spinal cord injury - bowen university

MANAGENT OF SPINAL CORD INJURY

ODEBODE T.O.

1

Outline

• Definition/Introduction • Epidemiology • Causes of SCI • Relevant anatomy • Pathophysiology of SCI • Mechanisms of spine injuries • Classification of SCI • (a)Primary and secondary SCI • (b)Complete and incomplete SCI • Treatment of SCI • Rehabilitation

2

Definition & Introduction

• Spinal cord injury (SCI) is an insult to the spinal cord

resulting in a change, either temporary or permanent,

in the cord‘s normal motor, sensory, or autonomic

function.

• Traumatic spinal cord injury (SCI) is a life changing

neurological condition with substantial

socioeconomic implications for patients and their

care-givers.

• Patients with SCI usually have permanent and often

devastating neurologic deficits and disability.

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Definition & Introduction

• Recent advances in medical management of SCI has

significantly improved diagnosis, stabilization,

survival rate and well-being of SCI patients.

• However, there has been only small progress made on

treatment options for improving neurological

outcomes of SCI patients

• Most important aspect or focus of clinical care is

prevention of complications related to disability.

• Supportive care has been shown to decrease

complications related to mobility

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Epidemiology

• Trauma to the spine occurs in approximately 2-5/100,000 population in the US

• About 12,500 new cases of SCI occur each year in North America

• Incidence in our setting not yet determined

• More than 90% of SCI cases are traumatic in origin

• They are due to traffic accidents, violence, sports or falls

• Male-to-female ratio = 2:1

• SCI occurs more frequently in adults than children

• Men are mostly affected during their early and late adulthood (3rd and 8th decades of life)

• Women are at higher risk during their adolescence (15–19 years and 7th decade of life)

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Epidemiology

• Age distribution is bimodal

• 1st peak involves young adults & 2nd involves adults >60yrs

• Adults > 60 years who suffer SCI have worse outcomes

than younger patients

• Their injuries usually result from falls & age-related bony

degenerative changes

• SCI outcomes depend on severity & location of lesion

• May include partial or complete loss of sensory and motor

function below the level of injury.

• Majority of SCI do not affect the spinal cord or exiting

nerve roots (i.e. only bones being affected in a majority)

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Epidemiology

• Generally, lower thoracic lesions cause paraplegia while cervical lesions result in quadriplegia

• About 10% of cases of SCI will result in quadriplegia

• Single most commonly affected vertebral level is C5

• Cervical spine is typically most affected (50%)

• Thoracic spine (35%)

• Lumbar spine (11%).

• Survival rates for patients with tetraplegia and paraplegia is 91.2% and 95.9%, respectively→

• 40-year survival rate of these individuals (with tetra/paraplegia) = 47% and 62% respectively

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Causes of SCI: Traumatic

• N.B: Damage to the vertebrae, ligaments or discs of the spinal column & the spinal cord results most commonly from trauma than from non-traumatic causes.

• Traumatic causes of SCI

• MVA (Auto & motorcycle): Commonest → fractures, subluxation, dislocations, crushes, or compression

• Gunshot

• Physical assaults with stab/knife wound (penetrating injury)

• Falls

• Sporting

• Industrial accidents

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Non-traumatic causes

• Arthritis

• Cancer

• Inflammation

• Infections

• Disc degeneration

• Polio

• Spina bifida

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SPINAL ANATOMY

Vertebral canal: formed by vertebral

foramina of 7 cervical, 12 thoracic, 5

lumbar, and 5 sacral vertebrae

Spinal cord (SC): is located within the

canal

Extends from foramen magnum to level

of 1st & 2nd lumbar vert. below

At birth extends to 2nd/3rd lumbar vert.

Divided into 31 segments; each with

pair of ant. (motor) and dorsal (sensory)

spinal nerve roots. Include:

8 cervical (C) segments

12 thoracic (T) segments

5 lumbar (L) segments

5 sacral (S) segments

1 coccygeal (Co) segment - mainly

vestigial

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Cervical Vertebrae

N.B: Generally, Neurosurgeons manage all cervical pathologies while the

Orthopedic and traumatology Surgeons handle thoraco-lumbosacral

pathologies (except tumours).

Cervical vertebrae

• There are 7 cervical vertebrae

• They extend from base of skull above to 1st thoracic vertebra below

• Consist of 4 typical and 3 atypical vertebrae

• Typical C-vertebrae include C3, C4, C5 and C6.

• Atypical C-vertebrae include C1 (Atlas), C2 (Axis) and C7 (vertebra

prominens)

• All vertebrae except C1 and C2 consist of two broad portions:

Body: Large, central mass of bone.

Vertebral arch: consisting of

(a) a pedicle which connects the body to the articular processes

(b) a lamina that connects the articular processes to the spinous process. 11

Typical Cervical Vertebrae

(Typical Features)

Typical cervical vertebrae C3-C6 are characterized by:

1.Small size

2.Transverse foramina

3.Saddle-shaped body

4.Bifid spinous process that

bifurcates at its distal end

Exceptions to these are

C1 (no spinous process) &

C7 (spinous process is

longer than that of C2-C6

and may not bifurcate)

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Atypical cervical vertebrae [Features] Of the 7 cervical vertebrae,

Atlas (C1), axis (C2) and vertebra prominens (C7) are considered atypical

Atlas (C1):

Lacks a body and spinous process

Has anterior and posterior arches with lateral masses.

Superior articular surfaces articulate with occiput at the atlanto-occipital

joints.

Inferior articular surfaces articulate with the axis at the atlanto-axial joints.

Axis (C2): Unique with an odontoid process (the dens) projecting from its

superior surface.

