Spinal cord disorders Flashcards
Segments of the spinal cord
8 cervical
13 thoracic
7 lumbar
3 sacral
At least 2 caudal
Four functional regions of the spina cord
Cranial cervical (C1-C5)
Cervicothoracic (C6-T2)
Thoracolumbar (T3-L3)
Lumbosacral (L4-S3)
Lower motor neurons
Efferent neurons connecting the central nervous system to an effector organ
Cell bodies located within grey matter of cervicothoracic intumescence (C6-T2) for the thoracic limbs, and lumbosacral intumescence (L4-S3) for the pelvic limbs
UMN weakness
Refers to a lesion that interrupts the descending motor pathways from supraspinal neurons that converge on the LMN pool.
Clinical signs of UMN weakenss manifest as paresis and/or plegia with normal to increased spinal reflexes (hyperreflexia) and muscle hypertonia.
LMN weakness
Refers to a lesion of the ventral spinal cord grey matter and its axon coursing to the muscle through the spinal nerve roots and peripheral nerve.
Clinically manifests as paresis and/or plegia, decreased to absent spinal reflexes (hyporeflexia to areflexia), decreased muscle tone and muscle atrophy that is severe and rapid in onset.
C1-C5 lesions
Neck pain
Tetraparesis/plegia, ipsilateral hemiparesis/plegia, ataxia
- postural reaction deficits in all 4 limbs or in ipsilateral thoracic and pelvic limbs
- normal to increased spinal reflexes in all 4 limbs
- normal to increased tone in all 4 limbs
Ipsilateral Horner’s syndrome
Respiratory difficulty
Urinary retention
C6-T2 lesion
Neck pain
Tetraparesis/plegia, ipsilateral hemiparesis/plegia, ataxia
- postural reaction deficits in all 4 limbs or in ipsilateral thoracic and pelvic limbs
- decreased to absent reflexes in thoracic limbs, normal to increased reflexes in hind limbs
- decreased to absent tone in thoracic limbs, normal to increased tone in pelvic limbs
- muscle atrophy in thoracic limbs
Ipsilateral Horner’s syndrome
Respiratory difficulty
Urinary retention
T3-L3 lesions
Back pain
Paraparesis/plegia, ipsilateral monoparesis/plegia, ataxia
- postureal reaction deficits in both ot one pelvic limbs
- normal to increased spinal reflexes in pelvic limbs
- normal to increased tone in pelvic limbs
Schiff sherrington phenomenon possible in acute and severe lesion
Absent trunci reflex caudal to the level of the last in tact dermatome
Urinary retention (UMN bladder)
L4-S3 lesions
Back pain
Paraparesis/plegia, ipsilateral monoparesis/plegia, ataxia
- postural reaction deficits in both ot one pelvic limb
- decreased to absent spinal reflexes in hind limbs
- decreased to absent tone in pelvic limbs
- muscle atrophy in pelvic limbs
Urinary incontinence (LMN bladder)
Ataxia
Loss of proprioception, incoordination
Paresis
Reduced voluntary motor funtion
Paralysis
Absence of voluntary motor function
Schiff-sherrington posture
Lesion in thoracolumbar spinal cord segments alters the ascending inhibitory pathways from the border cells in the lumbar grey matter (L2-L4).
Axons of these cells ascend and terminate in the cervical intumescence.
Loss of this ascending inhibition to the thoracic limbs results in extension.
In spite of this increased in extensor tone the thoracic limbs are normal neurologically with respect to neuro function.
Vascular spinal diseases
Fibrocartilaginous embolic myelopathy
Infectious causes of spinal disease
Infectious meningo(encephalo)myelitis
Discospondylitis
Inflammatory causes of spinal disease
Steroid responsive meningitis
Meningo(encephalo)myelitis of unknown origin (MUO)
Idiopathic causes of spinal disease
(Sub)arachnoid diverticulum (SAD)
Traumatic causes of spinal disease
Vertebral fracture,
(sub)luxation
Spinal cord contusion
Haemorrhage
Traumatic disc herniation (Acute non-compressive neucleus pulposus extrusion - ANNPE)
Anomalous causes of spinal disease
Atlanto-axial instability
Vertebral and spinal cord anomalies
Syringohydromyelia
Neoplastic causes of spinal disease
Spinal tumours (extradural, extramedullary, intramedullary)
Nutritional causes of spinal disease
Hypervitaminosis A in cats
Degenerative causes of spinal disease
Inherited neurodegenerative diseases (storage diseases)
Intervertebral disc disease
Wobbler’s syndrome
Degenerative myelopathy
Lumbosacral stenosis
Spinal pain
Tissue damage or inflammation produces pain through stimulation of nociceptors
Most CNS parenchyma doesn’t have nociceptors - damage to grey and white matter is not painful
Meninges have a high density of nociceptors
What are the pain sensitive structures of the spine?
