4.

Spinal Pathology
Basic concepts:
Clinical embryology:
- Neural plate= formed by ectoderm triggered by inducing factors released by underlying
notochord.
Neural plate forms  neural groove and closure of neural folds creates neural tube
(neurulation)
Recent evidence: at least 5 waves of closure= required to produce neurulation- this
sequence of events= usually complete within 28 days of conception
- Neural tube gives rise  CNS (brain + spinal cord)
Neural crest give rise  peripheral nervous system
- Anterior neuropore closes @: 24 days
In adults: position = indicated by lamina terminalis
Failure of closure of anterior neuropore= results in forebrain defect + skull & facial
abnormalities
Anencephaly= most common brain defect
- Posterior neuropore closes at: 26-28 days- failure of closure  spina bifida
- Alpha- fetoprotein (AFP) + acetylcholinesterase obtained from amniocentesis= can
identify open neural tube defects in high risk mothers
Serum AFP is routinely measured at 16 weeks of pregnancy

- Role of folate
 Role of folate in neural tube defects= confirmed by several trials
 Recommended: women planning pregnancy= should consume 400 µg of folic acid daily.
 Peri-conceptual dietary folic acid supplementation= reduce incidence of neural tube
defects 50-70%
- Role of genes
 Mutations in genes (VANFL1)= recently identified in familial + sporadic types of neural
tube defects
- Other factors
 Anticonvulsants (especially valproate) taken during pregnancy
 Familial patterns

- Myelomeningocele and meningocele NB (vs)

 Myelomeningocele: a meningeal- lines sac containing spinal cord, spinal nerves or both
and herniates through a spinal body defect – is exposed to an open environment without
being covered by skin
 Meningocele: type of spinal dysraphysm where a sac meninges containing only CSF=
herniating through a bony defect. The sac is covered by normal skin

 Clinical features: NB
- If diagnosis was not made antenatally, on inspection, the placode is elevated from
skin surface (in contrast with meningocele which is covered by normal skin)
- Bulging fontanelle indicates: hydrocephalus
- Cardiovascular abnormalities (bradycardia, apnea) indicate symptomatic Chiari II
- Foot deformities may indicate segmental paralysis
- Neurological deficits= include severe motor and sensory deficits + urinary
abnormalities
Leg mvm in response to painful stimuli- may represent reflex and not voluntary
mvms
- Other abnormalities include: Chiari II hydrocephalus, gyral abnormalities + cardiac/
renal defects
Significant percentage of newborns (20-40%) also have: latex allergy
 Treatment:
- Primarily: surgical closure
If diagnosed prenatally: Caesarean section= preferred in centre with
resident neurosurgeon
Collaboration with plastic surgeons + use of rotational flap = results in
aesthetically good outcome
- Closure should be performed in <24h (6-12h ideal)
If infant has other abnormalities- which do not allow GA- closure can be
delayed+ further under cover of broad spectrum antibiotics
- Prognosis has improved in last few years
If untreated: 1yr 30% survival, 2 yr 20% survival
After prompt and continuous tx: >85% of children= alive at 5yr age
± 70% = IQ > 80
- Lipomyelomeningocele
 Lipomyelomeningocele= herniation of adipose tissue, attached caudally
to conus/ dorsally to spinal cord, through bony defect to sacrolumbar
subcutaneous tissue- commonly leads to  spinal cord tethering
 Clinical features:
- Physical findings include presence of a midline/ paramedian
lumbosacral subcutaneous lipoma, skin, haemangiomas and skin
dimples
- Orthopaedic findings include scoliosis and foot deformities
- Neurological findings include asymmetrical motor deficits, patchy
sensory deficits and urinary bladder symptoms
 Treatment:
- Either conservative mx with close follow up/ early surgical
intervention with untethering of spinal cord
 Prognosis:
- Children with LMM have normal IQ + can walk (95%)- but have
significant risk of bladder dysfunction and frequent UTI’s

