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Neuro D&D > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

How many Americans does stroke Kill every year?

A
  • Almost 130,000 Americans

* That’s 1 out of every 19 deaths

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2
Q

How many people in the US have a stroke every year?

A

*More than 795,000 people

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3
Q

How many strokes occur in the people who have had a previous stroke?

A

*About 185,000 (nearly 1 of 4)

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4
Q

What is the leading cause of serious long term disability?

A

Stroke!

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5
Q

What are the risk factors of stroke that CANT be changed?

A
  • Age
  • Gender
  • Prior Stroke, TIA or heart attack
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6
Q

How is Age a risk factor of stroke?

A

*Risk doubles for each decade of life after age 55

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7
Q

How is gender a risk factor of stroke?

A
  • Stroke is more common in men than women

* Women: use of birth control pills and pregnancy pose special stroke risks for women

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8
Q

What is a TIA?

A

*Transient ischemic attack or “Mini stroke” that resolves within 24 hours

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9
Q

How is a prior stroke, TIA, or heart attack a risk factor of stroke?

A
  • A person whose had one or more TIA’s is 10x more likely to have a stroke than someone of the same age/gender who has not
  • If the pt had a heart attack, 3x higher risk of having a stroke
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10
Q

How is a TIA often caused?

A

*caused by atherosclerosis

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11
Q

What part of the country has the highest death rate from stroke?

A

*Southeastern United states

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12
Q

What is the risk of stroke for african americans compared to caucasian americans?

A

*AA risk of having a first stroke is nearly twice as high and they’re more likely to die following a stroke

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13
Q

Where does a hispanic americans risk of stroke fall compared to Caucasian and African Americans?

A

*Their risk falls between them

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14
Q

What is the fourth leading cause of death among Americans?

A

Stroke

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15
Q

What risk factors of stroke CANT be changed but CAN be Treated?

A
  • Sickle Cell Anemia
  • *AA and Hispanic Children
  • *Sickle cells tend to stick to blood vessel walls, which block arteries and cause a stroke
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16
Q

What are the risk factors of stroke that CAN be changed, treated or controlled?

A
  • High Blood Pressure
  • Cigarette Smoking
  • Diabetes Mellitus
  • Carotid or other Artery Disease
  • Atrial Fibrillation
  • High blood cholesterol
  • Poor Diet
  • Physical inactivity and obesity
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17
Q

How can a carotid artery be effected by disease?

A

*When narrowed by atherosclerosis (plaque buildups in artery walls) may become blocked by a blood clot

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18
Q

What is peripheral artery disease?

A

*The narrowing of blood vessels carrying blood to leg and arm muscles (plaque in artery walls); higher risk of artery disease and thus stroke

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19
Q

How is poor diet a risk factor of stroke?

A
  • High in saturated fat and cholesterol
  • High sodium (salt)
  • Diets with excess calories > obesity
  • 5 or more servings of fruits and vegetables per day may reduce the risk of stroke
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20
Q

How is physical inactivity and obesity a risk factor of stroke?

A
  • Being inactive, obese, or both can increase your risk of hypertension, high blood cholesterol, diabetes, heart disease, and stroke
  • Recommendation: at least 30 min of activity on most or all days
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21
Q

What percent of strokes are ischemic strokes?

A

*83-87% of all strokes

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22
Q

What is an ischemic stroke?

A

*When blood flow is blocked to the brain (lack of O2)

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23
Q

What are the two types of Ischemic strokes?

A
  • Cerebral Thrombus- blood vessel narrows from atherosclerosis
  • Cerebral embolism- Clot from heart, upper body, or neck dislodges and move to the brain to block artery
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24
Q

What percent of strokes are Hemorrhagic?

A

*17% of all strokes

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25
Q

What is a hemorrhagic stroke?

A
  • Weakened vessel that ruptures and bleeds into the surrounding brain
  • blood accumulates and compresses the surrounding brain tissue
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26
Q

How do weakened blood vessels occur in a hemorrhagic stroke?

A
  • Aneurysm: Ballooning of weakened region of a blood vessel
  • Arteriovenous Malformation (AVM): A cluster of abnormally formed blood vessels. The vessels can rupture, causing bleeding into the brain
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27
Q

What is the most common location of a stroke?

A

*Middle cerebral artery

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28
Q

About how many days does it take to see a MCA stroke on a CAT scan?

A

After day 3 you can see the bleed

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29
Q

What are the symptoms you’d see in a post- MCA stroke?

A
  • loss of vision on the contralateral side. Optic radiation = Homonymous Hemianopia
  • left side of the brain is the dominant area for speech in right handed people so this would cause Broca’s (area 44 and pt can’t form words but understands them) or Wernicke’s area (area 22- person can speak but content doesn’t make sense).
  • On a left hand dominant person then their speech is 50/50 on either side (you’d have to do a study to determine which side is dominant).
  • Sensory modalities (hot, cold, light touch, pin prick, etc.) can be effected contralaterally
  • Contralateral hemiparesis, arm then leg
  • Apraxia = inability to plan or carry out a motor plan (ideomotor or ideational)
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30
Q

What does the MCA supply and what will damage to it result in?

A
  • Supplies the internal capsule and basal ganglia

* Damage to it results in both UE and LE involvement

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31
Q

What are the symptoms of an ACA stroke?

