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Exam 2 Flashcards

1
Q

Stroke Death Prevelence

A
  • stroke kills almost 130,000 americans each year
  • 1 out of every 19 deaths
  • every year, more than 795,000 people in the US have stroke
  • 185,000 strokes (1 in 4) are people who have had previous stroke
  • stroke is a leading cause of serious long-term disability
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2
Q

Risk factors of Stroke that CANNOT be changed

A
  • age: risk doubles for each decade of life after age 55
  • gender: more common in men than women, women use of birth control pills and pregnancy pose stroke risks though
  • prior stroke, TIA, or heart attack: person with 1+ TIA is 10X more likely to have a stroke than someone of same age/gender. if patient has had heart attack, 3X higher risk of having a stroke
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3
Q

TIA

A
  • transient ischemic attack

- aka “mini stroke’

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4
Q

Can stroke risk be influenced by race and ethnicity?

A
  • YES
  • risk of first stroke is nearly twice as high for African Americans and African American’s are more likely to die following a stroke than caucasians
  • hispanic americans’ risk for stroke falls between caucasians and african americans
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5
Q

CVA Risk Factors that CANNOT be changed but CAN be TREATED or controlled

A
  • sickle cell anemia
  • african american and hispanic children more common
  • sickle cells tend to stick to blood vessel walls, which block arteries and cause a stroke
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6
Q

CVA Risk factors that CAN be CHANGED, TREATED, AND CONTROLLED

A
  • high blood pressure
  • cigarette smoking
  • diabetes mellitus
  • carotid or other artery disease (peripheral)
  • atrial fibrillation
  • high blood cholesterol
  • poor diet
  • physical inactivity/obesity
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7
Q

Carotid artery

A
  • narrowed by atherosclerosis
  • plaque builds up in artery walls
  • may become blocked by blood clot
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8
Q

Peripheral Artery Disease

A
  • narrowing of blood vessels carrying blood to leg and arm muscles
  • plaque in artery walls
  • higher risk of artery disease and therefore stroke
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9
Q

Poor Diet that increases stroke risk

A
  • high in saturated fat and cholesterol
  • high sodium (salt)
  • diets with excess calories > obesity
  • 5+ servings of fruits and vegetables per day may reduce the risk of stroke
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10
Q

Physical inactivity and obesity effects on stroke

A
  • being inactive, obese, or both can increase risk of high blood pressure, high blood cholesterol, diabetes, heart disease, and stroke
  • recommendation: at least 30 minutes of activity on most or all days
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11
Q

Ischemic Prevelence with strokes

A
  • ischemic: lack of blood

- 83-87% of all strokes are ischemic strokes, when blood flow to brain is blocked

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12
Q

Two types of ischemic strokes

A
  • cerebral thrombus

- cerebral embolism

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13
Q

Cerebral Thrombus

A
  • type of ischemic stroke
  • blood vessel narrows
  • from atherosclerosis
  • thrombosis = blood clot
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14
Q

Cerebral embolism

A
  • type of ischemic stroke

- clot from heart, upper body, or neck dislodges and move to brain and blocks artery

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15
Q

DVT

A
  • deep vein thrombosis
  • expect swelling, red and warm to touch, paon
  • don’t vigorously exercise with DVT!
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16
Q

Hemorrhagic Stroke

A
  • 17% of all strokes
  • weakened vessel that ruptures and bleeds into the surrounding brain
  • blood accumulates and compresses the surrounding brain tissue
  • weakened blood vessels are from aneurysms or arteriovenous malformations (AVMs)
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17
Q

Aneurysm

A
  • ballooning of a weakened region of a blood vessel
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18
Q

Arteriovenous Malformation (AVM)

A
  • a cluster of abnormally formed blood vessels

- the vessels can rupture, causing bleeding into the brain

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19
Q

MCA

A
  • middle cerebral artery

- most common stroke location

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20
Q

Areas affected by a MCA stroke

A
  • optic radiation = homonymous hemianopia (contralateral visual fields cut)
  • broca’s and wernicke’s area = expressive and receptive aphasia
  • motor and sensory homunculus
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21
Q

Broca’s Area #

A

44

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22
Q

Wernicke’s Area #

A

22

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23
Q

Homonymous Hemianopsia

A
  • due to a stroke involving the optic tract or radiations on the opposite side
  • usually from MCA
  • homonymous hemianopsia is when you cannot see the same 1/2 of each eye (i.e. both eyes lose their field of vision of the R side)
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24
Q

Unilateral optic field loss

A
  • i.e. left optic nerve compression
  • this is when you can see completely out of one eye but not at all out of the other
  • eye that is blind is one with nerve compression
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25
Q

Bitemporal hemianopia

A
  • chiasmal compression from “pituitary tumor”

- means both the outside/lateral visual fields are blinded/blocked

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26
Q

Contralateral Hemiparesis and Sensory impairment due to MIDDLE Cerebral Artery affects what areas first

A
  • arm > leg
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27
Q

Apraxia

A
  • can be caused by MCA stroke
  • inability to plan or carry out a motor plan
  • ideomotor apraxia
  • ideational apraxia
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28
Q

What does the MCA supply?

A
  • supplied internal capsule and basal ganglia
  • damage will result in both UE and LE involvement
  • remember: internal capsule deals with a lot of motor output
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29
Q

Contralateral Hemiparesis and Sensory impairment due to ANTERIOR cerebral artery affects what areas first

A
  • leg > arm
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30
Q

Anterior Cerebral Artery Stroke impairments

A
  • contralateral hemiparesis
  • contralateral sensory impairments
  • loss of bowel/bladder control
  • apraxia
  • mental impairment with perseveration, confusion, memory loss
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31
Q

Perseveration

A
  • do the same thing or say the same words repeatedly
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32
Q

Posterior Cerebral Artery Stroke Impairments

A
  • contralateral homonymous hemianopia
  • Dyslexia
  • Memory deficits
  • Topographical disorientation
  • cranial nerve III Palsy (oculomotor)
  • contralateral hemiparesis
  • Thalamic Syndrome
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33
Q

Thalamic Syndrome

A
  • can be due to posterior cerebral artery stroke
  • sensory impairments in all modalities
  • pain
  • paresthesias
  • pain and temperature sensory loss
  • ataxia, athetosis, choreiform movement
  • visual agnosia: not recognizing familiar object with vision
  • tactile agnosia: not recognizing object based touch
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34
Q

Dyslexia

A
  • learning disorder characterized by difficulty reading due to problems identifying speech sounds and learning how they relate to letters and words
  • also called specific reading disability
  • common learning disability with children
  • can be from posterior cerebral artery stroke
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35
Q

Patesthesia

A
  • an abnormal sensation such as tingling, tickling, pricking, numbness or burning of a person’s skin
  • can be symptom of thalamic syndrome due to posterior cerebral artery stroke
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36
Q

