Exam 4 Flashcards

(73 cards)

1
Q

UMN tract for cranial nerves

A

corticobrainstem tracts

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2
Q

UMN tracts that don’t guide movement. Partially depolarize LMN to enable quick action

A

nonspecific activating tracts

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3
Q

partial loss of muscle strength

A

paresis

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4
Q

complete loss of muscle strength

A

paralysis (-plegia)

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5
Q

which motor neurons will have more severe atrophy if damaged

A

lower motor neurons

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6
Q

the atrophy of denervation is associated with which motor neurons

A

LMN

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7
Q

short-lived involuntary contraction of muscle tissue often due to metabolic or muscular issues

A

muscle spasm

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8
Q

a prolonged contraction of muscle tissue often due to metabolic or muscular issues

A

muscle cramp

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9
Q

involuntary contractions of entire motor units. Generally indicate irritation of motor neuron. Can be benign or pathologic

A

fasciculations

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10
Q

involuntary contraction of multiple muscles (limb or whole body) that typically occurs between sleep and wake state. No proximate cause

A

myoclonus

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11
Q

generally indicative of neural damage

can be resting or intention: suggestive of pathology in the cerebellum

A

tremors

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12
Q

very important diagnostic finding that cannot be observed. The spontaneous contraction of 1 muscle fiber that has lost its nerve. Indicates denervation (muscle fiber has lost it’s nerve)

A

fibrillations

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13
Q

type of hypertonia where if a muscle is moved slowly, there is no hypertonia. When a muscle is quickly stretched, the muscle overreacts.

A

velocity dependent

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14
Q

type of hypertonia where speed doesn’t matter, there is always high tone

A

velocity independent

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15
Q

posturing due to too much activity from the brainstem UMN. Involuntary continuous contraction of extensor muscles in UE and LE

A

decerebrate

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16
Q

posturing where connection from cortex to brainstem has been severed. Pattern is involuntary hypertonia in flexion of arms and extension of legs.

A

decorticate

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17
Q

potential sources of damage to LMN

A
Trauma (sharp or blunt) 
Infection (e.g., polio)
Degenerative disorders (e.g., ALS)
Vascular disorders
Tumors
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18
Q

a tremor at rest suggests what pathology

A

Parkinson’s Disease

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19
Q

an intention tremor is suggestive of pathology of the _____

A

cerebellum

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20
Q

Signs and symptoms of LMN disorder

A

Loss of reflexes
Atrophy (more likely atrophy of denervation)
Flaccid paralysis: low tone inability to move
Fibrillations

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21
Q

potential sources of damage to UMN

A
Spinal cord injury
Cerebral palsy
Multiple sclerosis
Degeneration (e.g., Parkinson’s Disease)
Trauma
Loss of blood supply (e.g., Stroke)
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22
Q

Signs and symptoms of UMN disorder

A
paresis
paralysis 
loss of "fractionated" movement 
abnormal cutaneous reflexes (babinski response...limb withdrawal)
muscle stretch hyperreflexia 
clonus 
clasp-knife response
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23
Q

what does the process of collateral sprouting create

A

giant motor unit (one axon innervates more muscle fibers than normal)