A
  • Contralateral hemiparesis affecting leg > arm
  • Contralateral sensory impairment affecting leg > arm
  • Loss of bowel/bladder control
  • Apraxia
  • Mental impairment with perseveration, confusion, memory loss
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32
Q

What is perseveration?

A

Do the same thing or say the same words repeatedly. They can’t let a topic go, they’re stuck on it

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33
Q

What are the effects of a PCA stroke?

A
  • Contralateral homonymous hemianopia
  • Dyslexia
  • Memory deficits
  • Topographical disorientation
  • Cranial nerve III palsy (oculomotor)
  • Contralateral hemiparesis
  • Thalamic syndrome
  • Pain and temperature sensory loss
  • Ataxia, athetosis, or choreiform movement
  • Visual agnosia
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34
Q

What is dyslexia?

A

*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, dyslexia is a common learning disability in children.

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35
Q

What occurs in thalamic syndrome?

A
  • Sensory impairment in all modalities
  • Pain
  • Paresthesias
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36
Q

What is paresthesia?

A

*An abnormal sensation such as tingling, tickling, pricking, numbness or burning of a person’s skin

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37
Q

What is athetosis?

A

*A symptom characterized by slow, involuntary, convoluted, writhing movements of the fingers, hands, toes, and feet and in some cases, arms, legs, neck and tongue (big, large, writhing movements)

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38
Q

What is the one sensory modality that doesn’t go through the thalamus?

A

*Smell

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39
Q

What are choreform movements?

A

*Involuntary, forcible, rapid, jerky movements which are mostly manifestations of basal ganglia diseases (relatively small amplitude)

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40
Q

What is visual agnosia?

A

An impairment in recognition of visually presented objects.

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41
Q

What is tactile agnosia?

A

Putting something in someone’s hand and they can’t recognize it

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42
Q

What is topographical disorientation?

A

Losing sense of direction, not being able to orient themselves

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43
Q

What is a carotid arteriogram?

A

*It’s a picture showing the carotid arteries

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44
Q

What can occur with a basilar artery (brainstem) stroke?

A
  • Coma
  • Quadriplegia
  • “locked in” syndrome - intact consciousness but no motor ability other than eye blinks to respond
  • Bilateral cerebellar ataxia
  • Thalamic pain syndrome
  • Diplopia or other visual field deficits including blindness
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45
Q

What occurs with a vertebral artery stroke?

A
  • Ataxia
  • Vertigo
  • Nausea
  • Vomiting
  • 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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46
Q

What is the vertebral artery test?

A
  • you’re rotating and extending away from the side that you’re testing. You’re looking for the pupil to dilate or dizziness, etc to test for occlusion/blockage of the vertebral artery
  • When people get dizzy/nauseaus when they’re washing their hair or shaving their face (bc of the extension) then they need to go to the doctors!!
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47
Q

If you have a lesion to the R optic nerve, what will be the deficits?

A

You will be blind in the Right eye

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48
Q

If you have a lesion to the optic chiasm what are the deficits?

A

You loose your peripheral vision, causing tunnel vision

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49
Q

If you have a lesion to the R optic tract, what are the deficits?

A

Left homonymous hemianopsia- the person can’t see to the left

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50
Q

If you have a lesion to the R optic radiations, what are the deficits?

A

Left homonymous hemianopsia- the person can’t see to the left

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51
Q

What are the visual deficits to a lesion of the the right occipital lobe?

A

*L homonymous hemianopsia- can’t see to the left

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52
Q

what are the visual deficits of a right temporal lobe lesion?

A

Left upper quadrant homonymous hemianopsia- person can’t see to the left above cheek bone level

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53
Q

What are the visual deficits of a Right parietal lobe lesion?

A

Left lower quadrant homonymous hemianopsia

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54
Q

How do you screen for the Optic Nerve?

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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55
Q

What muscle fiber type is I?

A

*Slow, oxidative

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56
Q

What motor unit type is I?

A

Slow

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57
Q

What muscle fiber type is IIA?

A

Fast, oxidative-glycolytic

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58
Q

What motor unit fiber type is IIA?

A

Fast, fatigue-resistant

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59
Q

What motor unit fiber type is IIB?

A

Fast, fatigable

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60
Q

what muscle fiber type is IIB?

A

fast, glycolytic

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61
Q

What is Henneman Principle?

A
  • There exists an order to motor unit recruitment when gradual control of tension is important
  • Small motor units are recruited 1st and larger ones are last
  • Larger motor units are de-recruited 1st and smaller ones are last
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62
Q

When is the Henneman Principle violated?

A

When one is performing ballistic or relatively fast movements because all motor units are required immediately

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63
Q

What is the order of recruitment as you gradually do tension?

A

*1st slow fibers, then fatigue resistant, and lastly the fast fatigable fibers

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64
Q

When does scapular subluxation occur?

A
  • When the rotator cuff muscles are weak because they keep the humeral head in the glenoid fossa
  • After stroke
  • Spasticity can pull the humerus into an abnormal postion
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65
Q

What is the most common type of shoulder subluxation?

A

*Inferior subluxation

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66
Q

What are the abnormal positions of the scapula that can be from shoulder subluxation?

