Chapter 15 Flashcards
1
Q
What is cognitive behavioural functional competence?
A
Integrated processes of cognitive, sensory and motor systems
2
Q
Full Consciousness
A
State of awareness of oneself and appropriate responses to the environment
3
Q
What are the 2 components of Consciousness?
A
Arousal
Awareness
4
Q
Arousal
A
State of awakeness
5
Q
Awareness
A
Content of thought
6
Q
How are structural alterations divided?
A
According to their location of dysfunction
7
Q
What are the 2 divisions of structural alterations?
A
Supratentorial disorders
Infratentorial disorders
8
Q
What are Supratentorial disorders?
A
Above tentorium cerebelli
-Produces changes in arousal
9
Q
What are Infratentorial disorders?
A
Below tentorium cerebelli
-Produces decline in arousal by dysfunction of the reticular activating system or brainstem
10
Q
What do metabolic alterations in arousal produce?
A
Disorders produce a decline in arousal by alterations in the delivery of energy substrates
11
Q
What are the five patterns of neurological functions?
A
- Level of consciousness
- Pattern of breathing
- Pupillary reaction
- Oculomotor responses
- Motor responses
12
Q
What is the most critical index of the nervous system function?
A
level of consciousness
13
Q
What do changes in the level of consciousness indicate?
A
Indicate improvement or deterioration
14
Q
What is the highest level of consciousness?
A
Person is alert and oriented to oneself, others, place and time
15
Q
How does the level of consciousness diminish from the normal state level?
A
Normal state level —> confusion —> Disorientation —> Coma
16
Q
What is normal breathing?
A
Rythmic pattern
17
Q
How does breathing respond to consciousness diminishing?
A
Breathing responds to changes in PaCO2 levels
18
Q
What is Cheyne-Stokes?
A
Altered period of tachypnea and apnea directly related to PaCO2
19
Q
What are other patterns related to reduced arousal related to breathing?
A
Apneusis
Ataxic breathing
20
Q
Apneusis
A
Prolonged inspiratory time and a pause before expiration
21
Q
Ataxic breathing
A
Complete irregularity of breathing with increasing periods of apnea
22
Q
What does Pupillary reaction indicate?
A
Presence/level of brainstem dysfunction
23
Q
The brainstem area that controls arousal also controls?
A
Pupils
24
Q
What happens to the pupils during Ischemia?
A
Dilated/fixed pupils
25
What happens to the pupils during Hypothermia or opiates?
Pinpoint pupils
26
What changes at various levels of brain dysfunction?
Oculomotor responses
-resting, spontaneous and reflexive eye movements
27
What is the normal oculomotor response?
Eyes move together to side opposite from the turn of the head
28
What is the abnormal oculomotor response?
Eyes do not turn together
29
What is the absent oculomotor response?
Eyes move in the direction of head movement
30
What is the caloric Ice water test?
Ice water is injected into the ear canal to test oculomotor responses
31
What is a normal oculomotor response to the caloric ice water test?
Eyes turn together to the side of the head where ice water is injected
32
What is an abnormal oculomotor response to the caloric ice water test?
Eyes do not move together
33
What is an absent oculomotor response to the caloric ice water test?
No eye movement
34
What do motor responses determine?
Determines brain function and indicates the most severely damaged side of the brain
35
What are the 3 possible patterns of motor response?
1. Purposeful
2. Inappropriate, generalized movement
3. Not present
36
What do motor signs indicate a loss of?
Cortical inhibition
37
What does a loss of cortical inhibition mean?
Decreased consciousness associated with the performance of primitive reflexes and rigidity (paratonia)
38
What is vomiting, yawning and hiccups?
Complex reflex-like motor responses integrated in the brainstem
39
A compulsive/repetitive production of vomiting, yawning and hiccups is caused by what?
A dysfunction of medulla oblongata
40
What are the two categories of outcomes of alterations in arousal?
Disability (morbidity) and mortality
41
What do outcomes of alterations in arousal depend on?
Cause
Damage
Duration of coma
42
What happens to some individuals who never retain consciousness?
Neurological death
43
What are the 2 forms of neurological death?
1. Brain death
2. Cerebral death
44
What is the neurological determination of death (NDD)?
Total brain death
45
What is brain death/
Brain is damaged and can't recover (irreversible) and can no longer maintain homeostasis
46
What is the Canadian criteria for NDD?
1. Unresponsive coma
2. No brainstem functions
3. No spontaneous respiration (apnea)
47
What parts of brain die during cerebral death?
Cerebral hemispheres die
-Brainstem and cerebellum still alive
48
What is cerebral death?
