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118 Cards in this Set

  • Front
  • Back
two main structural divisions of the nervous system
central nervous system
peripheral nervous system
what are the two main divisions of the peripheral nervous system
afferent - to brain from periphery
efferent -= to periphery from brain
what are the two main divisions of the efferent nervous system?
autonomic - automatic
somatic - voluntary
what are the two main divisions of the autonomic nervous system
parasympathetic - cholinergic/rest & digest

sympathetic - adrenergic/fight or flight
what are the protective structures of the CNS?
cerebrospinal fluid
bony structures
what are the meninges and their purposes?
dura mater: outmost, tough and thick layer
arachnoid space: not true space = potential space - only if pathology does space become evident
pia mater: attached to brain, conforms to every sulcus/gyrus
where is the favored place for csf samling?
from the large subarachnoid cistern at the end of the spinal cord at L1, L2
what structure produces CSF?
How much CSF is produced every day?
choroid plexus
500 mL/day
describe the arterial blood supply to the cns
2 pairs of arteries
• Internal carotids (anterior circulation)
• Vertebral arteries (posterior circulation
describe Production of CSF
production independent of BP or intraventricular pressure
Will continue to produce even when circulation/absorption blocked
-↑CSF with pathology=hydrocephalus
Which cells line the BBB? Which molecules get through
*Cells that line CSF spaces: very tight, difficult to penetrate = **Blood Brain Barrier (BBB): astrocytes maintain integrity by extending “feet” to capillaries
Lipid-soluble molecules pass easier than water-soluble ones. Polar/charged molecules
do not pass
General functions of:
• Cerebrum
Example: frontal lobe, motor cortex responsible for complex thought, behavior, morality
o Example: limbic structures: memory, emotion
Broca/Wernicke’s Area: language
Basal ganglia: coordination of movement
• Parkinson’s disease pathology happens here
General functions of:
• • Cerebellum
Execution of movement, moment-to-moment adjustments (proprioception)
General functions of:
• • Diencephalon
Thalamus, hypothalamus, pineal gland, hypothalamic extension to pituitary
• Hypothalamic extension: responsible for ANS functions (sleep, temperature, appetite, sex drive, regulation of BP, somolarity, blood O2 & CO2, pH, temperature
general functions of the brainstem
“Stalk” between upper spinal cord and diencephalon
• Vital centers for respiratory/CV function
what is the vagus nerve significance. Which cranial nerve is it.
Cranial nerve X (VAGUS NERVE) is critical to CV, resp, GI function
afferent neurons lead from:

efferent neurons take information from to?:
to brain from periphery

information away from CNS to periphery
Muscles, glands, postganglionic
autonomic nervous sytem does what in general
mediate autonomic or involuntary processes
nicotinic receptors are part of which division of the nervous system and are located where?
the somatic nervous system
skeletal muscle
nicotinic receptors receive what neurotransmitter and are excitatory or suppressor in effect?
Ach - excitatory
muscarinic receptors are part of which divition of the nervous system, and are located where?
the parasympathetic ns
the autonomic organs
muscarinic receptors receive what nt's and are excitatory or suppressor in effect?
Ach - suppressor
differentiate between neurons and glial cells
Neurons: generate + transmit impulses
• Glial Cells: supportive, don’t transmit impulses
what generates membrane potential in the neuron?
K+ greater in ICF
• Na+ greater in ECF
o K+ moves to ECF in concentration gradient, generates
Membrane potential (-70mV);
what stimulates release of nt's
Open voltage-gated Ca+2 channels simulate release of neurotransmitters…they move to next synapse, Na+ then rushes in, impulse moves down dendrite
what enzymes break down Ach
Acetylcholinesterase (AchE): quickly degrades Ach after release into synapse to limit duration of action. After degradation, immediately resynthesized
what enzymes break down dopamine?
