Neurophysiology Flashcards

(465 cards)

1
Q

<p>What is the function of the Frontal Lobe?</p>

A

<ol> <li>Cognitive function</li> <li>Movement control (primary motor cortex)</li> <li>motor programming of speech (Broca's area)</li></ol>

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2
Q

<p>what are some of the functions of the Parietal lobe?</p>

A

<ol> <li>major sensory center</li> <li>somatosensory integration (temperature, taste, touch and movement)</li> <li>Language comprehension (Wenicke's area)</li></ol>

<p></p>

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3
Q

<p>what are the main functions of the temporal lobe?</p>

A

<ol> <li>memory center</li> <li>auditory center</li> <li>taste, sound, sight and touch integration</li></ol>

<p></p>

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4
Q

<p>what is the main function of the occipital lobe?</p>

A

<p>primary visual center</p>

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5
Q

<p>from most lateral to most medial, what body structures are somatopically mapped at the precentral gyrus?</p>

A

<ol> <li>Mouth <ol> <li>swallowing</li> <li>tongue</li> <li>jaw</li> <li>lips</li> </ol> </li> <li>Face</li> <li>HAND</li> <li>arm</li> <li>Trunk</li> <li>Lower extremity</li></ol>

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6
Q

<p>what body structure would you expect to see somatopically mapped in the longitudinal fissure of the precentral gyrus?</p>

A

<p>(betweenL and R sides)</p>

<p>hip, knee, ankle and toes</p>

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7
Q

<p>from most lateral to most medial, describe where body structures are represented somatopically at the postcentral gyrus</p>

A

<p>most laterally to medially</p>

<ol> <li>intra-abdominal</li> <li>phayrnx</li> <li>mouth</li> <li>Face</li> <li>Arm</li> <li>Trunk</li> <li>Leg (at the top)</li></ol>

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8
Q

<p>what arteries make up the anterior circulation of the brain?</p>

A

<ol> <li>Internal carotid arteries</li> <li>Anterior Cerebral arteries</li> <li>Middle Cerebral arteries</li></ol>

<p></p>

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9
Q

<p>What arteries make up the posterior circulation of the brain?</p>

A

<ol> <li>Vertebral arteries</li> <li>Posterior and Anterior Inferior Cerebellar Arteries</li> <li>Basilar artery</li> <li>Pontine arteries</li> <li>superior cerebellar arteries</li> <li>Posterior Cerebral artery</li></ol>

<p></p>

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10
Q

<p>What are the 3 major arteries that supply our cerebrum?</p>

A

<ol> <li>Anterior Cerebral artery</li> <li>Middle Cerebral artery</li> <li>Posterior Cerebral artery</li></ol>

<p></p>

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11
Q

<p>What areas of the brain are perfused by the anterior cerebral artery?</p>

A

<ol> <li>anterior and medial surface of the brain</li> <li>from frontal lobe to anterior parietal lobe</li> <li>subcortical structures <ol> <li>basal ganglia (anterior internal capsule, inferior caudate nucleus),</li> <li>anterior fornix</li> <li>corpus callosum<span></span></li> </ol> </li></ol>

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12
Q

<p>What are the functions of the areas perfused by the anterior cerebral artery?</p>

A

<ol> <li>frontal lobe→ cognitive and motor functions</li> <li>parietal lobe→ sensory center</li> <li>corpus callosum→ two way highway that allows hemispheres to communicate</li></ol>

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13
Q

<p>what are some signs and symptoms of a stroke involving the Anterior Cerebral Artery?</p>

A

<ol> <li>contralateral hemiparesis or hemiplegia</li> <li>contralateral hemisensory loss</li> <li>apraxia</li> <li>problems w/bimanual tasks</li> <li>sig. cognitive deficits</li> <li>lack of spontaneity, motor inaction, slowness and delay</li> <li>difficulty with executive function tasks</li> <li>transcoritical aphasia</li> <li>contralateral grasp reflex</li> <li>Alien Hand syndrome</li> <li>Urinary incontience</li></ol>

<p></p>

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14
Q

<p>what is contralaleral hemiparesis or hemipelgia?</p>

<p>what brain structures are involved?</p>

A

<ol> <li>weakness effecting one side of the body</li> <li>motor cortex (frontal lobe)</li></ol>

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15
Q

<p>what is apraxia? what brain structures are involved with it?</p>

A

<ol> <li>motor agnosia→ knowledge of how to perform a skilled movement is lost</li> <li>supplementary motor area and corpus callosum</li></ol>

<p></p>

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16
Q

<p>An ACA stroke involving the pre-frontal cortex will include what symptoms?</p>

A

<ol> <li>lack of spontaneity</li> <li>motor inaction</li> <li>slowness and delay</li> <li>difficulties with executive function tasks (attention)</li></ol>

<p></p>

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17
Q

<p>what is transcortical aphasia and what brain structures does it involve?</p>

A

<ol> <li>aphasia→ loss of ability to produce or understand speech <ol> <li>this doesn't tend to be as severe as Broac's apahsia (motor) in that they can function a bit better</li> </ol> </li> <li>supplementay motor area (dominant hemisphere)</li></ol>

<p></p>

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18
Q

<p>what area's/structures of the brain are involved in the contralateral grasp reflex (sucking reflex)?</p>

A

<p>No well understood</p>

<p>maybe corpus callosum and frontal lobe?</p>

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19
Q

<p>what is alien hand syndrome and what regions of the brain are involved with it?</p>

A

<ol> <li>involuntary, uncontrollable movement of the upper limb</li> <li>supplemental motor area</li></ol>

<p></p>

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20
Q

<p>List some ACA treatment strategies</p>

A

<ol> <li>structure environment to minimize external distractions</li> <li>closed chain "big muscle" exercises</li> <li>bimanual activities to tackle UE deficits</li> <li>function-based training</li></ol>

<p></p>

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21
Q

<p>what areas of the brain does the middle cerebral artery (MCA) perfuse?</p>

A

<p>two branches</p>

<ol> <li>entire lateral aspect of the cerebral hemisphere (frontal, temporal, and parietal lobes)</li> <li>subcortical structures, <ol> <li>internal capsule (posterior portion)</li> <li>corona radiata</li> <li>globus pallidus (outer part),</li> <li>most of the caudate nucleus,</li> <li>putamen</li> </ol> </li></ol>

<p></p>

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22
Q

<p>what are the signs and symptoms of MCA syndrome?</p>

A

<ol> <li>Contralateral paresis</li> <li>Contralateral sensory loss</li> <li>Motor speech impairment</li> <li>receptive speech impairment</li> <li>global aphasia</li> <li>perceptual deficits</li> <li>apraxia</li> <li>visual deficits</li> <li>loss of conjugate gaze to opposite side</li> <li>pure motor hemiplegia (lacunar stroke)</li></ol>

<p></p>

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23
Q

<p>what brain structures are involved with motor speech impairment from MCA syndrome?</p>

A

<p>Broca's area (dominant hemisphere)</p>

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24
Q

<p>what brain structures are involved with recepive speech impairment with MCA syndrome?</p>

A

<p>Wenicke's area (dominant hemisphere)</p>

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25

What is global aphasia and what brain structures are involved with it?

  1. also called total apashia
    1. cannot speak fluentyly
    2. cannot communicae verbally
    3. cannot understand language
  2. Broca's and Wernicke's areas involved 
26

what are some examples of perceptual deficits observed with MCA syndrome?

  1. unilateral neglect → tendency to behave as if one side of the body and/or one side space does not exist. 
  2. depth perception issues 
  3. spatial relations issues 
27

what brain structures are involved with perceptual deficits observed with MCA syndrome?

parietal sensory association cortex (non-dominant hemisphere)

28

what brain structures are involved with visual deficits observed with MCA syndrome?

optic radiation in internal capsule

29

what is "loss of conjugate gaze to opposite side" and what brain structures are involved with it?

  1. conjugate gaze is the ability of the eyes to work together/in unison
  2. frontal eye fields or decending tracts

 

30

what brain structure are involved with pure motor hemiplegia (lucunar stroke)?

upper portion of posterior limb of internal capsule

31

what are the small perforating arteries off of the MCA?

lenticulostriate arteries → supply deep structures within the cerebrum 

basal ganglia and internal capsule

32

what is a major symptom of a lacunar infarct?

pure motor hemiparesis

33

List some treatment strategies when treating an stroke involving the MCA

  1. Incorperate speech strategies into actions
  2. UE functional strengthening
  3. sensory reintegration is key

 

34

what regions of the brain are perfused by the posterior cerebral artery (PCA)?

  1. occipital lobe
  2. posteromedial temporal lobes
  3. thalamus

 

35

what are some signs and symptoms that would be observed following a PCA stroke?

