Spinal Disease Flashcards

1
Q

What is syringomyelia

A

development of a fluid containing cavity within the parenchyma of the spinal cord as a result of abnormal CSF flow.

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2
Q

Description of Chiari-like malformation

A

Complex cause of caudal fossa crowding
- Occipital dysplasia (change to dorsal opening of foramen magnum - cerebellar compression)
- abnormally small caudal fossa
- Secondary cerebellar herniation

–> displacement of cerebellar vermis into the spinal canal
–> abnormal CSF flow dynamics associated with differencein pressure b/w the artery and CSF –> formation of syrinx (which possibly contains extracellular fluid and not CSF (supporting the theory of shift in fluid movement out of vascular space due to alterations in CSF pressure

50-70% of CKCS with CM develop a syrinx but clinical signs are not universally observed

No single morphometric characteristic evaluated thus far has been found to be a primary factor of syrinx development

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3
Q

Other craniocervical junction abnormalities that can occur (with or without CLM)

A

Atlanto-occipital overlap (atlas displaced cranially compressing caudal cerebellum)

Dorso-atlantoaxial bands (compress subarachnoid space)

Congenital dorsal angulation of the dens (decreases vertebral diameter)

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4
Q

Potential clinical signs of CLM/SM

A

Neuropathic pain - paraesthesias reported in humans, dermatomal hypersensitivity
Pain can also be nonspecific, intermittent, and spontaneous (e.g.,not caused by an obvious stimulus)

Phantom scratching unique clinical sign of CM/SM in dogs. A defining feature of phantom scratching, is that no contact is made with the skin and phantom scratching is typically oriented toward only one side of the body

Cervical myelopathy

Brainstem

Cerebellar dysfunction

Vestibular

Seizures rarely reported but referrable to CSF obstruction

Clinical signs may be exacerbated by excitement/stress or contact with neck or sometimes changes in barometric pressures

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5
Q

MRI findings of CLM/SM

A

Attenuation of dorsal subarachnoid space at cervicomedullary junction

Rostral displacement of caudal cerebellum by malformed occipital bone

Obstructive hydrocephalus

Caudal cerebellar vermis herniation

SM is a T2W hyperintensity linear lesion in spinal cord most commonly at C1-4 but also T1-L2 reported so whole spinal cord should be imaged
Large asymmetrical syrinx is the strongest predictor of pain

Not always assoc with clinical signs in the CKCS

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6
Q

Possible aetiologies of Syrinx formation

A

Abnormal CSF hydrodynamics - turbulent flow at foramen magnum

Cerebellar pulsation - subtle movement of cerebellum caudally with systolic filling of blood vessels causing a high pressure pulse wave of CSF with each cardiac cycle
–> arrives out of phase with arterial peak pressure –> arrives when arteries are small causing ECF fluid leak

CLM causes reduced compliance leading to larger pressure gradients between cranial and spinal systems

Reduced reabsorption of ECF fluid due to altered venous sinus formation

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7
Q

Treatment options sor SM pain and amount of evidence for them

A

Gabapentin/Pregabalin –> commonly prescribed, inhibits opening of specific Ca channels thus reducing neuronal excitability and release of NTs. Seem to help with phantom scratching symptoms

Topiramate - AED that increases frequency of GABA binding its receptor and antagonises the AMPA receptors (blocking glutamate transmission)

Amantadine - inhibits NMDA receptor by stabilising closed state of the ion channel –> reducing excitation. Most often used as adjunct. Little evidence as sole therapy

COXi - anecdotal evidence only, physiologically there is not a good justification for their use.

Steroids - little evidence for efficacy, may be better as pulse therapy during severe episodes. Inhibit PLA2 and COX enzymes, also reduce CSF production and substance P

PPi - thought to potentially reduce CSF production through activity in choroid plexus (inhibition of Na/K ATPase)
–> reported with IV administration but unknown effect of long term oral treatment

Maropitant NK1 antagonist. NK1R are in dorsomedial superficial spinal cord and involved in perception of itch
–> need more studies.

