Final Exam Study Guide
Neurological
Clinical Manifestations for alterations in arousal
o Changes in LOC is the most critical piece on information we have
o LOC: are early changes, first thing you will see when something goes wrong
neurologically
o Pattern of breathing: assess the rate, rhythm and pattern; can have changes in any
of those. Respiratory rate can be low or labored. Could have Cheyne stroke
respirations
o Pupillary Changes: biggest thing to look for fixed and dilated pupils. (Pupils are wide
and don’t move). This is not good, its sign of brain hypoxia or ischemia.
o Oculomotor Responses: just looking for changes and or things your not supposed to
have.
Resting, spontaneous, reflexive eye movements
o Motor Responses: Can help evaluate level of dysfunction and damaged side ( just
looking for changes or things that shouldn’t be there)
Purposeful, inappropriate, or not present
o Consciousness: state of awareness of oneself and the environment
Arousal: state of being awake and being able to respond
Awareness: state of being aware
These are all mediated by the RAS, in brainstem
If you get damage to cerebrum then the RAS will maintain you in a vegetative
state- will keep you alive if something happens severely to your brain tissue.
o Structural: could be due to a tumor, bleeding in the brain
o Metabolic: anything that effects the metabolism like hypoxia, electrolyte changes,
medications or drugs
o Psychogenic: patients with psychiatric diseases like schizophrenia
o Outcomes: Long-term disabilities, or patients could die.
Brain Death: body can no longer maintain internal homeostasis
o Occurs when the brain has been damaged so severely that it can never recover.
Death or damage to the brain stem. These patients are considered legally dead
Cerebral death : irreversible damage to the cerebrum but the cerebellum and brain stem
maintain intact- because the cerebellum and brainstem are intact, all vitals can be
maintained, your still alive, just not where you want to be
o 4 types:
o Remain in coma for life: they will have vital signs, but will not move, talk or open
their eyes etc.
o Emerge into a persistent vegetative state: the only thing they can do is open their
eyes and have normal sleep patterns. Will have vital signs
, o Progress into a minimal conscious state (MCS): may follow simple commands, may
have small motor movements, and could be able to say yes or no.
o Locked in syndrome: patient is fully conscious but completely paralyzed, only thing
they can do is move their eyes. They are completely aware of what’s going on. They
will be in this syndrome for the rest of their life.
Seizures: sudden transient (temporary) alteration of brain function caused by an abrupt
explosive, disorderly discharge of cerebral neurons. – Usually a small group of neurons
o Cause: could be tumor, trauma, a chemical disorder, or due to flashing lights, loud
noises.
o Epilepsy: a disease, someone has seizures but do NOT know the cause. Could be
genetic combined with environmental factors.
Epileptic neurons: hyper sensitive and fire more frequently
o Phases – Tonic clonic: has two phases
Tonic phase: the phase of continuous muscle contractions
Clonic phase: alternating of contraction and relaxation. The neurons that
aren’t part of seizure are trying to stop the seizure activity.- the periods of
relaxation will get longer and longer until the seizure stop.
Neurons cannot bring seizure to an adrupt stop, that’s why you get periods
of relaxation.
o post-ictal: the phase that immediately following the end of the seizure, this is when
seizure stops. Patient can be semi conscious, fatigued
o Manifestations
Aura: sign or symptom that the patient will have right before the seize.
(Seconds). It’s the warning sign that a seizure is coming
Prodroma: sign or symptom that occurs hours or days before a seizure. Could
be a headache, or feeling of malaise, it’s a warning sign of seizure coming.
Increase in oxygen consumption: a lot of oxygen is used during seizure
because of a lot of energy is being used.