Irreversible coma
Permanent brain damage in which an individual never responds in a significant way. May continue to maintain homeostasis
49
What are the cerebral death states?
1. Persistent vegetative state
2. Minimally conscious state (MSC)
3. Locked in Syndrome
50
What is a persistent vegetative state?
Complete unawareness of self or environment
Does not speak
Sleep-wake cycles present
cerebral function absent
51
What is a Minimally conscious state (MSC)?
Follow simple commands
Manipulate objects
Give yes/no responses
52
What is locked in syndrome?
Complete paralysis of voluntary muscles except for eye movement
Intact content of thought and level of arousal
Fully conscious
Blinking = communication
53
What is awareness?
Content of thought
54
What does awareness encompass?
All cognitive function
55
What mediates awareness?
Executive Attention Networks (EAN)
56
What are Executive Attention Networks (EAN)?
Networks include selective attention and memory and involve abstract reasoning, planning, decision-making, judgement and self-control
57
What is selective attention (orienting)?
Ability to select specific information and focus on related specific task
Also includes selective visual and auditory attention
58
What are the 3 executive attention deficits?
Initial detection
Mild deficit
Severe deficit
59
What is the initial detection of executive attention deficits?
Person fails to stay alert and orientate to stimuli
60
What is a mild deficit?
Grooming and social graces are lacking
61
What is a severe deficit?
Motionless
Lack of response
Doesn't react with surroundings
62
What are some characteristics of executive attention deficits?
Inability to maintain sustained attention and inability to set goals and recognize when the goal is achieved
63
What is memory?
Recording, retention and retrieval of information
64
What is amnesia?
Loss of memory
65
What is retrograde amnesia?
Difficulty retrieving past memories
66
What is anterograde amnesia?
Inability to form new memories
67
What are Data-processing deficits?
problems associated with recognizing and processing sensory information
68
What are the 5 states of data-processing deficits?
1. Agnosia
2. Dysphasia
3. Acute Confusional State and delirium
4. Dementia (Alzheimer's)
5. Frontotemporal Dementia
69
What is Agnosia a defect of?
Pattern recognition
70
What is Agnosia?
Failure to recognize the form and nature of objects
-Normally one sense affected
71
Example of agnosia?
Unable to identify a safety pin by touching it but able to name it when looking at it
72
What is agnosia associated with?
Cerebrovascular accidents in specific brain areas
73
What is Dysphasia?
Impairment of comprehension or production of language
74
What are the two types of dysphasia?
Expressive dysphasia
Receptive dysphasia
75
What area of the brain is affected to cause expressive dysphasia?
Broca's area
76
What is expressive/Broca dysphasia?
Loss of ability to produce spoken or written language
-Verbal comprehension is usually present
77
What area of the brain is affected to cause Receptive dysphasia?
Wernicke's area
78
What is Receptive/Wernicke dysphasia?
inability to understand written or spoken language
Speech is fluent but words and phrases have no meaning
79
The pathology of dysphasia is due to what?
The occlusion of the middle cerebral artery
80
What is the middle cerebral artery?
One of three major arteries supplying blood to the brain
81
What are the Acute Confusional States and Delirium?
Transient disorders of awareness may have a sudden or gradual onset.
82
What causes acute confusional states and delirium?
Drug intoxication, alcohol withdrawal, post anesthesia
and electrolyte imbalance
83
What areas of the brain are disrupted to cause acute confusional states?
Reticular system
Thalamus
Cortex
Limbic system
84
What is delirium?
Hyperactive Acute confusional state
85
Where does delirium most commonly occur?
In Critical Care units over 2-3 days
86
What is disrupted to cause delirium?
Neurotransmitters: acetylcholine and dopamine
87
What is Excited Delirium Syndrome?
AKA agitated delirium
Hyperkinetic delirium that can lead to sudden death
88
What are the signs/symptoms of Excited Delerium Syndrome?
Rapid breathing
High pain tolerance
Superhuman strength
89
How does delirium manifest?
Terrifying dreams
Hallucinations
Gross alteration of perception
Individuals can't sleep
90
How is delirium evaluated?
CAM-ICU: Confusion Assessment Method for Intensive Care Unit (ICU)
91
What is dementia?
Deterioration/progressive failure of many cerebral functions
92
What causes dementia?
Cerebral neuron degeneration, atherosclerosis and genetics
93
Does dementia have a cure?
No specific cure exists
-help the family to understand
94
How is dementia treated?
Maximizing remaining capacities
95
What is Alzheimer's disease?
The leading cause of severe cognitive dysfunction in older adults
96
What is the cause of Alzheimer's?
