Chapter 15 - Cognitive Systems and Motor Function Flashcards

1
Q

Cognitive behavioural functional competence

A

integrated processes of cognitive, sensory, and motor systems

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2
Q

What systems get manifested through the motor network?

A

behaviours that appropriate to human activity

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3
Q

Full Consciousness

A

state of awareness of oneself and appropriate responses to environment

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4
Q

What are the two components of consciousness?

A

arousal and awareness

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5
Q

Arousal

A

state of awakeness

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6
Q

Awareness

A

content of thought

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7
Q

How are structural alterations divided?

A

by their location of dysfunction

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8
Q

Where do supratentorial disorders affect?

A

above the tentorium cerebelli

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9
Q

What do supratentorial disorders produce change in?

A

arousal

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10
Q

Where do infratentorial disorders affect?

A

below the tentorium cerebelli

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11
Q

What do infrantentorial disorders do?

A

produce decline of arousal by RAS dysfunction

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12
Q

Metabolic alterations produce a ________ in arousal by altering…

A

decline; delivery of energy substrates

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13
Q

How many patterns of neurological functions are critical to evaluation process?

A

5

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14
Q

Which function is the most critical index of nervous system function?

A

level of consciousness

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15
Q

Changes in level of consciousness indicate _________ or _________

A

improvement or deterioration

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16
Q

What are characteristics of highest level of consciousness?

A

when the person is alert and orientated to oneself, others, place, time

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17
Q

What does level of consciousness diminish to?

A

confusion, then disorientation, then coma

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18
Q

Normal breathing is a __________ pattern

A

rhythmic

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19
Q

Diminished consciousness leaves breathing responding to changes in _________ levels

A

PaCO₂

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20
Q

Cheyne-Stokes Respirations

A

altered period of tachypnea and apnea related directly to PaCO₂

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21
Q

Apneusis

A

prolonged inspiratory time and a pause before expiration

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22
Q

Ataxic Breathing

A

complete irregularity of breathing with increased periods of apnea

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23
Q

What does pupillary reaction indicate?

A

presence and level of brainstem dysfunction

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24
Q

Where is the brainstem area that controls pupils?

A

adjacent to the areas controlling arousal

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25
Q

How does ischemia affect the pupils?

A

makes them dilated/fixed

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26
Q

What causes pinpoint pupils?

A

hypothermia or opiates

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27
Q

Oculomotor Responses

A

resting, spontaneous, and reflexive eye movements

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28
Q

Normal Oculomotor Response

A

eyes move together to side opposite from turn of head

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29
Q

Abnormal Oculomotor Response

A

eyes do not turn together

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30
Q

Absent Oculomotor Response

A

eyes move in the direction of head movement

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31
Q

What is the caloric ice water test used to measure

A

oculomotor response

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32
Q

How does the caloric ice water test work?

A

ice water is injected into the ear canal

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33
Q

Normal Caloric Ice Water Test Response

A

eyes turn together to side of head where ice injected

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34
Q

Abnormal Caloric Ice Water Test Response

A

eyes do not move together

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35
Q

Absent Caloric Ice Water Test Response

A

no eye movement

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36
Q

What do motor responses tell us about brain dysfunction?

A

severity and which side of the brain is damaged

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37
Q

Motor response patterns may be ________, __________, or _____________

A
  1. purposeful
  2. inappropriate
  3. not present
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38
Q

Paratonia

A

form of hypertonia with an involuntary variable resistance during passive movement

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39
Q

Slide 13 - § Motor signs indicating loss of cortical inhibition
= decreased consciousness / associated with the
performance of primitive reflexes and rigidity
(paratonia)????

A
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40
Q

Dysfunction of the medulla oblongata may manifest as?

A

compulsive/repetitive vomiting, yawning, hiccups

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41
Q

Alterations in arousal may result in ________ (morbidity) or _______

A

disability or mortality

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42
Q

Outcomes of arousal alterations depend on the ________, _________, ________ of the coma

A

cause, damage, duration

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43
Q

What are the two forms of neurological death?

