2021 paraplegia uptodate

1. Dr. Bikal Lamichhane
PGY-2
NAMS Internal Medicine
Approach to Paraplegia/Paraparesis

2.  The word plegia comes from a Greek word
meaning “to strike,” and the word “palsy” is from
an old French word that has the same meaning as
paralysis.
 Paralysis means loss of voluntary movement as a
result of interruption of one of the motor pathways
at any point from the cerebrum to the muscle fiber.
A lesser degree of weakness is spoken of as
paresis

3.  Based on the location and distribution of the muscle weakness weakness
can be calssified further as follow:-
 1. Monoplegia:-
 refers to weakness or paralysis of all the muscles of one leg or arm.
 2. Hemiplegia:-
 commonest form of paralysis, involves the arm, the leg, and sometimes
the face on one side of the body.
 3. Paraplegia :-
 indicates weakness or paralysis of both legs.
 It is most often the result of diseases of the thoracic spinal cord, cauda
equina, or peripheral nerves, and rarely, both medial frontal cortices.

4. 4. Quadriplegia (tetraplegia):-
denotes weakness or paralysis of all four extremities.
result from disease of the peripheral nerves, muscles, or myoneural
junctions; gray matter of the spinal cord; or the upper motor
neurons bilaterally in the cervical cord, brainstem, or cerebrum.
Diplegia:-
is a special form of quadriplegia in which the legs are affected more
than the arms.
Triplegia:-
occurs most often as a transitional condition in the development of,
or partial recovery from, tetraplegia.
.

5. 5. Isolated paralysis of one or more muscle groups due to
disease of muscle, anterior horn cells, or nerve roots.
6. Nonparalytic disorders of movement (e.g., apraxia,
ataxia, rigidity).
7. Hysterical paralysis

6. Neuroanatomy of Spinal Cord
 Cylindrical in shape.
 Extent:- From foramen magnum in the skull (Medulla
oblangata of brain) to L1.
 Lies in the vertebral canal.
 Average length – 45 cm in adult male & 42-43 cm in adult
female.
 Weight = approx 30 gms

7.  Although it is a continuous and non-segmental
structure, 31 pair of originating nerves give it
segmental appearance.
 Occupies only 2/3rd of Spinal cord, thus the vertebral
spine level and spinal segment level are different.
 31 pair of spinal nerves:-
 8 Cervical
 12 Thoracic
 5 Lumbar
 5 Sacral
 1 Coccygeal

8.  All spinal nerves, except the first, exit below
their corresponding vertebrae.
 In the cervical segments, there are 7 cervical
vertebrae and 8 cervical nerves .
 C1-C7 nerves exit above their vertebrae whereas
the C8 nerve exits below the C7 vertebra.
 It leaves between the C7 vertebra and the first
thoracic vertebra.
 Therefore, each subsequent nerve leaves the cord
below the corresponding vertebra.

9.  Therefore, the root filaments of spinal cord
segments have to travel longer distances to
reach the corresponding intervertebral foramen
from which the spinal nerves emerge.
 The lumbosacral roots are known as the cauda
equina

10. SPINAL CORD LEVELS RELATIVE
TO THE VERTEBRAL BODIES
SPINAL CORD LEVEL CORRESPONDING
VERTEBRAL BODY
Upper cervical Same as cord level
Lower cervical +1
Upper thoracic +2
Lower thoracic + 2 to 3 levels
Lumbar T 10 – T 12
Sacral T 12 – L1

13. Regions of the Spine
 Cervical
 Upper cervical: C1-C2
 Lower cervical: C3-C7
• Thoracic: T1-T12
• Lumbar: L1- L5
• Sacrococcygeal: 9
fused vertebrae
in the sacrum
and coccyx.

14. Cervical Lordosis 20°- 40°
Thoracic Kyphosis 20°- 40°
Lumbar Lordosis 30°- 50°
Sacral Kyphosis
Sagittal Plane Curves

15. Regions of the Spine
Line of gravity
Auricle of the ear
Odontoid
Body of C7
Anterior to
thoracic spine
Posterior to
L3
Mid femoral
heads

16. Functions of the Spine
Protection of
 spinal cord and nerve
roots
• internal organs

17. Functions of the Spine
 Flexibility of motion in six degrees of freedom
Left and Right
Side Bending
Flexion and Extension
Left and Right
Rotation

18. Spinal Injuries:-

19. Internal Structure of the Spinal Cord
 A transverse section of the adult spinal cord shows
white matter in the periphery, gray matter inside,
and a tiny central canal filled with CSF at its center.
 Surrounding the canal is a single layer of cells,
the ependymal layer.
 Surrounding the ependymal layer is the gray
matter – a region containing cell bodies –
shaped like the letter “H” or a “butterfly”.
 The two “wings” of the butterfly are connected
across the midline by the dorsal gray commissure
and below the white commissure.

20.  The shape and size of
the gray matter varies
according to spinal cord
level.
 At the lower levels, the
ratio between gray matter
and white matter is
greater than in higher
levels, mainly because
lower levels contain less
ascending and
descending nerve fibers.

21. White Matter
 The white matter, which consists of longitudinal
bundles of nerve fibres, is divided into three
columns on each side.
 Anterior column
 Lateral column
 Posterior column
 Anterior column:-
 contains ascending and crossed fibres in the
ventral spino-thalamic tract, along with the
descending fibres in the olivo-spinal, vestibulo-
spinal, tecto-spinal, and ventral cortico-spinal
tracts.

