Part of the Veteducation Live Online Web-Seminar Series · The Veteducation International Online Veterinary Conference 2011 Part of the Veteducation Live Online Web-Seminar Series

The Veteducation International Online

Veterinary Conference 2011

Part of the Veteducation Live Online Web-Seminar Series

Dealing with Spinal PatientsWith Dr Sam Long BVSc PhD DipECVN

The University of MelbourneAustralia

Dealing with spinal patients:

• Where’s the problem?• How do we make a diagnosis?• How do we treat?

Sam Long BVSc PhD [email protected]

The layout

• What we’re going to cover:– Where’s the problem?

• Localising the lesion: a neuroanatomy refresher and theneurological exam

– How do we make a diagnosis?• What tests can we use? How good are they?

– How to treat?• What’s on the differential list?• The end of the controversy – steroids and intervertebral disc

disease• Other more common conditions• Upcoming developments

The Diagnostic Process• Following the plan:

• History

• Signalment

• Physicalexamination

• Neurological Examination

• Lesion localisation

• List of PossibleCauses/DifferentialDiagnoses

• Problem List

• Data Collection

Two Questions

• Where is the lesion?

• What is the nature of the lesion?

Clinical Signs of Spinal Cord Disease

• Neurological Exam– Functions Carried by the Spinal cord Which help us

• Proprioception:– Which limbs are normal and which are abnormal?

• Motor function (Upper motor neuron/Lower motor neuron (ART)):– More precise localisation

• Presence/absence of deep pain sensation– Severity

– Localisation to:• C1-C5

• C6-T2

• T3-L3

• L4-S3

• OR: multifocal/diffuse

Proprioception• Proprioceptive pathways:

– Concious vs unconscious proprioception:

• Dorsal funiculus– Fasciculus gracilis (m) and cuneatus (l)

– Mechanoreceptors skin, joints

– Ultimate destination: sensorimotor cortex (forebrain)

• Lateral funiculus– Dorsal and ventral spinocerebellar tracts (hl)

– Cranial spinocerebellar and cuneospinocerebellar (fl)

– Muscle spindles and golgi tendon organs

– Ultimate destination: cerebellar cortex

Motor Control•Upper motor neuron vs Lowermotor neuron

–UMN inhibits the LMN

–LMN function: Ach release at NMJ

•Signs of disease:

Upper MotorNeuron

Lower MotorNeuron

MuscleAtrophy

None/mild Severe

Reflexes Normal orincreased

Decreased

Muscle Tone Normal orincreased

Decreased

Pain Sensation• Thin, unmyelinated Aδ and C fibres

– Bilateral, multisynaptic pathways

– Three pathways - all funiculi involved:• Spinothalamic – lateral WM

• Spinocervicothalamic – dorsal WM

• Spinomesencephalic – ventral WM

– Loss of pain sensation: major transverse lesion

– Pain sensation gives information on severity, NOT location

The Neurological Examination

• Proprioception function tests

The Neurological Examination

• Reflex Testing– FL:

– Extensor carpi radialis– Biceps tendon reflex– Triceps tendon reflex– Withdrawal

– HL:– Patellar tendon– Gastrocnemius tendon– Cranial tibial– Withdrawal

– Other reflexes:– Panniculus– Anal

Localising Lesions: relationship toanatomy

Telencephalon

Diencephalon

Vestibular

Metencephalon/Myelencephalon

Cervical(C1-C5)

Mesencephalon

Cerebellar Cervicothoracic(C6-T2)

Thoracolumbar

( T3-L3)

Lumbosacral(L4-S3)

Cervical (C1-C5) syndrome

C1-C5 Clinical Signs• Weakness or paralysis in all four limbs

(tetraparesis/tetraplegia) or hemiparesis/hemiplegia• Proprioceptive deficits in limbs on the same side as the

lesion or in all limbs• Normal or increased reflexes and muscle tone in all limbs,

extensor rigidity in limbs on the same side as the lesion• Cervical muscle spasms, pain and/or rigidity (animals may

resist neck flexion/extension)• Respiratory difficulty – phrenic nerve damage (C5)

