Spinal Cord Injury Lecture Notes

Spinal Cord Injury

Demographics and Etiology

• 17,730 new cases of spinal cord injury (SCI) occur annually (National Spinal Cord Injury Statistical Center, 2019).
• More than 291,000 people are living with SCIs (National Spinal Cord Injury Statistical Center, 2019).
• Bimodal distribution of age at injury:
  • First peak: young adults between 15 and 29.
  • Second peak: older adults (65 or older).
• 78%-81% Male (National Spinal Cord Injury Statistical Center, 2019).
• Two broad etiological categories: traumatic and nontraumatic.

Demographics and Etiology: Trauma

• Most frequent cause of injury in adult rehabilitation populations.
• Most common causes of SCIs in the United States (National Spinal Cord Injury Statistical Center, 2019):
  1. Motor vehicle accidents (39.3%).
  2. Falls (31.8%).
  3. Acts of violence (13.5%).
  4. Sports and recreation related injuries (8.0%).
  5. Medical and surgical complications (4.3%).
• Falls are the most common cause of SCI in older adults.

Demographics and Etiology: Nontraumatic

• Approximately 38% of all SCIs.
• Adult populations generally result from disease or pathological influence.
• Vascular Dysfunction (arteriovenous malformation, thrombosis, embolus, or hemorrhage).
• Spinal Stenosis.
• Spinal Neoplasms (new or abnormal growth of tissue in the spinal cord).
• Syringomyelia (cyst or cavity in spinal cord).
• Infection.

Syringomyelia

• Neurological disorder in which a fluid-filled cyst (syrinx) forms within the spinal cord.
• Causes include congenital (from birth) brain defects, spinal cord trauma, spinal cord tumor, and infection.

Nontraumatic SCI (Pediatric Population)

• Congenital
  • Spina Bifida: A condition that affects the spine and is usually apparent at birth; a type of neural tube defect (NTD).

• AFP (alpha-fetoprotein): A simple blood test that measures how much AFP has passed into the mother’s bloodstream from the baby.
• A high level of AFP might mean that the baby has spina bifida.

Clinical Features of Myelomeningocele (MMC)

• Neurologic defects and impairments.
• Musculoskeletal impairments.
• Osteoporosis risk.
• Spinal deformities: congenital or acquired scoliosis.
• Arnold-Chiari malformation:
  • Arnold-Chiari type II malformation involves the cerebellum, the medulla, and the cervical part of the spinal cord.
  • A child with spina bifida, MMC, and an Arnold-Chiari type II malformation has a greater than 90% chance of developing hydrocephalus.

Hydrocephalus

• Can occur in children with MMC with or without the Arnold-Chiari malformation.
• Treated neurosurgically with the placement of a ventriculoperitoneal shunt, which drains excess CSF into the peritoneal cavity.

Nontraumatic SCI Pediatric population

• Tumor
• Infections - viral: poliomyelitis
• Inflammatory - transverse myelitis
• Spinal Cord Injury without Radiographic Abnormality (SCIWORA):
  • Term that denotes objective clinical signs of posttraumatic spinal cord injury without evidence of fracture or malalignment on plain radiographs and computed tomography (CT) of the spine.
  • Spinal cord injury without radiographic abnormality is more common in the pediatric population due to increased ligamentous laxity and increased head-to-body ratio in children; children aged less than 8 years are more vulnerable.

Classification of Spinal Cord Injuries

• Two broad functional categories: tetraplegia and paraplegia.
  • Tetraplegia: motor and/or sensory impairment of all four extremities and trunk, including the respiratory muscles, results from lesions of the cervical cord.
  • Paraplegia: motor and/or sensory impairment of all or part of the trunk and both lower extremities (LEs), resulting from lesions of the thoracic or lumbar spinal cord or cauda equina (the spinal roots at L1 or below).
• Review of Anatomy
  • The spinal cord exits the foramen magnum and extends to approximately the L1 vertebral level.
  • In fetal development, the cord fills the entire length of the vertebral canal, and the spinal nerves run in a horizontal direction.
  • As the vertebral column elongates with growth, the spinal cord (does not elongate at the same rate) is drawn upward.
  • Nerve roots become increasingly oblique and downward, running in an almost vertical direction in the lumbar area, giving the appearance of a “horse’s tail” (cauda equina).