22.  Lateral column:-
 contains the major descending motor pathway, lateral
cortico-spinal tract, with the smaller descending
rubro-spinal tract and the ascending and crossed
spinothalamic tract.
 Dorsal column:
 contains the uncrossed gracile and cuneate
fascicles.
 In the lateral cortico-spinal tract the descending
motor neurons destined for the lumbo-sacral segments
run laterally to those destined for the cervical
segments.
 In posterior columns fibres from the lower limbs lie

23. Arrangement of fibers
Posterior column-
As they do not cross at the entry point in the
spinal cord segments, the fibres from the
lower limbs are placed more medially near the
central canal.
The fibres from the upper limbs are placed
more laterally.
- Medial to lateral at cervical level: Sacral,
lumbar, thoracic, and cervical respectively.
- Central canal to dorsum: (anterior to posterior)

24. Medial to lateral at
cervical level:
 Sacral, lumbar,
thoracic, and
cervical
respectively.(SLTC)
Central canal to
dorsum: (anterior to
posterior) touch,
position, movement,
vibration and pressure

25. Lateral column and anterior column:-
- Corticospinal tract
- Spinothalamic tract
 As the fibers cross in the spinal cord, the lower limb
fibers are placed more laterally, and the upper limb
fibers are placed more medially at the cervical level.
 Medial to lateral- Cervical, thoracic, lumbar and
sacral(CTLS)

26. Corticospinal tract
Spinothalamic tract
 As the fibers cross in the
spinal cord, the lower
limb fibers are placed
more laterally, and the
upper limb fibers are
placed more medially at
the cervical level.
 Medial to lateral-
Cervical, thoracic,
lumbar and
sacral(CTLS)

27. Spinal Cord Nuclei and Laminae
 Spinal neurons are organized into nuclei and laminae.
 Nuclei
 The prominent nuclear groups of cell columns within the
spinal cord from dorsal to ventral are the:
- marginal zone
- substantia gelatinosa
- nucleus proprius
- dorsal nucleus of Clarke
- intermediolateral nucleus
- lower motor neuron nuclei.

28. Rexed Laminae-anatomy and function
The distribution of cells and fibers within the
gray matter of the spinal cord exhibits a
pattern of lamination.
The cellular pattern of each lamina is
composed of various sizes or shapes of
neurons (cytoarchitecture) which led, Rexed
to propose a new classification based on 10
layers (laminae).

29. Rexed Laminae-cont
• Laminae I to IV- are
concerned with
exteroceptive sensation.
• Laminae V and VI are
concerned primarily with
proprioceptive sensations.
• Lamina VII- acts as a relay
between muscle spindle to
midbrain and cerebellum.
• Laminae VIII-IX- The axons of
these neurons innervate mainly
skeletal muscle.
• Lamina X surrounds the
central canal and contains
neuroglia.

30. MENINGES
• Within the spinal canal, the spinal cord is
surrounded by the EPIDURAL SPACE, filled with
fatty tissue, veins, and arteries.
• The fatty tissue acts as a shock absorber.
• The spinal cord is covered by MENINGES which
has three layers.

31. MENINGES
Subdural
space
Arachnoid
layer
Dura mater
Subarachnoid
space: filled
with CSF
Pia
mater

32. Blood supply of spinal cord
 Anterior spinal artery
 Posterior spinal
arteries
 Segmental spinal
arteries
- radicular arteries
 Feeder arteries
- Adamkiewicz

33. Blood supply of spinal cord
 The spinal arteries are reinforced at each intervertebral
foramen by segment arteries derived from :-
 verterbral
 costo-cervical trunk,
 intercostal and
 lumbar arteries.

35. Blood supply-cont
 At spinal cord regions below upper cervical levels,
the anterior and posterior spinal arteries narrow
and form an anastomotic network with radicular
arteries.
 The posterior spinal arteries are paired and form
an anastomotic chain over the posterior aspect
of the spinal cord.
 A plexus of small arteries, the arterial
vasocorona, on the surface of the cord
constitutes an anastomotic connection between
the anterior and posterior spinal arteries.
 This arrangement provides uninterrupted

37. Artery of Adamkiewicz
 The artery of Adamkiewicz (also arteria
radicularis magna) is the largest anterior
segmental medullary artery.
 The artery is named after Albert Adamkiewicz.
 It typically arises from a left posterior intercostal
artery which branches from the aorta at the level of
the T9 and L2, and supplies the lumbar
enlargement .
 It is also known as
- Great radicular artery of Adamkiewicz.
- Major anterior segmental medullary artery.

38. posterior 3rd of spinal cord
dorsal column
penetrating branches
•anterior and part of gray matter
circumferential branches
• anterior white matter

39. Venous Drainage
 The spinal veins derived from the spinal cord substance
terminate in a plexus in the pia mater where there are
six tortous, often plexiform longitudinal channels,
-one along the anterior median fissure
- a second along the posterior median sulcus
- two situated on either side,
- one pair just behind and the other just in front of the
ventral and dorsal nerve roots.
 These six vessels communicate freely with one other
and above pass into the corresponding veins of the
medulla oblongata and drain into the intracranial
venous sinuses.

40. Batson’s Plexus
• The AZYGOS SYSTEM is a large network of
veins draining blood from the intestines and
other abdominal organs back to the heart.
• The segmental veins drain into the azygos vein
located on the right side of the abdomen, or
into the hemiazygos vein located on the left
side.