Cervicothoracic(C6-T2) syndrome

C6-T2 Signs

• Tetraparesis/tetraplegia, hemiparesis/hemiplegia,monoparesis/monoplegia (thoracic limbs)

• Postural reaction deficits in one thoracic limb, in limbs onthe same side, or in all limbs

• LMN signs in thoracic limb(s), muscle atrophy after 1-2weeks

• UMN signs, without muscle atrophy, in pelvic limb(s)

• Root signature sign – thoracic limb held up due to pain

Other features– Pain (hyperesthesia) at level of lesion– Reduced sensitivity (hypesthesia) behind level of

lesion– Persistent scratching at one side of the

shoulder/neck region– Cutaneous trunci reflex depressed or absent

(unilaterally or bilaterally)– Horner's syndrome

• Miosis• Enophthalmos• Ptosis• Protrusion of third eyelid

Thoracolumbar (T3-L3) Syndrome

T3-L3 Signs• Paraparesis/paraplegia/monoparesis/monoplegia

(affecting one pelvic limb)• Proprioceptive deficits in pelvic limbs• UMN signs in the pelvic limbs:

– Normal/Increased muscle tone– Pelvic limb reflexes normal or brisk

• may see clonus or crossed extensor reflex

– No muscle atrophy in pelvic limbs

• Reduced/absent cutaneous trunci reflex behind level oflesion

• Increased local sensitivity (hyperesthesia) at level of lesion• Reduced sensitivity (hypesthesia) behind level of lesion• Urinary incontinence• + Schiff-Sherrington posture (severe lesions)

Lumbosacral (L4-S3) Syndrome

L4-S3 Clinical Signs

– Paraparesis/paraplegia/monoparesis/ monoplegia(affecting one pelvic limb)

• Tail often affected• Often see dropped hock in cats

– Proprioceptive deficits in pelvic limbs– LMN signs in pelvic limbs:

• Depressed pelvic limb reflexes• flaccid muscle tone• Neurogenic muscle atrophy in pelvic limbs, and/or hip muscles

– Dilated anal sphincter with poor anal reflex– Reduced sensitivity (hypesthesia) in perineal area,

pelvic limbs, or tail– Urinary incontinence– Faecal incontinence– Root signature sign

How do we make a diagnosis?

• What are the tools?

– Bloodwork

– Serology

– DNA testing

– Plain radiographs

– Radiographs + contrast (myelography)

– CSF analysis

– CT

– MRI

– Biopsy

Serology• Infectious causes of spinal cord disease:

– Bacterial (discospondylitis, empyema,osteomyelitis)

– Viral – distemper, rabies, FIV/FeLV-associatedtumours

– Protozoal – toxoplasmosis, neosporosis

– Rickettsial – lyme disease (not ANZ)

– Fungal – fungal hyphae, cryptococcosis

Serology• Serology vs PCR:

– Serology available• Toxoplasma• Neospora• Cryptococcus (antigen)• IgA levels (SRMA)

– PCR• Toxoplasma• Neospora• Cryptococcus• Borrelia burgdorfii• FIV• FeLV

• How to interpret?– Antigen within the CNS – almost certainly infection– Rising titres over 1 month or more – probable infection if clinical signs fit– Low to moderate titres – probable evidence of previous exposure?– PCR: low PPV if disease is uncommon

Plain radiographs• The good:

– Cheap

– Accessible

– Bony/calcified structures

• The bad:– Exposure to radiation!

– Easy to do badly• Positioning!

• General anaesthesia

– No information about soft tissue

Sacrocaudal dysgenesis

Vertebral osteosarcoma

Contrast radiography

• Myelography– The good:

• More information than plain radiographs (about spinal cord)

• Relatively accessible

• Relatively cheap

– The bad:• More exposure to radiation

• Less information than other imaging techniques

• Adverse effects: seizures, transient worsening of clinical signs, iatrogenichaemorrhage, iatrogenic central canal dilation, brain herniation

• Sometimes contrast material doesn’t go where we want it to:– Epidural

– Subdural

– Nowhere near the lesion (spinal cord oedema)