A

brain death and cerebral death

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44
Q

Brain Death = ________ brain death

A

total

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45
Q

NDD

A

neurological determination of death

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46
Q

Brain death is _______

A

irreversible

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47
Q

Brain death occurs when the brain cannot maintain __________

A

homeostasis

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48
Q

What is the criteria for NDD in Canada?

A
  1. unresponsive coma
  2. no brainstem functions
  3. no spontaneous respiration (apnea)
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49
Q

Cerebral death = ___________ coma

A

irreversible

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50
Q

Which part of the cerebral hemisphere is not involved in cerebral death?

A

brainstem and cerebellum

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51
Q

With cerebral death it is possible for the brain to continue __________ maintenance

A

homeostasis

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52
Q

With a persistent vegetative state the person is completely _________ of their self or environment.

A

unaware

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53
Q

What are 3 factors in a persistent vegetative state?

A

-no speech
-no cerebral function
-yes sleep-wake cycles

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54
Q

3 factors of a minimally conscious state (MSC)

A

-follow simple commands
-manipulate objects
-give yes/no responses

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55
Q

Locked in syndrome involves the complete paralysis of voluntary muscles except for…

A

eye movement

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56
Q

With locked in system the person is fully ________

A

conscious

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57
Q

How do people with locked in syndrome communicate?

A

blinking

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58
Q

Awareness encompasses all _________ function

A

cognitive

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59
Q

What mediates awareness?

A

executive attention networks (EAN)

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60
Q

Executive Attention Networks (EAN)

A

selective attention and memory involving abstract reasoning, planning, decision making, judgement, self-control

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61
Q

Selective Attention

A

ability to select specific information and focus on related task

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62
Q

Initial Executive Attention Deficit Detection

A

person fails to stay alert and orientate to stimuli

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63
Q

Mild Executive Attention Deficit Detection

A

grooming and social graces are lacking

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64
Q

Severe Executive Attention Deficit Detection

A

motionless, no response, no reaction to surroundings

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65
Q

Attention Deficits are characterized by an inability to maintain __________ attention and set ________

A

sustained; goals

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66
Q

Memory

A

recording, retention, retrieval of information

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67
Q

Amnesia

A

loss of memory

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68
Q

Retrograde Amnesia

A

difficulty retrieving past memories

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69
Q

Anterograde Amnesia

A

inability to form new memories

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70
Q

Data-Processing Deficits

A

problems associated with recognizing and processing sensory information

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71
Q

Agnosia is a defect of _________ recognition

A

pattern

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72
Q

Agnosia is characterized by the failure to recognize ______ and ______ of objects

A

form and nature

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73
Q

Agnosia only affects _____ sense most times

A

one

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74
Q

Agnosia Example

A

can’t identify a safety pin by touching it but can name it when looking at it

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75
Q

Agnosia is associated with _______________ accidents

A

cerebrovascular

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76
Q

Dysphasia

A

impairment of comprehension or production of language

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77
Q

Expressive Dysphasia aka _____ dysphasia

A

Broca

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78
Q

Expressive dysphasia results in the lost ability to…

A

produce spoken or written language

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79
Q

With expressive dysphasia, ________ comprehension is usually present

A

verbal

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80
Q

Receptive dysphasia aka ___________ dysphasia

A

wernicke

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81
Q

Receptive dysphasia results in the inability to…

A

understand written or spoken language

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82
Q

People with receptive dysphasia are fluent with speech but the words have no __________

A

meaning

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83
Q

Which artery is responsible for the pathology of dysphasia?

A

middle cerebral artery

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84
Q

How many major arteries supply blood to the brain?

A

3

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85
Q

Transient (acute) disorders of awareness have _______ or _______ onset

A

sudden or gradual

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86
Q

What causes transient awareness disorders?

A

-drug intoxication
-alcohol withdrawal
-post anesthesia
-electrolyte imbalance

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87
Q

Acute Confusion and Delirium result from disruption of the _____, ________, ________, and _________

A

thalamus, cortex, RAS, limbic system

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88
Q

Delirium aka ___________ Acute Confusional State

A

Hyperactive

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89
Q

Where does delirium most commonly occur?

A

critical care units over 2-3 days

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90
Q

Hyperactive Delirium results from a disruption of which neurotransmitters?

