Rehabilitation of SCI for all syudent.pptx

Rehabilitation of SCI for all syudent.pptx

1. Rehabilitation of SCI

2. HO is the formation of lamellar bone within the soft tissue surrounding a joint The incidence ranges between 13% and 57% is usually found in the first 6 months (peak at 2 months) after injury HO may occur beyond 1 year and is usually associated with a newly developed PU, DVT, or fracture. Heterotopic Ossification

3. Risk factors for HO older age (children and adolescents have a lower incidence) neurological complete lesions male gender Spasticity DVT pressure sores These risk factors may be cumulative.

4. Most of the cases of HO will have only radiological findings and are not clinically significant. Up to 20% will present with a limitation of the ROM, up to 8% progressing to joint ankylosis Only joints below the NLI will develop heterotopic bone, with the most common location being the hips ( anteromedial aspect) , followed by the knees, then shoulders.

5. The joint may appear warm and swollen must therefore be differentiated from a septic joint, cellulitis , DVT, fractures, and inflammatory arthritis. The patient may experience Pain Malaise low-grade fever an increase in spasticity.

6. Causes No definitive explanation established. Possibly due to alteration in neuronal control over the differentiation of mesenchymal cells into osteoblasts , which form new bone A decrease in tissue oxygenation or induced changes in multipotential connective tissue cells in which new bone forms in planes between connective tissue layers

7. When passive ROM is delayed more than 1 week after injury, patients are more likely to develop HO It is also possible that forced ROM of contracted limbs may cause micro trauma and bleeding, leading to HO In severe cases, adjacent neurovascular structures may be compromised leading to distal extremity swelling and nerve entrapment

8. Diagnosis Bone scans are also the most useful technique to assess maturity of the heterotopic bone Plain x-rays become positive approximately 2 to 6 weeks after a triple phase bone scan first reveals HO or 1 to 10 weeks after clinical presentation A triple phase bone scan is the most sensitive imaging study in diagnosing early HO, and can detect disease activity before calcification becomes apparent on plain x-ray

9. The first two phases of the bone scan measures the increase in blood flow to a joint during the early inflammatory period. The third phase , or static bone phase , is more specific since it measures the incorporation of the radionuclide into the bony matrix but may take another 3 weeks before it is positive Plain film detects HO in at least 7–10 days after clinical signs are observed.

10. Ultrasonography may be positive early and has the advantage of being a relatively inexpensive examination without requiring radiation MRI , with an increased T2 signal (edema) in muscles, fascia, and subcutaneous tissue can be helpful in diagnosing HO acutely CT scan may be used to determine the volume of bone needed for planning surgical resection.

11. Serum alkaline phosphatase increases at 2 weeks , exceeds normal levels at 3 weeks , peaks at 10 weeks , and returns to normal before HO matures. Not specific for HO. CRP and ESR : can be elevated but not specific for HO CRP is a more reliable predictor of disease activity, with normalization of the CRP correlating with resolution of the inflammatory phase of HO An elevation of serum creatinine phosphokinase (CPK) may be a more reliable predictor of HO

12. Treatments include ROM with gentle stretching after the acute inflammatory period is over (1 to 2 weeks), bisphosphonates , NSAIDS (e.g., indomethacin ) if not contraindicated, radiation therapy , and surgical excision

13. ROM Passive and active assistive ROM to the affected limb is necessary to prevent further loss of ROM. Aggressive ROM (beyond the initial end-point), especially during the acute inflammatory phase, is not recommended

14. Treatment with bisphosphonates to decrease the rate of new bone formation in patients with HO has no effect on bone which has already been deposited. Disodium etidronate inhibits osteoclastic activity and conversion of calcium phosphate to hydroxyapatite . Although IV administration of etidronate reportedly led to quicker resolution of edema with less rebound formation after the medication was discontinued , it is no longer available.