41.  The azygos system also communicates with a valveless
venous network known as BATSON’S PLEXUS.
 When the vena cava is partially or totally occluded, Batson’s
plexus provides an alternate route for blood return to the
heart.
 The vessels of Batson’s plexus may be referred to as epidural
veins Batson’s
plexus

42. Communications and Implications
 Valveless vertebral system of veins communicates:
- Above with the intracranial venous sinuses.
-Below with the pelvic veins, the portal vein, and the
caval system of veins.
 The veins are valveless and the blood can flow in
them in either direction.
 Such flow are clinically important because they
make possible spread of tumors or infections.

43. AscendingAnd Descending
tracts

46. ascending sensory pathway
( in general form )
from sensory endings
to
cerebral cortex
( note the three neurons chain )

47. Pain and temperature pathways

48. Clinical application destruction of LSTT
Loss of
 pain and thermal sensation
 on the contralateral side
 below the level of the lesion
Patient will not
respond to pinprick
recognize hot and cold

49. Touch and pressure pathways ASTT

50. Clinical application
destruction of ASTT
loss of touch and pressure sense
below the level of lesion
on the contralateral side of the body

51. Pathways for conscious proprioception discriminative touch vibratory sense

52. Clinical application
destruction of
fasciculus gracilia and cuneatus
 loss of muscle joint sense, position
sense, vibration sense and tactile
discrimination
 on the same side
 below the level of the lesion

53. Posterior and anterior spinocerebellar
tract
Transmit unconscious proprioceptive information
to the cerebellum.( length and tension of muscle
fibers)
Receive input from muscle spindles, Golgi Tendon
Organs and pressure receptors.
Involved in coordination of posture and movement
of individual muscles of the lower limb.

54. Muscle, joint sense pathways to cerebellum

55. Spinoreticular tract
 The spinoreticular tract is an ascending pathway in the
white matter of the spinal cord, positioned closely to
the lateral spinothalamic tract.
 The tract is from spinal cord—to reticular formation to
thalamus.
 It is responsible for automatic responses to pain, such
as in the case of injury .

58. Extrapyramidal Tracts
 The extrapyramidal tracts originate in the brainstem,
carrying motor fibres to the spinal cord.
 They are responsible for the involuntary and automatic
control of all musculature, such as muscle tone,
balance, posture and locomotion.
 There are four tracts in total.
The vestibulospinal and reticulospinal tracts do not
decussate, providing ipsilateral innervation.
The rupbrospinal and tectospinal tracts do decussate,
and therefore provide contralateral innervation.

61. Paraplegia
 Definition : Impairment in motor function of lower
extremities with or without involvement of sensory
system.
 Usually caused by involvement of :
 cerebral cortex
 spinal cord
 nerves supplying muscles of of lower limbs
 or due to involvement of muscles directly

62. Paraplegia
Spastic (UMN type) Flaccid (LMN type)
Paraplegia in Extension Paraplegia in Flexion

63.  Spastic paraplegia
 Weakness of muscle along with increased tone
 Occurs in upper motor neuron (UMN) disease due
to loss of inhibition of contraction
 Findings
 Increased muscle tone
 Exaggerated deep tendon reflexes
 Extensor planter response

64. Flaccid paraplegia
 Decreased tone and contractility of muscles
along with weakness
 Occurs in LMN lesions
 Due to loss of stimulatory innervation to muscle
 Findings
 Decreased muscle tone
 Atrophied muscle
 Absent deep tendon reflexes
 Flexor or equivocal planters
 With or without fasciculations

65. Causes of Paraplegia
 Due to upper motor neuron lesion (spastic paralysis)
 Intracranial/Cerebral
 Spinal (myelopathy)
 Non compressive
 Compressive
 Due to lower motor neuron lesion (flaccid paralysis)
 Anterior horn cells
 Roots
 Peripheral nerves
 Myo-neuronal junction
 Muscles
 Functional or hysterical

66. CEREBRAL CAUSES :
A. Causes in parsagittal Region
1. Traumatic :
• depressed fracture of vault of skull, subdural hematoma
2. Vascular : Superior sagittal sinus thrombosis
3. Inflammatory : Encephalitis, meningocephalitis
4. Neoplasm : Parasagital meningioma
5. Degenerative : Cerebral palsy
B. Causes in Brain Stem
• Syringobulbia and midline tumors

67. SPINAL CAUSES
Compressive Non-compressive
myelopathy myelopathy

68. Spinal cord
Non-compressive myelopathy
 Infections
 Bacterial: tubercular, syphilis
 Viral: EBV, CMV, HIV, HSV-1, VZV, HTLV-1 (Tropical spastic
paraplegia)
 Vascular
 Thrombosis of anterior spinal artery
 Embolism: Leriche’s syndrome (Saddle shaped thrombus at
bifurcation of aorta)
 Iatrogenic: after surgery for aorta (Co-arctation or aneurysm)
with prolonged clamping
 Vasculitis: Antiphospholipid antibody syndrome (APLA)

69.  Demyelinating disorders
 Multiple sclerosis
 Post infectious demyelination
 Post vaccine demyelination
 Toxic
 Lathyrism
 Metals: arsenic, bismuth, lead
 Uremia
 Toxemia of pregnancy

70.  Nutritional
 Pellagra
 Sub acute combined degeneration of spinal cord
 Nutritional myelopathy
 Traumatic
 Electric: electric shock, lightening
 Radiation
 Chemical: intrathecal methotrexate, penicillin
 Degenerative: motor neuron disease
 Hereditary
 Herditary spino-cerebellar ataxia
 Hereditary spastic paraplegia
 Freidrich’s ataxia
 Neoplasm
 Paraneoplastic syndrome

