Flashcards in Neuromuscular Cases Deck (45):
Sings of UMN weakness
- inability to control muscles
- normal/^ tone
- no muscle tone
Signs of LMN weakness?
- inability to contract the muscles
- muscle atrophy if chronic
Where do UMNs travel?
- 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
How long does neurogenic atrophy take to occour?
- within 2 weeks
- ongue paresis
- Pupuil dilation and sluggish PLR
- poor tail tone
- poor anal tone
- generalised flaccid paraylsis
- atypical myopathy
- exertional rhabdomyolysis
- equine motor neuron disease
- myasthenia gravis? (never confirmed in a horse)
What 3 ways may clostridium botulinum intoxicate a horse?
- 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)
What type of bacteria is clostridium and what toxins are involved in botulism?
- spore forming anaerobe found in soil and decaying corposes
- toxins B and C
- antitoxin (US) preformed Ab from horses
- Abx esp if recumbent (^ pneumonia risk)
- NG feeding
- 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)
How can atypical myopathy/exertional rhabdomyolysis be r/o as NMJ/muscular causes of weakness?
- CK and AST levels on bloods
How does botulinum exert its effects?
- prevents release of Ach
Wha is equine moor neuron disease and what is it also known as?
- generalised moto neuropathy
= amyotrophic lateral sclerosis (AML?) in humans
What are the 2 forms of myasthenia gravis? Is this common in horses?
- Genetic and acquired (lack of post-synaptic Ach receptors or Abs against receptors
> profound, rapid exercise intolerance
What toxin other than botulinum may cause myopathies?
- Digitalis (fox glove)
> cardiac arrhythmias and skeletal muscle changes
What are the 3 forms of grass sickenss? Aetiology?
- 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
Clinical signs of grass sickness?
- ileus and gastric reflux (potential rupture if not NGT)
- ddx SI entrapment/strangulation, ex lap needed to r/o
- v poor prog
- mild colic
- v poor prog
- mm. fasciculations
- patchy sweating
- mm. atrophy d/t v eating? or neurogenic?
- RHINITIS SICCA
Dx of grass sickness?
- clinical signs
- ileal biopsy (v mesenteric plexus neurons on IHC)
Potential grass sickness prevention?
- vax currently being trialled
Clinical signs of equine motor neuron disease?
- 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)
Ddx equine motor neuron dz?
- myopathy eg. PSSM longerm
- chronic grass sickness
How can EMND and grass sickness be differentiated?
- chronic grass sickness v apetite, pick at food, can't swallow
- EMND ravenous apetite and no problems swallowing
Potential cause of EMND? Which other disease is this pdf seen in ?
- low serum vit E eg. v intake if stabled
> EDM -> spinal ataxia d/t v vit E when young
Dx of EMND?
Biopsy tail head (sacrocaudalis dorsalis medialis m.)
What types of horses is tetanus commonly seen in?
- shoddy yard, gypsy horses
- unvaccinated animals (though can occour in vax)
- often distal limb d/t poor blood supply -> ^ risk anaerobic environment
Pathogenesis of tetanus?
- deep penetrating wound ~1week previously
- clostridium tetani (anaerobe)
Clinical signs of tetanus
- prolapse of TE 9comes out as normal but gets stuck)
- muscle rigidty (saw horse stance or sardonic grin) flared nostrils
- tetanus toxoid (inactivated toxin to stimulate better immune response)
- antitoxin (Abs) intrathecally (into the subarachnoid space)
- environmental management (minimise muscle activation, calm quiet environement)
How does the pathogensis of botulism and tetanus differ?
- prevents reelease of ACh
- carried retrograde axonal transport -> ventral hornm grey matter (LMN cell body)
- leaves, gets into inhibitory interneuron
- prevents INHIBITION at level of SC
-> constant excitation
What is stringhalt ?
- 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)
What is shivers?
- 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
Potential cause of group of horses affected by a generalised NM condition?
> Lathyrism (lathyrism hirsutus) sweet pea plant cutting
-> spastic paraparesis like tetanus
- B oxalylamino L alanine acid
- excitatory effects CNS and neurotoxic effects
Is the simplistic view of central v peripheral useful?
Yes but not realistic
- eg. LMN peripheral mostly but cell bodies are central
- tetanus toxin works cenrally on peripheral nn.
What condition is seen in scandanavian horses?
Scandanavian knuckling horses
- polyneuropathy d/t toxin
What is stiff horse syndrome?
- intermittent exensory hyper-ridgidity (stiff horse syndrome)
- Abs attack glutamic acid decarboxylase (inhibits NTs in SC)
- disinhibition -> stiffness
If all 4limbs are affected is 2 lesions or generalised NM disorder more likely?
What is acute polyradiculoneuritis? Dx?
> acute generalised rapidly progressive LMN paresis
> stabilises after 4-5d
- ^ CSF protein (non-specific)
- EMG for dx
Localise the lesion that causes dropjaw
- 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
What is acute trigeminal neuropathy?
- idiopathic, self limiting, acute onset
- d/t neuiritis? lymphoma?
> supportive tx. feed meatballs!
Where is the lesion: horse L head tilt + horizontal nystagmus to the R
- left sided peripheral vestibular
Ddx: petrous temporal bone fx, temporohyoid OA, idiopathic vestibular syndrome, ostitis media/interna
Where is the lesion: sheep with tetraparesis and ataxia all 4 limbs
Ddx: trauma, abscess
Where is the lesion: cow bizarre behavioural abnormalities and intermittent depression and hyperaesthesia
Ddx: lead poisoning, cerebrocortical necrosis, BSE
Where is the lesion: horse with focal muscle atrophy over the left epaxial muscle in the saddle area
- LMN T3-L3
Ddx: trauma, articular process joint vertebral arthropathy, focal grey matter SC (ventral horn)
- Ddx: EPM
Where is the lesion: horse with normal PLR but absent menace response in R eye
- left sided cortical lesion. Amaurosis can be seen temporarily in post ictal phase of seizures
Where is the lesion: horse with generalised weakness and profound mm atrophy of entire body
- generalised LMN or 1* myopathy
- consider other causes of weight loss
- Ddx: EMND, chronic grass sickness
Where is the lesion: horse with horners syndrome and sweating around the base of the ear
- 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