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
2
Q
systems get manifested through motor network. which are…
A
behaviours that are appropriate to human activity
3
Q
full consciousness
A
state of awareness of oneself and appropriate responses to the environment
4
Q
two components of consciousness
A
- arousal (state of awakeness)
- awareness (content of thought)
5
Q
alterations in arousal
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- structural alterations
- metabolic alterations
6
Q
structural alterations
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divided according to their location of dysfunction
1. supratentorial disorders
2. infratentorial disorders
7
Q
supratentorial disorders (cerebrum)
A
above the tentorium cerebelli. produce changes in arousal
8
Q
infratentorial disorders (cerebellum)
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below tentorium cerebelli. produce decline in arousal by dysfunction of reticular activating system or brain stem
9
Q
metabolic alterations
A
disorders produce a decline in arousal by alterations in delivery of energy substrates
10
Q
5 patterns of neurological functions that you evaluate
A
- level of consciousness
- pattern of breathing
- pupillary reaction
- oculomotor responses
5 motor responses
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
12
Q
evaluating pattern of breathing
A
normal breathing = rhythmic pattern
- when consciousness diminishes = breathing responds to changes in PaCO2 levels
13
Q
cheyene- stokes
A
altered period of tachypnea and apnea directly related to PaCO2 (deep and shallow)
14
Q
apneusis
A
prolonged inspiratory time and a pause before expiration
15
Q
ataxic breathing
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complete irregularity of breathing with increasing periods of apnea
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
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
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
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)
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
21
Q
outcomes of alterations in arousal
A
- disability (mortality)
- mortality
outcomes depend on cause, damage and duration of coma. some individuals never retain consciousness and experience neurological death
22
Q
2 forms of neurological death
A
- brain death
- cerebral death
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
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
25
cerebral death states
1. persistent vegetative state
2. minimally conscious state
3. locked-in syndrome
26
persistent vegetative state
complete unawareness of self or environment
- does not speak
- sleep-wake cycles present
- cerebral function is absent
27
minimally conscious state
follow simple commands, manipulate objects, give yes/no responses
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locked in syndrome
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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awareness
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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selective attention
ability to select specific information and focus on related specific task
- also includes selective visual and auditory attention
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executive attention deficits
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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executive attention deficits: initial detection
person fails to stay alert and oriented to stimuli
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executive attention deficits: mild deficit
grooming and social graces are lacking
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executive attention deficits: severe deficit
motionless, lack of response, doesn't interact with surroundings
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memory
recording, retention and retrieval of information
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amnesia
loss of memory
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retrograde amnesia
difficulty retrieving past memories
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anterograde amnesia
inability to form new memories
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data processing deficits
problems associated with recognizing and processing sensory information
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5 data processing deficits
1. agnosia
2. dysphasia
3. acute confusional state and delirium
4. dementia (alzheimer's)
5. frontotemporal dementia
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agnosia
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
dysphasia
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
2 types of dysphasia
1. expressive dysphasia (broca dysphasia)
2. receptive dysphasia (wernicke dysphasia)
44
expressive dysphasia (broca)
loss of ability to produce spoken or written language
- verbal comprehension is usually present
45
receptive dysphasia (wernicke)
inability to understand written or spoken language
- speech is fluent but words and phrases have no meaning
46
acute confusional states of delirium
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
pathophysiology of confusional states and delirium
- 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
dementia
deterioration/progressive failure of many cerebral functions
- causes: cerebral neuron degeneration, atherosclerosis, and genetics
49
alzheimer's disease
leading cause of severe cognitive dysfunction in older adults
- exact case unknown
50
3 forms of alzheimer's
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
pathophysiology of AD
- 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