Athetosis

A
  • slow, characterized by slow, involuntary, convoluted, writhing movements of the fingers, hands, toes, and feet
  • in some cases arms, legs, neck and tongue
  • can be symptom of thalamic syndrome post posterior cerebral artery stroke
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37
Q

Choreiform movements

A
  • involuntary, forcible, rapid, jerky movements which are mostly manifestations of basal ganglia diseases (relatively small amplitude)
  • can be from thalamic syndrome from posterior cerebral artery
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38
Q

Carotid Arteriogram

A
  • arteriogram of the R carotid artery showing a severe narrowing (Stenosis) of the internal carotid artery just past the carotid fork
  • there is enlargement of the artery after the stenosis
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39
Q

Basilar Artery Stroke Impairments

A
  • brainstem
  • coma
  • quadriplegia
  • “locked in” syndrome
  • bilateral cerebellar ataxia
  • thalamic pain syndrome
  • diplopia or other visual field deficits including blindness
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40
Q

Locked-in syndrome

A
  • can be from basilar artery stroke
  • pure motor
  • can’t move but they might be able to move their eyes and possibly communicate through the movement of their eyes
  • intact consciousness
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41
Q

Vertebral Artery Stroke Impairments

A
  • ataxia
  • vertigo
  • nausea
  • vomitting
  • nystagmus
  • impaired pain and temperature sensation in ipsilateral face
  • Horner’s syndrome (sympathetic dysfunction causing ptosis)
  • dysphagia
  • sensory impairment in contralateral arm, trunk, and leg
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42
Q

Vertebral Artery Test

A
  • rotating away from side that testing, and extending of cervical vertebra
  • look for pupil to dilate, for dizziness of individual
  • can also check for nystagmus
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43
Q

Muscle Fiber type I

A
  • slow, oxidative

- motor unit is slow

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44
Q

Muscle fiber type IIA

A
  • fast, oxidative glycolytic

- motor unit is fast, fatigue-resistant

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45
Q

Muscle fiber type IIB

A
  • fast, glycolytic

- motor unit fast, fatigable

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46
Q

Slow oxidative muscle fiber info (SO, Type I)

A
  • motor units: many
  • muscle fibers: few
  • axon diameter: small
  • tetanic tension: low
  • fatigability: low
  • speed of contraction: slow
  • muscle fiber diameter: small
  • capillarization: rich
  • mitochondria: many
  • ATPase: low
  • oxidative enzymes: high
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47
Q

FF Motor Unit/FG Muscle Fiber Info (Type IIB)

A
  • motor units: few
  • muscle fibers: many
  • axon diameter: large
  • tetanic tension: high
  • speed of contraction: fast
  • muscle diameter: large
  • capillarization: poor
  • mitochondria: few
  • ATPase: high
  • Oxidative enzymes: low
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48
Q

Henneman Principle

A
  • there exist an order to motor unit recruitment when GRADUAL CONTROL OF TENSION is important
  • small motor units are recruited 1st and larger last
  • large motor units are de-recruited 1st and small de-recruited last
  • *THIS ORDER IS VIOLATED WHEN ONE IS PERFORMING BALLISTIC OR RELATIVELY FAST MOVEMENTS
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49
Q

Henneman Principle slope

A
  • shows the control of speed of muscle force generation (graded)
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50
Q

Tactile Sensation

A
  • identify pattern of sensory loss
  • glove-like or sock-like loss = cortical lesion
  • cortical lesion
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51
Q

Scapula Subluxation

A
  • common occurrence after stroke
  • humerus subluxes inferiorly out of glenoid fossa
  • due to weakness or spasticity
  • weight of humerus causes upward rotation of inferior angle of scapula
  • abnormal position of scapula
  • flaccid or low tone or weak muscles at shoulder and trunk lead to altered alignment of scapula and humerus
  • dynamic stabilizers not present
  • reliance on static stabilizers which overstretch due to weight of arm in dependent position
  • inferior subluxation is most common
  • assume due to low tone, but also hypertonicity pullin scap up that may not even be related to RCM
  • best to position sidelying or with table/armrest under
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52
Q

Impairment if have an optic nerve lesion

A
  • blind in one eye
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53
Q

Impairment if have an optic chiasm lesion

A
  • Bilateral temporal field deficit

- i.e. blind in the outside/lateral of both eyes

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54
Q

Impairment if have an optic tract, optic radiations, and/or occipital lobe lesion

A
  • L homonymous hemianopsia

- cannot see the L half of the visual field for BOTH eyes

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55
Q

Temporal lobe lesion eye impairment

A
  • L upper quadrant homonymous hemianopsia

- Cannot see the upper left 1/4 in BOTH eyes

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56
Q

Parietal lobe lesion visual impairments

A
  • L lower quadrant homonymous hemianopsia

- cannot see in the lower left 1/4 of visual field in BOTH eyes

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57
Q

occipital lobe lesion visual impairments

A
  • homonymous hemianopsia
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58
Q

Optic Nerve Testing

A
  • usually test with glasses on
  • screen both eyes at the same time
  • if deficit noted, test each individual eye
  • know the optic nerve pathway (optic nerve, chiasm, tract, radiation)
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59
Q

Test 1 for Optic Nerve

A
  • determine peripheral vision “edges”

- find the visual deficit in which quadrant

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60
Q

Test 2 optic nerve test

A
  • which finger moving in each quadrant
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61
Q

Test 2/3?

A
  • number of fingers held up in each quadrant
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62
Q

TBI cause

A
  • caused by a bump, blow or jolt to the head or a penetrating head injury that disrupts the normal function of the brain
  • altered consciousness (no matter how brief)
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63
Q

CHI of TBI

A
  • closed head injury
  • no skull fracture or laceration of the brain
  • coup-countercoup
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64
Q

OHI of TBI

A
  • Open head injury

- meninges have been breached, brain is exposed

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65
Q

Coup-countercoup

A
  • coup: primary injury at impact in one direction from blow

- countercoup: secondary injury on the opposite side from bounce back/counteraction of forces

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66
Q

TBI prevelance

A
  • 1.7 million TBIs occur either as an isolated injury or along with other injuries each year
  • about 75% of TBIs that occur each year are concussions or mild TBI
  • TBI is a contributing factor to about 1/3 (30.5%) of all injury-related deaths
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67
Q

TBIs by AGE

A
  • 3 large peaks in lifetime of TBI
  • children 0-4 years
  • older adolescents 15-19
  • adults afed >65 years
  • *adults 75+ have highest rates of TBI-related hospitalization and death
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68
Q

TBI by GENDER

A
  • in every age group, TBI rates are higher for males as compared to females
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69
Q

Costs of TBI

A
  • direct medical costs and indirect costs such as lost productivity totaled an estimated $76.6 billion in the USA in 2000
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70
Q

