1. 1. Rehabilitation _TBI R
2. 2.
3. 3. ?
4. 4. Rancho Los Amigos (96-2-65) III IV V VI
5. 5. Rancho Los Amigos scale Rancho Los Amigos Head Injury Treatment team VI VII
6. 6. I II ( ) III
7. 7. IV V 2~3 VI
8. 8. VII VIII
9. 9. traumatic brain injury (97-1-56) (spasticity) Parkinsonism epilepsy headache
10. 10. traumatic brain injury (97-2-58) cognition seizure hydrocephalus hypotension
11. 11. Complications include the following: 1. Posttraumatic seizures: Frequently occur after moderate or severe TBI 2. Hydrocephalus 3. Deep vein thrombosis 4. Heterotopic ossification: Incidence of 11-76%, with a 10-20% incidence of clinically significant heterotopic ossification 5. Spasticity 6. Gastrointestinal and genitourinary complications: Among the most common sequelae in patients with TBI 7. Gait abnormalities 8. Agitation: Common after TBI
12. 12. Long-term physical, cognitive, and behavioral impairments 1. Insomnia 2. Cognitive decline 3. Posttraumatic headache: Tension-type headaches are the most common form, but exacerbations of migraine-like headaches are also frequent 4. Posttraumatic depression: Depression after TBI is further associated with cognitive decline,anxiety disorders, substance abuse, dysregulation of emotional expression, and aggressive outbursts
13. 13. seizure (97-2- 59) 2 Carbamazepine
14. 14. Incidence Varies greatly according to the severity of the injury, the time since the injury, and the presence of risk factors (see below). 5% of hospitalized TBI patients (closed-head injury) have late PTS. 45% of hospitalized TBI patients have 1 or more seizures in the first week after the injury (early PTS) (Rosenthal et al, 1990). 5066% of PTS occur within 1 year; 7580% occur within 2 years - Most PTS occur 13 months after injury. 50% patients with PTS will have only 1 seizure, and 25% have no more than 3 episodes.
15. 15. Therapeutic anticonvulsant medications are usually started once late seizures occur. In the TBI population, carbamazepine (partial seizures) and valproic acid (generalized seizures) are often preferred to medications that are more sedating or associated with cognitive impairment (such as phenobarbital and phenytoin). Their superiority over phenytoin has been debated, but the differences among these 3 agents are probably minimal; carbamazepine may be as sedating as phenytoin (Brain Injury Special Interest Group of the AAPM&R, 1998).
16. 16. Important to remember that all anticonvulsants may cause some degree of sedation and cognitive deficits (usually psychomotor slowing). Phenobarbital is clearly associated with greater cognitive impairment and should not be used as first choice of anticonvulsant therapy in the TBI patient. Long-term use of phenytoin has been associated with adverse cognitive effects. Animal and clinical (extrapolated from strokes) studies suggest that phenytoin may impede recovery from brain injury (Dikmen, 1991).
17. 17. Second-generation anticonvulsants, such as gabapentin and lamotrigine, may also be used for treatment of PTS as adjuvant agents (not approved yet for monotherapy). These agents appear to have fewer cognitive side effects but are still under investigation in the TBI population.
18. 18. Risk Factors Associated With Late Posttraumatic Seizures
19. 19. indifference pseudo-depression (96-2-58) frontal lobe temporal lobe parietal lobe occipital lobe
20. 20. (100-2-67)
21. 21. HETEROTOPIC OSSIFICATION (HO) HO is the formation of mature lamellar bone in extra skeletal soft tissue. Common in TBI: incidence of 1176%. Incidence of clinically significant cases is 10 20%.
22. 22. Risk Factors Prolonged coma (> 2 weeks) Immobility Limb spasticity increased muscle tone (in the involved extremity) Associated long-bone fracture Pressure ulcers Edema Period of greater risk to develop HO: 3 to 4 months postinjury
23. 23. Signs/Symptoms Most common: pain and decreased ROM. Also: local swelling, erythema, warmth in joint, muscle guarding, low-grade fever. In addition to pain and decreased ROM, complications of HO include bony ankylosis, peripheral nerve compression, vascular compression, and lymphedema. Joints most commonly involved: 1. Hips (most common) 2. Elbows/shoulders 3. Knees
24. 24. Diagnostic Tests Serum Alkaline Phosphatase (SAP) SAP elevation may be the earliest and least expensive method of detection of HO. It has poor specificity (may be elevated for multiple reasons, such as fractures, hepatic dysfunction, etc.)
25. 25. Bone Scan Sensitive method for early detection of HO. HO can be seen within the first 24 weeks after injury in Phase I (blood-flow phase) and Phase II (blood-pool phase) of a triple phase bone scan, and in Phase III (static phase/delayed images) in 48 weeks with normalization by 7 to 12 months. Plain X-Rays Require 3 weeks to 2 months postinjury to reveal HO. Useful to confirm maturity of HO.
26. 26. Fever (100.5F) and left knee pain developed in 22-y-old man after closed cranial trauma, raising concern about osteomyelitis or other local infection. Initial radiography findings were normal. (A) 67Ga image shows intense increased uptake in anteromedial aspect of distal left thigh. (B) From left to right, selected flow study images, blood pool images, and delayed bone scan images obtained shortly thereafter show increased flow, hyperemia, and increased uptake, respectively, also in anteromedial aspect of distal left knee. (C) Subsequently obtained radiograph shows HO at this site. (D) Three-phase bone scan 18 mo after injury shows significantly less abnormal activity on (from left to right) flow study images, blood pool images, and delayed bone scan images. (Reprinted with permission of (58).)
27. 27. HO Prophylaxis ROM exercises Control of spasticity Nonsteroidal anti-inflammatory drugs (NSAIDs) Radiation used perioperatively to inhibit HO in total hip replacement patients; concerns about decreased risk of neoplasia limit its use in younger patient populations. Radiation in TBI patients for HO prophylaxis would require essentially irradiation of the whole body (as HO can develop practically at any joint), which is not practical.
28. 28. Treatment Bisphosphonates and NSAIDs (particularly indomethacin) have been used on patients to arrest early HO and to prevent postop recurrence, but their efficacy has not been clearly proven (TBI population). ROM exercises: used for prophylaxis and treatment for developing HO to prevent ankylosis. Surgical resection of HO indicated only if function is the goal (eg, hygiene, ADLs, transfers). Surgical resection usually postponed 12 to 18 months to allow maturation of HO.
29. 29. traumatic brain injury (96-2-59) amnesia Glasgow blink reflex
30. 30. spasticity (102-2-59) 1. 2. 3. 4.