3. Early stages
Following fertilisation, the nervous system begins to form in the 3rd week of
development.
At the end of week two, a structure called the primitive streak appears as a groove
in the epiblast layer of the bilaminar disk.
Cells within the epiblast migrate downward through the primitive streak, giving rise
to three layers from the initial two.
4. Early stages
These three germinal layers form the trilaminar embryonic disk:
1. Endoderm – innermost layer
2. Mesoderm – middle layer
3. Ectoderm – outermost layer
The nervous system is derived from the ectoderm, which is the outermost layer of
the embryonic disc.
5.
6. Notochord development
Cranially, in the embryonic disc,
endoderm cells contribute to the
prechordal plate, an important
organizing center for head and brain
development.
Caudally, endoderm cells in the midline
detach from the endoderm to form the
notochord.
The notochord is considered to be a
mesoderm derived structure.
7. Notochord and prechordal plate are organizing centers, that produce the
morphogen, Sonic hedgehog (Shh)
Shh is essential for normal development of the brain and head region as well as
the spinal cord, spine and major musculoskeletal elements of the torso and limbs.
8. By the 19th day, there are three distinct columns on either side of the midline
1. Medial paraxial columns, which give rise to the somites
2. Intermediate mesodermal columns, which form the urogenital organs
3. Lateral mesodermal plates, which form the gut cavities.
In considering the development of the spine, attention is focused on the medial
paraxial columns.
The juxtaposition to the intermediate columns may help explain, however, why
abnormalities of the urogenital tract are frequently associated with vertebral
anomalies.
9.
10. Neurulation
Neurulation is the process that initiates development of the nervous system.
It begins in the 3rd week with the appearance of the neural folds in response to
sonic hedge hog (Shh), secreted by the notochord.
11. Under the influence of Sonic hedgehog (Shh) secreted by the notochord, midline
surface ectoderm thickens to become neural ectoderm.
The raised lateral edges of the neural ectoderm are called the neural folds.
Neural folds become elevated and approach one another dorsally in the midline,
surrounding the neural groove.
Eventually the neural folds meet in the posterior midline, where they fuse to form
the neural tube.
As the neural folds fuse, cells at the lateral edges undergo epithelial to
mesenchymal transformation and become detached to form the neural crest.
Neural crest cells migrate throughout the body of the embryo to form components
of the peripheral nervous system among other important tissues.
14. Neural tube
Fusion of the neural folds occurs simultaneously in
rostral (cranial) and caudal directions.
At day 23, the middle of the neural tube has sunk
beneath the surface ectoderm and is flanked on each
side by somites.
Cranially, the unfused neural folds surround the
anterior neuropore. Caudally, they surround the
posterior neuropore.
Completion of the cranial end of the neural tube is
around day 25 with closure of the anterior neuropore.
The caudal end of the neural tube is complete with
closure of the posterior neuropore around day 28 at
the end of the 4th week.
15. Failure of the anterior neuropore to close results in profound malformations of the
brain and skull, a condition referred to as anencephaly.
Failure of the posterior neuropore to close results in spina bifida, characterized by
defects of the vertebrae of the caudal end of the vertebral column, meningeal
herniation among others.
16. Later development
Cranial end of the neural tube forms the brain and cerebellum.
Caudal end develops to form the spinal cord.
Cells on the dorsal side form the alar plate, which subsequently becomes the
dorsal horn.
Cells at the ventral end form the basal plate, which then becomes the ventral horn.
17. Somites
The dorsolateral cells become the dermomyotomes. These eventually give rise to
the skin (lateral) and muscle (medial) overlying the spine.
The ventromedial cells within the somite become the sclerotomes. These are the
precursors of the skeletal components (vertebrae) of the spine.
The neural tube is fated to become the spinal cord.
20. The spinal cord is a continuation of the brainstem.
It extends from Foramen magnum at the base of the skull to the L1/L2 vertebra
where it terminates as the conus medullaris (medullary cone).
A thin thread called filum terminale extends from the tip of the conus medullaris all
the way to the 1st coccygeal vertebra and anchors the spinal cord in place.