Degraded by catechol-O-methyltransferase (COMT)
what does dopamine affect?
the CNS muscle regulation
what is an example of abnormal dopamine metabolism
parkinson's, schizophrenia
what is NE degraded by?
Degraded by catechol-O-methyltransferase (COMT)
if a amine neutotransmitter is not broken down in ECF, can be broken down in presynaptic nerve by
monoamine oxidase (MAO)
List the amine neurotransmitters
Dopamine (DA): CNS muscle regulation
 Degraded by catechol-O-methyltransferase (COMT)
 Abnormal DA metabolism=pathology
• Example: Parkinson’s, Schizophrenia
o Norepinepherine (NE)
 Degraded by catechol-O-methyltransferase (COMT)
o Epinepherine
o Serotonin (5-hydroxytryptamine, 5-HT)
 Sleep, mood, pain control
o Histamine
o Endorphins
Ca++ channels allow:
NT into the synaptic cleft
define ischemia
occurs when the delivery of oxygenated blood is below the level needed to meet the metabolic demands of the tissue "inadequate blood flow"
define hypoxia
a reduction in oxygen at the cellular level
which comes first, ischemia or hypoxia?
ischemia leads to hypoxia
why is neuronal tissue especially susceptible to hypoxic damage?
Has a limited capacity for anaerobic metabolism
during ischemia
 Uses 20% of total body O2 consumption
 Is dependent on glucose for ATP production
 Has little glycogen for storage
what is the mechanism of cellular damage from ischemia?
ischemia leads to cell hypoxia. O2 is needed to accept electrons in the TCA/Krebs Cycle. with reduced ATP production and glycolysis running out, H+ accumulates and acidosis occurs. Also, mitochondria fail leading to impaired Ca++ pumps, cuasing Ca++ overload, leading to free radical production and cell death
define CVA
The onset and persistence of neurological
dysfunction lasting longer than 24 hours and
resulting from disruption of blood supply to the brain
define hemorrhagic stroke
Leakage of blood or blood vessel and hemorrhage into brain
tissue, which causes edema, compression of brain tissue, and
spasm of adjacent blood vessels
 Can occur outside the dura, beneath the dura ( subdural), in
, ),
the subarachnoid space, or within the brain substance itself
define ischemic stroke
Partial or complete occlusion of the cerebral blood
flow to an area of the brain
what are the two possible causes of ischemic strokes?
Thrombus, most common, generally due to an
atherosclerotic plaque in a cerebral artery usually at a
point of bifurcation, occurs over several days
 Embolic, a moving clot of cardiac origin, frequently from
a-fib that travels quickly to the brain and lodges in a small
artery, occur suddenly, immediate and maximum deficits
which kind of stroke is associated with a greater morbidity and what is it almost always caused by?

caused by Hypertension
clinical manifestations of CVAs
Severe HA, paresthesia, weakness, loss of motor
ability on one side of the body, difficulty in
swallowing, aphasia (expressive, receptive, global),
visual difficulties, loss of half of a visual field, double
vision, altered cognitive abilities
what is the treatment goal for strokes?
save the penumbra (the area of eschemia in which cells are still viable and have the potential to be saved via reperfusion (initiate RX within 3 hours)
what is the significance of the optic nerve in a stroke?
↑ICP leads to: HA, vomiting, altered LOC, blurry vision, papilledema (optic disc swelling that is caused by increased intracranial pressure), pupil responsiveness
to light
what is the cushing reflex
last ditch effort of the body to maintain cerebral perfusion through clamped vessels = extreme somatic nervous sytem response which causes systolic blood pressure to rise above 200 mmHg
Define TIA
A transient ischemic attack (TIA) is an acute episode of
temporary and focal loss of cerebral function of vascular
(occlusive) origin.
 TIAs are rapid in onset; symptoms reach their maximal
manifestation in fewer than 5 minutes (usually <1 min).