The exact cause is unknown
97
What are the three forms of Alzheimer's?
1. Nonhereditary sporadic late-onset AD
2. Early-onset Familial AD
3. Early-onset AD
98
What is the most common form of Alzheimer's?
Nonhereditary sporadic late-onset AD
70%-90%
-Has no specific genetic association
99
What is early-onset familial AD linked to?
Chromosomal 21 mutations
100
What form of Alzheimer's is very rare?
Early-onset AD
101
What is Early-onset AD linked to?
Chromosomal 19 mutations
102
What is the same across all forms of Alzheimer's?
Pathological alteration
103
What accumulates to lead to Alzheimer's?
Accumulation of toxic fragments of amyloid plagues
104
What is there a loss of to lead to Alzheimer's?
Loss of acetylcholine in forebrain cholinergic neurons
105
What are amyloid plagues?
Aggregates of misfolded proteins
106
What happens when there is a loss of acetylcholine in forebrain cholinergic neurons?
Death of neurons
107
What increases neural death to cause Alzheimer's?
Tau proteins (microtubule) form neurofibrillary tangles within the neuron
108
Where are neuroibrullary tangles concentrated?
In the cerebral cortex
109
As neural death increases what happens to the brain?
Brain atrophy via widening of sulcus and shrinking of gyrus
Sulcus = grooves
Gyrus = Folds on the outermost layer of the brain
110
What are the first symptoms of Alzheimer's?
Memory loss
Impaired learning
111
How do symptoms of Alzheimer's continue?
Decrease in language, reasoning, social behaviour, dyspraxia (loss of movement and coordination) may occur
112
What is ALzheimer's progression of?
Short-term memory loss to total loss of cognitive function
113
When can pathophysiological changes occur in dementia?
Decades before dementia
114
What is Frontotemporal dementia?
Previously known as Pick Disease
115
What is the second most common form of dementia?
Frontotemporal dementia
116
What is Frontotemporal dementia an umbrella term for?
Disorders that affect frontal and temporal regions of the brain
117
What are the first symptoms of Frontotemporal dementia?
Apathy
Poor judgement/reasoning
Break laws
118
Does genetics determine frontotemporal dementia?
There is a genetic component
119
When does the onset of frontotemporal dementia occur?
At less than 60 years old
120
What genes are mutated in frontotemporal dementia?
Mutation of tau encoding genes
121
What do seizures represent?
Represent a manifestation of a disease, not a specific
122
What are seizures?
Sudden disruption in brain electrical function caused by abnormal excessive discharges of cortical neurons (interneurons)
123
What is Epilepsy?
Recurrence of seizures where no known cause for seizures can be found
124
What are convulsions?
Jerky, contact-relax movements associated with seizures?
125
What is the probable cause of seizures in young adults?
Alcohol/drug withdrawal
Brain tumour
Peri-natal insults (occurring between 28 weeks of gestation to 28 days after birth)
126
What is the probable cause of seizures in older adults?
Alcohol/drug withdrawal
Metabolic disorders
CNS degeneration
127
What is the epileptogenic focus?
Brain site where the seizure originates
-aka Epileptogenic zone
128
What happens to neurons in the epileptogenic focus?
They are hypersensitive and activated by numerous stimuli
Fire more frequently and with greater amplitude than other neurons
129
During a seizure what can the focus be determined by?
Activated SPECT
-a test that detects blood flow changes in the brain
130
What are the 2 phases of a seizure?
Tonic
Clonic
131
What is the tonic phase?
Muscle contraction with increased muscle tone
– associated with loss of consciousness
132
What is the clonic phase?
Alternating contraction and relaxation of muscles
133
What does the clonic phase begin with?
Begins when inhibitory neurons in thalamus and basal ganglia react to cortical excitation
134
What is the result of the clonic phase?
Seizure discharge is interrupted = intermittent contractions that diminish and finally cease
135
If the number of seizures increases, what else increases?
Brain damage
136
How do seizures end?
Epileptogenic neurons are exhausted
137
What happens to the brain during the clonic phase?
Reduced oxygen causes a switch to anaerobic metabolism and an accumulation of lactic acid
138
What are the 3 injury states that Cerebral Blood Flow (CBF)?
1. Inadequate cerebral perfusion
2. Normal perfusion but with elevated intracranial pressure (ICP)
3. Excessive blood volume (CBV)
139
What is normal ICP?
1-15 mmHg
140
How does increased ICP occur?
Increase in intracranial content
-Tumour, edema, hemorrhage, etc.
141
What is displaced to try to make room for the increased intracranial content?
