Dr. M. A Sofi MD;FRCP(London);FRCPEdinFRCSEdin

PARAPLEGIA AND SPINAL CORD SYNDROMES

Information highway between brain and body Extends through vertebral canal from foramen

magnum to L1 Each pair of spinal nerves receives sensory

information and issues motor signals to muscles and glands

Spinal cord is a component of the Central Nervous System while the spinal nerves are part of the Peripheral Nervous System

Overview of Spinal Cord

• The spinal cord has two major functions:

Carrying information: Spinal cord transmit information from body organs and external stimuli to the brain and send information from the brain to other areas of the body

• Coordinating reflexes: coordinates reflexes without the involvement of the brain, thus, the spinal cord has both communicative and integrative functions. Reflex actions are

automatic, unlearned, involuntary, and inborn responses.

These actions are sudden in nature and have a purpose of protecting the individual or his organs from sudden danger

Functions of the Spinal Cord

Somato-sensory Organization

Somato-sensory OrganizationPyramidal Tracts

Lateral Coticospinal TractAnterior Corticospinal Tract

RubrospinalReticulaospinal

OlivospinalVestibulospinal

Extrapyramidal Tracts

Descending Tracts

Somato-sensory OrganizationAscending tractsSensory & Ascending

PathwaysDorsal Column Medial Lemniscus

Gracile fasciculus Cuneate fasciculus

Spinocerebellar Tracts Posteriors pinocerebellar Anterior spinocerebellar

Anterolateral System

Lateral spinothalmic tract Anterior spinothalmic tract Spino-olivary tract

BLOOD SUPPLY SPINAL CORD

Spinal shock is a loss of sensation accompanied by motor paralysis with initial loss but gradual recovery of reflexes, following a spinal cord injury (SCI) – most often a complete transaction.

Reflexes in the spinal cord caudal to the SCI are depressed hyporeflexia/areflexia), while those rostral to the SCI remain unaffected.

‘Shock' in spinal shock does not refer to circulatory collapse, and should not be confused with neurogenic shock.

Paraplegia & Spinal cord syndromes

Phase Time Physical exam findingUnderlying physiological event

1 0-1dAreflexia/Hyporeflexia

Loss of descending facilitation

2 1-3d Initial reflex returnDenervation supersensitivity

3 1-4w Hyperreflexia (initial)Axon-supported synapse growth

41-12m

Hyperreflexia, Spasticity

Soma-supported synapse growth

Paraplegia & Spinal cord syndromesClassification of etiology

LMN type/Flaccid paraplegia

UMN type/ Spastic paraplegia

Cortical lesion Spinal cord lesion

Non-compressive Myelopathy

Compressive Myelopathy

Tumor Falx CerebriSuperior Sagital

Sinus Thrombosis

Paraplegia & Spinal cord syndromesClassification of etiology

COMPRESSIVE MYELOPATHY

EXTRAMEDULLARY INTRAMEDULLARY

EXTRADURAL INTRADURAL

Syringomyelia, Ependymymoa,

Glioma, Astrocytoma

DISC VERTEBRALMeningoma,

Neurofibroma, Arachnoditis

Paraplegia & Spinal cord syndromesClassification of etiology

Non-compressive myelopathies

INFAMMATORY NONINLAMMATORY

INFECTIOUS: VIRAL, BACTERIAL ,FUNGAL PARASTIC AUTOIMMUNE: SLE, SJOGREN, SARCOIDOSIS, BECHET S, MCTDDEMYELINATING: MS,NMO, ADEM, POST VIRAL POST VACCINIALPARANEOPLASTIC

INHERITED: HSP, INHERITED METABOLIC DISORDERSMETABOLIC: VIT B12,COPPER,FOLATE ,AIDS ASSOCIATED, VIT E DEFICIENCYTOXIC: CASSAVA, LATHYRISM,FLUOROSIS,SMON, NITROUS OXIDEVASCULAR: ANT SPINAL ARTERY THROMBOSIS, AVM, DURAL AV FISTULA

Paraplegia & Spinal cord syndromesDifferences between extradural and intradural lesions

Extradural Mnemonic – (3 Ps)

Pain present - (root pain & spinal tenderness)

Pyramidal involvement – early Protein in CSF high

Intradural Dissociated anesthesia

Bladder involvement early Not so high protein

Symmetrical involvement Trophic ulcers common

Determining level of lesion in cord compression

Sensory level Motor level Reflex level

Root pain – dermatome Type of bladder involvement

Sensory level – below that level, sensory impairment of loss

Motor level – Beevor’s sign indicates T10 lesionReflex level – Inverted supinator