15. Current recommendation is for oral administration of etidronate 20 mg/kg/d for 6 months if the CPK level is elevated at the time of diagnosis 20 mg/kg/d for 3 months , followed by 10 mg/kg/d for an additional 3 months if the initial CPK level is normal With this regimen, there was faster resolution of edema with less rebound formation after the medication was discontinued.

16. If CPK is elevated , or CRP greater than 8 , some recommend addition of a NSAID until the CRP less than 2 or CPK normalizes Surgical excision should be reserved for patients with severely limited ROM that causes functional limitations Most clinicians recommend waiting until after the ectopic bone is mature by bone scan, which may take up to 12 to 18 months to occur.

17. Complications of surgery include significant blood loss, infection, and recurrent HO Postop treatment includes NSAIDS for at least 6 weeks, bisphosphonates for 3 to 12 months, and/ or radiation While radiation decreases the degree of recurrence of HO, complications include delayed wound healing, osteonecrosis , and the risk of developing sarcoma

18. Prophylaxis of HO in SCI patients has been studied using several agents including etidronate and indomethacin (75 mg daily for 3 weeks within 5 weeks of injury), with less HO formation as compared with placebo Warfarin may also be an effective agent by inhibiting the formation of osteocalcin Despite the available therapeutic options, prophylaxis is still not routinely used because of the relatively low incidence of morbidity

19. When the core temperature is cool and requires an adjustment, the hypothalamus, which regulates body temperature, employs shivering and vasoconstriction to increase temperature. Similarly, sweating and vasodilatation decreases temperature through increased heat loss. After a SCI above the T6 level, the ability of the hypothalamus to direct the periphery is impaired. Thermoregulation

20. This results in the patients being partially poikilothermic , in that they may have difficulty maintaining a normal core temperature in response to environmental change in temperature People with SCI therefore tend to have a higher body temperature in warm environments and a lower temperature in cold environments. This is termed poikilothermia

21. This is an important factor to keep in mind In addition, patients should be cautioned to wear appropriate clothing depending on the setting/ environment they are in. Patients with chronic tetraplegia also frequently have subnormal body temperatures (<97.7°F) in a normal ambient environment

22. Anemia is a common finding following acute SCI, and is usually normochromic and normocytic Serum iron,and transferrin are usually low. Although the exact cause is not known, bleeding may be a factor in some cases. By 1 year post injury, anemia improves in the majority of patients and if it persists it is usually associated with chronic inflammatory complications such as PUs or frequent UTIs Anemia

23. Pressure ulcers are lesions in the integument caused by external pressure . External pressure causes local tissue ischemia and occurs typically over bony prominences . Although it is established that persons with SCI are highly susceptible to developing pressure ulcers because of impaired mobility and sensation, pressure ulcers can be prevented with proper care. Pressure Ulcers

24. PUs are one of the most common and potentially serious complications of SCI Approximately 24% of patients developed at least 1 PU during their initial rehabilitation The longer time injured, the greater the risk of developing an ulcer, as up to 80% of persons with SCI develop a PU at some point in their lifetime, with a community prevalence of approximately one third Skin issues are the second most common etiology for rehospitalization in chronic SCI

25. PUs are classified using the National Pressure Ulcer Advisory Panel (NPUAP) staging system, The NPUAP includes the original four stages and additional two categories on deep tissue injury and unstageable PUs

26. Deep tissue injury refers to a purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. Unstageable wounds occur when not enough slough and/or eschar is removed to expose the base of the wound, and therefore the true depth can not be determined and therefore staged.

27. PUs develop over bony prominences . The most common location in persons with SCI within the first 2 years is the sacrum , followed by the ischium , heels, and trochanters . After 2 years , the ITs are the most common site of development. In children up to age 13 years, the occiput is the site of most frequent development.

28. Mechanisms of developing a pressure ulcer Local soft tissue ischemia results due to prolonged pressure over bony prominences, that exceed supracapillary pressure > 70 mm Hg. 1. Ischemia: lack of blood supply to the tissue Frequently associated with hyperemia in the surrounding tissue. Increased local O2 consumption occurs. .