TBI causes

A
  • MVA >60% (auto 70%, pedestrian 5%, motocycle 25%)

- other <40%

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71
Q

TBI Prevention

A
  • risk of brain injury in hospitalized motorcyclists is 2X for un-helmed vs. helmeted motorcyclists
  • acute care costs for unhelmeted drivers are 3X cost
  • in Cali, first year’s implementation of 1992 helmet law resulted in 37.5% DECREASE in statewide crash fatalities
  • 140,000 head injuries per year are attributed to children and adolescents in bicycle accidents (estimated 74-85% mod-severe TBIS are prevented by bike helmets)
  • 14% decrease in fatality for front passangers wearing seat belts
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72
Q

General Risk Factors of TBI

A
  • young (avg TBI = 29 yo)
  • male
  • risk taking behaviors
  • low income, urban
  • substance abuse (50% hospitaliations for TBI associated with alc)
  • availability of firearm
  • previous TBI (sports-related concussions)
  • older age (more susceptible to tearing of blood vessels, declines in cerebrovascular circulation)
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73
Q

Skull Fractures

A
  • 24% of all patients admitted for CNS trauma sustained a skull fracture
  • 38% of fractures were open
  • 10% were depressed (<3 mm)
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74
Q

Location of Skull fractures in order most to least common

A
  • frontal
  • basilar
  • parietal
  • occipital
  • temporal
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75
Q

Extracranial Injuries with TBI

A
  • 82% at admission had one or more extra-cranial injury with TBI
  • most common: head laceration (61%)
  • facial fractures 13%
  • hemo/pneumothorax 9%
  • rib fx/long contusion 10%
  • spleen 4%
  • liver or bowel 11%
  • genitourinary 3%
  • UE fracture 14%
  • LE fracture 19%
  • pelvic fracture 4%
  • hip fracture 2%
  • other laceration 20%
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76
Q

Scapula Subluxation

A
  • common occurrence after stroke
  • humerus subluxes inferiorly out of glenoid fossa
  • due to weakness or spasticity
  • weight of humerus causes upward rotation of inferior angle of scapula
  • abnormal position of scapula
  • flaccid or low tone or weak muscles at shoulder and trunk lead to altered alignment of scapula and humerus
  • dynamic stabilizers not present
  • reliance on static stabilizers which overstretch due to weight of arm in dependent position
  • inferior subluxation is most common
  • assume due to low tone, but also hypertonicity pullin scap up that may not even be related to RCM
  • best to position sidelying or with table/armrest under
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77
Q

Impairment if have an optic nerve lesion

A
  • blind in one eye
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78
Q

Impairment if have an optic chiasm lesion

A
  • Bilateral temporal field deficit

- i.e. blind in the outside/lateral of both eyes

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79
Q

Impairment if have an optic tract, optic radiations, and/or occipital lobe lesion

A
  • L homonymous hemianopsia

- cannot see the L half of the visual field for BOTH eyes

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80
Q

Temporal lobe lesion eye impairment

A
  • L upper quadrant homonymous hemianopsia

- Cannot see the upper left 1/4 in BOTH eyes

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81
Q

Parietal lobe lesion visual impairments

A
  • L lower quadrant homonymous hemianopsia

- cannot see in the lower left 1/4 of visual field in BOTH eyes

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82
Q

occipital lobe lesion visual impairments

A
  • homonymous hemianopsia
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83
Q

Optic Nerve Testing

A
  • usually test with glasses on
  • screen both eyes at the same time
  • if deficit noted, test each individual eye
  • know the optic nerve pathway (optic nerve, chiasm, tract, radiation)
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84
Q

Test 1 for Optic Nerve

A
  • determine peripheral vision “edges”

- find the visual deficit in which quadrant

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85
Q

Test 2 optic nerve test

A
  • which finger moving in each quadrant
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86
Q

Test 2/3?

A
  • number of fingers held up in each quadrant
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87
Q

TBI cause

A
  • caused by a bump, blow or jolt to the head or a penetrating head injury that disrupts the normal function of the brain
  • altered consciousness (no matter how brief)
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88
Q

CHI of TBI

A
  • closed head injury
  • no skull fracture or laceration of the brain
  • coup-countercoup
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89
Q

OHI of TBI

A
  • Open head injury

- meninges have been breached, brain is exposed

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90
Q

Coup-countercoup

A
  • coup: primary injury at impact in one direction from blow

- countercoup: secondary injury on the opposite side from bounce back/counteraction of forces

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91
Q

TBI prevelance

A
  • 1.7 million TBIs occur either as an isolated injury or along with other injuries each year
  • about 75% of TBIs that occur each year are concussions or mild TBI
  • TBI is a contributing factor to about 1/3 (30.5%) of all injury-related deaths
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92
Q

TBIs by AGE

A
  • 3 large peaks in lifetime of TBI
  • children 0-4 years
  • older adolescents 15-19
  • adults afed >65 years
  • *adults 75+ have highest rates of TBI-related hospitalization and death
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93
Q

TBI by GENDER

A
  • in every age group, TBI rates are higher for males as compared to females
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94
Q

Costs of TBI

A
  • direct medical costs and indirect costs such as lost productivity totaled an estimated $76.6 billion in the USA in 2000
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95
Q

TBI causes

A
  • MVA >60% (auto 70%, pedestrian 5%, motocycle 25%)

- other <40%

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96
Q

TBI Prevention

A
  • risk of brain injury in hospitalized motorcyclists is 2X for un-helmed vs. helmeted motorcyclists
  • acute care costs for unhelmeted drivers are 3X cost
  • in Cali, first year’s implementation of 1992 helmet law resulted in 37.5% DECREASE in statewide crash fatalities
  • 140,000 head injuries per year are attributed to children and adolescents in bicycle accidents (estimated 74-85% mod-severe TBIS are prevented by bike helmets)
  • 14% decrease in fatality for front passangers wearing seat belts
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97
Q

General Risk Factors of TBI

A
  • young (avg TBI = 29 yo)
  • male
  • risk taking behaviors
  • low income, urban
  • substance abuse (50% hospitaliations for TBI associated with alc)
  • availability of firearm
  • previous TBI (sports-related concussions)
  • older age (more susceptible to tearing of blood vessels, declines in cerebrovascular circulation)
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98
Q

Skull Fractures

A
  • 24% of all patients admitted for CNS trauma sustained a skull fracture
  • 38% of fractures were open
  • 10% were depressed (<3 mm)
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99
Q

Location of Skull fractures in order most to least common

A
  • frontal
  • basilar
  • parietal
  • occipital
  • temporal
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100
Q