71. Compressive myelopathy
Extramedullary extradural
 Trauma: fracture dislocation of vertebral column
 Infection
o Epidural abscess
o Tuberculosis: cold abscess, collapse of vertebral
column
 Tumors
o Lipomas, neurofibromas, meningioma
o Metastasis causing fracture dislocation of vertebral
column
 Others

72. Extramedullary intradural
 Arachnoiditis: tuberculosis, syphilis, pyogenic, cryptococcus,
toxoplasmosis, fungal, chemical
 Tumors: lipoma, neurofibroma, meningioma
Intramedullary
 Syringomyelia
 Infections: tuberculosis, syphilis
 Tumors: glioma, lipoma
 Trauma: hematomyelia
Others: hemangioma, A-V malformation

73. Lower motor neuron lesion
 Anterior horn cells
 Infectious: polio, HIV, HTLV-1
 Motor neuron disease
 Roots
 Guillain Barre Syndrome
 Infection: Tabes dorsalis, HZV, EBV, CMV
 Cauda equina syndrome
 Prolapsed intervertebral disc
 Diabetic amyotrophy

74.  Peripheral nerves
 Peripheral neuritis
 Myo-neuronal junction
 Myasthenia Gravis
 Eaton Lambert syndrome
 Periodic paralysis
 Muscles
 Polymyositis
 Myopathy, myositis
 Muscular dystrophy

75. Based on onset :-
Acute paraplagia
I. Upper motor neuron lesion
A. Intracranial
-thrombosis of unpaired anterior cerebral artery
-thrombosis of superior sagittal sinus
B. Spinal
I. Non compressive myelopathy
- Acute transverse myelitis
- Infections
- vascular
- demyelinating diseases: MS, post infections, vaccination
- traumatic
II.Compressive myelopathy
- Extramedullary intradural: Arachnoiditis
- Extramedulary extradural: fracture
dislocation of vertebral column, epidural
abscess

76. II. Lower motor neuron lesion
Roots:
- Gullian Barre syndrome
- viral radiculitis
- prolapsed intervertebral disc
Myoneural junction:
-periodic paralysis

77. If the onset is acute
 Difficult to distinguish spinal from neuropathic
paralysis because of spinal shock, causing flaccidity
and abolished reflexes
 Involvement of corticospinal tracts causes paralysis
or weakness affecting all muscles below a given
level
 If white matter is extensively damaged, sensory level
below a circumferential level on trunk is also present
 In bilateral disease of the spinal cord, bladder and
bowel are affected

78. Gradual onset of paraplagia
1. UMN Lesion
Intracranial: Tumour of fax cerebri(meningioma),SOL
over motor area
Spinal
i. Non compressive myelopathy
- Toxic: lathyrysm, fluorosis
- Nutritional: pellegra
- Motor neuron disease
- Hereditary spastic paraplagia, spinocerebellar ataxia,
fredrich’s ataxia

79. ii. Compressive myelopathy
-Extramedullary extradural:
-Infections (TB cold abscess, collapse of vertebra)
-tumours, Aortic aneurysm, fluorosis
-Extramedullary
Intradural: Arachnoiditis, Tumours,
Intramedullary: syringomyelia, infections,
tumours

80. II. Lower motor neuron
A. Anterior horn cell: polio, motor neuron disease
B. Roots: Tabes dorsalis, diabetic amyotrophy,
cauda equina syndrome
C. Peripheral neuropathy
D. Myoneural junction
E. Muscle: polymyositis, myopathy, muscular
dystrophy

81.  Cerebral paraplegia
 There may be weakness of upper limbs along with other
features ie. Mental retardation, delayed milestones, seizures,
altered sensorium etc.
 Spinal paraplegia
 Spasticity, exaggerated DTR, radicular pain, dermatomal
sensory involvement with specific motor weakness
depending on level of lesion
 Peripheral nerve involvement
 Distal weakness, sensory loss, muscle atrophy, absent
tendon reflexes

82. Stages of paraplegia
 Stage of spinal shock
 Paraplegia in extension and
 Paraplegia in flexion

83. Spinal shock
 Loss of motor function at the time of injury
 Loss of all sensation below a level
corresponding to spinal cord lesion, muscular
flaccidity, and almost complete suppression of
reflex activity below the lesion
 Duration: 1 to 6 weeks
 First reflex to return is bulbocavernous reflex
 Spinal shock is believed to be due to
interruption of suprasegmental descending
fibres

84. Paraplegia in extension
Occurs in initial stages or partial
transection of spinal cord
Involvement of pyramidal tract
Hypertonia is more in extensor group
of muscles

85. Paraplegia in flexion
 Occurs as the disease or lesion progresses
further or with complete transection of
spinal cord
 Extrapyramidal tracts are involved leading
to hypertonia in flexor group of muscles
resulting in flexed posture of limbs

86. Paraplegia in
extension
Paraplegia in flexion
Cause Pyramidal lesion Pyramidal and extrapyramidal
lesion
Hypertonia More in extensors More in flexors
Position of lower
limbs
Extended Flexed
Deep tendon
reflexes
Exaggerated Present but diminished
Clonus Present Absent
Planter response Extensor Extensor but may be associated
with flexor spasm
Mass reflex Absent May be present

87. Approach
 History
 Onset
 Acute (within minutes or hours)
 Trauma: fracture dislocation of vertebrae
 Infection: epidural abscess
 Vascular: Thrombosis of ASA
 Transverse myelitis
 Subacute (within days or weeks)
 Pott’s paraplegia, Spinal epidural abscess, spinal cord tumors
 Chronic (within months or years)
 Familial spastic paraplegia, Amyotropic lateral sclerosis,
Craniovertebral anomalies

