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COMP EXAM > neuro rehab > Flashcards

neuro rehab Flashcards

1
Q

where do the lowest level reflexes originate?

A

spinal cord (then brainstem, then midbrain/cortical areas)

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2
Q

true or false, fast movements can be performed without sensory feedback

A

true (open loop control)

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3
Q

open loop control systems

A

instructions for the action (motor programs) are prepared in advance and carried out without feedback

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4
Q

feedforward control

A

“setting” of muscles prior to initiation of movement

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5
Q

closed loop is used ____ (more/less) during learning

A

more because we need the feedback when we are learning a movement

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6
Q

true or false, it is impossible for the brain to store motor programs for every movement

A

true, this is a limitation on this idea

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7
Q

which theory talks about times of stability and instability

A

dynamic systems theory

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8
Q

discrete tasks

A

have a beginning and end

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9
Q

serial tasks

A

discrete movements strung together

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10
Q

continuous movements

A

no recognizable beginning or end

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11
Q

open environment

A

unpredictable

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12
Q

closed environment

A

predictable

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13
Q

intrinsic feedback

A

from sensory receptors

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14
Q

extrinsic feedback

A

supplied from external sources

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15
Q

which type of feedback schedule is most effective?

A

faded

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16
Q

external focus of attention is better for learning (T/F)

A

true

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17
Q

which type of task works better for massed practice?

A

discrete, or for a novel skill

fatigue can be an issue for continuous

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18
Q

massed or distributed practice are about ….

A

the amount of time of practice vs. rest

massed is more practice than rest

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19
Q

meissner’s corpuscle

A

fine, discriminative touch

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20
Q

merkel’s disc

A

fine touch, superficial pressure

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21
Q

pascinian corpuscle

A

deep pressure, vibration

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22
Q

Ruffini corpuscles

A

stretch, vibrations

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23
Q

which type of reflex is monosynaptic?

A

deep tendon reflex (stretch)

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24
Q

function of the brainstem

A

receives and integrates somatosensory, vestibular, and visual inputs for postural control

regulate cardiovascular, respiratory and visceral activity

regulates arousal and awareness through ascending reticular system

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25
Q

basal ganglia goes with which cortical area?

A

supplementary motor

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26
Q

cerebellum goes with which cortical area?

A

premotor

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27
Q

vicarious function theory

A

assumes that functions can be learned or taken over by areas not previously done

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28
Q

CNS redundancy theory

A

CNS has back-up systems

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29
Q

functional substitution

A

areas of the brain become reprogrammed (increased sensitivity of hands as sensory information for the blind)

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30
Q

wallerian degeneration

A

the distal end that was separated (cut) will degenerate

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31
Q

recovery of synaptic effectiveness

A

edema resolves and function is restored

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32
Q

synaptic hyper effectiveness

A

when one presynaptic branch is destroyed, the rest release more NT

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33
Q

denervation super-sensitivity

A

increase in number of receptors on postsynaptic membrane

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34
Q

recruitment of silent synapses

A

unmasking, functional connections were silent before injury

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35
Q

axonal regeneration

A

sprouts from injured axons grow to form new synapses with other cell

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36
Q

collateral sprouting

A

presynaptic will sprout to synapse with a postsynaptic neuron that lost its presynaptic

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37
Q

angiogenesis and what substances promote it

A

formation of new blood vessels

BDNF and TGFa

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38
Q

retentive memory

A

immediate recall

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39
Q

recent memory

A

recall immediate and then 5 min later

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40
Q

remote memory

A

chronological order of events

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41
Q

difference between non-equilibrium and equilibrium coordination

A

equilibrium requiers upright balance

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42
Q

what does a wide based gait and ataxic movement indicate?

A

cerebellar issue

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43
Q

what is the gait speed of a community ambulatory?

A

.8 m/s

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44
Q

what is the tinetti used for?