Vertebra prominens (C7):

Has the longest and most prominent spinous process of all cervical vertebrae.

However, the spinous process remains non-bifid.

(N.B: The above features gave rise to its name)

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Atypical cervical vertebrae - C1 & C2

C1 – atlas C2 – axis

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Atypical cervical vertebrae - C7

(Vertebral Prominens)

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Thoracic vertebrae

• Thoracic vertebrae have bodies of intermediate size.

• Distinguished by their

• Long, slender spines

• Presence of facets on the sides of the bodies articulating with the heads of the ribs

• Facets on the transverse processes articulating with the tubercles of ribs

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Atypical thoracic vertebrae

• Of the twelve thoracic vertebrae, five are alleged to be atypical.

• They are T1 & T9-T12

• While sharing many similarities with the 7 typical thoracic vertebrae, T1 and T9 to T12 have specific characteristics that make them easily identifiable.

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Lumbar Vertebrae

• The lumbar spine (lower back) begins below the T12 (or last) thoracic vertebra and ends at the top of the sacrum (S1).

• Most people have 5 lumbar levels (L1-L5), but it is not unusual to have 6.

• Each lumbar spinal level is numbered from top to bottom—L1 through L5, or L6.

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Sacral vertebrae

Sacrum forms lowest end of spine

Lies between 5th lumbar vert. (L5) and

the coccyx (tailbone).

Triangular in shape

Consists of five segments (S1-S5) that

are fused together.

Components

First 3 sacral vert. have transverse

processes that form lateral wings or

‗alae‘ which articulate with the ilium

(via sacroiliac joint) of the pelvis

Forms posterior wall of pelvis

Contains four openings on each side of

midline thru which sacral nerves and

blood vessels run.

The Sacral canal which runs thru the

center of sacrum represents the end of

the vertebral canal.

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Spinal Cord Anatomy

• Spinal cord: extends from below the medulla oblongata (base of skull) above and terminates at the conus medullaris (lower margin of L1 or upper margin of L2 vertebral body) below.

• Below this level, spinal canal contains the lumbar, sacral, and coccygeal spinal nerves constituting the cauda equina.

• Injuries below L1 (termination of SC) are therefore not considered as spinal cord injuries ‗cause they involve segmental spinal nerves and/or cauda equina.

• Injuries above L1 (termination of SC), often involve a combination of spinal cord, segmental root or spinal nerve injuries.

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Spinal cord and nerve roots-anatomy

The spinal nerves consist of:

Sensory nerve roots: enter spinal cord at each level while

Motor roots: emerge from the cord at each level.

Spinal nerves: are named and numbered according to the site of their emergence from the vertebral canal.

C1-7 nerves emerge above their respective vertebrae.

C8 emerges between the seventh cervical and first thoracic vertebrae.

Remaining nerves emerge below their respective vertebrae.

On each side, the anterior and dorsal nerve roots combine to form the spinal nerve as it exits from the vertebral column through the neural foramina.

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Neural Pathways

Spinal cord: Is organized into a series of tracts/neural pathways caring motor (descending) and sensory (ascending) information.

Corticospinal tracts:

Descending motor pathways located anteriorly within SC

Axons extend from cerebral cortex, decussate in the medulla before entering the spinal cord → enter into corresponding spinal segment & synapse with motor neurons of the anterior horn cells.

Lateral spinothalamic tracts:

Transmit pain and temperature sensation.

Usually decussate within 3 segments of their origin as they ascend.

Anterior spinothalamic tract: Transmits light touch

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Neural Pathways

Dorsal columns

Constitute ascending sensory tracts

Transmit light touch, proprioception, vibration information and position sense to the sensory cortex.

They do not decussate until they reach the medulla.

Autonomic function

Autonomic function is transmitted in the anterior interomedial tract.

Sympathetic nervous system fibers exit from the spinal cord between C7 and L1.

Parasympathetic system nerves exit between S2 and S4. Therefore,

Progressively higher spinal cord injury → ↑sing degrees of autonomic dysfunction.

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Pathologic Anatomy

• Injury to the corticospinal tract or dorsal columns, respectively, results in ipsilateral paralysis or loss of sensation of light touch, proprioception, and vibration.

• Injury to the lateral spinothalamic tract causes contralateral loss of pain and temperature sensations.

• Because the anterior spinothalamic tract also transmits light touch information, injury to the dorsal columns may result in complete loss of vibration sensation and proprioception but only partial loss of light touch sensation.

• Anterior cord injury: causes paralysis and incomplete loss of light touch sensation.

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Pathologic anatomy Vascular supply of SC: consists of 1 anterior and 2 posterior

spinal arteries.

Ant. & Post. spinal arteries arise from the vertebral arteries in the neck

They descend from the base of the skull.

Various radicular arteries branch off the thoracic and abdominal aorta to provide collateral flow.

Anterior spinal artery → supplies anterior 2/3rds of the cord.

Ischemic injury to anterior spinal artery → dysfunction of corticospinal, lateral spinothalamic, and autonomic interomedial pathways.

Anterior spinal artery syndrome → paraplegia, loss of pain and temperature sensation, and autonomic dysfunction.

Posterior spinal arteries → supply dorsal columns.

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Segmental motor/reflex levels

• The cell bodies of ventral (motor) roots

• Are in the anterior horn of the cord parenchyma.

