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Neuro D&D > Exam 1 Quiz > Flashcards

Exam 1 Quiz Flashcards

1
Q

Name a presynaptic and postsynaptic acting disorder and explain how each works specifically and what each causes generally.

A

Pre- botulism–blocks Ach from binding the presyanptic membrane for release into synaptic cleft so nerve impulse fails to be transmitted across neuromuscular junction which causes muscle paralysis.
Post- MG– antibodies to ACh change the shape of the post synaptic membrane to be wider and have less receptors so ACh has less chance of finding a receptor to bind before it is hydrolyzed by AChesterase which causes increased muscle weakness.

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2
Q

Name 2 types of MG

A

ocular–symptoms in extraocular muscles only= diplopia and ptosis (10-15% of cases) and generalized (85%)

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3
Q

Where does MG weakness symptoms start?

A

BUE and BLE weakness starts proximal and moves distal

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4
Q

What is the action of recovery from botulism?

A

create NEW terminal nerve filaments and formation of NEW synapses at the NMJ

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5
Q

When using BOTOX as a tx what happens in PT?

A

as soon as BOTOX starts to take effect in 4-7 days PT is MANDATORY. should utilize active stretching with care to not overstretch and tear weak muscles, + reciprocal inhibition and serial casting/dynasplint if necessary AND strengthen the ANTAGONIST muscle

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6
Q

What kinds of pts can use BOTOX?

A

SCI, TBI, CVA, MS, Dystonia, hypertonicity–focal spasticity

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7
Q

How long does BOTOX tx last? how long until NMJ takes up? How long until see effects in pt?

A

3-4 months, 12 hours, 4-7 days

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8
Q

How does one contract botulism?

A

food bourne, improperly preserved foods/canned foods, wounds

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9
Q

Prevention for botulism?

A

no honey for <1 y/o, wounds clean, boil food for 10 minutes

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10
Q

Onset and Recovery time frame for botulism

A

12-36 hours for sxs, gradual full recovery in wks/months

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11
Q

Intervention for MG?

A

thymectomy(10-15% have tumor, 70% have enlargement)
anticholinesterase drugs
immunosuppressives-prednisone, cyclosporine, mycophenolate, azathioprine
IVIG
plasmaphoresis–lasts 4-6wks

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12
Q

Dx of MG?

A

Ab in blood for ACh receptors
Decremental EMG–decreased strength in repeated stimulation
Tensilon test–Achesterase inhibitor, so it acts to prevent ACh breakdown which will allow more time for it to bind to receptors= increased strength/endurance
Muscle biopsy- count ACh receptors

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13
Q

Symptoms of botulism

A 
flaccid symmetrical paralysis
diplopia, blurred vision, ptosis
dry mouth N&amp;V
lethargy
difficult swallow and speech
Respiratory distress
Autonomic involvement--symp/parasymp
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14
Q

Symptoms of MG

A 
ocular--diplopia, ptosis=CN3
facial weakness=CN7
oropharyngeal weakness
chewing/swallowing/speaking difficulty
BUE/BLE weakness starts prox to dist
respiratory muscle weakness
Fluctuates over days/hours--better in AM, declines with day/exercise
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15
Q

What type of population does MG affect?

specific term needed

A

Bimodal–30 year old women, 60 year old men
1 in 10-20,000 in US
15-30, 60-75 y/o
females>males 3:2

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16
Q

What is normal in both botulism and MG?

A

sensory. MG also reflexes and coordination

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17
Q

MG crisis

A

respiratory or choking

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18
Q

Intervention for Botulism

A

ABE serum antitoxin, antibiotics, debridement, gastric lavage, IV, mechanical vent

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19
Q

example of dendritic arborization

A

purkinje cell in cerebellum, tree like, many inputs to 1 output for slots of integration of information

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20
Q

neurons–types and where seen

A

multipolar- motor neurons–many dendrite 1 axon
bipolar–interneuron, 1 dendrite, 1 axon
unipolar–sensory–many dendrites 1 axon, cell body is removed usually in DRG

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21
Q

Glial cells 4 functions

A

structure and support
nutrients and oxygen
myelination
destroy pathogens, remove dead cells

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22
Q

Glial cell types and where found

A

PNS-Schwann cells

CNS-oligodendrocytes, astrocytes, microglia

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23
Q

Schwann cell functions

A

myelination of 1 neuron–wraps around axon, forms nodes of Ranvier

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24
Q

Oligodendrocyte functions

A

myelination of MANY neurons
insulate and protect
increase NCV
involved in Alzheimer’s and MS

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25
Q

what is the most common glial cell?