A

fall risk in the elderly

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45
Q

tests to determine risk…

A 
TUG
functional reach
tinoetti
Berg
BESTest
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46
Q

floor effect

A

they will score too low

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47
Q

ceiling effect

A

they will score too high

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48
Q

SIRS

A

systemic inflammation response syndrome

severe infection

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49
Q

risk for ICU acquired weakness goes up after how long

A

1 week

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50
Q

what is early mobility? how early?

A

within 24-48 hours after admission

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51
Q

PICS

A

post intensive care syndrome

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52
Q

who gets SCI?

A

young males, often preventable causes

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53
Q

what level are wedge compression fractures most common in?

A

thoracic

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54
Q

___ has regeneration, ___ has reorganization

A

PNS, CNS

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55
Q

spinal shock is caused by … and is…

A

edema,
temporary suppression of SC ruction at and below level
first to come back are sacral reflexes

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56
Q

spinal precautions

A

No BLT
bending
lifting more than 10 lbs
no twisting

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57
Q

who would you expect to have issues with generating a forceful cough (SCI level)?

A

above C6

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58
Q

level of autonomic dysreflexia

A

above T6

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59
Q

what to do for autonomic dysreflexia

A

raise HOB to decrease BP
look for noxious stimuli
keep checking vitals
ER immediately if BP does not come down

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60
Q

spasticity is ___ dependent

A

velocity

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61
Q

neuropathic pain therapies

A

anticonvulsants

tricyclic antidepressants

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62
Q

Brown-sequard syndrome

A

SC hemisection

ipsilateral: motor at that level and below, DCML below, AL at the level
contralateral: AL at level and below

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63
Q

anterior cord syndrome

A

AL loss at and below level, motor at and below

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64
Q

central cord syndrome

A

loss of motor pools at the level, loss of AL at the level (crossing fibers)

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65
Q

posterior cord syndrome

A

loss of DCML below lesion

likely have antalgic gait as a result

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66
Q

cauda equina

A

LMN

sensory impairment and flaccid paralysis

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67
Q

conus medularis

A

UMNs and LMNs

maybe see spasticity, hyperreflexia

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68
Q

root escape

A

preservation or return of function of nerve roots at, or near, level of lesion

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69
Q

neurologic level of inury

A

loest segment w/ normal sensory and or motor function (3/5) on both sides of the body

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70
Q

ASIA levels

A 
A = complete
B = sensory only
C = less than 1/2 motor normal
D = more than 1/2 motor normal
E = normal
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71
Q

how much HS length does an SCI patient need for functional long-sit?

A

110-120

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72
Q

secondary complications of SCI (think bone)

A

heterotrophic ossification

osteoporosis

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73
Q

sympathetic affects on bladder

A

hypogastric nerve –> relaxes bladder muscles and contracts internal urethral sphincter

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74
Q

parasympathetic effects on bladder

A

pelvic nerve –> contracts detrusor muscle –> voiding

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75
Q

somatic effects on bladder

A

pudendal nerve –> contracts external urethral sphincter (voluntary control)

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76
Q

location of lesion for spastic bladder

A

above conus medullar is because micturition reflex is still intact

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77
Q

location of lesion for flaccid bladder

A

lesion of conus medlars or cauda equina (the reflex is disrupted)

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78
Q

failure to store urine can be from 2 causes

A 
detrusor hyperreflexia
sphincter incompetence (corticospinal tract damage or sympathetic denervation)
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79
Q

failure to empty bladder

A

hyporeflexia of detrusor
outlet obstruction
spastic external sphincter

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80
Q

location of lesion for spastic bowel

A

lesion within SC above conus medullaris

intact defecation reflex

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81
Q

bowel program success

A 
SELF
Schedule
exercise
liquids
food
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82
Q

reflexogenic erections happen from

A

direct stimulation to the genital area

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83
Q

psychogenic erection happen from

A

result of audiovisual stimuli or fantasy (from brain)

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84
Q

NIHSS score is for what?