Anaerobic metabolism: If your patient runs out of oxygen then they
will start building up lactic acid
o Prolonged seizure can cause brain damage
Dysphasia: problem with communication (speech) – 3 types
o Agnosia- a problem with the ability to recognize patterns or objects. Theres a
problem with one of there senses,
have to use one of there other senses to recall. Ex) see pen, can see it but
cant recall what it is
o Expressive dysphasia-problem with brocas area- they know what they want to say
but they cant express themselves
Deficit of expression
, o Receptive dysphasia- problem with wernicke area- problem with comprehension –
when someone speaks you have no idea what they are saying (almost like they are
speaking in another language)- see a lot of with stroke patients.
Deficit of comprehension
o Transcortical dysphasia (not as common)- echolalia-repeats a word or phrase over
and over-speech is clear but makes no sense – fixed on a certain word or syllable
Echolalia
Acute confusion state and delirium-
o Acute Confusion State: Transient (temporary) disorders of awareness that result
from cerebral dysfunction. Temporary state of confusion.
Cause: patient disease or condition, drugs
Wont be able to concentrate, restless, wont know where they are.
Ex: patient that keeps climbing out of bed or they need bed alarms or sitters
o Delirium: more severe state of confusion. – see this a lot with patients withdrawing
from drugs and alcohol.
Will be confused, irritable, mis-interrupt things, could hallucinate, hostile,
violent.
Alzheimer’s Disease: form of dementia (umbrella term), most common form of dementia
o Don’t know the cause: could be chemical problem in brain, too much trauma. Could
be genetic ( 2 chromosomes)
o Pathologic Features:
Neurofibrillary tangles: tangles of protein on the neurons themselves.
Neuritic plaques: deposits of protein in the brain
Neural Degeneration: destruction of the neurons
o Pathologic features leads to:
o Neuron Death: when neurons die and get a loss of neurotransmitters- the
brain will atrophy
CM: Start with forgetfulness and emotional upset- they are going to get upset that
they are forgetting things.
Progressive CM: memory loss, confusion, mood changes, problem solving, they
become completely different
Increased intracranial pressure (ICP): caused by increase in intracranial content
o Stage 1: no change in pressure due to body compensating. Blood vessels in brain
constrict in attempt to keep pressure low.
o Stage 2: Expansion of intracranial content.
Slight pressure rise and subtle CM
Will have change in LOC.
o Stage 3: Pressure continues to increase, becomes hypoxic and patient deteriorates
o Pupil changes, respiratory changes, motor response changes
o Stage 4: Pressure in cranium is so high that brain tissue herniates
, Herniation of brain tissue- the brain tissue goes somewhere else ( the
foramen magnum)
Herniation= death
Cerebral edema: increase in the fluid content (intracellular or extracellular) within the brain
tissue itself.
o Occurs after brain injury
o **Vasogenic: Most common/important, increased capillary permeability
Brain got injured, inflammatory response became stimulated, get vasodilation
that increased capillary permeability and leaks fluid into the tissue
Hydrocephalus: excess fluid around the brain
o Cause: the flow of CFS- not being absorbed, your making too much or there is an
obstruction.
o CM: headache, changes in LOC, vomiting
o If adult gets this: they will have unsteady gait, signs that mimic dementia and bowel
or bladder incontinence.
o Infant gets this: head circumference will get bigger. Bones of skull havent fused
together yet. When they get excess fluid in cranium. Its going to get bigger. Brain will
get bigger.
Huntington’s Disease: also known as chorea
o Autosomal dominant genetic disease
o Severe degeneration/destruction of basal ganglia (these control your movement)
o CM:
Chorea- irregular excessive movements that begin in arms and face (constant
motion)
Athertosis: writhing movements- sliding down chair and needs to get back up
(wiggling of the body)
Ballism: flinging movements- arms coming up
Parkinson Disease: disorder of movement
o Unknown cause: could be genetic/ environmental factors.
o Severe degeneration of basal ganglia
o Key: these patients get a loss of dopamine- a neurotransmitter , the neurons that
produce dopamine get destroyed
o Loss of dopamine is what causes manifestations
o CM: bradykinesia- slow movements
Rigid
Shuffling gait
Most common: resting tremors – known as rolling pill tremors
Can get impaired speech, swallowing