A

acetylcholine and dopamine

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91
Q

Excited Delirium Syndrome aka _________ delirium

A

agitated

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92
Q

Agitated delirium is hyperkinetic and can lead to…

A

sudden death

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93
Q

How does excited (agitated) delirium syndrome manifest?

A

-rapid breathing
-high pain tolerance
-superhuman strength

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94
Q

Acute Confusional States and Delirium Manifest as:

A

-terrifying dreams
-hallucinations
-gross alteration of perception
-insomnia

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95
Q

How is delirium evaluated?

A

CAM-ICU - Confusion Assessment Method for Intensive Care Unit

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96
Q

Dementia

A

the deterioration or progressive failure of many cerebral functions

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97
Q

What are some possible causes of dementia?

A

-cerebral neuron degeneration
-atherosclerosis
-genetics

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98
Q

Is there a cure for dementia?

A

no

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99
Q

With dementia it is important to maximize ____________ capacities

A

remaining

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100
Q

What is the leading cause of severe cognitive dysfunction is older adults?

A

Alzheimer’s Disease

101
Q

What causes Alzheimers disease?

A

unknown

102
Q

How many forms of Alzheimers disease exist?

A

3

103
Q

What is the most common form of Alzheimer’s?

A

Nonhereditary sporadic late-onset AD

104
Q

Which form of Alzheimer’s has no genetic association?

A

Nonhereditary sporadic late-onset

105
Q

Early-onset familial AD is associated with a mutation on chromosome ___

A

21

106
Q

Early-onset AD is linked to a mutation on chromosome ___

A

19

107
Q

How common is early-onset AD?

A

not

108
Q

The pathology of the 3 different types of Alzheimer’s is _______

A

the same

109
Q

4 Key Pathophysiological Components of Alzheimer’s Disease

A
  1. accumulation of toxic amyloid plague fragments
  2. loss of ACh in the forebrain cholinergic neurons (neuronal death)
  3. Tau Proteins form neurofibrillary tangles in neuron (=death)
  4. Brain atrophy
110
Q

Amyloid Plagues

A

aggregates of misfolded proteins

111
Q

Where are neurofibrillary tangle concentrated?

A

cerebral cortex

112
Q

With brain atrophy, the sulci _________ and the gyri _________

A

widen; shrink

113
Q

What is the first symptoms of Alzheimer’s?

A

memory loss and impaired learning

114
Q

What continuation of symptoms result from Alzheimer’s?

A

loss of language, reasoning, social behaviour, dyspraxia

115
Q

Dyspraxia

A

loss of movement and co-ordination

116
Q

Alzheimer’s progresses from _____-term memory loss to ____ loss of cognitive function

A

short-term; total

117
Q

Do pathophysiological changes occur before or after dementia syndrome?

A

decades before usually

118
Q

What is the second most common form of dementia?

A

Frontotemporal Dementia

119
Q

Frontotemporal Dementia was previously known as…

A

Pick Disease

120
Q

Frontotemporal Dementia is an umbrella term for disorders that…

A

affect the frontal and temporal brain regions

121
Q

What is the first symptoms of Frontotemporal Dementia

A

apathy, poor judgement and reasoning, breaking laws

122
Q

The genetic component of frontotemporal dementia is associated with onset at less than ____ years of age

A

60

123
Q

Frontotemporal dementia involves a mutation of which encoding genes?

A

Tau

124
Q

Seizures are a _________ of disease, not a disease themselves

A

manifestation

125
Q

What is a seizure?

A

a sudden disruption in brain electrical function caused by abnormal excessive discharges of cortical neurons

126
Q

Cortical neurons = ____neurons

A

inter

127
Q

What is epilepsy?

A

a disorder characterized by the recurrence of seizure where no known cause for the seizures is found

128
Q

What are convulsions?

A

jerky, contact-relax movements associated with seizures

129
Q

What are 4 probable causes of seizure in young adults?

A
  1. alcohol withdrawal
  2. drug withdrawal
  3. brain tumour
  4. peri-natal insults
130
Q

Peri-natal insults

A

insults occurring between 28 weeks of gestation to 28 days after birth

131
Q

What are 4 probable causes of seizures in older adults?

