeks. Anti inflamm and pain relief.
  2. Dorsal laminectomy surgery
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22
Q

Complications of Dorsal laminectomy

A

Treatment for Lumbosacral stenosis (or conservative!)
IMMEDIATE= seroma
DELAYED= Discospondylitis (decrease blood supply)
or lamina formation/ fibrosis.
If severe LMN deficits are present/ chronic urinary incontinence = emergency and less fav prog.

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23
Q

Polyneuritis Equi clinical signs

A 
Tail paresis (easily missed)
Dilated anus
Faecal retention
Perineal loss of sensation
Muscle atrophy if chronic
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24
Q

Ddx for Polyneuritis Equi

A

Trauma- sacral fracture - common
EHV1= myeloencephalopathy = highly infectious / fatal
Primary or secondary cystitis

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25
Q

Pathogenesis of Polyneuritis Equi

How to diagnose

A

Immune mediated damage to peripheral nerves of caudal equine.
May follow adenovirus (??)
Diagnosis: Tail head muscle biopsy- Lymphocytic infiltrate seen around intramuscular nerves

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26
Q

Treatment of Polyneuritis Equi

A

Usually supportive.
Immunosuppressives are not usually effective.
Prog: ok for life, poor for return to function

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27
Q

Drugs to relax bladder

A

Phenoybenzamine (blocks sympathetic receptors)

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28
Q

Typical history of neuromuscular disease

A

LMN in fore and hind = tetraparesis. think neuromuscular (or 2 lesions)
Weakness, difficulty rising, exervise intolerance, regurgitation, lameness and pain.
Altered voice
Altered respiratory effort or inspiratory stridor

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29
Q

if paresis without ataxia likely to be ___

A

Muscular in origin.

Neuromuscular disease is tetraparesis +- proprioceptive ataxia

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30
Q

What changes to the pupil, tear production and HR would you expect with neuromuscular disease

A
  • Dilated pupil
  • Decreased tear production
  • Bradycardia
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31
Q

Gait for neuromuscular disease

A 
Paresis +- ataxia
Frequent sitting down
Exercise intolerance 
Low head carriage
Chopping and stilted gait (hypometria)
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32
Q

Normal EMG is

A

EMG: Electromyogram,

Normally Silent

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33
Q

EMG Fibrillation potentials

A

Caused by denervation and inflammation. Biphastic.
Sounds like rain on a tin roof.
Sponataneous action potentials of single myofibres

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34
Q

Positive sharp waves sound

A

Like a racing car driving by,
Dull thud or chug.
Caused by denervation.

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35
Q

EMG sounding like a machine gun would be indicitive of

A

Complex repetitive discharges.

Many myofibres in near synchrony.

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36
Q

How to calculate mean nerve conduction velocity

A

MNCV = Distance in mm / (prox latency - distance latency)

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37
Q

An action potential is a sudden increase in the permeability of

A

Action potential= sodium channels open = increase permeability.

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38
Q

How does Botulism cause tetraplegia?

A

Clinical signs vary from mild paresis to tetraplegia. LMN signs.
Found in soil. Equine botulism only toxin B found.
Toxin blocks the release of acetylcholine at NMJ IRREVERSIBLY

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39
Q

3 clinical form,s of bolulism

A

1) ingested toxin (all ages) - outbreaks. Only reported form in UK
2) Toxico-infectious - young foals. Spores ingested- organism prolifs in intestine
3) wound botulism (very rare)

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40
Q

In the UK botulism has only been reported in horses with access to ____

A

Big bale silage or haylage. C
aused by soil contaimination/ animal or bird carcasses.
pH <5.3 inhibits spores

41
Q

Diagnosis of Botulism in horses

A

Reduced tongue tone - remove tongue from mouth, will not retract. and history of exposure to silage.

42
Q

Treatment of Botulism in horse

A

Antiserum containing antibody to toxin B (only found in UK) C and D.
Broad spec antibiotics for pneumonia NOT PROCAINE AND AMINOGLYCO.
Fluid therapy.
Prog is GUARDED.

43
Q

What is Tensilon testing

A

AKA Edrophonium,
Tests for Myasthesia gravis.
Inhibits acetylcholinesterase therefore prolongs present of neurotransmitter acetylcholine - increase muscle strength,.
NOT SPECIFIC for MG.

