ch15: alterations in cognitive systems, cerebral hemodynamic, and motor functions Flashcards
what is consciousness?
awareness of oneself and the environment
what are three types of responses a pt can exhibit when faced with a stimuli?
- no response
- appropriate response
- inappropriate response
what is arousal?
a state of awakeness and the ability to respond to stimuli
vegetative state
opposite of dormant; cells are functioning but pt can’t respond to stimuli
“quasi waking state”
what maintains a vegetative state?
the reticular activating system (RAS)
what is awareness/content of thought?
awareness of self, environment, moods…
what controls awareness and conscious mind?
the cerebrum (supratentorially)
what controls unconscious homeostatic functions?
brainstem
what are structural alterations of arousals?
- supratentorial dysfunction
- infratentorial dysfunction
- metabolic dysfunction
supratentorial dysfunction
issue is at cerebrum above tentorial plate
infratentorial dysfunction
issue is below tentorial plate and affects the brainstem and cerebellum
metabolic dysfunction
alcohol, drugs –> affect state of arousal in different ways
- can affect ion concentrations that affect the brain
what is a psychogenic alteration of arousal?
not easy to assess clinically; psychology affects the state of arousal (mental illness) but pt can be “faking it”
6 steps when assessing arousal state
- LOC
- breathing pattern
- size/reactivity of pupils
- eye position/reflexive responses
- vomiting (yawning, hiccups)
- skeletal muscle motor responses
posthyperventilation apnea (PHVA) - explain
goes hand in hand with cheyne strokes respirations
hyperventilating → blowing off too much CO2 → pH goes up → stop breathing → start hyperventilating again bc of CO2 accumulation
oculocephalic test
turn head from center, left, right –> eyes should be able to focus on one object
abnormal: eyes follow head direction
oculovestibular test
inject cold water into patient’s ear, eyes should look in the direction of the water
what are 3 outcomes of alterations of arousal?
- brain death
- cerebral death
- cognitive disorders
what happens with brain death?
- what are signs of it?
brain can’t maintain homeostasis –> irreversible autolysis of brain
- no spontaneous respirations
- pupils dilated and fixed with no response
- flat EEG
- persistence 6-12hrs after onset
what is a symptom usually associated after pt has a seizure and why?
fatige: cells in brain consume A LOT of O2 –> rest of the body feels deprived
what happens with cerebral death?
death of cerebrum (NOT cerebellum or brainstem); could possibly have spontaneous muscle movements
what can a survivor of a coma progress to?
- vegetative state
- minimally conscious state
- locked in syndrome
vegetative state (VS)
maintain homeostasis, but higher level responsiveness is gone
minimally conscious state (MCS)
some part of the cerebrum still functions, only some response to some stimuli meant to target the cerebrum
locked in syndrome
mentally aware but cannon physically respond; communicate through blinking
what are some cognitive disorders (and what part of the brain do they affect)
affects the cerebrum
- selective attention deficits
- executive attention deficits
- retrograde amnesia
- anterograde amnesia
selective attention deficit
inability to preferentially attend to relevant aspects of a task and to ignore irrelevant information
ex. not being able to listen to music while driving, not being able to talk to friend in a crowded place
executive attention deficits
when a person’s brain has difficulty performing assorted important functions (ADHD, ADD)
- ex. can’t start or finish tasks, can’t stay on track, can’t follow multi-step instructions
retrograde amnesia
can’t remember the distant past
anterograde amnesia
can’t form new memories
what are cognitive disorders caused by?
- direct physical damage
- hypoxic/ischemic damage (O2 deprivation)
- chemical/toxic damage (drugs, alcohol, ion imbalances)
agnosia
- who is it more common in?
common in dementia pts: impaired detection, can’t recognize common objects or ppl you used to know
dysphasia
difficulty sending or receiving verbal cues
what are three types of dysphasia?
- expressive dysphasia
- receptive dysphasia
- global dysphasia
dementia
loss of more than one cognitive function
primary dementia
usually idiopathic; easily mistaken for alzheimers
how detect true alzheimer’s in patients?
need autopsy of the brain
secondary dementia
obvious defined cause for dementia
- stroke, neurodegenerative disease
progressive dementia
often irreversible; possible infection of prions
acute confusional states (ACS)
- what is the most common feature
precursor to diagnosis of agnosia, dysphasia
- impaired detection is the most common feature
what can ACS lead to
delirium
key feature of delirium
hyperactivity/agitation with impaired detection
developments of ACS
- physical injury to nervous tissue
- ischemic/hypoxic damage
- chemical/toxin damage
- “activation” of suppressed brain section
what are some degenerative disease?