• Clinically relevant spinal reflex center levels are as follows:

• Biceps - C5/6

• Brachioradialis - C5/6

• Triceps - C7 (C6-8)

• Finger flexors - C8 (C7-T1)

• Knee - L3 (L2-L4)

• Ankle - S1 (L5-S2)

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Clinically important dermatomes

Upper extremity –

• C2 and C3 – Post. head & neck

• C4 and T2 - Adjacent to each

• other in the upper thorax

• C5 (anterior shoulder),

• C6 (thumb)

• C7 (index and middle fingers)

• C 7/8 (ring finger)

• C8 (little finger)

• T1 (inner forearm)

• T2 (upper inner arm)

• T2/3 (axilla)

• T4 or T5 – Nipple

• T10 - Umbilicus

Lower extremity –

• L1 (anterior upper-inner thigh)

• L2 (anterior upper thigh),

• L3 (knee)

• L4 (medial malleolus)

• L5 (dorsum of foot)

• L5 (toes 1-3)

• S1 (toes 4-5; lateral malleolus)

• S3/S1 - Anus

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SPINAL CORD INJURY (SCI) MECHANISMS

• Mechanism of injury determines the type of vertebral

injury and neurological damage that follows

• The spinal cord can be damaged by trauma thru:

• (a) direct compression by bone fragment/ligament/disc

• (b) interruption of vascular supply

• (c )Traction

• SCI can be classified according to the underlying

mechanism of injury→

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CERVICAL SPINE INJURY MECHANISMS

Flexion and flexion-rotation injuries

Most frequent mechanism of C-Spine injuries

Most common site is C5/6

Subluxation and/or dislocation of one or both posterior facets may occur and they may be locked

There is extensive posterior ligamentous damage

Injuries are usually unstable

Spinal cord may be compressed and distracted thereby sustaining:

a) direct damage and

b) vascular impairment from involvement of anastomotic segmental vessels or feeders

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Compression injuries: Associated with Decreased vertebral height due to compression

Comminuted with posterior part encroaching on SC

C5/6 is most frequent fracture level

Usually stable b/c posterior elements & longitudinal ligaments are intact

‗tear-drop‘ fracture may occur when flexion is combined with rotation force (due to separation of a small antero- inferior fragment)

About ½ the resulting cord injuries cause complete neurological deficit below the level of the lesion.

Remainder being incomplete with major damage to the anterior cord

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Hyperextension injuries

Most common in older age groups especially those with

degenerative spinal canal stenosis

Bony injury is not often demonstrated on imaging [SCIWORA]

The major damage is to the anterior longitudinal ligament 20 to

hyperextension

Most injury result in incomplete cord damage from cord

compression b/n degenerative body/disc anteriorly and

hypertrophic ligamentum flavum posteriorly

Injuries are nearly always stable

Central cord syndrome is the most common neurological

impairment associated with hyperextension injuries.

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Thoracolumbar Injury Mechanisms

• Flexion rotation injuries:

• Occur most commonly at T12/L1 level

• Result in anterior dislocation of T12 on L1 vertebral

body

• Usually associated with disruption of posterior

longitudinal ligament and posterior bony elements

• Inferior vertebral body sustains antero-superior

wedge fracture and compression

• Injuries are unstable and usually result in complete

neurological deficit of either spinal cord, conus or

cauda equina.

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Thoracolumbar Injury Mechanisms

Compression injuries

Common with decrease in height of vertebral body

Usually stable injuries

Neurological damage is uncommon

Hyperextension injuries

Very uncommon mech. of injury at thoracolumbar spine

Involves rupture of (a) anterior longitudinal ligament & (b) intervertebral disc plus (c ) fracture thru anterior segment of involved vertebral body

Injuries are usually unstable

Cord injury is usually severe

Open missile penetrating injuries: from e.g. stab, cutlass or gunshot with cord damage usually due to:

(a) blast injury

(b) vascular damage and

(c ) cord penetration by the missile or bony fragments

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Pathophysiology of SCI

• Pathologic Mechanism of SCI

Direct force to the Spinal Cord or

Ischaemia due to vascular injury

20 haemorrhage in or around the cord

N.B: Degree of neurological injury is determined by extent of severity of above severity of above mechanism.

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• In the past few decades, considerable efforts have been made by SCI researchers to elucidate the pathophysiology of SCI and unravel the underlying cellular and molecular mechanisms of tissue degeneration and repair in the injured spinal cord.

• To this end, a number of preclinical animal and injury models have been developed to more closely recapitulate the primary and secondary injury processes of SCI

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Initial mechanical forces delivered to the spinal cord at the time of injury is known as primary (10) injury

In 10 injury ―displaced bone fragments, disc materials, and/or ligaments bruise or tear into the spinal cord tissue‖

Four main characteristic mechanisms of primary injury have been identified that include:

1. Impact plus persistent compression

2. Impact alone with transient compression (e.g. hyperextension inj.)

3. Distraction (when two adjacent vertebrae are pulled apart)

4. Laceration/transection (thru missile injuries, sharp bone fragment, severe dislocations)

• Most common form of primary injury is impact plus persistent compression

• It typically occurs through burst fractures with bone fragments compressing the spinal cord or through fracture-dislocation injuries

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• Regardless of the form of primary injury, these forces

directly damage ascending and descending pathways

in the spinal cord and disrupt blood vessels and cell

membranes causing spinal shock, systemic

hypotension, vasospasm, ischemia, ionic imbalance,

and neurotransmitter accumulation .

• To date, the most effective clinical treatment to limit

tissue damage following primary injury is the early

surgical decompression (< 24 h post-injury) of the

injured spinal cord.

• Overall, the extent of the primary injury determines

the severity and outcome of SCI.

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Secondary Mechanisms of Spinal Cord Injury

• Secondary injury begins within minutes following the initial primary injury and continues for weeks or months causing progressive damage of spinal cord tissue surrounding the lesion site

• Concept of secondary SCI was first introduced by Allen in 1911.

• While studying SCI in dogs, he observed that removal of the post traumatic hematomyelia improved neurological outcome.