A
  • 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.
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67
Q

What is important when positioning a patient with a shoulder subluxation?

A

*You need to make sure the weight of the humerus is supported so that the scapula is maintained in a proper position

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68
Q

What is the abnormal muscle tone pattern in a CVA?

A
  • Hypotonia with cerebral shock followed by hypertonia

* Brunnstrom stage progression

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69
Q

What is the flexion synergy pattern of the UE?

A
  • Scapula = elevation and or/retraction
  • Shoulder = ABD, ER (hyperextension)
  • Elbow = Flexion
  • Forearm = supination
  • Wrist and hand = Wrist flexion and/or mass finger flexion
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70
Q

What is the extension synergy of the UE?

A
  • Scapula = Depression and/or protraction
  • Shoulder = ADD, IR
  • Elbow = Extension
  • Forearm = Pronation
  • Wrist and hand = Wrist extension and/or mass finger flexion
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71
Q

What is the flexion synergy pattern for the LE?

A
  • Hip = Flexion, ABD, ER
  • Knee = Flexion
  • Ankle = Dorsiflexion
  • Foot = Inversion and mass flexion of toes
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72
Q

What is the extension synergy pattern for the LE?

A
  • Hip = Extension, ADD, IR
  • Knee = Extension
  • Ankle = Plantarflexion
  • Foot = Inversion and extension of toes
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73
Q

What stage of Brunnstrum do you start the testing?

A

*Stage 4 then work down or up from there

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74
Q

When is it appropriate to strength test post CVA?

A

*When a pt is categorized as brunnstrum stage 6/7 or not influenced by the synergies

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75
Q

What is a TBI?

A
  • TBI is caused by a bump, blow or jolt to the head or a penetrating head injury that disrupts the normal function of the brain (CDC 2013).
  • Altered consciousness (no matter how brief)
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76
Q

What is a Closed head injury?

A
  • no skull fracture or laceration of the brain
  • coup-countercoup
  • Primary injury at impact
  • Secondary injury on the opposite side
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77
Q

What is an open head injury?

A

*Meninges have been breached, brain is exposed

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78
Q

What is a Coup injury?

A

*the direct blow. Ex: if a person is in a car and they hit their head on the dashboard then that direct blow is the coup injury.

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79
Q

What is a counter-coup injury?

A
  • indirect blow, the brain slams into the skull forward, then slams into the back of the skull. If you’re hit from the side then the brain may go side to side. This could result in a global head injury
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80
Q

How many TBI’s occur every year?

A

*At least 1.7 million either as an isolated injury or with other injuries

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81
Q

How many TBIs are concussions or mild TBIs each year?

A

About 75% of TBI’s

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82
Q

What percent of all injury related deaths is TBI a contributing factor for?

A

*to 1/3 (30.5%)

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83
Q

What age of adults have the highest rates of TBI-related hospitalization and death?

A

*Adults aged 75 and older

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84
Q

How do most children get a TBI age 0-4?

A

*Risk of falls, shaken baby syndrome, etc

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85
Q

How do older adolescents (15-19) get a TBI?

A

*Driving, risk of sports

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86
Q

How do adults 65 and older get a TBI usually?

A

*They’re at an increase risk for falls

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87
Q

Are TBI rates higher for males or females?

A

*Males

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88
Q

What was the total of direct medical costs and indirect medical costs (lost productivity) due to TBI’s?

A

*$76.5 BILLION

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89
Q

What are the most common causes of TBI’s?

A
  • Motor Vehicle Accidents: more than 60%
  • Automobile (70%): 79% wearing seatbelts
  • Pedestrian (5%)
  • Motorcylce (25%): 92% wearing helmets
  • Other is the other 40%
  • falls
  • Assault/violence
  • Domestic accidents
  • Sports
  • industrial accidents
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90
Q

What is the risk of TBI for motorcyclists that don’t wear a helmet?

A

*2x greater than helmeted motorcyclists

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91
Q

What is the cost of acute care for unhelmeted drivers compared to helmeted drivers?

A

*3x greater!

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92
Q

The first year of the helmet law resulted in what percent decrease of motorcycle crash fatalities?

A

*A 37.5% decrease in fatalities!

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93
Q

How many head injuries per year are attributed to children in bike accidents?

A

*140,000 head injuries a year

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94
Q

What percent of moderate to severe TBIs are prevented by bike helmets?

A

*74-85% of TBIs

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95
Q

What percent of fatality is decreased for front seat passengers if they wear their seat belt?

A

*14% decrease of fatality!

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96
Q

What are the risk factors of getting a TBI?

A
  • Young (average age of TBI = 29 YO)
  • Male
  • Risk taking behaviors
  • Low income, urban
  • Substance abuse (50% hospitalizations for TBI associated with alcohol intoxication)
  • Availability of firearm
  • Previous TBI (e.g. sports-related concussions)
  • Older age (more susceptible to tearing of blood vessels, declines in cerebrovascular circulation)
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97
Q

What is the order of the mot common skull fracture?

A
  • 1st: Frontal
    2nd: basilar
    3rd: parietal
    4th: occipital
    5th: temporal
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98
Q

What percent of patients admitted for CNS trauma sustained a skull fracture?

