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Pathophysiology > Chapter 15 - Alteration In Cognitive Systems, Cerebral Hemodynamics And Motor Function > Flashcards

Chapter 15 - Alteration In Cognitive Systems, Cerebral Hemodynamics And Motor Function Flashcards

1
Q

Cogntivie behavioural functional competence =

A

Integrated processes of cognitive, sensory and motor systems

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2
Q

Systems get manifested through motor network =

A

Behaviours that are appropriate to human activity

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3
Q

Full consciousness

A

State of awareness of oneself and appropriate responses to envuroennt

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4
Q

Two components of consciousness

A

Arousal (awake) and awareness (thought)

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5
Q

Structural alterations are divided according to their

A

Location of dysfunction

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6
Q

Supratentorial disorders

A

Produce changes in arousal
-above tentorium cerebelli

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7
Q

Infratentorial disorders

A

Produce decline in arousal by dysfunction of reticular activating system or brain stem
-below tentorium cerebelli

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8
Q

Metabolic alterations

A

Disorders procuring a decline in arousal by alterations in delivery of energy substrates

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9
Q

Five patterns of neurological functions critical to evaluation process

A
  1. Level of consciousness
  2. Pattern of breathing
  3. Pupillary reaction
  4. Oculomotor response
  5. Motor response
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10
Q

Msot critical index of nervous system function

A

Level of consciousness

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11
Q

Level of consciousness

A

Changes = improvement or deterioration
-person alert/orientated to oneself, place, others, and time

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12
Q

Level of consciousness: from normal state level it diminishes to

A

Confusion —> disorientation —> coma

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13
Q

Pattern of breathing: normal breathing =

A

Rhythmic pattern

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14
Q

Pattern of breathing: when consciousness diminishes =

A

Breathing repsonds to changes in PaCO2 levels

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15
Q

Cheyne stokes

A

Altered periods of tachypnea and apnea directly related to PaCO2

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16
Q

Apneusis

A

Prolonged inspiratory time and a pause before expiration

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17
Q

Ataxic breathing

A

Complete irregularity of breathing with increasing periods of apnea

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18
Q

Pupillary reaction indicates..

A

Indicate presence or level of brain stem dysfunction

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19
Q

Brain stem area controlling arousal is adjacent

A

To area controlling pupils

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20
Q

Pupillary reaction in ischemia

A

Dilated or fixed pupils

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21
Q

Pupillary reaction in hypothermia/opiates

A

Cause pinpoint pupils

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22
Q

Oculomotor response :

A

Resting, spontaneous and reflexive eye movements change at various levels of brain dysfunction

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23
Q

Oculomotor response : normal response

A

Eyes move together to side opposite from turn of head

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24
Q

Oculomotor response : abnormal response

A

Eyes do not turn together

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25
Q

Oculomotor response : absent response

A

Eyes move in direction of head movement

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26
Q

Oculomotor response : caloric ice water test

A

Ice water injected into ear canal

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27
Q

Oculomotor response : caloric ice water test: normal response

A

Eyes turn together to side of head where ice injected

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28
Q

Oculomotor response : caloric ice water test : abnormal response

A

Eyes do not move together

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29
Q

Oculomotor response : caloric ice water test : absent response

A

No eye movement

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30
Q

Motor responses determine

A

Brain dysfunction and indicates most severely damaged side of brain

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31
Q

Motor response: pattern of response may be

A
  1. Purposeful
  2. Inappropriate or generalized movement
  3. Not present
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32
Q

Motor signs indicating loss of cortical inhibition =

A

Decreased consciousness
-associated with performance of primitive reflexes and rigidity

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33
Q

Paratonia

A

Rigidity
-involuntary resistance during passive movement

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34
Q

Vomiting, yawing and hiccups

A

Complicated reflex like motor responses integrated in brain stem
-dysfunction of medulla oblong = compulsive and receptive production of these responses

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35
Q

Coma Outcomes depend on

A

Cause, damage, and duration of coma
-some individuals never retain consciousness and experience neurological death

