Off hindlimbs WS + Off all limbs WS

CASE 1

5 year old female neuter Dachshund Sudden onset of left hind monoparalysis 24 hours prior to presentation. No history of trauma. Paralysis occured whilst out unaccompanied in the garden, but a yelp was heard. Neurological examination:

•General examination NAD

•Left hind absent voluntary movement, absent withdrawal, absent myotatic reflexes, deep pain present.

•No spinal pain

•Panniculus reflex intact

•Forelimb and right hindlimb examination within normal limits

•Cranial nerve examination NAD

THOUGHTS...

-Absence of reflexes suggest LMN

-localisation: L4-S3 as normal FL and HL affected

-left side affected

-only patella and withdrawal reflex affected so L4-S1 affected

-perineal reflex not mentioned so likely intact so less likely S2-S3

-sciatic and femoral nerves may be affected

-IVDD seen in Dachshunds but maybe would see both limbs affected

-helping with pain suggests trauma which may have caused spinal compression, fracture of vertebral column, disc extrusion which Dachshunds are prone

-stroke to spinal cord will likely affect one side more than the other (stroke can be haemorrhagic or ischaemic)

-ischaemia is more common in spinal cords such as fibrocartilaginous embolism (FCE) but need MRI to confirm and we will see a hyperintense small area

-FCE has sudden onset and affects one side

-radiograph rules out fracture

-check for even gaps in the vertebral column

case 1 ddx

Degenerative: IVDD-> but only one limb

Anonmalous

Metabolic

Neurologial: nerves in the limb

Idiopathic

Trauma: fracture-> limb or spinal -> not likely spine, m injury

Vascular: ischemia, haemorrhage, embolism (FCE)

case 1 xray

• To look for fractures/ ovious trauma -> rule out ddx

• Follow to ventral spinal canal= even

• Assess gaps between VB are even = vertebral disc

• Horsehead= facets grasp

• Want straight line and even

• Theres no fracture here

case 1 likely outcome

• Vascular most likely= ischeamic myopathy= fec

• Localisation= lmn l4-s1

• Pain sensation maintain -> so better prognosis

• Conserbvtive managemetn and nsaids

• Physio to maintain strength and rehanbilitation of limb

• Mri-> definitive diagnosis -> can refer

for ischaemic myopathy (FEC) what is it likely to be due to in cats and dogs

• Cats= can have a primary cause

• Dogs= more likely a sporadic event

CASE 2

3 month old chocolate labrador Progressive history of dificulty walking on the hindlimbs, progressing over 2 weeks Neurological examination:

•General examination NAD

•Forelimb examination NAD

•Hindlimb extensor rigidity such that unable to walk

•Difficult to demonstrate withdrawal or myotatic reflexes and resents attempts to flex hindlimbs

•Pain sensation from paws apparently present

•No spinal pain

•Panniculus reflex intact

THOUGHTS...

-progressive

-both HL affected

-localised to a neuromuscular condition and not spinal

-spastic paralysis which suggests UMN but with UMN should be able to flex the limbs

-Panicculus pathway= sensory pathway into the sc and a motor pathway back to the cutaneous trunci m -> localise lesions if an affected area is absent

ddx for case 2

D: hip dysplasia

A: congenital abnormality of sc or vb column

M

N:

I: neosporum

t:

V;

case 2 radiography

potential hip problem, everything else fine

what is the outcome for case 2

• Neospora canis

• Neuromuscular localisation= issue with m n or joint

• Vertical transmission from mother

• Unusual gait= rigidity and m atrophy

• Can test the mother

how does neiospora infect puppies

Congenitally infected puppies

The majority present as muscle atrophy with hyperextension of hindlimbs, ataxia, hindlimb paresis, a 'bunny-hopping' gait, ascending to paralysis, head tilt, difficulty in swallowing, etc.

There may be neonatal death with generalized pneumonia, myocarditis, encephalitis, hepatitis, etc.

Multiforme signs may be seen in animals with encephalomyelitis.

infection can cause fetal death.

Cutaneous neosporosis may be manifested by pyogranulomatous ulcerative dermatitis.

how does neospora present in older dogs

In adult dogs it causes more brain issues

CASE 3

Rapidly progressive paraparesis

3 year old castrated male DSH Rapidly progressive paraparesis (weakness or partial loss of voluntary movement in both hindlimbs) developing over 48 hours. Non-ambulatory paraparesis. Neurological examination:

•General examination NAD

•Cranial nerve examination NAD

•Fore limb examination NAD

•Hind limbs non-ambulatory (cant walk) paraparesis with increased hindlimb tone.

