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Spinal cord injury 2012 intern


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Spinal cord injury 2012 intern

  1. 1. Spinal Cord InjuryPartial or complete disruption of spinal cord resulting inparalysis, sensory loss, altered autonomic and reflex activities.A report by: Kenneth Pierre M. Lopez
  2. 2. Complete Lesion Incomplete Lesion• A lesion to the spinal cord • A lesion to the spinal cord where there is no with incomplete damage preserved motor or to the cord. There may be sensory function below scattered motor function, the level of lesion sensory function or both below the level of lesionIntroduction :2 General Classifications
  4. 4. • Cauda Equina Injuries: a term • Neurectomy: A surgical removal used to describe injuries that of a segment of a nerve in order to occur below the L1 level of the decrease spasticity and improve spine (LMN) function• Dermatome: Designated sensory • Neurologic level: the lowest areas based on spinal segment segment of the spinal cord with innervation intact strenth and sensation.• Myelotomy: A surgical procedure Muscle groups at this level must that severs certain tracts within receive a grade of 3 the spinal cord in order to • Paraplegia: a term used to decrease spasticity and improve describe injuries that occur at the function level of the thoracic lumber or• Myotome: Designated motor sacral spine areas based on spinal segment innervation
  5. 5. • Rhizotomy: a surgical resection of the sensory component of a spinal nerve in order to decrease spasticity and improve function• Tenotomy: a surgical release of a tendon in order to decrease spasticity and improve function• Zone of preservation: a term used to describe poor or trace motor or sensory function up to three levels below the neurologic level of injury
  7. 7. • Incidence of SCI is lowest for persons under the age of 15 and highest for persons 16-30 years of age.• 80% of all SCI occurs in males• Motor Vehicular Accidents = 48%• Falls = 16% (most common in pts over 45)• Sports Injuries = 16%• Violence = 14% (most common in urban communities)• Quadriplegia = 55% • Complete = 49% • Incomplete = 51%• Paraplegia = 45% • Complete = 62% • Incomplete = 38% • Spinal Areas of greatest frequency of injury: C5, C7, T12 and L1
  9. 9. • Gross Anatomy • Sagittal Diameter: 7-12 mm • Cervical Enlargement: C3-T2 level • Lumbar Enlargement: T10-T12 level • Length: approximately 45cm. From foramen magnum to L1-L2 vertebrae• Vascular Supply • 1 anterior spinal artery which supplies the anterior 2/3 of the cord • 2 posterior spinal arteries which supply the posterior 1/3 of the cord • Both anterior and posterior arteries receive reinforcement from the Radicular Artery • Spinal vertebral venous plexus to the azygous vein
  10. 10. • Internal Anatomy • Gray Matter – neuronal cell bodies & synapses • Anterior Horn – motor neurons • Posterior Horn – sensory neurons • White Matter – ascending & descending fiber pathways • Ascending – relays sensory information to the brain • Descending – relays motor information down to the cord
  11. 11. ASCENDING TRACTSConsists of axons that conduct action potentials orimpulses towards the brain (afferent)
  12. 12. • Pain and Temperature • Lateral Spinothalamic Tract – Main Pathway • Ventral Spinothalamic Tract • Both tracts cross to the contralateral side of the cord about 2-3 cord levels above as it travels up the cerebral cortex (Area 3,1,2) • Lesion of this tract presents with loss of contralateral pain & temperature below the level of injury
  13. 13. • Proprioception and Stereognosis • Posterior Column – ascends up the spinal cord and crosses to the contralateral side at the level of the medulla to the cerebral cortex (Area 3,1,2) • Fasciculus Cuneatus – laterally located; UE proprioception • Fasciculus Gracilis – medially located; LE proprioception • Lesion of Posterior Column: Loss of ipsilateral proprioception & stereognosis below the level of injury
  14. 14. • Lateral & Anterior Spinothalamic Tracts • Pain & temperature sensation and crude touch• Dorsal Column • Fine touch, proprioception, two-point discrimination• Dorsal & Ventral Spinocerebellar Tracts • Proprioceptive and exteroceptive stimuli for movement and position sense• Spinoreticular Tract • Deep and chronic painSummary Ascending Tracts
  15. 15. DESCENDING TRACTSConsists of axons that conduct action potentials orimpulses away from the brain (efferent)
  16. 16. • Lateral Corticospinal Tract – main pathway• Ventral Corticospinal Tract • Both tracts decussate from the cerebral cortex (area 4,6) at the level of the medulla as it descends to the cord ipsilaterally • Lesion of corticospinal tract: loss of ipsilateral motor function below the level of injuryMotor Pathway
  17. 17. • Rubrospinal Tract • Serves as motor junction • For large muscle movement & fine motor control • Facilitates flexion & inhibits extension of upper extremities• Reticulospinal Tract • For modulation of sensory transmission esp. pain; spinal reflexes• Tectospinal Tract • For reflex head turning • Mediate reflex postural movements of the head in response to visual & auditory stimuli• Medial Longitudinal Fissure • For coordination of head and eye movementsSummary Descending Tracts
