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. 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

5. 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

6. Somato-sensory Organization

7. BLOOD SUPPLY SPINAL CORD

8. Paraplegia & Spinal cord syndromes
Paraplegia is an impairment in motor or sensory function of the lower extremities.
It is usually caused by spinal cord injury or a congenital
condition such as spina bifida that affects the neural elements of
the spinal canal.
The area of the spinal canal that is affected in paraplegia is either
the thoracic, lumbar, or sacral regions.
If all four limbs are affected by paralysis, tetraplegia is the proper
terminology.
If only one limb is affected, the correct term is monoplegia.
Spastic paraplegia is a form of paraplegia defined by spasticity of the affected muscles, rather than flaccid paralysis

9. Paraplegia & Spinal cord syndromes
Spinal shock was first defined by Whytt in 1750 as 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 transection.
Reflexes in the spinal cord caudal to the SCI are depressed (hyporeflexia) or absent (areflexia), while those rostal to the SCI remain unaffected.
‘Shock' in spinal shock does not refer to circulatory collapse, and should not be confused with neurogenic shock, which is life threatening.
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

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

11. 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

12. 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

13. 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

14. 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
Medular compression:
Epidural abscess
Subdural abscess
Spondilodiscitis

15. 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.

16. 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?

17. 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?

18. 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?

19. 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?

20. 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 Gullian Barre Syndrome

21. 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

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

23. 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.

24. Right Dorsal Column Lesion
DRG R L L1
Dorsal column lesion
Ipsilateral loss of light touch, vibration, and position sense
generalized below the lesion level
Below T6 only the fasciculus gracilis is present.
Common causes include MS, penetrating injuries, and compression from tumors.

25. 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.

26. 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.

27. 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.

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

29. R L
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.

30. Right Lateral Spinothalamic Tract Lesion
DRG R L L1
Lateral spinothalamic tract lesion
Contralateral loss of pain and temperature sense
Common causes include MS, penetrating injuries, and compression from tumors.

31. 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.

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

33. 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.

34. 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

35. Hemicord Lesion (Brown-Sequard Syndrome)
UMN
DRG R L
DRG L1
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
Hemicord lesion

36. 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.

37. Transverse Cord Lesion
Dorsal column lesion
Bilateral loss of light touch, vibration, and position sense
Common causes include trauma, tumors, transverse myelitis, and MS.
Lateral corticospinal tract lesion
Bilateral upper motor neurons signs
Lateral spinothalamic tract lesion
Bilateral loss of pain and temperature sense

38. Transverse Cord Lesion
UMN
UMN
DRG
DRG R L
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
Transverse cord lesion

39. 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.

40. 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).

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. 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.

43. 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

44. THANK YOU
FOR
YOUR ATTENTION

45. Paraplegia & Spinal cord syndromes
60 year old female presented with hand clumsiness, worsening handwriting, difficulty with grasping and holding objects, diffuse numbness in the hands, and increasing difficulty with balance and ambulation. Physical examination revealed unsteadiness, broad-based gait, increased muscle tone, weakness and wasting of the upper and lower limbs, and diminished sensation to light touch, temperature, proprioception, and vibration.
What is the likely diagnosis?
What are imaging features?
What is recommended treatment?

46. Paraplegia & Spinal cord syndromes
72-year-old man NIDDM, dyslipidemia and psoriasis. He was referred for left- side weakness that had been worsening since 6/12
O/E
The left pupil was smaller, 3 millimeters reactive to 2.
Mild left eye ptosis.
Hyperreflexia more on the left than the right.
Bilateral planter up going
Left hemisensory syndrome.
Mildly spastic gait
What is diagnosis?
What is cause of ptosis?
What is treatment of choice?