CSF analysis

• Why do it?– Inflammatory diseases: GME, protozoa, SRMA

– Neoplastic diseases: lymphoma, oligodendroglioma,choroid plexus papilloma

– Infectious diseases: empyema

– Degenerative diseases: IVDD

• Normal values:– WCC <5 cells/ul

– Protein < 25mg/dl (0.25 g/l)

CT scanning

• An X-ray machine withideas above its station– The good:

• Even better imaging ofmineralised material

• Some capacity to image softtissue

• Reformatting in multiple planes

• Speed (nowadays…)

– The bad:• EVEN MORE radiation

• The spinal cord is SURROUNDEDby bone…

MRI

• How it works:

– Body region to be imaged placed in a large magnetic field

– Alignment of all magnetisable atoms within the body parallel to magnetic field(Hydrogen)

– Application of radiofrequency pulse to excite those atoms

– Collection of subsequent emitted electromagnetic radiation from the sameatoms allows localisation

– Since the most common magnetisable atom in the body is hydrogen in water,MRI tells the difference between different tissues based largely on their watercontent

MRI• The good:

– Since bone has low water content, essentially invisible to MRI– Superior soft tissue contrast = LOTS of information about the spinal cord– Special sequences for: fat suppression, CSF suppression, detection of

blood/blood products– Collection of images from any plane without reconstruction– Sagittal plane scans can give you virtual myelography without the need to

inject contrast

• The bad:– Lack of availability dt expense of the magnet:

• Small bore magnets are harder to get good images from

– Expense of the magnet = expense of the test– Some dangers – no metal objects or pacemakers– Slower than CT– Less information about bone

Biopsy

• Biopsying the spinal cord????

Common Differentials for Spinal Cord Disease

Degenerative/DevelopmentalConditions

Degenerative myelopathySyringomyeliaCervical SpondylomyelopathyLumbosacral stenosis

Anomalous conditionsAtlantoaxial SubluxationSpina bifida/sacrocaudal dysgenesisArachnoid cysts

Metabolic conditionsNone

Nutritional/Neoplastic conditionsNone

NeoplasiaPrimary/secondary tumoursMetastatic disease

Idiopathic/Inflammatory conditionsGranulomatous meningoencephalomyelitisDiskospondylitis and epidural empyemaInfectious diseases: distemper/FIP/FeLV

Trauma/ToxinsIntervertebral disk diseaseSpinal FracturesBrachial plexus avulsion

Vascular conditionsFibrocartilaginous Embolism (FCE)

Intervertebral Disk Disease

•Pathogenesis and classification•Chondroid metaplasia

•Fibroid metaplasia

•Hansen Type 1 (usually chondrodystrophoid)

–Dachshunds, corgis, cocker spaniels, basset hounds, lhasas apsos,shitzus etc

•Hansen Type 2 (usually non chondrodystrophoid)

•ANNPE: Acute non-compressive nucleus pulposus extrusions

Intervertebral Disc Disease– Location

• Cervical

– C2-3 most common

– Decreasing frequency further caudal

• Thoracolumbar

– 85% between T11 and L3

– 50% at T13-L1 or L1-2

– Diagnosis

• History, Signalment and Clinical Signs – apparent discomfort…

• Grading: which scale to use??

Grade 1 Painful only

Grade 2 Pain and paraparesis but still able to walk

Grade 3Pain and paraparesis – unable to walk but voluntary motor functionpresent

Grade 4 Paraplegia – deep pain sensation present

Grade 5 Paraplegia – deep pain sensation absent

NB: Grade 5 constitutes a true Neurological emergencyRefer as soon as possible!


– Imaging• Radiography

1. Narrowed intervertebral disk space

2. Calcified material in the disk space

3. Possible calcified material within the canal

Correct localisation 30% of the time

• Myelography

» Dorsal displacement of the ventral dye column

• CT

» Plain or with contrast (myelogram)

» Very sensitive to mineralised disk material

• MRI

» Best for assessing spinal cord (oedema, hrrg)



• Treatment:

– Conservative• STRICT cage rest: 4-6 weeks

• Analgesia – only to alleviate discomfort

– Surgical:• Decompression –

– Cervical: Ventral Slot

– Thoracolumbar: Dorsolateral hemilaminectomy


•Complications–Ascending-descending myelomalacia:

•5-6% of all Grade 5 cases

–Iatrogenic trauma

–Sepsis

•Prognosis

Grade Conservative therapy Surgery

1 100% 97%

2 84% 95%

3 84% 93%

4 81% 95%

5 5% 50-60%*

*If decompression performed within 24 hours of onset


• Recovery

– Essentially complete by90 d

– Better grading systems?