Periosteum of the vertebrae
Blood vessels
Meninges
Nerve roots
Intervertebral discs
Neurodiagnostic investigation of the spine
Haematology, serum biochemistry, urinalysis
Chest x-rays, abdominal U/S
Survey spinal radiographs
CSF (cell count, cytology, protein conc.)
Myelography, CT, or MRI
Culture, serology, PCR
Prognosis of spinal diseases
Progressive compressive extradural spinal cord disease - order of losses
- concious proprioception
- motor function
- bladder function
- deep pain perception
Assessment of pelvic limb pain sensation in paraplegic animals good prognosticator
Tetraplegic animals at risk of respiratory failure due to paresis of intercostal muscles and diaphragm, atelectasis as a result of recumbency
Pathogenesis of Fibrocartilaginous embolic myelopathy (FCE)
Fibrocartilage identical to the nucleus pulposus, embolises to the spinal cord vasculature, producing an area of ischaemic necrosis centred on the spinal cord grey matter.
Signs are often lateralised, as the embolus usually lodges in one branch of the ventral spinal artery
Epidemiology of Fibrocartilaginous embolic myelopathy (FCE)
Young and non-chondrodystrophic breeds
Rare in cats
Clinical signs of Fibrocartilaginous embolic myelopathy (FCE)
- per-acute onset, excersise at onset
- non-painful
- lateralised neurological herniation
Differential diagnoses of Fibrocartilaginous embolic myelopathy (FCE)
Traumatic disc (acute non-compressive nucleus pulposus extrucrion, ANNPE)
Acute disc herniation
Diagnosis of Fibrocartilaginous embolic myelopathy (FCE)
X-ray and myelogram show no evidence of compression (diagnosis by exclusion)
Infarcted are is visible on MRI (hyperintense on T2 weighted images)
Prognosis of Fibrocartilaginous embolic myelopathy (FCE)
Depends on extent of injury
GOod prognosis when preservation of deep pain perception
Guarded prognosis in absence of deep pain sensation
Treatment of Fibrocartilaginous embolic myelopathy (FCE)
Rehabilitation, improvement can be dramatic over the first 7 days and will continue for 1-3 months after injury
Pathogenesis of Discospondylitis
Infection of the intervertebral disc and adjacent vertebrae by
1. haematogenous spread from distant foci of infection
2. penetrating wounds or plant material
3. iatrogenic (surgery)
Immunosuppression is considered a predisposing cause
Staphylococcus intermedius is the most common aetiolgical agent of canine discospondylitis
Epidemiology of Discospondylitis
Multifocal in the vertebral column
Most frequently in large male intact middle aged dogs, less common in cats
Most commonly affected site in L7-S1
Clinical signs of Discospondylitis
Spinal pain (+++)
Fever - systemic signs 30% (fever, weight loss, endocarditis)
Combination of neurological deficits regarding the spinal cord segment affected
Diagnosis of Discospondylitis
Leucocytosis
Blood and urine culture
Spinal radiographs
- narrowing or enlarged disc space
- may not be evident in first 2-4 weeks
- entire spine should be radiographed as can be multifocal
Scintigraphy
Myelogram/CT/MRI
MRI with contrast
Abdominal/cardiac U/S
Thoracic radiographs
Prognosis of Discospondylitis
Very good unless fungal aetiology
Treatment of Discospondylitis
Antibiotics (cephalosporins, amoxicillin) for min 2 months
Cage rest
Analgesics (NSAIDs)
(Surgical decompression)
Pathogenesis of Steroid-responsive meningitis-arteritis
Suspected immunological cause, resulting in vasculitis and meningitis
Epidemiology of Steroid-responsive meningitis-arteritis
Predisposition in Beagles, Bernese Mountain Dogs, Boxers (BBB), other breeds
Young adults (<2 years)
Clinical signs of Steroid-responsive meningitis-arteritis
Acute form: febrile, anorexia, neck pain
Chronic form (rare): neurological deficits - meningomyelitis
50% concurrent polyarthritis (IMPA, immune mediated polyarthritis)
Diagnosis of Steroid-responsive meningitis-arteritis
Neutrophilia (left shift)
High CRP in serum
CSF: neutrophilic pleocytosis and protein elevation