88.  History of trauma
 Fall from height/ road traffic accident/ direct injury
 History of back pain
 Duration,
 Maximum intensity and
 History of spinal surgery
 Is there any girdle pain or sensation
 Any pain around the thorax or abdomen
 Is it unilateral or bilateral
 Does it increase with coughing or sneezing

89.  History of root pain
 Is it unilateral or bilateral
 Does it radiate to limbs
 Does it aggravate with coughing
 Any pyramidal tract involvement
 Slipping of slippers
 Tripping on small objects
 Any lower motor neuron involvement
 Loss of tone
 Wasting and
 Fasciculations

90.  Any dorsal column involvement
 Swaying while washing face or
 Difficulty in walking at night
 Any cerebellar involvement
 Any swaying while walking
 Inability to sit upright
 Incoordination
 Any bladder involvement
 Retention of urine
 Overflow incontinence
 Bladder sensation

91. Any bowel involvement
 Constipation
 Bowel incontinence
 Bowel sensation
Autonomic dysfunction
 Excessive or absence of sweating
History of
 Viral infection
 Vaccination
 Tuberculosis
 Malignancy

92.  Dietary history
 veg/non veg
 alcohol intake in excess
 Smoking
 History suggestive of malignancy
 swelling or bone tenderness
 Surgery for tumors
 Chemotherapy or radiation
 Family history
 Neurofibromatosis, hypercoagulability, bleeding
diathesis

93. NEUROLOGICAL
EXAMINATION
 Higher mental function status
 Affected in cerebral and degenerative diseases
 Cranial nerve examination
 Affected in brain stem leisons
 Tone
 Increased in UMN disease
 Decreased in LMN disease

94.  DTR
 Exaggerated in UMN leisons
 Absent in LMN leisons and spinal shock
 Sensory examination
 T
oassesparticular sensorylevel
 T
ofind the extent of sensory loss
 Proper examination of skull andspine
 T
olook for any localized tenderness
 Depressed fracture
 Deformity

95. Determining the Level of the
Lesion
 Sensory level:
 horizontally defined level below which sensory,
motor, and autonomic function is impaired, is a
hallmark of spinal cord disease
 Sensory loss below this level is due to
damage to the spinothalamic tract on the
opposite side

96.  Lesions transecting the cord produces
autonomic disturbances:
 Absent sweating below the cord level and
 Bowel, bladder and sexual dysfunction
 Lesions transecting corticospinal tract
produces LMN lesions signs

97.  Segmental signs:
 Correspond to disturbed motor or sensory
innervation
 Band of altered sensation (hyperalgesia and
hyperpathia) at upper end of sensory disturbance
 LMN lesions sign in muscles supplied by the
segments
 Severe and acute transverse lesions
 Limbs may initially be flaccid rather spastic known as
“spinal shock”
 Lasts for several days, rarely weeks

98.  Cervical cord lesions
 Quadriplegia and weakness of diaphragm
Level Weakness
C5-C6 Biceps
C7 Finger and wrist extensors
and triceps
C8 Finger and wrist flexion
Any level Horner’s syndrome

99.  Thoracic cord lesions
 Localized by the sensory level on trunk and
Level Involvement
Nipple T4
Umbilicus T10
Paralysis of lower
abdominal muscles
T9-T10

100.  Lumbar cord lesions
Level Weakness
L2-L4 Flexion and adduction of thigh, weaken
leg extension at knee, and abolish the
patellar reflex
L5-S1 Paralyze movement of foot and ankle,
flexion at knee, and extension of thigh
and abolishes ankle jerks

101. Sacral cord / conus medullaris
 Tapered termination of spinal cord is conus
medullaris and comprises of sacral and single
coccygeal segments
 Syndrome
 Prominent bladder and bowel dysfunction (urinary retention and
incontinence with lax anal tone) and
 Impotence
 Bulbocavernous (S2-S4) and anal reflexes (S4-
S5) are absent
 Muscle strength preserved
 Sensory abnormality precede motor and reflex
changes by many months

102. Cauda equina lesion
 Low back and radicular pain
 Asymmetric leg weakness and sensory
loss
 Variable arreflexia in lower extremities and
relative sparing of bowel and bladder
function

103. Cauda equina Vs. Conus medullaris
Conus medullaris Cauda equina
syndrome
Onset Sudden and bilateral Gradual and unilateral
Aetiology Intramedullary SOL;
glioma
PID, metastases
Root pain Usually absent Severe low back
Motor involvement Not marked Asymmetric limb
weakness
Sensory loss Bilateral saddle
anesthesia
Asymmetric sensory
loss
Bladder and bowel
function
Early and marked Late and less marked
Deep reflexes Knee jerk normal,
ankle jerk lost
Ankle and knee jerks
absent
Trophic changes Prominent Less
Planter response Extensor Flexor or no response

104. Determination of state of bladder function
• Bladder during Spinal Shock
• Bladder is ACONTRACTILE & AREFLEXIC
• Detrusor is paralysed, sphincter is also paralysed
but regains its tone early leading to urinary
retention.
• In complete suprasacral spinal spinal cord lesions
this period may last up to 2-6 weeks, but may last up
to 1 or 2 years
• It may last a shorter period of time in incomplete
suprasacral lesion

105. Innervation of the urinary bladder and its sphincters

108. Stage of reflex activity
⚫Smooth muscles regain functional activity first
⚫Automaticevacuationof urinary bladderand bowel
⚫Sympathetic toneof blood vessels is regained
⚫BP is restored to normal
⚫In skin sweating starts, bed sores heal up

