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Patho II Final > Neuro Mod 8 > Flashcards

Neuro Mod 8 Flashcards

1
Q

Primary injury to the spinal cord?

A

Direct physical impact immediately damages spinal cord cells (neurons/glial cells) and causes necrosis

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2
Q

Secondary injury to the spinal cord occurs within ______

A

hours

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3
Q

Secondary injury to the spinal cord?

A

Cellular necrosis from primary injury causes immune/inflammatory cascade, neuro excitatory responses to ischemia (further damage area adjacent to primary injury)

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4
Q

Medical strategies for primary spinal cord injury?

A

Stabilize injury, address emergency life threatening concerns

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5
Q

Medical strategies for secondary spinal cord injury?

A

Neuroprotective therapy to minimize: acute-phase procedural/surg intervention, systemic pharm agents, cell-based therapies
-high dose IV steroids used in past (unclear evidence, guidelines do not support)

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6
Q

What is spinal shock?

A

Acute loss of motor, sensory, reflex functions below level of injury:
-areflexia (including bulbocavernosus reflex)
-flaccid paralysis (all muscles below injury, bowel/bladder dysfunction, resp. dysfunction if high cervical injury)
-Complete anesthesia

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7
Q

When does spinal shock occur?

A

Immediately after acute spinal cord injury
*not usual w gradual injury (tumors, etc.)

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8
Q

Phase 1 of spinal shock?

A

Areflexia/hyporeflexia: immediate

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9
Q

Phase 2 of spinal shock?

A

Initial reflex return: first one to return is bulbocarvernosus (w/in 24-48 hr), usually a marker for end of spinal shock
*deep tendon reflexes remain absent

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10
Q

How to check for bulbocarvernosus reflex?

A

compress glans penis or clitoris and observe for anal sphincter contraction
*another method: tug on foley catheter

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11
Q

Phase 3 of spinal shock?

A

Early hyperreflexia: some DTRs return gradually (1-4wks) after injury and are hyper reflexic (transition phase from hyporeflexia to hyperreflexia)

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12
Q

Phase 4 of spinal shock?

A

Final hyperreflexia/spasticity: all DTR below level of injury return/are hyperreflexic
*flaccid paralysis is replaced by hypertonicity/spasticity 1-12 months post injury

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13
Q

What is neurogenic shock a result of?

A

acute spinal cord injury or sometimes non-traumatic causes of SCI (anesthesia, infection, toxins, etc)

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14
Q

How does neurogenic shock manifest?

A

Hypotension, bradyarrhythmia, temp dysregulation

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15
Q

Neurogenic shock occurs in what % of SCI?

A

</=10%

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16
Q

Neurogenic shock is associated w/ what kind of SCI?

A

cervical high thoracic (SCI above T6)

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17
Q

Neurogenic shock is ____ ____ if not managed immediately?

A

Potentially fatal

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18
Q

Pathophys of neurogenic shock?

A

Disrupts sympathetic pathways in upper SC, leads to severe loss of sympathetic function while parasympathetic is intact

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19
Q

Loss of sympathetic tone allows for ______ parasympathetic activity

A

Unopposed

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20
Q

What does unopposed parasympathetic activity lead to?

A

Hypotension (systolic <100), Bradycardia, Hypothermia

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21
Q

Management goal of neurogenic shock?

A

Restore hemodynamics

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22
Q

How to manage hypotension w/ neurogenic shock?

A

(MAP 85-94), IV fluids, vasopressors, inotropes (inc strength of cardio contraction)
*too much fluid can cause overload/pulm edema

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23
Q

How to manage bradycardia w/ neurogenic shock?

A

Anticholinergics (atropine, glycolpyrolate)

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24
Q

What is autonomic dysreflexia?

A

Extreme HTN w/ bradycardia
*potentially life threatening

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25
Q

Autonomic dysreflexia is a complication of SCI above the T6 level and rare if it occurs below _____

A

T10

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26
Q

What % of SCI will develop autonomic dysreflexia?

A

20-70%

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27
Q

A hx of autonomic dysreflexia is a potential complication for what?

A

Med procedures, surgeries, labor

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28
Q

Pathophys of autonomic dysreflexia?

A

Cutaneous or visceral stimulation below level of injury –> stimulates sympathetic reflex activity

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29
Q

Cutaneous/visceral stimulation of autonomic dysreflexia pathophys?

A

Bladder/rectum: distend, foley catheter, impaction
Cutaneous: pain, cold, pressure ulcers, etc.
Injuries: fx, etc.
UTIs

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30
Q

Sympathetic reflex activity of autonomic dysreflexia pathophys?