– Spinal walking?

The controversy: steroids or not?

• Methylprednisolone - the evidence in people:– NASCIS (National Acute Spinal Cord Injury Studies) trials:

• I: 1979 (330 patients)– 100mg vs 1000mg SID IV 10d

– No statistical difference

• II: 1985 (487 patients)– 30mg/kg bolus then 5mg/kg/hr CRI 23hrs vs naloxone

– Improvement in sensation/motor at 6m and 1yr: magnitude of differencesmall

– Significant errors in trial design: randomisation, statistical analysis,sampling, patient management

• III: 1991 (499 patients)– 30mg/kg bolus then 23hr CRI vs 30mg/kg bolus then 48hr CRI vs

30mg/kg bolus then tirilazad CRI

– No difference between any groups

– Higher incidence of infections, pneumonia

– Other studies have failed to reproduce the NASCIS findings

The controversy: steroids or not?

• The evidence in dogs?– Olby et al: Multi-centre randomised, placebo controlled, double blinded

clinical trial (ongoing)• Grade V severity IVDD• Methylprednisolone vs polyethylene glycol vs saline: 100 dogs per group• Intermediate analysis (May 2011): no significant difference between groups;

trial to close early

– Oral prednisolone?• No prospective, randomised clinical trials• Experimental evidence of decreased gluconeogenesis long term• Effects of euphoria plus analgesia

– What do I do?• There is NO evidence that steroids improve recovery• Good analgesia + STRICT rest

– The future:• 4-aminopyridine derivatives (4-AP)

Things that look like compressivedisc disease but aren’t:

• ANNPE:– Acute Non-compressive Nucleus Pulposus Extrusion:

• ‘Traumatic’ intervertebral disc extrusion:– Normal nucleus pulposus extrusion during violent exercise– History of acute onset of spinal cord signs– Usually non painful (after first 24 hrs), asymmetric signs– Signs occur due to contusion rather than compression– Diagnosis: MRI– Prognosis good - depending on severity

• FCE:– Fibrocartilaginous embolism:

• Vascular – focal segmental ischaemia within cord:– Thought to be due to disc material migration into vascular supply– History of acute onset, non painful myelopathy– Also non-painful, asymmetric– Diagnosis: MRI (more often norm)– Prognosis good – depending on severity

Atlantoaxial subluxation• Pathogenesis:

1. Failure of formation of the dens (46%)

2. Fracture/separation of the dens (30%)

3. Failure of formation/rupture transverse ligaments (24%)

• Diagnosis:• History, signalment, clinical findings

– <6m age

– Toy breeds – yorkshire terriers, chihuahuas

• Plain radiographsDO NOT anaesthetize if you suspect A-A subluxation

Neutral positioning sufficient

Atlantoaxial subluxation

Normal

AA Subluxation

Dens

Atlantoaxial subluxation

• Treatment• Conservative

– External fixation (brace)

– Some dogs may recover long term?

• Surgical– Wiring

– Ventral screw fixation C1-C2

• Prognosis– Good provided surgery is successful

Degenerative Myelopathy

• Signalment• GSDs, corgis, boxers, chesapeake bay

retrievers, rhodesian ridgebacks

• Middle-aged/older (>9y), no sex predilection

• Pathogenesis• Degenerative changes (wallerian degeneration, axonal spheroids):

T3-L3 WM

• Motor and sensory regions of WM dorsolateral/ ventromedianfuniculi

• Etiology• Previous theories: nutritional/ immune mediated/ axonal

transport

• Mutation in Cu/Zn Superoxide Dismutase1 (SOD1)

• Canine version of amyotrophic lateral sclerosis (motor neurondisease)?