C5 lesion

Vascular disorders of spinal cordIschemic disorders of spinal cord

a) Primary ischemia: atherosclerosis/vasculitis

b) Secondary ischemia: SOL, disorders of aorta

Decompression sickness Spinal hemorrhage: SAH,

SDH, EDH, hematomyelia Spinal AVM/Dural AV

fistula

Inflammatory disorders spinal cord

Acute TM: viral, bacterial, fungal, post-infectious

Myelitis of chronic disorders: MS

Myelitis of systemic disorders: Behcet’s

Medulary compression: Epidural abscess Subdural abscess Spondilodiscitis

Paraplegia & Spinal cord syndromes

Non-inflamatory spinal space occupying lesions

Disc prolapse NeoplasmsNon-spinal disorders Acute poliradiculitis

Guillain Barre Hyper/Hypokalemic

paralysis Parasigital cortical

syndromes: Bilateral infarctions

Toxic or allergic disorders of spinal cord

Subacute-myelo-optico-neuropahty (SMON) caused by clioquinol

Late myelopathy after chemonucleolysis

Elsberg phenomena:In cervical myelopathy there

is first weakness ipsilateral arm, then ipsilateral leg

then contralateral leg and lastly contralateral arm.

Paraplegia & Spinal cord syndromes

Clinical approach to Spinal cord syndromes

What is the onset of paraplegia

Is it acute within minutes or hours?

Is it sub-acute within days or weeks?

Is it chronic within months or years?

Was there a history of trauma?

Fall from a Height? Road traffic accident?

Direct injury to spine?

Clinical approach to Spinal cord syndromes

Symmetry of symptoms?

Is motor weakness symmetrical?

Is sensory symptoms symmetrical?

Or they are asymmetrical?

Any wasting or fasciculations?

Anywhere in the body?

Small muscles of the hand?

Thigh and gluteal muscles?

Clinical approach to Spinal cord syndromes

Is there a history of root pains?

Is it unilateral orbilateral?

Does it radiate to Limbs?

Does it aggravate with coughing?

Any pyramidal tract involvement?

Buckling of knees while walking?

Slipping of footWear?

Tipping on smallObjects?

Clinical approach to Spinal cord syndromes

History of vaccinations?

Anti Rabies Vaccination? Polio vaccination? Others?

History of increased ICT

Fever and headache? Projectile vomiting? Seizures or loss of consciousness?

Clinical approach to Spinal cord syndromes

What is the nature of neurological deficit?

Is it a?

Paraplegia?

Tetraplegia?

Brain stem lesion?

Consider and exclude Guillian Barre Syndrome

Cerebral diplgia?

Clinical approach to Spinal cord syndromesWhat is the mode of onset of paraplegia

Acute within daysTransverse myelitisAnterior spinal artery syndromeTraumatic paraplegia

Sub-acute 2- 6 weeksPott’s paraplegiaSpinal epidural abscessSpinal cord tumors

Chronic ˃ 6weeksFamilial spastic paraplegiaAmyotrophic lateral sclerosisCranio-vertebral junction anomalies

Legend

First-order neuron

Second-order neuron

Third-order neuronPain stimulus

Lesion

Sensory impairmentFunction intact

Function lost

Light touch stimulus

Lesion of the right dorsal column at L1 produces what impairment?

Damage to the right dorsal column at L1 causes the absence of light touch, vibration, and position sensation in the right leg. Only fasciculus gracilis exists below T6.

R L

Right Fasciculus Cuneatus Lesion

Fasciculus cuneatus lesion

Ipsilateral loss of light touch, vibration, and position senseIn the right arm and upper trunk

R LDRG

C3

Common causes include MS, penetrating injuries, and compression from tumors.

Lesion of the right fasciculus cuneatus at C3 produces what impairment?

Damage to the right fasciculus cuneatus at C3 causes the absence of light touch, vibration, and position sensation in the right arm and upper trunk.

R L

Lesion of the right lateral corticospinal tract at L1 produces what impairment?

Damage to the right lateral corticospinal tract at L1 causes upper motor neurons signs (weakness or paralysis, hyperreflexia, and hypertonia) in the right leg.

R L

R L

UMN

Lateral corticospinal tract lesion

Ipsilateral UMN signs below the lesion levelWeakness (Spastic paralysis) Hyperreflexia (+ Babinski, clonus) Hypertonia

Right Lateral Corticospinal Tract Lesion

L1

Common causes include penetrating injuries, lateral compression from tumors, and MS.

Damage to the right lateral spinothalamic tract at L1 causes the absence of pain and temperature sensation in the left leg.

Lesion of the right lateral spinothalamic tract at L1 produces what impairment?

R L

L4

R L

Lateral spinothalamic tract lesion

Contralateral loss of pain and temperature sense

Right Lateral Spinothalamic Tract Lesion

L1

Common causes include MS, penetrating injuries, and compression from tumors.