44
Q

Diagnosis of Myasthesia gravis

A
  1. Tensilon testing (Edrophonium cholride)

2. Check for paraneoplastic (thymoma!)

45
Q

Treatment of IM MG

A

> 3MNTS, gsd, labradors, golden retrievers
Pyridostygmine (start low and increase dose)
Immunemodulatory drugs

46
Q

3 forms of Immune mediated MG

A
  1. Focal MG (megaoes with regurgi)
  2. Generalised MG, exercise intoler with megaoeso
  3. Fulimating form
47
Q

Signalment for Congenital MG

A

6-8 weeks old.
jack russel terrir, springer spaniel, miniature dachshund.
Decrease of AChR.
Treatment: Pyridostygmine

48
Q

Difference between Immune mediated and Congenital MG

A

IM: Autoantibodys against receptors
Congenital: Decrease of ACh receptors. 6-8 weeks

49
Q

Examples of Peripheral neuropathies in a) calves b) cows/horses

A

a) calves: femoral nerve paresis post parturition

b) Cows/Horses: Obturator nerve

50
Q

What is Sweeny

A

Suprascapular nerve damage with muscle atrophy of supra and infraspinatus

51
Q

Well muscled labrador, collapse 30 mins post exervise then short rest = mobile again. Likely Diagn=

A

Exerise intolerence.
Gene identified in labradors.
Treatment: exercise restriction.

52
Q

Clinical signs of Myopathic syndrome

A

Paresis. Exercise intolerence. Still, stilted gait.

Muscle atrophy or hypertrophy. Muscle pain on palpatation.

53
Q

Muscle tone in ipsilateral/contralateral limb for vestibular disease

A

Ipsilateral limb: decrease tone

Contralateral limb: exaggerated extensor tone.

54
Q

Gait in myopathic syndrome

A

Stiff, stilted gait.

55
Q

How does pacing in horses differ from pacing in dogs?

A

Pacing in horses= sign of ataxia = normal for some horses

Pacing in small animal = weakness (paresis)

56
Q

How does the organisation of white and grey matter differ in the brain and spinal cord?

A

Brain: Grey matter (cell bodies) OUTSIDE white matter

Spinal Cord: Grey matter INSIDE white matter

57
Q

Retractor oculi reflex=

A

Test for horse.
Press on cornea through eyelid, feel for retraction of the globe.
Afferent: Trigeminal
Efferent: Abducens (innervations retractor bulbi muscle)

58
Q

Stringhalt is the result of contraction of which muscles?

A

youtube HINDLIMBS Uncontrollable exaggerated movement of the digital extensor muscle OR when the digital flexor muscles lack sufficient opposition,

59
Q

Cause of Stringhalt

A

Toxicity - flat weed (false dandilion) = Hypochaeris radicata
Lesions of the scaitic nerve

60
Q

Diagnosis of Stringhalt

A

More exaggerated when turning or backing up.

Can be diagnosed with EMG (Electromyleogram)

61
Q

Treatment of Stringhalt

A

Surgical resection of a part of the tendon running along the hock
Or if caused by false dandilion remove from pasture

62
Q

Pathogenesis of Stringhalt

A

This faulty wiring of the spindles causes certain muscles to contract either too early or too late, or too much or too little, during certain phases of the gait. Leading to spasticity of the Biceps femoris muscle

63
Q

Why can a C6-T2 lesion cause Stringhalt signs?

A

C6-T2 lesion: Forelimb: LMN Hindlimb: UMN signs

Springhalt = Hindlimb, faulty spindles therefore of extensor muscle.

64
Q

Equine neuro exam, what else could be causing the weakness?

A 
Non-neurological reason for weakness?
Locomotor assessment.
Jaundice in horse than seems depressed?
Foot abscess??
Mentation: bright or depressed? Head pressing?
65
Q

Horse head turning during neuro exam would be suggestive of

A

forebrain.

66
Q

How common are Cerebellum neuropathies in horses?

A

Rare, Intention tremor, ataxia without weakness. Spastic/ exagerrated movements.

67
Q

Weakness and Ataxia in horse would be suggestive of

A 
Brainstem disease (includes pons and medulla)
Ascending proprioceptive pathways and descending motor pathway. Also contains cranial nerve nuclei therefore good cranial nerve exam can find position of lesion
68
Q

Ataxia clues in horses

A

Pacing

Circumduction`

69
Q

Lameness vs Ataxia

A

Lameness: normally regularly irregulat
Ataxia: Irregularly irregular

70
Q

Inflammation of a ligament is known as

A

Desmitis e.g. Bilateral pelvic limb suspensory ligament desmitis is a common cause of unusal ataxia-like deficit. = sacroiliac disease

71
Q

What can you assume about spinal reflex’ in standing horse

A

Standing horse assume spinal reflexes are intact. Withdrawal reflexes are still useful.

72
Q

8YO Gelding, pelvic limb lameness which doesn’t respond to NSAIds, Worse when head is lifted up. Imported from USA.. Ataxic front legs

A

Cerebellar disease v. unlikely in the horse.
Worse when lifting head = C1-C5.
Tail pull on right = weakness. Lateralising. No pain. Chronic.
Gluteal muscle atrophy = LMN. Ventral root (MOTOR)
Can’t explain with one lesion = Equine protozoal myeloencephalitis.