A

Massive vasoconstriction in lower 2/3 of body and extreme HTN –> stimulates parasympathetics to inhibit sympathetics in brainstem via barorecptors to compensate

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31
Q

Parasympathetic signals in autonomic dysreflexia pathophys cannot descend past _______

A

level of injury (allows sympathetic reflexes to remain active below this point, massive vasoconstriction and HTN persist here)

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32
Q

Treatment for autonomic dysreflexia?

A

Immediately sit patient up to decrease BP, Do not lay pt down, remove irritating stimuli asap
*bladder distention is mc cause: evaluate catheter
*bowel: constipation/impaction
*skin: clothes, pressure sores

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33
Q

If unable to resolve irritating stimuli causing autonomic dysreflexia, what should be done?

A

Transfer to emergency medical system ASAP

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34
Q

If not treated promptly, autonomic dysreflexia can lead to what?

A

Seizures, cerebral hemorrhage/stroke, potential death

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35
Q

What two areas do descending motor tracts originate in the CNS?

A

Motor cortex (primary motor area) or Brainstem (red nucleus, tectum, vestibular nuclei, reticular nuclei)

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36
Q

What are the two major descending motor tract pathways?

A

Lateral and medial (anterior) motor tracts

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37
Q

Lateral motor tracts & their control?

A

Lateral corticospinal tract & rubrospinal tract
Control fine motor movements of distal extremities

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38
Q

Anterior/medial motor tracts & their control?

A

Tectospinal, anteriomedial corticospinal, reticulospinal, vestibulospional tracts
Control axial/trunk and reflexes

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39
Q

Lateral corticospinal and rubrospinal tracts travel ________ in the _______ of the spinal cord

A

Next to each other in the lateral column

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40
Q

Lateral corticospinal tract pathway?

A

Motor cortex output –> internal capsule –> ipsilateral anterior brainstem –> cross midline in lower medulla –> descend in lateral spinal column –> terminate in anterior horn motor neurons to supply UE/LE muscles
*controls fine motor movement

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41
Q

What is a result of a lesion in the lateral corticospinal tract above the medulla (stroke, tumor of motor cortex, internal capsule, anterior brain stem)?

A

Contralateral hemiparesis

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42
Q

What is a result of a lesion in the lateral corticospinal tract below the medulla (SCI or MS/ALS in lateral spinal cord)?

A

Ipsilateral hemiparesis below lesion

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43
Q

Function of rubrospinal tract?

A

Supports fine motor movement, promotes UE flexors/inhibits US extensors
*more involved in UE than LE

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44
Q

Pathway of rubrospinal tract?

A

Originates in red nucleus of midbrain –> descends lateral column of spinal tract just anterior to lateral corticospinal tract –> terminates at anterior horn motor neurons that supply UE/LE

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45
Q

An isolated rubrospinal tract lesion is rare and would not cause ________

A

hemiparesis

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46
Q

A lesion in the lateral column (that affects both rubrospinal and lateral corticospinal tracts would result in what?

A

Hemiparesis

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47
Q

What is decerebrate posturing?

A

UE and LE extended

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48
Q

What is decorticate posturing?

A

UE flexed, LE extended

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49
Q

Decorticate and decerebrate posturing are associated with ____ outcomes

A

poor

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50
Q

Brainstem damage involving the red nucleus and below would result in what?

A

Decerebrate posturing
*red nucleus decreases UE flexor tone/allows UE extensor tone to dominate at elbow

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51
Q

Which is more severe/has a worse outcome: decerebrate or decorticate posturing?

A

Decerebrate

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52
Q

Brainstem damage above the red nucleus would result in what?

A

Decorticate posturing
*loss of normal cortex inhibition to red nucleus, excessive flexor tone of UE to dominate

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53
Q

The medial (anterior) motor tracts are involved in what?

A

Axial (trunk)/proximal limb control/balance

54
Q

The medial (anterior) corticospinal tract controls/maintains axial/proximal limb voluntary movement and works synergistically with what?

A

Lateral corticospinal tract’s control of distal voluntary motor movement

55
Q

Pathway of the medial (anterior) corticospinal tract?

A

Motor cortex to brain same as lateral *except does not cross midline at medulla –> descends in anterioromedial spinal cord –> terminates near medial ventral horn of most levels of the spinal cord (C1 to approx. L2/L3)

56
Q

Function of the tectospinal tract?

A

Visual reflexes/coordination of head and eye movement
*reflexive reactions to visual input

57
Q

Pathway of tectospinal tract?

A

Originates at superior colliculi of midbrain –> descends anteriomedial spinal cord –> terminates in cervical spine (supplies postural muscles of head/neck
*only found in cervical spine

58
Q

Function of reticulospinal tract?