29. 2. Pressure: Prolonged pressure over bony prominences, exceeding supracapillary pressure ( 70 mmHg pressure) continuously for 2 hours results in occlusion of the microvessels of the dermis with subsequent tissue ischemia Occlusion of the microvessels occurs when the force exerted on the vessel wall is greater than the intraarterial pressure. This results in immediate epidermal ischemia

30. Ischemia causes hyperemia of the surrounding tissue. Muscle is more susceptible to pressure ischemia than skin. 3. Friction (Shearing Forces): Removes corpus striatum (stratum corneum ) of the skin The most important risk factors for the development of PUs are pressure and shear

31. Other risk factors significant in SCI include level and severity of the injury, mobility status, gender, ethnicity, marital status, employment status, educational achievement,

32. tobacco and alcohol use, history of a prior PU, nutritional status, anemia, incontinence, smoking, and possibly psychosocial issues (i.e., depression). Secondary effects of PUs include further medical morbidity , pain (especially in incomplete lesions), increased spasticity, and wound infections .

33. Prevention PU prevention is critical , and education regarding this should begin as early as possible after injury. This includes continued observation of skin (teaching patients to use a mirror), avoidance of excessive pressure or shearing, proper turning frequency in bed and weight relief techniques when seated,

34. proper equipment (e.g., mattress, wheelchairs, cushions, and seating system), early recognition and treatment . In addition, maintaining proper nutrition and discontinuing smoking are recommendations that will help prevent and heal ulcers if they develop.

35. TREATMENT OF PRESSURE ULCERS Prevention of pressure ulcers should always be the first line of defense. Once a lesion has developed, however, treatment should be prescribed to reduce the progression of the ulcer. Extrinsic factors that contributed to the initial formation of the ulcer should be identified and treated

36. In general, healing will be promoted if the wound remains clean and moist, with debridement of necrotic and infected tissue as needed Stage I and II pressure ulcers: usually nonoperative Stage III ulcers may require surgical intervention (debridement, muscle/skin flaps). Stage IV wounds almost always require surgery.

37. Medications can be used for supplementation, particularly in severe cases: – MVI with minerals – Vitamin C 1 g/day – Zinc sulfate 220 mg/day – Copper 2 mg/day (zinc depletes copper) – Arginine (7–15mg/day) and glutamine (10–20 mg/day) – Increase protein intake Surgery does not treat the underlying cause of the ulcer. Postoperatively, this still needs to be addressed. An appropriate sitting program should be followed after these procedures

38. The incidence of concomitant TBI in those with a primary SCI is reported between 24% & 60% Historical factors such as mechanism of injury (i.e., high velocity impact), loss of consciousness prolonged extrication and/or Intubation at the scene higher NLI Dual Diagnosis: TBI in Person with SCI

39. presence of PTA , and impaired initial Glascow Coma Scale (GCS) score, should alert medical personnel of the possibility of a concomitant TBI

40. Deficits may be seen in attention, concentration, and memory, and can interfere with new learning and problem solving. Medical management of problems common to the SCI population such as pain, DVT prophylaxis, spasticity, and neurogenic bladder requires special consideration in the dual diagnosis patient.

41. Special care should be taken to utilize medications with minimal cognitive impact. Medications routinely used in SCI may have an impact on the recovering brain ( ie , baclofen and benzodiazepines). Elevated BP may signal the presence of AD in those with SCI at or above the T6 level However, those with concomitant TBI may experience transient elevation of BP secondary to a centrally driven “sympathetic storm.”

