Gaerlan D.

Inciong, MD
1
Integration, Coordination & Behavior
OS 211
Rehabilitation of Neurogenic Bowel and Bladder and the Spinal Cord

Lecture Outline
I. Spinal Cord
A. Anatomy
DEFINITIONS
B. Definition of terms A. Spinal shock
C. Pathophysiology of SCI
D. Epidemiology of SCI • A state of transient physiological (rather than
E. Classification of SCI anatomical) reflex depression of cord function
F. Syndrome of SCI
G. Assessment of SCI below the level of injury with associated loss of all
H. Systemic changes after SCI sensorimotor functions
I. Functional Outcome
J. Prognosis • Flaccid paralysis, including the bowel and bladder
II. Neurogenic Bladder
A. Bladder Innervation • Symptoms tend to last several hours to days until
B. Receptors of the Bladder the reflex arcs below the level of the injury begin
C. Micturition
D. Functional Classification of Voiding Dysfunction to function again (eg, bulbocavernosus reflex,
E. Evaluation of Voiding Dysfunction muscle stretch reflex [MSR]).
F. Diagnostics
G. Laboratory Examinations
H. Management Goals of Voiding Dysfunction B. Neurogenic shock
I. Management of Voiding Problems
III. Neurogenic Bowel • Manifested by the triad of hypotension,
A. Evaluation of Bowel Dysfunction bradycardia, and hypothermia
B. Management Goals of Bowel Dysfunction
C. Management of Bowel Dysfunction • Shock tends to occur more commonly in injuries
above T6, secondary to the disruption of the
SPINAL CORD sympathetic outflow from T1-L2 and to
unopposed vagal tone, leading to decrease in
vascular resistance with associated vascular
Main functions:
dilatation
• Sensory – Spinothalamic tract
• Neurogenic shock needs to be differentiated from
• Motor – Corticospinal tract spinal and hypovolemic shock.
• Autonomic: Bowel, bladder
• Hypovolemic shock (due to hemorrhage) tends to
Case Scenario be associated with reflex tachycardia (there is
sympathetic shut down, so parasympathetic will
• 25 yo sustained C5 cervical fracture secondary to
dominate, resulting to bradycardia)
fall last March 2, 2010
• No associated problems
PATHOPHYSIOLOGY OF ACUTE SCI
• Spontaneous breathing, follows commands, both Series of biochemical processes causing further neuronal
UE and LE = 0/5 damage
• Sensory evaluation (via pinprick): intact C2-C4, Vasoactive substances
LT and PP
• + BCR (bulbocavernosus reflex)
Vasoconstriction
• Determine the extent of damage using ASIA
• Determine the motor score, sensory score, motor
level, sensory level
Ischemia of gray matter

SPINAL CORD ANATOMY

• The spinal cord is the major bundle of nerves that Edema
carries impulses to/from the brain to the rest of
the body.
• It has 31 segments each defined by an exiting Excitatory amino acids
ventral motor root and entering dorsal sensory
root.
Increase in calcium
• It is surrounded by rings of bone-vertebra. They
function to protect the spinal cord.
• Cord structures (and brain) require continuous Inc extracellular K
blood circulation Activation of phospholipase A2, C space
• Neurons do not undergo regeneration. Other cells
will have to assume the lost function of necrotic Free radicals, FFA metabolites
cells (neuronal plasticity).

SPINAL CORD INJURY (SCI) Cell membrane damage

• An insult to the spinal cord resulting in a change,
either temporary or permanent, in its normal
motor, sensory, or autonomic function. Neutrophils at injury site
• Tetraplegia (replaced the term quadriplegia –
brain pathology; e,g, stroke syndrome affecting
all limbs) Lysosomal enzymes, oxygen radicals
• Paraplegia
• Injury to the spinal cord in the thoracic, lumbar, or
Macrophages phagocytose debris
sacral segments, including the cauda equina and
Schwann cells  Modify myelin sheaths, produce
conus medullaris.
neutrotrophic factors
• SCI can be sustained through different
Fibroblasts  Fibroblast growth factorangiogenesis,
mechanisms with the following 3 common
neovascularization
abnormalities leading to tissue damage:
Note: Demyelination within 24 hrs (if myelin is damaged,
1. Destruction from direct trauma
there is interruption of action potential); Wallerian
2. Compression by bone fragments, hematoma, or
degeneration in 3 weeks
disk material
3. Ischemia from damage or impingement on the
• Effects on Neurologic Tissue
spinal arteries
Hazel, JB, Anne and Nic Tuesday, 14 Dec. 2010 Page 1 of 9
 Gaerlan D. Inciong, MD
1
Integration, Coordination & Behavior
OS 211
Rehabilitation of Neurogenic Bowel and Bladder and the Spinal Cord