A

Modulates reflexive/automatic motor movement related to posture/gait (sensory input to reticular system modifies motor control, modulates flexor response to noxious pain input)

59
Q

Pathway of reticulospinal tract?

A

Originates reticular nuclei in lower 2/3 of brainstem –> descends in anteriomedial spinal cord –> terminates in motor nuclei of anterior horn in all levels of spinal cord

60
Q

Function of medial vestibulo spinal tract?

A

Controls head and neck movement/posture

61
Q

Pathway of medial vestibulo spinal tract?

A

Begins medial vestibular nuclei of medulla –> descends in anteriomedial spinal cord –> terminates on motor nuclei of neck muscles located in anterior horn of cervical spinal cord
*only found in cervical spine

62
Q

Function of lateral vestibulospinal tract?

A

Balance and extensor tone

63
Q

Pathway of lateral vestibulospional tract?

A

Begins lateral vestibular nuclei of medulla –> descends anteriomedial spinal cord –> terminates on motor nuclei of antigravity (extensors) muscles located in anterior horn in all levels of spinal cord

64
Q

The corticobulbar tract is a motor tract that originates in the ______ cortex and terminates on motor nuclei of cranial nerves ___, ____, ___, and ___

A

Primary. 5, 7, 10, 12

65
Q

What does the corticobulbar tract innervate?

A

Muscles of the tongue, face, jaw, pharynx/larynx

66
Q

The corticobulbar tract is the _____ version of corticospinal tracts

67
Q

Function of corticobulbar tract?

A

Bilateral voluntary movement of upper face/mouth/pharynx/larynx muscles
&
Contralateral voluntary movement of lower facial muscles (lower CN7) and tongue (CN12)

68
Q

Pathway of corticobulbar tract?

A

Primary motor cortex —> descends through internal capsule & anterior brainstem —> terminates in motor nuclei of CN 5, 7, 10, 12

69
Q

CN 7 innervation?

A

Bilateral innervation of upper facial muscles, and contralateral innervation of lower facial muscles

70
Q

CN12 innervation?

A

Contralateral innervation of tongue

71
Q

Lesion of the cortex or corticobulbar tract has what kind of affect on upper facial muscles?

72
Q

Lesion of the cortex or corticobulbar tract has what kind of affect on lower facial muscles?

A

Contralateral hemiparesis of lower facial muscles (CN7) and tongue (CN12)

73
Q

Corticobulbar tract lesion vs bells palsy?

A

Bells palsy damages CN7 itself (hemiparesis ipsilateral upper & lower facial muscles)
Corticobulbar tract lesion damages tract that innervates CN7 (hemiparesis contralateral lower facial muscles)

74
Q

What are upper motor neuron structures?

A

Cortex, IC, descending motor tracts in brainstem/SC, terminal end of descending neuron before synapse w motor nucleus in anterior horn

75
Q

What are lower motor neuron structures?

A

Anterior horn (motor nucleus), motor root, motor portion of spinal nerve root & peripheral nerve

76
Q

UMN lesion/damage to anything above anterior horn is caused by what pathologies?

A

Stroke, SCI, tumor, MS, ALS, etc

77
Q

Which pathology causes both UMN and LMN sx?

78
Q

Signs/sx of UMN lesion?

A

Hyperreflexia, hypertonicity/spasticity, spastic weakness/paresis, small amount of muscle atrophy d/t disuse

79
Q

What are present w/ UMN lesion?

A

Pathological reflexes: Babinski’s siogn, Hoffmans sign, etc (primitive signs normal in infants but normally disappear in adults)
*UMN lesions cause them to reappear/indicate loss of cortical inhibition

80
Q

What is babinskis sign?

A

Plantar reflex test (reflex hammer dragged from heel to ball of feet along lateral plantar surface) will stimulate extension of great toe and fanning of other toes
*present in healthy infants or UMN lesion
*normal reflex in adults: toe flexion

81
Q

What is hoffmans sign?

A

Flexion of thumb or index finger after performing hoffmans test (flick middle finger at DIP joint)
aka digital reflex

82
Q

LMN lesion/damage to peripheral motor pathway can result from which pathologies?

A

Radiculopathy, peripheral nerve entrapment, Guillain-barre, ALS

83
Q

Signs/sx of LMN lesion?

A

Hyporeflexia, hypo-tonicity, flaccid weakness, severe muscle atrophy (occurs quickly w/in 2 wks), pathological reflexes not present

84
Q

What is present in LMN lesions?

A

Fasciculations (small visible muscle twitches d/t involuntary contraction/relaxation of small bundle muscle fibers)

85
Q

Somatosensory refers to what sensations?

A

Touch, pain, temp, vibration, proprioception (joint-limb position sense)

86
Q

3 spinal cord pathways of somatosensory info going to the brain/brainstem?