•Resentment of spinal palpation, but generally resented whole examination

•Withdrawal reflexes and pain sensation present

•Absent tail movement

THOUGHTS...

-increased tone and reflexes present suggests UMN so T3-L3 as FL normal

-FIP

-may be tail pull injury and usually due to trauma

-lymphoma on differential so may do some screening/bloods/US however rapid onset makes neoplasia less likely

-radiograph allows us to rule out tail pull → sacrococcygeal junction (is fine ehre)

ddx for case 3

Anomalous = Congenital

Trauma = tail pull (absent tail mm)

Infectious - FIP, toxoplasma, FeLV, feline parvovirus, mycoplasma

Neoplasia = lymphoma (rapid onset so less likely)

Vascular = haemorrhage or FEC (pain present so does not fit), saddle thromboembolism

Degeneration = IVVD

if bloods show this

- Neutrophilia and serum protein and globin elevation

what are you sus of (outcome for case)

FIP

• causing pyogranulomatous meningomyelitis in dry form would suspect as young cat,

• pain on palpation,

• would do bloods and check for neutrophilia, globulins and serum protein elevation which would suggest FIP.

Localisation = T3 L3

Confirm - MRI, CSF (referral)

Long term course of antibiotics

What are the three types of ataxia?

-cerebellar

-propioceptive

-vestibular

CASE 4

Sudden onset hindlimb ataxia

5 year old female neuter Dachshund Sudden onset development of hindlimb ataxia 24 hours prior to presentation. Previous bout of apparent ataxia 2 week previously had resolved on conservative management.

THOUGHTS...

-video of gait shows back legs ataxia and some weakness

-Paresis with ataxia suggests spinal cord problem

Weakness and drunk= spinal region-> likely proprioceptive (affects ascending sensory tracts -> cant feel limbs to know where to position them)

No head tilt so not vestibular

case 4 ddx

Degenerative = IVDD

Neoplasia

Vascular = haemorrhagic + ischaemic FEC

Inflammatory + infectious

CASE 1

9 month old female Chihuahua:

Sudden onset of cervical pain with non-ambulatory tetraparesis (weakness and reduced voluntary movement in all 4 legs).

Owner concerned that they may have rolled on the dog overnight.

Neurological examination:

§General examination NAD

§All limbs voluntary movement.

§Withdrawal reflexes, myotatic reflexes and deep pain present in all limbs

§Resentment of cervical manipulation

§Cranial nerve examination NAD

Thoughts...

C1-C5

-UMN

-affecting all limbs

Toy breed= common for subluxation

ddx for case 1 chiuauwau

D  N/A

A  N/A

M  N/A

N  N/A

I  -MUO, bacterial meningitis, SRMA (steroid responsive meningitis arteritis)

T - atlantoaxial subluxation, ANNPE (acute non compressive nucleus pulposus extrusion-> is a form of IVDD)

V  N/A

outcome for case 1 chihuahua

Increased distance between the c1 and c2

 

Atlantoaxial subluxation: Diagnosis is supported by increased distance (> a few mm) between the dorsal aspects of C1 and C2 when viewed on a lateral survey radiograph

normal radiograph

treatment for case 1 chihuahua

• Conservative management - brace (avoid excessive mm ventro flexion esp)

• Pain killers - Nsaids, Gaba

• Referral- Atlantoaxial fusion or brace (care with swelling causing asphyxiation)

CASE 2

Sudden onset cervical pain

11 month old cocker spaniel

Rapid onset of cervical pain and lethargy, 2 days prior to presentation with no apparent progression

Neurological examination:

§T 39.5oC

§General examination otherwise NAD

§Resentment of cervical manipulation and palpation

§Proprioception and segmental reflexes NAD

§Cranial nerves NAD

Thoughts...

-pyrexia→ has infection?