1. Necrosis of the entire neuron • Complete – characterized as complete loss of

2. Dissolution of axon with Wallerian Degeneration. motor and sensory function below the level of the
3. Demyelination traumatic lesion; infection will most likely be on
the main artery thus occluding supply to the rest
• Force mechanism producing fractures and/or of the cord
dislocations of the spine • Incomplete – characterized by variable
1. Flexion—anterior compression fracture neurological findings with partial loss of sensory
2. Extension—ALL, avulsion and/or motor function below the lesion; a rim on
3. Rotation—more damaging to the ligaments the lateral or periphery will still have neuronal
activity

SYNDROMES
A. Incomplete Cord Syndromes
• Anterior Cord Syndrome
• Brown Sequard Syndrome
• Central Cord Syndrome
• Conus Medullaris Syndrome
• Cauda Equina Syndrome

Figure 1. Flexion, Extension, Burst Fracture and Chance fracture

1. ANTERIOR CORD SYNDROME
• Anterior cord syndrome involves variable loss of
4.Compression (axial loading)—burst fracture, may motor function
or may not cause SCI • Loss of pain and/or temperature sensation
5. Distraction or chance fracture • With preservation of proprioception and vibration.
6. Shear/Translational forces—spinal instabilities • Usually results from compression of the artery
Examples: that runs along the front of the spinal cord
• Cervical spine injuries • Compression of SC may be from bone fragments
a. Burst Fracture of atlas (C1)—Jefferson’s fracture or a large disc herniation
b. Fracture of neural arch of the axis (C2)— • Words of wisdom from Dr. Inciong: how do you
Hangman’s fatal know it’s the ventral horn? The breasts and
c. C3-C7—flexion/extension injuries vagina are anterior – use your imagination 

EPIDEMIOLOGY
• Annual incidence US: 40 cases/million
• Lowest in age <15 yrs; highest in 16-30 yrs
• Mean age: 35.9 years
• 80% males
• Causes: Vehicular accidents 50.4%
Falls 23.8%
Figure 2. Anterior cord syndrome
Violence 11.2%
Sports/Recreation 9.0%
Others 5.6%
2. BROWN-SEQUARD SYNDROME
• Extent Of Neurologic Deficit
• A relatively greater ipsilateral loss of
Tetraplegia 51.7%
proprioception and motor function (may affect
Incomplete 29.4%
ambulation)
Complete 20.7%
Paraplegia 45.9% • With contralateral loss of pain and temperature
Incomplete 18.6% sensation (sensory deficit may also lead to gait
Complete 26.3% problem)
Unconfirmed 2.4% • Recall: motor functions governed by the
Thus: Incomplete lesions > complete lesions corticospinal tract decussates at the cortico-
• Life Expectancy / Mortality / Factors medullary junction, while sensory functions
governed by the spinothalamic tract decussates
o Highest mortality 1st yr post-injury at two spinal segments above the exit of the nerve.
6.3% then declines For example: If the damage is in L2, L2 will not
o Predictors: older, male (more prone to be affected. L4 will be affected because it
suicide when they cannot perform social crosses at L2
functions), injured by violence, complete • A zone of partial preservation or segmental
injury, ventilator dependence (prone to ipsilateral lower motor neuron weakness and
having infections), high neurologic level analgesia may be noted.
o Top 3 Causes of Mortality:
• Loss of ipsilateral autonomic function can result
1. Pneumonia – for higher cervical/thoracic injuries; in Horner syndrome.
inadequate ventilation and clearance of mucus
• May range from mild to severe neurologic deficit.
secretions
• Bowel and bladder function preserved because
2. Heart Disease – individuals confined to a wheelchair,
the unaffected half can still serve these functions
so no physical exertion
3. Genitourinary system diseases – regular monitoring of
bacteria through urine culture every 3 months or KUB
ultrasound every year

CLASSIFICATION

Complete and Incomplete

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 Gaerlan D. Inciong, MD
1
Integration, Coordination & Behavior
OS 211
Rehabilitation of Neurogenic Bowel and Bladder and the Spinal Cord