Primary Ascending Tracts (Sensory)

• Dorsal column: conveys proprioception, vibratory sensation, deep touch, and discriminative touch.
• Anterolateral system - spinothalamic, spinoreticular, and spinotectal tracts (conveys pain, temperature, and crude touch).
• Dorsal and ventral spinocerebellar tracts (conveys unconscious proprioception).

Primary Descending Tracts (Motor)

• Lateral corticospinal (voluntary movement).
• Anterior corticospinal (voluntary movement of axial muscles, minimal functional significance due to small size).
• Medial vestibulospinal (positioning of head and neck).
• Lateral and medial vestibulospinal (posture and balance).
• Lateral and medial reticulospinal (posture, balance, automatic gait-related movements).
• Rubrospinal (movement of limbs).

Classification of Spinal Cord Injuries: Designation of Lesion Level

• American Spinal Injury Association (ASIA) developed a classification system: International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI).
• American Spinal Injury Association is the premier North American organization in the field of Spinal Cord Injury Care, Education, and Research.
• ISNCSCI provides a standardized examination method to determine the extent of motor and sensory function loss after a SCI.
• Promotes better communication between professionals.
• Provides guidance for establishing the prognosis.
• Important tool for clinical research trials.
• Neurologic level: According to ASIA 2019, it is the most caudal segment of the cord with intact sensation and antigravity (3 or more) muscle function strength, provided that there is normal (intact) sensory and motor function rostrally respectively.
• The sensory level is determined by assessing both light touch and pinprick sensation bilaterally in the extremities and trunk; The sensory level is the most caudal level with normal light touch and pinprick sensation.
• Motor level for the right and left sides: lowest key muscle with a manual muscle testing grade of fair (3/5), provided that the key muscles above this level have intact (normal, 5/5) strength.

Classification of Spinal Cord Injuries: Designation of Lesion Level

• Muscles chosen are consistently innervated by the designated segments of the spinal cord and are easily tested in a clinical setting (easily accessible to test in supine, and they are significant in terms of functional mobility).

• ISNCSCI key muscles have two levels of innervation, adding to the validity of the scoring.

• Assigning a single muscle to represent one myotome is a generalization.

• In areas where no specific myotomes exist to test (i.e., C1–C4, T2–L1, and S2–S5), the motor level is presumed to correspond to the sensory level if the muscles above that level are judged to have normal strength.

• The motor and sensory levels may differ and may be different between the left and right sides of the body

• In some cases, the neurological level assignment can be misleading; A patient may have a mixed presentation of intact motor and/or sensory function below that level.

Classification of Spinal Cord Injuries: Complete Injuries, Incomplete Injuries, and Zone of Partial Preservation

• Complete injuries:
  • Sensory and motor function will be absent below the level of the injury and in the lowest sacral segments of S4 and S5 (no sacral sparing); most often the result of complete spinal cord transection, spinal cord compression, or vascular impairment.
  • An individual with a complete injury may have partial innervation of motor or sensory function in up to three segments below the injury site.
• Incomplete injuries:
  • Injuries in which there is partial preservation of some motor or sensory function below the neurologic level and in the lowest sacral segments of S4 and S5 (sacral sparing).
  • Sacral sparing: sensory function at S4–5 dermatome, ability to feel deep anal pressure, or voluntary anal sphincter contraction.
  • The clinical picture of incomplete injuries is highly variable and unpredictable.
    *Clinical findings that help to confirm a diagnosis of an incomplete injury:
  • Sacral sparing: sacral tracts run most medially within the spinal cord, they are often salvaged.
  • Abnormal tone or muscle spasticity: Resistance to passive stretching, clonus, increased deep tendon reflexes, and muscle spasms (possible explanations for these findings: Decreased inhibition from descending supraspinal pathways, loss of sensory information associated with weight bearing, increased responsiveness to neurons distal to the injury).