73
Q

Tail pull while walking tests =

A

UMN

74
Q

Tail pull while standing =

A

LMN

75
Q

Horse tests positive for Equine protozoal myeloencephalitis- what is pathogenesis?

A

Affects grey and white matter.
No horse to horse transmission so no need to quarantine
Faecal contam from birds.

76
Q

Treatment of EPM

A

Equine Protozoal Myeloencephalitis. Affects sensory and motor.
Treamtment: Inhibitors of folate metabolism - sulfadazine
Coccidiostats (Ponazuril)
NSAIDs
Steroids (only if deteriorating)
Guarded prog (esp as LMN signs - muscle atrophy)

77
Q

Sarcocystis neurona

A

= Protozoa causes Equine protozoal myeloencephalitis

78
Q

Main DDx of EDM is ___

A

Main differential for Equine Degenerative myeloencephalitis is Cervical Veterbral malformation/ stenosis

79
Q

2 types of Cervical Vertebral Stenosis

A

Static: Significant spinal cord compression on neutral (normal) radiograph (and flexed)
Dynamic: Instability only, seen on radiograph when next is flexed (NOT WHEN NEUTRAL)

80
Q

Wobblers syndrome =

A

Cervical vertebral stenosis. Most commonly C3-C6. 4 -23 months.
Diet too high in energy/ calcium
Also seen in dogs but normally C6-T2

81
Q

Type of radiograph to diagnose ‘wobblers’

A

CVS can be diagnosed with lateral cervical radiographs.

Most commonly affects C3 - C6.

82
Q

Equine Degenerative Myopathy pathogenesis

A

Affects white matter. Caused by vit E deficiency in the diet. (continually stabled horses)
Birth to 2 years old. Most are 6-12 months.
Spastic paraparesis + pelvic limb ataxia

83
Q

Most common cause of facial nerve paralysis in dogs

A

Otitis media

84
Q

What does a) sigamore b) false dandelion cause in horses

A

a) Sigamore- autumn- atypical myopathy

b) false dandelion (hypochaeris radicata) - Stringholt

85
Q

Difference between Stringholt and Fibrotic myopathy

A

Stringholt: hypermetric gate due to hypocharesis radicata- false dandilion
Fibrotic myopathy: slapping down of foot (norm semimembranous, semitendinous or gracalis) due to muscle tear, IM injection or neuropathy.

86
Q

Vit E deficiency causes_______

A

Nutritional myopathy in horses

87
Q

Why is Gabapentin a useful add on for epilepsy in dogs?

A

Renally excreted so avoids hepatotox

88
Q

Ddx for hypoglycaemia induced seizure

A

INSULINOMA
Toxicology (esp Xilitol)
Hypoadrenocorticism

89
Q

Recurrent Exertional Rhabdomyolsis

A

Exertional Rhabdomyolysis can be acquired (eccentric contraction, oxidative injury, metabolic exhaustion) or inherited (defective calcium reg e.g. RER!) OR polysaccharidge storage myopathy

90
Q

Prevention of recurrent exertional rhabdomyolysis

A

RER: Inherited (defective calcium reg OR polysacch storage myo)
for defective Ca regulation:
Oral Dantrolene (calcium release channel blocker)
and HIGH FAT/LOW CARB diet
Reg exercise/ turn out

91
Q

PSSM1

A

–>Mutation in glycogen synthase gene in skeletal muscle.

PSSM/EPSM are heritable. High prevalence in some draft breeds

92
Q

Presentation and Treatment of Supraspinatus/Infraspinatus contracture

A

Abduction extension

Tx: tenotomy

93
Q

Myosites ossificans

A

Secondary to trauma

94
Q

Which types of horses get fibrotic myopathy? and which type of dogs

A

a) Fibrotic myopathy: Quarterhorses- semitendinous/semimembranous
b) dog: GSD/Doberman/Rottweilers = gracilis

95
Q

Fibrotic myopathy gait

A

INT/EXT/INT ROTATION. STIFLE/HOCK/FOOT

96
Q

Pathogenesis of Lumbosacral stenosis

A

CHECK BLADDER FUNCTION: pudendal s1-s3
1. Hansen type II disk degen (AF) / protrusion
2. Subluxation of articular facets
3. Thickening of interarcutae ligaments = epidural fibrosis
Can lead to spondylosis/instability

97
Q

Why might you consider radiograph for horse with suspected polyneuritis equi?

A

Main Ddx: Sacral fracture (common)
also EHV-1 (csf tap)
or cystitis

98
Q

Syringomyelia pathogenesis

A

Associted with Chiari like malformation.
Syrinx formation is associated with obstruction of CSF flow at the foramen magnum.
Intermittent yelping due to neck pain, phantom scratching of neck.
Arachnoid diverticulum congenitally predisposes

VetMed Year 4- Term 1 (12 decks)

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