dermatomes and myotomes of the affected

Figure 3. Brown Sequard Syndrome
segments.
• Cauda equina lesion is a LMN lesion because the
Causes of Brown-Sequard Syndrome nerve roots are part of the PNS.
A. Common cause - traumatic injury: • Both clinical syndromes of the spinal cord;
a. Stab or gunshot wound
b. A unilateral facet fracture and A. Conus Medullaris Anatomy
dislocation due to a motor vehicle • Cone tipped end of the Spinal cord
accident • Note it ends at level of T12-L2 vertebra
c. Fall • Link of CNS with PNS thru the Filum Terminale
B. Patient is normally able to walk although some Conus Medullaris Syndrome (CMS)
bracing or stability devices may be required • Low back pain
• Usually bilateral sciatica
3. CENTRAL CORD SYNDROME • Anal sensory disturbances
• Central cord syndrome usually involves a cervical • Bladder and bowel dysfunction
lesion, with greater motor weakness in the upper • Symmetric lower extremity motor and sensory
extremities than in the lower extremities. loss.
• May result from cervical hyperextension causing • Combined UMN (clinically: hyperspastic) and
ischemic injury to the central part of the cord LMN presentation
• The pattern of motor weakness shows greater
distal involvement in the affected extremity than B. Cauda Equina Anatomy
proximal muscle weakness. • The cauda equina (CE) is formed by nerve roots
• Sensory loss is variable, and the patient is more caudal to the level of spinal cord termination.
likely to lose pain and/or temperature sensation • Consists of lumbar and sacral roots
than proprioception and/or vibration. • At level of L2 – Sacrum
• Dysesthesias, especially those in the upper Cauda Equina Syndrome (CES)
extremities (eg, sensation of burning in the hands • Low back pain
or arms), are common. • Unilateral or usually bilateral sciatica
• Sacral sensory sparing usually exists • Saddle sensory disturbances
• Example: Syringohydromyelia – Abnormal • Bladder and bowel dysfunction
widening of the central canal creates a cavity • Variable lower extremity motor and sensory loss.
where CSF may accumulate and cause
• Mainly LMN presentation (clinically: flaccid)
compression.
• Patient is usually able to ambulate Table 1. Comparing CMS and CES
Syndromes CES CMS
Presentation Sudden and Gradual and unilateral
bilateral
Reflexes Knee jerks Both ankle and knee
preserved but jerks affected
ankle jerks
affected
Radicular pain Less severe More severe
Sensory S/Sx Numbness tends Numbness tends to be
to be more more localized to saddle
localized to the area;
perianal area; Asymmetrical, may be
FIGURE 4. Central cord syndrome. Recall the representation of the Symmetrical and unilateral;
cervical, thoracic, lumbar, and sacral spinal segments. Match the bilateral; No sensory dissociation;
localization of the edema to know the region affected. Sensory Loss of sensation in
dissociation specific dermatomes in
Causes of CCS occurs lower extremities with
• Most common cause of CCS is trauma. numbness and
• In older adults, premorbid cervical spondylosis is paresthesia;
Possible numbness in
a significant risk factor.
pubic area, including
• Accordingly, even minor falls may result in glans penis or clitoris
tetraplegia in populations with a narrowed spinal Motor Strength Typically Asymmetric;
canal due to arthritis symmetric; Areflexic paraplegia that
• In younger age groups, major trauma with high Hyperreflexic is more marked;
incidence of cervical fractures leads to CCS. distal paresis of Fasciculations rare;
lower limbs that is Atrophy more common
• Simple whiplash injury or cervical osteoarthritis less marked;
can lead to an nervous system pathology Fasciculations
may be present
ASSESSMENT OF SCI

4. CAUDA EQUINA AND CONUS MEDULLARIS Timing of Examination

SYNDROMES • Should be done at 72 hours after injury (after
• Pathophysiology: The conus medullaris part of resolution of spinal shock/onset of BCR)
the spinal cord obtains its blood supply primarily • Immediate examination limited by:
from 3 spinal arterial vessels—the anterior 1. Associated injury
median longitudinal arterial trunk and 2 2. Level of alertness
posterolateral trunks. 3. Presence of drugs/alcohol
• Conus Medullaris syndrome is a combination of 4. Evolving neurologic deficits
upper motor neuron (UMN) and lower motor
neuron (LMN) symptoms and signs in the Spinal Shock

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 Gaerlan D. Inciong, MD
1
Integration, Coordination & Behavior
OS 211
Rehabilitation of Neurogenic Bowel and Bladder and the Spinal Cord