• He hypothesized that presence of some ―biochemical factors‖ in the necrotic hemorrhagic lesion causes further damage to the spinal cord

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Secondary SC injury

• The term of secondary injury is still being used in

the field and is referred to a series of cellular,

molecular and biochemical phenomena that

continue to self-destroy spinal cord tissue and impede

neurological recovery following SCI

• Diagram below shows the key pathophysiological

events that occur after primary injury and lead to

progressive tissue degeneration.

• Vascular disruption and ischemia occur immediately

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Secondary SC injury

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Secondary SC injury

• Secondary injury can be temporally divided into

• acute, sub-acute, and chronic phases.

Acute phase begins immediately following SCI and includes:

• Vascular damage

• Ionic imbalance

• Neurotransmitter accumulation (excitotoxicity)

• Free radical formation

• Calcium influx

• Lipid peroxidation

• Inflammation

• Edema, and

• Necrotic cell death

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Secondary SC injury

• As injury progresses,

Sub-acute phase sets in & involves:

Apoptosis,

Demyelination of surviving axons,

Wallerian degeneration,

Axonal dieback,

Matrix remodeling, and

Evolution of a glial scar around the injury site

Chronic phase: Further changes which occur in this phase of injury include:

Formation of a cystic cavity,

Progressive axonal die-back, and

Maturation of the glial scar

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Cell Death in Spinal Cord Injury

• Cell death is a major event in the secondary injury mechanisms that affects neurons and glia after SCI

• Cell death can happen through various mechanisms in response to various injury-induced mediators; examples include:

Necrosis & Apoptosis [were originally identified as two major cell death mechanisms]

Additional forms (12) defined (in 2012) by ―Nomenclature Committee on Cell Death‖ (NCCD) include:

Necroptosis, (= highly regulated, caspase-independent programmed necrosis executed by regulated mechanisms)

Pyroptosis, and

Netosis.

More extensively studied mechanism of cell death to date include:

Necrosis,

Necroptosis,

Apoptosis, and

Autophagy

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Cell Death in Spinal Cord Injury

• Following SCI, neurons and glial cells die thru necrosis from

mechanical damage at 10 injury

• This process continues to acute and subacute stages of injury.

• Necrosis may also be due to other factors including:

Accumulation of toxic blood components,

Glutamate excitotoxicity and

Ionic imbalance,

ATP depletion,

Pro-inflammatory cytokine release by neutrophils, lymphocytes &

Free radical formation.

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SCI: Classification systems

• Classification systems:

• The first classification system, ―Frankel Grade,‖ was developed by Frankel

and colleagues in 1969

• Others that came later include:

• Late 1970's; Lucas and Ducker (Maryland Institute for Emergency

Medical Services)

• Early 1980s; Klose and colleagues at the University of Miami Neuro-

spinal Index (UMNI)

• 1981; Chehrazi and colleagues (Yale Scale)

• 1987; Bracken et al. at Yale University School of Medicine

• The 1984 system, developed by the American Spinal Injury Association

labelled ―American Spinal Injury Association (ASIA) Scoring System‖ in

1984 is currently the most widely accepted and employed clinical scoring

system for SCI

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Classification of Spinal Cord Injury

• SCI can be classified into complete and incomplete

spinal cord injuries based on ASIA definition

• Complete: Absence of sensory and motor functions

in the lowest sacral segments

• Incomplete: Preservation of sensory or motor

function below the level of injury, including the

lowest sacral segments

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Types of neurological impairment by

ASIA Impairment Scale

• Extent of injury by American Spinal Injury Association

(ASIA) Impairment Scale (modified from the Frankel classification)

• A = Complete: No sensory or motor function is preserved in

sacral segments S4-S5

• B = Incomplete: Sensory, but not motor function is preserved

below the neurologic level and extends through sacral

segments S4-S5

• C = Incomplete: Motor function is preserved below the

neurologic level, and most key muscles below the neurologic

level have a muscle grade of less than 3

• D = Incomplete: Motor function is preserved below the

neurologic level, and most key muscles below the neurologic

level have a muscle grade that is greater than or equal to 3

• E = Normal: Sensory and motor functions are normal

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Principles of ASIA scoring and neurological recovery

• Initial neurological assessment using ASIA scoring system

should be determined at 72 h after SC injury.

• This time-point has been shown to provide a more precise

assessment of neurological impairments after SCI

• Most functional recovery occurs during the first 3 months

• Reaches a plateau by 9 months after injury in most cases

• Additional recovery may occur up to 12–18 months of SCI

• Patients with incomplete paraplegia have good prognosis in

regaining locomotor ability (~76% of patients) within a year.

• While complete paraplegic patients experience limited

recovery of lower limb function if their lesion is above T9.

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Types of Neurological Deficits in SCI

• Spinal shock or ‗Altered Reflex Activity‘

Transient depression in segments caudal to spinal

cord lesion

Due to sudden withdrawal of predominantly

facilitating or excitatory influence from supra-spinal

centers

Characterized by areflexic flaccid paralysis

Duration: varies from minimal reflex activity

appearing in 3-4 days or delayed to 6-8 weeks

(average of 3-4 weeks)

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COMPLETE LESIONS

• Most severe form of spinal injury is complete transverse myelopathy

• All neurological function including motor, sensory and autonomic below level of lesion is absent.