Degenerative Myelopathy

• History/Clinical Signs• Progressive (up to 2 years) hindlimb paresis• Predominantly T3-L3 localisation BUT:

– possible patellar and other reflex deficits– Muscle wastage consistent with LMN disease– urinary/fecal continence retained– Eventual progression to involve FL, brainstem

• NOT painful

• Diagnosis• Exclusion: Myelography/MRI, CSF tap• Genetic testing now available

– Homozygosity for SOD1 mutation

• Treatment/Prognosis– None– Physiotherapy

Chromosome 31 (Mb)

Sequencing• University of Missouri Project, led by Dr Joan Coates, in collaboration with Broad

Institute:

– PBWC

– Boxers

• Genome Wide Association Studies

– PBWC

• Fine mapping

– Multiple breeds

• Other breeds added:

– Chesapeake bay retrievers

– German shepherds

– Boxers

– Ridgebacks

27896 25324

A1

L2

1A1X

35232 33648

N2

1Z

34779

34525

34780

I2

34775

34776 34778

1C

B2

34773

J2

34781 34782

34769

1Y

34772 3506235231

C2

35259 35095

D1

3478634788 34768

28999

U1

P1 2M

1Q

30561

Q1

29006

2368

1E

1F F1

2H

H1

28650 26248

M1

28648 28644

E1

28235

225599

N1

1O S1

29870

1D

1H

1K

2G

28646

231163

1G

1I

30551 3154431483

1L

G11J

1MI1

4444644447

?

1N

1PJ1

1RK1

L11S

332390 35090 32391

1T

O1

40882

1U

1V

R1

T1

31523

1W

W1

V1

31522 3154931528

X12A

C12J

25528

?

25395

25683 25628 2539726253 25396

Pembroke Welsh Corgi Family #1-Degenerative Myelopathy

Coates JR, et. al. J Vet Int Med 2007

Region of Haplotype Association

SOD1 Candidate Gene

• Known to cause Amytrophic Lateral Schlerosis (motorneuron disease or ALS) in humans

• Mutation identified in exon 2:– SOD1:c.118G>A– Predicted to result in a missense mutation: p.E40K

glutamate to lysine– p.E40K amino acid very highly conserved across all

mammal species

• Mutation defines a new haplotype

SOD1 (Cu-Zn Superoxide Dismutase 1 )• Free radical scavenger that convert superoxide radicals to hydrogen

peroxide and oxygen.

• SOD1 protein expressed abundantly and ubiquitously in spinal cord

• Human SOD1 11kb chromosome 21

• Coding region organized with 5 exons

• Homodimeric enzyme

• 8-stranded antiparallel β-barrel

• Canine SOD1 AA position 40 lies within the short “Greek key” – stabilizesalignment between sets of β-strands

Rosen DR, et al. Nature 1993Sandelin E, et. Al. J Biol Chem 2007

Green SL, et al. J Hered 2002; Boissinot M, et al. EMBO J 1997;Sandelin E, et. Al. J Biol Chem 2007

G/G G/GG/G

A/G A/GA/G

A/A A/AA/A

RR

BPWCRR

LRLR

Syringomyelia/Caudal Occipital Malformation Syndrome

• Epidemiology/signalment:• Almost exclusively CKCS, some yorkshire terriers• Extremely common – possibly ‘the norm’ for breed• Signs usu present by 2-3 yrs age, some dogs by 6 months

• Etiology:• Poorly understood, likely to be small caudal fossa as a result of breeding which

leads to crowding of cerebellum and herniation• Secondary syrinx formation within the spinal cord (+/- hydrocephalus)

• Pathophysiology:• Multiple theories for development of syrinx:

– The ‘water-hammer’ theory– The ‘suck-effect’ theory– The ‘piston’ theory– The ‘intramedullary pulse pressure’ theory

Syringomyelia/Caudal Occipital Malformation Syndrome

• History and clinical signs:• Scratching (shoulders most commonly) (65%)

• Neck pain (57%)

• Unlocalisable pain: (39%)

• Scoliosis (spine twisting) (13%)

• Unsteady hindlimb gait (ataxia) (22%)