• Immediate loss of neurological level, and at least half of key muscles below
1. Sensation the neurological level have a muscle grade of 3 or more.
2. Motor function E = Normal: motor and sensory functions are normal.
3. Muscle tone
4. Reflex activity Importance of Comprehensive Neurological Exam - ASIA
• Ends after return of bulbocavernosus reflex • Evidence-based
o Patients are usually on polycatheter. • Valid, reliable, consistent
While wearing glands, pull the • Allows for prognosis
polycatheter with your right hand and o Neurological
feel for the bulbocavernosus response/ o Functional (Rehabilitation goals)
”anal wink” • Allows study of interventions
o Rehabilitation
Terminologies o Drugs
1. Zone of partial preservation – dermatomes and
myotomes caudal to the neurological level that 1. ASIA Sensory Exam
remain partially innervated • Sensory Exam
2. Rectal examination o 28 sensory “points” do the
• Sensation present if deep anal sensation or
inching/dangkal/Inciong method 
sensation of anal mucocutaneous junction is
 Test T2 on the axilla, not on the
present
thorax because there is
• Complete lesion - absence of sensory/motor
overlapping
function in lowest sacral segment
 T3 is located 2 fingerbreadths
• Incomplete lesion - either sensory/motor function
above the nipple
is present (Sacral sparing
 Umbilicus is T10, below
3. Motor level - Determined by the most caudal key umbilicus, use 3 fingerbreadths
muscles that have muscle strength of 3 or above o Test light touch & pin/pain
while the segment above is normal (= 5) o Dermatomal areas
4. Motor index scoring - Using the 0-5 scoring of  C2 – occipital protuberance
each key muscle with total points being  C3 – supraclavicular fossa
25/extremity and a total possible score of 100  C4 – top of the acromioclavicular joint
 C5 – lateral side of antecubital fossa
5. Sensory level - Most caudal dermatome with a  C6 – thumb
normal score of 2/2 for both pinprick and light  C7 – middle finger
touch (there are 31 spinal nerves, only 28  T1 – medial antecubital fossa
dermatomes, S3-S5 merge, and no C1)  T2 – apex of axilla
 T3
6. Sensory index scoring - Total score from  T4 – nipple
adding each dermatomal score with possible total  T5
score (=112 each for pinprick and light touch)  T6
Note: multiply the number of all the dermatomes (28) by 2 (to  T7 – 7th intercostal space
account for laterality) = 56. Since the highest possible grade for
a dermatome is 2/2, 56 x 2 = 112.  T8 – 8th intercostal space
7. Neurologic level of injury - Most caudal level at  T9 – 9th intercostal space
which both motor and sensory levels are intact,  T10 – umbilicus
with motor level as defined above and sensory  T11 – 11th intercostal space
level defined by a sensory score of 2  T12 – inguinal ligament
8. Skeletal level of injury - Level of greatest  L1 – upper anterior thigh
 L2 – mid anterior thigh
vertebral damage on radiograph
 L3 – medial femoral condyle
9. Lower extremities motor score (LEMS) - Uses  L4 – medial malleolus
the ASIA key muscles in both lower extremities  L5 – dorsum 3rd MTP joint
with a total possible score of 50 (i.e., maximum  S1 – lateral heel
score of 5 for each key muscle L2, L3, L4, L5,  S2 – popliteal fossa
and S1 per extremity)  S3 – ischial tuberosity
a. A LEMS score of 20 or less indicates  S4, S5 – perianal area
patients are likely to be limited o Importance of sacral pin testing
ambulators (limited ambulation = only o 3 point scale (0,1,2)
able to stand; will be dependent on 0 - absent
braces). 1 - imparied/hyperesthesia
b. A LEMS of 30 or more suggests that 2 - intact
patients are likely to be community • “Optional”: proprioception & deep pressure to
ambulators (3/5 on both sides, able to index and great toe (“present vs. absent”)
resist gravity) • Deep anal sensation recorded “present vs.
absent”
American Spinal Injury Association (ASIA) Impairment
Scale 2. ASIA Motor Exam –Myotomes: 10 “key” muscles
A = Complete: No motor or sensory function is preserved • C5 - Biceps L2 – Iliopsoas
in the sacral segments S4-S5 (0/5, no sensation at all) • C6 - ECRL L3 - Quadriceps
B = Incomplete: Sensory but not motor function is • C7 - Triceps L4 – Tibialis anterior
preserved below the neurological level and includes the
sacral segments S4-S5.
• C8 – FDP (3rd) L5 - EHL
C = Incomplete: Motor function is preserved below the • T1 – ADM S1 – Gastrocsoleus
neurological level, and more than half of key muscles • Sacral exam: voluntary anal contraction
below the neurological level have a muscle grade less (present/absent)
than 3. • “Optional m’s: diaphragm (VC), abdominal
D = Incomplete: Motor function is preserved below the (Beevors test), hip adductors