42. Spasticity is a syndrome of different components, including a velocity-dependent increased resistance to passive motion, involuntary muscle contractions or spasms, and hyper reflexia The incidence of spasticity in UMN-related SCI is approximately 70%, with roughly half the patients requiring pharmacological intervention While spasticity may occasionally contribute to improved function (i.e., transfers, standing, ambulation, and assisting in ADL) Spasticity

43. Complications including contractures, pain, impaired function, and decreased QOL. Spasticity occurs more frequently in persons with cervical and upper thoracic SCI than in those with lower thoracic and lumbosacral SCI, more significant in persons with certain incomplete injuries, AIS grades B and C , than in persons with grades A or D .

44. Before initiating treatment, potential nociceptive sources should be evaluated and if present, they should be treated . Common causes include UTI, bladder calculi, PUs, abdominal pathology, ingrown toenails, hemorrhoids, and bowel impaction.

45. Treatment Stretching of spastic muscles is the mainstay of treatment of spasticity for virtually all persons with SCI. Steady static stretching, to the limits of the ROM of a joint, has been shown to result in a reduction of reflex activity that can last for several hours after the exercise ROM exercises should be performed regularly on all affected joints by members of the rehabilitation team, support staff, or family members, after instruction in proper technique.

46. Proper positioning , in bed or in wheelchairs, can effectively control increased muscle tone, as well as provide a prolonged static stretch to spastic muscles. Modalities have been used including cold and ES, usually with short-term benefits Inhibitive casting, splinting, and orthotic management of muscles and joints at risk for contracture may be helpful in reducing tone

47. Oral baclofen to be the first-line pharmacologic treatment for spinal spasticity. a structural analog of γ- aminobutyric acid (GABA) the main inhibitory transmitter of the SC binds to GABA B receptors 10 to 15 mg/day in divided doses, with gradual increases as clinically indicated. maximum recommended dose is 80 mg/day

48. Adverse effects of baclofen include fatigue and dizziness, while seizures can occur with abrupt withdrawal Intrathecal baclofen (ITB) is of benefit for persons with SCI, with effective control of spasticity in the lower limbs being greater than in the trunk and upper limbs

49. Diazepam and other benzodiazepines bind to the GABA A receptor. Benzodiazepines can cause physical dependence, as well as lethargy and diminished concentration Tizanidine hydrochloride is a central α2-adrenergic agonist that has been shown to be effective in treating spasticity after SCI Adverse effects of tizanidine include sedation and liver function abnormalities

50. Gabapentin (especially at higher doses of >1,800 mg/d) and pregabalin , both anticonvulsants, have antispasticity benefits in persons with SCI Dantrolene may be of special benefit in persons with concurrent SCI and TBI, since its effects are peripheral rather than in the central nervous system

51. Alcohols injected perineurally or directly into muscles destroy nerve axons and muscle in a nonselective manner. The clinical effect of an alcohol injection is more variable , with reported effectiveness persisting from 1 month to several years Botulinum toxin , which can be injected into the affected muscle, blocks neuromuscular transmission by inhibiting the release of acetylcholine into the synapse.

52. It has an onset of action of 4 to 10 days , the effect lasts on an average for 3 months , and it has shown efficacy in improving UE and LE functions Follow-up stretching, which may include dynamic splinting or serial casting, is recommended to optimize function.

53. Surgical interventions , including cordectomy and myelotomy , have been performed to reduce spasticity, but with limited long-term success Dorsal rhizotomy , and dorsal root entry zone (DREZ) procedures, have been proposed to control spasticity by decreasing the afferent component of spasticity, although these should only be considered if all previous treatments have failed.

54. Thank You

55. The most common cause of progressive myelopathy after a SCI is post-traumatic syringomyelia (PTS). PTS may develop at any time, from 2 months to decades post injury PTS presents as neurologic decline in up to 8% of patients, but is more frequently first seen on MRI as an elongated cavity in a much higher percentage of cases. Post-Traumatic Syringomyelia

56. The pathogensis of past-traumatic syringomyelia is not entirely understood. Cavitation of the spinal cord usually occurs at the level of the injury. Cavity formation may be secondary to liquefaction of the spinal cord or from central hematoma present at the initial injury. The lesion usually progresses in a cephalad direction.