A 
stroke severity 
0 = no symptoms
1-4 = minor stroke
5-15 = mod stroke
16-20 = mod to severe 
21-42 = severe stroke
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85
Q

ASTRAL score is for what?

A 
stroke
Age
Severity (NIHSS)
Time delay
pResence of visual field deficit
glucose at Admission
Level of consciousness
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86
Q

an embolism is a clot that comes from…

A

the heart normally

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87
Q

intracerebral hemorrhage

A

blood vessels within brain rupture

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88
Q

subarachnoid hemorrhage

A

blood vessels outside of the brain ruptures, filling subarachnoid space with blood

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89
Q

Arteriovenous malformation

A

congenital defect consisting of abnormal tangle of blood vessels that pass blood directly from arteries to veins
CAN RUPTURE
common stroke seen in young people

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90
Q

watershed strokes

A

affect areas of the brain supplied by the most distal branches of major cerebral arteries
-proximal arm and leg weakness (man in a barrel)

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91
Q

warning signs of stroke

A 
FAST
Face
Arms
Speech
Time

worst headache of their life

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92
Q

what type of drugs do you give someone with a TIA of cardiac origin?

A

anticoagulants (warfarin, heparin)

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93
Q

what type of drug is aspirin?

A

platelet antiaggregant (antiplatelet, antithrombotic)

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94
Q

When do you use thrombolytic therapy?

A

tPA, altaplase… within 4.5 hours of an ischemic stroke

95
Q

what is a cryptogenic stroke?

A

the underlying cause is unknown after extensive testing

96
Q

what to do for intracerebral hemorrhagic stroke

A

stop antithrombotics, debased BP, decrease ICP

97
Q

dorsolateral prefrontal cortex deficit

A 
executive functioning(memory retrieval)
perseveration, disinhibition
98
Q

ventromedial prefrontal cortex deficit

A

motivational aspect of decision making
impulsive, risk-taking
inability to interpret emotions or act appropriately

99
Q

anterior cingulate cortex is important for

A

connected with VMPC and DLPFC and limbic system
shifting attention, awareness of emotion
(considered part of limbic system)

100
Q

posterior cingulate cortex is important for

A

working memory, comparing, evaluating info, orienting objects in space mentally

101
Q

declarative memory

A

facts and events

102
Q

nondeclarative memory

A

procedural and emotional learning

103
Q

non-associative learning

A

habituation and sensitization

104
Q

associative learning

A 
classical and operant conditioning
cellular mechanisms (LTP and LTD)
105
Q

where does long term potentiation happen?

A

hippocampus and neocortex

106
Q

where does long term depression happen?

A

cerebellum and hippocampus

107
Q

bottleneck theory

A

two tasks with similar neural network requirements create a bottleneck during dual tasking (decreasing performance in one or both tasks)

108
Q

capacity sharing model

A

processing capacity for an individual is limited… multiple tasks could require more capacity

109
Q

at the areas of broca’s and wernicke’s on opposite hemisphere, what do they do?

A

nonverbal planning (broca’s) and nonverbal interpretation (wernicke’s)

110
Q

verbal dorsal stream processing…

A

transforms what we want to say to sentences

111
Q

verbal ventral stream processing…

A

converts what is said into its meaning and plans what we want to say

112
Q

anomic aphasia

A

inability to retrieve words an individual wants to say

most common after stroke

113
Q

conduction aphasia

A

thought to be due to damage to arcuate fibers connecting broca’s and wernicke’s
speak in gibberish

114
Q

wernicke’s allows for repeating words (T/F)

A

true

115
Q

transcortical motor aphasia

A

disconnected broca from BG or premotor… non-fluent aphasia, but can repeat words

116
Q

transcortical sensory aphasia

A

fluent aphasia, but can repeat words, often echolalia

117
Q

mixed transcortical aphasia

A

least common (isolation aphasia)
all areas intact, but isolated
can repeat
can’t comprehend or produce spontaneous speech

118
Q

global aphasia

A

most severe, large left hemisphere lesion
can improve sometimes
no speech made or understood