A

astrocyte

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26
Q

what is the NCV of both myel/nonmyel neuron and types of each

A

myelinated–72-120 know 100ms, alphaMN, 12-20 diam.

unmyelinated–.5-2 know 1ms, c-sensory, chronic pain, 1-diameter

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27
Q

astrocytes function

A

fill brain space–support and insulation
maintain BBB
divide and wall off areas of damage from inflamm/injury
scavenge–remove NT’s from synaptic cleft, clean up debris in development/injury

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28
Q

microglia

A

phagocytosis!!!
protective- mobilize after injury/infect/disease
phagocytose bacteria and cells, important in devel.
destructive–in Alzheimer’s/aging=release toxins
in HIV/AIDS=cellular breakdown

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29
Q

how does MS tie into glial cells?

A

damage to myelin sheath in CNS
oligodendrocytes are attacked by own immune system Ab.
yields patches of demyelination= plaques in white matter

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30
Q

Where does Na and K influx/efflux occur during depolarization and what kind of conduction is it?

A

at the Nodes of Ranvier

Saltatory conduction

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31
Q

Name the 4 main symptoms of PD and how many for Dx?

other diagnostics

A

2/4
bradykinesia
resting tremors-pill rolling
posture instability–hypometric anticipatory adjustment
rigidity-cog-wheeling, lead pipe
can get CT or MRI to rule out other disease
positive response to DA-like medication

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32
Q

Name all 5 reflexes and spinal level

A 
C5- biceps
C6-brachioradialis
C7-triceps
L3/4-quads
S1-achilles, ankle jerk, PF's
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33
Q

What are common causes of nerve root compression? effects?

A

tumor, disc protrusion, closing of facets

decreased myotome, DTR, dermatome-sensory loss, often pain

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34
Q

Name the myotomes and spinal level

A 
C4- shoulder shrug
C5-shoulder abduction
C6-wrist extension
C7- elbow extension
C8-finger flexion/wrist flexion
T1-abd/add of fingers
L1/2-hip flexion
L3/4-knee extension
L5-S2-knee flexion
S1/2-PF
S2/3-abduction of toes
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35
Q

Neuro level C5

A

deltoid and bicep

bicep reflex

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36
Q

Neuro level C6

A

biceps, Wrist extensors(ECRL,ECRB)

brachioradialis reflex

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37
Q

Neuro level C7

A

triceps, wrist flexors, finger extensors

triceps reflex

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38
Q

Neuro level C8

A

interossei muscles

no DTR

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39
Q

Neuro level T1

A

interossei muscles

no DTR

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40
Q

Neuro level L4

A

Tib. Ant–inversion

Quad reflex

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41
Q

Neuro level L5

A

Extensor Hall. Longus

No DTR

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42
Q

Neuro level S1

A

Peroneus L and B–eversion

Achilles reflex

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43
Q

LMN signs and symptoms

A

Atrophy, weakness/paralysis, hypotonic DTRs, decreased muscle tone, fasciculations-rapid, fine, contractions of muscle fibers, painful/painless

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44
Q

UMN sxs

A

spasticity, hypo/hypertonic DTRs, clonus, +babinski/hoffman, weakness, synergistic movement patterns

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45
Q

Which type gives glove/sock like sensory loss

A

UMN

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46
Q

Motor loss occurs where

A

pre central gyrus Broadman area 4

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47
Q

sensory loss occurs where

A

post central gyrus Broadman area 3,1,2

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48
Q

Radial nerve

A

C6-8 T1
elbow extension, wrist/finger ext., supination
sensory-thumb web

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49
Q

Ulnar Nerve

A

C8 T1
interossei, little finger abd.
sensory- pinky finger

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50
Q

Median nerve

A

C6-8 T1
wrist flexion, long finger flexors, pronation
sensory- palm and tips of 1-3, 1/2 of 4th digit

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51
Q

Common peroneal

A

L4-5 S1-2
motor-DF, eversion, toe extension
sensory- lat. knee

52
Q

Deep peroneal

A

DF, toe extension (extensors hallucis, digitorum)

sensory- between digits 1-2

53
Q

superficial peroneal

A

Eversion (peroneus longus and brevis)

sensory- entire lat. leg

54
Q

Tibial

A

L4-5, S1-3
Ankle PF, Inversion, toe flexion
Sensory-sole and heel

55
Q

Hoehn and Yahr stages

A

1- unilateral, inconvient, mild, not disabling, tremor of 1 limb
2- bilateral, minimal disability, posture and gait affected
3- significant slowing of movement and QOL effect, moderately severe disability
4- Severe symptoms, rigidity, bradykin, limited ability to walk, cannot live alone
5- totally dependent-cannot stand or walk

