Exam 1 Quiz Flashcards

(127 cards)

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
what is the most common glial cell?
astrocyte
26
what is the NCV of both myel/nonmyel neuron and types of each
myelinated--72-120 know 100ms, alphaMN, 12-20 diam. | unmyelinated--.5-2 know 1ms, c-sensory, chronic pain, 1-diameter
27
astrocytes function
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
28
microglia
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
29
how does MS tie into glial cells?
damage to myelin sheath in CNS oligodendrocytes are attacked by own immune system Ab. yields patches of demyelination= plaques in white matter
30
Where does Na and K influx/efflux occur during depolarization and what kind of conduction is it?
at the Nodes of Ranvier | Saltatory conduction
31
Name the 4 main symptoms of PD and how many for Dx? | other diagnostics
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
32
Name all 5 reflexes and spinal level
``` C5- biceps C6-brachioradialis C7-triceps L3/4-quads S1-achilles, ankle jerk, PF's ```
33
What are common causes of nerve root compression? effects?
tumor, disc protrusion, closing of facets | decreased myotome, DTR, dermatome-sensory loss, often pain
34
Name the myotomes and spinal level
``` 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 ```
35
Neuro level C5
deltoid and bicep | bicep reflex
36
Neuro level C6
biceps, Wrist extensors(ECRL,ECRB) | brachioradialis reflex
37
Neuro level C7
triceps, wrist flexors, finger extensors | triceps reflex
38
Neuro level C8
interossei muscles | no DTR
39
Neuro level T1
interossei muscles | no DTR
40
Neuro level L4
Tib. Ant--inversion | Quad reflex
41
Neuro level L5
Extensor Hall. Longus | No DTR
42
Neuro level S1
Peroneus L and B--eversion | Achilles reflex
43
LMN signs and symptoms
Atrophy, weakness/paralysis, hypotonic DTRs, decreased muscle tone, fasciculations-rapid, fine, contractions of muscle fibers, painful/painless
44
UMN sxs
spasticity, hypo/hypertonic DTRs, clonus, +babinski/hoffman, weakness, synergistic movement patterns
45
Which type gives glove/sock like sensory loss
UMN
46
Motor loss occurs where
pre central gyrus Broadman area 4
47
sensory loss occurs where
post central gyrus Broadman area 3,1,2
48
Radial nerve
C6-8 T1 elbow extension, wrist/finger ext., supination sensory-thumb web
49
Ulnar Nerve
C8 T1 interossei, little finger abd. sensory- pinky finger
50
Median nerve
C6-8 T1 wrist flexion, long finger flexors, pronation sensory- palm and tips of 1-3, 1/2 of 4th digit
51
Common peroneal
L4-5 S1-2 motor-DF, eversion, toe extension sensory- lat. knee
52
Deep peroneal
DF, toe extension (extensors hallucis, digitorum) | sensory- between digits 1-2
53
superficial peroneal
Eversion (peroneus longus and brevis) | sensory- entire lat. leg
54
Tibial
L4-5, S1-3 Ankle PF, Inversion, toe flexion Sensory-sole and heel
55
Hoehn and Yahr stages
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
Meds for parkinsons and how they work
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
Surgery for PD and how\/why better
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
PD--how much decrease in neurons or DA b4 sxs?
80% for both
59
Other PD tx?
external sensory cues--laser cane--visual cue for floor, music therapy-pulse or beat...Dr. Ed Roth
60
What types of BG disorders and who is in what one?
Hypokinetic-PD | Hyperkinetic-Huntington's chorea, Dystonia, Tourette's
61
What is effected in PD BG?
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
What is effected in Huntington's chorea?
The striatal neurons to SNr and LGP are degenerated. which leads to under-inhibition of the thalamus and over-facilitation of the cortex
63
What is effected in Tourette's?
disturbance in limbic system circuits causes inhibition of SNc= less inhibition of thalamus, over-facilitation of cortex
64
What is effected in Dystonia?
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
PD sxs
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
Death in PD
usually choking, pneumonia, falls after ~20 yrs
67
Death in Huntington's
15-20 years after onset, probably from choking, weight loss
68
Death in Freiderich's ataxia
HEART DISEASE/ATTACK
69
Onset for PD..How?
idiopathic-unknown | MPTP
70
How does Sinemet work?
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
Dystonia sxs
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
Tx for Dystonia?
BOTOX for focal General-baclofen, artane, sinemet, klonopin DBS of GP, or Rhizotomy
73
Dystonia types
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
Tourettes sxs
impulsions/compulsions to perform fragments of motor programs TICS- skipping, jumping, touching, vocalization
75
Huntington's sxs
``` 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
Huntington's onset
after ~30 y/o death 15-20 years later. Mauritius has high population 1 in 2,166
77
HC Early stage
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
HC middle stage
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
HC late stage
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
HC medication
``` cholinergic-GABA containing perphenazine haloperidol reserpine riluzole ```
81
unified HD rating scale UHDRS
``` motor assess cog assess behavioral assess independence scale functional scale total functional capacity ```
82
parts of a neuron...go
dendrite, cell body, axon hillock, axon, node of ranvier, myelin sheath, presynaptic terminal, presynaptic membrane, synaptic cleft, post synaptic membrane
83
functions of both neo and spino
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
How much time does it take to correct an action in the moment?