  1. contralateral homonymous hemianopia 
  2. cortical blindness
  3. visual agnosia
  4. prosopagnosia
  5. dyslexia
  6. memory deficit
  7. topographic disorientation

 

36

what is homonymous hemianopia? what brain structures are involved with this?

  1. loss of visual information from the same visual field in both eyes 
  2. visual cortex or optic radiation
37

what is cortical blindness? What structures/regions of the brain are impacted?

  1. person has no awareness of any visual information due to a lesion in the brain
  2. bilateral occiptal lobe

 

38

what is visual agnosia? What regions/structures of the brain are involved?

  1. inability to visually recognize objects despite having intact vision
  2. occipital lobe (dominant side)

 

39

what is prosopagnosia? what regions/structures of the brain are involved?

  1. a highly specific type of visual agnosia → person is unable to visually ID people's faces, despite being able to correctly interpret emotional facial expressions and being able to visually recognize other items in environment
  2. visual association cortex

 

40

what region of the brain is involved with dyslexia resulting from PCA syndrome?

dominant calcarine lesion

posterior part of corpus callosum

41

what regions/structures in the brain are responsible for memory deficits observed with PCA syndrome?

lesion of inferomedial potions of temporal lobe (dominant side)

42

what is topographic disorientation? what brain regions/structures are involved?

  1. inability to orient in the surrounding and find your way around even in a familiar area
  2. nondominant visual area

 

43

a stroke involving the PCA and affecting the thalamus would have what symptoms?

  1. central post-stroke (thalamic) pain
  2. involuntary movements 
    1. choreoarthetosis, intention tremor, hemiballismus)

 

44

describe/define each of the symptoms for a stroke involving the PCA and affecting the thalamus

  1. thalamic pain - neurogenic pain, very hard to control
  2. choreoathetosis - involuntary movements
  3. hemiballismus - big involuntary movements

 

45

List some treatment strategies for PCA syndrome

  1. Gradually increase visual challenges as both symptoms improve and/or pt. is able to habituate to symptoms
  2. visual deficts can significantly impact balance
  3. remember to give pt visual breaks
    1. eyes closed, shut off lights, etc
  4. may require external aids initially to assist in improving visual deficits

 

46

a stroke involving the vertebral arteries and basilar artery is called what?

vertebrobasialr artery syndrome

47

what is a standout symptom to a vertebrobasilar artery stroke?

locked-in syndrome

48

what is locked-in syndrome

pt is cognitively intact but loses ALL motion other than eyes

49

what are NCVs used for?

help diagnose nerve damage or disease

50

what are EMGs used for?

help determine if there is myopathic involvement in the disease

51

List some broad disease categories that electrodiagnostic testing can be helpful in diagnosing

  1. Motor neuron disease
  2. Radiculopathy
  3. Plexopathy
  4. Neuromuscular junction disease
  5. Muscle diseases
  6. Neuropathies
  7. Weakness in ICU

 

52

how can you further divide the categeory of neuropathy?

mononeuropathy

polyneuropathy

53

what are the 3 classifications for a mononeuropathy?

  1. Neuropraxia
  2. Axonotmesis
  3. Neurotmesis

 

54

what is neuropraxia?

pressure, compression or stretch injury

distorts myelin sheath w/o Wallerian degeneration

55

what is axonotmesis?

demyelination that causes axonal damage

axonal regeneration will occur over time along w/sprouting

56

What is neurotmesis?

severe injury to the nerve

axon, schwann cell and endoneurium are completly disrupted (like a complete cut)

57

what are the outcome measures we look at when interpreting NCVs?

  1. amplitude
  2. latency (proximal and distal)
  3. conduction velocity

 

58

what is amplitude a measure of?

the strength of the AP

related to the # of axons in the nerve being tested

59

what is latency a measure of?

the time it takes the AP to travel 

60

what is conduction velocity a measure of?

the velocity of the AP

takes the distance traveled by the AP and the latency into account

61

when performing an NCV would type of injury would most likely result in changes to latency?

demyelination in some capacity 

62

what type of damage to a nerve will affect the conduction velocity?

both demyelination and axonal damage

63

T/F: you can only test motor nerves with NCVs?

FALSE

can test both sensory and motor nerves but the set up is a bit different

64

what is the name for an AP generated during motor nerve testing? sensory nerve testing?

  1. motor → CMAP (compound motor action potential)
  2. sensory → SNAP (sensory nerve action potential)

 

65

SNAPs can be either ____________ or ______________

Orthodromic

Antidromic

66

what does Orthodromic mean?

it is traveling in the natural direction of a sensory AP

67

what does antidromic mean?

testing and recording opposite direction of sensory AP

possible b/c the AP generated during testing will be propogated in both directions

68

If there is suspected proximal damage what tests would we want to do?

  1. F-wave
  2. H-reflex
69

what is an F-wave?

retrograde "rebound" motor impulse

AP that travels the full length of the motor axon and back

(measures the latency of the antidromic CMAP)

70

T/F: the F-wave can be done on both sensory and motor nerve fibers?

FALSE

just motor

71

what types of damage/diseases is F-wave helpful in diagnosing?

  1. proximal damage/demyelination
  2. GBS/CDIP
  3. Radiculopathies
  4. Peripheral neuropathies 
72

What is an H-reflex?

stimualtes an AP that follows the muscle stretch reflex arc

73

what types of disorders would an H-reflex be helpful in diagnosing?

  1. evaluation of:
    • nerve root lesions
    • Upper motor neuron lesions
  2. commonly done on the S1 root
74

what types of diseases/disorders would an EMG test be most helpful in?

diseases that affect:

  1. the muscle (muscular dystrophies)
  2. the neuromuscular junction (myasthenia gravis)
  3. diffuse disorders that cause peripheal neuropathies
  4. disorders that affect the motor neurons in the spinal cord (ALS, ruptured spinal disc)

 

75

what does EMG asses?

the electrical activity (AP) of the muscle in several stages.

refer to the electical activity as a MUAP (motor unit action potential)

76

EMG will asses the electrical activity of a muscle in several stages, what are they?

  1. as the needle goes into the muscle (insertional activity)
  2. muscle at rest
  3. muscle with activation 
77

what type of activity will be observed in a normal/healthy muscle during the at rest phase of an EMG?

  1. insertional activity (50-200 ms = very short)
  2. should be silent following the crisp static sound of insertional activity
  3. normal spontaneous acitivity may be observed

 

78

list some normal spontaneously activity types that can be observed during the EMG at rest

  1. MEPPs - mini end plate potential
  2. EPPs - end plate potentials
  3. EPSs - end plate spikes

 

79

what would be considered abdnormal muscle activity at rest during EMG (3)?

  1. decrease in normal insertional activity
  2. increase in normal insertional activity
  3. prolonged insertional activity

 

80

what can cause a decrease in insertional activity during EMG?

  1. loss of muscle fibers (fibrosis, muslce atrophy)
  2. some metabolic disordes
81

what can cause an increase in insertional activity during EMG?

  1. neuropathic disorders
  2. myopathic disorders
82

what can cause prolonged insertional activity during EMG?

  1. post acute denervation 
  2. inflammatory muscle disorders
  3. muscular dystrophy 

 

83

what types of abnormal activity can be observed during rest in EMG testing?

  1. Fibrillations
  2. Positive Sharp waves
  3. Fasciculations 
  4. Complex regional discharge (CRD)
  5. Myokymic
  6. Myotonic

 

84

what is a fibrillation?

spontaneous discharge of one or a few muscle fibers

85

what are fibrillations associted with?

  1. muscle degeneration (myopathy)
  2. suggests a potential LMN problem (neuropathy)
  3. the size of the fibrillations usually directly correspond to the severity of the injury
86

what are fasciculations?

spontaneous, twitch like contraction

not necessarily indivitive of pathology (ex: eye twitch)

87

what types of disorders/diseases are fasciculations more common with?

  1. a disease involving alpha motor neurons
  2. chronic demyelination conditions
88

what might suggest to you that a fasciculation is normal rather than due to a disease?

it is singular in event, not multiple is short succession

89

what is a complex reptitive discharge (CRD)?

polyphasic waveforms with fairly fixed amplitudes that show up in a high but stable discharge rate

sounds like a machine gun 

spontaneous discharge of multiple different muscle fibers that are asychonous 

90

what types of conditions are CRDs observed in?

  1. neurogenic
  2. myopathic
  3. generally observed with chronic conditions 
  4. hereditory neuropathic diseases
91

what are Myokymic discharges?

groups of recurring spontaneous MUAP that fire in a brief repetitive burst pattern 

 

92

what are Myotonic potentials?

rhythmic electrical discharges that are arise from muscle fibers all over the place - super spontaneous

93

what types of disease are myotonic potentials related to?

myotonic diseases

94

an alternative way to group MUAPs observed at rest is by what?

whether they fire alone or in groups

95

what types of MUAPs fire alone at rest?