119
Q

dysarthria types

A

spastic (UMN)

flaccid (cranial nerves)

120
Q

diaschisis

A

loss of function in a remote area, but neuronally connected

121
Q

On day 2 post stroke, if the following are present, predicts independent gait at 6 months with 98% chance

A

independent sitting for 30s
25 degree motion of DF, Knee extension, hip flexion
palpable contraction of DF, KE, AND HF
fair+ strength in DF, KE, HF

122
Q

3 stages of stroke recovery according to Bobath

A

1: flaccidity
2: spasticity
3: relative recovery
(recovery continues for 1 year)

123
Q

muscles not included in the synergy patterns

A 
lats
teres major
serrates anterior
finger extensors
ankle evertors
HARD TO ACTIVATE
124
Q

UE movement is in ___ direction as other for unmasked reflexes post stroke

A

SAME

125
Q

LE movement is in the _____ direction as other for unmasked reflexes post stroke… except

A

OPPOSITE

except for ABD and ADD

126
Q

sougue’s phenomenon

A

raise arm above horizontal and get finger extension and abduction

127
Q

raimiste’s phenomenon

A

resisted abduction elicits abduction in the contralateral limb (same for add)

128
Q

perceptual deficits usually occur in the ____ lobe

A

right parietal

129
Q

asonognosia

A

denial of presence or severity of disability

130
Q

agnosia

A

dont know what to do with an object

131
Q

dysphagia

A

delayed triggering of the swallowing reflex

posture and head control can contribute

132
Q

which type of hemiplegics tend to be more impulsive?

A

L

133
Q

thalamic syndrome

A

severe burning pain in the area weeks or months after thalamic stroke

134
Q

Gordon’s Investment Principle

A

performance will degrade during learning process, then it will improve as it becomes integrated

135
Q

shoulder problems associated with hemiplegia

A

pain and subluxation

136
Q

body scheme

A

postural model of body, relationships between body parts

137
Q

body awareness

A

integration of tactile, proprioceptive and interoceptive sensation, in addition to feelings
(these legs are mine)

138
Q

somatognosia

A

failure to recognize a part of their body (maybe think dead person in bed), includes naming a body part

139
Q

where does a lesion causing unilateral neglect happen?

A

right posterior inferior parietal lobe (they think right said is dominant in choosing what to pay attention too)

140
Q

anosognosia

A

deny symptoms such as paralysis, safety problem, they will say it’s not their arm

141
Q

pusher syndrome

A

uses non paretic extremities to push away

142
Q

prosopagnosia

A

inability to recognize familiar faces

143
Q

perceptual disorder classifications (4)

A

body image/scheme
spatial relations
agnosias
apraxia

144
Q

screening is more than a test, it is a program (T/F)

A

true

145
Q

orientation

A

adjustment of the body and head to vertical

146
Q

stability

A

ability to maintain the center of mass within the base of support

147
Q

anterior canals detect

A

nodding your head

148
Q

posterior canals detect

A

side bend

149
Q

saccule detects

A

motion in the sagittal plane

150
Q

superior vestibular nucleus

A

VOR (semicircular)

151
Q

lateral vestibular nucleus

A

LVST (Utricle and saccule)

152
Q

medial vestibular nucleus

A

MVST (semicircular)

153
Q

inferior vestibular nucleus

A

RF, cerebellum, SC

154
Q

when learning new motor skills you rely more on (visual/somatosensory) input

A

visual (same with children)

155
Q

suspensory strategy for balance

A

lower the COG towards BOS, crouch down

156
Q

acoustic neuroma

A

tumor of vestibulocochlear nerve

157
Q

vestibular hypofunction (unilateral)

A

feels like you are moving toward uninvolved side (more activity)

158
Q

cupulolithiasis

A

dislodged otoconia adhere to cupula

159
Q

canalithiasis

A

dislodged otoconia are free-floating (more common)

