26 - spinal disorders

define spina bifida

birth defect where there is incomplete closing of the spine and membranes around spinal cord during early development in pregnancy

risk factors for spina bifida

low folic acid before and during early pregnancy

family history of birth defect

diabetes

obesity

sodium valproate (anti-seizure drug)

what is spina bifida aperta

open spina bifida

- meningocele and myelomeningoceles

what is spina bifida occulta

closed spina bifida

usually occurs in lumbosacral region

clinical picture of spina bifida

back swelling

lower motor limb deficit - paraparesis, paraplegia

sensory deficit - hypothesia, anaesthesia

sphincter if disturbance - incontinence or retention w/ overflow

associated back deformities - kyphosis or scoliosis/ clubbed feet/ hip anomalies

most common region for spina bifida to occur

lumbosacral region

meningocele open spina bifida

- site, sac coverings, trans-illumination, deficit, sphincters, hydrocephalus

site = lumbosacral

sac coverings = normal skin less likely to be membranous

sac contents = CSF

translucent

no deficit

usually sphincters intact

hydrocephalus is uncommon

myelomeningocele open spina bifida

- site, sac coverings, trans-illumination, deficit, sphincters, hydrocephalus

site - lumbosacral

membranous sac coverings

CSF and neural tissue contents

transopaque

neuro deficit

double incontinence - bladder and bowel

hydrocephalus is common

treatment of spina bifida

Surgical repair - closure within 24hrs

Ongoing assistance and occupational and physical therapy after repair

what is tethered cord syndrome

inelastic anchoring of caudal spinal cord by abnormally thick or fatty filum terminale - lumbosacral cord is abnormally stretched and elongated so cannot move properly (toward the head)

name the main spinal infections

pyogenic vertebral osteomyelitis and discitis

granulomatous infections

epidural infections

post op infections

what is the most prevalent symptoms or pyogenic vertebral osteomyelitis and discitis

AXIAL pain

most prevalent sign of pyogenic vertebral osteomyelitis and discitis

FEVER

neuro changes seen in pyogenic vertebral osteomyelitis and discitis

radicular weakness and muscle weakness

lab findings in pyogenic vertebral osteomyelitis and discitis

increased OR normal WBC

ESR - more sensitive

raised CRP

blood cultures reveal causative pathogen

urinalysis to rule out UTI infection spread

imaging for pyogenic vertebral osteomyelitis and discitis

plain X-ray

CT

MRI

treatment of pyogenic vertebral osteomyelitis and discitis

first line = IV broad spectrum Abx for 6-8 weeks

identify pathogen

immobilisation for reducing and stabilising pain

surgery indications in pyogenic vertebral osteomyelitis and discitis

appropriate medication fails

patient develops neuro deterioration

spinal instability/deformity

risk factors for post op spinal infection

increased age

obesity

diabetes

tobacco use

poor nutritional status

prolonged surgical time

placement of surgical instruments

what are posts op spinal infections associated with

longer hospital stays

higher complication rate

increased mortality

prevention of post op spinal infections

prophylactic antibiotics 60mins before spinal procedure e.g. flucloaxicillin

additional doses intraoperatively (for prolonged surgical procedures with significant blood loss or gross contamination)

treatment of post op spinal infection

open irrigation and debridement

IV antibiotics for minimum 6weeks then switch to oral

anatomical locations of spinal cord tumours

intradural

extradural

what spinal cord tumours are more common

extradural - metastases

types of intradural spinal tumours

intramedullary

- ependymoma

- astrocytoma

- hemangioblastoma

extramedullary

- meningioma

- neurofibroma

- schwannoma

imaging investigations for spinal cord tumours

plain X-ray and CT

MRI - gold standard

treatment of spinal cord tumours

surgical excision

biopsy

radiotherapy and chemo

clinical features of spinal haematoma

motor weakness

sensory or reflex deficits

acute bowel/bladder dysfunction

epidural and subdural spinal haematoma symptoms

intense knife like pain at location of haemorrhage

subarachnoid haemorrhage symptoms

Thunderclap headache

Worst headache ever experienced

Photophobic (Inability to look at bright lights)

