Spinal cord injury

spinal cord

1. MAN BAHADUR
PAUDYAL
Spinal Cord Injury

2. Anatomy
CNS: Brain & spinal cord
Base of the skull ( foramen magnum) to lower
margin of the L1 vertebral body as conus
medullaris.
Cauda equina:
Below L
1
Lumbar, Sacral & Coccygeal spinal nerves
Filum terminale

3. Neuroanatomy
Two enlargements:
Cervical:
C
3
to T
1
segments
innervates arm
via brachial plexuses
Lumbar:
L
1
to S
3
segments
innervates leg
via lumbosacral plexuses

4. 3 layers:
Pia
Arachnoid
Dura matter

5. Segments:
(31)
Cervical - C1- C8
Thoracic - T1- T12
Lumbar - L1- L5
Sacral - S1- S5
Coccygeal - 1
pair of spinal nerves (mixed)
ventral (motor)
dorsal (sensory)

7. Blood Supply
1 anterior and 2 posterior
spinal arteries which arise from
the vertebral arteries.
Various radicular arteries
branch off the thoracic and
abdominal aorta to provide
collateral flow.
Venous drainage is usually by 3
anterior and 3 posterior spinal
veins.

Spinal veins join the veins
draining the vertebral bodies to
form the internal vertebral
venous plexus.

8. Spinal Cord Injury

9. Spinal cord injury is a mortal condition and has been
recognised as such since antiquity.
In about 2500 BC, in the Edwin Smith papyrus, Egyptian
physician accurately described the clinical features of
traumatic tetraplegia (quadriplegia) and revealed an
awareness of the awful prognosis with the chilling advice:
“an ailment not to be treated”.

10. Pathophysiology
Spinal cord injury (SCI)
insult to the spinal cord resulting in a
change, either temporary or permanent, in its
normal motor, sensory or autonomic
function.
Types:
A.Complete –
complete loss of motor , sensory
function below the lesion.
Incomplete - partial loss of sensory and/or
motor function below the level of injury.

11. B.Primary & Secondary
Primary: from mechanical disruption, transection, or
distraction of neural elements.
-mostly by fracture and/or dislocation of the
spine or penetrating injury.
-extradural compression by hematomas, or
abscesses or metastasis.
Secondary:
-free radicals
-excess neurotransmitters, leading to
excitotoxicity (secondary damage from
overexcited nerve cells )
-immune cells enter the CNS and release
chemical mediators
-edema, ischemia, necrosis

13. SCI, as with acute stroke, is a dynamic process.
 In all acute cord syndromes, the full extent of injury
may not be apparent initially. Incomplete cord
lesions may evolve into more complete lesions. More
commonly, the injury level rises 1 or 2 spinal levels
during the hours to days after the initial event.
A complex cascade of pathophysiologic events related
to free radicals, vasogenic edema, and altered blood
flow accounts for this clinical deterioration.
Normal oxygenation, perfusion, and acid-base
balance are required to prevent worsening of the SCI.

14. Extent of injury
Frankel scale:
A: complete paralysis
B: sensory function only below the injury level
C: incomplete motor function below injury level
D: fair to good motor function below injury level
E: normal function

15. American Spinal Injury Association (ASIA)
ASIA Impairment Scale
Type of Injury Description
A=Complete
No motor or sensory function is preserved in the sacral
segments S4-S5.
B=Incomplete
Sensory but not motor function is preserved below the
neurological level and includes the sacral segment S4-S5.
C=Incomplete
Motor function is preserved below the neurological level, and
more than half of key muscles below the neurological level
have a muscle grade less than 3. Sensory function is
present below the neurological level and includes sacral
segments S4-S5.
D=Incomplete
Motor function is preserved below the neurological level, and
at least half of key muscles below the neurological level
have a muscle grade of 3 or more. Sensory function is
present below the neurological level and includes sacral
segments S4-S5.
E=Normal Motor and sensory function is normal

16. The incomplete SCI syndromes are further
characterized clinically as:
Anterior cord syndrome involves variable loss
of motor function and pain and/or temperature
sensation, with preservation of proprioception.
Brown-Séquard syndrome involves a relatively
greater ipsilateral loss of proprioception and motor
function, with contralateral loss of pain and
temperature sensation.