- alzheimer’s disease
- pick’s disease
- parkinson’s disease
- huntington disease
- multiple sclerosis
- amytrophic lateral sclerosis (ALS)
- myasthenia gravis
what can degenerative diseases lead to?
all may lead to various myopathies (disease condition of your muscle tissues)
____ can send multiple sclerosis into remission
pregnancy
alzheimer’s disease
ability to recognize ppl/objects can be transient (come and go)
what are neurofibrillary tangles?
in alzheimer’s disease: proteins begin to coagulate and polymerize and act as if they have been infected by prion
what proteins are involved in neurofibrillary tangles
misfolded tau proteins
senile plaques
see this in alzheimers disease patients
- one of the first thing noticed if autopsy in brain is done (NOT prion but BEHAVES like prion)
pick’s disease
- who is it more common in
more rare than true alzheimers; more common in younger ppl
- polymerization of tau proteins + neurons
- signs and symptoms similar to alzheimers but in younger
- possible progeria
progeria
condition where a kid ages quick
parkinson’s disease
idiopathic; muscle spasms and tremors (involuntary spastic movements when pt is trying to do smth)
- body has low amounts of dopamine
- spastic movements
huntington’s disease (chorea)
- what accumulates?
huntington protein accumulation –> due to genetic/heredity factors
what does it mean when huntington disease is an autosomal dominant condition
one bad huntington allele: you’ll get this disease
HH: huntington, hh: no huntington
multiple sclerosis (ms)
immune system is attacking myelin sheaths in neurons
what happens when there’s no myelin sheaths?
no myelin sheaths = nerve impulse less efficient or complete interruption
amyotrophic lateral sclerosis (ALS) “gehrig’s disease”
progressive loss of muscle tone
- slow motor neuron wasting –> lose ability to innervate
myasthenia gravis
deficiency of the thymus (t cell quality control)
- flunky t cells –> start attacking neuromuscular junction
cerebral blood flow
how efficiently is blood being applied to the brain
cerebral blood volume
how much blood in brain
cerebral perfusion pressure
pressure that circulatory system is exerting in cranial vault can affect ability to effect provide those tissues with O2 and other nutrients
cerebral oxygenation
O2 in the cerebrum
explain the effects of increased intracranial pressure
increased icp –> vasoconstriction –> decreased O2 to brain = decreased perfusion
how to relieve increased intracranial pressure
drain some CSF (decrease overall pressure by compensating somewhere else)
where is CSF made
in the ventricles of the brain
what is spina bifida
breach in formation of neural tube during development → no proper closure = babies can’t create CSF
cerebral edema
increased fluid content in brain tissue
what are 4 types of cerebral edema
- vasogenic edema
- cytotoxic (metabolic) edema
- ischemic edema
- interstitial edema (NCH)
vasogenic edema
problem with circulatory system that supplies blood to the brain
cytotoxic (metabolic) edema
imbalances in ion concentration at physiological level –> affect blood supply to brain
ischemic edema
problem with perfusion toward the brain (part of vasogenic family)
interstitial edema (NCH)
most rare; noncommunicable hydrocephalus
- CSF build up in meninges
- defect in replenishing CSF, ventricles keep making = accumulation
congenital hydrocephalus
rare; infectious disease (toxoplasmosis) –> mom passes onto kids
how does congenital hydrocephalus present in adulthood
asymmetry in facial features
noncommunicating hydrocephalus
old CSF not coming out = ventricles keep making CSF = impeding ability for old to come out
communicating hydrocephalus
old stuff can get out, ventricles keep making CSF and its overpowering release of old CSF
acute hydrocephalus
due to injury; rapidly developing
seizure
sudden discharge of cerebral neurons
convulsions (paroxysms)
random disordered muscle movements; eyes roll to back of head, drooling
epilepsy
usually idiopathic; a disorder in which nerve cell activity in the brain is disturbed, causing seizures
what can cause seizures?
- cerebral lesions
- biochemical disorders
- cerebral trauma
- epilepsy
epileptogenic focus
hypersensitive area of neurons, source area for seizure
- mirror foci development
phases of seizure?
- preictal (prodromal) phase
- tonic phase
- clonic phase
- postictal phase
preictal phase
signs that seizure may begin
- aura
- vision blurs
tonic phase
sudden stiffness or tension in the muscles of the arms, legs or trunk.
clonic phase
start to see alternating contracting and relaxing spasms of muscles (can be very subtle)
postictal phase
after seizure; extreme fatigue (bc O2 consumed is 60% above normal), headache, lousy mood
_____ provides temporary relief of seizure
pregnancy
hypotonia
decrease in muscle tone
hypertonia
tonic phase: increase in muscle tone
dystonia
certain postures, gaits; can tell you where issue may be in nervous system
hypokinesia
dysfunction of voluntary motor movement
akinesia
lack of voluntary motor movement
bradykinesia
slow voluntary movement
hyperkinesia
rapid and disorganized voluntary movement
what are 2 types of hyperkinesia
- paroxysmal dyskinesia(s)
2. tardive dyskinesia
paroxysmal dyskinesia(s)
tourette’s syndrome; involuntary movements of muscles other than facial muscles
tardive dyskineisa
involuntary movement of facial muscles
dystonia
whole body rigidity
decorticate posture
whole body rigidity (hands to chest)
decerebrate posture
whole body rigidity (hands on sides)
dysparaxia/apraxia
lack of/impeded movements for fine motor tasks (handling utensils, writing)