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 Gaerlan D. Inciong, MD
1
Integration, Coordination & Behavior
OS 211
Rehabilitation of Neurogenic Bowel and Bladder and the Spinal Cord

o Vessel wall damage

3. ASIA Motor Grading • Highest risk period: first 2 weeks (important to
• Motor Grading Scale test during this period)
o 6 point scale (0-5; avoid +/-’s) • Serious complication: Pulmonary embolism
o 0 = no active movement • Manifestations:
o 1 = muscle contraction o Lower extremity pain
o 2 = movement thru ROM w/o gravity o Limb swelling
o 3 = movement thru ROM against gravity o Limb tenderness (+) Homan’s sign
o 4 = movement against some resistance A positive sign is present when there is pain in the
o 5 = movement against full resistance calf or popliteal region with examiner's abrupt
dorsiflexion of the patient's foot at the ankle while
the knee is flexed to 90 degrees. However, this has
4. ASIA Impairment Scale: Summary a poor predictive value for DVT.
A = Complete – No Sacral Motor/Sensory o Pallor
B = Incomplete – Sacral sensory sparing o Decrease pulse/ pulselessness
C = Incomplete – Motor Sparing (<3) o Decrease sensation/ paresthesias
D = Incomplete – Motor Sparing (>3) • Diagnostics:
E = Normal Motor & Sensory o Doppler ultrasonography
• Notation in the Chart o Duplex ultrasound
• Ex. If the patient comes with paraplegia ASIA A, o Impedance plethysmography
then eventually improves, do not change to
• Contrast venography
paraparesis, instead, paraplegia ASIA C.
• Management
SYSTEMIC CHANGES IN SCI o Pharmacologic agents e.g. heparin,
Coumadin (titration needed and PTT is
Cardiovascular System requested every 6 hours)
A. Cardiac Arrhythmias o Prophylactic measures e.g. compression
• Common during the acute period (14 days post stockings, external pneumatic
injury) compression, continuous rotation beds
• Common in cervical and complete injuries o Avoid ROM and strengthening exercises
• Bradycardia is common (predominance of the on the affected limb – risk of embolism!
parasympathetics) o Bed rest until medications are given
• Cause: Imbalance of the autonomic nervous E. Pulmonary Embolism
system with ↓ sympathetic and ↑ parasympathetic • Occur in 5% of SCI patients
activity • Can present as cardiac arrhtymias and
• Other causes of bradycardia autonomic hyperreflexia
o Hypoxia • Diagnostics: Perfusion scan of the lungs or
o Suctioning pulmonary angiography
• Prevention • Treatment: Medications (anticoagulation therapy)
o Use of atropine
o Induced hyperventilation F. Autonomic Dysreflexia
• Usually resolved within 6 weeks after injury • Acute syndrome of massive sympathetic
discharges as a result of noxious stimuli
B. Orthostatic Hypotension • The only emergency in rehab (and Dr. Inciong had a
• Venous return is affected by skeletal muscle case during his toxic residency!)
contraction • Common at the level of T6
• Common in higher levels of SCI • Manifestations
• Features: Dizziness, sudden loss of o Hypertension
consciousness, lightheadedness, visual changes o Headache
• Cause: o Sweating
o Ineffective vasoconstriction o Nasal congestion
o Pooling of blood in the lower extremities o Facial flushing
• Treatment: o Piloerection
o Progressive elevation o Reflex bradycardia
o Use of compression stocking and • Pathophysiology
abdominal binders o Noxious stimuli below level of lesion
o Liberal salt and fluid intake enter posterior gray matter, initiate
o Elevated leg rests segmental reflexes and ascend in cord
o Medications e.g. NaCl tablets, ephedrine to synapse with neurons in
intermediolateral columns of thoracic
C. Hypertension cord resulting in vasoconstrictor reflexes
• Inactivity can lead to increase cholesterol levels Note: descending inhibitory impulses blocked at level of cord injury
autonomic reflexes uncontrolled
• Increased risk of coronary artery disease
• Common causes:
• Management:
o Bladder distention (non-flowing urine)
o Perform exercise tolerance test
o Bowel impaction
o Exercise
o Pressure sores
D. Deep Vein Thrombosis
o Urinary tract infection
• Incidence: 47%-100%
o Tight clothing/ shoes
• 3 important factors (Virchow’s triad)
o Ingrown nails
o Venous stasis
o Invasive procedures e.g. catheterization,
o Hypercoagulability
cystometrogram

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 Gaerlan D. Inciong, MD
1
Integration, Coordination & Behavior
OS 211
Rehabilitation of Neurogenic Bowel and Bladder and the Spinal Cord

