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patho > ch 15: alterations in cognitive systems, cerebral hemodynamics and motor function > Flashcards

ch 15: alterations in cognitive systems, cerebral hemodynamics and motor function Flashcards

1
Q

cognitive behavioural functional competence is…

A

an integrated process of cognitive, sensory and motor systems

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2
Q

systems get manifested through motor network. which are…

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 the environment

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4
Q

two components of consciousness

A
  1. arousal (state of awakeness)
  2. awareness (content of thought)
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5
Q

alterations in arousal

A
  1. structural alterations
  2. metabolic alterations
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6
Q

structural alterations

A

divided according to their location of dysfunction
1. supratentorial disorders
2. infratentorial disorders

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7
Q

supratentorial disorders (cerebrum)

A

above the tentorium cerebelli. produce changes in arousal

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8
Q

infratentorial disorders (cerebellum)

A

below tentorium cerebelli. produce decline in arousal by dysfunction of reticular activating system or brain stem

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9
Q

metabolic alterations

A

disorders produce a decline in arousal by alterations in delivery of energy substrates

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10
Q

5 patterns of neurological functions that you evaluate

A
  1. level of consciousness
  2. pattern of breathing
  3. pupillary reaction
  4. oculomotor responses
    5 motor responses
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11
Q

evaluating level of consciousness

A

MOST CRITICAL index of nervous system function
- changes indicate improvement or deterioration
- highest level of consciousness = person is alert/orientated to oneself, others, place, and time
- from normal state it diminishes to confusion, disorientation and coma

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12
Q

evaluating pattern of breathing

A

normal breathing = rhythmic pattern
- when consciousness diminishes = breathing responds to changes in PaCO2 levels

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13
Q

cheyene- stokes

A

altered period of tachypnea and apnea directly related to PaCO2 (deep and shallow)

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14
Q

apneusis

A

prolonged inspiratory time and a pause before expiration

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15
Q

ataxic breathing

A

complete irregularity of breathing with increasing periods of apnea

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16
Q

evaluating pupillary reaction

A

indicate presence/level of brainstem dysfunction
- brainstem area controlling arousal is adjacent to area controlling pupils
- ischemia =dilated/fixed pupils
- hypothermia/opiates cause pinpoint pupils

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17
Q

evaluation of oculomotor responses

A

resting, spontaneous, and reflexive eye movements change at various levels of brain dysfunction
- normal response: eyes move together to side opposite from turn of head
- abnormal response: eyes do not turn together
- absent response: eyes move in direction of head movement

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18
Q

oculomotor responses: caloric ice water test

A

ice water injected into ear canal
- normal response: eyes turn together to side of head where ice injected
- abnormal response: eyes do not move together
- absent response: no eye movement

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19
Q

evaluating motor responses

A

determine brain dysfunction and indicates most severely damaged side of brain
- pattern of response may be: purposeful OR inappropriate, generalized movement OR not present
- motor signs indicating loss of cortical inhibition = decreased consciousness associated with the performance of primitive reflexes and rigidity (paratonia)

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20
Q

vomiting, yawning, hiccups

A

complex reflex-like motor responses integrated in brain stem
- dysfunction of medulla oblongata = compulsive/repetitive production of these responses

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21
Q

outcomes of alterations in arousal

A
  1. disability (mortality)
  2. mortality
    outcomes depend on cause, damage and duration of coma. some individuals never retain consciousness and experience neurological death
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22
Q

2 forms of neurological death

A
  1. brain death
  2. cerebral death
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23
Q

brain death (total brain death)

A

neurological determination of death (NDD)
- brain damaged, cannot recover, and cannot maintain homeostasis
- canadian criteria for NDD: unresponsive coma, no brain stem functions, no spontaneous respiration

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24
Q

cerebral death (irreversible coma)

A

death of cerebral hemispheres except for brainstem and cerebellum
- permanent brain damage, individual never responds in a significant way
- brain may continue to maintain homeostasis

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25
Q

cerebral death states

A
  1. persistent vegetative state
  2. minimally conscious state
  3. locked-in syndrome
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26
Q

persistent vegetative state

A

complete unawareness of self or environment
- does not speak
- sleep-wake cycles present
- cerebral function is absent

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27
Q

minimally conscious state

A

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

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28
Q

locked in syndrome

A

complete paralysis of voluntary muscles except for eye movement
- content of thought and level of arousal are intact (fully conscious)
- blinking as means of communication

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29
Q

awareness

A

content of thought
- encompasses all cognitive function
- mediated by executive attention networks (EAN) which include selective attention and memory and involve abstract reasoning, planning, decision making, judgement, and self-control