Zone of Partial Preservation

• Most caudal segment with some sensory or motor function (or both).
• Areas of intact motor and/or sensory function below the neurological level; if an individual has motor and/or sensory function below the neurological level but does not have sacral sparing.
• Previously only recorded with complete injuries but more recently was expanded to include incomplete injuries, to give a more precise clinical picture.

ASIA Impairment Scale Grade

• A = Complete: No motor or sensory function is preserved in the sacral segments S4–S5.
• B = Sensory Incomplete: Sensory, but not motor, function is preserved below the neurologic level and includes the sacral segments S4–S5, and no motor is preserved more than three levels below the motor level on either side of the body.
• C = Motor Incomplete: Motor function is preserved below the neurologic level for voluntary anal contraction, or the patient meets criteria for sensory incomplete. Some sparing of motor function more than 3 levels below the ipsilateral motor level on the right or left. For AIS C, less than half of key muscles have a grade greater than 3/5.
• D = Motor Incomplete: Motor function is preserved below the neurologic level, and at least half of key muscle functions below the neurologic level have a muscle grade of 3 or greater.
• E = Normal: Motor and sensory functions are normal in all segments, and the patient had prior deficits.

Clinical Syndromes

*Brown-Séquard syndrome
* Injury involving half of the spinal cord.
* Common causes: penetrating injuries, such as injuries sustained from gunshot or stab wounds.
* Loss of motor function, proprioception, and vibration on the same side as the injury because the fibers within the corticospinal tract and dorsal columns do not cross at the spinal cord level.
* Pain and temperature sensations are absent on the opposite side of the injury a few segments lower; the lateral spinothalamic tract ascends several spinal segments on the same side of the spinal cord before it crosses to the contralateral side.
* A limited number of patients have the pure form of BSS; more common is Brown-Séquard-plus syndrome, which refers to a relative ipsilateral hemiplegia with a relative contralateral hemi-analgesia.
* Recovery with this type of injury is good; best prognosis for ambulation of the SCI syndromes; independent in activities of daily living (ADLs) and are continent of bowel and bladder.
*Anterior cord syndrome
* Results from a flexion injury to the cervical spine in which a fracture-dislocation of the cervical vertebrae occurs.
* The anterior spinal cord or anterior spinal artery may be damaged.
* Loss of motor, pain, and temperature sensations bilaterally below the level of the injury as a result of injury to the corticospinal and spinothalamic tracts.
* Retains the ability to perceive position sense and vibration below the injury; the prognosis for functional return is limited because all voluntary motor function is lost.
*Central cord syndrome
* The most common SCI syndrome; generally occurs from hyperextension injuries to the cervical region.
* Results from progressive stenosis (congenital or degenerative narrowing of the spinal canal) or compression that is a consequence of hyperextension injuries.
* Upper extremities are more severely involved than the lower extremities because cervical tracts are located more centrally in the gray matter.
* Damages three different motor and sensory tracts: spinothalamic tract, the corticospinal tract, and the dorsal column.
* Ambulation is possible. Functional independence in ADLs depends on the amount of upper extremity innervation the patient regains.
*Cauda equina injuries
* Direct trauma from a fracturedislocation below the L1 vertebrae; complete transections are rare.
* Not considered to be a true SCI.
* Often results in an incomplete lower motor neuron lesion; considered a pure LMN lesion (peripheral nerve injury), without UMN signs.
* Common clinical manifestations: saddle anesthesia, bladder and bowel dysfunction (areflexic bowel and bladder), and variable LE involvement that is often asymmetrical.
* Has the same potential to regenerate as peripheral nerves elsewhere in the body; Early surgical decompression is one of the most important predictors for favorable recovery
* Full return of innervation is not common because (1) there is a large distance between the lesion and the point of innervation, (2) axonal regeneration may not occur along the original distribution of the nerve, (3) axonal regeneration may be blocked by glial-collagen scarring, (4) the end organ may no longer be functioning once reinnervation occurs, and (5) the rate of regeneration slows and finally stops after about 1 year.
*Conus medullaris syndrome
* A very distal portion of the spinal cord is damaged; this type of injury often results in a mixture of LMN and upper motor neuron (UMN) damage.
* Injuries to the conus medullaris: back pain, flaccid paralysis, and areflexic bowel and bladder function; Sacral sensation is decreased.
*Dorsal column syndrome or posterior cord syndrome
* A rare incomplete injury that results from damage to the posterior spinal artery by a tumor or vascular infarct.
* Loss of the ability to perceive proprioception and vibration.