  1. EPSs
  2. Fibrillation potentials
  3. Myotonic Discharges

 

96

what types of MUAPs fire in groups?

  1. adjacent muscle fibers
    1. CRD
    2. insertional activity
  2. motor unit potentials 
    1. fasciculation potentials
    2. myokymic discharges
    3. neurotonic discharges

 

97

how would you describe the shape of a normal MUAP during muscle activation EMG?

  1. biphasic
  2. triphasic

 

98

when a neurogenic injury occurs, what changes will be observed immediately in an EMG?

reduced recruitment

increase in firing rates of MUAPs

99

when a neurogenic injury occurs, what changes will be oberved after collateral sprouting has occured?

the shape of the MUAP will change from triphasic to polyphasic 

(MUAPs will be out of sync) 

100

what are polyphasic MUAPs indicative of?

neurogenesis

collateral sprouting has most likely occured following a neurogenic injury and the new branches of the nerves are trying to figure out how to fire in sync again, they are disoriented

101

after a long time has passed following a neurogenic injury (>6 months) what changes will be observed on an EMG?

shape is once again triphasic

amplitude will be greater (1 nerve with 2x as many muscle fibers = must fire at a higher amplitude)

102

myopathic = decrease in _________

number of viable muscle fibers

103

what are the 5 primary categories of tests for cognitive status?

  1. consciousness
  2. orientation
  3. attention/concentration
  4. memory
  5. executive function

 

104

what are the levels of consciousness?

  1. alert/fully conscious
  2. lethargy = general slowing of cognitive and motor processes
  3. obtundation = dulled/blunted sensitivity, difficult to arouse
  4. stupor = semi-conscious state, aroused only w/deep pressure pain
  5. coma

 

105

what is the gold-standard test for levels of consciousness?

Glascow Coma Scale (GCS)

106

what are the 3 areas of consciousness measured in the GCS?

  1. eye opening
  2. motor response
  3. verbal response

*graded 3-15 (<8 = severe; 9-12 moderate; 13-15 mild)

107

What are the 3-4 primary areas of examination for orientation?

  1. Person
  2. Place
  3. Time
  4. Situation

 

108

what are the 4 different aspects of attention/concentration?

  1. sustained attention
  2. selective attention
  3. divided attention
  4. alternating attention

 

109

what is sustained attention? 

How can we test it?

ability to sustain and focus attention over a duration of time

tested via the Cancellation Test

110

what is the Cancellation test?

a method of testing sustained attention

instruct pt to inspect an image and circle all of the ______ in the image. Will take a lot of time and require a lot of attention

111

what is selective attention?

How can we test it?

ability to screen and process relevant sensory info about the task and environment while screening out irrelevant info

Test = Stroop Test

112

what is the Stroop Test?

used to test selective attention

look at a letter outloud and say the color of the word rather than the word itself

113

what is divided attention?

How can we test it?

ability to perform 2 tasks simultaneously

Walkie-Talkie Test

114

what is alternating attention?

How can we test it?

attention flexibility

shifting your attention back and forth between 2 different things

115

What is memory?

the capacity to store knowledge, experiences, and perceptions for recall and recognition

116

what are the 2 types of memory?

Declarative (Explict)

Non-declarative (Procedural/Implict)

117

what is declarative memory?

conscious recollection of facts and events 

118

what is non-declarative memory?

recall movements/movement schema without conscious recollections 

119

what is another 3 part classification of memory?

  1. immediate recall
    • "repeat after me" (seconds to minutes)
  2. short-term memory
    • recent or working memory (minutes to hours/days)
  3. long-term memory
    • remote memory (months to years)

 

120

What is executive function?

capacity to engage successfully in independent, purposeful, self-directed behavior

121

what are the different aspects of executive function?

  1. volition/planning
  2. problem solving/reasoning
  3. insight/awareness
    • poor judgement
  4. social pragmatics
    • inappropriate behaviors
  5. self-regulation/purposeful action
    • initiate, maintain, switch, and stop tasks

 

122

what is difference between sensation and perception?

sensation = raw data

perception = interpretation of data 

123

what are 2 critera for sensation to occur?

adequate arousal and selective attention

adequate stimulus level to activate sensory receptor

*entire pathway must work!

124

Give a working definition of perception

capacity to transform info from the senses and use it to interact appropriately with the environment 

selective, integrative, dynamic process that includes problem solving and memory

125

what type of sensations are carried in the spinothalamic tract?

  1. pain
  2. temperature
  3. crude touch

 

126

what types of receptors are utilized in the spinothalamic tract?

  1. free nerve endings
  2. cutaneous receptors in the skin

 

127

what are the afferent fiber characteristics in the spinothalamic tract?

small, thin, slow conducting

no myelination

128

where is the spinothalamic tract heading?

what are it's major connections?

  1. lower brainstem
  2. thalamus
  3. limbic system
  4. diffuse cortical areas

 

129

what types of sensations are carried by the dorsal column/medial lemniscus tract?

  1. discriminative touch (tactile location)
  2. proprioception
  3. kinesthesia
  4. vibration
  5. 2-point discrimination

 

130

what types of receptors are utilized in the dorsal column/medial lemniscus tract?

  1. muscle spindle
  2. GTOs
  3. joint receptors
  4. some cutaneous receptors in the skin

 

131

what are the afferent fiber types of the dorsal column/medial lemniscus tract?

large, thick, rapidly conducting

well myelinated

132

where is the dorsal column/medial lemniscus tract headed?

sensory cortex

133

what types of sensations are carried in the spinocerebellar tract?

"unconscious"

proprioception and kinesthesia

134

what types of receptors are utilized in the spinocerebellar tracts?

  1. muscle spindles
  2. GTOs
  3. joint receptors
  4. some cutaneous receptors in the skin

 

135

what are the afferent fiber types of the spinocerebellar tract?

fast, direct, heavily myelinated

136

where is the spinocerebellar tract headed?

cerebellum

137

What are the 4 major subcategories/components of the perceptual exam?

  1. Body scheme and body image impairments
  2. spatial relationships
  3. agnosias
  4. apraxia
138

what is the difference between body scheme and body image?

body image = visual/mental image of one's body

body scheme = postural model of body (body awareness)

139

Name a major impairment to body scheme/image

Unilateral Neglect

140

what is unilateral neglect?

failure to orient toward, respond to, or report stimuli on the contralateral side to the lesion

*despite normal sensory, visual and motor systems

141

Unilateral neglect occurs mostly with ________ lesions

R tempoparietal junction

posterior parietal 

(**R side most often)

142

what are the 2 classification systems for unilateral neglect?

  1. Modality
  2. Distribution

 

143

what are the 3 types of modality neglect?

  1. sensory
  2. motor
  3. representational

 

144

What is sensory neglect?

brain loses ability to maintain awareness of a specific sense as it comes in (can be visual, auditory, or tactile)

the sensation is fine but the perception is off

145

what is motor neglect?

"output neglect"

failure to generate a movement response to a specific stimuli even if the pt. is aware of the stimuli

ex: ball is thrown at you, you only raise 1 arm to catch it even though both arms have 5/5 strength

146

what is representational neglect?

loss of internally generated images 

ex: pt asked to recall and draw a clock. They draw a clock with all the numbers on 1 side of a circle

147

What are the two subcategories of distribution neglect?

  1. Personal
  2. Spatial

 

148

what is personal neglect?

individual lacks awares of entire contralateral side of their body

149

what is spatial neglect?

failure to acknowledge stimuli of the contralateral side of space

can be peripersonal (within reaching space)

extrapersonal (in far space)

150

Other than unilateral neglect. What are 4 other types of body scheme/body image impairments?