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30
Q

selective attention

A

ability to select specific information and focus on related specific task
- also includes selective visual and auditory attention

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31
Q

executive attention deficits

A

characteristics: inability to maintain sustained attention and inability to set goals and recognize when goal is achieved
types: initial detection, mild deficit, severe deficit

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32
Q

executive attention deficits: initial detection

A

person fails to stay alert and oriented to stimuli

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33
Q

executive attention deficits: mild deficit

A

grooming and social graces are lacking

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34
Q

executive attention deficits: severe deficit

A

motionless, lack of response, doesn’t interact with surroundings

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35
Q

memory

A

recording, retention and retrieval of information

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36
Q

amnesia

A

loss of memory

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37
Q

retrograde amnesia

A

difficulty retrieving past memories

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38
Q

anterograde amnesia

A

inability to form new memories

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39
Q

data processing deficits

A

problems associated with recognizing and processing sensory information

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40
Q

5 data processing deficits

A
  1. agnosia
  2. dysphasia
  3. acute confusional state and delirium
  4. dementia (alzheimer’s)
  5. frontotemporal dementia
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41
Q

agnosia

A

defect of pattern recognition
- failure to recognize form and nature of objects
- generally one sense is affected (unable to identify pin by touching but can name it when looking at it)
- associated with cerebrovascular accidents to specific brain areas

42
Q

dysphasia

A

impairment of comprehension or production of language
- pathophysiology is due to occlusion of middle cerebral artery (one of three major arteries supplying blood to brain)

43
Q

2 types of dysphasia

A
  1. expressive dysphasia (broca dysphasia)
  2. receptive dysphasia (wernicke dysphasia)
44
Q

expressive dysphasia (broca)

A

loss of ability to produce spoken or written language
- verbal comprehension is usually present

45
Q

receptive dysphasia (wernicke)

A

inability to understand written or spoken language
- speech is fluent but words and phrases have no meaning

46
Q

acute confusional states of delirium

A

transient disorders of awareness and may have a sudden or gradual onset
- causes: drug intoxication, alcohol withdrawal, post anesthesia, electrolyte imbalance
- manifestations: terrifying dreams, hallucinations, gross alteration of perception, no sleep
- evaluation: CAM-ICU (confusion assessment method for intensive care unit)

47
Q

pathophysiology of confusional states and delirium

A
  • disruption of reticular system, thalamus, cortex and limbic system
  • delirium (hyperactive acute confusional state): most commonly occurs in critical care units over 2-3 days = disruption of neurotransmitter acetylcholine and dopamine
  • excited delirium syndrome (agitated delirium): hyperkinetic delirium that can lead to sudden death. rapid breathing, high tolerance to pain, superhuman strength
48
Q

dementia

A

deterioration/progressive failure of many cerebral functions
- causes: cerebral neuron degeneration, atherosclerosis, and genetics

49
Q

alzheimer’s disease

A

leading cause of severe cognitive dysfunction in older adults
- exact case unknown

50
Q

3 forms of alzheimer’s

A
  1. non hereditary sporadic late-onset AD: 70-90%, most common form, no specific genetic association
  2. early onset familial AD: linked to chr 21 mutations
  3. early onset AD: linked to chr 19 mutations (rare)
51
Q

pathophysiology of AD

A
  • accumulation of toxic fragments of amyloid plaques (misfolded proteins)
  • loss of Ach in forebrain cholinergic neurons = death of neurons
  • tau proteins (microtubule) form neurofibrillary tangles within the neuron = increased neural death
  • neurofibrillary tangles are concentration in cerebral cortex
  • brain atrophy via widening of sulcus and shrinking of gyrus
52
Q

AD manifestations

A
  • first symptom: memory loss, impaired learning
  • continuation of symptoms: language, reasoning, social behavior, dyspraxia (loss of movement and coordination) may occur
  • progression from short term memory loss to total loss of cognitive function
  • pathophysiological changes can occur decades before dementia syndrome
53
Q

frontotemporal dementia

A

AKA pick disease
- 2nd most common form of dementia
- umbrella term for disorders that affect frontal and temporal regions of brain
- first symptom: apathy, poor judgement/reasoning, break laws, difference in personality/character
- genetic component with onset at less than 60 yoa
- involved mutation of tau encoding genes