• Treatment: 2. Training in proper transfer techniques

o Identify cause and remove the cause 3. Avoidance of vigorous PT
o Sit up the patient (only if the patient’s
spine is stable) Heterotopic Ossification (HO)
o Blood pressure monitoring • Definition: Development of ectopic bone within
o Medications e.g. nitrates, nifedipine, soft tissues surrounding the joints
prazosin • Incidence: 16-35% of SCI patients
o Manual bowel extraction (Sir did this ) • Onset: 6 months post injury
• Prevention • Greatest risk 1-4 months
o Proper bladder/ bowel mgt. • Common areas: Hip> Knee> Shoulder>Elbow
o Skin care • Etiology
o Patient and family education • Unclear
• Due to metabolic, biochemical, circulatory factors
Pulmonary System • Occurs extraarticular
• Muscles Involved • Presentation
1. Diaphragm o Heat and swelling
2. Intercostal muscles o Decrease in ROM/LOM
3. Abdominal muscles o Fever
4. Accessory muscles
• Differential Diagnosis: DVT, thrombophlebitis,
• Level of Lesions
cellulitis, bone tumor, fracture
o C4 - highest level with spontaneous
• Diagnostics: X-ray, Triple phase Bone scan,
ventilation
serum alkaline phosphatase
o Above C8 - loss of abdominal and
intercostal muscles • Complications: Peripheral nerve entrapment,
o T1-T12 pressure sores, ankylosis, ↑ risk of DVT, ulcer
 Impairment of some abdominal • Management
muscles 1. ROM Exercises
 Reduced cough 2. Medications e.g. disodium etidronate,
 Paradoxical retraction of chest indomethacin
wall during inspiration 3. Surgery for mature bone
o Below T12 - no impairment of
respiratory function Pressure Ulcers
o Complications: • Staging of Pressure Ulcers
 Higher levels: atelectasis, o I – Nonblanchable; erythema not
pneumonia, ventilatory failure resolved within 30 mins
 Thoracic levels: Pleural o II – Partial thickness skin loss; blisters
effusion, atelectasis, with erythema
pneumothorax, hemothorax o III – Full thickness destruction of the skin
• Management o IV – Deep tissue destruction
1. Position changes/Postural Drainage o Stage III-IV may need the help of a
2. Deep breathing exercises plastic surgeon for management
3. Use of incentive spirometry • Management
4. Cough assist o Wound Cleansing and Debridement
5. Glossopharyngeal breathing exercises (use  Use of Plain Normal Saline
your tongue to capture the air: just like a frog ) Solution (NSS)
6. Pneumobelt  Topical antibiotics e.g.
7. Phrenic nerve pacing Flammazine
8. Non-invasive ventilatory support  Debridement e.g. sharp,
mechanical, enzymatic
Musculoskeletal System o Wound dressings e.g. Transparent
Osteoporosis adhesive dressing, hydrocolloid,
• Occurs below the level of injury hydrogel
• Reduction of bone mineral content o Wound Care Modalities e.g Whirlpool,
• Increase risk of lower extremity fracture UV light, Ultrasound
• Management o Surgery e.g. skin grafts and skin flaps
o FES exercises
o Ambulatory activities Spasticity
o Medications: Calcitonin, Biphosphonates • Definition: velocity dependent increase in muscle
tone and in muscle stretch reflexes
Fracture after SCI • Treatment
• Occurs in chronic SCI 1. Avoidance of noxious stimuli
• Incidence of 4%-7% 2. Prolonged muscle stretching
• Common causes 3. Medications e.g. Baclofen, Diazepam,
1. Osteoporosis Dantrolene sodium
2. Falls 4. Cold modalities
3. Vigorous PT 5. Casting/ Splinting
4. Minor forces 6. Biofeedback
• Common in long bones of lower extremity, 7. Intrathecal Baclofen
supracondylar fractures 8. Motor point and nerve blocks
• Management: 9. Rhizotomy
1. Patient/ Family Education

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 Gaerlan D. Inciong, MD
1
Integration, Coordination & Behavior
OS 211
Rehabilitation of Neurogenic Bowel and Bladder and the Spinal Cord

NEUROGENIC BLADDER
adrenergic and alpha-adrenergic receptors stimulation

Bladder full

Any pathologic CNS/PNS condition Triggers stretch reflex by receptors in walls
 
Affects the nervous system Sacral segments of cord (PN)
 
Control of nerves to bladder/bowel Parasympathetic fibers (efferents) back to bladder
 