109. ⚫Once the stageof spinal shock has subsided, level and
type of cord or conus-cauda equina lesion, whether
completeor incomplete, are determining factors in
pathophysiologyof bladder

110. UMN Bladder
• Impliesa neurologicallycomplete lesion above the level
of sacro spinal cord that results in skeletal muscle
spasticity below the level of injury
• Features :
• Involuntary bladder filling
• Residual urinevolumegreater than 20% of bladder
capacity
• Refers to pattern of injury tosuprasacral spinal cord
afterperiod of spinal shock has passed
• Occurs with lesions between cervical and sacral spinal
cord

111. LMN Bladder
• Impliesa neurologicallycomplete lesion at the level of
sacrospinal cord orof thesacral roots
• Features:
• Results in skeletal muscle flaccidity below that level
• Detrusoraref lexia
• Whateverthe measures the patient may used to increased
intravesical pressure during attempted voiding are not
sufficient to decrease residual urinevolume.

112. Lapides classification
• Sensory neurogenic bladder
• Motorparalytic bladder
• Uninhibited neurogenic bladder
• Reflex neurogenic bladder
• Autonomous neurogenic bladder

113. Sensory neurogenic bladder
• Causes: DM, Tabes Dorsalis, MS, Subacutecombined
degeneration of cord
• Pathophysiology:
• Interrupts sensory fibers between bladderand
spinal cord or theafferent tractsof brain
• There’s lack of stretch signals from bladder preventing
•micturition reflex contraction.
• Features: Impaired sensationof bladderdistension
results in bladderoverdistension & hypotonicity.

114. Motor paralytic bladder
⚫Causes: Extensivepelvicsurgery/ trauma, herpes zoster
⚫Pathophysiology: Destructionof parasympathetic motor
innervation of the bladder
⚫Features: Painful urinary retention
⚫Relative inability to initiate & maintain normal
micturition.
⚫A large residual urine may result.

115. Uninhibited neurogenic bladder
•Causes:
•Injury or disease to Cortico regulatory tract.
•Brain or Spinal cord tumour-Parasagittal menigiomas,
•frontal lobe tumour. Parkinson’sdisease, Demyelinating
disease, anteriorcommunicating artery aneursyms.
• Features:
• Frequency, urgency, urge incontinence.
• Residual urine ischaracteristically low.
• The patientcan initiate bladdercontraction voluntarily,
•but is often unable todo so becauseof low urinestorage

116. Reflex neurogenic bladder
• Causes:
• traumaticspinal cord injury, transverse myelitis
• Pathophysiology: Describes postspinal shock condition
thatexists aftercomplete interruptionof sensory & motor
pathways between sacral spinal cord &the brain stem.
• Features: No bladdersensation
• Inabilityto initiatevoluntary micturition
• Therefore, INCONTINENCE WITHOUT SENSATION
results, becauseof lowvolume involuntarycontraction,
STRAINED SPHINCTER DYS-SYNERGIA is the rule

117. Autonomous neurogenic bladder
• Causes:
• Anydiseasewhichdamagesextensivelysacral cord/sacral roots, pelvic
surgery, pelvic malignant disease, spina bifida.
• Pathophysiology:
• Results fromcomplete & sensory seperationof bladderfrom spinal
cord.
• Features: Inabilitytovoluntary micturition intiation,
• no bladderreflex activity,
• nospecific bladdersensation
• Continous dribbling incontinence
• Considerable residual urinevolume
• Lossof sexual function.

118. Determining complications of
paraplegia
 Bed sores
 Contractures
 Urinary tract infection
 Pneumonia
 Deep venous thrombosis

119. Investigations
 Routine blood tests
 Blood chemistry (blood urea, creatinine, electrolytes etc.)
 Routine urine exam, urine for culture andsensitivity
 Plain X-ray Spine (Lateral and oblique view)
 CSFAnalysis
 ToR/O infection-bacterial/tubercular/viral meningitis
 CSFculture and sensitivity testing
 C.S.F.-Electrophoresis to show oligoclonal bands of
multiple sclerosis
 CTCranium/Brain

120.  MRI brain is more informative thanCT
 It helps in diagnosing
Degenerative/neoplastic/vascular/infective lesions
 Spinal MRI
 Sagittal views – differentiates Syringomyelia from
intramedullary tumours/transverse myelitis
 Italso shows cord compression whether internal or external
 Myelogram

121. MANAGEMENTOFPARAPLEGIA
1.General
• Frequent change of posture to guard against bed sores
• Care of skin
• Care of the bladder
• If there isretention, use a catheter to evacuate thebladder
• In case of urinary incontinence
• Frequent change of bed-sheets

122. 2.Physiotherapy
3.Symptomatic Treatment
• Analgesics and sedatives for pain
• Muscle relaxants for the spasticity
• Vitamins and mineral supplementation

123. 4.Specific Treatment (treatment of the cause)
• ATT+ Supportive measures in Pott's disease
• Drainage of paraspinal abscess
• Traumatic spine stabilisation
• Surgical management of some tumors
5. Rehabilitation
• Management of complications
• Occupational therapy
• Gait retaining

124. Special Patterns of Spinal Cord
Disease
Brown-Sequard Hemicord Syndrome
Ipsilateral
 Weakness (corticospinal tract) and
 Loss of joint position and vibratory sense (posterior
column)
Contralateral
 Loss of pain and temperature sense (spinothalamic
tract) 1-2 levels below the lesion

125. 125
 Segmental signs, such as
radicular pain, muscle
atrophy, or loss of a deep
tendon reflex, are
unilateral.
 Partial forms are more
common than the fully
developed syndrome.