Extracranial Injuries with TBI

A
  • 82% at admission had one or more extra-cranial injury with TBI
  • most common: head laceration (61%)
  • facial fractures 13%
  • hemo/pneumothorax 9%
  • rib fx/long contusion 10%
  • spleen 4%
  • liver or bowel 11%
  • genitourinary 3%
  • UE fracture 14%
  • LE fracture 19%
  • pelvic fracture 4%
  • hip fracture 2%
  • other laceration 20%
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101
Q

Primary vs. secondary TBI

A
  • primary: direct injury to the brain (i.e. impact, missile, shearing)
  • secondary: damage after the traumatic event caused by brain hypoxia (lack of oxygen), edema, herniation, hematoma, ischemia
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102
Q

Focal vs. Diffuse TBI

A
  • focal: localized trauma (small blow or tumor)

- diffuse: trauma over a large area (coup-countercoup)

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103
Q

Four Types of Hemorrhages

A
  • epidural hematoma
  • subdural hematoma
  • subarachnoid hemorrhage
  • intracerebral hematoma
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104
Q

Epidural Hematoma

A
  • in epidural space, between dura mater and skull
  • acute bleeding
  • common in temporal bone fracture
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105
Q

Subdural Hematoma

A
  • beneath the dura
  • laceration of cortical veins during sudden head deceleration
  • a feature of shaken baby syndrome
  • seen in children because of firm adherence of dura to the inner skull
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106
Q

Subarachnoid Hemorrhage

A
  • poor prognosis if bleeding into ventricular system
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107
Q

Intra-cerebral Hematoma

A
  • in brain parenchyma (neurons & glial cells)

- hematoma may enlarge during the first few days after injury

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108
Q

Concussion

A
  • mild TBI
  • alteration of consciousness and memory
  • CT or MRI usually normal
  • good prognosis
  • cumulative effects of repeated concussion (can cause dimentia)
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109
Q

Post-concussion

A
  • dizziness, disorientation, nausea, headache, fatigue
  • decreased control of emotions and personality changes
  • attention deficit
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110
Q

Altered Level of Consciousness

A
  • reduction in response to stimuli
  • arousal is associated with wakefulness and depends on an intact reticular formation and upper brainstem
  • coma rarely lasts > 4 weeks
  • DEPTH AND DURATION OF COMA IS USED TO DETERMINE CURRENT STATUS AND PROGNOSIS
111
Q

Coma

A
  • state of unresponsiveness

- not opening eyes

112
Q

Persistent Vegetative State

A
  • no evidence of cerebral cortical function

- eye opening with sleep-wake cycles

113
Q

Lethargy

A
  • severe drowsiness

- aroused by moderate stimuli and then drift back to sleep

114
Q

Confusion

A
  • disorientation, bewilderment, and difficulty following commands
115
Q

Glascow Coma Scale Overview

A
  • out of 15 points

- 3 sections: eye opening response, verbal response, motor response

116
Q

Eye Opening Response Glascow Coma Scale

A
  • spontaneous… open with blinking at baseline (4 pts)
  • to verbal stimuli, command, speech (3 pts)
  • to pain only (not applied to face) (2 pts)
  • no response (1 pt)
117
Q

Verbal Response Glascow Coma Scale

A
  • oriented (5 pts)
  • confused conversation, but able to answer questions (4 pts)
  • inappropriate words (3 pts)
  • incomprehensible speech (2 pts)
  • no response (1 pt)
118
Q

Motor Response Glascow Coma Scale

A
  • obeys commands for movement (6 pts)
  • purposeful movement to painful stimulus (5 pts)
  • withdraws in response to pain (4 pts)
  • flexion in response to pain (decorticate posturing) (3 pts)
  • extension response in response to pain (decerebrate posturing) (2pts)
  • no response (1 pt)
119
Q

Outcomes of the Glascow Coma Scale

A 
<8 ..... 70% mortality 
9-11 .... 6% mortality
12-13 ..... 1% mortality
>14 .... <1% mortality
- DEPTH and DURATION of coma is the MOST ACCURATE INDICATOR OF SEVERITY OF CNS DAMAGE
120
Q

Mild Concussion loss of consciousness, Glascow scale, memory loss, and prognosis

A
  • <30 minutes of loss of consciousness
  • 13-15 on Glascow scale
  • <24 hr memory loss
  • good prognosis, most recover completely
121
Q

Moderate Concussion loss of consciousness, Glasgow coma, memory loss, and prognosis

A
  • > 30 minutes but < 24 hours loss of consciousness
  • 8-12 glascow scale
  • > 24 hr <7 memory loss
  • good prognosis, learn to manage problems resulting from TBI
122
Q

Severe Concussion loss of consciousness, glasgow scale, memory loss, and prognosis

A
  • > 24 hours of loss of consciousness
  • <8 glasgow scale
  • > 7 days of memory loss
  • most impossible to recover completely and physical and/or cognitive disability
123
Q

Severe TBI

A
  • assess severity of brain injury
  • acute surgical care: expanding mass lesion from increasing ICP
  • address life-threatening injuries (ABC: airway, breathing, circulation)
  • prevent complications
  • preventative rehab interventions
124
Q

Cognitive Impairments with TBI

A
  • difficulties in:
  • attention
  • concentration
  • learning
  • memory
  • abstract thinking, information processing
  • problem solving
  • initiation, executive functions
125
Q

Rancho Los Amigos Cognitive Scale

A
  • best to wait at least 3 days before you use this test
  • I: no response
  • II: generalized response
  • III: localized response
  • IV: confused, agitated
  • V: confused, inapropriate
  • VI: confused, appropriate
  • VII: automatic, appropriate
  • VIII: purposeful, appropriate
126
Q

Rancho Los Amigos Cognitive Rating of I

A
  • no response

- patient appears to be in a deep sleep and is completely unresponsive to any stimulus

127
Q

Rancho Los Amigos Rating II

A
  • generalized response
  • patient reacts inconsistently and non-purposefully to stimuli in a non-specific manner
  • responses are limited and often the same regardeless of stimuli
  • responses may be physiological, gross body movements, or vocalization
128
Q

Rancho Los Amigos Rating III

A
  • localized response
  • patient reacts specifically but inconsistently to stimuli
  • responses are directly related to the type of stimulus presented
  • may follow simple commands such as closing the eyes or squeezing the hand in an inconsistent, delayed manner
129
Q

Rancho Los Amigos Cognitive Rating of IV

A
  • confused, agitated
  • patient in heightened state of activity
  • bizarre and non-purposeful behavior to environment
  • decreased attention span, aggressive
130
Q

Rancho Los Amigos Cognitive rating of V

A
  • confused, inappropriate
  • patient responds to simple commands fairly consistently
  • responses become random or non-purposeful when commands become more complex
  • gross attention intact but highly distractable
  • verbalization is often inappropriate and confabulated
  • memory and ability to learn new tasks severely impaired
131
Q