Neurogenic bladder and bowel Detrusor contraction

Common Causes of Neurogenic Bladder Micturtion / voiding
(Neuropathic Voiding Dysfunction)
1. Brain lesions above pontine micturition center FUNCTIONAL CLASSIFICATION OF VOIDING DYSFUNCTION
- Stroke patients because of vascular problems
2. Brain lesions below pontine micturition center and in spinal cord
3. Conus medullaris and cauda equina lesions • Failure to STORE (INCONTINENCE)
4. Peripheral neuropathy / other neuropathies, such as in diabetes • Suprapontine lesions
5. Bladder overdistention with disruption of intramural nexus • Suprasacral lesions below the pons
Note: Neurogenic bladder/bowel is not limited to spinal cord injuries
• Failure to EMPTY (RETENTION)
BLADDER INNERVATION • During spinal shock
Pelvic Nerves (PN) • Peripheral lesions (polyneuropathies)
PN • Failure of sphincter relaxation during bladder contraction
(Sensory/Motor - parasympathetic) 3. Combination
 • Incomplete emptying
Spinal Cord S2-S3 (in some books, S2-S4)
 EVALUATION OF VOIDING DYSFUNCTION
Detrusor Muscles (contraction) History
• Voiding/defecating complaints
Pudendal Nerves • Cognitive deficits: patients with spinal cord injuries also have
- Somatic nerve fibers to voluntary skeletal muscles & associated contusions, etc.
external bladder sphincter • Past history
- So we can control our urgers, enabling us to pee at the • Associated medical problems
right place and time
Physiatric Health
Hypogastric Nerves • Hand function: will have a bearing for future management
- Sympathetic innervation (independent catheterization program)
- Spinal cord T11-L2 • Dressing skills
- Sympathetic stimulation facilitates bladder • Sitting balance
storage/ retention
• Ability for transfers/ambulation
• Also evaluate patients’ reactions/coping mechanisms to stigma
RECEPTORS OF THE BLADDER
Physical Examination
• In a flaccid bladder, there is overdistention. We • Abdomen
want the flaccid bladder to contract, so the drug • External genitalia: check for indwelling catheters (retention),
to use can be a cholinergic agonist (to promote) diapers (incontinence)
or a parasympathomimetic (to block) • Perineal skin: check for bed sores  prone to infection in the
• Flaccid bladder = high volume, low pressure setting of incontinence
• Spastic bladder = low volume, high pressure • Rectum

Neurologic Examination
Beta Adrenergic (part of sympathetic) (β for BODY) 1. Motor and sensory examination
• Predominate in superior portion of bladder (body) 2. Cutaneous reflexes

• Stimulation causes smooth muscle relaxation DIAGNOSTICS

facilitating filling/storage • Determine underlying pathology
• Determine the consequences/ complications (UTI, lithiasis,
Alpha Adrenergic (α – CONTRACT – “AH!!”, relief by hydonephrosis, vesicoureteral reflux, renal failure are the
voiding) most common complications.)

• Predominate near base of bladder and prostatic LABORATORY EXAMINATIONS

urethra Upper Tracts
• Renal ultrasound
• Stimulation causes smooth muscle contraction • Intravenous pyelogram: viewing tract obstruction (lithiasis)
and facilitates filling/storage
Lower Tracts
• Urinalysis: check for UTI

Cholinergic • Urodynamic studies (cystometry): measures bladder capacity

(volume) and pressure; determine the functional problem of the
• Distributed throughout the bladder bladder urge to void normally occurs at 300-350 mL
• Stimulation causes detrusor contractions
• Facilitates emptying/voiding MANAGEMENT GOALS OF VOIDING DYSFUNCTION
1. Prevent upper and lower urinary tract infections
MICTURITION 2. Develop a bladder management program that will allow patient to
• Process by which urinary bladder empties when filled reintegrate back into the community
• Autonomic spinal cord reflex
• Inhibited and facilitated by higher centers MANAGEMENT OF VOIDING PROBLEMS
Phases
Medical
1. Bladder Filling (Storage)
• Sympathetic innervation
• Work around the receptors to manage the
neurogenic problem
2. Emptying (Voiding)
• Parasympathetic innervation • To treat RETENTION
o Cholinergics (detrusor contraction)
During bladder filling

o Alpha receptor antagonists (sphincter
Low intravesical pressure maintained by progressive increase in beta- relaxation)

Hazel, JB, Anne and Nic Tuesday, 14 Dec. 2010 Page 7 of 9

 Gaerlan D. Inciong, MD
1
Integration, Coordination & Behavior
OS 211
Rehabilitation of Neurogenic Bowel and Bladder and the Spinal Cord