A
  1. alcohol withdrawal
  2. drug withdrawal
  3. metabolic disorders
  4. CNS degeneration
132
Q

Epileptogenic Focus (zone)

A

brain site where seizure originates

133
Q

Neurons in the epileptogenic focus are ____sensitive and activated by numerous stimuli

A

hyper

134
Q

epileptogenic focus neurons fire ______ frequently and with ______ amplitude

A

more; greater

135
Q

How is the epileptogenic focus determined during seizures?

A

activated SPECT - test that detects blood flow changes in the brain

136
Q

What is the tonic phase of a seizure?

A

muscle contraction with increased muscle tone

137
Q

The tonic phase is associated with loss of _____________

A

consciousness

138
Q

What is the clonic phase of a seizure?

A

alternating contraction and relaxation of muscles

139
Q

The clonic phase begins when _______ neurons in the ________ and _________ react to cortical excitation

A

inhibitory; thalamus and basal ganglia

140
Q

The clonic phase results in the seizure discharge being ________ with intermittent ________ that diminish

A

interrupted; contractions

141
Q

Increase in the number of seizure = increase in ____________

A

brain damage

142
Q

What causes seizure cessation?

A

epileptogenic neurons becoming exhausted

143
Q

During a seizure, reduced oxygen to the brain forces cells to switch to __________ metabolism which causes a _____ ______ accumulation

A

anaerobic; lactic acid

144
Q

Cerebral blood flow (CBF) is related to 3 injury states: 1) inadequate cerebral p________ 2) normal perfusion but with elevated _______ ______ (ICP) 3) excessive ________ volume (CBV)

A

perfusion; intracranial pressure (ICP); blood volume (CBV)

145
Q

What is a normal ICP?

A

1-15 mmHg

146
Q

ICP results from an increase in intracranial _____ (ie. due to tumour, edema, hemorrhage)

A

content

147
Q

With increased content, something must be _________. First it is _______.

A

removed; CSF

148
Q

Continued high ICP results in cerebral blood _____ and _____ alterations

A

volume and flow

149
Q

Increased ICP results in the ______ stages of ____ that lead to death

A

4 stages of ICP

150
Q

Stage 1 ICP is characterized by cranial ______ and systemic adjustments to decrease ICP

A

vasoconstriction

151
Q

Stage 1 involves no detectable _____ of ICP

A

symptoms (person is awake, alert, with equal and reactive pupils, normal breathing, with normal pulse and BP)

152
Q

In Stage 2 ICP, intracranial contents continue to ______ and the ICP has _______ compensatory mechanisms (stage 1)

A

expand; exceeded

153
Q

With stage 2 ICP: pressure begins to affect neuron __________

A

oxygenation

154
Q

What are the manifestations of stage 2 ICP?

A

-confusion
-restlessness
-lethargy

155
Q

In stage 2 ICP, pupils and breathing are…

A

normal

156
Q

Surgical intervention is best during stage ___

A

2

157
Q

Autoregulation

A

mechanism to alter diameter of intracranial blood vessels to maintain a constant blood flow during ICP changes

158
Q

Autoregulation is lost in stage ____

A

3

159
Q

In stage 3, ICP approaches _______ pressure

A

arterial

160
Q

In stage 3, _______, ________, and acidosis occur which deteriorate the condition

A

hypoxia; hypercapnia

161
Q

In stage 3 the pupils are…

A

small and sluggish

162
Q

During stage 3, pulse pressure ________

A

widens

163
Q

Manifestations of stage 3 ICP:

A

-loss of peripheral vision/blindness
-tinnitus

164
Q

Surgical intervention is ________ in stage 3

A

needed

165
Q

During stage 4, brain tissue ______ from greater pressure to lesser pressure

A

herniates

166
Q

Herniated brain tissue results in a _______ of blood supply

A

reduction

167
Q

What do herniations rapidly increase?

A

ICP

168
Q

During stage 4, the pupils have progressed to…

A

bilateral dilation and fixation

169
Q

What is the breathing pattern during stage 4?