Damage to the anterior gray and white commissures at C5-C6 causes the absence of pain and temperature sensation in the C5 and C6 dermatomes in both upper extremities.

Lesion of the anterior gray and white commissures (central cord syndrome) at C5-C6 produces what impairment?

R L

C5-C6

Central Cord Syndrome

Lateral SpinothalamicTract

Impaired pain and temperaturesensation, C5-C6 dermatomes, bilaterally

DRG DRGR L

Common causes include posttraumatic contusion and syringomyelia, and intrinsic spinal cord tumors.

Postraumatic central cord syndromeMRI of the cervical spine focal posterior disc protrusion at C3/4 level causing spinal stenosis obliterating CSF space and impressing onto the spinal cord. There is increased intramedullary T2 signal without abnormal T1 signal noted

Damage to the right dorsal columns at L1 causes the absence of light touch, vibration, and position sense in the right leg. Damage to the lateral corticospinal tract causes upper motor neuron signs in the right leg (Monoplegia), and damage to the lateral spinothalamic tract causes the absence of pain and temperature sensation in the left leg.

Complete transection of the right half the spinal cord (Hemicord or Brown-Sequard syndrome) at L1 produces what impairments?

R L

R L

Hemicord Lesion (Brown-Sequard Syndrome)

Dorsal column lesionIpsilateral loss of light touch, vibration, and position senseLateral corticospinal tract lesion

Ipsilateral upper motor neurons signs

Lateral spinothalamic tract lesionContralateral loss of pain and temperature sense

Hemicord lesion

L1

Common causes include penetrating injuries, lateral compression from tumors, and MS.

Hemicord Lesion (Brown-Sequard Syndrome)

Cervical spine MRI showing a T2 hyperintense enhancing lesion at C2-3

Damage to the dorsal columns, bilaterally, causes the absence of light touch, vibration, and position sense in the both legs. Damage to the lateral corticospinal tracts, bilaterally, cause upper motor neuron signs in the both legs (Paraplegia), and damage to the lateral spinothalamic tracts, bilaterally, cause the absence of pain and temperature sensation in the both legs.

Complete transection of the spinal cord (Transverse cord lesion) at L1 would produce what impairments?

R L

An MRI showing a Transverse myelitis lesion (the lesion is the lighter, oval shape at center-right), this MRI was taken 3 months after patient recovered

Clinical approach to Spinal cord syndromesClinical features anterior, central, Brown-

Séquard syndrome

Anterior spinal cord syndrome is usually seen as a result of compression of the ASA. Sensory loss is incomplete. Sensitivity to pain and temperature are lost while sensitivity to vibration and position are preserved. Central cord syndrome is results impairment in the arms and hands and to a lesser extent in the legs. Loss of fine control of movements in the arms and hands, relatively less impairment of leg movements. Loss of bladder control may also occur, as well as painful parethesia.Brown-Séquard syndrome is a loss of sensation and motor function (paralysis and anesthesia) that is caused by the lateral hemisection (cutting) of the spinal cord.

Damage to the lateral corticospinal tracts cause upper motor neuron signs, bilaterally, below the lesion level. Damage to lower motor neurons in the ventral horns cause lower motor neuron signs, bilaterally, at the lesion level. Damage to the lateral spinothalamic tracts cause absence of pain and temperature sensation, bilaterally, below the lesion level. Sparing of the dorsal columns leaves light touch, vibration, and position sense intact throughout.

Complete transection of the lateral corticospinal and lateral spinothalamic tracts with sparing of the dorsal columns, bilaterally, (anterior cord syndrome) in the cervical region would produce what impairments?

R L

UMN

DRG

UMN

DRG

R L

Anterior cord lesion

Lateral corticospinal tract lesionIpsilateral upper motor neurons signs

Contralateral loss of pain and temperature sense

Lateral spinothalamic tract lesion

Anterior Cord Syndrome

Common causes include anterior spinal artery infarct, trauma, and MS.

Left: hyperintense intramedullary lesion in T2 at the level C3-C7 (arrows), indicate acute cervical spinal cord infarction. Right: MR sagittal T2: myelomalacia cavity C3-C7 in control after a month. The star indicates the infarcted area.

Anterior Cord Syndrome

R L

Posterior Cord Syndrome

DRGDRG

Dorsal column lesion (bilateral)

Bilateral loss of light touch, vibration, and position sense, generalized below lesion level

Common causes include trauma, compression from posteriorly located tumors, and MS.

Posterior Cord Syndrome

Damage to the dorsal columns (fasciculus gracilis and cuneatus), bilaterally, causes the absence of light touch, vibration, and position sense, bilaterally, from the neck down (below the lesion level).

Complete transection of the dorsal columns, bilaterally, (posterior cord syndrome) in the cervical region would produce what impairments?

R L