• Weak forelimb gait (17%)

• Diagnosis:• Imaging (MRI)

• MRI scanning of asymptomatic dogs:• 70% of unaffected cases have syringomyelia

• 17% of unaffected cases have occipital malformation but nosyringomyelia

• 13% of dogs anatomically ‘normal’

Syringomyelia/Caudal Occipital MalformationSyndrome

• Magnetic Resonance Imaging:

Mild occipital dysplasia,kinking of medulla

Moderate occipital dysplasia

Severe occipitaldysplasia with

cerebellarherniation and

syrinx formation

Syringomyelia/Caudal Occipital MalformationSyndrome

• Treatment:• Medical:

– Prednisone – anti-inflammatory doses

– Furosemide (2 mg/kg)

– Gabapentin (7-10 mg/kg BID-TID)

• Surgical:– Decompression caudal fossa

– Varying success rate:

» 85% in some cases

» Extremely high relapse rate by 2yrs

– Better for resolution of neurological deficits, but not forpain/pruritis

Cervical Spondylomyelopathy(CSM / Wobbler’s Syndrome)

• Diagnosis:– History, signalment and clinical signs– Imaging:

– Radiography1. Narrowed spinal canal2. Enlarged articular facet joints (VD)3. ‘Tipping’4. Wedge shaped vertebrae

– Myelography» Ventral extradural compression» ‘Hourglass’ compression» Variable number of spaces

– CT– MRI

• Traction views important – dynamic vs static


ab

c

d

e


• Treatment:• Conservative

• Surgical– Decompression – for static lesions

– Traction-fusion – for dynamic lesions

• Surgical approaches– Dorsal laminectomy – for dorsal lesions

– Ventral slot-based – for ventral or hourglass compression


• Distraction-fusion:


• Complications:• Sepsis

• Implant failure

• Poor implant positioning/iatrogenic damage

• Endplate fracture/resorption


• Prognosis

– Guarded:

• Single vs multiple lesions

• Ambulatory vs non-ambulatory

• Domino lesions:– Approximately 30%, between 6m and 4y after surgery

• With single lesions mildly affected and treated early,70-80% do well

• Longer term mortality 19% - 43%

Case Examples

Rizzo

• Signalment

– 4y FN french bulldog

• History

– Mild lameness day before presentation

– Sudden onset non ambulatory paraplegia

– Possibly fell down stairs


Telencephalon

Diencephalon

Vestibular


Cervical(C1-C5)

Mesencephalon


Thoracolumbar

( T3-L3)

Lumbosacral(L4-S3)

Rizzo

• Localisation?

• Diagnostics:

Rizzo

• Imaging

Fleur

• Signalment

– 3yo F american bulldog X

• History

– At end of walk this evening started to drag RHL

– No major exercise or other health issues


Telencephalon

Diencephalon

Vestibular


Cervical(C1-C5)

Mesencephalon


Thoracolumbar

( T3-L3)

Lumbosacral(L4-S3)

Fleur• Localisation

• Differentials• Diagnostics

Fleur

• Imaging

Surgical Treatment of spinal corddisease

Outline

• Surgical Anatomy

• Aims of surgery

• Focal spinal cord disease (Indications for spinal surgery)

• Treatment and prognosis

Surgical anatomy – cervical spine

• Vertebrae• Spinous processes

• Articular facets

• Lamina

• Pedicles

• Body

• Ligaments

• Disks

Surgical anatomy – cervical spine (cont)

• Spinal cord

– Spinal cord segments

– Cervicothoracic intumescence

– Meninges

• Nerves

• Blood supply

Surgical anatomy – cervical spine (cont)

Surgical anatomy – thoracic and lumbar spine

• Vertebrae• Spinous processes

• Articular facets

• Lamina

• Pedicles

• Body

• Ligaments

• Disks

Surgical anatomy – thoracic and lumbar spine(cont)

• Spinal cord

– Spinal cord segments

– Lumbosacral intumescence L4 - S3

– Meninges

• Nerves

• Blood supply

Aims of Surgery

• Biopsy - Diagnosis

• Decompression

• Prophylaxis(fenestration)