Nausea & Vomiting

Stiff neck

Confusion

Seizure

Loss of consciousness.

meningitis symptoms

imaging for spinal cord haematoma

MRI

treatment for spinal cord haematomas

correction of coagulopathy

emergency surgical decompression if emergent and neurological deficit present

-laminectomy w/o infusion

what is cauda equina syndrome

Surgical emergency results from compressive, ischemic and/or inflammatory neuropathy of multiple lumbar and sacral nerve roots in lumbar spinal canal 

symptoms and signs of cauda equina syndrome

leg pain

weakness

saddle anaesthesia - numb bum

bladder, bowel and sexual dysfunction

decreased anal tone

absence of ankle reflexes

types of cauda equina syndrome

incomplete

- loss or urgency or decreased urinary sensation without incontinence or retention

complete

- urinary and/or bowel retention or incontinence

investigations for cauda equina syndrome

MRI

treatment for cauda equina syndrome

surgical decompression WITHIN 24 HOURS

causes of cauda equina syndrome

Trauma (spinal fractures and dislocations) 

Hameorrhage (spinal epidural haematoma) 

Inflammatory disease (ankylosing spondyllitis) 

Infection (spinal extradural abscess) 

Degenerative spine disease  

Spine tumours (primary or metastasis) 

what are the reflexes

•Biceps reflex (C5-C6) 

•Supinator reflex (C6-C7) 

•Triceps reflex (C7-C8) 

 

•Abdominal reflex (T8-T9/T10-12) 

•Creamasteric reflex (L2-L3) 

 

•Knee jerk (L3-L4) 

•Ankle jerk (S1-S2) 

 

•Anal cutaneous reflex (S2,S3,S4) 

•Bulbocavernosus reflex (S2,S3,S4) 

loss of bulbocavenosus reflex is seen in

spinal shock

conus medullaris and cauda equina lesions

where does the spinal cord end in adults, newborn and fetus

adult - L1/L2

newborn - L3

fetus - S2

function of dorsal column

fine touch

joint position

vibration

proprioception

lateral spino-thalamic tract

pain and temperature

anterior spino-thalamic tract

light crude touch

spinal emergencies

spinal epidural compression: 

• Hematomas – spinal haematomas typically localised dorsally to spinal cord 

Subarachnoid haematomas can extend along the entire length of the subarachnoid space 

• abscess  

Cauda equina and conus syndromes 

primary spinal cord injury

trauma result in immediate death of local cells

• direct damage to cell bodies and/or neuronal processes

• damage to spinal axons -wallerian degeneration (axon and myelin breakdown away from neuron’s cell body)

secondary spinal cord injury

inflammation

vascular events - ischemia and secondary tissue damage

chronic phase of injury - demyelination - scar formation

spinal shock

– transient loss of all neurological function below level of spinal cord injury → flaccid paralysis and areflexia (loss of bulbocavernosus reflex) 

-hypotension (shock) systolic blood pressure usually 80 mmHg 

-duration: 72hrs, typically persists 1-2 weeks, occassionally several months 

causes of spinal shock

interruption of sympathetics - implies spinal cord injury ABOVE T1

loss of vascular tone (vasoconstrictors) - causes bradycardia

relative hypovolemia - skeletal muscle paralysis below level of injury result in venous pooling

true hypovolemia - due to blood loss from associated wouns

how is resolution of spinal shock seen?

return of the bulbocavernous reflex 

complete spinal cord injury

complete loss of motor and/or sensory function below level of injury in absence of spinal shock 

Poor prognosis 

incomplete spinal cord injury

any residual motor or sensory function below level of injury 

Sacral sparing (preserved sensation around anus) 

Voluntary anal sphincter contraction 

Voluntary toe flexion 

types of incomplete spinal cord injury

Central cord syndrome 

Brown-sequard syndrome (cord hemisection) 

