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46 Cards in this Set

  • Front
  • Back
cells excited by something
sensory- to brain
motor- to muscle
can be a single fiber (neuron)
or a collection of fibers (cluster)
nerves communicate with each other
terminal branches mesh with dendrites of next neuron to communicate
cell body- with nucleus center
axon- message sent through to terminal branches
humps synapse to next cell body
all nerves have some mylelin
white fiber that surrounds axon and terminal branches
prevents short circuits
the more myelin the faster the message gets sent
nonmyelinated- 1 layer of myelin
myelinated- 2 layers of myelin
Peripheral nervous system
nerve cells highly specialized
has healing capacity
healing rates:
1 inch/month
joint and roots are abbreviated
vertebrae are moveable
UMN: from brain to point in spinal cord where exists and interfaces with next neuron
LMN: cell body where dendrites are synapsing with spinal cord
reflex arch
serves brain functions for more important activities
saves time for reflex to take place
emergency shortcut
certain locations in body that because of where they are, can respond faster than any other place in body (knee reflex)
turns sensory input right into motor response
no need to go to brain
cross over
right side of brain controls left side of body
cross over takes place in spinal cord
motor crossover takes place at same point it exists
sensory crossover takes place about 2 levels above exit/entrance
Autonomic Nervous system
controlls: sweating, goosebumps, chills, heartbeating
involuntary nervous system
not consciously controlled
exist outside spinal cord
activated by sensory input, hormones and emotions
Autonomic Nervous subsystem
1. sympathetic
2. parasympathetic

one increases/starts, one decreases/ends
Autonomic dysreflexia
involutnary difficult reflexing
similar to reflex arch
not exactly sensory or motor
excessive response to stimulus because of lack of message to brain
brain moderates communication
when injury above T7, brain not able to communicate
Entrapment neuropathy
muscles and bones have a certain path that nerves follow if these get blocked by compression then problems arise
example: carpal tunnel syndrom
repetitive strain injury- compression of nerve
actual disease of tunnels and adds to disease of nerves- more difficulty
Guillain-Barre syndrom
autoimmune disease
upper GI infection
antibodies wiping out myelin
peripheral- outside nervous system
infectious polyneuritis (inflammation of many nerves)
starts infecting lower extremities and then 1-4 weeks, starts moving up body
progressive de-myelenization by on antibodies
return of functioning and myelin can happen
mostly no side effects
Transverse Myelitis
inflammation across spinal cord
tumors in spinal column
usually slow growing and once removed, recovery looks good
fast moving means
between mom and child
mom RH negative and baby RH positive
mom's blood begins to recognize babies blood as antigen and starts attacking it
attacking starts after birth and blood transfusion is needed
enzume attacking blood is called Bilireuben
Cerebral Palsy (CP)
prenatal, perinatal and postnatal damage occurs
up to age 8/9 years old
development during growth
disturbance in motor functioning
results from function of intracranial CNS tissue that is non-progressive and developed during growth and maturation stage of life

Type of CP
athetoid, spastic and ataxic at the same time

Type of CP
70% of cases
spasms in antogonistic muscles
rigid body
person has trouble doing what they want
can be so severe --> quadraplegic
scizzory gait
feet cross over
hemiplegia, hemiperesis
may have seizures

Type of CP
15% of cases
spasm in all 4 extremities
caused by kernicterus
problems speaking
facial grimacing
hearing loss
no seizures
intelligence is preserved
difficulty in life because of poor speech and language