High IgA levels in serum and CSF
Prognosis of Steroid-responsive meningitis-arteritis
Good if treated early and aggressively
Treatment of Steroid-responsive meningitis-arteritis
Long term (4-6 months) tapering immunosuppressive doses of corticosteroids
Pathogenesis of traumatic intervertebral disc disease
ANNPE: acute non-compressive nucleus pulposus extrusion
HNPE: Hydrated nucleus pulposus extrusion
ANNPE
Acute non-compressive nucleus pulposus extrusion
Intervertebral discs are mainly healthy or only mild/early signs of degeneration
There is traumatic rupture of the annulus fibrosus with acute extrusion of fluid healthy nucleus pulposus into the vertebral canal
Causes per-acute contusive but non-compressive myelopathy
HNPE
Hydrated nucleus pulposus extrusion
Gelatinous to liquid, histologically only partially degenerated nucleus pulposus extrudes causing contusive and compressive myelopathy
Unknown spontaneous cause, rarely to be associated with exercise or trauma
Epidemiology of traumatic intervertebral disc disease
ANNPE: classically in large breed dogs, non-chondrodystrophic, also in cats. Older adults (mean 7yr)
HNPE: any breed, and cats. Adults (5-12 yrs, median 9yrs)
Clinical signs of traumatic intervertebral disc disease
Common localisation at C1-C5
ANNPE: common to be lateralised and painful in the first 24 hrs, vocalisation at onset. Signs tend to stabilise or improve after 24-48hrs
HNPE: symmetric non-lateralised signs; spinal pain rarely detected
Diagnosis of traumatic intervertebral disc disease
MRI of the neuroanatomical localisation distinguishes ANNPE from HNPE and other myelopathies
Differentials are FCE, disc herniation
Treatment of traumatic intervertebral disc disease
ANNPE: supportive, it is mainly a spinal cord contusive injury
HNPE: supportive when mild to moderate signs or improving. Decompressive surgery can be attempted on non-improving severe cases
Prognosis of traumatic intervertebral disc disease
ANNPE and HNPE: good prognosis if deep pain is preserved
HNPE: unsuccessful if tetraplegia with respiration compromise (remember C1C5)
Pathogenesis of atlanto-axial instability
Subluxation of the atlantoaxial junction is a relatively common problem and usually results from a failure of ligamentous support and/or congenital absence or hypoplasia of the dens
Epidemiology of atlanto-axial instability
Classically young toy and small breeds
<2 years
Traumatic fracture of the dens and rupture of the ligaments can occur in any dog or cat
Clinical signs of atlanto-axial instability
Neck pain (do not flex head!)
Neurological deficits for C1C5
Diagnosis of atlanto-axial instability
Survey radiographs of the cervical spine (extreme care if sedated or anaesthetised, flexion of the neck can cause iatrogenic spinal cord damage)
- Lateral view: increased space between dorsal lamina of atlas and dorsal spinous process of the axis
- Ventrodorsal view: reduced size or absence of the dens
Treatment of atlanto-axial instability
Conservative: external splint/bandage from ears to shoulders minimum 2-3 months, plus strict rest
Surgical: reduction of subluxation and stabilisation with K wires, screws, and polymethacrylate
Prognosis of atlanto-axial instability
Conservative: often effective on short term, long term deficiency doubtful but possible
Surgical: excellent if mild neurological deficits, worse if severe and chronic neurological deficits. Risk of resp arrest and death in 48-hour post-operative period (20%)
Pathogenesis of spinal cord tumours
Primary:
- Extradural: verterbral tumours (sarcomas, multiple myeloma), lymphoma
- Intradural-extramedullary: meningiomas, nerve sheath tumours, nephroblastoma, lymphoma
- Intramedullary: ependymomas, gliomas, lymphoma
Secondary: metastatic
Epidemiology of spinal tumours
Older dogs and cats
Extradural lymphoma is the most common spinal tumours in cats. Most affected cats are <2yrs of age. FeLV has been associated.