  1. somatoagnosia
  2. R-L discrimination
  3. vertical disorientation/midline disorientation
  4. Pusher syndrome

 

151

what is somatoagnosia?

an impairment of body scheme

Lack of awareness of relationship of body parts

(how your shoulder relates to your elbow, difficult to differentiate from proprioception)

152

what portion of the brain is primarily/most often affected with somatoagnosia?

usually lesion to dominant parietal lobe

153

what is R-L discrimination?

decreased R/L differentiation with body parts and following directions

154

what portion of the brain is primarily/usually affected with R/L discrimination?

lesion to either parietal lobe

155

what is vertical disorientation/midline disorientation?

cannot ID when their body is in the middle 

156

what is Pusher Syndrome?

a subtype of vertical/midline disorientation

characterized by leaning and active pushing towards hemiplegic side w/o compensation for instability and with resistance to passive correction towards midline

 

157

what portion of the brain is primarily affected with pusher syndrome?

lesion to R hemisphere centered in area of posterolateral thalamus

tends to be more common when L hemiplegia is present alongside L spatial and sensory neglect

158

list the various spatial relationships impairments

  1. Figure ground
  2. spatial relations disorder
  3. position in space disorder
  4. topographical disorientation
  5. depth and distance perception

 

159

what is Figure ground?

the inability to distinguish a figure from the background in which it is embedded 

ex: pick a screwdriver out of a toolbox full of tools

160

what is spatial relations disorder?

the inability to percieve relationships of one object in space to another object, or to one's self

 

161

what primarily causes spatial relations disorder?

lesion in the R inferior parietal lobe 

162

what is position in space disorder?

decreased ability to perceive and interpret spatial concepts

can't distinguis between opposite directional/spatial concepts

ex: confused up and down 

163

what is topographical disorientation?

difficulty perceiving relationships from one location to another in the environment

164

what is depth and distance perception?

inaccurate judgement of directions, distance, and depth 

more broad than spatial relationship disorders, and deals with environmental cues (like difficulty negotiating a curb)

165

what is the primary cause of depth and distance perception issues?

lesion of R or bilateral visual assocaition cortex

166

what does the general term agnosias mean?

decreased ability to recognize stimuli despite intact sensory function. 

most commonly associated with damage to temporal lobe

167

what are the different types of agnosias?

  1. Sensory
    1. visual
    2. auditory
    3. tactile (asterognosis)
  2. Body scheme
    1. anosognosia
    2. somatagonsia 

 

168

what is visual agnosia?

inability to recognize familiar objects despite normal eye function

 

169

what type of lesion normally causes visual agnosia?

occipital and temporal lobe (R or L)

170

what is auditory agnosia?

inability to recognize non-speech sounds and discriminate between them

171

what type of lesion normally causes auditory agnosia?

left temporal lobe

172

what is tactile agnosia (astereognosis)?

inabilty to recongize objects when handling them, despite normal tactile sensation 

173

what types of lesions normally causes tactile agnosia?

parietal/temporal/occipital association areas (R or L)

174

what is anosognosia?

a severe condition in which an individual does not acknowledge, denies, or lacks awareness of presence/severity of one's deficits

175

define apraxia

impairment of voluntary, skilled, well-learned movement 

w/o deficits in motor function, sensory function, or coordination

176

what are the 2 types of apraxia?

ideomotor

ideational

177

what is ideomotor apraxia?

breakdown between concept (idea) and performance (motor execution)

178

what is ideational apraxia?

failure in the conceptualization of the task

179

what type of lesion normally causes apraxia?

left frontal or parietal lobes

180

what is an Upper Motor Neuron (UMN)?

descending axons from cortex to brainstem 

OR

from brainstem to spinal cord

181

what is a Lower Motor Neuron (LMN)?

axons exiting the CNS and innervating peripheral nerves

motor divisions of cranial nerves

182

is weakness a sign of an UMN or LMN Lesion?

Both

183

is atrophy a sign of an UMN or a LMN lesion?

LMN lesion

184

are fasiculations a sign of an UMN or LMN lesion?

LMN

185

are increased reflexes a sign of an UMN or a LMN lesion?

UMN lesion

(LMN have decreased reflexes)

186

is decreased tone a sign of an UMN or a LMN lesion?

LMN lesion

(increased tone = UMN lesion)

187

What are the 6 components of the whole clinical neurological exam?

  1. Mental Status
  2. Cranial Nerves
  3. Motor Exam
  4. Sensory Exam
  5. Reflexes
  6. Coordination/Gait

 

188

Which cranial nerves are pure sensory nerves?

  1. Olfactory (CN 1)
  2. Optic (CN 2)
  3. Auditory (CN 8)

 

189

which cranial nerves are pure motor nerves?

  1. Trochlear (CN 4)
  2. Abducent (CN 6)
  3. Accessory (CN 11)
  4. Hypoglossal (CN 12)

 

190

which cranial nerves are mixed nerves (both motor and sensory)?

  1. Trigeminal (CN 5)
  2. Facial (CN 7)
  3. Glossopharyngeal (CN 9)
  4. Vagus (CN 10)
  5. Occulomotor (CN 3)
191

Th test for olfaction (CN 1) includes what 2 tests?

  1. Tests for discrimination (contrast odors)
  2. Tests for arousal (noxious stimulant)

 

192

T/F: the CN 1 test is not often included in the cranial nerve screen

TRUE

this nerve tends to be spared from a lot of issues unless there is a specific pathology that impacts this sense

193

If a patient presents with unilateral or bilateral loss of smell but can still distinguish the smell what is the differential diagnosis?

a local nasal disease rather than a neural condition

194

When testing CN 1, what would suggest to you that there might be a neural pathology invovled?

if the pt has a distorted sense of smell for a neutral scent

195

List some possible mechanisms of injury to the olfactory nerve

  1. Parkinson's disease
  2. chronic meningeal inflammation
  3. tumors in sub frontal region
  4. head injuries
  5. heavy smoking

 

196

What tests are included in the CN 2 exam?

  1. Visual acuity
  2. Color discrimination
  3. Field Cuts
  4. Pupillary response to light accommodation 
  5. Visual Extinction 

 

 

197

What is visual acuity? How do we test it?

ability to see clearly

Snellin chart 

198

What is a visual field cut?

blindness in one of the 4 quadrants of the eye

this is due to damage to the optic nerve and is NOT the same as visual neglect

199

What is the visual extinction test?

a visual neglect test

helpful to include in testing the optic nerve and ruling out visual neglect over a visual field cut 

200

what cranial nerves are responsible for innervating the extraoccular muscles?

CN III
CN IV

CN VI

201

CN III innervates extraoccular muscles that perform what movements?

elevation

depression

ADDuction

(PSNS: pupil constriction - efferent limb of pupillary reflex)

202

CN IV innervates extraoccular muscles that perform what movements?

Depression/intorsion

203

CN VI innervates extraoccular muscles that perform what movements?

ABDuction

204

what test is performing the examination of CN 3, 4, and 6?

Big H test

205

if a patient presents with a gaze palsy in which both eyes are skewed in the same direction, what type of lesion are you suspecting?

UMN Lesion

(both eyes have dysconjugate gaze)

206

if a pt presents with a gaze palsy in which both eyes are dysconjugate but are skewed in different directions, what lesion do you suspect?

LMN lesion

207

if a pt presents with a gaze palsy in which only one eye has a dysconjugate gaze in a specific direction, what type of lesion are you suspecting?

LMN lesion

208

The trigeminal nerve is a mixed sensory and motor nerve. What afferent/efferent info does it carry?

Afferent:

  1. pain
  2. temperature
  3. joint position
  4. vibration
  5. anterior 2/3 tongue (somatosensory)
  6. nasal sinuses

Efferent

  1. muscles of mastication
  2. tensor tympani

 

209

How would you test the trigeminal nerve?

  1. Light tough to face
    • for all branches (V1, 2, 3)
  2. Bite strength 
    • for muscles of mastication
  3. Corneal reflex
    • tests both V and VII 
210

when is the corneal reflex test most often performed?

if a pt is obtunded

not commonly performed if a pt is alert 

211

the facial nerve is a mixed sensory and motor nerve. What are it's afferent and efferent branches?

afferent

  1. taste afferents for anterior 2/3 of tongue
  2. somatosensory for proprioception of facial muscles
  3. somatosensory for skin sensation of posterior ear and external auditory meatus
  4. motor for facial expression muscles
  5. autonomic motor to lacrimal and salivary glands

 

212

What is/are the methods for testnig CN VII?

  1. Observation
  2. Motor
    1. smile, raise eyebrows, puff out cheeks, purse lips, close eyes tightly
  3. Sensory
    1. taste (not typically done)
    2. secretomotor function
  4. Reflexes
    1. corneal reflex (CN V and VII)
    2. nasopalpebral reflex

 

213

why is taste not typically tested specifically?

pts wil often complain about it and will let you know if they have lose some taste

214

what is the formal way to test the salivary glands?

give the pt something spicy and then compare the either side of the inside of their mouth.

look for saliva secretion either side

215

When testing CN 7 how can you distinguish between an UMN and a LMN lesion?

look at the forehead

UMN = intact forehead muscle function

LMN = entire side of face will lose motor function

216

how is CN IX assessed/tested?

Palatal activation

inspect for symmetry → with a lesion, one side will deviate to uninvolved side

Gag reflex (sensory limb)

217

The gag reflex tests which cranial nerves?

CN IX (sensory afferent limb)

CN X (motor efferent limb)

218

how would you expect a pt with CN 9 and 10 dysfunction to sound?

hoarse

difficulty with speech production

219

how is CN 11 assessed?