25. Composed of 7 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 4–5 coccygeal vertebral
segments.
Highly specialized anatomy of the upper cervical spine allows weight transfer between
the head and neck, facilitates neck motion, and protects the neurovascular elements
from injury.
In the upper cervical spine, flexion is limited by the bony anatomy, while extension is
limited by the tectorial membrane.
Rotation and lateral bending are restricted by the contralateral alar ligaments.
The cruciate ligaments restrict potentially dangerous anterior translation during flexion,
while still allowing torsion around the dens.
Distraction >2 mm is prevented by the tectorial membrane and alar ligaments.
Translation is limited by the facet joints when the tectorial membrane and alar
ligaments are intact.
26. TR: Transverse atlantal ligament, part of cruciate ligament. Strong. Prevents atlantoaxial subluxation.
AP: Apical ligament
AL: Alar ligament
Tectorial membrane: Cranial continuation of posterior longitudinal ligament.
27. Thoracic and lumbar spine
Vertebral bodies are separated by intervertebral disks.
The posterior elements are composed of paired pedicles, lateral masses, facet
joints, laminae, transverse processes, and a single spinous process.
The transverse process contains the transverse foramen, through which the
vertebral artery (the first major branch of the subclavian artery) passes.
28. Thoracic and lumbar spine
The motion segments are stabilized by three structures:
1. Anterior longitudinal ligament running on the ventral aspect of the vertebral
bodies from the foramen magnum to the sacrum
2. Posterior longitudinal ligament running on the dorsal aspect of the vertebral
bodies from the foramen magnum to the sacrum (its cranial extent between
C2 and the occiput is referred to as the tectorial membrane)
3. Posterior ligamentous complex (PLC). The anatomical structures of the PLC
include the supraspinous ligament, interspinous ligament, ligamentum flavum,
and facet joint capsules
29.
30. Vertebral columns
● Anterior column
➔ Anterior longitudinal ligament
➔ Anterior annulus
➔ Anterior 2/3rd of vertebral body
● Middle column
➔ Posterior 1/3rd of vertebral body
➔ Posterior annulus
➔ Posterior longitudinal ligament
● Posterior column
➔ Posterior elements:
-Pedicles, facets
-Lamina
-Spinous process
➔ Posterior ligaments
Unstable: If middle column + Anterior OR Posterior column is damaged
35. Indirect trauma
Hyperflexion injury
● Fall in bent position
● Deceleration
● Wedge fracture
● Stable
● Usually no spinal cord injury
Hyperextension injury
● Sudden acceleration
● Blow on face
● Includes Hangman fracture
● Can cause fracture of arch of atlas
and axis
● Spinal cord may be injured
36.
37. Compression injury
● Fall from height on foot
● Fall on head
● Heavy object falling on head
Includes burst fracture
Usually stable fracture
Usually no spinal cord injury
42. Myotomes
Upper limbs
C5: Deltoid
C6: Wrist extensors
C7: Elbow extensors
C8: Long finger flexors
T1: Small hand muscles
Lower limbs
L2: Hip flexors
L3,4: Knee extensors
L4,5 - S1: Knee flexion
L5: Ankle dorsiflexion
S1: Ankle plantar flexion
43. Frankel classification of spinal injury
● Grade A: Complete neurological injury - No motor or sensory function
detected below level of lesion
● Grade B: Preserved sensation only - No motor function detected below
level of lesion, some sensory function below level of lesion preserved
● Grade C: Preserved motor, nonfunctional - Some voluntary motor function
preserved below level of lesion but too weak to serve any useful purpose,
sensation may or may not be preserved
● Grade D: Preserved motor, functional - Functionally useful voluntary motor
function below level of injury is preserved
● Grade E: Normal motor function - Normal motor and sensory function
below level of lesion, abnormal reflexes may persist
46. Suspect spinal injury
Head injury or severe facial or scalp lacerations
Recent trauma with neck/spinal pain
Inability to assess neck pain because of:
● Secondary distracting injury
● Abnormal neurological findings
● Transient neurological symptoms
Physical signs of spinal trauma (Ecchymosis or abrasions)
47. Spinal shock
Temporary dysfunction of spinal cord with loss of sensorimotor function and
reflexes caudal to the level of injury.