Clinical signs of spinal tumours
Spinal hyperaesthesia (extradural or intradural-extramedullary)
Neurological deficits depending on localisation
Pathological fractures of vertebral body results in acute onset of neurological deficits
Diagnosis of spinal tumours
Survey radiographs: vertebral tumours: lysis, pathological fractures
Abdominal U/S, chest radiographs
CT/MRI
Fluoroscopic-guided needle aspiration or surgical biopsy
Scintigraphy: vertebral tumours - metastasis
Bone marrow biopsy (myeloma, lymphoma)
Monoclonal gammopathy in serum and urine, Bence Jones proteinuria (myeloma)
Treatment of spinal tumours
Palliative, combination of surgery, irridation +/- chemotherapy
Prognosis of spinal tumours
Guarded to poor - depends on type of tumour, localisation, staging, and tumour size
Pathogenesis of degenerative intervertebral disc disease
Type 1 = extrusion
- central nuclear material of disc ruptured through dorsal fibrous structures into the vertebral canal
- nucleus pulposus ages prematurely in chondrodystrophic breeds so nucleus matrix degenerates and mineralises making them prone
Type 2 = protrusion
- disc ‘bulging’ into vertebral canal
- fibroid degeneration involves a progressive thickening of the dorsal annulus fibrosus and loss of elasticity
Epidemiology of degenerative intervertebral disc disease
One of the most common neurological disorders in dogs, less common in cats
Type 1: small breed dogs, unusual in dogs <2yrs
Type 2: large breed dogs, 5yrs or older, most commonly cervical and thoracolumbar region
Clinical signs of degenerative intervertebral disc disease
Type 1: acute, minutes-days
Type 2: chronic, slowly progressive (weeks-months)
Depends on localisation
Diagnosis of degenerative intervertebral disc disease
Survey spinal radiographs
- type 1: narrowing of intervertebral disc space, narrowing of the intervertebral foramen and presence of mineralised material within the vertebral foramen and mineralised material within canal and discc space
- type 2: spondylosis
Myelography, CT, or MRI
Treatment of degenerative intervertebral disc disease
Conservative:
- if first time with spinal pain, only mild-moderate paresis
- any time if still ambulatory
- if finacial restrictions
- Strict cage rest, then restricted exercise
- mandatory to support healthy micturition - bladder needs to be manually expressed 3-4x a day
Surgical
- spinal decompressive surgery
- removal of disc materal by ventral slot if cervical or hemilaminectomy if thoracolumbar
Prognosis of degenerative intervertebral disc disease
Depends on clinical signs good if ambulatory or non ambulatory paraparesis but gets worse if paraplegic and without deep pain response
Lumbosacral stenosis
Stenosis of vertebral canal or foramina and compression of the cauda equina
IV disc herniation (type II>type I)
Ventral subluxation of S1/instability/malalignment
Vertebral anomalies
Soft tissue proliferation
Osteophytosis
Osteochondrosis
Pathogenesis of degenerative myelopathy
progressive neurodegenerative disease in dogs with both upper and motor neuron involvement
Has been associated with a variation of the gene SODI with a missense mutation
Epidemiology of degenerative myelopathy
Severeal dog breeds, including GSD, boxer, chesapeake bay retriever
Usually 8yrs or older
Clinical signs of degenerative myelopathy
Insidious, progressive ataxia and paresis of the pelvic limbs (UMN) ascending to tetraparesis (LMN)
Control of urination or defecation may be affected late in the disease process
Differential diagnosis of degenerative myelopathy
Intervertebral disc disease or degenerative lumbosacral stenosis
Degenerative myelopathy is not painful!
Diagnosis of degenerative myelopathy
Ruling out other diseases causing progressive myelopathy
Genetic test: mutation in the SODI gene is a risk factor
Post mortem
Prognosis of degenerative myelopathy
Poor, dogs often lose the ability to ambulate within 6 months of diagnosis
Treatment of degenerative myelopathy
Regular exercise
Physiotherapy may improve the dogs quality of life
Disc associated cervical spondylomyopathy
Multifactorial/unknown aetiology
Large breed dogs
Middle-older age
C5-C7 (more caudal)
Mild pain - moderate (tetraparesis/’2-engine gait’/C6T2)
Osseous associated cervical spondylomyopathy
Multifactorial/unknown aetiology
Giant breed dogs
Young age
C3-C6 (more cranial)
Mild pain - moderate (tetraparesis/C1C5/C6T2)
Conservative mangement of cervical spondylomyopathy
Exercise restriction/rest
Anti-inflammatories (preds)
Physiotherapy
Surgical treatment of cervical spondylomyopathy
Severe progressive/relapses
Direct decompression
Indirect decompression