Cerebral spinal fluid
142
What happens when high ICP continues?
Alterations in cerebral blood volume and blood flow
143
What is the result of increased ICP?
Four stages of ICP that lead to Death
144
What is Stage 1 increased ICP?
Cranial vasoconstriction and systemic adjustments result in a decrease in ICP
ICP does not increase due to these compensations
No detectable symptoms of ICP
145
What is Stage 2 increased ICP?
Continual expansion of intracranial contents = ICP exceeds compensatory mechanisms
Pressure begins to affect neuron oxygenation
Manifestations of confusion, restlessness and lethargy
Pupils and breathing remain normal
Surgical intervention is best here
146
What is Stage 3 increased ICP?
Autoregulation: mechanism to alter diameter of intracranial blood vessels to
maintain a constant blood flow during changes in ICP
˜ Autoregulation is lost in Stage 3 = ICP approaches arterial pressure
˜ Severe hypoxia, hypercapnia and acidosis occur = severe deterioration of individual condition
˜ Pupils: small, sluggish
˜ Widening of pulse pressure
˜ Manifestations of loss of peripheral vision/blindness, tinnitus
˜ Surgical intervention needed here
147
What is stage 4 increased ICP?
˜ Brain tissue shifts (herniates) from greater pressure to lesser pressure
˜ Herniated brain tissue = reduction in blood supply
˜ Herniations rapidly increases ICP
˜ Pupils: progress to bilateral dilation and fixation
˜ Breathing: Cheyne-Stokes breathing /Mental status: progresses to deep coma
˜ Surgical intervention futile here / Death occurs
148
What are the 3 types of cerebral edema?
Vasogenic edema
Cytotoxic (metabolic) edema
Interstitial edema
149
What is most important type of edema?
Vasogenic
150
What causes vasogenic edema?
Increased capillary permeability
Disruption of BBB
151
What leaks into cranial ECF during Vasogenic edema?
Plasma proteins/fluid
152
What happens when fluid accumulates in white matter during vasogenic edema?
Separation of myelinated fibers
153
How does Vasogenic edema manifest?
Consciousness disturbances and increases in ICP
154
What is the resolution to Vasogenic edema?
Slow diffusion
155
What is brain edema?
Lateral ventricles compressed (long
arrows)
Gyri flattened (short arrows)
156
What is cytotoxic (metabolic) edema?
Toxic factors affect neural, glial, and endothelial cells = loss of active transport mechanisms
= loss of K+ and gain large amounts of Na+ = change in intracellular osmolarity = cells swell
157
What is interstitial edema?
Movement of cerebral spinal fluid from ventricles into interstitial space = edema
fluid volume increases around ventricles = increased pressure within white matters = disappearance of myelination
158
What is Hydrocephalus?
Condition of excess cerebral spinal fluid (CSF) in
ventricles or subarachnoid space.
159
What causes Hydrocephalus?
Increased CSF production
obstruction in ventricles
defective reabsorption of CSF fluid into systemic blood
160
What are the types of Hydrocephalus?
Communicating
Noncommunicating
161
What does 'communicating' mean?
refers to fact that CSF can still flow between the ventricles
162
Who is affected by communicating hydrocephalus?
Infancy through adulthood
163
What is communicating hydrocephalus?
Impaired absorption of CSF from
subarachnoid space
164
What causes communicating hydrocephalus?
Infection
165
Who is affected by noncommunicating hydrocephalus?
Adults
166
What is noncommunicating hydrocephalus?
Obstruction of CSF between ventricles
167
What causes noncommunicating hydrocephalus?
Congenital
-present from birth
168
What leads to Hydrocephalus (HC)?
Obstruction of CSF flow = increase pressure and dilation of ventricles
= atrophy of cerebral cortex and degeneration of white matter
169
How does acute hydrocephalus manifest?
Rapidly developing ICP = deep coma
170
How does normal pressure HC manifest?
Dilation of ventricles without increased pressure
HC develops slowly
Family notices declines in memory, etc.
Progression to triad symptoms: broad- based gate / falling / incontinence
171
How is Hydrocephalus treated?
Shunting procedure
172
What is the shunting procedure?
Shunt used for ventricular bypass into normal intracranial/extracranial channels where fluid can be absorbed
-One of three most common neurosurgical procedures
173
What is normal muscle tone?
Slight resistance to passive movement
resistance is smooth, constant, and even.
174
What is Hypotonia?
Decreased muscle tone
Tire easily
Difficulty rising from a sitting position
Muscle mass atrophy/muscles appear flabby and flat
Joints hyperflexible (can acquire positions requiring extreme joint mobility)
175
What is Hypertonia?