Spinal Cord Injuries - Mechanisms of Injury

• Cervical flexion and rotation injuries
  • The cervical region is the most common type of injury, one that involves flexion and rotation
  • Posterior spinal ligaments rupture, and the uppermost vertebra is displaced over the one below it, rupture of the intervertebral disc and anterior longitudinal ligament (severe cases).
  • Transection of the spinal cord is often associated with this type of injury
  • Rear-end motor vehicle accidents frequently produce flexion and rotation injuries.
• Cervical hyperflexion injuries
  • Pure hyperflexion force: anterior compression fracture of the vertebral body with stretching of the posterior longitudinal ligaments; ligaments remain intact
  • Leads to a wedge-type fracture of the vertebral bodies
  • This type of injury frequently severs the anterior spinal artery and results in an incomplete anterior cord syndrome
  • Cause: head-on collision or a blow to the back of the head
• Compression injuries
  • Diving accidents cause injuries that are a combination of compression and flexion forces
  • Fracture of the vertebral end plates and movement of the nucleus pulposus into the vertebral body; bone fragments can be produced and displaced outward; longitudinal ligaments are stretched but remain intact
  • Effects of osteoporosis, osteoarthritis, or rheumatoid arthritis can also produce an SCI in the older adult
• Cervical hyperextension injuries
  • Common in the older adult as a result of a fall
  • An individual’s chin often strikes a stationary object, and this leads to neck hyperextension
  • Ruptures the anterior longitudinal ligament and compresses and ruptures the intervertebral disc
  • The spinal cord can become compressed between the ligamentum flavum and the vertebral body, with a resulting central cord type of injury

Medical Intervention

• Acute SCI:
  • The patient should be immobilized and transferred to a trauma center
  • Monitoring the patient’s respiratory and neurologic function is critical
  • New pharmacologic interventions: to limit cell death at the site of injury and promote tissue sparing; Current guidelines discourage the administration of steroids after injury patient is medically stable
  • Stabilization of the spine to prevent further spinal cord or nerve root damage: strong evidence that early surgical stabilization of patients with unstable spinal columns has favorable outcomes
• Indications for surgery:
  • To restore the alignment of bony vertebral structures
  • To decompress neural tissue
  • To stabilize the spine by fusion or instrumentation
  • To minimize deformities
  • To allow the individual earlier opportunities for mobilization
    *During surgery:
  • Fusion of the fracture fragments; bone grafting from the iliac crests, combined with the placement of internal fixation devices
• Stabilization procedures:
  • Skeletal traction: an interim basis while the patient’s medical condition is fragile; can reduce the overlapping of fracture fragments and can assist with spinal alignment.
  • Surgery is not indicated: external fixation with a halo jacket, a hard cervical collar, or a rigid body jacket may be all that is needed to stabilize the involved spinal segments
  • The physical therapist assistant must look for and pay close attention to any restrictions listed in the medical record; check the patient's skin for redness or breakdown when the brace is being applied or removed (discuss with nursing and the physician if there are problems )

