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Neuro > Neuromuscular Cases > Flashcards

Neuromuscular Cases Flashcards

1
Q

Sings of UMN weakness

A
  • inability to control muscles
  • normal/^ tone
  • no muscle tone
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2
Q

Signs of LMN weakness?

A
  • inability to contract the muscles
  • facidity
  • muscle atrophy if chronic
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3
Q

Where do UMNs travel?

A
  • ventral funiculus of the white matter
  • synapse ventral horn of the grey matte (LMN cell bodies in grey)
  • LMN axons bunch up to make nerves
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4
Q

How long does neurogenic atrophy take to occour?

A
  • within 2 weeks
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5
Q

Ddx for:

  • Dysphagia
  • ongue paresis
  • Pupuil dilation and sluggish PLR
  • poor tail tone
  • poor anal tone
  • ecumbencey
  • generalised flaccid paraylsis
A
  • atypical myopathy
  • exertional rhabdomyolysis
  • botulism
  • equine motor neuron disease
  • myasthenia gravis? (never confirmed in a horse)
  • toxicity?
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6
Q

What 3 ways may clostridium botulinum intoxicate a horse?

A
  • forage poisoning (often silage) = ingestion of preformed toxin eg. decaying vermin in silage, common where farmers make their own silage!!
  • toxicoinfectious (foals) = eat bacteria, proliferation in GIT, toxins absorbed (d/t ^ absorption/v AB?)
  • wound (v rare) necrotic tissues needed (v poor blood supply)
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7
Q

What type of bacteria is clostridium and what toxins are involved in botulism?

A
  • spore forming anaerobe found in soil and decaying corposes

- toxins B and C

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8
Q

Tx Botulism

A
  • antitoxin (US) preformed Ab from horses
  • nursing
  • Abx esp if recumbent (^ pneumonia risk)
  • fluids
  • NG feeding
  • ventilation?
  • leave recumbent and quiet (though if becomes recumbent and cant get up, prog poor)
    > wai for toxin to clar and new NMJ to form (takes ~2weeks)
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9
Q

How can atypical myopathy/exertional rhabdomyolysis be r/o as NMJ/muscular causes of weakness?

A
  • CK and AST levels on bloods

- anything

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10
Q

How does botulinum exert its effects?

A
  • prevents release of Ach
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11
Q

Wha is equine moor neuron disease and what is it also known as?

A
  • generalised moto neuropathy

= amyotrophic lateral sclerosis (AML?) in humans

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12
Q

What are the 2 forms of myasthenia gravis? Is this common in horses?

A
  • Genetic and acquired (lack of post-synaptic Ach receptors or Abs against receptors
    > profound, rapid exercise intolerance
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13
Q

What toxin other than botulinum may cause myopathies?

A
  • Digitalis (fox glove)

> cardiac arrhythmias and skeletal muscle changes

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14
Q

What are the 3 forms of grass sickenss? Aetiology?

A

> acute
subacute
chronic
- aetiology unclear
- botulism type C? not yet proven but strong links
- regional distribution, some fields will repeatedly have problems
- hroses in contact with infected animals ^ resistnace to dz
- messing upi field (building, rotavating esp.) ^ risk
- young animals ^ risk

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15
Q

Clinical signs of grass sickness?

A 
> acute 
- ileus and gastric reflux (potential rupture if not NGT) 
- ddx SI entrapment/strangulation, ex lap needed to r/o 
- v poor prog
> subacute 
- mild colic
- v poor prog 
> chronic
- weakness 
- mm. fasciculations
- patchy sweating
- mm. atrophy d/t v eating? or neurogenic? 
- RHINITIS SICCA
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16
Q

Dx of grass sickness?

A
  • clinical signs

- ileal biopsy (v mesenteric plexus neurons on IHC)

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17
Q

Potential grass sickness prevention?

A
  • vax currently being trialled
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18
Q

Clinical signs of equine motor neuron disease?

A
  • generalised weakness tetraparesis
  • wastage of postural muscles
  • shifting weight, excessive recumbency
  • walk better than they stand
  • limbs tucked under body -> elephant on a drum
  • elevated tail head (muscles fibrose and can’t be pushed back down)
  • lowered head carriage
  • good apetite
  • retinopathy (brown pigment deposited in non-tapetal fundus in squiggly lines)
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19
Q

Ddx equine motor neuron dz?

A
  • myopathy eg. PSSM longerm

- chronic grass sickness

20
Q

How can EMND and grass sickness be differentiated?

A
  • chronic grass sickness v apetite, pick at food, can’t swallow
  • EMND ravenous apetite and no problems swallowing
21
Q

Potential cause of EMND? Which other disease is this pdf seen in ?

A
  • low serum vit E eg. v intake if stabled

> EDM -> spinal ataxia d/t v vit E when young

22
Q

Dx of EMND?

A

Biopsy tail head (sacrocaudalis dorsalis medialis m.)

23
Q

What types of horses is tetanus commonly seen in?

A
  • shoddy yard, gypsy horses
  • unvaccinated animals (though can occour in vax)
  • often distal limb d/t poor blood supply -> ^ risk anaerobic environment
24
Q

Pathogenesis of tetanus?