Acetazolamide - carbonic anhydrase inhibitor alters CSF composition. Limited evidence for use

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8
Q

When is surgery indicated in C
OMS

A

Refractory to medical management

Adverse drug effects

Progression of symptoms despite medical mgmt (56%)

Goal is to prevent progressive syrinx enlargement and reduce pain related behaviours

Short term success 80-94%
Long term there is a high relapse rate depending on surgery performed due to scarring

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9
Q

Types of IVDD

A

1 = accelerated intervertebral disc degeneration due to chondroid metaplasia and mineralisation of the nucleus pulposus
–> ultimate failure and extrusion into the vertebral canal through weakened annular fibres
–> acute focal compressive myelopathy (contusion or compression of spinal cord)
(Chondrodystrophic breeds: pekingese, mini poodle, Dachshund, Beagle, also GSD and Doberman)

2 = annular protrusion commonly associated with fibroid disc degeneration (generally slow)

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10
Q

Risk factors for type 1 IVDD

A

Chondrodystrophy breed

Miniaturisation

Obesity

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11
Q

Clinical signs of IVDD

A

Type 1 - peracute onset of spinal pain, paresis/plegia, urinary retention and neurological deficits correlating to location of extrusion
T3-L3 extrusion can cause schiff-Sherrington posture (flaccid HLs with reflexes, extensor rigidity in FLs)

(Type 2 - usually gradual onset of weakness/pain)

Imaging for diagnosis

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12
Q

ACVIM 2022 consensus imaging recommendations for IVDD comparison of CT and MRI

A

Magnetic resonance imaging, CT, CT-myelography or myelography are reasonable modalities for diagnosing TL-IVDE.

MRI sensitivity >98.5%, superior performance to CT for acute extrusion.
Also offers moderate level of prognostication
Superior ability to differentiate other possible DDx
Post-contrast imaging generally not needed.
( Limitations slower, limited availability)

When considering cases outside this typical clinical presentation, there is evidence to support the highest diagnostic sensitivity for high field MRI and higher risk of adverse events with myelo-graphy or CT-myelography

CT rapid acquisition,
Sensitivity 81%, Specificity 100% reported
–> better for chondrodystrophied subgroups where prevalence is higher.
Limited information on parenchymal injury or prognosis

Myelography - with CT sensitivity is 53-97%
Risk of seizures or causing spinal cord swelling and infiltration of contrast medium into spinal cord (bad)

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13
Q

Features of MRI assoc with IVDDD prognosis

A

Presence and extent of INTRAMEDULLARY hyperintensity on T2W
T2 hypointensity of spinal cord

Attenuation of CSF signal

All have been assoc with poorer Px

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14
Q

Medical vs surgical mgmt outcome based on THORACOLUMBAR IVDD neurological grade ACVIm 2022 consensus

A

Grade I (pain only) - 80% Medical, 98% surgical (lateralisation of disc reduces chance of medical mgmt working)

Grade II ( non-ambulatory paraparesis): 80% medical, 93% surgical (less complete recovery with medical management)

Grade III (Paraplegia with deep pain) - 60% medical, 93% surgery. Prolonged recovery with medical management

Grade IV (deep pain negative) - 21% medical, 61% surgery.

Recurrence rates for medical mgmt are 15-66%, so surgery should be considered in younger active dogs.

When consider-ing cases outside this typical clinical presentation, there is evidence to support the highest diagnostic sensitivity for high field MRI and higher risk of adverse events with myelo-graphy or CT-myelography (ACVIM consensus was only TL extrusion)

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15
Q

Is there evidence that timing affects surgical outcome in IVDD

A

Most larger and more recent studies suggest a lack of association

a number of dogs reported elsewhere to have been paraplegic DPN for as much as a week or more before surgery went on to recover ambulation. Surgical treatment should not be declined simply because the dog has been paralyzed for an extended period

Some evidence suggests that delayed decompression for DPN dogs may result in a longer time to achieve postoperative ambulation, which requires further investigation

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16
Q

Components of medical mgmt for TL IVDD (ACVIM consensus)

A

Few studies critically evaluate components so mostly anecdotal/expert opinion

Strict rest - 4-6 weeks with anti-inflammatory pain relief (NSAID for 7 days, if needing ongoing pain relief investigate further)
(though a study of >200 dogs found duration of rest not associated with outcome)
–> recommended to promote healing of annulus and resolution of inflammation (low LoE)

Other analgesia: gabapentin/pregabalin or muscle relaxants. low LoE for efficacy

If needing opioids for pain relief then need to reassess Dx or hospitalise until pain controlled adequately

Corticosteroids - no longer recommended for routine use in acute TL IVDD. Low LoE they are assoc with poorer outcome and lower QoL compared to NSAIDs

Rehab and Accupuncture - low LoE for both and neither a surrogate for Sx in severe cases. Physical therapy should be implemented after 4 weeks rest.