Rancho Los Amigos Cognitive Rating of VI

A
  • confused, appropriate
  • shows goal-directed behavior but is dependent on external input or direction
  • follows simple directions consistently and shows carryover for relearned tasks (i.e. self care)
  • responses may be incorrect due to memory deficits but are appropriate for the situation
132
Q

Rancho Los Amigos Cognitive Rating of VII

A
  • automatic, appropriate
  • patient appears appropriate and oriented within the hospital and home settings
  • goes through daily routine automatically
  • minimal to no confusion and has shallow recall of activities
  • shows carryover for new learning but at a decreased rate
  • able to initial social activities with structure
  • judgement remains impaired
133
Q

Rancho Los Amigos Cognitive Rating VIII

A
  • purposeful, appropriate
  • patient is able to recall and integrate past and recent events and is aware of and responsive to enviornment
  • shows carryover for new learning and needs no supervision once activities are learned
  • may continue to show a decreased ability relative to premorbid abilities, abstract reasoning, tolerance for stress, and judgement in emergencies or unusual circumstances
134
Q

Retrograde Amnesia

A
  • period of loss of recall of events prior to injury
135
Q

Post-Traumatic Amnesia (PTA)

A
  • period between the injury and time of continuous day to day memory
136
Q

STM

A
  • short term memory

- immediate past

137
Q

Short Term Working Memory

A
  • inability to learn new information
138
Q

LTM

A
  • long term memory
  • 1 min to 1 hour
  • may of may not include over-learned material
139
Q

Personality and Social impairments with TBI

A
  • disinhibition: “basic personality” emerges
  • inappropriate, excessive social behaviors
  • exaggerated dependency or more independent
  • irresponsible or lacks judgement
  • egocentric or inconsiderate
  • violent/aggessive
  • childishness
  • tactless
  • miss goodie two shoes
140
Q

Frontal Lobe TBI Signs

A
  • decreased ability to take cues from enviornment
  • silence: when say something embarrassing or inappropriate
  • blush: when embarrassed or something of sexual nature
  • angry look: patient bumps into someone with their wheelchair
141
Q

Sexual Behavior Issues with TBI

A
  • tactless attempts at intimacy
  • conversation with a lot of sexual content
  • inappropriate touching
  • crude remarks
  • indecent exposure
  • masturabation
  • frontal or temporal lobe
142
Q

Mood Behavior Changes with TBI

A
  • mood disturbances including depression and anxiety
  • irritability, rage, refuse to cooperate
  • euphoria: involuntary laughing or crying
  • apathy: indifference
  • motor, sensory, verbal perservation
143
Q

Perservation

A
  • uncontrollable repetition of a particular response, such as a word, phrase, or gesture despite the absence or cessation of a stimulus
144
Q

Decortical Posturing

A
  • seen with TBI

- flex BUE, Extend BLE

145
Q

Decerebrate Posturing

A
  • happens with TBI

- extend BUE and BLE

146
Q

Visual Impairments with TBI

A
  • neurological impairments: field cuts due to tract, radiation injuries, visual-perceptual deficits, diplopia, gaze palsies, nystagmus, tracking disorders, etc
  • ophthalmologica injuries: direct injury to the eye (globe, retina, intraoccular hemorrhage, glaucoma, etc)
147
Q

Neurological complications with TBI

A
  • infection: brain abscess, meningitis, wound infection, osteomyelitis of skull
  • recurrent hemorrhage, thrombus, aneurysm
  • hydrocephalus (increased ICP)
  • seizures
148
Q

Increased Intracranial Pressure

A
  • caused by swelling, fluid build-up in the brain and hematomas
  • increased ICP compresses the brain within the rigid skull
  • serious, life-threatening
  • ICP monitoring: medications, fluid management, decompressive craniectomy, shunt
149
Q

General Medical Complications with TBI

A
  • infection
  • drug toxicities
  • upper respiratory trauma, infection, obstruction
  • pulmonary embolism
  • endocrine-metabolic disorders
  • musculoskeletal disorders
  • skin disorders
  • autonomic disturbances
  • urinary tract disorders
150
Q

Movement Symptoms with CVA (TBI & CP)

A
  • abnormal movement synergies

- abnormal muscle tone: hypotonia with cerebral shock, followed by hypertonia, brunnstrom stage progression

151
Q

Abnormal Tone Scales/Tests

A
  • modified Ashworth Scale (MAS)
  • clonus
  • DTRs
  • UMN lesion: Babinski and Hoffmans
152
Q

Brunstrom Stages

A
  • Stage 1: flaccid
  • Stage 2: associated reactions/beginning spasticity (no voluntary movement)
  • Stage 3: synergy stage (voluntary movement present)
  • Stage 4: movements deviating from the basic synergies
  • Stage 5: relative independence of the basic synergies
  • Stage 6: near normal (impaired strength, coordination, speed)
  • Stage 7: normal (Except when fatigued)
153
Q

Brunnstrom UE Synergy Pattern for FLEXION

A
  • scap: elevation and/or retraction
  • shoulder: abduction, external rotation (hyperextension)
  • elbow: flexion
  • forearm: supination
  • wrist/hand: wrist flexion and/or mass finger flexion
154
Q

Brunnstrom UE Synergy Pattern for EXTENSION

A
  • scap: depression and/or protraction
  • shoulder: adduction, internal rotation
  • elbow: extension
  • forearm: pronation
  • wrist&Hand: wrist extension and/or mass finger flexion
155
Q

Brunnstrom LE Synergy Pattern for FLEXION

A
  • hip: flexion, abduction, external rotation
  • knee: flexion
  • ankle: dorsiflexion
  • foot: inversion and mass flexion of toes
156
Q

Brunnstrom LE Synergy pattern for EXTENSION

A
  • hip: extension, adduction, internal rotation
  • knee: extension
  • ankle: PF
  • foot: inversion and extension of toes
157
Q

What Brunnstrom stage do you usually start the testing at?