126. Central cord syndrome
 Selective damage to the gray matter nerve cells
and crossing spinothalamic tracts surrounding
the central canal
 In cervical cord produces
 Arm weakness out of proportion to leg weakness and
‘dissociated’ sensory loss-greater motor impairment in upper
limb compared with lower extremities
 Loss of pain and temperature sensations over the shoulders,
lower neck, and upper trunk (cape distribution) in contrast to
preservation of light touch, joint position, and vibration sense in
these regions

127. Anterior spinal artery
syndrome
 Bilateral tissue destruction at several
contiguous levels
 All sensation: Motor, sensory, and
autonomic are lost below the level of lesion
 Retained vibration and position sensation
(spares the posterior columns)

128. Foramen magnum syndrome
 Lesions interrupt decussating pyramidal
tract fibers for legs
 Quadriparesis
 Sub-occipital pain spreading to neck and
shoulders
 Marked imbalance
 Cerebellar and cranial nerve involvement if
they spread intracranially
 Classically produces “around the clock”
progression of weakness
 Elsberg’s phenomenon

129. 129
 Elsberg’s phenomenon -U pattern weakness.
 Ipsilateral upper limb
 Ipsilateral lower limb
 Contralateral lower limb
 Contrallateral upper limb

130. Differentiation of Intramedullary and
Extramedullary Syndromes
Intramedullary process
 Arises within the substance of the cord
 Produces
 Poorly localized burning pain rather than radicular pain
and
 Spare sensation in perineal and sacral areas (“sacral
sparing”)

132. Extramedullary
 Lie outside the cord and compress the spinal cord or
its vascular supply
 Radicular pain is prominent
 Early sacral sensory loss and spastic weakness in
the legs with incontinence due to superficial location
of the corresponding sensory and motor fibres in the
spinothalamic and corticospinal tract
 May be either
 Extradural: generally malignant
 Intradural: benign, neurofibroma commonly

133. Extramedullary vs. Intramedullary lesions
Extramedullary Intramedullary
Root pain Early and common Rare
Sensory deficit No dissociation of
sensation
Dissociation of sensation
common
Sacral sensation Lost (Early) Sacral sparing
LMN involvement Segmental Marked with widespread
atrophy
UMN involvement Early and prominent Less pronounced
Reflexes Brisk, early Less brisk, late feature
Autonomic involvement
(Bowel and bladder)
Late Early
Trophic changes Usually not marked Common
Vertebral tenderness May be present Absent
Changes in CSF Frequent Rare

134. Compressive Vs. non-
compressive
Compressive
 Warning signs of neck or back pain,
 Bladder disturbances, and
 Sensory symptoms that precede the development
of paralysis
Non-compressive
 Without antecedent symptoms

135. Spinal Cord Infarction
 Cord supplied by single anterior spinal
artery and paired posterior spinal artery
 Causes
 Aortic atherosclerosis
 Dissecting aortic aneurysm
 Vertebral artery occlusion or dissection in the neck
 Aortic surgery
 Profound hypotension from any cause
 Cardiogenic emboli
 Vasculitis
 Collagen vascular disease: SLE, Sjogren’s syndrome

136. Anterior spinal artery infarction produces
Paraplegia or quadriplegia of acute
onset
Dissociated sensory loss affecting
pain and temperature sense but
sparing vibration and position sense,
and
Loss of sphincter control
“Anterior cord syndrome”

137. Pott’s Disease
 Hematogenous spread or from adjacent paravertebral
lymph nodes
 Often involves two or more vertebral bodies.
 Lower thoracic and upper lumbar spine being most
common site for spinal TB.
 Collapsed vertebra or abscess cause compression of the
spinal cord leading to paraparesis
 X ray spine shows decreased vertebral height collapsed
vertebrae and irregular vertebral margins .
 CT and MRI spine reveals characteristic lesions.

138. Transverse Myelitis
 Sensory, motor or autonomic dysfunction attributable
to the spinal cord
 Bilateral signs and/or symptoms
 Clearly defined sensory level
 No evidence of compressive cord lesion
 Inflammation defined by CSF pleocytosis, elevated
IgG index or gadolinium enhancement on MRI
 Progression to nadir between 4 hours and 21 days

139. Multiple Sclerosis
Acute myelitis
 Partial > complete
 CSF
 May be normal,
 Mild mononuclear cell pleocytosis,
 Protein: normal or mildly elevated,
 Oligoclonal bands
 Initial treatment: IV methylprednisolone (500
mg qd for 3 days) followed by oral prednisone
 Plasma exchange if glucocorticoid are
ineffective

140. Post infectious myelitis
 Organisms:
 EBV, CMV, Mycoplasma, Influenza, Measles, Varicella,
Rubeola, and Mumps
 Begins as patient appears recovering from
febrile infection
 Infectious agent cannot be isolated from
CSF
 Myelitis represents an autoimmune disorder
triggered by infection and is not due to direct
infection of the spinal cord
 Treatment: Glucocorticoids or, in fulminant
cases, plasma exchange

141. Spondylotic Myelopathy
Most common cause of
 Chronic cord compression
 Gait difficulty in elderly
Early symptoms:
 Neck and shoulder pain with stiffness
Radicular arm pain most often C5 or
C6

142. Cervical cord compression
 Slowly progressive spastic paraparesis,
 Asymmetric and
 Paresthesias in the feet and hands
 Sensory level for vibration or pinprick on the
upper thorax
 Dermatomal sensory loss in the arms
 Atrophy of intrinsic hand muscles
 Increased deep-tendon reflexes in the legs,
and extensor plantar responses
 Urinary urgency or incontinence in
advanced cases

143. Vascular Malformations of the Cord
and Dura
Dural arteriovenous (AV) fistulas presents
as
 Middle-aged man with a progressive myelopathy that
worsens slowly or intermittently and may have
periods of remission resembling MS
 Incomplete sensory, motor, and bladder
disturbances.

