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Neuroscience > Exam 4 > Flashcards

Exam 4 Flashcards

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
Q

Exaggerated reflex response when descending inhibition is missing or much reduced or when UMN is damaged

A

muscle stretch hyperreflexia

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26
Q

2 ways to help muscle stretch hyperreflexia

A

don’t stretch quickly and use pharmacology to turn down LMN (act like GABA)

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27
Q

how do you elicit clonus

A

quick stretch

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28
Q

Rhythmic, repeating (usually involuntary) contraction

A series of hyperreflexia responses when there is a continuing stimulus of stretch

A

clonus

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29
Q

how to prevent clonus

A

Pharmacology
Position ankles in extreme dorsiflexion
Lift leg and set it back down slowly
Lean on that leg

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30
Q

when clonus is sustained, this is an indication of what

A

UMN damage

31
Q

example of hyperreflexic response to stretch that goes away (UMN damage)

A

clasp-knife response

32
Q

what are 2 ways that the muscle changes in response to lack of movement due to UMN injury

A

atrophy and increased mechanical stiffness/contracture

33
Q

what are different ways we can have hypertonia or spasticity

A

hyperreflexia or brainstem UMN overactivity

34
Q

types of brainstem overractivity

A

more tonic or resting (i.e. “rigidity” of PD)

more activity dependent (i.e. muscle overactivity of CVA that create abnormal synergies)

35
Q

where does the basal ganglia motor loop output to

A

cortical UMN via thalamus and brainstem UMN via pedunculopontine nucleus

36
Q

predict the effects of various actions, then make and execute action plans

A

basal ganglia

37
Q

piece of basal ganglia that malfunctiosn to cause PD

A

substantia nigra

38
Q

excitatory neurotransmitter that has input signals from other brain regions to Putamen

A

glutamate

39
Q

5 basal ganglia loops

A 
motor
oculomotor 
executive
behavior flexibility and control 
limbic
40
Q

loop from basal ganglia to pre central gyrus and back. Contains the plan to move

A

motor

41
Q

loop from basal ganglia to prefrontal cortex. Decides what to do

A

executive

42
Q

As a group, basal ganglia “loops” help with

A 
predicting future events
selecting desired behaviors
preventing undesired behaviors
motor learning (procedural memory)
shifting attention 
spatial working memory
43
Q

Motor “loop” regulates

A

Muscle contraction
Muscle force
Multijoint movements
Sequencing of movements

44
Q

is the basal ganglia motor loop excitatory or inhibitory

A

inhibitory

45
Q

pathology where there is death of dopamine producing cells in substantial nigra

A

akinetic/rigid PD

46
Q

excitatory and is the neurotransmitter that makes the basal ganglia circuitry work properly to plan movements. Without it, the basal ganglia malfunction

A

dopamine

47
Q

with dopamine gone, the output of basal ganglia increases, leading to

A

Too little activation of voluntary muscles
Too much activation of postural and girdle muscles
Too little activation of midbrain locomotor region

48
Q

signs and symptoms of akinetic/rigid parkinson’s disease

A

akinesia/hypokinesia
rigidity
postural instability
resting tremor

49
Q

hyperkinetic disorder involving the basal ganglia where it doesn’t output enough

A

Huntington’s disease

50
Q

degeneration of striatum and cerebral cortex

A

Huntington’s disease

51
Q

tremor of movement where you miss the target and correct it

A

action tremor

52
Q

inability to rapidly/smoothly alternate the direction of movement

A

Dysdiadochokinesia

53
Q

Wide-based, unsteady, staggering, veering gait

A

ataxic gait

54
Q

side effects of spinocerebellum damage

A

ataxic gait
dysdiadochokinesia
dysmetria
action tremor

55
Q

side effects of vestsbulocerebellum damage

A

Nystagmus
Dysequilibrium
Balance deficit (truncal ataxia)

56
Q

side effect of paravermis and hemisphere damage

A

Dysarthria (“ataxic”):

57
Q

side effect of cerebrocerebellar damage

A

Hand ataxia

Incoordination of fine finger movements

58
Q

side effect of spinocerebellar damage

A

gait ataxia

59
Q

strategies to improve function of pt with cerebellar damage

A

slow down
use vision to guide movement
think about what you’re doing
simplify movements

60
Q

what is damaged if a person has ataxia whether eyes are open or closed and their sensation tests have normal results

A

cerebellum

61
Q

what is damaged if a person has ataxia only when eyes are closed and their sensation tests have abnormal results

A

somatosensory

62
Q

all neural structures distal to the spinal nerves

A

peripheral nervous system

63
Q

surrounds individual axons

A

endoneurium

64
Q

surrounds bundles of axons

A

perineurium

65
Q

surrounds bundles of fascicles

A

epineurium

66
Q

All peripheral nerves have axons of ___, ____ and ____ (usually SNS) function

A

motor, sensory, autonomic

67
Q

A-alpha are

A

efferent, extrafusal

68
Q

Ia, Ib, II are

A

afferent, proprioception

69
Q

A-beta are

A

afferent, exteroception

70
Q

A-gamma are

A

efferent-intrafusal

71
Q

A-delta are

A

afferent- pain, temperature, viscera

72
Q

B are

A

efferent- presynaptic autonomic

73
Q

C are

A

afferent-pain, temperature, viscera

efferent-postsynaptic autonomic

Neuroscience (6 decks)

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