• Presents either as paraplegia or quadriplegia depending on spinal level

• Motor deficit: injury to Spinal Cord results in

• a) Upper motor neuron (UMN) paralysis with loss of voluntary function, increased tone, & hyperreflexia

• b) Injury to lumbar spine causing caudal equina syndrome →lower motor neuron (LMN), paralysis characterized by decreased muscle tone, wasting and loss of reflexes

• C) Thoracolumbar injury involving conus medullaris & cauda equina → combination of upper & lower motor neuron signs

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COMPLETE LESIONS

• Sensory deficits: afferent long tracts carrying

sensory appreciation of pain, temperature, touch,

position and tactile discrimination are interrupted and

abolished below the level of lesion

• Visceral sensation also lost

• Sensation may decrease over a few spinal segments

(residual sensation) before being lost altogether

• May occasionally have abnormally increased

sensation (hypereasthesia) and hyperalgesia at or just

below level of lesion

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COMPLETE LESIONS

Autonomic deficit: Vasomotor control:

Cervical & high thoracic lesions above sympathetic

outflow at T5 may lead to hypotension.

Interruption of sympathetic vasomotor control will

initially produce postural hypotension because of

impaired venous return

Temperature control: Patient with complete injury

looses satisfactory thermal regulation because of

impaired autonomic control of vasoconstriction &

vasodilation

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COMPLETE LESIONS

• Sphincter control: impairment of bowel & bladder control. In spinal shock patient develops acute retention with overflow incontinence

• As spinal shock phase passes, reflex activity returns in upper motor neuron lesion

• Because spinal micturition reflex arc is intact in a lesion above conus medullaris

• Leads to ‘autonomic’ bladder in which bladder empties involuntarily but bladder capacity may be less than normal but good voiding pressure is retained

• No sensation of bladder fullness

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COMPLETE LESIONS

• Lower Motor neuron lesion

• Because spinal micturition reflex is interrupted

• →autonomous bladder whose function is under control of myogenic stretch reflex inherent in detrusor muscle fibers

• Characterized by linear ↑se in intravessical pressure with filling till full capacity is reached.

• Urine then flows pass sphincter by overflow incontinence

• Mixed upper & lower MN lesion e.g. of conus medullaris & cauda equina : →→flaccid detrusor & spastic sphincter or the reverse

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INCOMPLETE SCI

• Anterior cervical spinal cord syndrome (ACSCS)

• Due to compression of anterior aspect of the cord

• →damage to corticospinal & spinothalamic tracts →motor paralysis below level of lesion

→loss of pain, temp & touch sensations with

• → relative preservation of proprioception, light touch,

• position sense & (carried by posterior columns)

• Exact pathophysiology of ACSCS →unclear

• Possible mechanism → (a) Stretch from attached dentate ligaments at equitorial plane (b) Ischaemia from compromise of anterior spinal artery (which supplies anterior 2/3rd of SC)

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INCOMPLETE SCI • Central spinal cord syndrome (CSCS)

• Usually involves a cervical lesion, most commonly hyperextension injury of

cervical spine → compression of SC between degenerative intervertebral

disc anteriorly & hypertrophied ligamentum flavum posteriorly

• Cord damage is predominantly central & the more central cervical tracts to

upper limbs suffer the most severe injury

• Result→ disproportionate weakness in upper vs. lower limbs b/w level of

lesion with greater motor weakness in the upper than lower extremities

• Greater distal than proximal muscle weakness in the affected extremity.

• Sacral sensory sparing

• Variable sensory loss: more likely to lose pain/temperature sensation than

proprioception and/or vibration.

• Dysesthesias (eg, sensation of burning) in the hands or arms are common

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INCOMPLETE SCI • Brown-Sequard Syndrome

• Results from hemisection of the cord caused by many factors

• Trauma: Commonest cause - often a penetrating stab or gunshot wound

• Occasional: unilateral facet #/dislocation from MVA or a fall

• Unusual: assault with a pen, removal of CSF drainage catheter after thoracic aortic surgery

• Infrequent: blunt injury or pressure contusion.

• Non-traumatic causes: – Tumor (10 or metastatic),

– Multiple Sclerosis,

– Disc herniation,

– Cervical spondylosis,

– Herniation of spinal cord thru a dural defect,

– Epidural hematoma,

– Transverse myelitis,

– Ossification of ligamentum flavum

– Others: radiation, meningitis, syphilis, TB,,

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INCOMPLETE SCI Brown-Sequard Syndrome (Physical features)

Involves a relatively greater ipsilateral loss of proprioception and motor function, with contralateral loss of pain and temperature sensation.

Anatomic mechanism

Interruption of lateral corticospinal tracts →

Ipsilateral (UMN) spastic paralysis (weakness)

Babinski sign

Hypertonia

Hyperreflexia,

Clonus,

Positive Hoffman sign below level of injury

Interruption of posterior white column →

Ipsilateral loss of proprioception, tactile discrimination, vibratory &

position sensation below level of lesion

Interruption of lateral spinothalamic tracts →

Contralateral loss of pain/temperature sensation (light touch, hot or

cold) usually occurring 2-3 segments below level of lesion

(may be absent, impaired or sometimes normal)

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INCOMPLETE SCI • Brown-Sequard Syndrome (Other features)

Pure Brown-Sequard Syndrome reflecting complete hemiseection of the cord is not often observed

Clinical picture composed of fragments of the hemisection syndrome plus additional symptoms and signs is more common

Posterior column interruption may not produce significant neurological deficit in complete hemisection because some fibers decussate while

Loss of vibratory sensation may accompany the more common incomplete hemisection

Partial segmental ipsilateral LMN weakness & analgesia sometimes occur

Loss of ipsilateral autonomic function can result in Horner‘s syndrome

Spasticity & hyperreflexia may be absent with an acute lesion

N.B: Clinical features may range from mild to severe

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Conus Medullaris Syndrome

• Conus Medullaris (CM) (Latin for ―medullary cone‖) or conus terminalis is the tapered, lower end of the spinal cord that ends below at the cauda equina (CE)

• CM is situated near L1 to L2 vertebral levels and sometimes lower with unclearly defined upper end.