17. Central cord syndrome
- usually involves a cervical lesion, with greater
motor weakness in the upper extremities than in
the lower extremities.

- pattern of motor weakness shows greater distal
muscle weakness than proximal.
- Sensory loss is variable, and pain and temperature
sensation more affected than proprioception and
vibration.
- Dysesthesias, especially in upper extremities (eg,
sensation of burning in the hands or arms), are
common.
- Sacral sensory sparing usually exists

18. Conus medullaris syndrome:
- is a sacral cord injury with or without
involvement of the lumbar nerve roots.
- characterized by areflexia in the bladder,
bowel, and to a lesser degree, lower limbs.
- motor and sensory loss in the lower limbs is
variable.
- the sacral segments occasionally may show
preserved reflexes (eg, bulbocavernosus and
micturition reflexes).
A spinal cord concussion is characterized by a
transient neurologic deficit localized to the spinal
cord that fully recovers without any apparent
structural damage.

19. Cauda equina syndrome:
- involves injury to the lumbosacral nerve roots
- characterized by an areflexic bowel and/or bladder,
with variable motor and sensory loss in the lower
limbs.
- Because this syndrome is a nerve root injury rather
than a true SCI, the affected limbs are areflexic
( LMN type). -is usually caused by a central
lumbar disk herniation.

20. SCIWORA
Longitudinal distraction with or without flexion and/or
extension of the vertebral column may result in primary
SCI without spinal fracture or dislocation.
more common in children.

21. Spinal shock
Spinal shock:
“a state of transient physiological (rather than
anatomical) reflex depression of cord function below
the level of injury with associated loss of all
sensorimotor functions.”
- An initial increase in blood pressure due to the
release of catecholamines, followed by hypotension.
- Flaccid paralysis, bowel and bladder involvement,
- sometimes sustained priapism develops.
- symptoms last several hours to days until the
reflex arcs below the level of the injury begin to
function again. (eg, bulbocavernosus reflex,
muscle stretch reflex [MSR]).

22. Neurogenic shock Vs Hemorrhagic shock
Neurogenic shock:
“triad of hypotension, bradycardia, and
hypothermia.”
-disruption of the sympathetic outflow from T1-L2
and due
to unopposed vagal tone, leading to decrease in
vascular resistance with associated vascular
dilatation.
-Shock tends to occur more commonly in injuries
above T6.

23. Hemorrhagic shock:
“hypotension, tachycardia, peripheral
vasoconstriction and shock.”
- Hypotension and/or shock with acute SCI at or below T6
is caused by hemorrhage.
- Hypotension with a spinal fracture alone, without any
neurologic deficit or apparent SCI, is invariably due to
hemorrhage.
- Patients with an SCI above T6 may not have the classic
physical findings associated with hemorrhage like
tachycardia or peripheral vasoconstriction.
- So, high index of suspision is required for this vital sign
confusion.

24. EPIDEMIOLOGY
M:F = 3:1
Age: > 50% of SCI occur in – age between16-30 years
Traumatic SCI is more common in <40 years,
Non-traumatic SCI is more common in > 40
years
Only about 5% of spinal cord injuries occur in
children, but usually complete injury.

Incidence: 30-60 cases / million population / year.

25. Common causes of SCI :
Motor vehicle accidents (44.5%)
Falls (18.1%) especially in persons aged 45 years
or older
Violence (16.6%)
Sports injuries (12.7%)
Other causes :
Vascular disorders
Tumors
Infectious conditions
Spondylosis
Iatrogenic injuries, especially after spinal
injections and epidural catheter placement
Vertebral fractures secondary to osteoporosis
Developmental disorders

26. Level and type of injury:
The most common levels are C4, C5 and C6
then thoracolumbar junction T12
July, Saturday

27. Injuries by ASIA classification
Incomplete tetraplegia - 29.5%
Complete paraplegia - 27.9%
Incomplete paraplegia - 21.3%
Complete tetraplegia - 18.5%
Leading cause of death in patients following SCI :
- pneumonia and other respiratory conditions,
- bed sore
- by heart disease, subsequent trauma, and
septicemia

28. Life expectancy
-Approximately 10-20% of patients who have
sustained SCI do not survive to reach acute
hospitalization.
Aged 20 years at the time of sustaining SCI
33 years as tetraplegics, 39 years as low tetraplegics,
and 44 years as paraplegics.
Aged 60 years at the time of injury
7 years as tetraplegics, 9 years as low tetraplegics, and
13 years as paraplegics.