57. As the lesion progresses and compromises more nerve fibers, symptoms may become more apparent The pathogenesis is unknown, but the cavity begins at the level of the cord injury in the gray matter between the dorsal horns and posterior columns.

58. The most common presenting symptom is pain , usually located at the site of the original injury or may radiate to the neck or upper limbs. The pain is described as aching or burning, worse with coughing, sneezing, straining, and in the sitting rather than in the supine position. The earliest sign is an ascending loss of deep tendon reflexes.

59. An ascending sensory level is common, typically with a dissociated sensory loss with impaired pain and temperature sensation but intact touch, position, and vibration sense . Loss of pain sensation can lead to a Charcot joint. Weakness occurs, but rarely in isolation.

60. Additional findings may include increased or decreased spasticity, hyperhidrosis , AD, neck muscle fatigue with prolonged sitting, loss of reflex bladder emptying, worsening OH, scoliosis, central and/or obstructive sleep apnea, new Horner’s syndrome, reduced respiratory drive, diaphragmatic paralysis, cranial nerve dysfunction, impaired vagal cardiovascular reflexes, and sudden death

61. MRI with gadolinium is the gold standard for diagnosing PTS. Neurologic monitoring is essential , and includes clinical examination, serial electrodiagnostic tests, and/or MRI. Conservative treatment includes close monitoring, pain control, activity restrictions, and providing rehabilitation interventions as needed (i.e., functional training and adaptive equipment).

62. Surgical treatment is usually indicated if there is an ongoing neurologic decline or severe intractable pain. Recurrence of neurologic symptoms is common (up to 50%).

63. PAIN AFTER SCI

64. The upper limbs in persons with SCI are used for weightbearing activities including weight shifts, transfers, and wheelchair propulsion as well as for ADL, thereby increasing the chances of overuse syndromes. Shoulder pain is the most commonly reported painful joint after SCI (382). Approximately 30% to 50% of patients complain of shoulder pain severe enough to interfere with function, with the prevalence increasing with time from injury (366,383). Pain during the first year after injury is more common in tetraplegics , but in later years it is more common in paraplegics. UE NeuroMusculoskeletal Pain

65. Two thirds of shoulder pain is due to chronic impingement syndrome and approximately half involves rotator cuff pathology. Bicipital tendonitis, subacromial bursitis, adhesive capsulitis , acromioclavicular osteoarthritis, and cervical radiculopathy are other common causes of shoulder pain in chronic SCI. Other causes that are specific to SCI include muscle imbalance, spasticity, contractures, HO, and the presence of a syrinx . If pain develops acutely, then referred pain should be excluded, including UTI, peptic ulcer disease, angina, and an acute abdominal problem. Pain associated with neurologic changes (i.e., weakness, sensory loss, and/or reflex changes) may be due to peripheral nerve entrapment, radiculopathy , or a post-traumatic syrinx .

66. Diagnostic tests shoul Diagnosis – Complete history and physical exam, including functional assessment, ROM, flexibility, and sensation testing – Radiological and electrodiagnostic testing as neededd be ordered as needed.

67. Relief of acute pain includes rest, icing, and other modalities along with pharmacologic intervention (NSAIDS, acetaminophen, muscle relaxants) and injections, as needed. Acupuncture may also be helpful (387,388). Once overuse problems arise, they can become a chronic problem if treatment is not focused on correcting the cause . the chronic upper limb musculoskeletal problems are due to the overuse from functional activities, it is vital that proper exercise techniques and shoulder protection, and conservation should be learned early during acute rehabilitation and reinforced frequently

68. Overuse injuries may also affect the elbow (32%), wrist, and hand (45%), including the development of carpal tunnel syndrome (CTS), ulnar nerve entrapment at the elbow and wrist, de Quervain syndrome or other tenosynovitis , osteoarthritis, and stress fractures (384). The most common source of elbow pain is overuse of the extensor and flexor tendons as they attach to the medial epicondyle . Ulnar neuropathy can lead to intrinsic hand weakness and medial hand numbness, and can impact ADL (366). The incidence of CTS is between 21% and 65%, with persons with paraplegia more affected than persons with tetraplegia (380), and with a higher incidence at longer times postinjury (393)