  18. 18. • Anterior Corticospinal (Direct Pyramidal Tract) • Pathway for control of voluntary motion • Conduct voluntary motor impulses from the precentral gyrus to the motor centers of the cord.• Lateral Corticospinal (Crossed Pyramidal Tract) • Pathway for control of voluntary motion • Provides fine motor control of limbs and digits• Vestibulospinal Tract • For postural reflexes • Facilitates extensor muscle tone & equilibrium• Spino-olivary Tract • Proprioception from muscles & tendons and cutaneous impulses to the olivary nucleusSummary Descending Tracts
  20. 20. • Lesion level indicates most distal uninvolved nerve root segment with normal function; muscles must have a grade of at least 3+/5 or fair + function• Tertraplegia (quadreplegia): injury occurs between C1 and C8, involves all extremities and trunk• Paraplegia: injury occurs between T1 and T12- L1; involves both lower extremities and trunk (varying levels)UMN Injury
  21. 21. Upper Motor Neuron (UMN) vs. Lower Motor Neuron (LMN) Syndrome UMN syndrome LMN SyndromeType of Paralysis Spastic Paresis Flaccid ParalysisAtrophy No (Disuse) Atrophy Severe AtrophyDeep Tendon Reflex Increase Absent DTRPathological Reflex Positive Babinski Sign AbsentSuperficial Reflex Absent PresentFasciculation and Absent Could beFibrillation Present
  22. 22. • 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 segments S4-S5• C= incomplete: motor functional is preserved below the neurological level, and most key muscles below the neurological level have a muscle grade <3• D= incomplete: motor function is preserved below the neurological level, and most key muscles below the neurological level have a muscle grade of ≤3• E= normal: motor and sensory function in normal American Spinal Injury Association
  24. 24. • An incomplete lesion that results from compression and damage to the anterior part of the spinal cord or anterior spinal artery. The mechanism of injury is usually cervical flexion. There is loss of motor function and pain and temperature sense below the lesion due to damage of the corticospinal and spinothalamic tracts Anterior Cord Syndrome
  25. 25. • A relatively rare syndrome that is caused by compression of the posterior spinal artery and is characterized by loss of pain perception, proprioception, two point discrimination, and stereognosis. Motor function is preserved. Posterior Cord Syndrome
  26. 26. • An incomplete lesion usually caused by a stab wound, which produces hemisection of the spinal cord. There is paralysis and loss of vibratory and position sense on the same side as the lesion due to the damage to the CST and dorsal columns. There is a loss of pain and temp sense on the opposite side of the lesion from damage to the lateral spinothalamic tract. Brown Sequard Syndrome
  27. 27. • An incomplete lesion that results from compression and damage to the central portion of the spinal cord. The mechanism of injury is usually cervical hyperextension that damages the spinothalamic tract, CST and dorsal columns. The upper extremities present with greater involvement than the lower extremities and greater motor deficits exist as compared to sensory deficits. Central Cord Syndrome
  28. 28. • An incomplete lesion that results from compression and damage to the central portion of the spinal cord. The mechanism of injury is usually cervical hyperextension that damages the spinothalamic tract, CST, and dorsal columns. The upper extremities present with greater involvement than the lower extremities and greater motor deficits exist as compared to sensory deficits Cauda Equina Injuries
  29. 29. • sparing of tracts to sacral segments with preservation of perianal sensation, rectal sphincter tone or active toe flexion. Sacral Sparing
  30. 30. WHAT TO EXAMINEThings to watch out for in a patient with SCI
  31. 31. • Vital Signs• Respiratory function: action of diaphragm, respiratory muscles, intercostals; chest expansion breathing pattern, cough, vital capacity; respiratory insufficiency or failure occurs in lesion above C4 (phrenic nerve, C3-5 innervation for diaphragm) Examine
  32. 32. • Skin condition, integrity: check areas of high pressure• Muscle tone and DTRs• Sensation/Spinal cord level of injury: check to see if sensory level corresponds to motor level of innervation (may differ in incomplete lesions) Examine
  33. 33. • Muscle Strength (MMT)/spinal cord level of injury: lowest segmental level of innervation includes muscle strength present at a fair + grade (3+/5); use caution when doing MMT in acute phase with spinal immobilization.• Functional status: full functional assessment possible only when patient is cleared for activity and active rehabilitation Examine
  34. 34. STANDARDIZED TESTS ANDMEASURESFor examination of patients with spinal cordinjury
  35. 35. • FIM/FAM (functional independence and functional assessment measures)• Wheelchair skills test provides for measurement of functional and wheelchair management skills for the patient who uses the wheelchair for primary mobility Functional Tests
  37. 37. • Spinal shock: A physiologic response that occurs between 30 and 60 minutes after trauma to the spinal cord and can last up to several weeks. Spinal shock presents with total flaccid paralysis and loss of all reflexes below the level of injury.• Neurogenic Bladder: the bladder empties reflexively for a patient with an injury above the level of S2. the sacral reflex arc remains intact.• Nonreflexive Bladder: the bladder is flaccid as a result of a cauda equina or conus medullaris lesion. The sacral reflex arc is damaged.