M if i f i bl d i d i ll l 2 15
Manifestations are of variable duration and typically last 2-minutes (rarely as long as 24 h). Most TIA durations are less than
1 hour; median duration is 14 minutes in the carotid distribution
and 8 minutes in vertebrobasilar ischemia.
 Temporary reduction or cessation of cerebral blood flow
adversely affects neuronal function in cortical, subcortical, and
nuclear regions of the CNS.
what makes a TIA different than a CVA?
Death does not occur directly from a single
episode of TIA. A TIA may be considered a sign
of generalized atherosclerotic disease
 Blood flow is re established before infarction
re-takes place, “brain angina”
 TIAs are important warning signs of a potential
impending stroke
what is meningitis?
Meningitis is an infection of the linings of the
brain and ventricles.
 Can be fungal, viral, bacterial
what is the mechanism of infection in the meninges?
Usually the brain is protected naturally from the
immune system by a barrier created by the meninges,
the blood brain barrier
 Evolutionarily, this was seen as an advantage, since the
barrier prevents the body from attacking itself
b h h h f d h
 However, bacteria or other organisms that have found their
way into the brain are isolated from the immune system and
can spread quickly.
 Once the body recognizes that there is an infection, as it tries
to fight the infection, the blood vessels become leaky,
and allow fluid, white blood cells, and other infection fighting
particles to enter the meninges and the brain, causing
swelling, decreased blood flow to parts of the brain, and
worsening symptoms of infection
what are the routes of infection in meningitis
Hematogenous spread
 Nose and throat
 Localized extension otitis media sinusitis mastoiditis
extension, media, sinusitis,  Bone fracture, head or neck surgery, penetrating bone injury, skull fracture
what is the triad of symptoms in meningitis?
Meningitis develops quickly with a classic triad:
1. fever
2. headache
3. stiff neck developing over several hours to one to
two days
what are other symptoms of meningits?
Other symptoms include nausea, vomiting,
photophobia, mental status change, sleepiness
 Petichial, purpuric rash esp with N. menindititis
 Two classic signs: Kernig, Brudzinski
describe kernig and brudzinski
Kernig's sign is assessed with the patient lying supine, with the hip and knee flexed to 90 degrees. In a patient with a positive Kernig's sign, pain limits passive extension of the knee. A positive Brudzinski's sign occurs when flexion of the neck causes involuntary flexion of the knee and hip
what cells would you see increases in a lumbar puncture lab result?
↑Neutrophils, ↑protein,(decreased glucose)
The principal damage from bacterial meningitis
is caused by the _____________ and not
the ___________________
inflammatory reaction

define parkinson's
Parkinson’s disease is a progressive neurodegenerative
disorder associated with loss of dopamine neurons
 Named after James Parkinson, English physician who first
described the shaking palsy in 1817
 The underlying etiology is unclear, possible virus
possible genetic susceptibility, possible toxicity from
pesticides, repeated head injury or other unknown
 Idopathic vs. acquired (infection, intoxification, trauma)
Two pathways exist within the basal ganglia circuit, one
stimulatory the other inhibitory, which NTs are which?
 Stimulatory: Ach
 Inhibitory: DA
what area of the brain is affected in Parkinsons'
the cerebral cortex
signs and symptoms of Parkinson's
 the tremor he is noticed in the hands, feet, head, face, lips
 The most noticeable tremor he is pill rolling
 Rigidity
 This is the resistance to movement of both flexor and extents muscles through
full range of motion jerky, ratchet like movement of the joints
 Bradykinesia
 slowness in the initiating or performing of conscious movements
 Shuffling gait, no swinging of the arms with walking
 The face lacks emotional expression, poor link reflects
 Tongue, palate, and throat muscles become rigid, frequent drooling,
speech becomes slow and poorly articulated
 Autonomic problems
 Orthostatic hypotension
 Excessive sweating, sebaceous gland secretions, salivation
 Swallowing delayed: aspiration risk
 Dementia
how is Alzheimer Disease diagnosed?