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24
Q

if a person had a stroke that only damaged the cortex, they would have ___

A

paresis

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25
Exaggerated reflex response when descending inhibition is missing or much reduced or when UMN is damaged
muscle stretch hyperreflexia
26
2 ways to help muscle stretch hyperreflexia
don't stretch quickly and use pharmacology to turn down LMN (act like GABA)
27
how do you elicit clonus
quick stretch
28
Rhythmic, repeating (usually involuntary) contraction | A series of hyperreflexia responses when there is a continuing stimulus of stretch
clonus
29
how to prevent clonus
Pharmacology Position ankles in extreme dorsiflexion Lift leg and set it back down slowly Lean on that leg
30
when clonus is sustained, this is an indication of what
UMN damage
31
example of hyperreflexic response to stretch that goes away (UMN damage)
clasp-knife response
32
what are 2 ways that the muscle changes in response to lack of movement due to UMN injury
atrophy and increased mechanical stiffness/contracture
33
what are different ways we can have hypertonia or spasticity
hyperreflexia or brainstem UMN overactivity
34
types of brainstem overractivity
more tonic or resting (i.e. "rigidity" of PD) | more activity dependent (i.e. muscle overactivity of CVA that create abnormal synergies)
35
where does the basal ganglia motor loop output to
cortical UMN via thalamus and brainstem UMN via pedunculopontine nucleus
36
predict the effects of various actions, then make and execute action plans
basal ganglia
37
piece of basal ganglia that malfunctiosn to cause PD
substantia nigra
38
excitatory neurotransmitter that has input signals from other brain regions to Putamen
glutamate
39
5 basal ganglia loops
``` motor oculomotor executive behavior flexibility and control limbic ```
40
loop from basal ganglia to pre central gyrus and back. Contains the plan to move
motor
41
loop from basal ganglia to prefrontal cortex. Decides what to do
executive
42
As a group, basal ganglia "loops" help with
``` predicting future events selecting desired behaviors preventing undesired behaviors motor learning (procedural memory) shifting attention spatial working memory ```
43
Motor "loop" regulates
Muscle contraction Muscle force Multijoint movements Sequencing of movements
44
is the basal ganglia motor loop excitatory or inhibitory
inhibitory
45
pathology where there is death of dopamine producing cells in substantial nigra
akinetic/rigid PD
46
excitatory and is the neurotransmitter that makes the basal ganglia circuitry work properly to plan movements. Without it, the basal ganglia malfunction
dopamine
47
with dopamine gone, the output of basal ganglia increases, leading to
Too little activation of voluntary muscles Too much activation of postural and girdle muscles Too little activation of midbrain locomotor region
48
signs and symptoms of akinetic/rigid parkinson's disease
akinesia/hypokinesia rigidity postural instability resting tremor
49
hyperkinetic disorder involving the basal ganglia where it doesn't output enough
Huntington's disease
50
degeneration of striatum and cerebral cortex
Huntington's disease
51
tremor of movement where you miss the target and correct it
action tremor
52
inability to rapidly/smoothly alternate the direction of movement
Dysdiadochokinesia
53
Wide-based, unsteady, staggering, veering gait
ataxic gait
54
side effects of spinocerebellum damage
ataxic gait dysdiadochokinesia dysmetria action tremor
55
side effects of vestsbulocerebellum damage
Nystagmus Dysequilibrium Balance deficit (truncal ataxia)
56
side effect of paravermis and hemisphere damage
Dysarthria (“ataxic”):
57
side effect of cerebrocerebellar damage
Hand ataxia | Incoordination of fine finger movements
58
side effect of spinocerebellar damage
gait ataxia
59
strategies to improve function of pt with cerebellar damage
slow down use vision to guide movement think about what you're doing simplify movements
60
what is damaged if a person has ataxia whether eyes are open or closed and their sensation tests have normal results
cerebellum
61
what is damaged if a person has ataxia only when eyes are closed and their sensation tests have abnormal results
somatosensory
62
all neural structures distal to the spinal nerves
peripheral nervous system
63
surrounds individual axons
endoneurium
64
surrounds bundles of axons
perineurium
65
surrounds bundles of fascicles
epineurium
66
All peripheral nerves have axons of ___, ____ and ____ (usually SNS) function
motor, sensory, autonomic
67
A-alpha are
efferent, extrafusal
68
Ia, Ib, II are
afferent, proprioception
69
A-beta are
afferent, exteroception
70
A-gamma are
efferent-intrafusal
71
A-delta are
afferent- pain, temperature, viscera
72
B are
efferent- presynaptic autonomic
73
C are
afferent-pain, temperature, viscera | efferent-postsynaptic autonomic