56
Q

Meds for parkinsons and how they work

A

Medication–L-dopa-breaks down b4 BBB-1% effective, sinemet–perfect design, decreases brady and rigid–other side effects though, ropinorole, pramipexole, neupro patch-last 3 cross BBB to stimulate DA receptors directly=less dyskinesia

DELICATE BALANCE/ON/OFF phenomenon/DRUG HOLIDAY

57
Q

Surgery for PD and how\/why better

A

DBS-deep brain stimulation
reversible, better for bilateral, fewer side effects, less severe fluctuations and amplitude, stim of GP or STN= decrease of all symptoms and decrease of dyskinesia

Stereotaxic- ablate a part of BG–GP-palladotomy=decrease brady, tremor, rigid. OR thalamotomy= decrease tremor

58
Q

PD–how much decrease in neurons or DA b4 sxs?

A

80% for both

59
Q

Other PD tx?

A

external sensory cues–laser cane–visual cue for floor, music therapy-pulse or beat…Dr. Ed Roth

60
Q

What types of BG disorders and who is in what one?

A

Hypokinetic-PD

Hyperkinetic-Huntington’s chorea, Dystonia, Tourette’s

61
Q

What is effected in PD BG?

A

The SNc is degenerated so it does not make enough DA and the thalamus is over-inhibited which leads to under-facilitation of cortex.

62
Q

What is effected in Huntington’s chorea?

A

The striatal neurons to SNr and LGP are degenerated. which leads to under-inhibition of the thalamus and over-facilitation of the cortex

63
Q

What is effected in Tourette’s?

A

disturbance in limbic system circuits causes inhibition of SNc= less inhibition of thalamus, over-facilitation of cortex

64
Q

What is effected in Dystonia?

A

unknown etiology–usually from vascular issue–stroke, TBI, anoxia
can be genetic–general dystonia–DYT1 gene–onset 8y/o
can be lesions of any/all BG–focal dystonia–affects 1 body part/joint/related joints, onset at 30-50y/o

65
Q

PD sxs

A

difficulty swallowing/chewing
speech impaired–too soft, monotone, hesitant, slurred
flat affect of face
fatigue, sleep problems
decreased strength of respiratory muscles
dimentia/cognitive problems
kyphosis, flexed trunk, forward head, crouched legs
micrographia-words are cramped and slow
Difficulty initiating GAIT-freezing, festinating–shuffle/fall
decreased trunk rotation and arm swing

66
Q

Death in PD

A

usually choking, pneumonia, falls after ~20 yrs

67
Q

Death in Huntington’s

A

15-20 years after onset, probably from choking, weight loss

68
Q

Death in Freiderich’s ataxia

A

HEART DISEASE/ATTACK

69
Q

Onset for PD..How?

A

idiopathic-unknown

MPTP

70
Q

How does Sinemet work?

A

carbidopa prevents levodopa from being broken down b4 it crosses the BBB, but carbidopa cannot cross too so L-dopa gets to breakdown once inside the brain.
lasts 4-5 years before tolerance generated.–2 thoughts: save for later, or use now b4 too few neurons in SNc

71
Q

Dystonia sxs

A

simultaneous contraction of agonist and antagonist muscle–sustained contraction at end ROM–involuntary
can be rapid or slow, rhythmic or unpatterned
can last minutes to hours +
rigidity, usually painful, contorted/twisted postures
can be onset by stress, purposeful mvmt, task-specific activity–musicians or writers
NOT FATAL- decreased with relax and sleep

72
Q

Tx for Dystonia?

A

BOTOX for focal
General-baclofen, artane, sinemet, klonopin
DBS of GP, or Rhizotomy

73
Q

Dystonia types

A

focal–pharyngeal, cervical–most common–not torticollis, writers cramp, musicians cramp–progresses for ~5 years–30% spontaneous recovery
General- entire body-genetic
begins in legs and progresses to rest of body. starts with a mvmt then twisted trunk, then to UE, LE

74
Q

Tourettes sxs

A

impulsions/compulsions to perform fragments of motor programs
TICS- skipping, jumping, touching, vocalization

75
Q

Huntington’s sxs

A 
Aspects of behavioral, cognitive, and motor
chorea-invol small amplitude, rapid mvmt
akinesia/bradykinesia
hypotonia
wide, staggering gait
speech lacks timing and rhythm
difficulty swallowing
saccadic eye mvmts
dementia, poor judgement, decreased long term memory, depression and irritability
76
Q