54
Q

seizure

A

sudden disruption in brain electrical function caused by abnormal excessive discharges of cortical neurons (interferons)

seizures represent a manifestation of a disease, not a specific disease entity

55
Q

epilepsy

A

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

56
Q

convulsions

A

jerky, contract-relax movements associated with seizures

57
Q

probable causes of seizures

A
  • young adults: alcohol, drug withdrawal, brain tumor, perinatal insults (occurring between 28 weeks of gestation to 28 days after birth)
  • older adults: alcohol/drug withdrawal, metabolic disorders, CNS degeneration
58
Q

anatomy of a seizure

A
  1. epileptogenic focus
  2. tonic phase
  3. clonic phase
59
Q

epileptogenic focus

A
  • focus: brain site where seizure originates (referred to as epileptogenic zone)
  • neurons in epileptogenic focus are hypersensitive and activated by numerous stimuli. they fire more frequently and with greater amplitude than other neurons
  • during seizure, focus can be determined by activated SPECT (test that detects blood flow changes in brain)
60
Q

tonic phase

A

muscle contraction with increased muscle tone - associated with loss of consciousness

61
Q

clonic phase

A
  • alternating contraction and relaxation of muscles
  • begins when inhibitory neurons in thalamus and basal ganglia react to cortical excitation
  • result: seizure discharge is interrupted = intermittent contractions that diminish and finally cease
  • increase in number of seizures = increase in brain damage
  • seizure cessation due to epileptogenic neurons being exhausted
  • brain: reduced oxygen = switch to anaerobic metabolism = accumulation of lactic acid
62
Q

cerebral blood flow (CBF) related to 3 injury states

A
  1. inadequate cerebral perfusion
  2. normal perfusion but with elevated intracranial pressure (ICP)
  3. excessive blood volume (CBV)
63
Q

increased intracranial pressure (ICP)

A
  • normal ICP = 1-15mmHg
  • ICP results from increase in intracranial content (due to tumor, edema, hemorrhage)
  • increased content = something must be removed. first is displacement of cerebral spinal fluid (CSF)
  • continued high ICP = alterations cerebral blood volume and blood flow
  • result: four stages of ICP that lead to death
64
Q

ICP: stage 1

A
  • cranial vasoconstriction and systemic adjustments result in a decrease in ICP
  • ICP does not increase due to these compensations
  • no detectable symptoms of ICP
65
Q

ICP: stage 2

A
  • 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
66
Q

ICP: stage 3

A
  • autoregulation is lost in stage 3= ICP approaches arterial 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 and tinnitus)
  • surgical intervention needed here
67
Q

autoregulation

A

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

68
Q

ICP: stage 4

A
  • brain tissue shifts (herniates) from greater to lesser pressure
  • herniated brain tissue = reduction in blood supply
  • herniations rapidly increase ICP
  • pupils: progress to bilateral dilation and fixation
  • breathing: cheyne-stokes breathing
  • mental status: progresses to deep coma
  • surgical intervention futile here, death occurs
69
Q

3 types of cerebral edema

A
  1. vasogenic edema
  2. cytotoxic (metabolic) edema
  3. interstitial edema
70
Q

vasogenic edema

A

MOST important type
- cause: increased capillary permeability/disruption of BBB
- plasma proteins/fluid leak into cranial ECF
- fluid accumulates in white matter = separation of myelinated fibers
- manifestations: consciousness disturbances and increases in ICP
- resolution: by slow diffusion

71
Q

cytotoxic edema

A

toxic factors affects neural, glial, and endothelial cells = loss of active transport mechanisms
- loss of K+ and gain lots of Na+ = change in intracellular osmolarity = cells swells

72
Q

interstitial edema

A

movement of cerebrospinal fluid from ventricles into interstitial space = edema
- result: fluid volume increases around ventricles = increased pressure within white matter = disappearance of myelination

73
Q

brain edema

A

lateral ventricles compressed and gyri flattened

74
Q

hydrocephalus

A

condition of excess cerebrospinal fluid (CSF) in ventricles or subarachnoid space

75
Q

cause of hydrocephalus

A

increased CSF production from an obstruction in ventricles or defective reabsorption of CSF fluid into systemic blood

76
Q

types of hydrocephalus

A
  1. communicating hydrocephalus
  2. noncommunicating hydrocephalus
77
Q

communicating hydrocephalus

A
  • infancy through adulthood
  • impaired absorption of CSF from subarachnoid space
  • cause: infection
  • communicating refers to the fact that CSF can still flow between the ventricles
78
Q

noncommunicating hydrocephalus

A
  • in adults
  • obstruction of CSF between ventricles
  • cause: congenital (present from birth)
79
Q

pathophysiology of hydrocephalus

A
  • obstruction of CSF flow = increase pressure and dilation of ventricles
  • atrophy of cerebral cortex and degeneration of white matter
80
Q

manifestations of HC

A
  • acute HC: rapidly developing ICP = deep coma
  • normal pressure HC: dilation of ventricles without increased pressure, HC develops slowly, family notices decline in memory, progression to triad symptoms (broad based gate, falling, incontinence)
81
Q

