MAN BAHADUR PAUDYAL

Spinal Cord Injury

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 L1

Lumbar, Sacral & Coccygeal spinal nerves

Filum terminale

Neuroanatomy

Two enlargements: Cervical:

C3 to T1 segments innervates armvia brachial plexuses

Lumbar: L1 to S3 segmentsinnervates legvia lumbosacral plexuses

3 layers: Pia Arachnoid Dura matter

Segments: (31) Cervical - C1- C8 Thoracic - T1- T12Lumbar - L1- L5 Sacral - S1- S5Coccygeal - 1

pair of spinal nerves (mixed) ventral (motor) dorsal (sensory)

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.

Spinal Cord Injury

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”.

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.

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

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.

Extent of injury

Frankel scale:A: complete paralysisB: sensory function only below the injury

levelC: incomplete motor function below injury

levelD: fair to good motor function below injury

levelE: normal function

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

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.

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

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.

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.

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.

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]).

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.

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.

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.

Common causes of SCI :Motor vehicle accidents (44.5%) Falls (18.1%) especially in persons aged 45 years or olderViolence (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

Level and type of injury:The most common levels are C4, C5 and

C6 then thoracolumbar junction T12

July, Saturday

Injuries by ASIA classificationIncomplete 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

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 SCI33 years as tetraplegics, 39 years as low tetraplegics, and 44 years as paraplegics.

Aged 60 years at the time of injury7 years as tetraplegics, 9 years as low tetraplegics, and 13 years as paraplegics.

Clinical featuresHistory:

-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

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.

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

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.

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

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

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.

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

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

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)

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.

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)

Management

Lab Studies: Hemoglobin and hematocrit levels Urinalysis Other routine investigations Radiology

Imaging StudiesX-ray C-spine:Standard 3 views:

APLateral Odontoid (Open-mouth)

Additional view:Swimmer’s view (for C7- T2)

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

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.

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.

Fracture Dislocation Fracture

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.

Treatment

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.

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

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

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.

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.

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.

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).

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.

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

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.

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

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 physiotherapySpinal immobility: Philadelphia collar, spinal orthosesAnalgesicsNutritional supportsPhysiotherapyPsychological supportRehabilitation

Spinal orthoses

Philadelphia Collar

Skull traction- Gardner Well’s tongue traction

Soft Collar

Cervical-Thoracic Orthosis (CTO)

Sterno-occipital mandibular immobilizer (SOMI)

Skull Calipers & Halo Traction

Cervico-thoraco-lumbosacral Orthosis (CTLSO)

Milwaukee Brace

Thoracolumbosacral Orthosis (TLSO)

Jewett Brace

TLSO brace

Lumbosacral Orthosis (LSO) 

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.

ComplicationsNeurologic 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

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

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

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.

Recent advances

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.

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.

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

2. Neural ProsthesesThese 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 StrokeSpinal Cord Injury: Emerging Concepts June, 2007

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

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

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

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.

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).

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.

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

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.

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.