Huntington’s onset

A

after ~30 y/o death 15-20 years later. Mauritius has high population 1 in 2,166

77
Q

HC Early stage

A

symptoms for DX–can continue work/drive/etc.
starts in EXTREMITIES–invol twitches of fingers/toes/face
subtle loss of coordination
harder to work and perform at usual cog level
difficult to think through complex tasks
depression, irritability, DISINHIBITION

78
Q

HC middle stage

A

loss of ability to work and drive
difficulty swallowing, slurred speech, staggering walk, CHOREA, weight loss
difficulty thinking clearly, organizing info, problem solving
increased APATHY, loss of interest in activities and increased depression, irritable, disinhibited more

79
Q

HC late stage

A

totally dependent, bed ridden, unable to speak, choke, tube fed
severe rigidity, dystonia, bradykin. Chorea usually gone
cannot initiate mvmt
cognitively debilitating–recognize faces, understand speech
depression fades, increased apathy, psychosis in some

80
Q

HC medication

A 
cholinergic-GABA containing
perphenazine
haloperidol
reserpine
riluzole
81
Q

unified HD rating scale UHDRS

A 
motor assess
cog assess
behavioral assess
independence scale
functional scale
total functional capacity
82
Q

parts of a neuron…go

A

dendrite, cell body, axon hillock, axon, node of ranvier, myelin sheath, presynaptic terminal, presynaptic membrane, synaptic cleft, post synaptic membrane

83
Q

functions of both neo and spino

A

comparator–compares actual outcome to intended motor program.
collects continuous info about desired program from M1, PMA, SMA cerebral cortex
collects continuous info from peripheral muscle spindles, GTO’s, proprioceptors, and tactile receptors about instant status of body–body parts, position, force, and rate of motion

84
Q

How much time does it take to correct an action in the moment?

A

100-200ms

85
Q

functions of both vestibulo and spino

A

excitatory influence on gamma motor neurons
with acute cerebellar damage, decreased excitation of gamma’s=decreased sensitivity of spindles=decreased tone-hypotonicity

86
Q

what part of brain contains more neurons than anywher?

A

Cerebellum

87
Q

8 cell types in cerebellum

A

Purkinje, Granule, Golgi, Parallel, Stellate, Basket, Mossy fibers, Climbing fibers-afferent input

88
Q

4 types of deep nuclei

A

fastigial
interposed-globose and emoliform
vestibular–flocculonodular
dentate-worm like

89
Q

Where are all the axons to/from cerebellum held?

A

in the peduncles

90
Q

Main function of cerebellum and how it does its job

A

vast integration of info concerning mvmt and complex computations of movement,
because of the infolding-gyri and sulci–all anatomically similar

91
Q

Vestibulocerebellum inputs and what they are bringing in

A

from vestibular nuclei to the focculonodular lobe

sense change in linear/angular head position, rotation, accel/deceleration

92
Q

Vestibulocerebellum outputs and function

A

from flocculonodular to vestibular nuclei
coordinates eye/head mvmt, equilibrium and balance, coordinates proximal musculature of axial body–head, neck, trunk, pelvis/hips, scap/shoulder
senses rapid position and direction changes

93
Q

Neocerebellum inputs and where

A

from ipsilateral cortex, to corticopontocerebellar tract to pontine nuclei to LATERAL ZONES–frontal and parietal lobe, motor, sensory, PMa, SMA

94
Q

Neocerebellar outputs

A

dentate nucleus to VL thalamus, to premotor and motor cortices

95
Q

Neocerebellar function

A

planning and timing of voluntary movements, particularly learned, skillful movement that becomes more rapid, precise, and automatic with practice
motor planning of sequential movement
onset, rate, amplitude, and duration of agonist and antagonist mm.
SO= associated with mvmt DECOMPOSITION, and DYSMETRIA

96
Q

Spinocerebellar inputs to vermis and what

A

dorsal spinocerebellar, cuneocerebellar, and trigeminocerebellar from head and trunk
Also, vestibular and tectocerebellar–from superior-visual and inferior-auditory- colliculi

97
Q

Spinocerebellar inputs to intermediate zone and what

A

dorsal spinocerebellar, cuneocerebellar from UE and LE

98
Q

Spinocerebellar outputs from vermis

A

GROUP A-GROSS MOTOR
thalamus->M1 area->Anterior CST
fastigial nuclei->reticular nuclei->CMRST
vestibular nuclei->vestibulospinal tract lat and med.