• It corresponds with spinal cord segments S1-S5

• Problems of CM often affect CE

• CMS is a secondary form of sacral cord injury, with or

without involvement of the lumbar nerve roots resulting from lumbar vertebral injuries.

• It also represents a type of incomplete SCI

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Conus Medullaris Syndrome

• Clinical Features: Characterized by areflexia in the bladder,

bowel, and to a lesser degree, lower limbs

• Sacral segments occasionally may show preserved reflexes

(eg, bulbocavernosus and micturition reflexes).

• Motor and sensory loss in the lower limbs usually variable.

• May include weakness, numbness in lower limbs

• There may be severe back pain, strange/jarring sensations in

the back (buzzing, tingling, numbness, unexplainable itching)

& sexual dysfunction

• CM typically produces sudden symptoms on both sides of the

body while cauda equina develops over time producing uneven

symptoms

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Diagnosis and Rx of Conus Medullaris

Syndrome • Diagnosis: Lumbosacral MRI

• Treatment: depends on causes.

• Usually a spinal decompression surgery

• Radiation if cancer

• Intravenous/oral antibiotics if infection is the cause

• Physical therapy

• Bowel & bladder care

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Cauda Equina Syndrome (CES)

• Cauda equina (Latin; Cauda = tail, equina = horse

→ horse‘s tail) is a bundle of intradural nerve roots

at the end of the spinal cord, in the subarachnoid

space distal to the conus medullaris.

• They are lower lumbar and all sacral nerve roots

which provide:

• (a) Sensory innervation to the saddle area

• (b) Motor innervation to sphincters and

• (c) Parasympathetic innervation to the bladder and

lower bowel from left splenic flexure to rectum

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Cauda Equina Syndrome : Clinical features

Simultaneous compression of multiple lumbosacral

nerve roots below conus medullaris result in

neuromuscular and urogenital symptoms including:

Low back pain,

Sciatica (unilateral or usually bilateral)

Saddle sensory disturbances (saddle anaesthesia)

Bladder and bowel dysfunction

Variable lower extremity motor and sensory loss

Though lesion in CES involves nerve roots & therefore

= a peripheral nerve injury, damage may be irreversible

making it a surgical emergency

65

Common causes of cauda equina syndrome [CES]

• Causes include any pathology that narrows the spinal canal and compresses nerve roots below the terminal end of the spinal cord.

Spinal trauma → # or subluxation with compression of cauda equina

Penetrating trauma and spinal manipulation → damage or compression

Lumbar stenosis (multilevel type)

Herniated nucleus pulposus

Neoplasms (10 astrocytoma, neurofibroma, meningioma or metastases) 20% spinal tumors are found in this area

Spinal infection/abscess, TB, Meningitis, CMV

Spinal bifida+ subsequent tethered cord syndrome

66

Spinal Cord concussion

A variant of mild SCI characterized by:

Transient paraplegia and neuropraxia

Variable degrees of sensory impairment and motor weakness

• Typically resolves within 24-72 hours without permanent deficits or apparent structural damage.

• Pathological process involved is poorly understood in comparison to brain concussion that is well defined

3 criteria for its diagnosis include:

Spinal trauma immediately precedes onset of neurological deficits

Neurological deficits are consistent with spinal cord involvement at the level of injury

Complete neurologic recovery occurs within 72 hours after injury.

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Spinal Cord concussion

• Graded into G1 to G3 based on duration of symptoms ranging from Grade I (<15 minutes), Grade II (between 15 minutes and 24 hours, Grade III (>24 hours)

• Predominantly a sport related injury including wrestling, hockey, gymnastics and diving.

• Most common in American football.

• Can also occur after minor car accidents as in ―whiplash injuries‖ and falls

• Thoracic portion of vertebral column = most frequent seat of trauma

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MANAGEMENT OF SCI

• Little can be done about the initial neurological

damage

• Major efforts are directed towards prevention of

further SC injury and complications from damage

• Management principles include:

• (a) Prevent further injury to SC

• (b) Reduction & stabilization of bony injuries

• (c ) Prevention of complications of SCI

• (d) Rehabilitation

69

Initial Treatment

• First aid:

• (a) Require utmost caution in turning and lifting patient

• (b) Handle spine with care: Avoid inflicting additional damage

• (c) Need help to provide horizontal stability and longitudinal

• traction without spine flexion when moving patient

• (d) Apply temporary neck collar if cervical injury

• (f) Assess associated injuries e.g. chest, abdomen, extremities

• (g) Assess for hypotension and hypoventilation which may be

life threatening and may ↑se neurological impairment

• Hypotension is usually 20 to loss of sympathetic tone →

vasodilatation and → peripheral vascular pooling

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Treatment : Resuscitation

• Ensure spine remains stable

• Administer O2

• Give ventilator assistance if respiratory insufficiency is present

Treat hypotension:

Intravenous volume expanders

-adrenergic stimulators

Intravenous atropine

Transvenous pacemaker (rarely necessary)

Preserve body temperature in cold and warm weather (patients with SCI become poikilothermic, loose temperature control & tend to assume temperature of the environment.

71

Treatment

• Pass a nasogatric tube [NGT] to prevent vomiting

that may result from gastric stasis & paralytic

ileus and lead to aspiration & chest infection.

• Pass a urethral catheter to prevent over-distention

of bladder and its complications [may change to

intermittent catheterization later]

• Commence anticoagulant for prophylaxis against

DVT and/or Pulmonary embolism. Use mini---

dose heparin (5000iu s/c b. d.)

• Apply compression stockings for lower limbs.