Shoulder Shrug (UTrap)

Side bend and rotate (SCM)

220

how would an UMN lesion impact CN 11?

pt will present with trapezius weakness 

BUT the SCM will be spared

221

how would a LMN lesion impact CN 11?

both the trapezius and SCM would be impacted

222

how is CN 12 assessed?

Stick out tongue (tongue protrusion)

direction may indicate UMN vs LMN

223

how will a pt present with an UMN lesion of CN 12?

tongue will deviate away from the side of the lesion 

(picture on the right)

224

how will a pt present with a LMN lesion of CN 12?

tongue will deviate toward the side of the lesion

atrophy and fasciculations will also be observed 

(left picture)

225

T/F: you can performm the motor exam part of the clincial neurological exam without even toughing the pt?

TRUE

226

what are the components of the Motor Exam?

  1. Inspection at rest
  2. Task Based observation
  3. Tone assessment
  4. MMT

 

227

what are you looking for during the inspection at rest portion of the Motor Exam?

  1. Muscle atrophy
  2. Fasiculation
  3. Hypertrophy
  4. Tremors
  5. Involuntary movements
  6. posturing

 

228

What is posturing?

occurs when a pt picks up a very specific position of their UE and LE base don where their inujury was

229

What are the 2 main kinds of posturing?

  1. Decorticate posture
  2. Decerebrate posture

 

230

Describe decorticate posture

pt has full flexion of the UE and they hold it there 

full extension of LE

 

231

What type of damage would result in decorticate posturing?

damage to brainstemm above the red nucleus

232

Describe decerebrate posture

pt has full extension of UE and LE 

might still have some finger flexion

233

What type of damage would result in decerebrate posture?

damage underneath/lower than the red nucleus in the brainstem

ex: pontine lesion

234

T/F: posturing has no prognostic value

FALSE

it is an indicator that the pt might not progress/get that much better

235

What is the distinction between the tone assessment and MMT?

tone assessment = resitance against passive movement

MMT = greater resistance, helps ID patterns of weakness

236

What is assessed during the Sensory Exam?

  1. Pain
  2. Temperature
  3. Vibration
  4. Proprioception
  5. Light touch/2 pt discrimination
237

How are reflexes graded?

0-5

0 = absent

1 = trace

2 = normal

3= brisk

4 = non-sustained clonus

5 = sustained clonus

238

If reflexes are abnormally increased this is indicative of what?

UMN lesion

239

if reflexes are abnormally decreased, this is indicative of what?

LMN lesion

but could be muscle, nerve fiber and NMJ

240

What are some primary neuromusclar impairments that can result from a neurological pathology?

  1. Muscle weakness
  2. Abnormal tone
  3. Coordination deficits
  4. involuntary movements

 

241

What are some secondary neuromusclar impairments that can result from a neurological pathology like an UMN lesion?

  1. ROM and alignment issues
  2. Endurance issues
  3. Pain

 

242

how would you define muscle weakness as a neuromusclar impairment?

inability to generate force or recruit/modulate motor units

243

list some neural contributions that can result in the primary neuromusclar impairment of muscle weakness

Change in:

  1. # of motor units recruited
  2. D/C frequency
  3. type of motor unit recruited

 

244

What are some potential neurological pathologies that can result in neuromusclar weakness as an impairment?

  1. Cortical lesions
  2. lesions in descending pathways
  3. disruption of impulses to alpha motor neurons
  4. peripheral nerve injury
  5. synaptic dysfunction at NMJ

 

245

Muscle weakness as a neurological impairment can result in what secondary impairments/observations?

  1. postural abnormalities
  2. asymmetrical weight bearing
  3. abnormal synergies

 

246

list 2 types of abnormal synergies

  1. Flexor synergy (UE)
  2. Extensor synergy (LE)

 

247

describe a flexory synergy?

scapular retraction and elevation

shoulder abduction and ER

elbow flexion

supination

wrist and finger flexion

248

describe an extensor synergy

hip extension, adduction and IR

knee extension

ankle PF and inversion

toe PF

249

what is tone?

muscles' resistance to passive stretch

250

Describe the continuum/varying levels of tone

From too little to too much

  1. Flaccid
  2. Hypotonicity
  3. normal
  4. hypertonic/spasticity
  5. Rigid 
251

what are the neural contributions to normal tone?

net balance of descending input on motor neurons from:

corticospinal tracts

rubrospinal tracts

reticulospinal tracts

vestibulospinal tracts

as well as the sensitivity of synaptic connections

252

what are the non neural contributions to normal tone?

  1. CT plasticity
  2. viscoelastic properties of the muscles, tendons, and joints

 

253

How is spasticity different from hypertonia?

spasticity is velocity dependent and hypertonia is not

254

Spasticity can sometime be described as a ___________

clasp-knife phenomenon

255

what is a typical cause of spasticity and a common result/association?

damage to pyramidal tract or other nearby descending paths

can be associated with clonus (commonly in distal > proximal extremities)

256

Describe the mechanism by which spasticity occurs

  1. changes in neural contributions
  2. results in decreased descending activity
  3. reduction of inhibitory synaptic input
  4. increases tonic excitatory input
  5. results in alterations to threshold of stretch reflex 
257

List 2 scales typically used to measure tone

  1. Modified Ashworth Scale
  2. Tardieu scale

 

258

which scale used to measure tone, also gives us info on spasticity?

Tardieau 

since we vary the velocities (V1, 2, 3)

259

which applied velocities equate to spasticity on the Tardieau scale?

V2 = speed of limb falling under gravity

V3 = fast as possible

260

In what muscle group is hypertonia typically observed?

Flexors

261

When testing hypertonia with movements, it can be described as _________ or _________

leadpipe or cogwheel

262

what is the difference between leadpipe and cogwheel hypertonia?

leadpipe = constant resistance to movements throughotu entire ROM

Cogwheel = alternating episodes of resistance and relaxation

263

what is hypertonia at rest called?

Posturing

264

What are the 2 types of posturing?

decorticate = UE flexion, LE extension/IR/PF

decerebrate = UE and LE extension

265

what type of posturing is due to a lesion at or above the level of the red nucleus?

decorticate posturing

266

characteristic of the tone abnormality depends on what factors?

  1. type and location of pathology
  2. Chronicity 
    • increases in nonneural changes = increased "stiffness"

 

267

List the type of abnormal tone that would result if a lesion occured at the cortical, brainstem, and basal ganglia level?

  1. cortical: pyramidal → change in descending inputs of alpha motor neurons → spasticity
  2. Basal ganglia: extra pyramidal → rigidity
  3. brainstem: above/below red nucleus → decorticate/decerebrate posturing 

 

268

List some pathologies in which hypertonicity is commonly observed

  1. CVA
  2. TBI
  3. MS
  4. Parkinsons Disease (rigidity)
269

define hypotonicity

reduction in resistance to lengthening

reduction in "stiffness"

270

hypotonicity can be described as _______ or _______

floppy = collapse into gravity, harder to excite

flaccidity = complete loss of muscle tone

271

what causes hypotonicity?

disruption of afferent input from stretch reflex →

lack of cerebellar efference influence →

result in decreased input to gamma motor neurons

272

List some pathologies where hypotonicity is commonly observed

  1. Cerebellar lesions
  2. down syndrome
  3. musclar dystrophies
  4. late stage ALS 
  5. post-polio
  6. Acute CNS injuries → typically end up resulting in hypertonicity/spasticity once subactue phase is over

 

273

what are the functional implications for increased tone?

  1. abnormal posturing
  2. misalignment
  3. high risk for injury during prolonged rest (skin breakdown)
  4. bias with recruitment
    1. increased likelihood of synergistic movement
  5. destabilization with changes in position (clonus, increased risk for contractures)

 

274

what are the functional implications for decreased tone?

  1. fall into gravity
  2. high risk for injury during dynamic tasks

 

275

define coordination

ability to use parts of the body together smoothly and efficiently

276

what are the critical components of coordination?

  1. sequencing
  2. timing
  3. grading

 

277

define incoordination

movements that are awkward, uneven, inaccurate

disrupting of sequencing, timing and grading

loss of coupling between synergistic joints and muscles

278

incoordination is typically observed with what types of lesions?

motor cortex

basal ganglia

cerebellar 

(proprioceptive lesions too)

279

the functional implications of incoordination can be divided into what categories?

  1. grading/scaling dysfunction
  2. timing difficulties
  3. activation and sequencing problems

 

280

what are the types of grading/scaling dysfunctions found with incoordination?

  1. dysmetria = under/overshooting intended position (a type of ataxia)
  2. hypermetria = moving beyond intended goal
  3. hypometria = moving short of intended goal

 

281

list some timing difficulties that are a result of incoordination

  1. increased reaction times
  2. slowed movement times
  3. difficulty terminating movements
  4. rebound phenomenon
  5. dysdiadochokinesia

 

282

list some activation and sequencing problems that occur with incoordination

  1. abnormal synergies
  2. coactivation
  3. impaired inter-joint coordination

 

283

what are the components of the coordination examination?