A
  • 24%

* 38% were open and 10% were depressed (< 3 mm)

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99
Q

What is the biggest danger of getting an open head fracture?

A

*The risk of infection getting into the brain

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100
Q

What percent of patients admitted to the hospital with a TBI also had extra-cranial injuries?

A

*82%

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101
Q

What percent of extra-cranial injuries were facial fractures?

A

*13%

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102
Q

What percent of extra cranial injuries were hemothorax/pneumothorax and what percent were rib fx/long contusion?

A
  • Hemothorax/pneumothorax: 9%

* Rib fx/long contusion: 10%

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103
Q

What percent of extra cranial injuries were spleen, liver/bowel, and genitourinary?

A
  • Spleen: 4%
  • Liver or bowel: 11%
  • Genitourinary: 3%
104
Q

What percent of extra cranial injuries were fractures of the UE, LE, Pelvis, and hip?

A
  • UE: 14%
  • LE: 19%
  • Pelvis: 4%
  • Hip: 2%
105
Q

What percent of extra cranial injuries were lacerations of the head or other?

A
  • Head: 61%

* Other: 20%

106
Q

What is the difference between a primary and secondary TBI injury?

A
  • Primary = direct injury to the brain (impact, missile, shearing)
  • Secondary = damage after the traumatic even caused by brain hypoxia, edema, herniation, hematoma, ischemia
107
Q

What is the difference between a focal and diffuse TBI?

A
  • Focal = localized trauma

* Diffuse = trauma over a large area

108
Q

What are hemorrhages named for and what ones are there?

A
  • *They’re named for where they occur
  • epidural hematoma
  • subdural hematoma
  • subarachnoid hemorrhage
  • intracerebral hematoma
109
Q

What are the characteristics of an epidural hematoma?

A
  • In epidural space, between dura mater and skull
  • Acute bleeding
  • Common in temporal bone fracutres
110
Q

What are the characteristics of a 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
111
Q

What is the prognosis of a subarachnoid hemorrhage?

A

*Poor prognosis if bleeding into ventricular system

112
Q

What are the characteristics of an intra-cerebral hematoma?

A
  • In brain parenchyma (neurons and glial cells)

* Hematoma may enlarge during the first few days after injury

113
Q

What is the most common head injury?

A

*concussion

114
Q

What are the effects of repeated concussions?

A

*Can cause dementia

115
Q

What are the typical characteristics of a concussion?

A
  • Alteration of consciousness and memory
  • CT and MRI usually normal
  • Good Prognosis
116
Q

How does a person act post-concussion?

A
  • dizziness, disorientation, nausea, headache, fatigue
  • Decreased control of emotions and personality changes
  • Attention deficit
117
Q

What are the characteristics of 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 last > 4 weeks
  • Depth and duration of coma is used to determine current status and prognosis
118
Q

What is a coma?

A

*State of unresponsiveness; not opening eyes

119
Q

What is a persistent vegetative state?

A

*No evidence of cerebral cortical function; eye opening with sleep-wake cycles

120
Q

What is lethargy?

A

*Severe drowsiness; aroused by moderate stimuli and then drift back to sleep

121
Q

What is confusion?

A

*Disorientation, bewilderment, and difficulty following commands

122
Q

What are the 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
123
Q

What are the characteristics of a 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

What are the cognitive impairments of a TBI?

A

Difficulties in:

  • Attention, concentration
  • Learning, memory
  • Abstract thinking, information processing
  • Problem solving
  • Initiation, executive functions
125
Q

What is the cognitive scale of Rancho Los Amigos?

A 
I.	no response
II. generalized response
III. localized response
IV. confused, agitated
V.	confused, inappropriate
VI.	confused, appropriate
VII.	automatic, appropriate
VIII.   purposeful, appropriate
126
Q

What is No response in RLA?

A

No Response: patient appears to be in a deep sleep and is completely unresponsive to any stimulus

127
Q

What is Generalized Response in RLA?

A

Generalized Response: Patient reacts inconsistently and non-purposefully to stimuli in a non-specific manner; responses are limited and often the same regardless of the stimulus presented; responses may be physiological, gross body movements, or vocalizations

128
Q

what is localized response in RLA?

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

What is Confused-agitated in RLA?

A

Confused-Agitated: patient in a heightened state of activity; bizarre and non-purposeful behavior to environment; decreased attention span; aggressive

130
Q

What is confused- inappropriate in RLA?

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

What is confused appropriate in RLA?

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 (e.g. self-care); responses may be incorrect due to memory deficits but are appropriate for the situation

132
Q

What is automatic-appropriate in RLA?

A

Automatic-Appropriate: patient appears appropriate and oriented within the hospital and home settings; does through daily routine automatically (robot-like); 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; judgment remains impaired

133
Q

What is Purposeful- appropriate in RLA?

A

Purposeful-Appropriate: patient is able to recall and integrate past and recent events and is aware of and responsive to environment; 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 judgment in emergencies or unusual circumstances

134
Q

How long should a person wait before administering the RLA test and what does it test for?

A
  • Wait at least 3 days

* It tests for Basic congnitive level of function

135
Q

What is retrograde amnesia?

A

*period of loss of recall of events prior to injury

136
Q

what is post-traumatic amnesia (PTA)?