 Spinal angiography

144. Tropical spastic paraparesis
 HTLV-1 associated
 Insidious onset, slowly progressive spastic
syndrome
 Half the patients have mild back or leg pain
 HIV-vacuolar degeneration of the posterior
and lateral tracts, resembling SCD

145.  Dx: HTLV-1-specific antibody in serum by ELISA/
Western blot
 CSF/ Serum antibody index may provide support by
establishing intrathecal synthesis of antibodies
favoring HTVL-1 myelopathy over asymptomatic
carriage
 No effective treatment, only symptomatic therapy

146. Syringomyelia
 Developmental cavity of the cervical cord
 May enlarge and produce progressive myelopathy
 Insidiously in adolescence or early adulthood
 Progress irregularly, and may undergo spontaneous
arrest for several years
 Associated with Chiari type 1 malformations
 Acquired:
 Trauma, myelitis, necrotic spinal cord tumors, and
chronic arachnoiditis due to tuberculosis

147. Syringomyelia…..
 Dissociated sensory loss
 Sensory deficit-cape distribution
 Begin asymmetrically with
unilateral sensory loss in the
hands
 Muscle wasting in the lower neck,
shoulders, arms, and hands with
asymmetric or absent reflexes in
the arms.
 Spasticity and weakness of the
legs
 Bladder and bowel dysfunction,
and
 Horner's syndrome

148. Familial Spastic Paraplegia
 Genetic in origin
 Progressive spasticity and weakness in the legs,
usually but not always symmetric
 Associated with seizure
 Mild or no sensory symptom
 Sphincter disturbances may be present

149. Degeneration
 Predominantly involve
 Posterior and pyramidal tracts
 Symmetric loss of reflexes and Babinski
signs
 Optic atrophy and irritability or other mental
changes
 Macrocytic red blood cells, a low serum B12
concentration, and elevated serum levels of
homocysteine and methylmalonic acid

150. Neurolathyrism
 Associated with prolonged consumption of
Lathyrus sativus.
 Slowly developing spastic paraparesis with
cramps, paresthesia, and numbness.
 Pathological studies shows loss of myelinated
fibres in corticospinal and spinocerebellar
tracts.
 Toxin: Neuroexcitatory amino acid, Beta-N-
Oxalylaminoalanine (BOAA)

151. Tabes Dorsalis
Symptoms:
 Fleeting and repetitive lancinating pain in legs,
back, thorax, abdomen
Cardinal Signs:
 Loss of reflexes in the legs
 Impaired position and vibratory sense
 Romberg's sign and
 Bilateral Argyll Robertson pupils

152. GBS
 Preceding Infections
 Ascending LMN type paralysis
 B/L facial palsy
 Dysautonomia
 Bulbar weakness
 Hypo or areflexia.
 Sensory intact
 Bladder involvement rare

153. Copyrights apply

154. Thank you!
 References
 Uptodate 2021
 Adams and Victor, Principle of neurology 11th
Edition
 Harrison’s Principles of Internal Medicine, 20th
Edition

155. Compressive

156. Non-compressive

157. Vestibulospinal tract
 There are two vestibulospinal
pathways; medial and lateral.
 They arise from the vestibular nuclei,
which receive input from the organs of
balance.
 The tracts convey this balance
information to the spinal cord, where it
remains ipsilateral.
 Fibres in this pathway
control balance and posture by
innervating the ‘anti-gravity’ muscles
(flexors of the arm, and extensors of the
leg), via lower motor neurones.

158. Reticulospinal Tracts
 The two recticulospinal tracts have differing functions:
 The medial reticulospinal tract arises from the pons. It facilitates
voluntary movements, and increases muscle tone.
 The lateral reticulospinal tract arises from the medulla. It inhibits voluntary
movements, and reduces muscle tone.
 Nerve cells in reticular formation
 Fibres pass through
 midbrain, pons, and medulla oblongata
 End at the anterior gray column of spinal cord
 control activity of motor neurons

159. Reticulospinal tract

160. Rubrospinal Tracts
 In the midbrain, it originates in the red nucleus, crosses
to the other side of the midbrain, and descends in the
lateral part of the brainstem tegmentum.
 The tract is responsible for large muscle movement as
well as fine motor control, and it terminates primarily in
the cervical spinal cord, suggesting that it functions in
upper limb but not in lower limb control.

161. Rubrospinal tract
 Nerve cells in red nucleus
( tegmentum of midbrain at the level
of superior colliculus )
 Nerve fibres / axons
 cross the mid line
 descend as rubrospinal
tract
 through pons and
medulla oblongata
Terminate in anterior gray
column of spinal cord
( facilitate the activity of flexor
muscles )

162. Tectospinal Tracts
 This pathway begins at the
superior colliculus of the
midbrain.
The superior colliculus is a
structure that receives input
from the optic nerves.
 The neurones then quickly
decussate, and enter the
spinal cord.
 They terminate at the
cervical levels of the spinal
cord.