  1. finger to nose
  2. alternating pronation/supination
  3. hand or foot tapping
  4. heel to shin

 

 

284

List several categories/types of involuntary movements that are primary neuromusclar impairments

  1. dystonia
  2. tremors
  3. choreiform
  4. athetosis

 

285

what is dystonia?

syndrome dominated by sustained muscle contractions 

causing twisting, repetitive movements, and abnormal postures

286

what region of the brain is dystonia correlated with?

basal ganglia

287

what are tremors?

rhythmic, involuntary oscillatory movement of a body part

can be intermittent or constant, sporadic or as a sequale to a disease or injury

288

what is the difference between a resting and active tremor?

resting = occurs in a body part that is not voluntarily activated (it's relaxed)

active = any tremor produced by voluntary contraction of muscle (can be postural or intention)

289

what is a postural tremor? Intention tremor?

postural = person maintains a part of body against gravity

intention = produced with purposeful movement 

290

what is a choreiform?

involuntary, rapid, irregular and jerky movements

seen with Huntingtons disease and is a SE of PD meds

291

what is athetosis?

slow, writhing and twisting movements 

UE > LE

common in CP

292

What causes endurance issues to be a secondary neuromuscular impairment?

  1. decrease in central drive to spinal cord motor neurons
  2. decrease in activity level/immobility
293

T/F: There is a greater proportion of our brain devoted to vision than any other sense?

TRUE

multiple concurrent visual processes are ongoing continuously like:

  1. conscious perception of visual image info
  2. conventional visual reflexes
  3. saccadic movements 
  4. regulation of sleep/wake 

 

294

A lesion to the optic nerve prior to the optic chiasm would result in what type of visual deficit?

blindness in the ipsilateral eye

295

what are the functional implications to ipsilateral blindness?

  1. poor depth perception
  2. small visual field 
  3. far peripheral vision is impacted = difficulty with driving and other higher level tasks
  4. potential musculoskeletal issues like pain from positioning to compensate

 

296

 compression of the optic chiasm would result in what visual defict?

binasal hemianopsia = loss of nasal fields bilaterally, temporal fields spared

297

what are the functional implications of binasal hemianopsia?

trouble with near vision and any tasks that utilize that like reading

difficulty concentrating

difficulty with ADLS

**these pts can usually learn to compensate pretty well  though

298

a lesion to the optic chiasm would result in what visual deficit?

bitemporal hemianopsia = results in loss of temporal fields, nasal fields spared

 

299

bitemporal hemianopsia is commonly seen with what type of injury?

pituitary tumors

300

what are the functional implications of bitemporal hemianopsia?

it's like having horse blinders on!

miss peripheral objects and trip on things 

miss doors

common fall risk

301

what do patients with bitemporal hemianopsia require?

prism glasses or other external aids to be safe on their feet

 

302

a lesion to the optic tract after the optic chiasm results in what type of visual deficit?

homonymous hemianopsia = complete loss in affected region of binocular visual field

 

Temporal half of R/L visual field + nasal half of L/R visual field

303

homonymous hemianopsia is common with what type of injury?

CVA

304

what are the functional implications of homonymous hemianopsia?

difficulty seeing everything on one side

must teach pt to turn towards the side they are missing

305

a lesion to the lower division of the optic radiations (in temporal lobe) results in what visual deficit?

upper quadrantopia 

306

what are the functional implications for someone with upper quadratanopia?

none really!

just mostly annoying to pts but they can function just fine

307

a lesion to the upper division of the optic radiation (temporal lobe) would result in what visual deficit?

lower quadrantanopia

308

what are the functional implications of lower quadrantanopia?

might just be an annoyance and pt can function/adapt just fine

BUT, pts often forget to compensate with this making tripping and falling more common

309

what causes homonymous hemianopia with macular sparring?

a lesion to both division of the optic radiations 

or a lesion to the visual cortex 

310

what are the functional implications to homonymous hemianopsia with maccular sparring?

the exact same as homonymous hemianopsia

311

what is the typical cause of monoaural hearing loss?

peripheral lesion/damage 

cochlear lesion or damage to CN VIII

312

what does having 2 ears help us with?

localization of source of sound

313

what are some common causes of acquired hearing loss?

  1. acoustic neuroma
  2. meniere's disease
  3. traumatic brain injury
  4. ototoxicity
  5. presbycusis

 

314

what are the functional implications of hearing loss?

can impact the ability to participate in social settings

but other than that none really/just annoying

315

T/F: if there is acquired hearing loss, vestibular loss/dysfunction is usually not far behind

TRUE

316

List the 3 vestibular reflexes

  1. Vestibulo-occular reflex (VOR)
  2. Vestibulospinal reflex (VSR)
  3. Vestibulocollic reflex (VCR)

 

317

what is the VOR?

allows us to stabilize gaze during head movements 

results in eye movements that equally coutner head movements 

318

describe how the VOR would work with L head turning

+L semicircular canals → +R abducens and +L occulomotor to move eyes 

 

-R semicircular canals → -L abducens and -R occulomotor 

319

Vestibular damage involving the VOR would most likely impact what structures?

  1. Central: damage to midbrain and pons
  2. Peripheral: CN VIII, labryinth structures 

 

320

damage to the VOR would result in what impairments?

  1. difficulty stabilizing image on retina while head is moving
  2. bilateral vestibular dysfunction 
    1. oscillopsia = bouncing vision
  3. unilateral vestibular dysfunction
    1. nystagmus
    2. saccedes

 

321

what do the VSR and VCR help with?

postural adjustments 

 

322

what structures are involved with the VSR?

  1. otoliths (utricle and saccule) project to LVN
  2. axons descend to antigravity muscles at all levels of the spinal cord

 

323

what structures are involved with the VCR?

  1. MVN axons descend in MLF to upper cervical levels of spinal cord
    • these help dictate head position in response to head rotation 

 

324

how does the VSR work?

Head is tilted to one side

  1. Canals and otoliths are stimulated ipsilaterally (and inhibited contralateral)
  2. Increased input through the vestibular nerve to the vestibular nuclei ipsilaterally
  3. Impulses transmitted through the lateral & medial vestibulospinal tracts to the spinal cord

** result in increased lateral extension of trunk on side of head tilt, increased flexion contralaterally

325

Damage to the VSR/VCR would result in what?

Postural instability, difficulty sensing falling/tipping

Truncal ataxia

326

what is truncal ataxia?

incoordination, unstable trunk movement during movement

327

what is the difference between unimodal and heteromodal corticies?

both are association corties

unimodal are modality specific

heteromodal are higher-order functioning

328

what is one reason for hemispheric specialization?

a reduction in the amount of time it would take to have both hemisphere's "talk to each other" to accomplish the task

329

T/F: there is bilateral representation of language centers in many right handers?

FALSE
it is observed in 60-70% of LEFT handers

330

what is our non-dominant hemisphere primarily responsible for?

  1. complex visual-spatial skills
  2. imparting emotional significance to events and language
  3. music perception

 

331

List some clinical features of a non-dominant hemisphere lesion

  1. visual-spatial analysis/constructional difficulties
  2. Gestalt difficulties
  3. tendency toward relatively severe personality and emotional changes
  4. increased likelihood to have delusions and hallucinations (when compared to the dominant hemisphere)

 

332

what is meant by constructional difficulties?

difficulty judging or matching orientation of lines displayed at different angles 

(this person would have a hard time drawing more complex shapes but could draw simple ones)

333

what are gestalt difficuties?

overall spatial arrangement difficulties

(a pt would have difficulty understanding how everything is organized in their visual field, ie. big picture)

334

List some odd nondominant syndromes 

  1. capgas syndrome
  2. fregoli syndrome
  3. reduplicative paramnesia
335

what is capgas syndrome?

patient insists that their friends and family members have been replaced by identical-looking imposters

336

what is fregoli syndrome?

patients belive that different people are actually the same person in disguise 

337

what is reduplicative paramnesia?

patient believes that a person, place, or object exists as two identical copies

338

List some dominant (usually left) hemisphere functions

  1. Language
  2. skilled motor function (praxis)
  3. Arithmetic: sequential and analytical calculating skills
  4. Musical ability: sequential and analytical skills in trained muscians 
  5. Sense of directions: following a set of written directions in sequence

 

339

List some non-dominant (usually right) hemisphere functions

  1. Prosody (emotion conveyed by tone of voice)
  2. visual-spatial analysis and spatial attention
  3. arithmetic: ability to estimate quantity and to correctly line up columns of numbers on the page
  4. musical ability: in untrained musicians, and for complex musical pieces in trained musicians
  5. sense of direction: finding one's way by overall sense of spatial orientation

 

340

how do Broca's and Wernicke's area communicate?

arcuate fasciculus

341

List all the regions of the brain associated with language

  1. inferior lateral primary motor cortex
  2. Frontal lobes
  3. supramarginal gyrus and angular gyrus
  4. visual cortex, visual association cortex
  5. Non-dominant hemisphere is also involved
  6. subcotical regions

 

342

what is the role of the Frontal Lobe with respect to language processing?