Anterior cord syndrome 

Posterior cord syndrome 

most common type of incomplete spinal cord injury

central cord syndrome because central region is a vascular watershed zone

usually results from hyperextension injury in older patients with pre-existing stenosis 

hyperextension injury can result in cord contusion

clinical picture of central cord syndrome

motor - weakness in UL > LL

sensory - loss below level of injury

sphincter - urine retention

recovery pattern of central cord syndrome

LL early recovery

UL late recovery

recovery usually incomplete

anterior spinal cord injury

cord infarction in territory supplied by anterior spinal artery 

causes:

• Occlusion of anterior spinal artery 

• Anterior cord compression e.g. dislocated bone fragment, traumatiic herniated disc 

Presents:

• Paraplegia or quadraplegia if higher than C7 

• Dissociated sensory loss below lesion – loss of pain nd temp sensation (spinothalamic tract lesion) with preservation of two point discrimination, joint position sense, deep pressure sensation (reserved posterior column fucntion) 

brown sequard syndrome

Ipsilateral loss of joint position sense, vibration sense and discrimination (posterior columns) 

Ipsilateral spastic paresis below level of lesion (pyramidal tract) 

Contralateral loss of pain and temp one level below lesion (lateral spinothalamic tract) 

spinal cord injury management

Airway  – hypoxia can further damage injured spinal cord 

Breathing – tension pneumothorax, open pneumo/haemothorax or flail chest should be diagnosed

Circulation – hypotension and bradycardia can be signs of neurogenic shock usually in lesions above C6 (disruption of sympathetic chain). Hypotenison should be treated aiming of MAP of 70 mmHg 

Immobilisation 

secondary assessment of spinal cord injury

Assessment of GCS 

Identify any:

–axial skeleton fractures 

-appendicular skeleton 

-pelvic fractures 

spinal cord injury imaging

• Xray 

AP view, lateral view, open mouth (odontoid view) 

• CT 

• MRI – shows cord compression, haematomas or signal change within the cord 

if a fracture is identified in one part of the spinal column..

the whole spine should be scanned

indications for early decompression

-incomplete spinal cord injury 

-patients with progressive neurological deterioration 

occipital condyle fracture

• Rare 

• Usually stable 

• Mostly due to direct blow to head 

Presentation: 

• Loss of consciousness 

• Cranio-cervical pain 

• Rarely with lower cranial nerve deficits (CN IX – XII) 

atlanto-occipital dislocation

Common in children due to smaller size of occipital condyles,soft tissue laxity 

Mechanism – hyperextension, distraction and rotation 

Clinically –instantly fatal 

-80% of survivors have neurological deficits (lower cranial nerve palsies, complete or spinal cord injuries 

-20% may have normal findings at presentation 

atlas (C1) fracture

anterior or posterior arch with:

intact transverse ligament (stable)

disrupted transverse ligament (unstable)

*Patients usually neurologically intact because the canal is capacious at C0-C1 

fractures of axis (C2)

Fractures of odonotid process

traumatic spondyloisthesis of the axis (hagman's fracture)

fractures of the body of the axis 

subaxial cervical spine fractures

Ligamentous (facet dislocations) 

Osseus (tear-drop and burst fractures) 

thoracolumbar spine injuries

Thoraco-lumbar junction (T12-L1) most frequently affected segment followed by lumbar and thoracic segments 

4 categories: compression, burst, seat belt, fracture-dislocations 

sacral spine injuries

zone 1-3

Zone 1 – rare, produce neurological deficits, either L5 nerve root or sciatic nerve damaged 

Zone 2 – higher incidence of neurological deficits but usually with no sphincter involvement 

Zone 3 – involve the area medial to the foramina and possibly the central canal, predictably have the highest rate of profound neurological deficits. Bowel and bladder dysfunction may also result 

indication for surgical treatment of spine fractures

Occipital condyle avulsion fractures 

Atlanto-occipital dislocation 

C1-C2 displacement more than 5 mm 

Neurological deficits 

Biomechanical instability 

Non-union after 12 weeks of immobilisation