- Tethered cord Syndrome (TCS) NB – Physical findings

 TCS= unelastic anchoring of caudal spinal cord by an abnormally thich/
fatty filum terinale/ by tumours, myelomeningoceles, LMM, scars +
dural bands
 As result” lumbosacral spinal cord= abnormally stretched+ elongated so
that it cannot move in cephalad direction during spinal mvms
 Patients may present with neurological, urological + orthopaedic
symotom + signs
 Clinical features: NB
- Physical findings: midline lipomas, dermal sinus tract, cutaneous haemangiomas +
lumbosacral hair patch
- Neurological findings : a mixed picture of upper+ lower motor neuron symptoms,
asymmetrical motor defects, usually patchy sensory deficits, unsteady gait + delayed
growth
- Orthopaedic findings : scoliosis, lumbosacral lordosis, pes cavus, claw toes, leg +
foot asymmetry’
- Urological findings : urinary incontinence, frequent urinary tract infections
 Treatment:
- Depends on number of factors- including presence of co-existing congenital
malformation, clinical course+ imaging features

- Degenerative spinal Disease NB know table

Cervical spondylosis:
 Cervical spondylosis= general term used to indicate:
age-related/ repeated stress- related degenerative
 changes of intervertebral discs, vertebral end-plates, facet and uncovertebral joints +
ligaments flavum, individually/ in combination= narrow spinal canal and/ or nerve root
foramina

 Epidemiology:
- More common in males, may be associated with lumbar stenosis
- Spondylotic changes occur in > 50% of patients after 5th decade,
- <20% become symptomatic

 Natural history:
- Onset= usually insidious – with progressive deterioration+ intervening stable
intervals
- Slow deterioration occurs in 20% of pt.’s, 5% remain static + 75% develop new
symptoms + signs
 Clinical presentation
- neck + shoulder pain associated with stiffness in most common presentation
- pt.’s often describe Lhermitte;s sign, on electric shock-like sensation traveling from
neck downwards with neck flexion
- radiculopathy secondary to n. root compression (usually at foramen)= typically
follows neck pain after months/ years
- symptoms may be similar to cervical disc prolapse-but onset= less acute
- pain is sharp + shooting + increased with neck mvm + coughing

- Typical findings in nerve root compression NB

Nerve root C5 C6 C7 C8 T1

Disc space C4/5 C5/6 C6/7 C7/T1 T1/2

Pain medial scapula, Medial scapula, Posterior arm Medial arm and Medial arm
upper arm arm and lateral forearm
hand
Weakness Shoulder Elbow flexion Elbow Finger Finger
abduction extension extensors abduction
Muscles. Deltoid, biceps Biceps, Triceps Wrist & finger Intrinsic mm.
Brachioradialis extensory carpi extensors & of hand
radialis flexors
Reflex None Biceps & Tricepts None None
bracioradialis
Numbness Over deltoid Thumb, lateral Index + middle 4th and 5th Axilla
border of hand fingers fingers
 Myelopathy – typically manifests with gait difficulties, asymmetric spastic paraparesis +
clumsy hands
acute neck hyperextensions- may produce “ man in the barrel” syndrome- arms very weak
( ant. Horn cells)- but leg function (lateral columns)= preserved
 Radiculopathy – can also occur
Pts. preent with LMN signs at level of impingements + UMN sings below this level
 Examination
 - Flexor mm. usually affected more than extensor mm.
- Ant. Column compression produces fasciculation’s and m. wasting
- Post. Column compression produces sensory ataxia + loss of joint position sense +
vibration
- Physical signs include:
 Babinsky sign
 Hoffman’s sign
 Clonus
 Clasp-knife rigidity
 Imaging
- T1W MRI can show disc bulges, bony osteophytes compressing nerve roots +
effaced CSF spaces around spinal cord
- T2W MRI may show high spinal cord signal (myelomalacia) in addition to n. root/
spinal cord compression
- T2 GRE shows uncovertebral joint hypertrophy better