Impact of Spinal Cord Injury: ICF Body Structure/Function Impairments

*Spinal Shock:
* After SCI, a period of areflexia occurs; the period of transient reflex depression is not clearly understood (result from the very abrupt withdrawal of connections between higher centers and the spinal cord)
* Characterized by the absence of all reflex activity and impairment of autonomic regulation, hypotension and loss of control of sweating and piloerection (goose bumps); loss of the bulbocavernosus reflex, cremasteric reflex, Babinski response, and a delayed plantar response
* Evolves over time:
* The initial period of total areflexia lasts approximately 24 hours.
* Gradual return of reflexes in 1 to 3 days.
* Period of increasing hyperreflexia lasting 1 to 4 weeks.
*Motor and Sensory Impairments:
* Complete (paralysis) or partial loss (paresis) of muscle function below the level of the lesion.
* Impaired or absent sensation below the level of the lesion.
* The clinical presentation of the patient will depend on the level and specific features of the lesion
*Autonomic Dysreflexia (Autonomic Hyperreflexia)
* Occurs in patients with injuries above T6 (above sympathetic splanchnic outflow)
* Mostly due to shunting of blood away from the splanchnic vasculature (which supplies the abdominal organs, including the liver, stomach, pancreas, spleen, small intestine, and large intestine) forcing it to enter the general circulation
* The result of disruption of the autonomic control of the cardiovascular system; over time, the spinal circuitry reorganizes, becoming hyperexcitable; hyperexcitability of the sympathetic reflexes, combined with the loss of descending control, results in abnormal reflex activation of the sympathetic system below the level of the injury when there is a noxious stimulus below the level of the lesion.

*Lack of inhibition from higher centers, hypertension will persist if not treated promptly
*Noxious sensory input causes autonomic stimulation, vasoconstriction, and a rapid and massive rise in the patient’s blood pressure.
*Typical (normal)response: increase in an individual’s blood pressure would stimulate the baroreceptors in the carotid sinus and aorta and would cause an adjustment in peripheral vascular resistance, thereby lowering the patient’s blood pressure
*In SCI: hypertension persists unless the noxious stimulus is removed or the patient receives medical intervention, and it should be treated as a medical emergency

*Common causes:
* Bladder or bowel distention
* Bowel impaction
* Disruption of the patient’s catheter
* Urinary tract infections, noxious cutaneous stimulation
* Pressure sores
* Kidney malfunction
* Environmental temperature changes
* Passive stretch is applied to the patient’s hip
*Symptoms of autonomic dysreflexia:
* Significant hypertension
* Severe and pounding headache
* Bradycardia
* Vasoconstriction below the level of the lesion
* Vasodilation (flushing)
* Profuse sweating above the level of the injury
* Constricted pupils
* Goose bumps (piloerection)
* Blurred vision
* Runny nose
*Immediate treatment and measures by the physical therapist assistant:
*First thing to do: look for the likely source of noxious stimulation; the patient’s catheter is kinked, or the catheter bag may need emptying; the source of the irritation that caused AD must be identified and eliminated.
*Monitoring the BP, loosening tight clothing or constrictive devices (eg, binder, stockings, or leg straps), getting the patient into the sitting position, making sure urine flow is unimpeded, and notifying the physical therapist, nurse, and physician.
*If the source of the problem cannot be identified immediately: try to lower the patient’s blood pressure by sitting or standing the patient
*Monitoring of the patient’s vital signs is necessary
*The patient’s primary nurse and physician must be notified as soon as possible
*Critical, emergency situation; Hypertension triggered by AD can result in seizures, cardiac arrest, subarachnoid hemorrhage, stroke, or even death
*Application of a nitroglycerin patch (vasodilator) or administration of antihypertensive drugs assist in lowering the patient’s blood pressure in the acute phase*
*Spastic Hypertonia
* Approximately 65% of people with SCI have spasticity, more common in people with cervical-level injuries
* Result of altered input at the spinal segmental level, which causes an imbalance between excitation and inhibition of the spinal motor neurons
* Spastic hypertonia typically emerges below the level of the lesion after spinal shock evolves; a plateau is usually reached 1 year after injury
* 50% of people with SCI report that their spasticity is problematic and negatively impacts their function
* Strong spasticity can be a deterrent to independent function or assist in functional activities (some patients may trigger spasm/spasticity - minimal/moderate involvement)
* Management includes a variety of methods, including stretch, modalities, and medications.
*Medications: muscle relaxants and spasmolytic agents such as baclofen,tizanidine,diazepam,and dantrolene sodium
* Intrathecal baclofen (where an implanted pump delivers small amounts of baclofen directly at the spinal cord level to minimize side effects) can be used in cases of severe spasticity when individuals do not respond well to oral administration
* Injection of botulinum neurotoxin can be used to manage focal spasticity
* Pharmacological management is often not successful in alleviating spasticity
*Cardiovascular Impairment
* The cardiovascular system is regulated by the brain stem and hypothalamus via the sympathetic and parasympathetic nervous system
* Parasympathetic signals to the heart via the vagus nerve (decreasing heart rate and contractility)
* Sympathetic outflow to the heart and blood vessels of the upper body comes from the cervical and upper thoracic region (above T6); blood vessels of the lower body come from below T5 (T6–L2)
* SCI (above T6): loss of sympathetic control to the heart and blood vessels below the level of the injury; intact parasympathetic input to the heart paradoxically, bradycardia is often associated with AD due to the parasympathetic nervous system attempting to control the sudden increase in BP).
* SCI at T6 and below: intact sympathetic and parasympathetic control to the heart; loss of sympathetic control to the blood vessels below the level of the injury
*Resulting imbalance between sympathetic and parasympathetic control of the cardiovascular system can result in a variety of cardiovascular impairments:
*Autonomic Dysreflexia, neurogenic shock, bradyarrhythmias, hypotension, orthostatic hypotension, and impaired cardiovascular reflexes