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36
Q

Brain death

A

-total brain death
Brain damaged—> irreversible —> cannot maintain homeostasis

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37
Q

NDD

A

Neurological determination of death

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38
Q

Canadian criteria for NDD

A
  1. Unresponsive coma
  2. No brain stem function
  3. No spontaneous respiration
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39
Q

Canadian criteria for NDD

A
  1. Unresponsive coma
  2. No brain stem function
  3. No spontaneous respiration
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40
Q

Cerebral death

A

Irreversible coma
-death of cerebral hemispheres (except for brain stem and cerebellum = remains homeostasis)

-permanent brain damage -> never responds in significant way

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41
Q

Persistent vegetative state

A

Complete unawareness of self or environment
-no speak or cerebral function
-sleep wake cycles present

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42
Q

MSC or minimally conscious state

A

Follow simple commands, manipulate object and give yes or no responses

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43
Q

Locked in syndrome

A

Complete paralysis of voluntary muscles except eye movement
-thought and arousal = fully conscious
-blinking is communication

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44
Q

Awareness if mediated by

A

Executive attention networks (EAN)

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45
Q

EAN networks

A

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

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46
Q

Selective attention

A

Ability to select specific information and focus on related specific task
-visual and auditory

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47
Q

Executive attention deficits: initial detection

A

Person fails to stay alert and orientate to stimuli

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48
Q

Executive attention deficits: mild deficit

A

Grooming and social graces are lacking

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49
Q

Executive attention deficits: severe deficit

A

Motionless, lack of response, doesn’t react with surroundings

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50
Q

Characteristics of executive attention deficits

A

Inability to maintain sustained attention
-inability to set goals and recognize when goal is achieved

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51
Q

Amnesia

A

Loss of memory

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52
Q

Retrograde amnesia vs anterograde amnesia

A

RETROGRADE- difficulty retrieving past memories

ANTEROGRADE- inability to form new memories

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53
Q

Data processing deficits

A

Problems associated with recognizing and processing sensory information

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54
Q

Agnosia

A

Defect of pattern recognition, form and nature of objects
-only one sense is affected

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55
Q

Agnosia is associated with

A

Cerebrovascular accidents to specific brain areas

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56
Q

Example of Agnosia

A

Unable to identify a safety pin by touching it but able to name it when looking at it

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57
Q

Dysphasia

A

Impairment of comprehension or production of language

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58
Q

Expressive dysphasia

A

Broca dysphasia
-loss of ability to produce spoken or written language
-verbally competent

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59
Q

Receptive dysphasia

A

Wernicke dysphasia
-inability to understand written or spoken language
-speech is fluent but has no meaning

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60
Q

Pathology of dysphasia

A

Occlusion of middle cerebral artery
-which is one of three major arteries supplying blood to brain

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61
Q

Acute confusional states and delirium

A

Transient disorders of awareness and may have a sudden or gradual onset

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62
Q

Causes of Acute confusional states and delirium

A

Drug intoxication, alcohol withdrawal, post anesthesia, electrolyte imbalance

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63
Q

Pathophysiology of Acute confusional states and delirium

A

Disruption of reticular system, thalamus, cortex and limbic system

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64
Q

Delirium most commonly occurs in

A

Critical care units over 2-3 days
-disruption of acetylcholine and dopamine

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65
Q

Delirium

A

Hyperactive acute confusional state

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66
Q

Excited delirium syndrome

A

Hyperkinetic can lead to sudden death
-rapid breathing, high pain tolerance, superhuman strength

“Agitated delirium”

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67
Q

Manifestations of Acute confusional states and delirium

A

Terrifying dreams, hallucination, gross alternation of perception
-cannot sleep

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68
Q

Evaluation for Acute confusional states and delirium

A

CAM-ICU or confusion assessment method for intensive care unit

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69
Q

Dementia

A

Deterioration/progressive failure of many cerebral functions

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70
Q

Cause of dementia

A

Cerebral neuron degeneration, atherosclerosis and genetics

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71
Q

Dementia manifestations

A

-no cure exists
-maximizing remaining capacities
-help family to understand

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72
Q

What is the Leading cause of severe cognitive dysfunction in older aldutls

A

Alzheimer’s (exact cause unknown)