29. Clinical features
History:
-begins with careful history taking,
-focus on symptoms related to the vertebral
column like pain and any motor or
sensory deficits.
-mechanism of injury
-level of injury / type of injury
-Complete bilateral loss of sensation or motor
function below a certain level indicates a
complete SCI.
-other associated injuries eg, head injury, chest
and abdominal injury

30. Physical examination
As with all trauma patients, initial clinical evaluation
begins with a primary survey.
- focuses on life-threatening conditions.
- assessment of airway, breathing, and circulation.
Careful neurologic assessment is required—
- to establish the presence or absence of SCI
- to classify the lesion according to a specific cord
syndrome.
- to determine the level of injury and
- to differentiate nerve root injury from SCI or
presence of both.

31. Clinical assessment of pulmonary function in acute SCI:
-careful history taking regarding respiratory
symptoms
- review of underlying cardiopulmonary comorbidity
such as COPD or heart failure
- evaluate respiratory rate, chest wall expansion,
abdominal wall movement, cough, and chest
wall and/or pulmonary injuries eg, pneumothorax,
hemothorax, or pulmonary contusion

32.  A direct relationship exists between the level of cord
injury and the degree of respiratory dysfunction.
high lesions (C1 or C2), vital capacity is only 5-10%
of normal, and cough is absent.
lesions at C3 - C6, vital capacity is 20% of normal,
and cough is weak and ineffective.
high thoracic cord injuries (T2 - T4), vital capacity
is 30-50% of normal, and cough is weak.
injuries at T11, respiratory dysfunction is minimal.
Vital capacity is essentially normal, and cough is
strong.

33. assessment of deep tendon reflexes and perineal evaluation is
critical.
The presence or absence of sacral sparing is a key prognostic
indicator.
The sacral roots may be evaluated by:
Perineal sensation to light touch and pinprick
Bulbocavernous reflex (S3 or S4)
Anal wink (S5)
Rectal tone
Urine retention or incontinence
Priapism

34. Level of injury
Neurologic level of injury - Most caudal level at
which both motor and sensory levels are intact.
Motor level - Determined by the most caudal key
muscles that have muscle strength of 3 or above while
the segment above is normal (= 5)
Sensory level - Most caudal dermatome with a normal
score of 2/2 for both pinprick and light touch
Skeletal level of injury - Level of greatest vertebral
damage on radiograph

35. Motor index scoring - Using the 0-5 scoring of
each key muscle with total points being
25/extremity and a total possible score of 100
Sensory index scoring - Total score from
adding each dermatomal score with possible total
score (= 112 each for pinprick and light touch)
Zone of partial preservation - This index is
used only when the injury is complete. All
segments below the neurologic level of injury with
preservation of motor or sensory findings.

36. Lower extremities motor score (LEMS) - Uses the
ASIA key muscles in both lower extremities with a total
possible score of 50 (ie, maximum score of 5 for each key
muscle L2, L3, L4, L5, and S1 per extremity).
- A LEMS score ≤20 : patients are likely to be limited
ambulators.
- A LEMS score ≥30 : patients are likely to be community
ambulators

37. Medical Research Council (MRC)
Muscle strengths are graded using the following
Medical Research Council (MRC) scale of 0-5:
5: Normal power
4+: Submaximal movement against resistance
4: Moderate movement against resistance
4-: Slight movement against resistance
3: Movement against gravity but not against
resistance
2: Movement with gravity eliminated
1: Flicker of movement
0: No movement