47. Paraplegia & Spinal cord syndromes
27-year (F) had a 2-week history of back and lower extremity pain with gradual weakness and paresthesias of the legs, accompanied by urinary retention. This progressed to involve all extremities and inability to stand. No antecedent neurological/respiratory or gastrointestinal illness. Four days prior to the onset of symptoms, she received the attenuated-virus nasal novel influenza A(H1N1) vaccine. Examination revealed
Mild proximal muscle weakness UL
Mild diminished sensation of the UL
Moderate proximal weakness LL
Profound sensory loss in the LL.
Sensations moderately diminished on the trunk.
T4 sensory level.
Diffuse hyperreflexia
Plantar response was silent and no clonus.
What is the diagnosis?
List 3 major investigations of choice?
What is treatment of choice?

48. Paraplegia & Spinal cord syndromes
48 year old male presented with sudden onset of:
Complete motor paralysis of
all 4 limbs
Loss of temperature and
pain sensation below T2
Retained proprioception &
vibratory sensation.
Areflexia
Flaccid anal sphincter,
urinary retention.
What is the diagnosis?
List 3 causes for this condition?
What treatment can be offered?

49. Paraplegia & Spinal cord syndromes
60 year old lady had H/O recurrent lower limb paralysis. Now presented with quadreparesis. She had for many years suffered from Rheumatoid arthritis and has been on NSAID on and off for years. She had been using artificial tears for grittiness and dryness of eyes. Not known to have DM or HTN.
O/E
Joint deformities of RA
Quadreparesis of UMN below C2
Dysesthesia of both lower extremities and the left trunk, weakness of the left leg, and urinary disturbance.
Decreased sensations for touch and pin prick glove and stocking type
Bilateral up-going planter response
Reflexes present symmetrical in all four limbs
What is diagnosis?
What is cause for recurrent Paraparesis?

50. Paraplegia & Spinal cord syndromes
68-year-old woman with a 9-month history of back pain and sensory loss, progressing to the point of loss of bowel and bladder function along with a sudden onset of paraparesis. The pain occurred both at rest and on exercise and at times radiated to lower limbs.
O/E
Grade IV weakness both LL
Sensory deficit to pin prick to D4
Hyper-reflexia knee & ankle jerks
Bladder incontinence
Bilateral extensor planter response
What are imaging abnormalities?
What is the cause of paraplegia?
What investigations are pertinent?

51. Paraplegia & Spinal cord syndromes
31 year old man presented history of dorsal pain that had progressed for 4/12. He complained of numbness of both lower limbs and had developed urinary incontinence and constipation. He had bilateral facial weakness a year earlier that had partially improved with steroid therapy. 6/12 ago he had painful redness of eye
O/E
Decreased sensation to pin prick, light touch, and impaired JPS & vibration to T7 – T8 bilaterally.
LL weakness grade IV.
Hyperactive tendon reflexes
Bilateral up going planters
Absent superficial abdominal reflexes
CSF: Cells 42 lymphocytes. Protein 1Gm/L
Case for discussion

52. Paraplegia & Spinal cord syndromes
A 56-year-old right-handed man with recurrent bilateral uveitis had memory disturbance, constructional and dressing apraxia at age 53. He presented with subacute spastic paraparesis and urinary retention age 56.
O/E Hyperreflexia in the lower limbs with bilateral extensor response. Memory disturbance, dressing and constructional apraxia. CSF mild lymphocytic pleocytosis. After intravenous methylprednisolone treatment, clinical symptoms resolved and abnormal intensities with enhancement of the cord disappeared.
What is the likely cause of his symptoms?
What is the likely cause of his MRI lesion?
What is long-term treatment modality?

53. Paraplegia & Spinal cord syndromes
30 year old lady presented with bilateral loss of vision and weakness of LL in 2010 that resolved in few weeks. 8/12 later she presented with LL weakness and urine incontinence improved with I/V prednisolone significantly. One year later she developed quadrepresis that showed some improvement with steroid + Azothioprin
What is the imaging feature in MRI?
What is the likely diagnosis?
Name two investigations of relevance?