A

*period between the injury and time of continuous day to day memory

137
Q

What is STM (short term memory)?

A

*Immediate past

138
Q

What is Short term working memory?

A

*Inability to learn new information

139
Q

What is LTM (long term memory)?

A
  • 1 min to 1 hour

- may or may not include over-learned material

140
Q

What occurs in disinhibition?

A

*“basic personality” emerges

141
Q

What are some inappropriate, excessive social behaviors with a TBI?

A
  • Exaggerated dependency or more independent
  • Irresponsible or lacks judgment
  • Egocentric or inconsiderate
  • Violent/aggressive
  • Childishness
  • Tactless
  • Miss goodie two shoes
142
Q

What are the Frontal lobe signs?

A
  • Decreased ability to take cues from environment
  • Silence - when say something embarrassing or inappropriate
  • Blush - when embarrassed or something of sexual nature
  • Angry look - patient bumps into someone with his wheelchair
143
Q

What are sexual behavioral issues with a TBI?

A
  • Tactless attempts at intimacy
  • Conversation with a lot of sexual content
  • Inappropriate touching
  • Crude remarks
  • Indecent exposure
  • Masturbation
  • *Can be caused by damage to the frontal or temporal lobe
144
Q

What are other behavioral changes often seen in a TBI?

A
  • Mood disturbances including depression and anxiety
  • Irritability; rage; refuse to cooperate
  • Euphoria; involuntary laughing or crying
  • Apathy; indifference
  • Motor, sensory, verbal perserveration
145
Q

What are some movement disorders associated with TBIs?

A
  • hemiplegia/hemiparesis
  • quadriplegia/quadriparesis (tetra)
  • triplegia/triparesis
  • monoplegia/monoparesis
  • bradykinesia
  • ataxia
  • apraxia
  • spasticity/rigidity
  • dyskinesias
  • tremors
  • athetoid, ballistic, chorea
146
Q

What is Decerebrate Posturing?

A

*Extend BUE and BLE

147
Q

What is Decortical Posturing?

A

*Flex BUE and extend BLE

148
Q

What are neurological impairments (visual) of a TBI?

A
  • Field cuts due to tract, radiation injuries
  • Visual-perceptual deficits
  • Diplopia
  • Gaze palsies
  • Nystagmus
  • Tracking disorders
  • Decreased visual acquity or blindness due to optic nerve injury
  • Cortical blindness (retain tectopulvinar vision)
  • Deficits in color vision
149
Q

What are opthalmologic injuries (direct eye injury)?

A
  • Retinal
  • Globe
  • Intra-ocular hemorrhage
  • Glaucoma
  • Diplopia due to extra-ocular muscle or orbit injuries
150
Q

What are neurological complications with a TBI?

A
  • Infection
  • Brain abscess
  • meningitis
  • wound infection
  • osteomyelitis of the skull
  • Recurrent hemorrhage, thrombus, aneurysm
  • Hydrocephalus (increased ICP)
  • Seizures
151
Q

What is the cause of ICP?

A

Swelling, fluid build-up in the brain and hematomas

152
Q

What occurs in ICP?

A
  • The fluid compresses the brain within the rigid skull

* Serious, life threathening

153
Q

How do you monitor ICP?

A
  • Medications
  • Fluid Management
  • Decompressive craniectomy
  • Shunt
154
Q

What kind of musculoskeletal disorders can occur with TBI?

A
  • heterotopic bone formation (HO)
  • osteoporosis
  • disuse muscle atrophy
  • contractures
  • secondary injuries – falls, burns, contusions, etc.
155
Q

What kind of skin disorders can occur with TBI?

A
  • decubitus ulcers
  • dependent edema
  • injuries: self-induced, restraints, equipment, shearing, etc.
156
Q

What autonomic disturbances can occur with TBI?

A
  • hypertension
  • sweating disorders (too little, too much)
  • hyperventilation
  • poor temperature control
157
Q

What urinary tract disorders can occur with TBI?

A
  • infection
  • calculi
  • neuropathic bladder/bowel/sexual dysfunction
158
Q

What is the incidence of SCI?

A
  • 40 cases per million population in US

* 12,000 new cases each year

159
Q

What is the prevalence of SCI?

A

*in 2012 there were 270,000 (236,000-327,000) persons alive with SCI in US

160
Q

What is the average age of injury for a SCI?

A

*41 years

161
Q

What is the percent of males/females with SCI?

A
  • 80.6% Males

* 19.4% Females

162
Q

What is the race/ethnicity percentages of SCI?

A
  • 66.0% Caucasian
  • 26.2% African American
  • 0.9% Native American
  • 2.1% Asian
  • 8.3% Hispanic
163
Q

What is the largest cause of SCI?

A
  • Vehicle accident (39.2%)
  • Falls (28.3%)
  • Violence (14.6%)
  • Sports (8.2%)
  • Other (9.7%)
164
Q

What are the different SCI’s and what are their prevalence?

A
  • Incomplete tetraplegia 40.8%
  • Complete paraplegia 21.6%
  • Incomplete paraplegia 21.4%
  • Complete tetraplegia 15.8%
165
Q

What is the length of stay for a SCI in a hospital?