 Treatment
- Conservative management: NB - Surgical management
Trial of NSAID’s + m. relaxants can Indication for surgery:
be tried initially. Non-  Persistent severe arm pain (>6weeks)
pharmacological, non-surgical mx  Motor/ significant sensory deficit
consist of:  Clinical Myelopathy
 Physiotherapy  Radiological spinal cord compression
 Soft+ rigid neck braces Possible surgical options include:
 Traction +manipulation  Laminectomy
 Thermal therapy  Laminoplasty
 Acupuncture  Corpectomy
 Facet block
 - Low back pain
 Epidemiology:
 Axial low back pain= 2nd most common cause for medical consultation (after UTI)=
affect 2/3 adults at least once in their lifetime
 LBP= most common + expensive work-related disability in patients <45 yrs old
 ± 90% of pt.’s with: non-specific LBP =recover in 2 weeks- recurrences= common (40%
within months)
 In pt.’s with improving symptoms- majority usually return to work <1month
 Examination
 History
- Thorough evaluation= required to exclude other degenerative spinal diseases, visceral
pathologies, spinal infections, spinal tumours + inflammatory spinal conditions.
Sciatic pain increases with increased intra-abdominal pressure (coughing, sneezing)
- Yellow flags: psychological risk factors, including: psychological distress,
compensation claims+ job dissatisfaction
 Can predict long-term outcome + indicate need: holistic approach
- Red flags: symptoms + signs  serious pathology: ± 33% of pt.’s = report risk
factor & 1-10% will have specific pathology
 Assess red flags regularly
 Physical examination
- Observe: walking, sitting and standing. Ax: Spinal mobility + spinal curvatures
- Ax: Paraspinal mm. + joints + straight- leg raise show: lumbosacral radiculopathy
- Peripheral pulses= assessed
- Full neurological examination= performed with emphasis on: motor and sensory
deficits
- Imaging:
 Plain x-rays= limited value except as an initial test to investigate bony
pathology, inflammatory sacro-illitis/ mobile spondylolisthesis
 CT better elucidates bony pathology
 MRI= show: n. root/ cord compression infection, tumour+ degenerative changes
 Treatment
 Pharmacological tx:
- NSAID’s can be effective
- M. relaxants can be moderately effective
- Tricyclic+ tetracyclic antidepressants = effective in treating pt.’s wiith acute LBP and
no clinical depression
 Physiotherapy can improve disability by 5-10%
 Pain clinic
 TENS can be effective
 Glucocorticoid/ anaesthetic injections to facet joint, epidural space/ trigger points =
limited improvement
 Surgical mx: acute LBP
- Indications remain controversial. Prerequisites in patient selection include:
Determination to improve Normal psychosocial history Absence: pending litigation/ claims
Lumbar disc disease
 Anatomy of lumbar disc:
 Central nucleus pulposus= surrounded by: annulus fibrosus  composed: 2 layers :
intertwined annular bands
 Inner layers= attached to cartilaginous end plates
 Outer layer= attached to vertebral end-plate
 Healthy adult disc: few (if any) blood vv.  derives nutrition from capillary beds of
interosseous aa. in vertebral end plates. Small-molecule nutrients: Oxygen & glucose=
supplied to disc cells by: diffusion
 Meningeal branch: spinal n. (Sino vertebral n.) enters spinal canal & divides  ascending
+ descending branches= fuse those from adjacent vertebrae.  give off transverse
branches  PLL and posterior layers of annulus fibrosus
Pathology:
 Lumbar disc degeneration + herniation= biomechanical + biochemical changes
 Disc generation starts with: breakdown of aggrecan molecule- present in: nucleus
pulposus + annulus fibrosis of mature disc decreased water content : nucleus
 Loss: hydration: nucleus pulposus= stress transmission to periphery rather than centre of
endplates= increased size: end plates+ decreased ROM
 Defect :annulus fibrosus =  disc herniation  induce: inflammatory response