R i hi l i l fi i l d
 Requires histological confirmation, only done
postmortem, but diagnosis can be made with high
certainty based upon a progressive cognitive decline
that is expressed in loss of memory, language skills, and
activities of daily living
describe the pathophysiology of AD
The classic neuropathological findings include
 amyloid plaque
 neurofibrillary tangles
 Tangles~ tau protein/neural thread protein
 Normally neural thread proteins bind/stablize microtubules--
essential for axon growth and development. In AD, tau twists
into paired helical filaments called neurofibrillary tangles
 synaptic and neuronal cell death.
 Brain in AD=ATROPY
 Changes in Cholinergic System
 choline acetylesterase
  Ach synthesis
what are the changes you see in the cholinergic system of someone with AD?
choline acetylesterase
  Ach synthesis
describe the amyloid plaques in AD
Beta amyloid protein
thought to cause
O id i f li id
 Oxidation of lipids
 Activation of apoptotic
 Disruption of cell
 Forms insoluble plaques
describe the neurofibrillary tangles
Neurofibrillary tangles are
deposited in neurons located
in the hippocampus,
temporal lobe, frontal lobe,
leading to cell death
signs and symptoms of AD
AD is a progressive dementia with memory loss as a major
clinical manifestation
 Language disturbance
 searching for words when naming objects is common and evolves into
communication breakdown as the patient struggles with a very limited
b l i l h i d d f t i l h i
vocabulary, nominal aphasia, and defects in language comprehension
 Behavioral problems are common throughout the disease process
 Early-stage disease shows disturbances of mood such as
depression, anxiety
 Late stage and manifest as delusions, hallucinations, psychosis,
aggression, and inappropriate sexual behavior
 End-stage disease has the patient in a vegetative like state, as
cognitive activity ceases
cause of death in AD is usually from:
differentiate btw concussion and contusion
 A sudden trauma induced alteration of the alert state
 No brain damage
 Contusion
 damage the cerebral cortex by bruising
 CT will show necrosis, laceration, bruising
 Cerebral contusions tend to occur at the tip of the frontal and
temporal lobes where they bang up against interior of the skull
 or the deep white matter can suffer diffuse axonal injury,
which can stretch, tear the axonal connection
discuss coup and contracoup
Contusion from direct
 Brain shifts side to side
 Shockwaves are sent to the
brain matter
 Even though the skull may
not be penetrated or
fractured, the forces imparted
to the brain can cause the
brain to collide against the
inside of the skull, coup, and
against the opposite area of
the brain =countercoup.
 Both areas of the brain will
be contused and subject to hemorrhage
define DAI
or the deep white matter can suffer diffuse axonal injury,
which can stretch, tear the axonal connection
 Diffuse Axonal Injury (DAI) occurs more towards the center of the
brain, where axons are subjected to maximal stretching, best example
is a whiplash injury
describe whiplash and its relationship to shaken baby syndrom
Whiplash, DAI
 The brain consists of billions
of nerve cells that
communicate by way of
 In a whiplash injury,
stretching, twisting, and
tearing of these axons and
their connections can occur
 Shaken baby syndrome is the
define epidural hematoma
EDH is a collection of blood which
occurs below the skull but above the
 This area of the brain is basically fluid
and acts as a shock absorber
 The veins that feed and drain the brain
which move through this area can be
EDH area, torn, resulting in a bleed
s/s and tx of epidural hematoma
These patients have a lucid interval
 Patient is struck in the head, short
period of unconsciousness, followed by
wakefulness and seeming normality,
then rapid deterioration
 This is from the gradual accumulation
of blood in this area which presses on
the brain over time, creating a mass
 Surgery is done to relieve the pressure,
if the person has progressed to coma
with GCS <9
define subdural hematoma
Between dura and outer
arachnoid membrane
 The source of the bleeding can
b f d h b i
be from damage to the brain
itself, damage to a vein,
 More common in elderly
patients after a fall
 The presence of blood directly
under the brain tissue is
thought to be an irritant to the brain, frequently causing a seizure
discuss the skull characteristics that make compensation difficult
Skull is a closed system
 Finite ability to compensate
 Brain parenchyma has little ability to volume
 CSF can shunt to venous system via arachnoid villi
 Blood vessels can vasoconstrict
what the ranges of ICP
Normal = 0-15mmHg
 > 20 abnormal
 >40 = neurological impairment ( decreased level of
consciousness, problems with breathing, pupil dilation,
compression of bringing on MRI, abnormal EEG
 >60 = fatal
what does high ICP cause?