38. Key muscles are tested in patients with SCI
1.C5 - Elbow flexors (biceps, brachialis)
2.C6 - Wrist extensors (extensor carpi radialis longus
and brevis)
3.C7 - Elbow extensors (triceps)
4.C8 - Finger flexors (flexor digitorum profundus) to
the middle finger
5.T1 - Small finger abductors (abductor digiti minimi)
6.L2 - Hip flexors (iliopsoas)
7.L3 - Knee extensors (quadriceps)
8.L4 - Ankle dorsiflexors (tibialis anterior)
9.L5 - Long toe extensors (extensors hallucis longus)
10.S1 - Ankle plantar flexors (gastrocnemius, soleus)

39. Sensory scoring for light touch and pinprick, as follows:
0 - Absent
1 - Impaired or hyperesthesia
2 – Intact
A score of zero is given if the patient cannot differentiate
between the point of a sharp pin and the dull edge.

40. Sensory testing levels (28 key sensory points)
C2 - Occipital protuberance
C3 - Supraclavicular fossa
C4 - Top of the acromioclavicular
joint
C5 - Lateral side of antecubital
fossa
C6 - Thumb
C7 - Middle finger
C8 - Little finger
T1 - Medial side of antecubital
fossa
T2 - Apex of axilla
T3 - Third intercostal space (IS)
T4 - 4th IS at nipple line
T5 - 5th IS (midway between T4
and T6)
T6 - 6th IS at the level of the
xiphisternum
T7 - 7th IS (midway between T6
and T8)
T8 - 8th IS (midway between T6
and T10)
T9 - 9th IS (midway between T8
and T10)
T10 - 10th IS or umbilicus
T11 - 11th IS (midway between
T10 and T12)
T12 - Midpoint of inguinal
ligament
L1 - Half the distance between
T12 and L2
L2 - Mid-anterior thigh
L3 - Medial femoral condyle
L4 - Medial malleolus
L5 - Dorsum of the foot at third
metatarsophalangeal joint
S1 - Lateral heel
S2 - Popliteal fossa in the
midline
S3 - Ischial tuberosity
S4-5 - Perianal area (taken as one
level)

42. Management
Lab Studies:
Hemoglobin and hematocrit levels
Urinalysis
Other routine investigations
Radiology

43. Imaging Studies
X-ray C-spine:
Standard 3 views:
AP
Lateral
Odontoid (Open-
mouth)
Additional view:
Swimmer’s view
(for C7- T2)

44. Thoracolumbar X-ray:
Anteroposterior and
lateral views of the and
lumbar spine are
recommended.
Radiographs must
adequately depict all
vertebrae.
A common cause of
missed injury is the failure
to obtain adequate images

45. CT scanning
CT scanning with sagittal and coronal reformatting is
more sensitive than plain radiography for the
detection of spinal fractures.
Indications:
Plain radiography is inadequate.
Convenience and speed: If a CT scan of the head is
required, then it is usually simpler and faster to obtain a CT
of the cervical spine at the same time.
Radiography shows suspicious and/or indeterminate
abnormalities.

46. Radiography shows fracture or displacement: CT scanning
provides better visualization of the extent and
displacement of the fracture.
To confirm SCI without radiologic abnormality
(SCIWORA), a CT scan documenting the absence of
fracture often is necessary.
Dynamic flexion/extension views are safe and
effective for detecting occult ligamentous injury of
the cervical spine in the absence of fracture.

47. Fracture Dislocation Fracture

48. MRI is best for suspected spinal cord lesions,
ligamentous injuries, or other soft tissue injuries or
pathology.
MRI should be used to evaluate nonosseous lesions,
such as extradural spinal hematoma; abscess or
tumor; and spinal cord hemorrhage, contusion, and
edema.
Neurologic deterioration is usually caused by
secondary injury, resulting in edema and/or
hemorrhage. MRI is the best diagnostic image to
depict these changes.

50. Treatment

51. Prehospital Care
Airway, respiration, and
circulation
Airway management in
the setting of SCI, with or
without a cervical spine
injury, is complex and
difficult.
The cervical spine must be
maintained in neutral
alignment at all times.