72

Investigations: Laboratory Studies

• Arterial blood gas (ABG) measurements - Useful to evaluate adequacy of oxygenation and ventilation

• Lactate levels - To monitor perfusion status; can be helpful in the presence of shock

• Hemoglobin and/or hematocrit levels - Measure initially and monitor serially to detect or monitor sources of blood loss

• Urinalysis – Initially to detect any associated genitourinary injury and later with M/C/S to detect urinary tract infection

• Clotting/coagulation profile: Including INR, PT, PTT, aPTT, PC, FIB, CT, BT

73

Radiological investigation

Plain radiography – C-spine (+abdomen &chest)

Only as good as the first and last vertebrae seen,

Radiographs must adequately depict all vertebrae

Computed tomography (CT) scanning –

Reserved for delineating bony abnormalities or fracture

Useful when plain radiography is inadequate or fails to visualize segments of the axial skeleton

Flexion/Extension study : If plain x-ray and CT scan show no anomaly, a flexion/extension study should be done to exclude instability due to ligamentous damage.

CT Myelography: fluoroscopy+ injected contrast material to evaluate spinal cord, nerve roots, meninges

Magnetic resonance imaging (MRI) – Useful for detecting suspected spinal cord lesions, ligamentous injuries, and other soft-tissue injuries or pathology

74

SPINAL REDUCTION & STABILIZATION

• After stabilizing systemic parameters the next step is

vertebral alignment and stabilization

• Can be achieved by applying skeletal traction or by

open or endoscopic surgery

• Cervical traction is light stretching action meant to

relieve pressure on compressed vertebrae while also

maintaining the health & placement of spinal discs

• Traction: Using a counter-weight attached to a pulley

system, the head is stretched away from the

shoulders, relieving disc compression and spinal pain.

75

Cervical Traction Devices

• Many have flooded the market

• Commoner devices include:

• 1. Gardner-Wells tongs [Introduced in 1973 by

Dr. James Gardner]

• 2. Crutchfield‘s caliper

• 3. Odebode-Agaja (O-A) adult cervical traction device [

• 4. Cone‘s caliper

• 5. Blackburn‘s caliper

• 6. Pronex Pneumatic Traction device

• 7. Saunder‘s cervical Hometrac traction device

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Functions of GWT & O-A Device

Gardner-Wells Tongs useful for:

Treatment of cervical spine #s/dislocations

Patient positioning and during surgery

To maintain skeletal traction during spinal deformity

(e.g. scoliosis) surgery

Reduction of subluxation/dislocation & facet joints

#/dislocation

Same usefulness applies for ‗Odebode-Agaja adult

cervical traction device for third world countries‘

Also similar technique of application

78

Application of GWT & O-A Device

• A bedside procedure

• The neck is stabilized in a rigid neck collar

• The scalp over temporo-parietal area above the pinna is shaved

• The skin is marked bilaterally symmetrically at a point where a horizontal line 2 finger-breadths above the pinna meets with a vertical line drawn along the axis of the ipsilateral tragus.

• Skin preparation of shaved area is done in routine manner (with savlon/povidone iodine/methylated spirit).

• The surgeon scrubs & gloves up and applies sterile drapes

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Application of GWT & O-A Device

• Skin over marked points is infiltrated with 2%

lignocaine raising a bleb.

• Sterilized GWT device is then positioned with

the tips of its tongs driven/screwed in through

the marked points on the scalp until further

advancement/skull penetration ceases.

• A stopper knot is screwed into position on

either sides to stabilize the tongs.

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Application of GWT & maintenance of traction

A strong rope attached to the hook of the device is

passed thru a pulley system at bed-head to carry a

weight calculated based on adjacent vertebral levels

involved in the cervical injury (e.g. fractures/

subluxation). Maintenance weight is calculated by:

1. Applying a maximum of 5 lb-weight (2.25kg) for

each cervical level below the occiput e.g. for C6;

weight = 5 x 6 lbs.= 30lbs or 13.6 kg

2. Dividing sum of levels (from 1-7) of 2 involved

adjacent vertebrae by 2 in Kg body weight. E.g. for

C5 on C6 subluxation, the weight = 5+6/2 =5.5 kg

wt. 81

Reduction of fracture/subluxation

• For reduction and alignment of subluxation, commence with 5kg-wt under x-ray or fluoroscopic guidance

• Gradually add more weights up to the maximum that would produce alignment

• Extreme caution must be exercised to avoid distraction at fracture site or of underlying cord

• The latter will worsen neurological damage

• Reduction of facet dislocation/locks may be more difficult or impossible,

• For such, some advocate neck manipulation under fluoroscopy or traction & reduction under GA.

• Traction under GA is practiced in Australia and Europe but not popular in the USA

• Open surgery is best option to reduce #-dislocation with locked or overriding facet joints

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Reduction of fracture/subluxation

• Following reduction, the alignment position is

protected and maintained for 6 weeks with

skeletal traction using calculated weights.

• Following six weeks of traction a flexion-

extension (F/E) dynamic/supervised study is

undertaken to assess stability of the spine

• Traction is discontinued if the study is satisfactory

• If not, traction can be continued extra 2 weeks

• If a repeat study remains unsatisfactory, surgery is

then indicated

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Advantages and complications of GWT

Advantages

The spring-loaded GWT has

become globally popular

because of following

advantages:

• Relative ease of application

and maintenance

• Sterile technique

• Lack of incisions

• Reduced screw pull-out

• Elimination of burr holes

Complications

• Complication rate is low

• Minor complications (37.5%)

Pin loosening

Asymmetrical pin positioning

Superficial infections

Major

Perforation of the skull

Brain abscesses

Neurovascular damage

Osteomyelitis

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Thoracolumbar Spinal Cord Injuries

• Management of T-L spine injuries usually

conservative

• Requires postural reduction in bed

• Correct positioning/posture must be maintained in

lateral, prone & supine positions by appropriate

placement of bolsters and pillows by the turning team

• Mandatory turning 2 hourly on regular/water/air beds.