High ICP will
 deform the brain and push tissue in such a way as to
cause herniation, or a shifting of the brain tissue under
pressure, which is tearing and stretching neurons
what is herniation in TBI
Complication of ↑ICP
 Protrusion through
opening in dura mater
Glasgow coma scale ranges
 15 = WNL
 Mild head injury = 13-15
pp p
 2 incomprehensible sounds
 1 no response
 Moderate head injury =
 <8 severe head injury
which is worse decorticate posturing or decerebrate?
what is the common denominator with all migraine headaches
Common denominator is meningeal instability/hyperexcitability that releases
several neurotransmitters:
 Dopamine
 Serotonin
 Histamine
 Prostaglandin
 All of these mediate the inflammatory response and cause vascular dilation
signs and symptoms of migraines
85% of migraineurs have HA without aura
 Pulsatile, unilateral (but can be bilat), throbbing, lasts 1-2 days, inc
pain with physical activity, +n/v from pain, photophobia, inc sound
15% f i i h HA i h a ra
 of migraineurs have with aura
 All of the above symptoms plus aura
 Spots, flashing lights, zig-zag/wavy lines cutting across
visual field
 Aura lasts < 1 hour
what is the significance of vasodilation in migraine?
Vasodilation causes more meingeal irritation trigeminal
instability NT release vasodilation… and a vicious
cycle is born which causes a self-sustaining HA that can go
on for days
So, a migraine is a neuro-vascular disorder at heart and is treated
as such
define multiple sclerosis
Primary demyelinating disease, acquired,
recurrent, multifocal
 often presents with optic neuritis but can present
with any neurologic abnormality
 any white matter can be involved, usually
periventricular, brainstem, optic nerve (optic neuritis
 onset at any age, peak 20-50, females 2x times more
likely to get than males
3 s/s
3 major symptoms: nystagmus, intention tremor,
scanning speech (monotonous or slurred speech
describe optic neuritis in MS
optic neuritis - papillitis acutely - central scotoma, decreased
visual acuity, Marcus-Gunn pupil, unilateral papilledem
what is the significance of placques in MS
MRI is diagnostic, looking for placques in the white matter on CNS
seizures are
Transient neurological events
 Excessive cortical electrical discharges
 Skeletal motor Fx
 Sensation
 Autonomic visceral Fx
 Behavior
 Consciousness
 Idiopathic, or with a known cause
 Environmental/physiologic/psychosocial
define epileptogenic focus
Neurons form an epileptogenic focus
 Area in brain where seizure begins
 Functions autonomously, emitting ↑↑discharges
 Can recruit neurons from opposite hemisphere
 Partial=focal; part of brain surface affected
 Generalized=entire brain surface affected
what happens if seizure is not treated in status epilepticus
Continued seizures without recovery period
 Can be life threatening!