Manifested by absence of anal wink, bulbocavernous reflex and flaccid paralysis.
Mechanism is unknown, may be due to effect on impulse conduction.
Phases 1-4
1: 24-48 hours. Areflexia or hyporeflexia
2: 1-2 days. Polysynaptic reflex return. Usually bulbocavernosus
3: 1-4 weeks. Hyperreflexia.
4: 1-12 months. Hyperreflexia and spasticity
48. Neurogenic shock
Hypotension + Bradycardia
Due to disruption of sympathetic pathway within the cord
Common in cervical and upper thoracic spinal cord injury
Hypotension due to decreased systemic vascular resistance
Bradycardia due to unopposed vagal activity
Can be differentiated from hypovolemic shock due to presence of relative
bradycardia.
49. Cauda equina syndrome
Etiology: Compression of cauda equina by
herniated disk, tumor, abscess
Clinical findings:
Urinary retention followed by incontinence
Post void residual urine >100mL
Bowel retention
Saddle anesthesia
Lower extremities flaccidity (LMN)
Loss of DTR
Loss of rectal tone
50. Conus medullaris syndrome
Conus medullaris lies opposite to vertebral bodies of T12 and L1
Caused by flexion distraction injuries and burst fractures
Both UMN and LMN deficits occur
Development of neurogenic bladder
52. ATLS protocol
Airway maintenance and cervical spine stabilization
Breathing and ventilation
Circulation with bleeding control
Disability/neurology assessment
Exposure and environment control
53. Radiology investigations
X-ray C-spine
Chest X-ray
Pelvis X-ray
CT Scan: Sagittal view detects 85% of spinal fractures
MRI: Soft tissue injuries, central canal compromise, Spinal cord injury and edema
57. Stabilization
First goal in treatment is stabilization.
Cervical traction and collar
Log roll for examination and transport
Long backboards: Used for transportation only, Decubitus ulcer can form after 30-
60 minutes.
58.
59. High dose methylprednisolone
National Acute Spinal Cord Injury Studies (NASCIS) II and III trials
Cochrane Database of Systematic Reviews article of all randomized clinical trials
Significant improvement in motor function and sensation in patients with complete
or incomplete spinal cord injuries (SCIs) who were treated with high doses of
methylprednisolone within 8 hours of injury.
Methylprednisolone 30 mg/kg bolus over 15 minutes and an infusion of
methylprednisolone at 5.4 mg/kg/h for 23 hours beginning 45 minutes after the
bolus.
60. Controversy regarding high dose steroids in SCI
Congress of Neurological Surgeons (CNS) has stated that steroid therapy "should
only be undertaken with the knowledge that the evidence suggesting harmful side
effects is more consistent than any suggestion of clinical benefit."
American College of Surgeons (ACS) has modified their advanced trauma life
support (ACLS) guidelines to state that methylprednisolone is "a recommended
treatment" rather than "the recommended treatment."
American Association of Neurological Surgeons (AANS) recommend against the
use of steroids early after an acute SCI. The guidelines recommend that
methylprednisolone not be used for the treatment of acute SCI within the first 24-
48 hours following injury.
62. Surgical intervention
Timing: No standard recommendations.
Surgical intervention for spinal injury can be deferred in presence of other life
threatening injuries.
Emergent decompression of the spinal cord
● Progressive neurologic deterioration
● Facet dislocation
● Bilateral locked facets
● Spinal nerve impingement with progressive radiculopathy
● Extradural lesions such as epidural hematomas or abscesses
● Cauda equina syndrome
63. Surgical Treatment for Acute Spinal Cord Injury Study (STASCIS)
Conducted by the Spine Trauma Study Group
Ongoing
Preliminary data
24% of patients who receive decompressive surgery within 24 hours of their injury
experience a 2-grade or better improvement on the ASIA scale, compared with
4% of those in the delayed-treatment group.
Cardiopulmonary and urinary tract complications were found to be 37% in the
early surgery group compared with the delayed group rate of 48.6%