A

Cheyne-stokes

170
Q

During stage 4, mental status progresses to…

A

a deep coma

171
Q

Surgical intervention during stage 4 is _______

A

futile (pointless)

172
Q

_______ results from stage 4

A

death

173
Q

What are the 3 types of cerebral edema?

A
  1. vasogenic
  2. cytotoxic
  3. interstitial
174
Q

Which type of cerebral edema is the most important?

A

vasogenic

175
Q

What causes vasogenic edema?

A

-increased capillary permeability
-BBB disruption

176
Q

During vasogenic edema, _____ ______ leak into the cranial ECF

A

plasma proteins

177
Q

During vasogenic edema, fluid accumulates in the ______ matter which leads to the separation of __________ fibers

A

white; myelinated

178
Q

What are the manifestations of vasogenic edema?

A

-consciousness disturbances
-ICP increase

179
Q

How is vasogenic edema resolved?

A

slow diffusion

180
Q

During cerebral edema the lateral ventricles are ______ and the gyri are ______

A

compressed; flattened

181
Q

Cytotoxic edema aka ______ edema

A

metabolic

182
Q

During cytotoxic edema, toxic factors affect neural, glial, and endothelial cells which results in the loss of ______ transport mechanisms

A

active

183
Q

Cytotoxic edema results from a loss of ____ and a gain of ____ which cause the cells to _____

A

K+, Na+, swell

184
Q

Interstitial edema results from the movement of ____ from ventricles into the interstitial space

A

CSF

185
Q

Interstitial edema causes a fluid increas around the ventricles which increases pressure in the _____ matter, causing ________ to disappear

A

white; myelination

186
Q

What is hydrocephalus?

A

condition of excess CSF into the ventricles or subarachnoid space

187
Q

What are 3 things that can cause hydrocephalus?

A
  1. Increased CSF production
  2. Obstruction in ventricles
  3. Defective reabsorption of CSF into systemic blood
188
Q

Hydrocephalus can be ___________ or __________

A

communicating or non-communicating

189
Q

What is “communicating” hydrocephalus?

A

when CSF can still flow between the ventricles

190
Q

Communicating hydrocephalus is caused by ________

A

infection

191
Q

Communicating hydrocephalus can occur anytime from ___________ to adulthood

A

infancy

192
Q

Communicating hydrocephalus is caused by impaired ___________ of CSF from the ______________ space

A

absorption; subarachnoid

193
Q

Non-communicating hydrocephalus only occurs in ________

A

adults

194
Q

Non-communicating hydrocephalus is caused by ___________ of CSF between ventricles

A

obstruction

195
Q

Non-communicating hydrocephalus is congenital meaning…

A

it is present from birth

196
Q

What does an obstruction of CSF do when it increases pressure in the brain?

A

causes dilation of the ventircles and atrophy of the cerebral cortx

197
Q

Hydrocephalus causes the degeneration of ________ matter

A

white

198
Q

Acute hydrocephalus results in a rapidly increasing _____ and places the person in a deep _____

A

ICP; coma

199
Q

Normal pressure hydrocephalus involves the dilation of ventricles without increased __________

A

pressure

200
Q

Normal pressure hydrocephalus develops _______

A

slowly

201
Q

What symptoms does the family notice with normal pressure hydrocephalus?

A

decline in memory

202
Q

Normal pressure hydrocephalus appears as a triad of symptoms that are: ______-_____ gate, f_______, in____________

A

broad-based gate, falling, incontinence

203
Q

How is hydrocephalus treated?

A

shunting - bypasses CSF into normal channels where it can be absorbed

204
Q

Shunt placement for hydrocephalus is one of ______ most common neurosurgical procedures

A

three

205
Q

Normal muscle tone has a slight ________ to passive movement, is smooth, constant, and even

A

resistance

206
Q

What is hypotonia?

A

decreased muscle tone

207
Q

People with hypotonia get _____ easily and have difficulty rising from a _______ position

A

tired; sitting

208
Q

Hypotonia causes muscle atrophy and muscles appear ________ and flat

A

flabby

209
Q

People with hypotonia have _____________ joints

A

hyperflexible

210
Q

What is hypertonia?