  1. higher-order motor aspects of speech formation and planning
  2. syntax

 

343

what is the role of the supramarginal and angular gyrus (parietal and tempral lobes) in language?

  1. lexicon
  2. writing

 

344

what is the role of the visual and visual association cortices in language?

reading

345

List some syndromes related to aphasia

  1. Alexia
  2. Agraphia
  3. Alexia with agraphia

 

346

what is alexia?

an impairment in reading ability

 

347

what is agraphia?

impairment in writing ability

348

alexia without aphasia will have a lesion where?

dominant occipital cortex extending to the posterior corpus callosum (often PCA infarct)

349

Agraphia without aphasia will often involve a lesion where?

lesion of inferior parietal lobule of language-dominant hemisphere 

350

what is alexia with agraphia? 

what regions of the brain does it impact?

aphasia absent or only mild dysnomia and paraphasias

lesions of dominant inferior parietal lobe, region of angular gyrus

351

what are the symptoms of gerstmann's syndrome?

  1. agraphia
  2. acalculia
  3. R/L disorientation
  4. Finger agnosia

 

352

a lesion to what region of the brain often results in gerstmann's syndrome?

dominant inferior parietal lobe

(right where the angular gyrus is)

353

List some disorders involving the primary visual cortex

  1. Cortical blindness
  2. Blindsight
  3. Anton's Syndrome

 

354

What is cortical blindness?

complete visual loss on confrontation testing

bilateral occiptial lobe lesion

355

what is blindsight and what causes it?

individual can perform a task without conscious visual perception

visual cortex lesion

356

What is Anton's Syndrome? What causes it?

Complete visual loss on confrontation testing + anosognosia

Bilateral occipital lobe lesion

357

List some disorders involving the Inferior Occipitotemporal Cortex

  1. Prosopagnosia
  2. Achromatopsia
  3. Micropsia, Macropsia
  4. Metamorphopsia
  5. Cerebral dipopia/polyopia

 

358

what is archromatopsia?

Difficulty with color perception

whole visual field involved = lesions in bilateral inferior occititotemporal cortex

one eye = contralateral cortical involvement

359

what is micropsia and macropsia?

objects appear unusually small or big

360

what is metamorphopsia?

objects have distorted shape or size

361

what causes cerebral diplopsia/polyopia?

occipital lobe lesion

362

List some syndromes of the Dorsolateral Parieto-Occipital Cortex

  1. Simultanagnosia
  2. Optic ataxia
  3. ocular apraxia
  4. Baliant's syndrome

 

363

what is simultanagnosia?

impaired ability to percieve parts of a visual scene as a whole

364

what is optic ataxia?

impaired ability to reach for or point to objects in space under visual guidance

365

what is occular apraxia?

difficulty voluntarily directing one's gaze towards objects in peripheral vision

366

what is Baliant's syndrome?

bilateral lesions of DL parieto-occipital cortex

presents with a clincial triad of the following symptoms:

  • simultanagnosia
  • optic apraxia
  • occular apraxia 

 

367

Functions of the frontal lobe can fit into 3 categories, what are they?

  1. restraint
  2. initiative
  3. order

 

368

list some restraint functions of the frontal lobe

  1. judgement
  2. foresight
  3. perseverance
  4. delaying gratification
  5. inhibiting socially inappropriate responses
  6. self-governance
  7. concentration

 

369

List some initiative functions of the frontal lobe

  1. curiosity
  2. spontaneity
  3. motivation
  4. drive
  5. creativity
  6. shifting cognitive set
  7. mental flexibility
  8. personality

 

370

list some Order functions of the frontal lobe

  1. abstract reasoning
  2. working memory
  3. perspective taking
  4. planning
  5. insight
  6. organization
  7. sequencing
  8. temporal order

 

371

what is the difference in symptoms between a dorsolateral and ventromedial orbitofrontal lesion?

DL = apthetic, abulic

VM = impulsive, disinhibited, poor judgement

 

372

what is the difference between a L and R hemisphere frontal lobe lesion?

left = associated with depression-like symptoms

right = more associated with behavioral disturbances like mania

373

frontal lobe syndromes are also known as ________________

dysexecutive syndrome

374

What types of symptoms are typically observed with an orbitofrontal lobe syndrome?

(disinhibited)

  1. impulsive behavior (psuedopsychopathic)
  2. inappropriate jocular affect, euphoria
  3. emotional lability
  4. poor judgement and insight
  5. distractibility

 

375

what types of symptoms are typically observed with frontal convexity syndrome?

(apathetic)

  1. apathy (pseudodepressive)
  2. indifference
  3. psychomotor retardation
  4. motor perseveration and impersistence
  5. stimulus-bound behavior 
  6. motor programming deficits
  7. poor word list generation

 

376

What are some additional frontal lobe lesion symptoms?

  1. disinhibition 
  2. inappropriate jocularity (witzelsucht)
  3. limited insight
  4. utilization behavior/environmental dependence
  5. frontal release signs
  6. paratonia
  7. frontal gait

 

377

what is the symptom of disinhibition?

silly behavior, crass jokes, aggressive outbursts

378

define inappropriate joculatiry (witzelsucht)

seemingly unconcerned about potentially serious matters

379

what is utilization behavior/environmental dependence?

respond to whatever stimuli at hand, even when not appropriate 

(also called new bed over syndrome)

380

List some frontal release signs

  1. palmar reflex
  2. grasp reflex
  3. sucking reflex

 

381

what is paratonia?

increase in tone, but in a manner in which patient appears to resist the movements of the examiner in almost a willful fashion

382

define Frontal gait

shuffling, unsteady, magnetic gait

383

what is being tested during the 

light touch: localization test?

dorsal column 

ability to detect and localize a light touch stimulus

384

what is being tested during the pin prick test?

spinothalamic tract

ability to detect difference between sharp and dull sensation

385

what is being tested during the hot:cold test?

spinothalamic tract

ability to detect between a hot and cold stimulus

386

what is being tested during a vibration test?

dorsal column/medial lemniscus

ability to detect a vibration (when it starts and when it stops)

387

what is being tested during the extinction test?

test for unilateral neglect

specifically tactile neglect

388

what is being tested during the 2-point discrimination test?

dorsal column/medial lemnsicus tract

ability to accurately distinguish between 1 or 2 points of contact

 

389

what is the normative data/distances for the 2-point discrimination test?

fingertips = 2-5 mm

palms = 8-12 mm

hand, extremities, trunk = 20-30 mm

390

what is being tested in the proprioception test?

dorsal column/medial lemniscus tract

ability to detect position of limb when it is changed slightly (up/down)

391

what is being tested during the stereognosis test?

dorsal column → integrative ability of the parietal cortex

ability to accurately ID common objects based off of touch alone (eyes closed)

392

what is being tested during the graphesthesia test?

dorsal column → integration at parietal cortex

ability to accurately ID a letter/number that is drawn on your hand w/eyes closed

393

what is being tested during the kinesthesia test?

dorsal column → integration at parietal cortex → motor cortex

ability to detect movement in space and then match it with the contralateral limb (eyes closed)

394

how are all sensations tests graded?

5/5 = normal

1 - 4/5 = impaired

0/5 = absent

395

what are the deep tendon reflexes for the UE/LE testing for?

presence or absense of an UMN/LMN lesion

396

what nerve roots are responsible for the patellar tendon reflex?

femoral nerve (L2, 3, 4)

397

what nerve roots are responsible for the achilles reflex?

tibial neve (S1, 2)

398

what nerve roots are responsible for the biceps brachii tendon reflex?

musculocutaneous nerve ((C5, 6)

399

what nerve roots are responsible for the brachioradialis tendon reflex?

radial nerve (C5, 6)

400

what nerve roots are responsible for the triceps tendon reflex?

radial nerve (C6, 7)

401

what are the grades/scores for reflex testing?

