Spinal Disease Flashcards
What is syringomyelia
development of a fluid containing cavity within the parenchyma of the spinal cord as a result of abnormal CSF flow.
Description of Chiari-like malformation
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
Other craniocervical junction abnormalities that can occur (with or without CLM)
Atlanto-occipital overlap (atlas displaced cranially compressing caudal cerebellum)
Dorso-atlantoaxial bands (compress subarachnoid space)
Congenital dorsal angulation of the dens (decreases vertebral diameter)
Potential clinical signs of CLM/SM
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
MRI findings of CLM/SM
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
Possible aetiologies of Syrinx formation
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
Treatment options sor SM pain and amount of evidence for them
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
When is surgery indicated in C
OMS
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
Types of IVDD
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)
Risk factors for type 1 IVDD
Chondrodystrophy breed
Miniaturisation
Obesity
Clinical signs of IVDD
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
ACVIM 2022 consensus imaging recommendations for IVDD comparison of CT and MRI
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)
Features of MRI assoc with IVDDD prognosis
Presence and extent of INTRAMEDULLARY hyperintensity on T2W
T2 hypointensity of spinal cord
Attenuation of CSF signal
All have been assoc with poorer Px
Medical vs surgical mgmt outcome based on THORACOLUMBAR IVDD neurological grade ACVIm 2022 consensus
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)
Is there evidence that timing affects surgical outcome in IVDD
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