1. PARAPLEGIA AND SPINAL CORD SYNDROMES
Dr. M. A Sofi MD;FRCP(London);FRCPEdin
FRCSEdin

2. Overview of Spinal Cord
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

3. Functions of the 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

4. Somato-sensory Organization

5. Lateral Coticospinal Tract Anterior Corticospinal Tract
Somato-sensory Organization
Descending Tracts
Pyramidal Tracts
Lateral Coticospinal Tract
Anterior Corticospinal Tract
Extrapyramidal Tracts
Rubrospinal
Reticulaospinal
Olivospinal
Vestibulospinal

6. Somato-sensory Organization
Sensory & Ascending Pathways
Ascending tracts
Dorsal Column Medial Lemniscus
Gracile fasciculus
Cuneate fasciculus
Spinocerebellar Tracts
Posteriors pinocerebellar
Anterior spinocerebellar
Anterolateral System
Lateral spinothalmic tract
Anterior spinothalmic tract
Spino-olivary tract

7. BLOOD SUPPLY SPINAL CORD

8. Paraplegia & Spinal cord syndromes
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.
Phase
Time
Physical exam finding
Underlying physiological event 1
0-1d
Areflexia/Hyporeflexia
Loss of descending facilitation 2
1-3d
Initial reflex return
Denervation supersensitivity 3
1-4w
Hyperreflexia (initial)
Axon-supported synapse growth 4
1-12m
Hyperreflexia, Spasticity
Soma-supported synapse growth

9. Paraplegia & Spinal cord syndromes
Classification of etiology
UMN type/ Spastic paraplegia
LMN type/Flaccid paraplegia
Cortical lesion
Spinal cord lesion
Non-compressive Myelopathy
Tumor Falx Cerebri
Superior Sagital Sinus Thrombosis
Compressive Myelopathy

10. Classification of etiology COMPRESSIVE MYELOPATHY
Paraplegia & Spinal cord syndromes
Classification of etiology
COMPRESSIVE MYELOPATHY
EXTRAMEDULLARY
INTRAMEDULLARY
Syringomyelia, Ependymymoa, Glioma, Astrocytoma
EXTRADURAL
INTRADURAL
DISC
VERTEBRAL
Meningoma, Neurofibroma, Arachnoditis

11. Classification of etiology Non-compressive myelopathies
Paraplegia & Spinal cord syndromes
Classification of etiology
Non-compressive myelopathies
NONINLAMMATORY
INFAMMATORY
INFECTIOUS: VIRAL, BACTERIAL ,FUNGAL PARASTIC
AUTOIMMUNE: SLE, SJOGREN, SARCOIDOSIS, BECHET S, MCTD
DEMYELINATING: MS,NMO, ADEM, POST VIRAL POST VACCINIAL
PARANEOPLASTIC
INHERITED: HSP, INHERITED METABOLIC DISORDERS
METABOLIC: VIT B12,COPPER,FOLATE ,AIDS ASSOCIATED, VIT E DEFICIENCY
TOXIC: CASSAVA, LATHYRISM,FLUOROSIS,
SMON, NITROUS OXIDE
VASCULAR: ANT SPINAL ARTERY THROMBOSIS, AVM, DURAL AV FISTULA

12. Paraplegia & Spinal cord syndromes
Differences 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 lesion
Reflex level – Inverted supinator C5 lesion

13. Paraplegia & Spinal cord syndromes
Vascular disorders of spinal cord
Ischemic disorders of spinal cord
Primary ischemia: atherosclerosis/vasculitis
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

14. Paraplegia & Spinal cord syndromes
Non-inflamatory spinal space occupying lesions
Disc prolapse
Neoplasms
Non-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.

15. 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?

16. Any wasting or fasciculations?
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?

17. Clinical approach to Spinal cord syndromes
Is there a history of root pains?
Is it unilateral or
bilateral?
Does it radiate to
Limbs?
Does it aggravate with coughing?
Any pyramidal tract involvement?
Buckling of knees while walking?
Slipping of foot
Wear?
Tipping on small
Objects?

18. History of vaccinations?
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?

19. Clinical approach to Spinal cord syndromes
What is the nature of neurological deficit?
Is it a?
Paraplegia?
Tetraplegia?
Brain stem lesion?
Cerebral diplgia?
Consider and exclude Guillian Barre Syndrome

20. Clinical approach to Spinal cord syndromes
What is the mode of onset of paraplegia
Acute within days
Transverse myelitis
Anterior spinal artery syndrome
Traumatic paraplegia
Sub-acute weeks
Pott’s paraplegia
Spinal epidural abscess
Spinal cord tumors
Chronic ˃ 6weeks
Familial spastic paraplegia
Amyotrophic lateral sclerosis
Cranio-vertebral junction anomalies

21. Legend First-order neuron Lesion Second-order neuron Pain stimulus
Third-order neuron
Light touch stimulus
Sensory impairment
Function intact
Function lost

22. 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.

23. Right Fasciculus Cuneatus Lesion
DRG R L C3
Fasciculus cuneatus lesion
Ipsilateral loss of light touch, vibration, and position sense
In the right arm and upper trunk
Common causes include MS, penetrating injuries, and compression from tumors.

24. R L
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.

25. 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.

26. Right Lateral Corticospinal Tract Lesion
UMN R L L1
Lateral corticospinal tract lesion
Ipsilateral UMN signs below the lesion level
Weakness (Spastic paralysis) Hyperreflexia (+ Babinski, clonus) Hypertonia
Common causes include penetrating injuries, lateral compression from tumors, and MS.

27. Lesion of the right lateral spinothalamic tract at L1 produces what impairment?
Damage to the right lateral spinothalamic tract at L1 causes the absence of pain and temperature sensation in the left leg.

28. Right Lateral Spinothalamic Tract Lesion
Contralateral loss of pain and temperature sense
Common causes include MS, penetrating injuries, and compression from tumors.

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

30. Central Cord Syndrome Impaired pain and temperature
DRG
DRG
C5-C6
Lateral
Spinothalamic
Tract
Common causes include posttraumatic contusion and syringomyelia, and intrinsic spinal cord tumors.
Impaired pain and temperature
sensation, C5-C6 dermatomes,
bilaterally

31. Postraumatic central cord syndrome
MRI 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

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

33. Hemicord Lesion (Brown-Sequard Syndrome)
Common causes include penetrating injuries, lateral compression from tumors, and MS.
Dorsal column lesion
Ipsilateral loss of light touch, vibration, and position sense
Lateral corticospinal tract lesion
Ipsilateral upper motor neurons signs
Lateral spinothalamic tract lesion
Contralateral loss of pain and temperature sense

34. Hemicord Lesion (Brown-Sequard Syndrome)
Cervical spine MRI showing a T2 hyperintense enhancing lesion at C2-3

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

36. 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

37. Clinical features anterior, central, Brown-Séquard syndrome
Clinical approach to Spinal cord syndromes
Clinical 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.

38. 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
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.

39. Anterior Cord Syndrome
UMN
UMN
DRG
DRG R L
Anterior cord lesion
Common causes include anterior spinal artery infarct, trauma, and MS.
Lateral corticospinal tract lesion
Ipsilateral upper motor neurons signs
Lateral spinothalamic tract lesion
Contralateral loss of pain and temperature sense

40. Anterior Cord Syndrome
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.

41. Posterior Cord Syndrome
DRG
DRG R L
Common causes include trauma, compression from posteriorly located tumors, and MS.
Dorsal column lesion (bilateral)
Bilateral loss of light touch, vibration, and position sense, generalized below lesion level

42. Posterior Cord Syndrome

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