Spinal Surgery Flashcards
Degenerative cervical spinal disease
A broad term encompassing a number of pathologies resulting in structural changes in the joints i.e. the intervertebral disc, facet joints and the uncovertebral joints which can potentially lead to compression of neural structures, deformity, pain and disability.
Factors affecting the rate of degenerative change
Load and intensity of use over time
Smoking, genetics, localised trauma, infection.
Pathophysiology of degenerative cervical spinal changes
Intervertebral discs bear the load of the head and neck.
Axial loading through the nucleus pulposus of the disc is converted to hoop stresses acting on the annulus fibrosus and the vertebral endplates.
This alters the cellular composition of the nucleus pulposus with reduction in hydrophilic proteoglycans and increased collagen.
The mechanical properties of the disc change with the loss of intervertebral height and cracks and fissures appearing predisposing to the pulposus herniation.
Consequences of altered mechanical stresses in degenerative cervical spinal disease
Transferred to the facet joints leading to segmental hypermobility with osteophytic spurs deposited in an adaptive remodelling process meant to confer increased stability.
Ligamentous hypertrophy also occurs
Commonest levels affected by degenerative cervical spinal disease
C5/6
C6/7
Cause of neural compression in the cervical spine of patients <55
Tends to be soft disc prolapse encroaching into the spinal canal or the neural exit foramina causing myelopathy or radiculopathy
Cause of neural compression in the cervical spine of patients >55?
Osteophytes and thickened annulus
Morphology of the degenerated cervical spine
Alters normal cervical lordosis leading to straightening or the adoption of kyphotic, hyperlordotic or scoliotic curvatures
At what degree of stenosis of the spinal canal does myelopathy result?
Reduction in the cross-sectional area >30%
Normal cervical canal diameter
18mm
Normal cervical cord diameter
10mm
Pathophysiological mechanisms contributing to cord injury in degenerative cervical myelopathy
Static compression results in direct trauma and chronic cord ischaemia
Dynamic compression results from excessive translational movements.
Neuroinflammatory response triggers a cascade of cellular events causing demyelination of the corticospinal tract, central grey matter degeneration with loss of interneurons, anterior horn cell atrophy and gliosis.
Symmetrical involvement of motor and sensory tracts
Bilateral weakness below the affected level
Paraesthesia, numbness, tingling and sensory loss with a discrete sensory level
?Cervical myelopathy
Examination findings in DCM
Increased tone
Brisk and pathological reflexes
Symptoms of difficulty with sphincter control
Symptom progression in DCM
Insidious onset with steady deterioration in hand control, progressive clumsiness, gait unsteadiness, falls.
What is the most common clinical presentation of degenerative cervical disease?
Radiculopathy from compression of a nerve root
Motor and sensory deficits with reduced deep tendon reflexes in the distribution of the affected nerve root
Pain with associated reduced movements radiating into the arm as brachalgia
Positive root compression tests can reproduce pain
?Cervical radiculopathy
Ix in diagnosis of degenerative cervical disease
MRI
Dynamic cervical spine radiographs can assist in operative planning
CT may be useful for assessing the degree of osteophytosis and the extent of foraminal stenosis
Myelography has excellent sensitivity for detecting SC compression
Surgical decompression in DCM
Indicated in most patients because the majority deteriorate over time.
Timing of intervention in DCM
Earlier intervention in symptomatic cervical myelopathy is associated with improved outcomes.
Chronic neurological deficit is unlikely to improve.
Conservative vs surgical Mx of cervical radiculopathy
RCTs have shown that surgery rapidly improves symptoms but in the long term PT and Sx are equally effective
Aim of surgical decompression in DCM?
Halt disease progression
Outcomes in DCM decompression
60-70% of patients improve
30% have stable disease
10% continue to progress
Outcomes in surgical treatment of cervical radiculopathy?
90% have improvement in arm symptoms
OPLL
Ossification of posterior longitudinal ligament
OLF
Ossification of ligamentum flavum
Pathophysiology of OPLL and OLF
NIDDM, IGT, excessive weight gain, hypoPTHism and hypophosphataemic rickets all implicated.