A
  • Median days hospitalized in the acute care medical/surgical unit (in model systems) is 11 days (2005)
  • Median days in rehab = 37 days
166
Q

What can often be a cause of death in SCI?

A
  • In the past, renal failure
  • Advances in urologic management
  • Currently, pneumonia & septicemia
  • Septicemia is caused when certain bacteria get into the bloodstream
167
Q

Above C8 where does the nerve root exit?

A

*Above it’s corresponding vertebrae
*so: C1 exits below the occiput and above cervical vertebrae 1
*C2 exits above cervical vertebrae 2
etc.
*C7 exits above cervical vertebrae C7
*C8 exits above thoracic vertebrae 1

168
Q

Below C8 where does the nerve root exit?

A
  • Below its corresponding vertebrae
  • T1 exits below thoracic vertebrae 1
  • T2 exits below T2 (etc.)
  • Hyper-extension of C4 on C5 would compress the C5 nerve root
169
Q

What problems would occur with injury at the Cauda Equina?

A

*Sexual function and bowel/bladder problems

170
Q

Above T3, how do the nerve roots exit?

A
  • the nerve roots exit immediately and horizontal to the corresponding spinal cord level.
  • Example: the C7 nerve root exits at the same level as the C7 spinal cord (intervertebral canal)
171
Q

Below T3, how do the nerve roots exit?

A
  • the nerve root runs parallel to the spinal cord for a distance before existing below the spinal cord level.
  • Example: the T9 nerve root runs several segments lower to exit through the intervertebral foramen between T9 & T10 vertebrae
172
Q

Below L2 where is the injury happen?

A

*Damage can only happen to the nerve roots (not the spinal cord) as they pass through the spinal canal

173
Q

What is a contusion?

A

*Bruising of SC following fractures and dislocations of the vertebrae

174
Q

What is the clinical presentation of a contusion?

A
  • Initially severe symptoms from loss of SC function (compression from swelling, etc.)
  • Usually, rapid return of function (weeks)
  • Amount of return depends on severity of injury
  • Contusion has the best prognosis since the SC is still intact
175
Q

How does a compression injury occur?

A
  • From fractures and dislocations of vertebrae, tumors, disc herniation
  • *Clinical Presentation
  • Amount of return depends on severity of injury
176
Q

How does a laceration occur?

A

*From knife, gunshot or other projectile/foreign object

177
Q

What is the clinical presentation of a laceration?

A
  • Partial to complete loss of function below level of lesion

* Impairment depends on extent of lesion

178
Q

How does a loss of vascular supply occur?

A

*From thrombosis, embolus, arteriovenous malformation or direct disruption of blood vessels

179
Q

What is the clinical presentation of loss of vascular supply?

A

Clinical Presentation:

Partial loss of SC function below level of lesion in distribution of blood supply

180
Q

What is a complete injury?

A
  • loss of all sensation and motor function below the level of the lesion
  • AIS A
181
Q

What is incomplete injury?

A
  • partial loss of sensation and motor function below the level of the injury
  • AIS B, C, or D
182
Q

AIS A?

A
  • Complete

* No sensory or motor function preserved

183
Q

AIS B?

A
  • Incomplete
  • sensory preserved but no motor function
  • Bowel/bladder function; violate “NOON” sign
184
Q

AIS C?

A
  • Incomplete

* Motor preserved with majority of muscles graded < 3 (0,1,2)

185
Q

AIS D?

A
  • Incomplete

* Motor preserved with majority of muscles graded > 3 (3, 4, 5)

186
Q

AIS E?

A

Normal

187
Q

What is the NOON sign?

A

*Pt is ASIA A if they have all No’s and 0’s, but if they have any Yes’s or 1’s (or higher) then they violate the NOON sign and they’re ASIA B

188
Q

What occurs at a C2-C3 injury?

A

*Ventilator dependent, total care

189
Q

What occurs at C3-5?

A

Phrenic nerve, independent breathing, off ventilator

190
Q

What occurs at C5 injury?

A

Can raise shoulders and flex arm to use a joystick on a power w/c, possibly manual w/c with adaptations

191
Q

What occurs at C6 injury?

A

*Have wrist extension so weak, functional, tenodesis grasp (wrist extends, passive finger flexion due to contracted finger flexors)

192
Q

What occurs at C7 injury?

A

*Have triceps, can preform pressure relief and transfers and to help self prevent ulcers

193
Q

What occurs at a thoracic region injury?

A

*Adds postural stability and respiration function (accessory breathing muscles)

194
Q

What occurs at T6-12 injury?

A
  • Abdominal function

* Start getting slips of function at T6

195
Q

What occurs at L2 injury?

A

Hip flexion

196
Q

What occurs at S2-4 injury?

A

Sacral region is important for bowel/bladder/sexual function

197
Q

What occurs in the DCML?

A

proprioception, vibration, fine discrimination, two-point touch

198
Q

What occurs in the antero-lateral system?

A

crude touch, sharp/dull, temperature, pain, tickle and itch, sexual sensations

199
Q

What is 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
200
Q

How does Anterior Cord Syndrome occur?

A
  • Most common injury of cervical spine
  • Mechanism of injury- Flexion
  • Flexion teardrop or burst fracture
  • Infarct or compression of anterior spinal arteries
201
Q

What is 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
202
Q

What occurs in 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)

203
Q

Where does Central Cord syndrome usually occur and what happens?