69. Upper Extremity Compression Neuropathies • Nearly 2/3 of patients with SCI develop UE compression neuropathies. • Increases with the length of time from injury and includes most commonly median and ulnar neuropathies. • The incidence of carpal tunnel syndrome (CTS) is between 21–65% with persons with paraplegia, who are more affected than persons with tetraplegia . – CTS is due to recurrent stress from transfers, wheelchair propulsion and pressure relief. – Treatment includes analgesics, NSAIDs, splinting (especially at night), injections (anesthetic and/or corticosteroid), physical modalities (ultrasound, friction massage, etc), and education regarding transfers to avoid end range stress. – Padded glove use may decrease the trauma of wheelchair propulsion. – Surgical release may be required, with the postoperative recovery time being weighed against the long term benefits of the procedure. • Ulnar neuropathy is also common. • 25% bilateral UE are affected.

70. Surgical Interventions of the UE in Tetraplegia

71. SCI is a life-altering event for patients and their families A person who sustains a SCI is at risk for the “ four D syndrome ”; dependency , depression , drug addiction, and, if married, divorce Depressive disorders are the most common form of psychological distress after SCI, estimated to affect 20% to 45% of those injured, and usually occurs within the first month Psychological issues

72. Risk factors for depression include a prior history or family history of depression pain female gender lack of social support multiplicity of life stresses concurrent medical illness, and alcohol or substance abuse.

73. Additional factors include having a complete neurological injury medical comorbidity with TBI a low level of autonomy poor education unemployment, having a poor social network and family support few financial resources architectural barriers vocational difficulties, and the need for personal and transportation assistance.

74. The suicide rate for individuals with SCI is approximately five times the age-sex specific suicide rate in the United States. It is the leading cause of death in individuals with SCI in the youngest age groups, and is highest 1 to 5 years postinjury (22,436,437). The suicide rate is higher for those “marginally” injured (incomplete injuries) who have a near complete recovery (438). In addition to depression, lack of social support, history of suicide attempt, and a feasible plan for inflicting harm to self are risk factors for suicide. Substance abuse, which is increased in the SCI population, is also a major risk factor for suicide. It is imperative that physicians and other health care personnel continue to monitor patients for depression well after the acute phase of injury.

75. Anxiety and post-traumatic stress disorder (PTSD) have been reported in up to 20% of persons with SCI (439). Symptoms of PTSD may be higher in those with features of depression and/or anxiety The treatment for psychological disturbances after SCI includes counseling and pharmacological intervention. The medications should continue for at least 4 months (441,442), and be tapered slowly as discontinuation early is associated with a high rate of relapse (443 After this initial period, medication may need to be continued to prevent recurrence of symptoms. A psychiatrist should be consulted if the patient has suicidal ideation or presents with psychotic features, and/or the patient does not respond to one or two of the trials of antidepressant medications. Recurrence rates for depression are common

76. remove Substance Abuse

77. Cardiovascular Disease, Obesity, and Diabetes After SCI

78. Long-term follow-up with a SCI specialist is extremely important, especially with shorter LOS in acute rehabilitation after injury Initially, visits should occur on a monthly basis , especially while the person is on outpatient therapy. This allows for monitoring of medical issues reevaluation of the therapy program updating goals and equipment prescriptions Long-Term Follow-Up

79. This includes Bowel Bladder spasticity changes the possible development of HO Hypercalcemia and AD After medical issues have stabilized and outpatient therapy has concluded, visits are recommended every 3 to 6 months throughout the first year and at least yearly visits are recommended.