HC treatment

A

shunting procedure:
- shunt used for ventricular bypass into normal intracranial/extracranial channels where fluid can be absorbed
- 1 of 3 most common neurosurgical procedure

82
Q

alterations in muscle tone

A

normal muscle tone = slight resistance to passive movement
- resistance is smooth, constant and even

83
Q

hypotonia

A

decreased muscle tone
- tire easily
- difficulty rising from sitting position
- muscle mass atrophy - muscles flabby and flat
- joints hyperflexible (can acquire positions requiring extreme joint mobility)

84
Q

hypertonia

A

increased muscle tone
- passive movement occurs with increased resistance
- symptoms: enlargement of muscle mass, development of firm muscles, muscle spasms

85
Q

alterations in muscle movement causes

A
  1. neurotransmitter dopamine involved in several disorders (too little or too much)
  2. other disorders are neurological = excessive or insufficient movement
86
Q

hyperkinesia

A

excessive, purposeless

87
Q

3 types of dyskinesias

A
  1. paroxysmal dyskinesias
  2. tardive dyskinesias
  3. ballism
88
Q

paroxysmal dyskinesias

A

involuntary movements that occur as spasms

89
Q

tardive dyskinesias

A
  • involuntary movement of face, lips, tongue and extremities
  • often caused by prolonged antipsychotic medication
  • characteristic: rapid repetitive stereotypical movements (continually chewing or tongue protrusions)
  • tourette syndrome
90
Q

ballism

A

muscle disorder with wild flinging movement of limbs

91
Q

huntington’s disease (AKA chorea)

A
  • symptoms are hallmark of hyperkinesia
  • relatively rare degradative hyperkinetic disorder
  • involved basal ganglia and cerebral cortex
  • onset 25-45 yoa
92
Q

manifestations of HD

A
  • begins in face and arms (eventually whole body)
  • thinking is slow
  • alterations in euphoria and depression are common
  • involuntary fragmented movements
93
Q

pathophysiology of HD

A
  • inherited disease, autosomal dominant trait
  • mutation in chr 4 results in abnormally long protein caused by a CAG trinucleotide
  • altered amino acid chain = protein toxic to neurons
  • age of onset determined by number of repeated amino acid chains (increased chains = increased toxicity of protein = earlier age of onset)
94
Q

hypokinesia (decreased movement)

A

loss of voluntary movement despite preserved consciousness
1. akinesia: lack of spontaneous movement(facial expressions) or associated movements (arm swinging while walking)
2. bradykinesia: slowing of performed movements

95
Q

parkinson’s disease

A

complex motor disorder accompanied by systemic non motor and neurological symptoms

96
Q

primary PD

A

begins after 40 yoa with increased incidence after 60 yoa
- leading cause of neurological disability in people ver 60

97
Q

secondary PD

A

parkinson’s caused by disorder other than PD (head trauma, infections, toxins, medication intoxication)
- medication intoxication PD is second most common form and is most reversible. it is caused by neuroleptics (antipsychotics to treat hallucinations and delusions)

98
Q

PD pathophysiology

A
  • several gene mutations
  • pathology: basal ganglia dysfunction due to misfolded proteins
  • result: loss of dopamine producing neurons in substantia nigra
  • loss of dopamine (inhibitory neurotransmitter) and excess production of cholinergic (excitatory neurotransmitters) = symptoms of muscle tremors and rigidity
  • these symptoms produce abnormal movement called parkinson’s
99
Q

PD manifestations

A
  • classic: resting tremor
  • dysarthria: loss of control of muscles you speak with = slurring speech
  • loss of smell can be early symptom
  • disorders of equilibrium (cannot make appropriate postural adjustments to tilting - fall like a post)
100
Q

amyotrophic lateral sclerosis (ALS)
AKA Lou Gehrig’s

A
  • principle feature = degeneration of both lower and upper motor neurons
  • upper: decrease in larger motor neurons in CNS. motor neurons death results in demyelination and glia proliferations and sclerosis (scarring)
  • lower: denervation of motor units
101
Q

ALS manifestations

A
  • muscle weakness starting in arms and legs and progressing to difficulty speaking and swallowing
  • no associated mental or sensory symptoms
102
Q

treatment

A

medication Rilutek extends time before ventilatory assistance is required

patho (4 decks)

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