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73
Q

Three forms of Alzheimer’s

A
  1. Non hereditary
  2. Early onset familial
  3. Early onset AD
74
Q

Non hereditary sporadic

A

-late onset 70 to 90 percent
-most common form
-no specific genetic association

75
Q

Early onset familial AD

A

Linked to chromosomal 21 mutations

76
Q

Early onset AD

A

Very rare
-linked to chromosomal 19 mutations

77
Q

Pathology of AD

A

Accumulation of toxic fragments of amyloid plagues

-loss of acetylcholine in forebrain cholingeric neurons causing death

78
Q

Pathology of AD

A

Accumulation of toxic fragments of amyloid plagues

-loss of acetylcholine in forebrain cholingeric neurons causing death

79
Q

Amyloid plagues

A

Aggregates of midfolded proteins

80
Q

After death of neurons in AD, what occurs

A

Tau proteins from neuroofibrillary tangles within the neuron, increasing neural death

81
Q

Where are neruofibrillary tangles concentrated

A

In cerebral cortex

82
Q

AD brain atrophy occurs via

A

Widening of sulcus (grooves) and shrinking gyrus (folds on outermost of brain)

83
Q

First symptom of AD

A

Memory loss and impaired learning

84
Q

Continuation of symptoms in AD

A

Language, reasoning, social behaviour, dyspraxia

85
Q

Dyspraxia

A

Loss of movement and coordination

86
Q

Pathophysiological changes can occur ___ before dementia syndrome

A

Decades

87
Q

Second most common form of dementia

A

Frontotemporal dementia otherwise known as pick disease

88
Q

Frontotemporal dementia (3)

A

Umbrella term for affecting frontal and temporal regions of brain
-mutation of tau encoding genes
-genetic, onset within <60 yoa

89
Q

First symptom of Frontotemporal dementia

A

Apathy, poor judgment and reasoning, break laws

90
Q

Seizures represent

A

Manifestation of disease, not a specific disease entity

91
Q

Seizure

A

Sudden disruption in brain electrical function caused by abnormal discharge of cortical neurons

92
Q

Epilepsy

A

Recurrence of seizures where no known cause for seizures can be found

93
Q

Convulsion

A

Jerky, contact relax movements associated with seizures

94
Q

Probable causes of seizures in YA

A

Alcohol, drug withdrawl, brain tumour, perinatal insults

95
Q

Probable causes of seizures in OA

A

Alcohol, drug withdrawl, metabolic disorders, CNS degeneration

96
Q

Focus

A

Brain site where seizure originates
-epileptogenic zone

97
Q

Epileptogenic focus

A

Neurons are hypersensitive and activates by numerous stimuli
-fire more frequently and w greater amplitude

98
Q

How can focus be determined during a seizure

A

Activated SPECT
-detecting blood flow changes in brain

99
Q

Tonic phase

A

Muscle contraction with inc muscle tone
-loss of consciousness

100
Q

Clonoc phase

A

Alternating contraction and relaxation of muscles

101
Q

Clonic phase begins when

A

Inhibitory neurons in thalamus and basal ganglia react to cortical excitation

102
Q

Clonic phase: seizure discharge is interrupted =

A

Intermittent contractions that diminish and finally cease

103
Q

Inc in # of seizures =

A

Inc in brain damage

104
Q

Seizure cessation is due to

A

Epileptogenic neurons being exhausted

105
Q

What happens when the brain has reduced oxygen

A

Switches to anaerobic metabolism and an accumulation of lactic acid

106
Q

Normal intracranial pressure

A

1-15 mmHg

107
Q

ICP results from increase in

A

Intracranial content
-tumour, deems, hemorrhage

108
Q

Inc content =

A

Something must be removed
-displacement of cerebral spinal fluid

109
Q

Continued high ICP =

A

Alterations cerebral blood volume and blood flow

110
Q

Four stages of ICP leads to

A

Death

111
Q

ICP stage one

A

Cranial vasoconstriction and systemic adjustment result in a decrease in ICP
-no detectable symptoms