52. To maintain airway patency and to
prevent aspiration clearing of oral
secretions and/or debris is essential.
The modified jaw thrust and insertion of
an oral airway may be all that is required
to maintain an airway in some cases.
However, intubation may be required in
unconscious patients.
Suction should be avoided when
possible as it may stimulate the vagal
reflex, aggravate preexisting
bradycardia, and occasionally precipitate
cardiac arrest

53. Spine should be immobilised with a
cervical hard collar and patient on a
hard backboard.
Commercial devices are available to
secure the patient to the board
 Spinal immobilization protocols
should be standard in all prehospital
care systems.
 log rolling

54. Log rolling should ideally be performed
by a minimum of four people in a
coordinated manner, ensuring that
unnecessary movement does not
occur in any part of the spine.

55. Hypotension may be hemorrhagic and/or neurogenic in
acute SCI.
Due to the vital sign confusion in acute SCI and the high
incidence of associated injuries, a diligent search for
occult sources of hemorrhage must be made.
Common causes of occult hemorrhage are chest, intra-
abdominal, or retroperitoneal injuries and pelvic or
long bone fractures.

56. Investigations, including radiography or CT scanning,
diagnostic peritoneal lavage or bedside FAST
(focused abdominal sonography for trauma)
ultrasonographic study may be required to detect
intra-abdominal hemorrhage.
Once neurogenic shock is diagnosed, initial treatment
focuses on fluid resuscitation.
Judicious fluid replacement with isotonic crystalloid
solution to a maximum of 2 liters is the initial
treatment of choice.

57. Therapeutic goal for neurogenic shock is adequate
perfusion with the following parameters:
- Systolic blood pressure (BP) should be 90-100
mm Hg to maintain adequate oxygenation and
perfusion of the injured spinal cord.
- Heart rate should be 60-100 beats per minute
in normal sinus rhythm
- Hemodynamically significant bradycardia may
be treated with atropine.
- Urine output should be more than 30 mL/h
- Prevent hypothermia(patient is poikilothermic due to
impaired vasomotor responses).

58. Associated head injury occurs in about 25% of SCI
patients. A careful neurologic assessment for
associated head injury is compulsory.
Noncontrast head CT scanning may be required.
Placement of a NG tube is essential to prevent
aspiration pneumonitis, antiemetics should be used
when necessary.
Prevent pressure sores by frequent change in position
every 1-2 hours. Pad all extensor surfaces/ bony
surfaces.

Remember Logrolling.

59. High doses of methylprednisolone
National Acute Spinal Cord Injury Studies (NASCIS) II
and III, a Cochrane review of all randomized clinical
trials and other published reports , have verified
significant improvement in motor function and
sensation in patients with complete or incomplete SCIs
who were treated with high doses of methylprednisolone
within 8 hours of injury .
Mechanism: - antioxidant properties,
- inhibition of inflammatory response,
- reduces the damage to cellular membranes
(membrane stabilizing action)
- a role in immunosuppression

60. Should be initiated within 8 hours of injury with the
following steroid protocol:
-inj methylprednisolone 30 mg/kg bolus over one hour,
and
- an infusion of methylprednisolone at 5.4 mg/kg/h for
next 23 hours if started within 3 hours of injury and
47 hours if started within 3 - 8 hours.

61. Treatment of pulmonary complications and injury:
- supplementary oxygen for all patients
- chest tube thoracostomy for pneumothorax /
hemothorax
Emergency intubation in the setting of SCI
- fiberoptic intubation with cervical spine control is
the ideal technique ( but no proven benefit
than orotracheal intubation).
Indications for intubation in SCI are
- acute respiratory failure,
- decreased level of consciousness (Glasgow score
<9), - increased respiratory rate with hypoxia,
- PCO2 > 50mmHg, and vital capacity < 10 mL/kg.
- maxillofacial injury

62. Inpatient Care
 Depending on the level of neurologic deficit and
associated injuries, the patient may require
admission to the ICU, neurosurgical observation unit,
or general ward.
Care to prevent bed sores- every 2 hourly position
change
Prevent chest infection- chest physiotherapy
Spinal immobility: Philadelphia collar, spinal
orthoses
Analgesics
Nutritional supports
Physiotherapy
Psychological support
Rehabilitation