-UMN (still has intact reflexes)

Hunched

Stiff/slow to sit

Resentment - pain

High temperature = infection

No localisation

Pain in neck - joints, IV disc, muscle, + soft tissues

Acute onset on pyrexia + neck pain = meningitis (infectious/inflammatory)

ANNPE Acute Non-Compressive Nucleus Pulposus Extrusion

ddx for case 2 cocker spaniel

D  IVDD (likely too young), syringomyelia (unlikely if not CKCS)

A  Congenital issue

M  N/A

N  Lymphoma

I - discospondylitis, , bacterial/viral meningitis

T  ANNPE (likely too young) soft tissue injury, fracture / subluxation (unlikely)

V  N/A

Infectious/inflammation - bacterial/viral meningitis

Immune mediated - steroid response meningitis arteritis SRMA

X-ray for disco (osteomyelitis), CSF for SRMA (neutrophilic)

what is srma

This is a neurological immune mediated disorder causing inflammation of the meninges and associated blood vessels in the brain and spinal cord. non-infectious and responds well to steroids.

case 2 further diagnostics

CSF = 1000WBC/ul = neutrophilla

IgA serum/csf

C reactive protein increase

outcome?

SRMA - Steroid responsive meningits arteritis

Immune system attack meninges and cause inflammation + fever

Prednisolone = 24 mg/kg/day for 12 weeks, then taper to alternate day

therapy and decreasing doses over several months

Additional immunosuppression - azathioprine or ciclosporine is considered on

a case-by-case basis in cases refractory to prednisolone.

syringomyelia

caused by chiari like malformation in ckcs-> blocks CSF and builds up in sc

Discospondylitis

• • Bacterial infection and subsequent abscess formation of the vertebral bodies and/or intervertebral disc, with or without extension into the spinal canal and compression or trauma of the spinal cord.

  
  

  
  

how is meningioencephalitis different to SRMA

is non-infectious and doesn't respond to steroids. We see inflammation in meninges and parenchyma.

CASE 3

Sudden onset/progressive nonambulatory tetraparesis

§Sudden onset of cervical pain following running into tree at exercise 3 days ago.

§Progression to non-ambulatory tetraparesis on recovery from GA to obtain radiographs

§Neurological examination: not performed

Thoughts...

trauma

differentials for case 3 caesar

D  N/A

A  N/A

M  N/A

N - vertebral osteosarcoma w/ pathological fracture

I 

N/A

T  ANNPE, fracture / subluxation

V - vertebral haematoma

case 3 xrays

diagnosis and treatment?

C2 = large dorsal process

Fragment = C3

Narrowed disc space

Hairline fracture C3

Spinal stabilisation w/ hemilaminectomy for fracture, or conservative

management w/ neck brace

hemilaminectomy ?

A hemilaminectomy is a minimally invasive spinal decompression surgery in which a surgeon removes only one side of the vertebral lamina to relieve nerve compression

how has the anaesthtic made this case 3 worse

(Anaesthesia makes subluxation worse as relaxed muscles cannot hold discs in place but this image is a full fracture and not subluxation)

CASE 4

Rapid onset/progressive non-ambulatory tetraparesis

§2 week progressive history inability to walk.

§Initially just affecting hindlimbs progressing to affect forelimbs

§General examination NAD

Neurological examination

-Video shows generalized weakness of FL +HL but not neck

Cannot stand

Alert + distressed

Weakness

Neuromuscular - nerves, junction + muscle

Tetanus would be rigidity, MG as would get worse with exercise and improve

with rest

ddx for case 4 cat lily

D  N/A

A  N/A

M  renal disease →Hypokalaemia = ventroflexion

N  N/A

I - idiopathic polyradiculoneuritis (immune mediated disease, causes inflam of the peripheral n roots -> progresive m weakness and paralysis), Immune mediated polyneuropathy (targets the peripheral n), FIP, tetanus, botulism, myasthenia gravis (autoimmune, skeletal m weakness

T  botulism which is a progressive generalised weakness caused by toxin ingestion

V  N/A

how is muscular weakness in cats diff in the neck

-important to note that cats do not have nuchal ligament in neck so when they have muscular weakness they cannot lift their head

what is myasenthia gravis

causes generalised weakness but they get weaker with exercise and diagnosed with blood test

what is idiopathic polyradiculoneuritis

starts distally and progresses,

no diagnostic test and requires conservative managment

case 4 lily outcome

Immune mediated polyneuropathy -> treat with immunosuppressives, (preds)

What is wobbles?

CCSM (caudalcervical spondilo myolopathy)

-compression of spinal cord in caudal spine due to overgrowth of bone

-short movement in FL, long movement in HL

-Ataxia in all limbs

-could be caused by disc protrusion causing overgrowth of ligaments around spine and instability of vertebrae