• To treat INCONTINENCE • Frequency, duration, technique bowel care

o Anticholinergics (detrusor relaxation) • Lifestyle goals (stigma issues)
o Alpha receptor agonists (sphincter • Rectodynamics
contraction) o Measures expulsive and resistive
o Others: antispasmodics forces/pressures in anorectum
Behavioral • Bowel evacuation mechanics
• Must be explained well and acceptable to the o Studies sequence of defecation
patient
• Catheterization programs MANAGEMENT GOALS OF BOWEL DYSFUNCTION
o Once the pt is UTI free, independent Figure 4. Margie, celebrating her 21st birthday.
intermittent catheterization every 4/6
hours, if the patient has hand function Happy 22nd birthday, Margaret Rose!
We love love love you!
o Limitation of fluid intake
o Use of a voiding diary Forever bubbly, forever Schuschulle!
• Timed voiding We approve 
o Schedule voiding
o Use of a voiding diary • Achievement of continence of stool
• Bladder training programs • Simple willful independent defecation
• Maneuvers
• Prevention of gastrointestinal complications
o Valsalva maneuver, suprapubic
(fecal impaction- most common complication)
application of pressure, tug pubic hair
(but not pull out! ) MANAGEMENT OF BOWEL MOVEMENTS
• Use of appliances Once you see a patient with SCI, manage right away! Do
o Condom, foley, straight catheters not wait for fecal impaction or urine retention!
Note: Medical intervention is always done in conjunction
with behavioral intervention. Medical
• Rectal suppositories, laxatives
Surgical • Oral medications (watch out for diarrhea)
• When above strategies fail
o Augmentation cystoplasty Behavioral
o Interruption of innervation • Timing of bowel care
o Neurostimulation o Take advantage of the gastrocolic
o Artificial sphincter reflex
o Sphincterotomy • Dietary modification
o Pudendal neurectomy o High fiber diet, increase fluid intake
o Bladder outlet surgery • Digital stimulation
o Balloon dilatation o Gloved hand  circular motion at anal
NEUROGENIC BOWEL sphincter
• Manual extraction
• Bowel training programs
COMMON CAUSES
1. Lesions rostral to pons Surgical
2. Frontal lobe lesions • Colostomy
3. Peripheral neuropathy o Creation of a stoma at the side of the
4. Between pons and sacral spinal cord (most abdomen for another exit point of the
common in SCI) poop poop goes out of the plastic bag
5. With enteric nervous system attached to the stoma!
o Also done for patients with imperforate
EVALUATION OF BOWEL DYSFUNCTION anus
• Defecating patterns (check for pre-morbid
defacating patterns, fecal consistency), ASSESSMENT OF THE CASE
abdominal symptoms (distention, abdominal ASIA Scoring
pain), effect of body position, time of day, diet, Incomplete because + BCR
bowel care, urinary function Motor score 50
• Gastrocolic reflex – tends to go to the CR right Sensory score 12 impaired on both sides = 24… 88
after eating Motor level – none
• Associated symptoms Sensory level – T9 (no myotome)
o Autonomic dysreflexia (check for hx)
o Abdominal wall spasticity Tips for the exam
o Spastic lower extremities (cannot sit • 10 items. Questions on dermatomes, myotomes,
down properly) ASIA, case scenario.
o Fever, weight change, check for
nutritional status
• Change in medication (cholinergics can cause
constipation), bowel program, living situation
(bathroom location)
• Premorbid bowel function
• Impact of symptoms
• Type of diet, fluid/fiber intake, use of medications
• Stool consistency

Hazel, JB, Anne and Nic Tuesday, 14 Dec. 2010 Page 8 of 9

 Gaerlan D. Inciong, MD
1
Integration, Coordination & Behavior
OS 211
Rehabilitation of Neurogenic Bowel and Bladder and the Spinal Cord

------------------------END OF TRANS------------------------
Trans concerns? Nic: 09189178361
Greetings!
Hazel: Merry Christmas, 2014!  Happy birthday Marj!
JB: Happy birthday Margie! Yahoo! Christmas na! hi Marcus! Yiiii bati na ulit tayo!
Congrats to the pasad team and the raft  to berne, super fun last night! Patrick
salamat sa sosyal ko na snacks! Tel, enjoy the fondue pot! Buddy Alex and Mama Sam,
hi! Merry Christmas classmates! Ther, get me a good gift! Hi to my yuletide season
seatmates Ricky, Leeann, Lance, Patrick, AA and Roland! Hi Carlo! And to my
snowflake R_ _ _r, hope you like what I gave you!
Anne: Happy birthday Margie!!! Carlos, thanks for the classy drinks! BERNE!!! Ang saya
ng Yakimix Party, may gift-snatching involved, haha! Next year ulit! “Yayakapin ang
buong pamilya…at kukwentuhan sila ng walang sawa.” Enjoy the holidays 2014
Nic: It’s almost my favorite time of the year! For He is the reason for the season 
Carlos, thank you for teaching me about muddling. BERNE, what can I say, thank you
for the possible pound or two I gained in Yakimix during our dinner, but lost again after
the rucus that was our exchange gift bit. Brifer, Bombombuño, Joeyboy: thanks for
heading the façade, and congratulations! Today: Adopt-a-Ward, UPCM Christmas Party
(new auditorium, wow!). Thursday: UPM Lantern Parade and lastly, Friday: 2014
Christmas Party and UPD Lantern Parade! Whattaweek. Thank You!

Hazel, JB, Anne and Nic Tuesday, 14 Dec. 2010 Page 9 of 9