More common in Japan.
Ectopic bone forms within the ligaments, with ossification, ligamentous hyperplasia, cell proliferation and vascular ingrowth seen.
Classification of OPLL
Based on CT findings
Hirbayashi
Hirayabashi classification of OPLL
a) Continuous type
b) Segmental
c) Circumferential (confined to disc space)
d) Mixed type
Impact of OPLL on surgery
Complicates anterior surgical decompression and dramatically increases the risk of intraoperative durotomy.
When ossification bridges the disc spaces, segmental mobility is reduced and the PLL fuses with thecal sac.
Posterior approach is inidcated
Pathology of RA
Involves novel antigenic expression by synovial cells, leading to persistent cellular activation and immune complex production (RF- IgM).
Cytokine mediated chronic inflammation is initiated (IL-1, 6, TNF-alpha)
Results in granulation deposition within the synovium (rheumatoid pannus) which produces proteolytic enzymes capable of destroying adjacent cartilage, ligaments, tendons and bone.
Consequence of RA in the cervical spine
Destructive synovitis leads to ligamentous laxity and bony erosions with subsequent instability and subluxation.
Compression of neural structures can result from instability or from direct pannus compression.
Why are the upper cervical articulations primarily affected in rheumatoid cervical spinal disease?
Occiput/C1 and C1/2 because the normal ligamentous structures surrounding the occipito-atlantoaxial region conferring its significant strength and stability are degraded as part of the disease process.
What are the most common cervical spine pathologies in RA
C1/2 instability (65%)
Basilar invagination (20%)
Subaxial subluxation
Cause of C1-2 instability (atlantoaxial subluxation)
Results from the destruction of the transverse, apical and alar ligaments e.g. from rheumatoid pannus.
Also occurs in AS, achondroplasia, Down’s syndrome, Morquio’s syndrome and secondary to trauma.
Radiographic features of atlantoaxial subluxation
Plain XR
In a non-traumatic setting flexion and extension views may be performed. The expected distance between anterior arch of C1 and the dens in the fully flexed position should be <3 mm in an adult (~5 mm in a child).
In a vertical subluxation, the dens is often above the McGregor line by over 8 mm in men and 9.7 mm in women.
Atlantoaxial subluxation
Normal ADI in adults should be <3mm
Atlantoaxial subluxation
On CT, C1 is not orientated in line with the head. The head may be pointed anteriorly, C1 is turned. If this is a fixed defect, C2 is rotated in conjunction with C1.
Indications for surgical stabilisation of atlantoaxial subluxation
Asymptomatic with ADI >8mm
All patients with cervical myelopathy.
Normal posterior atlanto-dental interval?
>14mm
Basilar erosion
Occurs from erosion of occiput/C1 and C1/2 joints such that the dens migrates into the foramen magnum
May present with HCP, syringomyelia, progressive myelopathy
Chamberlain’s line
Extends from the hard palate to the opisithion (back of the foramen magnum)
The dens should be <3mm above this line
McGregor’s line
Extends from the hard palate to the most caudal point of the occipital curve
The dental tip should be <4.5mm above this line
McRae’s line
Drawn from the basion (front of the foramen magnum) to the opisthion (back of the foramen magnum)
The odontoid tip should not be above this line, is normally 5mm below.
Additional use of McRae’s line
Used to diagnose Chiari 1 malforamations where the cerebellar tonsils are seen to descend more than 3mm in children or 5mm in adults, below this line.
What is the difference between basilar impression and basilar invagination
The basilar impression is caused by softening of the bones of the skull base rather than migration of the dens upwards due to ligamentous instability
There can be brainstem compression as a result of the basi-occiput and condylar segment of the occipital bone leading to infolding of the foramen magnum.