Type of CP
5% of cases
feet set far apart
wide based walking
poor balance
difficulty reaching
causes of CP before birth
6-7 million births
prenatal: before birth
apoxia of mother- lack of oxygen
tortia- twisting of umbilical cord
intrauterine infection
breach birth
premature baby
low birth weight
placenta plevia- detached from uterus
other problems with CP
1. intelligence:
1/3 unaffected
1/3 mild MR
1/3 moderate to severe
2. seizures- 50%
3. visual problems
awkward gaze
strabismus- crossed eyes
4. hearing problems
5. dysarthria
6. personality and behavioral disorders
Gran Mal Seizure
Tonic- Clonic Seizures
aura before seisure
becomes weak, dizzy, and fall to floor
tonic contractions
generalized rigidity
clonic contractions
occurring in adulthood
loss of control, lose consciousness
status epilepticus
if tonic clonic seizure (grand mal) last more than 4 minutes
becomes dangerous and may die
Petite mal
mostly children
very brief, few seconds
others may not know
mal= storm, turmoil
absence of seizures
loss of consciousness
head drooping
stagger in walk
fixed daze
focal seizure
maybe combined with gran mal
involuntary motor activities that are localized
muscle group
half body- one arm, one leg
abnormal, involuntary motor act
when goes to both halves- lose consciousness
twilight state of consciousness
perform inappropriate acts
not really with it
strong emotion
hallucinations- visual and auditory
autonomic epilepsia
involuntary symptom
bradycardia- slow heartbeat
tachycardia- fast heartbeat
many symptoms can occur
blue or red in face
sudden flushing
treatment of seizures
1. medications- CNS depressants
2. combination of meds
3. 5-10% cannot be controlled
4. Take away drivers license until no seizure in 12 month period
seizure onset in adults
head trauma
seizure onset in adolescents
withdrawal from barbituates and alcohol
seizure onset in elderly
vascular disease
seizure onset in infancy
birth injury
congenital malformation
seizure onset in childhood
3-5% of children have seizure disorders
majority outgrow
due to fever
types of seizures
1% of general population have seizure disorder
1. gran mal (tonic clonic)
2. petite mal (absence seizure)
3. jacksonian (focal seizure)
4. psychomotor
5. autonomic epilepsia
explanation of seizure disorder/epilepsy
symptom, not disease itself
bad sudden brain rhythms
sudden discharge in CNS activity
gray matter
checmical signs and symptoms that interfere with normal functioning
Parkinson's disease
later in life- 50-70s
men and women equally
part of brain called substantia nigra starts to deteriorate
body stops producing dopanine in this area and problems start
dopamine can be taken but only works for short time
degeneration of brain
1st treatment- levadopa- dopamine replacement
Progression of Parkinson's
decrease in ADL
decrease in incoordination
initially minor, but then progresses
facial blinking
dull affect/no facial expression
initiating movement/stopping
shuffling gait
bradycarnsia- slow motor functioning
slow speech- dysarthria
small writing- micrographia
slow movements- bradykinesia
tremors when sleep
pellrose- fingers roll
occurs earlier in life
meds may work for a little longer
same symptoms
due to designer drugs/boxing
multiple sclerosis
the most recurrence- worst off person is
could be viral infection
overreaction to autoimmune
most common neurological disease
3 times more common in northern parts of US and Europe
affects myelin of the body
antigen enters, attacks myelin, body makes enzyme to kill antigen but then also kills myelin
myelin can regenerate
early signs: numbness, atoxia, speech, emotional

Types of MS
most common
sudden onset and relapse and remission
no permanent damage until next occurance
exacerbation- when things get worse
secondary progressive

Types of MS
many/all started as second type
but after 5+ years, problems accumulate
start with relapse
remittal- gets worse
slow worsening of ability without clear cut worsening
Amytrophys Lateral Sclerosis
Lou Gherig's Disease
disease of cell bodies
no known cause
motor neurons degenerate after age 40
starts in lower body and progression upwards in 3 years and then death
no treatment
no cure
progress upwards to brainstem
decreasing in breathing
motor neuronsn in spinal cord only
poliomyelitus (polio)
polio= gray
affects cell body
disease of cell body
virus --> contagious
destruction of nerves for few days.. then subsides
cell bodies completely destroyed and nothing to regenerate from
prognosis depends on how many dead cell bodies
attacks lowermotor neurons
post-polio syndrome
normal diminishing of neurons
person had polio at young age and it resulted in some defecits
as person goes through aging process, more deficits onset
they think they are going through it again
Myasthenia Gravis
diesase of myoneural junction
where muscle and nerve meet
fluid at this spot is not being produced properly
weakness in muscles
progrressive condition
disease where inability for impulse to travel
Muscular Dystrophy
genetically determined
progressive deteriorazation of muscles
children- male
wheelchair bound
early death
low IQ
no problem in brain
progressive weakness
infant- delayed milestones
face, shoulder and upper body
males and females
longer lifestyle