A
  • Most often in the cervical region
  • Pronounced weakness in the UEs > LEs
  • Sparing of sacral motor and sensory function
  • Hyperextension injuries in elderly or any age
  • Contusion of central region of SC
  • Can be from MVAs, but reduced frequency since head rests in cars
204
Q

What is a Brown-Sequard Hemisection?

A
  • Damage to one side of the SC

* Ipsilateral DCML, Ipsilateral CST, and Contralateral ALS

205
Q

What occurs with Brown-Sequard Ipsilateral DCML?

A

*Loss of proprioception, vibration, fine discriminatory, 2-point touch

206
Q

What occurs with Brown-Sequard ipsilateral CST?

A

*Loss of voluntary motor control

207
Q

What occurs with Brown-Sequard Contralateral ALS?

A

*Crude touch, sharp/dull, temperature, pain, tickle and itch, sexual sensations

208
Q

What is the Mechanism of injury for a Brown-Sequard?

A
  • 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
209
Q

How do Brown-Sequards occur?

A

*Traumatic SCI, Penetrating injuries (gunshot, knife wound), burst fractures

210
Q

What is the Acute management of SCI?

A
  • ABCs: Airway, Breathing, Circulation
  • If necessary to move, log roll maintaining spine in neutral (“Matt”)
  • Immobilize
  • Monitor BP & ECG
  • X-ray, CT and/or MRI
211
Q

What are the indications for surgery?

A
  • Bone fragments and disk 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.
212
Q

What are Harrington Rods (thoracolumbar surgeries)?

A
  • Stainless steel rods with hooks on either end placed on either side of injury area
  • Distracts spine until proper alignment is achieved
  • Pts can get hypermobile above and below the rods but CAN NOT move where the rods are.
213
Q

What types of surgeries need to be immobilized and for how long?

A
  • Stable fracture with no surgery
  • 6-12 weeks
  • Cervical Fusion
  • 3-4 months using a halo or SOMI (sterno-occipital-mandibular immobilizer)
  • Thoracolumbar Fusions
  • 4-6 months using a rigid body jacket (TLSO)
214
Q

When is the onset to Spinal shock?

A

Immediately post- injury

215
Q

What is the duration of Spinal shock?

A

1 week- several months (mean of 6 weeks)

216
Q

What occurs in spinal shock below the level of the lesion?

A
  • Flaccid paralysis
  • No reflex activity
  • Absent bowel and bladder tone
  • Decreased blood pressure
217
Q

When does spasticity occur in spinal shock?

A

*Occurs AFTER spinal shock ends!

218
Q

What injuries can cause respiratory system problems?

A
  • Phrenic nerve = C3, 4, 5
  • So individuals with C1-3 SCI are on a respirator/ventilator because they have no or minimal diaphragm function
  • C4-5 (even C6-T1): may need respirator permanently or at least temporarily
  • C8-T12 injuries: when intercostal and abdominal muscles are lost, 20-70% decrease in vital capacity
219
Q

What can be problems with the circulatory system?

A
  • Bradycardia
  • Dysrhythmias
  • Orthostatic hypotension
  • Low BP (especially 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 (pooling)
220
Q

What are complications with the circulatory system?

A
  • Increased risk for DVTs and pulmonary emboli (deep vein thrombosis)
  • DVT: warm and red in area (very localized)
221
Q

What is the intervention for circulatory system?

A
  • Heparin
  • Anti-embolism stockings (TED hose)
  • Abdominal binder (increases blood flow)
222
Q

What changes can occur in the gastrointestinal system?

A

*Loss of bowel control

223
Q

What complications can occur with the gastrointestinal system?

A
  • Incontinence
  • Constipation
  • Bowel obstructions
  • Bowel accidents are often due to use of medications needed to treat constipation
  • Oral medications
  • -Colace as a stool softener and Metamucil to produce well-formed soft stool
  • Suppositories: e.g. Dulcolax, for bowel program
  • High fiber diets
224
Q

What changes can occur with the Urologic system?

A
  • Urinary incontinence
  • Flaccid Neurogenic Bladder (“Arefelxic bladder”)
  • Reflexic Neurogenic Bladder (“spastic bladder”)
225
Q

What is Flaccid Neurogenic Bladder (“arefexic bladder”)?

A
  • 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 artificially
  • Some patients may be able to learn to do self-catheterization (increased risk of bladder infection)
226
Q

What is Reflexic Neurogenic Bladder (“Spastic bladder”)?

A
  • 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
227
Q

What are the complications with the urologic system?

A
  • UTI (urine is cloudy)
  • Kidney Stones
  • Bladder Stones
228
Q

What is the potential for recovery of sensation and motor below the level of the lesion?

A
  • Most likely in zone of injury (1-3 neurological levels below the neurological level of injury)
  • Intense rehabilitation programs
229
Q

What is Neuropathic Pain?

A
  • Experienced by 90% of all SCI patients at least intermittently below level of lesion
  • Burning sensation
230
Q

What can spasticity/hypertonicity interfere with?

A

*Can interfere with positioning, transfers, maintenance of joint ROM, and with active motion

231
Q

What is the definition of spasticity?