112
Q

ICP stage 2

A

ICP exceeds compensatory mechanisms
-pressure affects neuron oxygenation
-confusion, restlessness, lethargy
-pupil + breathing normal

113
Q

Stage 2: surgical intervention is

A

Best here

114
Q

Auto regulation

A

Mechanism to alter diameter of intracranial blood vessels to maintain constant blood flow during changes in ICP

115
Q

Stage 3

A

-auto regulation is lost, approaches arterial pressure
-pupils: small, sluggish
-widening of pp

-loss of peripheral vision/blindness, tinnitus

116
Q

Stage 3

A

-auto regulation is lost, approaches arterial pressure
-pupils: small, sluggish
-widening of pp

-loss of peripheral vision/blindness, tinnitus

117
Q

Stage 3: surgical intervention is

A

Needed here

118
Q

ICP stage 4

A

Brain tissue shifts (herniates = inc ICP)
-reduction in blood supply
-pupils: bilateral dilation+fixation
-Cheyenne stokes
-progress to coma

119
Q

Surgical intervention in stage 4

A

Futile here, death occurs

120
Q

Most important type of cerebral edema

A

Vasogenic edema

121
Q

Brain edema

A

Lateral ventricles compressed
-gyri are flattened

122
Q

Causes of vasogenic edema

A

Increased capillary permeability, disruption of BBB

123
Q

Vasogenic edema

A

Plasma proteins and fluid leak into cranial ECF
-accumulates in white matter = separation of myelinated fibres

124
Q

Manifestation of vasogenic edema

A

Consciousness disturbances and increases in ICP

125
Q

Vasogenic edema resolution

A

Slow diffusion

126
Q

Cytotoxic edema

A

Toxic factors affects neural glial and endotherlial cells causing loss of active transport mechanisms

127
Q

Cytotoxic edema: loss of K+ and gain large amounts of Na+ causing…

A

Change in intracellular osmolarity and cells swell

128
Q

Interstitial edema

A

Movement of cerebral spinal fluid from ventricles into interstitial space

129
Q

Result of interstitial edema

A

Fluid volume increases around ventricles = inc pressure within white matters = disappearance of myelination

130
Q

Result of interstitial edema

A

Fluid volume increases around ventricles = inc pressure within white matters = disappearance of myelin at ion

131
Q

Hydrocephalus

A

Excess CSF in ventricles or subarachnoid space

132
Q

Cause of hydrocephalus

A

Inc CSF production, obstruction in ventricles, defective reabsorption of CSF fluid into systemic blood

133
Q

Communicating hydrocephalus

A

Infancy through adulthood
-impaired absorption of CSF from subarachnoid space

Usually due to infection

134
Q

Non communicating hydrocephalus

A

Adults
-obstruction of CSF between ventricles

Cause: congenital (present since birth)

135
Q

The word communicating refers to the fact that CSF can

A

Still flow between ventricles

136
Q

Obstruction of CSF flow =

A

Inc pressure and dilation of ventricles
-atrophy of cerebral cortex and degeneration of white matter

137
Q

Manifestation of acute HC

A

Rapidly developing ICP
-deep coma

138
Q

Manifestation of acute HC

A

Rapidly developing ICP
-deep coma

139
Q

Manifestation of normal pressure HC

A

Dilation of ventricles w/o inc pressure
-slow development
-decline in memory
-triad symptom progression

140
Q

TX HC

A

shunt procedure
-ventricular bypass into normal intracranial channels where fluid is absorbed

141
Q

___ is one of three most common neurosurgical procedures

A

Shunting

142
Q

Normal muscle tone is

A

Having slight resistant to passive movement
-resistant is smooth consistent and even

143
Q

Hypotonia

A

Dec muscle tone
-tire easily, have difficulty rising from sitting position
-muacsle mass atrophy, flabby and flat
-hyper flexible joints

144
Q

Hypertonia

A

Inc muscle tone
-increased resistance
-enlargement, firm muscles and muscle spams