158
Q

Post Brain Injury Medication ANTIDEPRESSANTS

159
Q

Post-Brain Injury Medications ANTICONVULSANTS

A
  • Phenobarbital
  • Dilantin
  • Tegretol
160
Q

Post-brain injury medications that control spasticity

A
  • Dantrium
  • Lioreseal (baclofen)
  • Valium
161
Q

Tranquilizer Medications for Post-Brain Imjury

A
  • Thorazine
  • Haldol
  • Mellaril
162
Q

When in Brunnstrom Stages is it appropriate to do MMT

A
  • at stage 6 when you know the strength is not influenced by any muscle synergies/tone
163
Q

SCI Incidence

A
  • about 40 cases per million population in USA

- 12,000 new cases each year

164
Q

SCI Prevalence

A
  • 270,000 individuals alive with SCI in USA
165
Q

SCI avg age

166
Q

SCI gender stats

A
  • 80.6% male

- 19.4% femlase

167
Q

SCI race/ethnicity

A
  • 66 white
    1. 2 AA
  • 0.9 native americans
  • 2.1% Asian
  • 8.3% Hispanic
168
Q

Causes of SCI

A
  • vehicular: 40%
  • falls: 28%
  • violence: 15%
  • sports: 8%
  • other: 9%
169
Q

Amount of incomplete and complete SCI

A
  • incomplete tertraplegia: 40%
  • complete paraplegia: 21%
  • incomplete paraplegia: 21%
  • complete tetraplegia: 16%
170
Q

SCI length of stay

A
  • median days hospitalized in acute care medical/surgical unit is 11 days
  • median days in rehab: 37 days
171
Q

Cost of care of SCI

A
  • C1-C4 highest cost

- incomplete motor functional at any level has lowest cost

172
Q

Cause of death with SCI

A
  • currently pneumonia and specticemia
  • specticemia is caused when certain bacteria get into bloodstream (skin/wound/respiratory management)
  • renal failure, advances in urologic management
173
Q

Hyper extension of C4 on C5 would compress what nerve root?

A

C5!

- because nerve roots are above their spinal vertebrae

174
Q

Contusion Injury with SCI

A
  • bruising of SC following fractures and dislocations of the vertebrae
  • initially severe symptoms from loss of SC function (compression from swelling)
  • usually rapid return of function in weeks
  • amount of return depends on severity of injury
  • contusion has the best prognosis since the SC is still intact
175
Q

Compression injury with SCI

A
  • from fractures and dislocations of vertebrae, tumors, disc herniation
  • amount of return depends on severity of injury
176
Q

Laceration injury with SCI

A
  • from knife, gunshot, or other projectile/foreign object
  • partial to complete loss of function below level of lesion
  • impairment depends on extent of lesion
177
Q

Loss of vascular supply with SCI

A
  • from thrombosis, embolus, arteriovenous malformation or direct disruption of blood vessels
  • partial loss of SC function below level
178
Q

Complete loss SCI

A
  • loss of all sensation and motor function below the level of the lesion
  • ASI A
179
Q

Incomplete loss SCI

A
  • partial loss of sensation and motor function below the level of the injury
  • AIS B, C, or D
180
Q

ASI A

A
  • complete SCI
  • no sensory or motor function preserved
  • NOON sign
181
Q

ASI B

A
  • incomplete SCI
  • sensory preserved but no motor function
  • bowel/bladder function; violate NOON sign
182
Q

ASI C

A
  • incomplete SCI

- motor preserved with majority of muscles graded less than 3

183
Q

NOON sign

A
  • turn them on their side
  • expose anal sphincter
  • act like you are stopping a bowel movement and watch for contraction
  • if yes, violated noon sign! ASI B
  • if get 1 or 2 (have sensation to light touch around anal area) then violated noon sign! ASI B
  • if get 1 or 2 with pin prick around anal
  • put finger into deep anal area and press around and ask for sensation
  • if spell noon…then have ASI A
  • if cannot spell noon….then have ASI B
184
Q

ASI D

A
  • incomplete SCI

- motor preserved with majority of muscles graded greater or equal to 3

185
Q

ASI E

186
Q

C2-C3

A
  • ventilatory dependent

- total care

187
Q

C3-C5

A
  • phrenic nerve
  • independent breathing
  • off ventilator
188
Q

start getting slips of abs at what level

A

usually T6

189
Q

DCML

A
  • dorsal column medial lemniscus
  • proprioception
  • vibration
  • fine discrimination
  • two-point touch
190
Q

Antero-lateral System

A
  • crude touch
  • sharp/dull
  • temperature
  • pain
  • tickle
  • itch
  • sexual sensations
191
Q

Anterior Cord Syndrome

A
  • damage to the anterior (ventral) spinal cord
  • Partial or full loss of bilateral ALS & lateral CST below level of lesion
  • Preserved posterior columns (DCML) bilaterally below level of lesion
  • Most common injury of cervical spine
  • Mechanism of Injury – Flexion (Flexion teardrop or burst fracture…Infarct or compression of anterior spinal arteries)
192
Q

Posterior Cord Syndrome

A
  • Damage to the posterior (dorsal) spinal cord
  • Loss of DCML sensory modalities below the level of lesion
  • Preservation of bilateral ALS sensory modalities
  • Partial or full preservation of CST motor function bilaterally
  • Mechanism of injury: Hyperextension
193
Q

Central Cord Syndrome

A
  • central SC hemorrhage and necrosis
  • sparing of the peripheral areas of the spinal cord (central area more susceptible to damage due to poor arterial supply)
  • most often in cervical region
  • pronounced weakness in the UEs > LEs
  • sparing of sacral motor and sensory functions
  • hyperextension injuries in the elderly or any age
  • more common in cervical spine
  • Contusion of central region of SC
  • Can be from MVAs, but reduced frequency since head rests in cars
194
Q

Spinal Stenosis

A
  • there is compression all around the outside of the SC
  • pressure is uniform on all sides
  • b/c center of SC is much less well vascularized, so similarly looks like central cord syndrome (?) i think
195
Q

Incidence of SCI

A
  • 40 cases per million population in US

- 12,000 new cases each year

196
Q

Prevelence of SCI

A
  • 2012: 270,000 persons alive with SCI in US
197
Q

SCI average age at injury

A
  • 41 years old
198
Q

SCI prevalence in gender

A
  • 80.6% males

- 19.4% females

199
Q

SCI prevalence in race/ethnicity

A
  • 66% caucasions
  • 26.2% african americans
  • 0.9% Native American
  • 2.1% Asian
  • 8.3% hispanic
200
Q

Causes of SCI

A
  • vehicle (40%)
  • falls (30%)
  • violence (15%)
  • sports (8%)
  • other (9%)
201
Q

Percent Incomplete and Complete Tetraplegia of SCI

A
  • 40.8% incomplete tetraplegia

- 15.8% complete tetraplegia

202
Q

Percent incomplete and complete paraplegia

A
  • 21.6% complete paraplegia

- 21.4% incomplete paraplegia

203
Q

Length of Stay in Hospital for SCI

A
  • median days hospitalized in the acute care medical/surgical unit (in model systems) is 11 days
  • median days in rehab = 37 days
204
Q

Cause of death for SCI

A
  • in the past, renal failure (advances in urologic management)
  • currently pneumonia and septicemia
  • septicemia is caused when certain bacteria get into the bloodstream
205
Q

Types of Spinal Cord Injuries

A
  • contusions
  • compression
  • laceration
  • loss of vascular supply
206
Q

SCI Contusions

A
  • bruising of SC following fractures and dislocations of the vertebrae
  • initially severe symptoms from loss of SC function
  • usually rapid return of function within weeks
  • amount of return depends on severity of injury
  • has the best prognosis since the SC is still intact
207
Q