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.

232
Q

What is Gamma Spasticity?

A
  • Most common and predominate theory
  • 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
233
Q

Who does Autonomic Dysreflexia Occur in?

A

*In persons with lesions ABOVE T6

234
Q

What is Autonomic Dysreflexia?

A
  • Consequence of over-activity of the ANS (autonomic nervous system) (elevated BP)
  • Precipitated by a noxious stimulus (triggers)
  • Can escalate into a medical emergency
235
Q

What are some triggers for Autonomic dysreflexia?

A
  • Full bladder or blocked catheter, UTI (most common)
  • Constipation, distention, hemorrhoids
  • Infection or irritation (e.g. appendicitis)
  • Sunburn
  • Tight clothing
  • Pain (e.g. childbirth, fracture, bruise, cut)
  • Prolonged pressure by object: tight shoe, ill=fitting brace
  • Pressure sores (decubitus ulcer)
  • Ingrown toenails
236
Q

How does AD happen?

A
  • Some stimulus triggers a sympathetic (ANS) response (elevated BP)
  • Sympathetic system can only be adjusted above the level of the lesion; reflex cannot be turned off below the level of the lesion
237
Q

What are the Signs and symptoms of AD?

A
  • Pounding headache(caused by the elevation in blood pressure)
  • Goosebumps
  • Sweating above the level of injury
  • Nasal Congestion
  • Blotching of the skin
  • Restlessness
  • Hypertension
  • Flushed (reddened) face
238
Q

Why do people lose the ability to control body temperature?

A

*due to inability to sweat or shiver below level of lesion

239
Q

What are the complications of temperature control?

A

*Less able to tolerate extremes in temperature

240
Q

What are the interventions for temperature control?

A
  • Avoid extreme hot/cold temperatures
  • Separate heating or air conditioning may be a necessity
  • Dress extra warm in winter
  • Spray bottle of water
241
Q

What are the problems with the Integumentary system?

A
  • Decubitus ulcers

* Cuts, burns, etc. occur before patient is aware of them

242
Q

What are the interventions for integumentary system?

A
  • Prevention of pressure sores
  • WC and bed cushions
  • Pressure relief techniques – “mini-lab”
  • Good transfer techniques to avoid sheer forces
  • Teach awareness and protection of insensate body parts to prevent injuries
243
Q

What are the changes in the musculoskeletal system?

A
  • Loss of calcium from bone occurs following injury
  • Complications:
  • Hypercalcemia (high blood calcium levels)
  • –can cause cardiac arhythmias
  • Osteoporosis (DEXA scans: < -3.5 at risk for fractures)
  • Heterotopic ossification
244
Q

What is the intervention for Osteoporosis?

A

*Weight bearing in all positions

245
Q

FES Cycling

A
  • Helps prevent and treat osteoporosis

* FES also adds muscle bulk which can help prevent decubiti

246
Q

What is Heterotopic ossification?

A
  • Calcium deposits in soft tissues around joints that receive stress (e.g. hip joints)
  • Marked limitation of ROM
247
Q

What is the treatment for HO?

A
  • Didronel and radiation therapy to inhibit osteoblast function (slows HO, but doesn’t stop it)
  • Maintain ROM if possible (gentle but firm PROM)
  • If surgically removed, likely to come back and be worse
248
Q

What occurs in the reproductive system in women with an 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)
  • Delivery
  • -Many have normal vaginal delivery
  • -Autonomic dysreflexia may occur during labor  C-section to deliver baby quickly
249
Q

What occurs in the reproductive system in males with a SCI?

A
  • Reflexogenic (controlled at S2-4, must be intact)
  • Spontaneous (secondary to internal stimulation (e.g. full bladder)
  • Ejaculation usually does not occur unless sacral sensation is intact
250
Q

What is a central pattern generator? (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
251
Q

What are Evarts-spinal rhythm generators?

A

*A group of neurons that inherently present a pre-arranged sequence of muscle activity arranged temporally and spatially.

252
Q

What happened in the dog spinal transection?

A
  • stimulation to flank produces rhythmic scratching

* range and frequency of rhythmic flexion and extension (scratching) is dependent on strength of stimulus

253
Q

What occured in the spinal testing of cats? Specifically the Shik study?

A
  • Shik preparation (midbrain, cerebellum and spinal cord are areas of stimulation)
  • cerebral cortex cannot communicate with spinal cord in humans
254
Q

What is suggested about humans and CPGs?

A
  • it is suggested that the gait CPG extends higher into MI area (Brodmann area 4), but may not
  • Humans- un-weighted gait in the clinic
255
Q

How do you get cat to begin gait while it’s suspended over a treadmill?

A
  • If apply brief electrical current (or L-DOPA) at level of transection
  • Produces stepping by just starting treadmill usually with manual assistance
  • -At first clumsy and feet trailing but eventually crude stepping
256
Q

What happens if you increase the speed of a treadmill while a cat is on it?

A

*cat walked faster eventually transitioning to a trot, then later a gallop (thus, different patterns of gait are present at a spinal level)

257
Q

Where are the CPG neural networks for gait in a cat?

A

*In the spinal cord, midbrain, and cerebellum

Neuro D&D (4 decks)

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