80. Deterioration of the neurologic status may be secondary to a tethered cord, syringomyelia , or peripheral problems, such as median or ulnar nerve entrapment, or other musculoskeletal complications As a greater proportion of persons with SCI are surviving after their injury, the importance of their follow-up visits to maintain their QOL cannot be over emphasized

81. Yearly evaluations should include the patient’s current condition and concerns, medications, review of systems (ROS), and age-appropriate screening Specifics include dental, vision, and hearing screens, evaluating for cognitive slowing, depression, and suicide Questions related to smoking, alcohol and drug use, exercise, and current employment status also should be included

82. In addition to a general physical examination, areas to examine include the skin, oral cavity in smokers, digital rectal examination for men over age 50, the SCI-specific neurological examination, and a musculoskeletal examination to identify problems related to aging with SCI and pain A gynecologic evaluation is recommended for a clinical breast exam for women over 50 and a pelvic examination .

83. Recommendations for the general medical screening should be followed in persons with SCI, including screening for colon cancer with a flexible sigmoidoscopy for those over age 50 , and colonoscopy if at high risk. Mammography is recommended for women every 1 to 2 years between the ages of 50 and 69.

84. Fasting glucose every 3 years for those over age 40 or annually for persons with risk factors for type-II diabetes screening for nutritional deficiencies with complete blood count, albumin and iron levels (if at risk), fasting lipid profile for men over 40 and for women over 50, prostate-specific antigen testing in men between age 50 and 70 or after age 45 if at increased risk, are also recommended Counseling is an important aspect of follow-up visits, both for medical as well as physical and social issues

85. Secondary medical complications are extremely common in patients with chronic SCI The most common reasons for rehospitalization include GU complications, PUs, and respiratory complications Pneumonia is more common in persons with tetraplegia while pressure sores are more common in persons with paraplegia

86. Rehospitalization rates have remained static over the last 10 years Patients from skilled nursing facilities, with lower motor FIM scores, or using state or federal health insurance plans, have higher rehospitalization rates

87. The quest for cure is as strong as ever, with many new advances constantly being made. Over the last decade, there is increased knowledge regarding the basic pathophysiology of SCI and new pharmacological strategies in the acute and chronic treatment to enhance neurological and functional recovery. The future

88. In animal models, scientists have successfully used antibodies to block growth inhibitors, applied growth factors, implanted cells and peripheral nerve bridges, and used gene therapies to stimulate spinal cord regeneration. Some advances are nearly ready for application in the clinical setting. The key factors for cure include minimizing secondary effects of injury, neutralizing the effects of substrates that inhibit CNS regeneration, delivery of regeneration-promoting substances to the injured spinal cord, allowing a bridge to which the spinal cord axons can attach and grow along after injury, and determining the genes that may allow for “turning on” axonal growth after injury

89. Basic science research continues to make progress with the ultimate goal of a cure for SCI. Rehabilitation is a crucial part of any cure treatment strategy and is what we currently have available to maximize functional potential. Rehabilitation professionals should be involved in the research but remain committed to the patients and their needs. Caring for the acute and long-term medical issues, as well as assisting the patient to be active in all domain including social, recreational, and vocational activities, is what rehabilitation is all about!

90. Thank You

91. Before a patient is diagnosed as having a dual disabilitybased on behavioral issues, the clinician should seek other causes for such behavior including the possibility of seizures, post traumatic hydrocephalus, intracranial pathology, neuroendocrine disturbance, metabolic disturbance, side effects of centrally acting medications, hypoxemia, and infectious issues.

92. Fever may represent infection, poikilothermia , or “central fever” which occurs in TBI. Once the former two etiologies have been excluded, treatment with a b-blocker can be considered .

93. If initial interventions to treat AD do not improve the patient’s BP, pharmacotherapy should be initiated. Agitation is common in those with TBI and should be managed similarly in those with dual diagnosis. Behavioral interventions such as redirection and decreasing environmental stimulation are first-line treatments. Pharmacotherapy is appropriate when behavioral modifications are ineffective.