145
Q

Two major causes for alterations in muscle movement

A
  1. Dopamine (too little or too much)
  2. Neurological disorders (excessive or insufficient movement)
146
Q

Two major causes for alterations in muscle movement

A
  1. Dopamine (too little or too much)
  2. Neurological disorders (excessive or insufficient movement)
147
Q

Hyperkinesia

A

Excessive, purposeless movement

148
Q

Paroxysmal dyskinesias

A

Involuntary movements that occur as spasms

149
Q

Tardive dyskinesias

A

Involunatary movement of face lips tongue and extremities
-antipsychotic medication
-rapid receptive stereotypical movements (chewing or tongue protrusions)

150
Q

Common example of tardive dyskinesias

A

Tourette syndrome

151
Q

Ballism

A

Muscle disorder with wild flinging movement of limbs

152
Q

Huntingtons disease (chorea)

A

hyperkinesia
-involves basal ganglia and cerebral cortex
25-45 yoa

153
Q

Manifestations of HD

A

Face and arms (eventually whole body)
-slow thinking, euphoria and depression
-involuntary fragmented movements

154
Q

Pathophysiology of huntingtons disease

A

Autosomal dominant trait
-mutant in chromosome 4 = abnormally long protein due to CAG trinucleotide
-alters aa = protein toxic to neurons

155
Q

Age of disease onset =

A

Number of recreated amino acids chains
-increased chains = inc toxicity of protein = earlier age of onset

156
Q

Hyperkinesia

A

Loss of voluntary moment despite preserved consciousness

157
Q

Akinesia

A

Lack of spontaneous movement (facial expressions) or associated movements (arm swinging while talking)

158
Q

Bradykinesia

A

Slowing of performed movements

159
Q

Parkinson’s disease

A

Complex motor disorder accomplished by systemic non motor and neurological symptoms

160
Q

Primary PD

A

Begins after 40 yoa with inc incidence after 60 yoa

161
Q

Primary PD

A

Begins after 40 yoa with inc incidence after 60 yoa

162
Q

What is the leading cause of neurological disability in people over 60 yoa

A

Primary PD

163
Q

Secondary PD

A

Parkinson’s caused by disorder other than PD
-head trauma, infections, toxins, medication intoxication

164
Q

What is the most common cause of secondary PD

A

Medicication intoxication
-reversible

165
Q

Medication intoxication PD is caused by

A

-neuroleptics (antispychotics, hallucinations, delusions)
-antiemetics
-anti hypertensives

166
Q

Pathophysiology of PD

A

Several gene mutations
-basal ganglia dysfunction due to msifolded proteins

167
Q

Result of PD

A

Loss of dopamine producing neurons in substantial nigra

168
Q

PD: loss of

A

Dopamine and excess production of cholinergic = symptoms of muscle tremors and rigidity

169
Q

Dopamine vs cholinergic

A

D- inhibitory

C- excitatory

170
Q

What are the tell tale symptoms of abnormal movement in Parkinson’s

A

Muscle tremors and rigidity

171
Q

Classic manifestations of PD

A

Resting tremor, rigidity, bradykinesia, dysarthria

172
Q

Dysaerthria

A

Loss of control of muscles you speak with
-slurring of speech

173
Q

Early symptom of PD

A

Loss of smell

174
Q

Disorders of equilibrium in PD

A

PD can’t make appropriate postural adjustments to tilting
-falls like a post

175
Q

Lou Gehrig’s disease

A

Degeneration of both lower and upper motor neurons

176
Q

Upper ALS

A

-Dec in large motor neurons in CNS
-motor neuron death = demyelination and glia proliferations, sclerosis

177
Q

Upper Lou gherig

A

-Dec in large motor neurons in CNS
-motor neuron death = demyelination and glia proliferations, sclerosis

178
Q

Lower lou gherig

A

Enervation of motor units

179
Q

Manifestations of lou gehrig

A

Muscle weakness in arms and legs, that progresses to speaking and swallowing
-no mental or sensory symptoms

180
Q

TX for lou gherig

A

Medication rilutek extends time before ventilator assistance is required

Pathophysiology (20 decks)

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