Causes of basilar invagination
Most common is RA
Klippel-Feil
Osteogenesis imperfecta
Achondroplasia
Chiari malformations
Cleidocranial dysostosis
Schwartz-Jaempl Syndrome 2
Morquio’s syndrome
HyperPTH
Osteomalacia
Paget’s
Morquio’s syndrome
Morquio syndrome, also known as Mucopolysaccharidosis Type IV (MPS IV), is a rare metabolic disorder in which the body cannot process certain types of sugar molecules called glycosaminoglycans (AKA GAGs, or mucopolysaccharides). In Morquio syndrome, the specific GAG which builds up in the body is called keratan sulfate. This birth defect, which is autosomal recessive, is a type of lysosomal storage disorder. The buildup of GAGs in different parts of the body causes symptoms in many different organ systems.[2]:544 In the US, the incidence rate for Morquio is estimated at between 1 in 200,000 and 1 in 300,000 live births.
Klippel Feil syndrome
Klippel Feil syndrome (KFS) is a congenital, musculoskeletal condition characterized by the fusion of at least two vertebrae of the neck. Common symptoms include a short neck, low hairline at the back of the head, and restricted mobility of the upper spine.
Cleidocranial Dysostosis
Cleidocranial Dysplasia (cleido = collar bone, + cranial = head, + dysplasia = abnormal forming), also known as Cleidocranial Dysostosis and Marie-Sainton Disease, is a condition characterized by defective development of the cranial bones and by the complete or partial absence of the collar bones (clavicles).
Schwartz-Jampel syndrome
Schwartz–Jampel syndrome (SJS) is a rare genetic disease caused by a mutation in the perlecan gene (HSPG2)[1] which causes osteochondrodysplasia associated with myotonia.[2] Most people with Schwartz–Jampel syndrome have a nearly normal life expectancy
Def: Platybasia
Flattening of the skull base
Usually asymptomatic unless associated with other abnormalities.
Skull base angle is formed by a line joining the nasion with the centre of the pituitary fossa and a line joining the anterior border of the foramen magnum with the centre of the pituitary fossa
Platybasia is present if this angle is >143
When should surgical correction of AS kyphotic spine be considered?
Only if concomitant thoracolumbar and hip/knee joint abnormalities excluded.
AS also leads to bony osteopenia which influences planning of instrumentation
Forestier Disease
Diffuse idiopathic skeletal hyperostosis
Presence of non-marginal syndesmophytes at three successive levels involving four contiguous vertebrae
Appears radiologically as flowing anterior ossification of the ALL with disc space preservation.
There is an absence of facet joint ankylosis, SI erosion, sclerosis and intra-articular osseous fusion
Surface landmarks:
C3/4 level
Caudal to hyoid bone
Surface landmarks:
C4/5
Thyroid cartilage
Surface landmarks:
C5/6
Cricothyorid membrane
Surface landmarks:
C6/7
Cricoid cartilage
What is this muscle?
What is its innervation?
Longus colli
Anterior rami of C2-6
What may result with excessive posterior cervical muscle stripping and adjacent facet joint exposure?
Instability and progressive deformity (post-laminectomy kyphosis and swan-neck deformity)
What is the lateral limit for cervical laminectomy
Medial border of the lateral masses
Approach to Margerl’s C1/2 stabilisation
A single screw on each side is placed through the pars interarticularis of C2 passing through the C1/2 joint directed at the lateral mass of C1
It provides the most stable and rigid fixation biomechanically of the C1/2 joint with almost complete obliteration of rotation.
Approach to Magerl’s transarticular screws
Prone, skull clamp, flexed.
C1 posteiror arch and lateral masses, C2 laminae, C2 pars and C2/3 facet joints are exposed.
Caudal stab incisions may be required to obtain screw trajectory (usually 1-2cm lateral to the C7/T1 spinous process).
C1/2 joint capsule can be opened to denude the articular surface.
Drilling is fluoroscopic guided.
A bone graft can be sited on exposed surfaces to supplement the fusion
Fixation often supplemented with a Dickmann=Sonntag posterior sublaminar wire.