A

increased muscle tone

211
Q

Hypertonia causes increased _______ with passive movement

A

resistance

212
Q

What are the symptoms of hypertonia?

A

-enlarged muscle mass
-firm muscles
-muscle spasms

213
Q

___________ is a neurotransmitter that in high or low amounts can cause alterations in muscle movement

A

dopamine

214
Q

Some muscle disorders are ___________

A

neurological

215
Q

What is hyperkinesia?

A

excessive, purposeless muscle movement

216
Q

What are the 3 types of hyperkinesia?

A
  1. paroxysmal dyskinesia
  2. tardive dyskinesia
  3. ballism
217
Q

With paroxysmal dyskinesia, muscle movement occurs as _________

A

spasms

218
Q

Tardive dyskinesia occurs as involuntary movement of the _____, lips, tongue, and __________

A

face, lips, tongue, extremities

219
Q

________ dyskinesia is often caused by prolonged antipsychotic medication

A

Tardive

220
Q

Tardive dyskinesia appears as rapid repetitive ___________ movements like continually _______ or tongue protrusions

A

stereotypical; chewing

221
Q

Tourette syndrome is a type of _______ dyskinesia

A

tardive

222
Q

What is Ballism?

A

a muscle disorder with wild flinging movements of the limbs

223
Q

What is another name for Huntington’s disease?

A

chorea

224
Q

Huntington’s disease symptoms are a hallmark of ____________

A

hyperkinesia

225
Q

Huntington’s disease involves which areas of the brain?

A

basal ganglia and cerebral cortex

226
Q

What age does the onset of Huntington’s disease occur?

A

25-45 years

227
Q

Huntington’s disease involves involuntary fragmented movements of the _____ and ____ (eventually whole body), slowed ______, and alterations in euphoria and ________.

A

face and arms; thinking; depression

228
Q

Huntington’s disease is inherited by an autosomal _________ trait

A

dominant

229
Q

With HD, there is a mutation on chromosome ___ that results in an abnormally ______ protein caused by a cytosine-adenine-guanine (CAG) trinucleotide.

A

4; long

230
Q

The altered protein chain created by the HD mutation is ______ to neurons

A

toxic

231
Q

What determines the onset age of HD?

A

the number of repeated amino acid chains (increased chains = increased protein toxicity = earlier onset)

232
Q

A heathy gene repeats ____-____ times.

A

10-26

233
Q

Hypokinesia is…

A

loss of voluntary movement despite perceived consciousness (↓ amplitude of movement)

234
Q

What are the two types of hypokinesia?

A

akinesia and bradykinesia

235
Q

Akinesia is a _____ of spontaneous movement (facial expressions) or associated movements (_________ while walking)

A

lack; arm swinging

236
Q

Bradykinesia is the slowing of ________ movements

A

performed

237
Q

What are the manifestations of Parkinson’s disease?

A

-resting tremor
-rigidity
-bradykinesia
-dysarthria (difficulty speaking)

238
Q

Dysarthria

A

slurred speech due to lost control of speech muscles

239
Q

What is an early symptom of Parkinson’s disease?

A

loss of smell

240
Q

When tilting, people with PD often fall like a post because they can’t make proper _________ adjustments.

A

postural

241
Q

Amyotrophic Lateral Sclerosis (ALS) aka ______________ disease

A

Lou Gehrig’s

242
Q

ALS involves degeneration of which type of neurons?

A

upper and lower motor neurons

243
Q

How does ALS affect upper motor neurons?

A

-decrease in large motor CNS neurons
-demyelination, glia proliferations, sclerosis of neurons

244
Q

Sclerosis = _______

A

scarring

245
Q

How does ALS affect lower motor neurons?

A

denervation of motor units

246
Q

Symptoms of ALS:

A

-muscle weakness starting in arms and legs
-difficulty speaking and swallowing

247
Q

Does ALS involve mental or sensory symptoms?

A

no

248
Q

How is ALS treated?

A

Rilutek medication

249
Q

What is the purpose of Rilutek for ALS?

A

extend the time before ventilatory support is needed