Increased muscle tone
Passive movement occurs with increased
resistance
Symptoms: enlargement of muscle mass, development of firm muscles, muscle spasms
176
What causes alterations in Muscle Movement?
1. Neurotransmitter dopamine involved in several disorders (too little or too much dopamine)
2. Other disorders are neurological disorder = excessive or insufficient movement
177
What is Hyperkinesia?
Excessive, purposeless movement
178
What are the 3 types of Hyperkinesia?
Paroxysmal dyskinesias
Tardive dyskinesias
Ballism
179
What is Paroxysmal dyskinesias?
Involuntary movements that occur as spasms
180
What is Tardive dyskinesias?
Involuntary movement of face, lips, tongue and extremities
181
What causes tardive dyskinesias?
Prolonged antipsychotic medication use
182
What is a characteristic of tardive dyskinesias?
Rapid, repetitive stereotypical movements
-Continually chewing, or tongue protrusions
183
What syndrome is associated with tardive dyskinesias?
Tourette Syndrome
184
What is Ballism?
Muscle disorder with wild, flinging movement of limbs
185
What is the other name for Huntington's disease?
Chorea
186
What is HD symptoms the hallmark of?
Hyperkinesia
187
What is Huntington's disease?
relatively rare degrative hyperkinetic disorder
188
What part of brain is involved in Huntington's?
Basal ganglia and cerebral cortex
189
When is the onset of HD?
25-45 years old
190
What is the most common manifestation of huntington's disease?
Begins in face and arms and eventually whole body is affected
191
What are manifestations of HD?
Thinking is slow
Alterations in euphoria and depression are common
Involuntary fragmented movements
192
How does one get Huntington's?
Inherited
-Autosomal dominant trait
193
What causes Huntington's?
Mutation in chromosome 4 results in abnormally long protein caused by a cytosine-adenine-guanine (CAG) trinucleotide
194
The altered amino acid chain in HD does what to neurons?
It is toxic to neurons
195
How is the age of onset of HD determined?
by the number of repeated amino acid chains
= increased chains = increased toxicity of protein = earlier age of onset.
196
How many repeats does a healthy gene have vs HD gene?
Healthy = 10-26 repeats
HD = 37-80
197
What is Hypokinesia?
Decreased movement
Loss of voluntary movement despite preserved consciousness
198
What are the 2 types of Hypokinesia?
Akinesia
Bradykinesia
199
What is Akinesia?
lack of spontaneous movement (facial expressions) or associated movements (arm swinging while walking)
200
What is Bradykinesia?
Slowing of movement
201
What is Parkinson's?
Complex motor disorder accompanied by systemic nonmotor and neurological symptoms
202
What is Primary parkinson's?
Begins after 40 yoa with increased incidence after 60 years old
-Leading cause of neurological disability in people over 60 yoa
203
What is Secondary PD?
Parkinson’s caused by disorder other than PD (head trauma, infections, toxins, medication intoxication)
204
What is the most common secondary PD?
Medication intoxication
-Most often reversible
205
What medications lead to medication intoxication?
-Neuroleptics: antipsychotics (treat hallucinations, delusions, etc.)
-Antiemetics: prescribed to address nausea and vomiting
-Anti-hypertensives
206
What is Parkinson's disease due to?
Several gene mutations
207
What causes PD?
Basal ganglia dysfunction due to misfolded proteins
208
What do misfolded proteins due in regards to PD?
Loss of dopamine-producing neurons in substantia nigra
209
What causes tremors and rigidity associated with PD?
Loss of dopamine (inhibitory neurotransmitter) and excess production of cholinergic (excitatory neurotransmitters)
210
What is the classic manifestation of PD?
resting tremor, rigidity, bradykinesia
(slowness of movement), dysarthria
211
Dysarthria
loss of control of muscles you speak
with = slurring speech
212
What can be an early symptom of PD?
Loss of smell
213
What can't people with PD make adjustments to?
Tilting
-Fall like a post
214
What is the principal feature of ALS/Lou Gehrig's?
Degeneration of both lower and upper motor neurons
215
What happens to upper motor neurons in ALS?
Decrease in large motor neurons in CNS
-Motor neurons death results in demyelination and glia proliferations and sclerosis (scarring)
216
What happens to lower motor neurons in ALS?
Denervation of motor units
217
How does ALS manifest?
-Muscle weakness starting in arms and legs and
progressing to difficulty speaking and swallowing
-No associated mental or sensory symptoms
218
How is ALS treated?
Medication Rilutek extends time before ventilatory
assistance is required