  38. 38. • Can occasionally be useful to a patient with a SCI however more often serves to interfere with functional activities. Spasticity can be enhanced by both internal and external sources such as stress, decubiti, urinary tract infections, bowel or bladder obstruction, temperature changes or touch.• Increased involuntary contraction of muscle groups, increased tonic stretch reflexes, excessive deep tendon reflexes.• Treatment: medications are usually administered in an attempt to reduce the degree of spasticity (Dantrium, Baclofen, Lioresal). Aggressive treatment includes rhizotomies, myelotomies, and other surgical intervention. Physical therapy intervention includes positioning, aquatic therapy, weight bearing, FES, ROM, resting splints and inhibitive casting. Spasticity
  39. 39. • (hyperreflexia): an emergency situation in which a noxious stimulus precipitates a pathological autonomic reflex with symptoms of paraoxysmal hypertension, bradycardia, headache, diaphoresis, flushing, diplopia, or convulsions; examine for irritating stimuli; treat as a medical emergency, elevate head, check and empty catheter first.• Treatment: the first reaction to this medical crisis is to transfer the patient to a sitting position and then immediately check the catheter for blockage. The bowel should also be checked for impaction. A patient should remain in sitting position. Lying a patient down is contraindicated and will only assist to further elevate blood pressure. The patient should be examined for any other irritating stimuli. If the cause remains unknown the patient should receive immediate medical intervention. Autonomic Dysreflexia
  40. 40. • Abnormal bone growth in soft tissues; examine for early changes- soft tissue swelling, pain, erythema, generally near large joint; late changes- calcification, initial signs of ankylosis• Treatment: Drug intervention usually involves diphosphates that inhibit ectopic bone formation. Physical therapy and surgery are often incorporated into treatment. Physical therapy must focus on maintaining functional range of motion and allowing the patient the most independent functional outcome possible. Heterotopic Bone Formation
  41. 41. • Results from the formation of a blood clot that becomes dislodged and is termed an embolus. This is considered a serious medical condition since the embolus may obstruct a selected artery. A pateint with a spinal cord injury has a greater risk of developing a DVT due to the absence or decrease in the normal pumping action by active contractions of muscles in the lower extremities.• Treatment: once a DVT is suspected there should be no active or passive movement performed to the involved lower extremity. Bed rest and anticoagulant drug therapy are usually indicated. Surgical procedures can be performed if necessary. Deep Vein Thrombosis
  42. 42. • Occurs due to a loss of sympathetic control of vasoconstriction in combination with absent or severely reduced muscle tone. Venous pooling is fairly common during the early stages of rehab. A decrease in systolic blood pressure greater than 20mmHG after moving from supine to sitting is typically indicative of this.• Treatment: Monitoring vital signs assists with minimizing the effects of orthostatic hypotension. The use of elastic stockings, ace wraps to the lower extremities, and abdominal binders are common. Gradual progression to a vertical position using a tilt table is often indicated. During intervention may be indicated in order to increase blood pressure Orthostatic Hypotension
  43. 43. • Caused by sustained pressure, friction, and/or shearing to a surface. The most common areas susceptible to pressure ulcers are the coccyx, sacrum, ischium, trochanters, elbows, buttocks, malleoli, scapulae, and prominent vertebrae. Pressure ulcers require immediate medical intervention and can often significantly delay the rehab process.• Prevention is of greatest importance. A patient should change position frequently, maintain proper skin care, sit on an appropriate cushion, consistently weight shift, and maintain proper nutrition and hydration. Surgical intervention is often necessary with advanced pressure ulcers. Pressure Ulcers
  45. 45. • Deep breathing exercises, strengthening exercises to respiratory muscles; assisted coughing, respiratory hygiene (postural drainage, percussion, vibration, suctioning) as needed to keep airway clear; abdominal supportImprove RespiratoryCapacity
  46. 46. • Prevent contracture: PROM, positioning, splinting, selective stretching to preserve function (tenodesis grasp)Maintain ROM
  47. 47. • Free of pressure ulcers and other injury positioning program, pressure relieving devices (cushion, ankleboots) patient education: pressure relief activities (pushups) and skin inspection; provide prompt treatment of pressure soresMaintain Skin Integrity