AD manifestations
- 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
frontotemporal dementia
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
seizure
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
epilepsy
recurrence of seizures where no known cause for seizures can be found
56
convulsions
jerky, contract-relax movements associated with seizures
57
probable causes of seizures
- 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
anatomy of a seizure
1. epileptogenic focus
2. tonic phase
3. clonic phase
59
epileptogenic focus
- 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
tonic phase
muscle contraction with increased muscle tone - associated with loss of consciousness
61
clonic phase
- 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
cerebral blood flow (CBF) related to 3 injury states
1. inadequate cerebral perfusion
2. normal perfusion but with elevated intracranial pressure (ICP)
3. excessive blood volume (CBV)
63
increased intracranial pressure (ICP)
- 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
ICP: stage 1
- cranial vasoconstriction and systemic adjustments result in a decrease in ICP
- ICP does not increase due to these compensations
- no detectable symptoms of ICP
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ICP: stage 2
- 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
ICP: stage 3
- 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
autoregulation
mechanism to alter diameter of intracranial blood vessels to maintain a constant blood flow during changes in ICP
68
ICP: stage 4
- 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
3 types of cerebral edema
1. vasogenic edema
2. cytotoxic (metabolic) edema
3. interstitial edema
70
vasogenic edema
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
cytotoxic edema
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
interstitial edema
movement of cerebrospinal fluid from ventricles into interstitial space = edema
- result: fluid volume increases around ventricles = increased pressure within white matter = disappearance of myelination
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brain edema
lateral ventricles compressed and gyri flattened
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hydrocephalus
condition of excess cerebrospinal fluid (CSF) in ventricles or subarachnoid space
75
cause of hydrocephalus
increased CSF production from an obstruction in ventricles or defective reabsorption of CSF fluid into systemic blood
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types of hydrocephalus
1. communicating hydrocephalus
2. noncommunicating hydrocephalus
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communicating hydrocephalus
- 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
noncommunicating hydrocephalus
- in adults
- obstruction of CSF between ventricles
- cause: congenital (present from birth)
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pathophysiology of hydrocephalus
- obstruction of CSF flow = increase pressure and dilation of ventricles
- atrophy of cerebral cortex and degeneration of white matter
80
manifestations of HC
- 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
HC treatment
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
alterations in muscle tone
normal muscle tone = slight resistance to passive movement
- resistance is smooth, constant and even
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hypotonia
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)
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hypertonia
increased muscle tone
- passive movement occurs with increased resistance
- symptoms: enlargement of muscle mass, development of firm muscles, muscle spasms
85
alterations in muscle movement causes
1. neurotransmitter dopamine involved in several disorders (too little or too much)
2. other disorders are neurological = excessive or insufficient movement
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hyperkinesia
excessive, purposeless
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3 types of dyskinesias
1. paroxysmal dyskinesias
2. tardive dyskinesias
3. ballism
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paroxysmal dyskinesias
involuntary movements that occur as spasms
89
tardive dyskinesias
- 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
ballism
muscle disorder with wild flinging movement of limbs
91
huntington's disease (AKA chorea)
- symptoms are hallmark of hyperkinesia
- relatively rare degradative hyperkinetic disorder
- involved basal ganglia and cerebral cortex
- onset 25-45 yoa
92
manifestations of HD
- begins in face and arms (eventually whole body)
- thinking is slow
- alterations in euphoria and depression are common
- involuntary fragmented movements
93
pathophysiology of HD
- 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
hypokinesia (decreased movement)
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
parkinson's disease
complex motor disorder accompanied by systemic non motor and neurological symptoms
96
primary PD
begins after 40 yoa with increased incidence after 60 yoa
- leading cause of neurological disability in people ver 60
97
secondary PD
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
PD pathophysiology
- 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
PD manifestations
- 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
amyotrophic lateral sclerosis (ALS)
AKA Lou Gehrig's
- 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
ALS manifestations
- muscle weakness starting in arms and legs and progressing to difficulty speaking and swallowing
- no associated mental or sensory symptoms
102
treatment
medication Rilutek extends time before ventilatory assistance is required