• Neurogenic shock: systolic blood pressure below 100 mm Hg and heart rate below 80 beats per minute; SCI (above T6) may result in neurogenic shock because sympathetic output to the heart is lacking and vagal (parasympathetic) input is unopposed *Orthostatic (postural) hypotension: defined as a 20 mm Hg or greater decrease in systolic blood pressure or a 10 mm Hg decrease in diastolic blood pressure. *Lack of a efficient skeletal muscle pump, combined with an absent vasoresponse in the lower extremities, leads to venous pooling *Careful monitoring of blood pressure responses must occur during treatment activities *Application of an abdominal binder before beginning upright activities promotes venous return by minimizing the drops in intraabdominal pressure *Elastic stockings may be worn to prevent venous pooling in the lower extremities *Medications (vasopressors or mineralocorticoids) increase a patient’s blood pressure and Increasing fluid intake: presence of hypovolemia* *Pulmonary Impairment
  • Ventilatory and respiratory function varies considerably according to the level of lesion involved
  • High spinal cord lesions at C1 and C2:
    • Phrenic nerve innervation and spontaneous respiration are lost
    • An artificial ventilator or phrenic nerve stimulator is required to sustain life
  • Expiration is passive, often requiring assistance for airway clearance
  • Injuries at C5–C8:
    • Have a fully innervated diaphragm (C3-C5) and many accessory muscles of inspiration
    • Are not likely to require ventilator support
    • Forced expiration is severely impaired; some cough ability is preserved, usually weak (WHY?)
      *Pressure ulcers
  • Develop over bony prominences in response to the patient’s inability to perceive the need to shift weight or relieve pressure
  • Changes in collagen degradation and decreased peripheral blood flow make the skin more vulnerable to injury
  • Poor nutrition, complete injuries, those who smoke, and those who do not follow their self-care and skin care programs are more susceptible to developing pressure ulcers
  • Patients must be instructed in pressure relief techniques; family members and caregivers must be taught how to assist patients with weight-shifting activities
  • 1 minute of pressure relief for every 15 to 30 minutes of sitting
  • Perform skin inspection independently with the use of a handheld mirror, if possible
  • Protective padding, including specialized beds, mattresses, custom wheelchairs, cushions, and lower extremity splints and padding, are utilized for pressure reduction
    *Bladder and Bowel Impairment
    Bladder Dysfunction
  • A serious medical complication requiring consistent and long-term management
  • Urinary tract infections (UTIs) are a major cause of mortality and morbidity
  • Spinal control for micturition originates from the sacral segments of S2, S3, and S4
  • Spastic or hyperreflexic bladder (UMN bladder): lesions that occur above the conus medullaris and sacral segments; contracts and reflexively empties in response to a certain level of filling pressure
  • Flaccid or areflexic bladder (LMN bladder): lesion of the sacral segments or conus medullaris; the bladder remains flaccid, requiring manual emptying at predetermined time periods
    *Bladder Management
  • Primary Goal: Prevent or minimize urinary tract complications
  • Intermittent catheterization: most frequently used method of bladder management; patient is stable during rehabilitation
  • Suprapubic tapping: tapping directly over the bladder with fingertips, causing a reflexive emptying of the bladder; only works for individuals with an UMN bladder without dyssynergia between the detrusor and sphincter
  • Performing a maneuver called crede: pressing on the bladder forces urine out
  • Valsalva maneuver: Individuals with an areflexive bladder can use the Valsalva maneuver, which is done by straining
    Bowel Dysfunction