Management of UMN bladder if present - alpha antag +/- skeletal muscle relaxant. Combined with intermittent catheterisation or manual expression

17
Q

Surgical technique that may reduce the risk of IVDD recurrence

A

fenestration of the extruded disc at time of decompression

(odds of recurrence 5.8x higher if not done)

18
Q

Prognosis for bladder function recovery

A

Lags behind return of normal voiding and can be abnormal still 6 weeks postop.

Suboptimal continence is reported in dogs with severe lesions even if motor and sensory function returns

19
Q

Pathogenesis of ascending-descending ischaemic necrosis (myelomalacia)

A

Progressive necrosis , ischaemia and haemorrhage of the spinal cord (expanding cranially and caudally) following TL IVDD (not seen typically with cervical disc extrusion)
–> affects motor and sensory fibres.

thought to be a result of vascular lesion causing severe ischaemia

More likely to occur in paraplegic DPN dogs (10-33% reported).

Clinical signs develop within 1 week of injury

20
Q

Ways to reduce risk of ascending-descending myelomalacia

A

Use of corticosteroids reduced risk of occurrence

Concurrent durotomy at time of hemilaminectomy also reported to reduce risk

21
Q

Differences in outcome of cervical protrusion/extrusion disc disease

A

Protrusion more likely to be associated with cervical spondylomyelopathy (in older large breed dogs)

Extrusion surgery is indicated if ongoing pain or if neurological deficits present. Medical mgmt is otherwise the same
JVIm - older than dogs with TL disease, often less severe and longer duration. Overall better outcome. Not associated with chondrodystrophy phenotype

22
Q

Differences in management of type II IVDD TL

A

TL Protrusions are more difficult to manage and less likely to have full recovery due to secondary spinal cord injury and more aggressive surgery often needed to stabilise the spine.

23
Q

2 presentations for cervical spondylomyelop[athy

A

Instability of caudal cervical

Young-adult giant breeds
Osseous associated compression –> due to proliferation of vertebral arch
–> C6-7

Middle age dog (Dobermans)
Disc associated compression –> disc protrusion and hypertrophy of interarcuate ligaments

24
Q

Clinical signs of cervical spondylomyelopathy

A

Chronic progressive gait deficits - 2 engine

HLs proprioceptive ataxia and long strides. Normal to increased reflexes.

FL short choppy strides.. +/- reduced flexor withdrawals

Cervical hyperaesthesia is common

25
Q

Cause of lumbosacral stenosis

A

Biomechanical instability contributes to abnormal motion at lumbosacral articular processes → proliferative fibrosis through microtrauma and development of osteophytes
–> entrapment of L7 nerves.

Type II Hansen disc protrusion

26
Q

Typical presentation for LSS and Tx

A

Lumbosacral pain

Pelvic limb weakness, abnormal proprioception
but no ataxia

Stiff HL gait

Paresis only late in disease process.

Lesions present in many older dogs, severity of changes not always correlating with CS.
Epidural steroids, strict rest and NSAIDs.

Sx only in severe cases

27
Q

Pug Thoracolumbar myelopathy

A

A constrictive myelopathy involving a fibrous band that is around the spinal cord

Presents with chronic TL myelopathies and often incontinence

28
Q

Degenerative myelopathy: presentation, proposed cause and affected breeds

A

Primary central axonopathy that begins in TL spinal cord and ascends/descends –> axon and myelin degeneration and eventual complete loss

An immune mediated mechanism is hypothesised

Begins as mild proprioceptive ataxia and paraparesis that progresses over 6-12mo with lack of spinal pain and normal to increased HL reflexes and increased extensor tone
(making other spinal dz less likely)

Breeds: GSD, Corgi, Rhodesian Ridgeback, Boxers
–> genetic test for GSD.

Dx based on exclsion of other causes of myelopathy –> normal imaging and CSF.
EMG –> evidence of denervation atrophy with spontaneous activity

No Tx

29
Q

Pathogenesis of SRMA

A

Presumed immune mediated process due to response to steroids and lack of other cause identified. dogs with SRMA present with a predominating B- over T-lymphocyte ratio in blood and CSF as well as in meningeal lesions of acute SRMA (this changes in the chronic form)
Also high IgA levels (although not thought to be part of disease pathogenesis).
Inflammatory lesions in the leptomeninges and associated arteries with a necrotising vasculitis.