 If not treated for 30-40 minutes
 Ischemic brain damage
#1 nursing intervention in seizures
#2 Protect from injury
significance of aura/prodrome in seizures
Aura/Prodrome associated with seizures
 Subjective sense of impending seizure
 Prodromal period: HA, myoclonic jerking, lethargy,
mood change, palpitations, epigastric sensations
 Can last several hours
 Aura: odd sensory experience before seizure
 Patient remembers this after recovery
what are the psycotic illnesses
delusional disorder
bipolar disorder
what are the non-psycotic illnesses
anxiety disorders (panic d.o, ocd)
personality d.o.'s
eating disorders
NT comprimised in Schizophrenia
definition of Schizophrenia
Disturbance/deterioration of cognitive, social, emotional functioning
More of a syndrome than a single illness
Pathophys of schizoprenia
Exact cause unknown. Probably presynaptic dysregulation of DA in D1 and D2 receptors. Excessive DA D2 receptor activity produces more noticeable symptoms
s/s of schizophrenia
Disorganized thinking, unusual speech (invented words), odd behavior, delusions, hallucinations
Delusion=systematic fixed false beliefs. Can be religious, grandiose, and persecutory

Neologisms=invented words with invented special, private meanings

Hallucinations: breakdown of perceptual selectivity, can affect 5 senses
anhedonia absence of pleasure, interest
Self-identity disturbance= lack of identity; cannot tell self from others
Autism=profound detatchment
NT comprimised in Delusional D.O.
definition of delusional d.o.
Similar to schizophrenia. Systematic false beliefs. Persist despite evidence demonstrating otherwise. Can dramatically reshape personality and character. Person’s life shapes the delusion; life then confirms the delusion. A defense mechanism?
s/s of delusional d.o.
Systematic delusions/not bizarre
Impaired reality testing
NT comprimised in depression
serotonin (5-HT)
definition of depression
A multi-faceted disorder characterized by: Low energy, inability to experience joy, difficulty initiating tasks, reduced decision-making ability, difficulty sleeping, poor appetite, weight loss, and decreased libido. Thoughts may focus on guilt, futility, emptiness, hopelessness, helplessness, and suicide
pathophysiology of depression
Low CNS 5-HT transmission: brain serotonin activity via excessive pre-synaptic uptake. OR, could be through stress-related down regulation of post-synaptic receptors
s/s of depression
Sleep disturbance (melatonin from Pineal Gland)
Depressed mood; loss of interest (anhedonia), fatigue not relieved by rest, restless/irritable/agitated/pacing, impaired concentration, low self-esteem, negative thinking, vegetative state, appetite disturbance, psychosis
difference btw minor and major depression
Minor depression: symptoms usually resolve in 1-2 years. Also known as dysthymia
Major depression: symptoms last for 2+ years
NT comprimised in Bipolar d.o.
Serotonin, Norepi (NE), Dopamine
definition of bipolar d.o.
Depression and/or elation (mania), often mistaken as schizophrenia. A mood disorder connected to diencephalon dysfunction.
pathophysiology of bipoloar d.o.
Neurotransmitter deficit~depression
Neurotransmitter overactive~mania
s/s of bipolar
Mania, or hypomania. Depression, or euphoria
Seemingly limitless energy level, impervious to fatigue
Speech disturbances, hallucinations/delusions, impulsive action, impaired judgment, sleep disturbance, hypersexuality. Appetite decreased because they are too distracted to eat
NT comprimised in anxiety do's
5HT primarily
s/s of anxiety do's
Panic 5HT Physical (resp. distress, palpitations, choking); Fearful; exaggerated startle response
Generalized GABA, NE, 5HT Muscle tension, sweating, palpitations, Uncontrollable worry
OCD 5HT, DA Compulsions (repetitive rituals), Obsessions (uncontrollable)
NT compromised in personality do's
HPA axis, 5HT
s/s of personality do's
borderline = Combination of psychosis/neurosis, alienation, impulsiveness; Manipulation, self-harm, Devalues others (splitting)
Antisocial = “psychopath”, “sociopath”, disregard for others
NT compromised in Eating do's
Related to depression
s/s of anorexia
Severe ritualistic restriction of caloric intake, binging/purging, body dysmorphia; cardiac arrhythmias, K+
s/s of bulimia