0-1+ = LMN

2+ = norma

3+ = Brisk

4+ and 5+ = UMN lesion

402

what is the purpose of the Hoffman's sign?

it is a pathological reflex that indicates the presence or absence of an UMN/LMN

flexion of 1,2 phalanx = a positive sign

 

403

what is the purpose and grading of the Babinski's sign?

tests for the presence/absence of an UMN/LMN

splaying of toes and ext of hallux is a positive sign

404

what is the UE and LE synergy test for?

it tests the corticospinal tract and isolation of movement at a joint

 

405

what is considered an abnormal result for an UE and LE synergy test?

movement in two or more joints in compensatory/synergistic pattern 

this indicates an UMN lesion

406

what does dysmetria (for UE and LE) test for?

cerebellar coordination/functioning

407

what are abnormal results for dysmetria UE/LE?

hypometria = undershooting 

hypermetria = overshooting, varying course of movement, disintegration of pattern

408

what does dysdiadochokinesia test for?

cerebellar coordination/functioning 

409

what is included in a spasticity test?

  1. shoulder FLX/EXT
  2. elbow FLX/EXT
  3. wrist FLX/EXT
  4. thumb flexors
  5. finger flexors
  6. hip FLX/EXT
  7. hip ABD/ADD
  8. knee FLX/EXT
  9. ankle DF/PF
  10. clonus

 

410

what does spasticity test for?

velocity dependent tone

presense of an UMN lesion

411

how are spasticity tests measured?

Modified Ashworth Scale

412

what results indicate the presence of clonus?

repeated bouncing of foot (plantarflexors)

413

what results are you looking for when testing the papillary reflexes?

direct and consensual constriction

accommodation

414

what is considered an abnormal result when testing the papillary reflex?

absense of constriction (direct/consensual)

absense of accommodation

415

what is tested when performing the big H test?

EOMs

pursuit eye movements

416

what are considered abnormal results from the big H test?

any asymmetry in movement

gaze palsies

2 or more of the following: nystagmus, strabysmus, saccades, and double vision

417

what gaze palsies can be observed as an abnormal result from a big H test?

UMN = same direction limitation

LMN = opposite direction limitation or in one eye

 

418

what are the grades that can be assigned during a Weber and Rinne test?

normal

conductive loss

sensoryneuro loss

419

what suggests conductive hearing loss during a Weber test?

positive is louder in affected ear

420

what suggests neurosensory hearing loss during a Weber test?

positive weber = louder in unaffected ear

421

what suggests conductive hearing loss during a Rinne test?

hear sound only in mastoid process

no sound heard when tuning fork is placed in front of auricle

422

what suggests neurosensory hearing loss during a Rinne test

no sound hear at either the mastoid or in front of the ear

423

when testing CN XI what indicates and UMN or LMN?

asymmetry in strength

UMN = trap is weak but SCM is spared

LMN = both are weak/absent

424

define dysesthesia

unpleasant and abnormal sensation

can be evoked or spontaneous

425

what are the 2 types of dyesthesia?

  1. allodynia
  2. hyperalgesia

 

426

what is allodynia?

pain evoked by stimulus that is not usually noxious

(a cotton ball evoking pain)

427

what is hyperalgesia?

excessive sensitivity to stimuli that are normally mildly painful

428

T/F: when a part of the body is injured, special pain receptors convey the pain message to your brain

FALSE

incomplete concept

pain is a perception/experience

nociceptive fibers carry sensations that can be later interrpreted as pain

429

what evidence is there that type C and A-delta fibers do not carry pain signals?

if they carried pain fibers then every time they were stimulated, the result should be the same pain.

Not the case, the same injury in the same person can cause different levels of pain depending on the context

430

T/F: pain only occurs when you are injured

FALSE

injury or degeneration may be present in the absence of pain

significant pain may be present with no identifiable disease process or even after tissue healing

431

pain is an emotional experience and can develop due to emotional overload. However it is important to not classify it as _____________

a psychosomatic issue

432

T/F: the timing and intensity of pain matches the timing and number of signals in nociceptors 

FALSE

repeated signals from nociceptors to the dorsal horn of spinal cord can result in action potential windup leading to heightened sensitization

433

what is action potential windup?

repeated stimulation of nociceptors to the dorsal horn of the spinal cord resulting in a progressive increase in action potentials 

434

what can action potential windup cause?

heightened sensitization

death of interneuron in dorsal horn ⇒ decreased ability to modulate response

2nd order neuron receptors get replaced with receptors that increase danger messages to the brain

435

T/F: Nerves have to connect a body part to your brain in pain

FALSE

phantom limb pain

 

436

T/F: in chronic pain , the CNS becomes more sensitive to nociception

TRUE

due to:

  1. action potential windup
  2. changes at the interneuron ⇒ increased sensitization
  3. changes in descending modulation of pain

 

437

how does changes at the dorsal horn interneurons come about? How does this result in increased sensitization?

persistent input from C-fibers → changes interneuron

→ changes in 2nd order neuron receptors → sprouting and expansion of receptor fields → increased sensitization

438

T/F: the body tells the brain when it is in pain?

FALSE

the brain tells the body

 

439

T/F: the brain sends messages down your spinal cord that can increase the nociception going up your spinal cord?

TRUE

changes in the CNS as a result of AP windup allow for increased info to be processed in the brain

440

T/F: nerves adapt by increasing their resting level of excitment

TRUE

ion channels possess neuroplastic characteristics 

441

how often does ion expression change on a nerve?

continuously

half-life reported to be 48 hours

442

T/F: Chronic pain mean that an injury hasn't healed properly

FALSE

injury and pain are not synonymous

not uncommon for a chronic pain pt to have no injury history

443

T/F: receptors on nerves work by opening ion channels in the walls of the nerve

TRUE

ion channel expression constantly changes

ion channels are found on axons

444

what is ion channel expression dependent on? 

genetic coding 

and

the brain's expression of the survival needs of the individual

445

how is increased expression of certain ion channels impactful to chronic pain?

increased expression of certain ion channels may result in the development of sensitivity to the stimulus that opens that specific channel

446

T/F: the brain decides when you will experience pain

TRUE

pain is a brain construct based on perception of threat

447

T/F: worse injuries always result in worse pain

FALSE
stepping on a lego vs soldier not noticing getting shot

448

T/F: when you are injured, the environment that you are in will not have an effect on the amount of pain you experience

FALSE

injuries in high stress environments are 7-8x more likely to result in persistent pain

449

T/F: it is possible to have pain and not know about it

FALSE

the decision to produce pain is a conscious decision by the brain

this is why you aren't in pain while under anesthesia

450

T/F: Nerves can adapt by making more ion channels

TRUE

451

T/F: 2nd order nociceptor post-synaptic membrane potential is dependent on descending modulation

TRUE

452

how should the placebo effect be viewed?

an endogenous mechanism to modulate the pain experience

453

T/F: Nerves adapt by making ion channels stay open longer

TRUE

G-protein channels can remain open for minutes

in persistent pain, a greater concentration of G-protein channels may be seen in 2nd order neurons

can contribute to the windup effect

454

T/F: when you are injured, chemicals in your tissues can make nerves more sensitive

TRUE

various chemicals can influence opening/closing of specific ion channels

Adrenaline and cortisol

455

T/F: in chronic pain, chemicals associated with stress can directly activate nociception pathways

TRUE

the stress response 

456

using a the lion metaphor, describe the stress response if "the lion enters the room and follows you around for months/years"

if the stressors remain present for months, the stress response of increased adrenaline is then followed by cortisol changes in your body

457

what is the IASP definition of pain?

pain is an unpleasant sensory and emotional experience which follows actual or potential tissue damage or is described in terms of such damage

458

List 2 key things to keep in mind when defining what chronic pain is

  1. it can be thought of as maladaptive neuroplasticity (increased sensitivity)
  2. associated with abnormal intracortical inhibitory mechanisms 
    1. smudging

 

459

List the PNE Principles (summary)

  1. pain is an output of the brain
  2. pain is not always an indicator of tissue damage
  3. the amount of pain you percieve does not = the amount of damage
  4. in chronic pain, the brain believes you are in danger and need protecting
  5. context of pain experience is vital

 

460

what is fibromyalgia?

chronic disorder

widespread pain, abnormal pain processing (pain amplification and impaired descending inhibition), sleep disturbances and fatigue

461

what is chronic regional pain syndrome (CRPS)?

syndrome resulting in pain, vascular changes and atrophy

occurs in a regional distribution as opposed to a peripheral nerve or nerve root distribution

S/S worse in distal extremities

462

when does CRPS usually occur?

secondary to trauma (surgery, fracture, crush injury, sprain)

 

463

what is the primary complaint for CRPS?

severe, spontaneous pain, out of proportion to the injury

464

what are the S/S of CRPS?

  1. sensitivity to cold, pressure and touch
  2. early symptoms:
    1. red/pale skin
    2. excessive sweating
    3. edema 
    4. skin atrophy
  3. later signs
    1. skin becomes dry and cold and joints become stiff and swollen
  4. motor signs (paresis, spasms, and tremor)

 

465

what is the primary precipitating factor for CRPS?

disuse