Epidemiology
 Sciatica from herniated lumbar disc= most common cause for: radicular pain, usually
affecting: 1%: population/ year
 Incidence peaks: between: 24-45yrs: age
 Slight male predominance (1,3-2:1)
 95% of herniations occur with equal frequency @: L4-L5 + L5-S1 levels
Natural history vs surgery
 Maine Lumbar Spine Study=10yr prospective cohort study- outcomes: pt’s with sciatica
from lumbar disc herniation. Analysed: tx: surgically + non-surgically
 Surgical treated pt.’s= more complete pain relieved+ improved F+ satisfaction
 Improvement of symptoms + work+ disability outcomes= similar in 2 groups

Clinical features:
 Presentation:
 Onset: acute/ gradual
 Distribution: pain & motor & sensory deficits= determined by root involved
 
In lumbar spine: n. root exist around pedicle of corresponding cephalad vertebra
e.g.: L4 root exist in L4/5 space
 Physical examination:
 Pt. should be observed for spinal alignment + pelvic tilt
 Same check list as with LBP

 Clinical features of herniated lumbar discs NB

Nerve root L3 L4 L5 S1
Disc space L2/3 L3/4 L4/5 L5/S1
Weakness Hip flexion Ankle dorsiflexion Great toe Ankle plantar flexion
Knee extension extension
Muscles Iliopsoas, Medial hamstrings, Ext. halluces Gastrocnemius
quadriceps tibialis anterior longus
Reflex Knee Med. hamstrings Achilles
Numbness Ant. Thigh Med. malleolus Dorsum of foot Lateral foot
Med. knee

 Imaging:
 x-rays= reveal loss: disc height, facet hypertrophy, end-plate sclerosis+ spondylolisthesis
 Myelography: (rarely used) show: prolapsed discs as extradural mass pressing on theca
 CT show: prolapsed dics as soft tissue mass at. To t heca
 MRI:
 T1W shows prolapsed disc as isointense soft tissue mass
 T2W shows iso-or hyperintese signal
 Herniated disc material- does not enhance with contrast
 Treatment
 Conservative
 Surgical- laminectomy + discectomy

- Cauda equine syndromes (CES) NB

 Usually secondary to central/ centrolateral lumbar disc herniation + includes:
- Low back pain/ sciatic
- Motor deficits (may progress to paraplegia)
- Sensory deficits (± saddle anaesthesia
 - Bladder &/or bowel dysfunction + erectile dysfunciton
 Not all disturbance required to diagnose CES but: bladders &/or bowel dysfunction
typically herald CES onset- more implicit in CES diagnosis
 Incomplete CES:
- Altered urinary sensation
- Loss of desire to void, Poor urinary stream
- Need to strain to micturate
 Complete CES:
- Painless retention
- Dribbling due to overflow incontinence
 Epidemiology:
- Only 2% of all herniated lumbar discs=  CES
- Incidence: ± 1/ 50000 people
- Delay in mx: CES= reason for: medicolegal claims 50% :claims= successful
 Pathophysiology:
- Parasymhatic involvement of sphincters + perineal anaesthesia= at all level- but:
motor deficits= not always present. Lower level=less likely: motor deficit
- Pain + parasympathetic function= subserved by small myelinated+ unmyelinated
fibres sensitive to compression/ ischaemia- but not power, light touch, joint position
sense= subserved bylarge fibres resilient to pressure
 Imaging:
- MRI = need to be obtained without delay when suspect CES
Levels of prolapsed disc/ unusual causes: CES= easily demonstrated
 Treatment:
- Urgent surgical decompression with laminectomy + discectomy = standard tx
 Risk: continuing deficits for pt.’s who underwent surgery after >48hrs
compared to pt. who underwent surgery <48 hrs were:
 Urinary deficits x 2.5
 Rectal dysfunction x9.5
 Motor deficits x9.1
 Sensory deficits x 3.5
- Red flags in spinal disease:
1. Cancer/ infection 2. Spinal fracture 3. Cauda equine
 Age>50 or <20 yrs  History of significant trauma syndrome
 History of cancer  Prolonged use of steroids (CES)
 Unexplained weight loss  Age > 70 yrs
 Immunosuppression
 UTI, IV drug abuse, fever/ chills
 Back pain- not improved with rest
- Acute Spinal Cord Injuries
 ASIA/ ICoS exam chart (ASIA Impairment Scale):
Grade A - Complete lack: motor and sensory function below
level of injury (including anal area)
Grade B - Some sensation below level of injury (including
anal sensation)
Grade C - Some m. mvm is spared below level of injury
- 50% of mm. below level of injury= cannot move
@ gravity
Grade D - Most ( >50%) of mm. spared below level of
injury= strong enough to move @ gravity
Grade E - All neurologic Function has returned