160
Q

Meniere’s Disease

A

fluctuations in fluid and electrolyte control in inner ear

161
Q

stupor

A

barely conscious state, can only be aroused briefly

162
Q

obtunded

A

sleeps often, and when aroused has decreased alertness

163
Q

post-traumatic amnesia

A

period of both retrograde and anterograde amnesia after mod/severe TBI

164
Q

Glascow Coma Score

A 
13-15 = mild concussion
9-12 = moderate 
3-8 = severe
165
Q

Ranchos Level 1

A

no response

166
Q

Ranchos Level 2

A

general response (inconsistent, nonpurposeful)

167
Q

Ranchos Level 3

A

localized response (specifically, but inconsistently)

168
Q

Ranchos Level 4

A

confused - agitated (bizarre, nonpurposeful)

169
Q

Ranchos Level 5

A

confused - inappropriate

170
Q

Ranchos Level 6

A

confused - appropriate (dependent on external input or direction)

171
Q

Ranchos Level 7

A

automatic - appropriate (shows carryover for NEW learning, impaired judgement)

172
Q

Ranchos Level 8

A

purposeful - appropriate (needs no supervision once activity is learned)

173
Q

key to manage agitation

A

prevent escalation, modify environment

174
Q

key to manage confusion

A

external structure

175
Q

key to manage impulsivity

A

consistency across caregivers, verbal rehearsal

176
Q

key to manage disinhibition

A

calm, provide concrete feedback

177
Q

key to manage perseveration

A

curing and pacing to interrupt repetitive behavior, stimulus to move onto next step

178
Q

key to manage confabulation

A

may be serving a purpose like reducing anxiety… ignore it if low functioning, nonthreatening feedback of inaccuracy in higher functioning, redirection

179
Q

key to manage inability to self-reflect

A

use concrete goals

180
Q

key to manage apathy

A

treatment should target choices and acknowledge accomplishment

181
Q

key to mange lack of initiation

A

cueing to start activity

182
Q

anoxic brain injury

A

incidents that alter the amount of oxygen in the blood (poor prognosis)

183
Q

most adult tumors are ___(supra/infra)tentorial

A

supra, children are more likely infra (cerebellum, brainstem)

184
Q

adenoma

A

gland (usually benign)

185
Q

blastoma

A

malignant tumor whose cells have underdeveloped characteristics

186
Q

glioma

A

any tumor that arises from supportive tissue of the brain (can be benign or malignant)

187
Q

most common type of glioma

A

astrocytoma

188
Q

most common malignant primary CNS tumor in children

A

medulloblastoma

189
Q

most common benign CNS tumor

A

meningioma

190
Q

craniotomy

A

resection of skull overlying tumor and replacement of bone flap

191
Q

normal ICP

A

0-15, emergency is over 20

192
Q

ALS

A

most common form of adult-onset progressive motor neuron disease, UMN and LMN, spreads from one focal region to another adjacent area, axonal degeneration distal to proximal

193
Q

ALS on EMG

A

spontaneous potentials at rest (acute denervation)
reduced motor recruitment (reduced number of motor units)
re-innervation changes (chronic denervation with re-innervation)

194
Q

ALS on nerve conduction study

A 
reduction combined motor AP (fewer functioning motor axons)
normal latency and velocity (myelin unaffected)
normal sensory (unaffected)
195
Q

ALS on muscle biopsy

A

grouping of fiber types (checkerboard)

196
Q

ALS disease modifying drugs

A

Rilutek and Radicava

197
Q

exercise guidelines for ALS

A

concentric
moderate intensity
energy conservation

198
Q

post-polio syndrome

A

overwork weakness of giant motor units 20-40 years after resolution, energy conservation is big for this group

199
Q

GBS

A

autoimmune disease, progressive muscle weakness and respiratory paralysis (PNS)