100-200ms
85
functions of both vestibulo and spino
excitatory influence on gamma motor neurons with acute cerebellar damage, decreased excitation of gamma's=decreased sensitivity of spindles=decreased tone-hypotonicity
86
what part of brain contains more neurons than anywher?
Cerebellum
87
8 cell types in cerebellum
Purkinje, Granule, Golgi, Parallel, Stellate, Basket, Mossy fibers, Climbing fibers-afferent input
88
4 types of deep nuclei
fastigial interposed-globose and emoliform vestibular--flocculonodular dentate-worm like
89
Where are all the axons to/from cerebellum held?
in the peduncles
90
Main function of cerebellum and how it does its job
vast integration of info concerning mvmt and complex computations of movement, because of the infolding-gyri and sulci--all anatomically similar
91
Vestibulocerebellum inputs and what they are bringing in
from vestibular nuclei to the focculonodular lobe | sense change in linear/angular head position, rotation, accel/deceleration
92
Vestibulocerebellum outputs and function
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
Neocerebellum inputs and where
from ipsilateral cortex, to corticopontocerebellar tract to pontine nuclei to LATERAL ZONES--frontal and parietal lobe, motor, sensory, PMa, SMA
94
Neocerebellar outputs
dentate nucleus to VL thalamus, to premotor and motor cortices
95
Neocerebellar function
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
Spinocerebellar inputs to vermis and what
dorsal spinocerebellar, cuneocerebellar, and trigeminocerebellar from head and trunk Also, vestibular and tectocerebellar--from superior-visual and inferior-auditory- colliculi
97
Spinocerebellar inputs to intermediate zone and what
dorsal spinocerebellar, cuneocerebellar from UE and LE
98
Spinocerebellar outputs from vermis
GROUP A-GROSS MOTOR thalamus->M1 area->Anterior CST fastigial nuclei->reticular nuclei->CMRST vestibular nuclei->vestibulospinal tract lat and med.
99
Spinocerebellar outputs from intermediate zone
GROUP B-FINE MOTOR thalamus->M1 area and SMA->Lateral CST reticular nuclei->CPRST interposed nuclei->red nuclei->rubrospinal tract
100
Spinocerebellar function from vermis
GROSS MOTOR MVMT coordination of axial and girdle musculature regulates rhythmic walking--CPG's of gait adjusts timing of locomotor mvmt interlimb coordination
101
Spinocerebellar function from intermediate zones
FINE MOTOR MVMT | coordination of distal musculature of distal extremities, hands and feet
102
Name the lobes and zones of cerebellum
anterior lobe, posterior lobe, flocculonodular lobe | vermis, intermediate zone, lateral zones
103
What will happen with damage to cerebellum?
poor coordination without overt muscle weakness
104
Hypotonicity
decreased firmness and tone during PROM, pendular DTR's, decreased extensor tone=trouble remaining upright
105
Asthenia
general weakness or decreased activity and easy fatigue
106
intention tremors and amplitude
3-5 Hz, amplitude increases as effector approaches target
107
disturbances of posture and balance
flexed posture, wide BOS, poor equilibrium and balance especially in axial body and rapid changes VESTIBULOCEREBELLUM
108
Dysmetria
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
Dysdiadochokinesia
rapid alternating supination/pronation shin test deficit in coordination--errors in rate/timing, range/amplitude
110
Ataxic gait
disruption in rhythm of gait, wide based gait, unsteady falls are back and toward side of lesion SPINO-VERMIS
111
Movement Decomposition
disruption in sequence in a multi step task, breaking a multi-joint movement into a series of seperate movements NEOCEREBELLUM
112
Poor coordination of muscles associated with speech
dysarthria-slurred | explosive/staccato speech
113
Eye movements
gaze evoked nystagmus, ocular dysmetria, disrupted smooth pursuit, poor coordination of eye/head movement. VESTIBULOCEREBELLUM maybe more
114
TIme asymetric velocity profiles
normal=equal time in accel./decel. mild= more time in decel. severe= more time in accel.
115
Delays in force production and error in force maintenance
difficulty generating enough force, matching to the wt. of the object, and maintaining that force
116
Friederich's ataxia onset
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
Friederich's ataxia sxs
``` 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
FA life expectancy
60-70 if no Heart attack | progressive disease where you eventually lose ability to walk and confined to wheelchair in 10-20 years
119
Cerebellar stroke
less than 5% of all strokes involve Post/inf, Ant/inf, or superior cerebellar arteries if deep cerebellar nuclei are involved->px worse
120
Cerebellar tumor
Children more common but have better PX b/c usually benign and removed with surgery Adults--more likely aggresive cancer--poor Px
121
Static balance T
maintain a position over time--time is the measure
122
Static balance R
maintain a position against resistance | rhythmic stabilization and alternating isometrics
123
Static Balance AFF
maintain a position while reaching within arms length | Anticipatory feed forward
124
Dynamic Balance RFB
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
Dynamic Balance AFF
anticipatory feed forward | sitting/standing--reach in various directions beyond arms length to elicit various trunk and arm balance reactions
126
Protective reactions
slow/quick displacement of COM outside BOS to elicit a change--placing a hand or foot out to catch the body
127
Functional balance
AFF and RFB --utilizing effective balance strategies while performing a set of functional tasks that increases in difficulty