  • Spinal cord lesions above S2: spastic or reflex bowel (UMN lesion)
  • S2–S4 or cauda equina (peripheral nerves) lesions: a flaccid or areflexive bowel (LMN lesion)
    Bowel Management
  • Establishing a daily (or every other day) pattern of eliciting a bowel movement; the exact time of day is chosen by the patient based on lifestyle needs and should be done consistently at the same time of day
  • Reflex bowel: use of suppositories and digital stimulation techniques to cause a reflex defecation
  • Nonreflex bowel: manual evacuation techniques and gentle Valsalva
    *Sexual Dysfunction
    Male
  • Erectile capacity is greater in UMN lesions than in LMN lesions and greater in incomplete lesions than in complete lesions
  • Reflexogenic erections: response to external physical stimulation of the genitals or perineum. An intact reflex arc is required (mediated through S2, S3, and S4.)
  • Psychogenic erections: cognitive activity such as erotic fantasy, mediated from the cerebral cortex either through the thoracolumbar or sacral cord centers
    Female
  • Also follow a pattern related to the location of the lesion
  • Sexual arousal in (UMN) patients through reflexogenic stimulation
  • Fertility is not affected
    *
    *Pain
  • A common occurrence following SCI both in the acute and chronic stages of recovery
    *Nociceptive Pain:
  • Musculoskeletal injuries are often due to overuse or poor posture
    *Neuropathic Pain:
  • Caused by injury to the central or peripheral nervous system; can occur below, at, or above the level of the spinal cord lesion
  • May be burning, shooting, or sharp
  • May take the form of allodynia (central pain in response to a normal non-painful stimulation) or hyperalgesia (increased sensitivity to pain caused by damage to nociceptors)
    *Impaired Temperature Control
  • After a SCI, the hypothalamus can no longer control cutaneous blood flow or level of sweat
  • Loss of Autonomic Nervous System (sympathetic) results in loss of internal thermoregulatory response of “sweat secretion”
  • The degree of impairment will be determined by the level of the injury and if its complete or incomplete
  • Cervical-level and complete injuries demonstrate more impairments
    *
    *Contractures are secondary to the prolonged shortening of structures across and around a joint, resulting in limitation in motion
    *Heterotopic (Ectopic) Ossification
  • Osteogenesis in soft tissues, usually near joints, below the level of the lesion; unknown etiology
  • Most often occurs in the hip and knee joints
  • Early symptoms: include swelling, joint and muscle pain, decreased ROM, erythema, and local warmth near a joint
  • Careful with passive range of motion (PROM); too vigorous may cause trauma
    *Deep vein thrombosis
  • Greatest risk during the acute-care phase because patients are often immobile, which is both a common and life-threatening complication
  • Management includes: receiving low-molecular-weight-heparin to prevent blood clotting; the application of pneumatic compression devices (sequential compression devices), with or without compression stockings, should be applied to the lower extremities as soon as possible to reduce venous stasis; Surgical implantation of a temporary vena cava filter may be necessary in patients who are unable to tolerate anticoagulation to decrease the risk of pulmonary embolus
    *Osteoporosis and Skeletal Fracture
  • Rapid bone mineral loss occurs in the first 4 to 6 months after injury
  • Bone mineral density (BMD) continues to decrease up to 3 years after injury and may continue longer
  • Most common in the LEs, although osteoporosis may also occur in the UEs in people with cervical SCIs
  • The reduction in BMD places people with SCI at a significant risk for fracture; when bone mineral density has decreased 37%, the fracture index has been exceeded, and the person is at risk for fractures
  • Early mobilization, therapeutic standing, use of