200
Q

types of GBS

A

AIDP: demyelination, better prognosis
AMAN: axon, nodes of ranvier

201
Q

medical treatment of GBS

A

plasmapheresis
intravenous human immunoglobulin
NOT COTRICOSTEROIDS

202
Q

PT for acute GBS

A

pain management
ROM
positioning
gentle stretching

203
Q

peripheral nerve injury seddon classification

A

neurapraxia
axonotmesis
neurotmesis

204
Q

peripheral nerve sunderland classification

A

1-5

205
Q

mononeuropathy multiplex

A

asymmetrical involvement of several nerves

206
Q

polyneuropathy

A

distal and symmetrical involvement of many nerves

207
Q

MS

A

most common inflammatory demyelinating disease of CNS
early symptom: optic neuritis (cellophane in one eye)
HEAT INTOLERANCE, fatigue, ANS dysfunction

208
Q

Diagnosis of MS

A 
dissemination in space (2 sites) and time (1 month apart) 
periventricular
juxtacortical
infratentorial
spinal cord
209
Q

primary vs. secondary progressive MS

A

secondary is when you start out with relapsing-remitting and then start just progressing over time

210
Q

treatment of relapse in MS

A

corticosteroids

211
Q

risk factors in MS

A

living far from equator (Vit. D)

epstein barr

212
Q

types of MS

A

clinically isolated syndrome
RRMS
PPMS
SPMS

213
Q

how many drugs are there to treat MS

A

22

214
Q

uthoff’s sign

A

worsening of neuro symptoms in MS due to heat intolerance

215
Q

which drug is used for PPMS

A

ocrevus

216
Q

when is PT contraindicated for MS?

A

acute exacerbation + corticosteroids

217
Q

cardinal motor signs of PD

A 
TRAP
tremor at rest
rigidity
akinesia/bradykinesia
postural instability
218
Q

types of PD

A

primary
secondary (from brain injury)
parkinson-plus

219
Q

parkinson-plus syndromes

A

progressive supranuclear palsy
multiple system atrophy
corticobasal ganglionic degeneration
Lewy body dementia

220
Q

which circuits are involved in PD

A 
motor
associative (DLPFC = executive functioning)
limbic = emotional regulation effects
221
Q

where are lewy bodies first seen?

A

low in brainstem, work their way up, see symptoms in midbrain,
more cognition problems towards end due to cortical areas

222
Q

cogwheel vs. lead pipe rigidity

A 
cogwheel = jerky
leadpipe = constant, uniform resistance
223
Q

microgrpahia

A

writing starts out big but gets smaller

224
Q

hypophonia

A

voice amplitude is smaller

225
Q

PD prodromal symptoms that occur before motor

A

OH, bladder dysfunction, constipation, anosmia (loss of smell), excessive daytime somnolence, rapid eye movement

226
Q

progresive supranuclear palsy

A 
most common PP
supranuclear ophthalmoplegia (cant look down), postural instability
227
Q

multiple system atrophy

A

dont respond to levodopa, hyperkinetic dysarthria (6 years survival)

228
Q

corticobasal ganglionic degeneration

A

cortical atrophy of frontal and parietal + loss of D in SN

early cognitive dysfunction

229
Q

dementia with lewy bodies

A

early cognitive symptoms
visual hallucinations
really exaggerated responses to antipsychotics

230
Q

diagnosis of PD

A

must have bradykinesia w/ tremor and/or rigidity, absence of secondary cause, definite dx made w/ autopsy

231
Q

HD

A

HD gene, more than 40 repeats will causes disease
more repeats = younger onset
early: loss of GABA pathway neurons (D2) –> more movement
late: loss of D1 and D2 –> less movement
can have movement, cognitive, and psychiatric issues
age of onset 30-50

232
Q

how does HD present in kids (less than 20 y.o.)

A

more like PD

233
Q

HD dx

A

family history, presence of extrapyramidal movement disorder

234
Q

medical treatment for HD

A

chorea: DA blockers and DA-depleting drugs
depression: tricyclic antidepressants
irritability/aggressive behaviors: atypical antipsychotics

COMP EXAM (18 decks)

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