Frankel Classification of spinal Cord injury:

A. Complete: no motor or sensory function

B. Sensory only: some sensation preserved

No motor function
C. Motor useless: some sensory and motor function
but motor function not useful
D. Motor useful: sensory function preserved. Motor
function weak but useful
E. Intact: normal sensory and motor function

- Central cord injury

Pneumonics: MUD
 motor >sensory loss
 upper> lower extremity loss
 Distal > proximal m. weakness
 Classically occurs with hyperextension injuries of cervical spine

- Anterior Cord Syndrome

 loss of motor function + pain & temperature sensation
 preservation of light touch, vibratory sensation + proprioception

- Brown- Sequard Lesion

 Loss: ipsilateral, proprioception, light touch, motor function
 Loss: contralateral pain + temperature sensation
 Due to hemisection of cord due to penetrating injury
 Incomplete lesions= most common

- Conus medullaris syndrome

Injury to sacral cord, lumbar nerve roots, causing:
 Areflexic bladder
 Loss of control of bowels
  Knee jerk reflexes preserved, ankle jerk absent
 Signs similar to cauda equine syndrome except more likely to be bilateral

- Cauda Equina Syndrome

 Injury to n. roots and not spinal cord itself
 M. weakness + decreased sensation unaffected dermatomes
 Decreased bowel and bladder control

- Spinal shock
 Temporary COMPLETE cessation of spinal cord function
 Occurs IMMEDIATELY after injury
 Complete loss of all reflexes- including: bulbocavernosus
 Flaccidity of all mm.
- Neurogenic Shock
 Caused by high spinal cord injury
 Slow pulse
 Low blood pressure
 Treatment:
 R/O haemorrhage + other causes of hypotension
 Fluids, Trendelenburg
 Alpha adrenergic drugs
 Other problems:
 Inadequate ventilation
 Change in clinical signs due to absent sensation

Spinal shock vs. neurogenic shock:

Spinal shock
- Due to acute spinal cord injury
- Absence of all voluntary + reflex
neurologic activity below level of
injury:
 Decreased reflexes
 Loss of sensation
 Flaccid paralysis below injury
- Last days to months (transient)
- Spinal shock and neurogenic shock
can in be in same pt. BUT not
same disorder
Neurogenic shock
- Hemodynamic phenomenon:
 Loss of vasomotor tone
 Loss of sympathetic nervous system tone
 Impaired cellular metabolism
- Critical features:
 Hypotension: due to massive vasodilation
 Bradycardia: due to unopposed parasympathetic
stimulation
 Poikilothermia: unable to regulate temperature
- Occurs:
 Within a 30min cord injury level T5/ above: last up to
6 weeks: also due to effect some drugs that effect
vasomotor center of medulla as opioids,
benzodiazepines
- Management:
 Airway support
 Fluids as needed – typicall 0.9 NS, rate depends upon
need
 Atropine for bradycardia
 Vasopressors as phenylelphrine: neo-synephrine for
Bp support