Neurological deficits (general proprioceptive ataxia, and limb paresis/paralysis) are more likely to be seen in the chronic form - which causes fibrosis of the meninges that may compress the vasculature or obstruct the flow of cerebrospinal fluid (CSF), which further compromises blood flow to certain CNS structures in particular motor neurons resulting in neurological deficits.

usually characterised by a systemic inflammatory response with pyrexia and an inflammatory leukogram with left-shift neutrophilia in addition to the neurological disease

30
Q

Vet Journal Biomarker for SRMA summary

A

At present, a confirmation of the clinical suspicion is based essentially on a CSF analysis demonstrating inflammatory features
–> polymorphonuclear pleocytosis (nondegenerate in acute form) or mononuclear in chronic form,

CRP has been shown to be significantly higher in dogs with SRMA in comparison to other neurological diseases and increases with relapse so could be a useful monitoring marker.

Antibodies:
Increased IgA concentrations in both serum and CSF are characteristic for dogs with SRMA, and can be found not only in the acute stage but also the chronic, even after treatment with corticosteroids
sensitivity of 91% and specificity of 78% for SRMA when applying paired serum and CSF IgA results
both serum and CSF IgA measurements are needed to distinguish SRMA from other inflammatory CNS conditions with this marker as CSF levels are not different b/w diseases.

IgA levels remain high in spite of clinical resolution of disease

Cytokines - highly sensitive to Tx, time of sampling and other systemic disease.
IL8 is increased (neutrophil chemotaxis) but lacks specificity

31
Q

Clinical findings of discospondylitis

A

Slowly progressive
Spinal pain +/- neurological deficits
+/- fever
Most often thoracolumbar in dogs and cats

French BD, English setter, Irish Wolfhound and Greyhound overrepresented

CRP was reported to be a sensitive but nonspecific biomarker
DDx SRMA (usually more cervical)

Imaging: MRI still more sensitive than CT, but as some dogs have multifocal localisation can be costly and time consuming to perform MRI of entire spine.
Radiographs have the lowest sensitivity and compared to MRI reported to have poor agreement

Cultures: blood, disc, urine.

32
Q

Recent case series on Discospondylitis and reports of culture positivity

A

Vet record 2023 - 120 cases retrospective review
Positive cultures from >1 site in 42%
Not all cultures performed in all cases
Disc culture positive in 33%, blood in 32% and urine in 24%

JVIM study was larger but still retrospective multi-institutional study and not all dogs had all tests
28% positive urine, 27% positive blood, 41% positive disc aspirate.

Initial reports of culture positivity in up to 75% of cases in a small study

33
Q

Treatment of Discospondylitis

A

Various durations reported.

Cephalosporins considered reasonable first line

G+ cocci (Staph and Strep) are most common isolates.
Ideally base on culture where possible

Duration and use of repeat imaging is not well established, some report use of ABx based on resolution of systemic inflammatory markers or presence of pain

Imaging changes can take a long time to resolve and generally never look normal

34
Q

Recent case series on cat discospondylitis

A

2 series from same institution

1 - imaging characteristics in 17 cats.

2 - clinical features and outcome in 17 cases.
Similar presentation to dogs.
All Tx with antibiotics for median of 3 months. Empirical therapy used for most as only 2/17 cultured positive.

Excellent outcome in 12 cats with available follow up.

35
Q

Types of spinal tumours and progression

A

Extradural - arising from bone or soft tissues, metastatic disease and lymphoma. Account for 50%
Usually rapid progression or can cause fracture of vertebrae or spinal cord compression from haemorrhage

Intradural-extramedullary
= meningioma, nephroblastomas
Very slow progression

Intramedullary = gliomas, ependyomas, astrocytoma, metastatic.
Most often slow growing but some have rapid onset and progression

36
Q

Most common spinal tumour in cats and Dx/Tx options

A

Lymphoma - often FeLV positive and young (older cats more likely meningioma)

May get Dx on CSF if do lumbar tap, can do flow or PARR to look for malignant characteristics

Tx with chemo and RT reported to be successful at inducing remission in some.

37
Q

Causes of vascular spinal cord disease - and prognostic factors in general

A

ISCHAEMIC MYELOPATHY
Thromboembolism - due to underlying coagulopathy, fibrocartilagenous embolism (GSD, Mini Schnauzer, Irish Wolfhound), hypertension, hypothyroidism

Haemorrhage - due to systemic hypocoagulability, neoplasia, anomalous vessels, disc herniation, trauma, angiostrongylus migration

Loss of deep pain has a poorer prognosis as do lesions of the intumescence (ie those with LMN signs).
Because there is less scope for plastic responses to ameliorate the functional deficits if gray matter regions have been destroyed