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Indications for surgical intervention

• Absolute indications:

• 1. Progression of neurological deficit especially when

compressive lesion is demonstrated on CT or MRI

scan. Should be treated as an emergency.

• 2. Patients with partial neurological injury &

preservation of some distal function usually due to

extrinsic compression from herniated cervical disc,

depressed lamina or osteophytic bar

• 3.Open injury due to stab wound/gunshot :

exploration, removal of foreign elements, and repair

of dura

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Indications for surgical intervention

• 4. Most common indication for surgery is the need for

stabilization if

• (a) gross instability especially after incomplete injury

• (b) failure of closed reduction of locked facets

(posterior reduction and fusion

• (c ) Operative procedure to stabilize unstable C-spine

and reduce length of hospital stay

87

Pharmacological Treatment of SCI

Glucocorticoids: Methylprednisolone prescribed as a

bolus intravenous injection of 30mg/kg body weight

over 15 minutes within 8 hours of closed SCI

Followed 45 minutes later by an infusion of 5.4 mg

/kg per hour for 23 hours

Diuretics

Local hypothermia

Barbiturates

Endogenous opiate-antagonists

Steroids & diuretics are particularly useful for spinal

cord edema 88

Further Conservative Measures

General: Maintain general and metabolic wellbeing

• Maintain positive nitrogen balance

• Assess for and treat anaemia

• Prevent urinary, chest and other infections

• Skilled counseling + emotional support to patient & relatives during RX & rehab

• Padding of pressure points (prevent pressure sores)

Gastrointestinal complications: acute gastric dilatation and paralytic ileus

• Rx: Pass NGT to alleviate vomiting & aspiration of intestinal contents

89

Further Conservative Measures

Bladder complications: Urinary retention/ neurogenic bladder etc.

• Place a urethral catheter for drainage.

• May be continuous but preferably intermittent

• Follow-up by bladder training and management depending on whether neurogenic bladder has resulted from upper or lower motor neuron lesion + results of cystometrogram showing intravessical volume/pressure relationship.

Limb care: Physiotherapy: To prevent contracture as tone returns and spasticity develops

90

Special C-Spine fractures

Jefferson’s fracture: bilateral fracture of posterior arch of the atlas due to direct vertical blow on the head (head pressing down on the S. column & atlas squeezed between occipital condyles and axis e.g. axial load injury during a diving)

• Grooves for the vertebral arteries = weakest sites of the arches of the atlas & fractures usually occur here → burst fragments displaced outwards

• Always necessary to assess for vertebral artery injuries via a CTA neck

• If vertebral artery dissection is confirmed, patient requires anticoagulation with heparin and further evaluation by interventional radiology.

• Patients without widened atlanto/dens interval (ADI) and disruption of the transverse ligament on MRI can be managed with cervical collar.

• Otherwise, may need a halo immobilizer and finally undergo posterior C1-C2 lateral mass internal fixation.

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Jefferson’s fracture

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Hangman’s fracture Hangman’s fracture = avulsion of the laminar arches of

C2 + dislocation of C2 vertebral body on C3

• Traumatic spondylolisthesis of the axis (Hangman's Fracture) - Spine ...

• This is the characteristic lesion resulting from judicial hanging

• There is a fracture through bilateral pedicles of C2 with the fracture line extending through the right foramen transversarium and right intertubercular lamina.

• On the left, the fracture line involves the posterior tubercle The medial aspect of the fractured right pedicle is displaced medially into the spinal canal contacting but not significantly effacing the theca sacof the left transverse process.

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Imaging Considerations

Open Mouth Odontoid Radiograph:

• Reveals asymmetry of the spaces between the dens (located on C2 and

projecting up) and the lateral masses of C1.

• The lateral masses are usually extended out laterally with respect to the

margins of C2 because the C1 fragments spread radially.

CT Scan & MRI:

• Both modalities help to determine if fracture line involves both the anterior

and posterior arches

• But an MRI can be more useful in providing more information on local

soft-tissue injury (e.g. pre-vertebral hemorrhage or swelling plus

ligamentous injury)

CT angiogram: Given the mechanism of injury, a CT angiogram of the

neck should be considered, especially if there are new neurologic deficits.

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Hangman’s fracture

• This fracture is associated with subtle widening of the C2/3 facet joints greater on the left, suspicious for bilateral facet joint subluxation.

• There is an associated hematoma that measures up to 3 mm in maximum depth that elevates the posterior longitudinal ligament and tectorial membrane.

• Opacity at the C3/4 intervertebral disc level with resulting mild compression of the cervical cord may be due to hematoma or disc protrusion.

• No other cervical spine fracture is identified.

• There is no significant prevertebral hematoma

95

Hangman’s fracture

96

Special C-Spine fractures Odontoid peg fractures:

• May occur at (a) the tip (Type-I) (b) base of dens (Type-II) or (c) base extending to adjacent C2 vertebral body (Type-III)

• Type-II fracture to the base is most common

• May cause disruption of blood supply to the dens resulting in non-union of the fracture

• Rx: Immobilization in firm halo-brace for 4 months would suffice in many cases

• If non-union or instability occurs: →Posterior C1/2 fusion

• Also advocated is trans-oral internal fixation of odontoid #

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Odontoid process fractures

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Odontoid process fractures on open-mouth

radiography

99

•Thanks for your attention

100

spinal cord injury - bowen university

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