SCI Compression

A
  • from fractures and dislocations of vertebrae, tumors, disc herniation
  • amount of return depends on severity of injury
208
Q

SCI Laceration

A
  • from knofe, gunshot, or other projectile/foreign object
  • partial to complete loss of function below level of lesion
  • impairment depends on extent of lesion
209
Q

SCI Loss of vascular supply

A
  • from thrombosis, embolus, arteriovenous malformation or direct disruption of blood vessels
  • partial loss of SC function below level of lesion in distribution blood supply
210
Q

Complete Injury of SCI

A
  • loss of all sensation and motor function below the level of the lesion
  • AIS A
211
Q

Incomplete injury of SCI

A
  • partial loss of sensation and motor function below the level of the unjury
  • AIS B, C, or D
212
Q

AIS A

A
  • complete SCI injury

- no sensory or motor function preserved

213
Q

AIS B

A
  • incomplete SCI injury
  • sensory preserved but no motor function
  • bowel/bladder function
  • violates NOON sign
214
Q

AIS C

A
  • incomplete SCI injury
  • motor preserved with majority of muscles graded <3
  • violates NOON sign
215
Q

AIS D

A
  • incomplete SCI injury
  • motor preserved with majority of muscles graded >3
  • violates NOON sign
216
Q

AIS E

217
Q

C2-3 care

A
  • ventilator dependent, total care
218
Q

C3-5 Care

A
  • phrenic nerve
  • independent breathing
  • off ventilator
219
Q

C5 care

A
  • can raise shoulders and flex arm to use a joystick on a power WC, possibly manual WC with adaptations
220
Q

C6 care

A
  • have wrist extension so weak, functional, tenodesis grasp

- wrist extends, passive finger flexion due to contracted finger flexors

221
Q

C7 Care

A
  • have triceps

- can perform pressure relief and transfers and to help self prevent ulcers

222
Q

Thoracic region care

A
  • adds postural stability and respiration function

- acessory breathing muscles

223
Q

T6-T12 Care

A
  • abdomminal function
224
Q

L2 Care

A
  • hip flexion
225
Q

DCML

A
  • proprioception
  • vibration
  • fine discrimination
  • two-point touch
226
Q

Antero-lateral system

A
  • crude touch
  • sharp/dull
  • temperature
  • pain
  • tickle and itch
  • sexual sensations
227
Q

Anterior Cord Syndrome

A
  • damage to the anterior (ventral) spinal cord
  • partial or full loss of bilateral ALS and lateral CST below level of lesion
  • preserved posterior columns (DCML) bilaterally below level of lesion
  • most common injury of cervical spine
  • mechanism of injury: flexion
  • flexion teardrop burst fracture
  • infarct or compression of anterior spinal arteries
228
Q

Posterior Cord Syndrome

A
  • damage to the posterior (dorsal) SC
  • loss of DCML sensory modalities below the level of lesion
  • preservation of bilateral ALS sensory modalities
  • partial or full preservation of CST motor function bilaterally
  • mechanism of injury: hyperextension
229
Q

Central Cord Syndrome

A
  • central SC hemorrhage and necrosis
  • sparing of peripheral areas of the SC (central area more susceptible to damage due to poor arterial supply)
  • most often in teh cervical region
  • pronounced weakness in UEs > LEs
  • sparing of sacral motor and sensory function
  • hyperextension injuries in the elderly or at any age
  • more common in cervical spine
  • contusion of central region of SC
  • can be from MVAs, but reduced frequency since head rests in cars
230
Q

Brown - Sequard

A
  • hemisection (damage to one side) of the SC
  • ipsilateral DCML: loss of proprioception, vibration, fine discriminatory, 2-point touch
  • ipsilateral CST: loss of voluntary motor control
  • contralateral ALS: crude touch, sharp/dull, temperature, pain, tickle and itch, sexual sensations
  • traumatic SCI, pretending injuries (gunshot, kife wound), burst fractures
  • mechanism of injury: rotation
  • pure rotation injury is more common in cervical spine, but occurs most often with flexion injuries
  • not much rotation possible in thoracic and lumbar regions
231
Q

Acute Management of SCI

A
  • ABCs: airway, Breathing, Circulation
  • if necessary to move, log roll, maintaining spine in neutral
  • immobilie
  • monitor BP & ECG
  • x-ray, CT, and/or MRI
232
Q

Indications for Surgery with SCI

A
  • bone fragments and disc material in spinal canal
  • unstable fracture
  • progression of neurologic deficit (even if spinal column is stable)
  • decompression due to edema, increased blood in area, etc
233
Q

Harrington Rods

A
  • stainless steel rods with hooks on either end placed on either side of injury area
  • distracts spine until proper alignment is achieved
  • just above and below the rods pts tend to be hypermobile
234
Q

Stable fracture with no surgery immobilization

A

6-12 weeks

235
Q

Cervical Fusion Immobilization

A
  • 3-4 months using a halo or SOMI (sterno-occipital-mandibular immobilizer)
236
Q

Thoracolumbar Fusions Immobilization

A
  • 4-6 months using a rigid body jacket (TLSO)
237
Q

Spinal Shock

A
  • onset: immediately post-injury
  • duration: 1 week to several months (mean = 6 wks)
  • below level of lesion: flaccid paralysis, no reflex activity, absent bowel and bladder tone, decreased blood pressure.
  • spasticity develops AFTER spinal shock ends
  • true spinal shock = no tone at all originally
238
Q

Respiratory System Changes with SCI

A
  • phrenic nerve = C3/4/5
  • those with C1-3 sCI are on respirator/ventilator b/c they have no or minimal diaphragm function
  • C4-5 (even C6-T1): may need respirator permanently or at least temporarily (b/c chest accessory mm loss)
  • C8-T12: when intercostal and abdominal muscles are lost, 20-70% decrease in vital capactiy
239
Q

Physiological Changes in Circulatory System with SCI

A
  • bradycardia
  • dysrhythmias
  • orthostatic hypotension
  • low BP (esp when elevating head, coming to upright)
  • cause: loss of sympathetic input below lesion level
  • prolonged bed rest decreases vascular tone
  • loss of muscle pumping action to return blood from LEs
  • blood pools in feet, watch for S&S, take BP before during and after intervention
240
Q

Complications in Circulatory System SCI

A
  • increased risk for DCTs and pulmonary emboli

- DVT: warm and red in area (very localized)

241
Q

Intervention for Circulatory System With SCI

A
  • heparin
  • anti-embolism stockings (TED hose)
  • abdominal binder (increases blood flow)
242
Q

Gastrointestinal Changes with SCI

A
  • loss of bowel control
  • incontinence
  • constipation
  • bowel obstructions
  • bowel accidents are often due to use of medications needed to treat constipation
  • spasticity increases when bladder problems
243
Q