99
Q

Spinocerebellar outputs from intermediate zone

A

GROUP B-FINE MOTOR
thalamus->M1 area and SMA->Lateral CST
reticular nuclei->CPRST
interposed nuclei->red nuclei->rubrospinal tract

100
Q

Spinocerebellar function from vermis

A

GROSS MOTOR MVMT
coordination of axial and girdle musculature
regulates rhythmic walking–CPG’s of gait
adjusts timing of locomotor mvmt
interlimb coordination

101
Q

Spinocerebellar function from intermediate zones

A

FINE MOTOR MVMT

coordination of distal musculature of distal extremities, hands and feet

102
Q

Name the lobes and zones of cerebellum

A

anterior lobe, posterior lobe, flocculonodular lobe

vermis, intermediate zone, lateral zones

103
Q

What will happen with damage to cerebellum?

A

poor coordination without overt muscle weakness

104
Q

Hypotonicity

A

decreased firmness and tone during PROM, pendular DTR’s, decreased extensor tone=trouble remaining upright

105
Q

Asthenia

A

general weakness or decreased activity and easy fatigue

106
Q

intention tremors and amplitude

A

3-5 Hz, amplitude increases as effector approaches target

107
Q

disturbances of posture and balance

A

flexed posture, wide BOS, poor equilibrium and balance especially in axial body and rapid changes
VESTIBULOCEREBELLUM

108
Q

Dysmetria

A

over or under shooting, left or right,up or down
past-pointing
force issue—triphasic EMG–AG1, ANTAG and AG2 not programmed correctly
NEOCEREBELLUM

109
Q

Dysdiadochokinesia

A

rapid alternating supination/pronation
shin test
deficit in coordination–errors in rate/timing, range/amplitude

110
Q

Ataxic gait

A

disruption in rhythm of gait, wide based gait, unsteady
falls are back and toward side of lesion
SPINO-VERMIS

111
Q

Movement Decomposition

A

disruption in sequence in a multi step task, breaking a multi-joint movement into a series of seperate movements
NEOCEREBELLUM

112
Q

Poor coordination of muscles associated with speech

A

dysarthria-slurred

explosive/staccato speech

113
Q

Eye movements

A

gaze evoked nystagmus, ocular dysmetria, disrupted smooth pursuit, poor coordination of eye/head movement.
VESTIBULOCEREBELLUM maybe more

114
Q

TIme asymetric velocity profiles

A

normal=equal time in accel./decel.
mild= more time in decel.
severe= more time in accel.

115
Q

Delays in force production and error in force maintenance

A

difficulty generating enough force, matching to the wt. of the object, and maintaining that force

116
Q

Friederich’s ataxia onset

A

hereditary, 5-15 y/o, 25% of offspring
lesions affect cerebellum
DRG-sensory
dorsal columns-conc. prop., fine touch, vibration
spinocerebellar tracts-unconcious proprioception
some corticospinal tract involvement

117
Q

Friederich’s ataxia sxs

A 
ataxia of gait 1st then extremities
clumsiness, intention tremor
loss of extrem sensation
\+babinski
decreased DTRs
tone is normal at rest
nystagmus and impaired smooth pursuit
HEART DISEASE
easily fatigued
scoliosis
slurred difficult speech
118
Q

FA life expectancy

A

60-70 if no Heart attack

progressive disease where you eventually lose ability to walk and confined to wheelchair in 10-20 years

119
Q

Cerebellar stroke

A

less than 5% of all strokes involve Post/inf, Ant/inf, or superior cerebellar arteries
if deep cerebellar nuclei are involved->px worse

120
Q

Cerebellar tumor

A

Children more common but have better PX b/c usually benign and removed with surgery
Adults–more likely aggresive cancer–poor Px

121
Q

Static balance T

A

maintain a position over time–time is the measure

122
Q

Static balance R

A

maintain a position against resistance

rhythmic stabilization and alternating isometrics

123
Q

Static Balance AFF

A

maintain a position while reaching within arms length

Anticipatory feed forward

124
Q

Dynamic Balance RFB

A

reactive feedback
sitting/standing–manually place COM to edges of BOS to elicit an equilibrium reaction–movement of trunk, arms, legs to counteract the balance point

125
Q

Dynamic Balance AFF

A

anticipatory feed forward

sitting/standing–reach in various directions beyond arms length to elicit various trunk and arm balance reactions

126
Q

Protective reactions

A

slow/quick displacement of COM outside BOS to elicit a change–placing a hand or foot out to catch the body

127
Q

Functional balance

A

AFF and RFB –utilizing effective balance strategies while performing a set of functional tasks that increases in difficulty

Neuro D&D (3 decks)

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