63. Spinal orthoses
Philadelphia Collar
Skull traction- Gardner
Well’s tongue traction
Soft
Collar

64. Cervical-Thoracic Orthosis (CTO)
·Sterno-occipital
mandibular immobilizer
(SOMI)
·Skull Calipers & Halo
Traction

65. Cervico-thoraco-lumbosacral Orthosis (CTLSO)
Milwaukee Brace

66. Thoracolumbosacral Orthosis
(TLSO)
Jewett Brace
TLSO brace

67. Lumbosacral Orthosis (LSO)

68. Eemergent surgical decompression/ spine fixation
Incomplete SCI
extradural lesions, such as epidural hematomas or abscesses
 facet dislocation, bilateral locked facets, or cauda equina
syndrome.
Impingement of spinal nerves or acute neurologic deterioration.

69. Complications
Neurologic deficit often increases during the hours to
days following acute SCI, despite optimal treatment.
- neurological level usually rises by 1-2 segments
on repeat examination.
Pressure sores: denervated skin is particularly prone
for sore
 Prevent hypothermia by using external rewarming
techniques and/ warm humidified oxygen.
Pulmonary complications

70. Pulmonary complications:
- Atelectasis secondary to decreased vital capacity
and decreased functional residual capacity
Ventilation-perfusion mismatch due to
sympathectomy and/or adrenergic blockade
Increased work of breathing because of decreased
compliance
Decreased coughing, which increases the risk of
retained secretions, atelectasis, and pneumonia
Muscle fatigue

71. Prognosis
Patients with a complete cord injury have a less than
5% chance of recovery.
If complete paralysis persists at 72 hours after injury,
recovery is essentially zero.
The prognosis is much better for the incomplete cord
syndromes.
If some sensory function is preserved, the chance that
the patient will eventually be able walk is greater than
50%.
Ultimately, 90% of patients with SCI return to their
homes and regain independence

72. In the early 1900s, the mortality rate 1 year after injury in
patients with complete lesions approached 100%.
Currently, the 5-year survival rate for patients with a
traumatic quadriplegia exceeds 90%. The hospital mortality
rate for isolated acute SCI is low.

73. Recent advances

74. 1. Drugs
The NASCIS II (National Acute Spinal Cord Injury
Study II) trial, a multicenter clinical trial comparing
methylprednisolone to placebo and to the drug
naloxone.
methylprednisolone given within 8 hours after injury
significantly improves recovery in humans.
Completely paralyzed patients:
- recovery of about 20 % of their lost motor
function Vs 8 p% in untreated patients.
Paretic (partially paralyzed) patients:
- recovery of average of 75 % of their function Vs
59 % in untreated patients.

75. Patients treated with naloxone, or methylprednisolone
more than 8 hours after injury, did not improve
significantly than patients given a placebo.
Lazaroid, a potent inhibitor of lipid peroxidation without
glucocorticosteroid activity might be desirable.
GM-1 ganglioside, is useful in preventing secondary
damage in acute spinal cord injury, and may also improve
neurological recovery from spinal cord injury during
rehabilitation.

76. Calpain and Caspase, are Ca-dependent cysteine protease,
which cleaves many cytoskeletal and myelin proteins and
calpastatin, an endogenous calpain-specific inhibitor.
Spinal cord injury (SCI) evokes an increase in intracellular free
Ca level
↓
Activation of Calpain and Caspase leading g to cleavage of the key
cytoskeletal and membrane proteins in spinal cord.
↓
disturbed integrity and stability of CNS cells leading to cell death &
↑ Apoptosis.
Administration of cell permeable and specific inhibitors of calpain
and caspase-3 in experimental animal models of SCI has
provided significant neuroprotection.
Brain Research Reviews Vol 42, Issue 2, May 2003, Pages 169-185

77. 2. Neural Prostheses
These electrical and mechanical devices connect with
the nervous system to supplement or replace lost
motor and sensory functions.
One such neural prosthesis allows rudimentary hand
control, was recently approved by the United States
Food and Drug Administration (FDA).
Patients control the device using shoulder muscles.
With training, most patients with this device can
open and close their hand in two different grasping
movements and lock the grasp in place by moving
their shoulder in different ways.
National Institute of Neurological Disorders and
Stroke
Spinal Cord Injury: Emerging Concepts June, 2007