Interventions for Gastrointestinal changes iwith SCI

A
  • oral meds: colace as a stool softener and metamucil to produce well-formed soft stool
  • suppositories: i.e. dulcolaz, for bowel program
  • high fiber diets
244
Q

Urologic Changes with SCI

A
  • urinary incontinence
  • flaccid neurogenic bladder
  • reflexic neurogenic bladder
245
Q

Flaccid Neurogenic bladder

A
  • areflexic bladder
  • neurological injury at S2-4 level
  • only empties a little when it “overflows” so it must be artificially or manually emptied
  • bladder fill to normal or larger capacity before being emptied articifialy
  • some patients may be able to learn to do self-catheterization (increased risk of bladder infection)
246
Q

Reflexic Neurogenic Bladder

A
  • spastic bladder
  • S2-4 reflexes must be intact (all SC level injuries above S2)
  • MOST COMMON
  • detrusor muscle becomes spastic and contracts
  • empties at smaller than normal volumes some patients may be able to stimulate reflex emptying
247
Q

Complications in Urologic System with SCI

A
  • UTI
  • kidney stones
  • bladder stones
248
Q

Loss of Sensation with SCI

A
  • complete or partial loss of sensation below the level of the SCI
249
Q

MOtor Function with SCI

A
  • complete or partial loss of muscle function below the level of the SCI
  • decreased strength remaining, innervated muscles
  • potential for recovery below level of lesion
  • nmost likely in zone of injury (1-3 neurological levels below the neurological level of injury)
  • intense rehab programs
250
Q

Neuropathic Pain

A
  • experienced by 90% of all SCI patients at least intermittently below level of lesion
  • burning sensation
  • some are on medical maryJ for this
251
Q

Spasticity/Hypertonicity with SCI

A
  • can interfere with positioning, transfers, maintenance of joint ROM, and with active motion
252
Q

Spasticity Definition

A
  • a motor disorder characterized by a velocity dependent increase in tonic stretch reflexes with exaggerated deep tendon (phasic) reflexes resulting from the hyper-excitability of the monosynaptic stretch reflex as one component of the UMN syndrome
253
Q

Gamma Spasticity

A
  • most common and predominate theoryu
  • normal inhibition to gamma MNs from higher CNS is not functioning; resulting in excess gamma MN firing
  • supersensitive muscle spindle
  • continual firing of monosynaptic reflex arc
254
Q

Autonomic Dysreflexia (AD)

A
  • occurs in persons with lesions above T6
  • consequence of over-activity of ANS (elevated BP)
  • precipitated by a noxious stimulus (triggers)
  • full bladder or blocked catheter, UTI (most common)
  • constipation, distention, hemorrhoids
  • infection or irritation
  • sunburn
  • tight clothing
  • pain
  • prolongued pressure by object
  • pressure sores
  • ingrown toenails
  • DO NOT LAY THESE pts DOWN!!!
255
Q

How AD Happens:

A
  • some stimulus triggers a sympathetic (ANS) response (elevated BP)
  • sympatheticc system can only be adjusted above the level of the lesion; reflex cannot be turned off below the level of the lesion
256
Q

Autonomic Dysreflexia S&S

A
  • pounding headache (caused by the elevation in the blood pressure)
  • goosebumps
  • sweating above the level of injury
  • nasal congestion
  • blotching of the skin
  • restlessness
  • hypertension
  • flushed (reddened face)
257
Q

Temperature control problems with SCI

A
  • loss of ability to control body temp due to inability to sweat or shiver below level of lesion
  • less able to tolerate extremes in temperature
258
Q

Intervention for temperature control with SCI

A
  • avoid extreme hot.cold temperatures
  • separate heating or air conditioning may be a necessity
  • dress extra warm in winter
  • spray bottle of water
259
Q

Integumentary Changes with SCI

A
  • decubitus ulcers

- cuts, burns, etc occur before patient is aware of them

260
Q

Intervention for Integumentary System with sCI

A
  • prevention of pressure sores
  • WC and bed cushions
  • pressure relief techniques
  • good transfer techniques to avoid sheer forces
  • teach awareness and protection of insensate body parts to prevent injuries
261
Q

Musculoskeletal Changes with SCI

A
  • loss of calcium from bone occurs following injury
  • hypercalcemia (high blood calcium levels)
  • can cause cardiac arhythmias
  • osteoporosis (if DEXA scans less than -3.5 then high risk for fracture)
  • heterotopic ossification
262
Q

FES cycling

A
  • helps prevent and treat osteroporosis

- adds muscle bulk which can help prevent decubiti

263
Q

Heterotropic Ossification

A
  • calcium deposits in soft tissues around joints that recieve stress
  • marked limiation of ROM
  • treatment: didronel and radiation therapy to inhibit osteoblast function (slows HOLD ON A SEC but doesnt stop it)
  • maintain ROM if possible
  • if surgically removed, likely to come back and be worse
264
Q

Female Reproductive system with SCI

A
  • menses typically returns in 3-6 months
  • women CAN GET PREGNANT even if they cannot feel or move below the level of injury
  • many have normal vaginal deliveryu
  • autonomic dysreflexia may occur during labor = C-section to deliver baby quickly
265
Q

Males reproductive system with SCI

A
  • reflexogenic (controlled at S2-4, must be intact)
  • spontaneous (secodary to internal stimulation)
  • ejaculation usually does not occur unless sacral sensation is in tact
  • fertility of sperm decreases significantly over time
266
Q

Central Pattern Generators (CPGs)

A
  • groups of neurons and interneurons that produce rhythmic or oscillatory motor activity
  • hard-wired, less variable, less flexible than more complex, goal-directed motor control
  • used in body weight support treadmill training (BWSTT)
267
Q

Evarts of CPGs

A
  • Evarts are spinal rhythm generators
  • a group of neurons that inherently present a pre-arranged sequence of muscle activity arranged temporally and spatially
  • need some type of trigger to start off the neural network and keep it going
268
Q

Example of CPGs with dog

A
  • spinal transection
  • stimulation to flank produces rhythmic scratching
  • range and frequency of rythmic flexion and extension (scratching) is dependent on strength of stimulus
269
Q

Example of CPGs with cats

A
  • spinal cats
  • shik preparation (midbrain, cerebellum, and spinal cord)
  • cerebral cortex cannot communicate with spinal cord
270
Q

Halo

A
  • screwed into skull
  • stabilizes cervical spine
  • balance is thrown off because so top-heavy
271
Q

TLSO

A
  • thoracic-lumbosacral stabilizer
272
Q

SOMI

A
  • cervical/thoracic stabilizer
273
Q

need at least what % in what broadmanns area to initiate gait?

A
  • 10-20% input to broadmanns area 4 to initiate gait

Neuro D&D (3 decks)

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