• Stabilization

Therapy

Surgical Procedures

• Ventral Slot:

Surgical Procedures

• Ventral Slot (cont):

Surgical Procedures

• Dorsolateral hemilaminectomy:

Surgical Procedures

• Dorsolateral hemilaminectomy:

Lumbosacral stenosis• Etiology:

• Probably related to CSM: instability at the LSjunction

• Resultant changes:» Stenosis vertebral canal

» Disk protrusion-extrusion L7-S1 (L6-7)

» Subluxation/osteophytosis/thickening articularprocesses

» Soft tissue proliferation (joint capsule)

» OCD sacrum

» Instability and malalignment L7-S1

Lumbosacral stenosis

• Diagnosis:

– History, signalment, clinical findings– Usu large breed dogs, esp GSDs

– Pain the main presenting sign

– Variable L4-S3 signs including urinary/fecal incontinence

– Imaging– Plain radiographs insufficient – possibly associated with

spondylosis, transitional vertebrae

– Myelography, epidurography, discography

– CT

– MRI

Lumbosacral stenosis

Normal foraminal fat around nerve roots

Lumbosacral stenosis• Treatment and prognosis

– Conservative:• 4-6 weeks STRICT cage rest followed by gradual return to exercise

(2wks on lead)

– Surgical:• Dorsal laminectomy

• Foraminotomy

• Possible stabilization

Prognosis good for return to normal life unless severe LMNsigns

Spinal trauma• Etiology:

• Utes, Toorak tractors, Trains etc….

• Diagnosis:• History, clinical findings (important to grade)

• Plain radiographs without sedation/anesthesia –immobilize first (strap to board)

– Normal alignment does not rule out cord transection

– Myelography may be necessary

Spinal trauma

• Treatment and prognosis• Treat systemically first!

– Stabilise BP/hypovolaemia/shock– Look for intraabdominal/intrathoracic problems

• 3 compartment theory:1. Dorsal: spinous process, lamina, articular processes2. Middle: pedicles and floor of spinal canal3. Ventral: body of vertebra and disk

Disruption of 2 or more: unstable fracture

• External coaptation possible for stable fractures with mildclinical signs

• Internal fixation necessary for unstable fractures/severe clinicalsigns

Prognosis depends on severity and locationBeware ascending-descending myelomalacia

Steroid Responsive Meningitis Polyarteritis

• Signalment:• Large breeds, typically around 1y age, no sex

predilection; also relatively common in beagles

• Etiology:• Immune mediated – very high levels of intrathecal IgA

production

• History/Clinical Signs:• Pain – typically on neck flexion; low head carriage

• Pyrexia

• Usually no significant neurological deficits

Steroid Responsive Meningitis Polyarteritis

• Diagnosis:• Negative findings on imaging

• CSF tap: VERY increased WBC, neutrophilic pleocytosis

• Elevated CSF/Serum IgA level

• Treatment:• Corticosteroids:

– I/S doses: 1mg/kg BID 2wks, 0.5 mg/kg BID 4wks, 0.5 mg/kgSID 4 wks, 0.5 mg/kg EOD 8wks

– Monitor CSF/Serum IgA levels q4wks

Neoplasia

• Etiology:• Commonly:

– Peripheral nerve sheath tumor, meningioma, lymphoma,nephroblastoma, osteosarcoma, fibrosarcoma

– Glial tumors less commonly

• Location:– Extradural: 45-50%

– Intradural (extramedullary): 35%

– (intradural) Intramedullary: 15-20%

Neoplasia

• Diagnosis:• History, signalment, clinical findings

– Important to look for systemic signs: chest rads, abdo U/S,CBC, check lymph nodes

• Imaging– Plain radiographys

– Myelography/CT/MRI

– Definitive diagnosis: biopsy or FNA (fluoroscopy guided)

• Treatment and prognosis:• Surgery, radiation therapy (except lymphoma)

• Guarded-poor, dependent on tumor type, severity

Neoplasia

Documents

Part of the Veteducation Live Online Web-Seminar Series · The Veteducation International Online Veterinary Conference 2011 Part of the Veteducation Live Online Web-Seminar Series