A
  • deep penetrating wound ~1week previously

- clostridium tetani (anaerobe)

25
Q

Clinical signs of tetanus

A
  • hyperalert
  • tense
  • prolapse of TE 9comes out as normal but gets stuck)
  • opisthotonus
  • muscle rigidty (saw horse stance or sardonic grin) flared nostrils
26
Q

Tx tetanus

A
  • penicillin
  • tranquiliser
  • tetanus toxoid (inactivated toxin to stimulate better immune response)
  • antitoxin (Abs) intrathecally (into the subarachnoid space)
  • environmental management (minimise muscle activation, calm quiet environement)
27
Q

How does the pathogensis of botulism and tetanus differ?

A

> Botulism
- prevents reelease of ACh
Tetanus
- carried retrograde axonal transport -> ventral hornm grey matter (LMN cell body)
- leaves, gets into inhibitory interneuron
- prevents INHIBITION at level of SC
-> constant excitation

28
Q

What is stringhalt ?

A
  • hyperflexion pelvic limbs esp. hock and knee
  • hypochaeris Radicata (false dandelion) cause but lots has o be consumed before clinical signs seen
    = lesion of afferent neuron of reflex pathway with spindle fibre
  • commonly seen bilaterally in Australia
  • Seen more often at walk than trot
  • unilateral seen d/t trauma of the cranial/dorsal aspect of the hock (may remain or resolve spontaneousl)
29
Q

What is shivers?

A
  • reflex arc defect? cerebellar defect? NT defect?
    > horses don’t want to pick up feet voluntarily
    > tail head may elevate concurrently with picking up back leg
    > trembling of HLs and tailhead
  • starts as an adult
  • progressive
30
Q

Potential cause of group of horses affected by a generalised NM condition?

A

> Lathyrism (lathyrism hirsutus) sweet pea plant cutting

  • > spastic paraparesis like tetanus
  • B oxalylamino L alanine acid
  • excitatory effects CNS and neurotoxic effects
31
Q

Is the simplistic view of central v peripheral useful?

A

Yes but not realistic

  • eg. LMN peripheral mostly but cell bodies are central
  • tetanus toxin works cenrally on peripheral nn.
32
Q

What condition is seen in scandanavian horses?

A

Scandanavian knuckling horses

- polyneuropathy d/t toxin

33
Q

What is stiff horse syndrome?

A
  • intermittent exensory hyper-ridgidity (stiff horse syndrome)
  • Abs attack glutamic acid decarboxylase (inhibits NTs in SC)
  • disinhibition -> stiffness
34
Q

If all 4limbs are affected is 2 lesions or generalised NM disorder more likely?

A

generalised NM

35
Q

What is acute polyradiculoneuritis? Dx?

A

> acute generalised rapidly progressive LMN paresis
stabilises after 4-5d
- ^ CSF protein (non-specific)
- EMG for dx

36
Q

Localise the lesion that causes dropjaw

A
  • brain or
  • trigem (mandibular branch) bilaterally
    > CN deficits combined w/ postural deficits or mentation etc indicates central
    > if rest of neuro exam normal suggests peripheral
37
Q

What is acute trigeminal neuropathy?

A
  • idiopathic, self limiting, acute onset
  • d/t neuiritis? lymphoma?
    > supportive tx. feed meatballs!
38
Q

Where is the lesion: horse L head tilt + horizontal nystagmus to the R

A
  • left sided peripheral vestibular

Ddx: petrous temporal bone fx, temporohyoid OA, idiopathic vestibular syndrome, ostitis media/interna

39
Q

Where is the lesion: sheep with tetraparesis and ataxia all 4 limbs

A
  • C1-C5

Ddx: trauma, abscess

40
Q

Where is the lesion: cow bizarre behavioural abnormalities and intermittent depression and hyperaesthesia

A
  • forebrain

Ddx: lead poisoning, cerebrocortical necrosis, BSE

41
Q

Where is the lesion: horse with focal muscle atrophy over the left epaxial muscle in the saddle area

A
  • LMN T3-L3
    Ddx: trauma, articular process joint vertebral arthropathy, focal grey matter SC (ventral horn)
  • Ddx: EPM
42
Q

Where is the lesion: horse with normal PLR but absent menace response in R eye

A
  • left sided cortical lesion. Amaurosis can be seen temporarily in post ictal phase of seizures
43
Q

Where is the lesion: horse with generalised weakness and profound mm atrophy of entire body

A
  • generalised LMN or 1* myopathy
  • consider other causes of weight loss
  • Ddx: EMND, chronic grass sickness
44
Q

Where is the lesion: horse with horners syndrome and sweating around the base of the ear

A
  • sympathetic fibres to the eye
  • most likely 3* neurons as sweating not further down the neck
  • cranial sympathetic ganglion in wall of GP might be affected
  • Ddx: abscess, fungal dz, tumour
45
Q

Where is the lesion: cow with unilateral mm atrophy of left masseter and loss of sensation over side of the face

A
  • left trigem - mandibular division

- no other CN deficits or ataxia - likely peripheral

Neuro (30 decks)

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