  48. 48. • Strengthen all remaining innervated muscles use selective strengthening during acute phase to reduce stress on spinal segments; resistive training to hypertrophy musclesImprove Strength
  49. 49. • Tilt table, wheelchair, use of abdominal binder, elastic lower extremity wraps to decrease venous pooling; examine for signs and symptoms of orthostatic hypotension (light headedness, syncope, mental or visual blurring, sense of weaknessReorient Patient toVertical Position
  50. 50. • Emphasis on independent rolling and bed mobility assumption of sitting, transfers, sit-to-stand, and ambulation as indicated• Tolerance, postural control, symmetry, and standing balance as indicatedPromote early return ofADLs
  52. 52. • Pt with high cervical lesions (C1-C4) require electric wheelchair with tilt-in space seating or reclining seat back; microswitch or puff and sip control, portable respirator may be attached• Pt with cervical lesions, shoulder function, elbow flexion (C5): can use a manual chair with propulsion aids independent for short distances on smooth flat surfaces; may choose electric wheelchair for distances and energy conservation
  53. 53. • C6: manual wheelchair with friction surface hand rims; independent• C7: same for C6, but with increased propulsion• Patients with hand function C8-T1 and below: manual wheelchair, standard hand rims• Significant changes in lighter, more durable, sports-oriented chairs
  55. 55. • management of wheelchair parts, turns, propulsion, all surfaces indoors and outdoors, safe fall out of and return to wheelchair.
  57. 57. • Pt’s with midthoracic lesions (T6-9): supervised ambulation for short distances (physiological, limited household ambulatory); requires bilateral knee-ankle-foot orthoses and crutches, swing-to gait pattern; requires assistance; may prefer standing devices/ standing wheelchairs for physiological standing
  58. 58. • Pt’s with high lumbar lesions (T12-L3); can be independent in ambulation all surfaces and stairs; using a swing-through or four-point gait pattern and bilateral KAFOs and gait orthoses with walker with or without FES system. Typically independent house hold ambulators; wheelchair use for community ambulation
  59. 59. • Patients with low lumbar lesions (L4-5); can crutches or canes. Typically independent community ambulators; may still use wheelchair for activities with high-endurance requirements.• High rate of rejection of orthoses/ambulation in favor of wheelchair mobility and energy conservation
  61. 61. • Methods: arm crank ergometry; functional electrical stimulation- leg cycle ergometry hybrid: arm crank ergometry and functional electrical stimulation- leg cycle ergometry wheelchair propulsion• Precautions: individuals with tetraplegia and high- lesion paraplegia experience blunted tachycardia, lack of pressure response, and very low VO2 peak, substantially higher variability of most responses
  62. 62. • Trunk stabilization and skin protection important• Vascular support may be needed (elastic stockings, abdominal binder).• Absolute contraindications to exercise testing and training of individuals with SCI (from American College of Sports Medicine, ACSM) • Autonomic dysreflexia • Sever or infected skin on weight-bearing surfaces • Symptomatic hypotension • Urinary Tract Infection • Uncontrolled Spasticity or Pain • Unstable Fracture • Uncontrolled hot and humid environments • Insufficient ROM to perform exercise task
  64. 64. • (Body Weight Support)• Indications: incomplete cervical/thoracic injuries (ASIA levels B,C and D)• Promotes spinal cord learning/activation of spinal locomotor pools• Uses body harness to support weight; variable levels of loading from 40% decreasing to 10% to full loading• Early training: therapists assist with foot placement• High Frequency (4days/week): moderate duration (30 minutes); typically for 8-12 weeksTreadmill Training UsingBWS
  66. 66. • In home and community environment; assist patient in community reintegration; ordering of proper equipment, home modification.• Provide psychological and emotional support, encourage socialization and motivation • Reorient and reassure • Promote independent problem solving, self-direction • Provide patient and family education. Focus on strategies to prevent skin breakdown, and maintain ROM, strength, and functionPromote MaximumMobility
  67. 67. • References:• PTEXAM the complete study guide Scott M. Gilles 2011• IQ PT/OT Reveiwer 2010• NPTE – Mark Dutton 2010• NPTE Review & Study Guide Sullivan & Siegelman 2011• Physical Rehabilitation 5th Edition :Susan O’Sullivan• Physical Medicine & Rehabilitation :Braddom• Clinical Neuroanatomy : Richard Snell• Clinical Neuroanatomy made ridiculously simple: Stephen GoldbergThank You!