78. activities such as using silverware, pouring a drink,
answering a telephone, and writing a note.
Other types of neural prostheses currently being
developed aim to improve respiratory functions,
bladder control, and fecal continence
Functional electrical stimulation (FES): electric
stimulation of innervating nerves helps in
strengthening the lower extremities, increases muscle
mass, improves blood flow, and better bladder and
bowel function.
electrical stimulation of S2, S3, and S4 roots can
improve bladder and bowel function

Spinal-cord injury. Lancet 359: 417–425, 2002

79. 3. Neuronal Regeneration
combination of embryonic stem cells and growth
factors like retinoic acid, rolipram and db cAMP can
produce motoneurons in the spinal cord
these motoneurons sent axons out of the spinal roots
to reinnervate muscle and restore function as shown
in experimental rats.
Whittemore SR, et al. Optimizing stem cell grafting
into the CNS. Methods Mol Biol 198: 319–325, 2002

80. combination of Schwann cells with db cAMP and
rolipram produced the best regeneration.
Pearse and Bunge from the Miami
Project
the combination chondroitinase and lithium work
better than either of the therapies alone (exciting
because lithium has long been used to treat manic
depression)
Yick, Wu, and So in Hong Kong
University

81. 4. Myelination of spinal axons
Remyelination is one of the crucial goals of spinal cord
injury.
Many cells have now been reported to remyelinate spinal
axons like Schwann cells, oligodendroglial precursor cells
obtained from embryonic or fetal neural stem cells,
olfactory ensheathing glia, and even enteric glia.

82. 5. Reversal of axonal growth
inhibitors
 a protein called Nogo in myelin that inhibits axonal
growth
reversing the effects of Nogo will promote axonal
growth
- antibodies against Nogo itself (called IN-1, this
is now in Phase 1 clinical trials in Switzerland),
- a bacterial toxin called Cethrin that has
inhibitory effects,
- Nogo receptor blockers (including Nogo-66 an
antibodies against a co-receptor
Lingo), and
- chondroitinase (a bacterial enzyme mentioned
above that breaks down chondroitin-6-
sulfate-proteoglycan).

83. 6. Bridging the Gap: Transplant
Strategies
fetal spinal cord transplants
olfactory ensheathing cells
Human neural progenitor cells and embryonic stem
transposition of the omentum
artificial material, such as biodegradable hydrogels
or combinations of hydrogels and cells
Zompa EA, et al, Transplant therapy: recovery of
function after spinal cord injury. J Neurotrauma
14: 479–506, 1999.

84. 7. Bowel & bladder control
Functional electrical stimulation (FES):
-electrical stimulation is delivered to the sacral
anterior roots to induce bladder contraction for
bladder emptying
The Brindley bladder stimulator:
-bilateral S2-S4 sacral anterior nerve roots with
posterior rhizotomy
-delivers intermittent stimulation to the anterior
sacral roots
-The stimulus parameters can be adjusted and
set specifically for individual use

85. 8. Management of male infertility
VIBRATORY STIMULATIONS:
-Vibration applied to the head and shaft of the penis
can stimulate ejaculation in men
with loss of control of an
intact ejaculatory reflex
-semen sample is then processed for either IUI or
IVF.
ELECTROEJACULATION:
- Rectal probe electroejaculation to get semen
SPERM HARVESTING:
-Sperm may be removed from any site along the
path of ejaculation, including the
vasdeferens, epididymis, and
directly from the testis.

86. 9. Newer Technology
lighter weight wheelchairs that are easier to maneuver.
-significantly improve the quality of life from a practical,
everyday standpoint of being comfortable and getting around .
Voice-activated computer technology:
-assistance of a computer can make many of the daily
tasks of living and working possible such as answering and
dialing the phone or using a computer to e-mail messages and
pay bills.
treadmill-assisted walking may also greatly improve
ambulation. This therapy is based on the theory that a central
pattern generator (CPG) resides in the spinal cord that controls
rhythmic locomotion patterns such as walking or running.
Repetitions of walking are believed to reactivate the CPG so the
injured patient can re-learn the stepping mechanism and walk.