A

Dorsal column-medial lemniscus system, spinocerebellar tracts, spinothalamic tracts

87
Q

Function of dorsal column-medial lemniscus system?

A

Transmits discriminating touch (well localized touch), pressure, vibration, proprioception from brain to body

88
Q

Pathway of dorsal column-medial lemniscus system?

A

Sensory info enters posterior horn –> ascends in ipsilateral posterior column —> medulla, crosses midline —> thalamus —> projects to primary somatosensory cortex (3,1,2)

89
Q

Lesion of dorsal column-medial lemniscus system above the medulla results in what?

A

Contralateral loss of proprioception (discriminating touch/vibtaion)

90
Q

Lesion of dorsal column-medial lemniscus system below the medulla results in what?

A

Ipsilateral loss of proprioception (discriminating touch/vibtaion) below the lesion

91
Q

Vibration sense test for dorsal column-medial lemniscus system?

A

tuning fork (128 hz) over bony prominence

92
Q

Joint position sense test for dorsal column-medial lemniscus system?

A

Contact side of finger/toe & move it up/down and assess if pt can determine direction

93
Q

Discriminating touch tests for dorsal column-medial lemniscus system?

A

2 pt discrimination: moving vs static, monofilaments

94
Q

Romberg’s test for dorsal column-medial lemniscus system?

A

Stand feet close together, observe amount of trunk sway
*safely guard and ask pts to close eyes & observe for sway/loss of balance

95
Q

Positive rombergs test (rombergs sign)?

A

Increased trunk sway or loss of balance w/ eyes closed when compared to eyes open

96
Q

Function of spinocerebellar tracts?

A

Transmit unconscious proprioception to cerebellum

97
Q

Pathway of spinocerebellar tracts?

A

proprioceptive info enters SC –> ascends in ipsilateral lateral column –> ascend to brainstem/cerebellum

98
Q

Isolated lesion of the spinocerebellar tracts is _____

99
Q

Lesion of spinocerebellar tracts may cause what?

A

Small amount of ataxia (uncoordination)
*but lateral column injury/lesion would probably involve lateral corticospinal tract resulting in hemiparesis that would overshadow ataxia

100
Q

Spinothalamic tracts are also known as what?

A

Anterolateral tracts or anterolateral system

101
Q

Function of spinothalamic system?

A

Transmit pain and temp

102
Q

Which two pathways form the spinothalamic/anterolateral system?

A

Lateral spinothalamic tract & anterior spinothalamic tract

103
Q

Function of lateral spinothalamic tract?

A

Fast pain away: immediate localized pain associated w/ tissue damage/injury
*detect/localize pain/temp of body & mediates discriminative pain/temp aspects from body

104
Q

Lateral spinothalamic tract pathway?

A

Nociceptive info enters SC/cross midline immediately –> ascends contralateral lateral column —> thalamus –> projects to primary somatosensory cortex (3, 1, 2)

105
Q

Lesion of lateral spinothalamic tract would result in what?

A

Contralateral loss of pain/temp below level of lesion

106
Q

Lateral spinothalamic tract tests?

A

Pinprick/pinwheel test: detect ability to sense sharp pain
Temp test: compare warm vs cold object

107
Q

Function of anterior spinothalamic tract?

A

Slow pain away: delayed/unpleasant and diffuse sensation associated w/ tissue damage/injury
*mediaste visceral, consciousness, autonomic, and emotional/behavioral rxns to pain
*involved in central modulation of pain

108
Q

Pathways of anterior spinothalamic tract?

A

Nociceptive info enters posterior horn/immediately crosses midline in SC –> ascends contralaterally in anterior column –> terminates at many diff structures (reticular nuclei, tectum, pretecal, thalamus/project to limbic)

109
Q

Reticular termination of anterior spinothalamic tract controls what info?

A

Autonomic responses, arousal, alertness, pain modulation

110
Q

Tectum termination of anterior spinothalamic tract controls what info?

A

Visual reflexes

111
Q

Pretectal (periaqueductal gray) termination of anterior spinothalamic tract controls what info?

A

Pain modulation

112
Q

Thalamus/projection into limbic system termination of anterior spinothalamic tract controls what info?

A

Emotional/behavioral aspects of pain (diffuse poorly localized pain)

113
Q

Anterior spinothalamic tract clinical tests?

A

Pain response: such as glasgow coma scale
*require pathways of anterior spinothalamic tracts to be functioning along w other structures necessary (eye, verbal, motor)

114
Q

Region of SC damaged in Brown sequard syndrome?

A

Incomplete lesion: 1/2 (R/L) of cord is damaged

115
Q

Motor dysfunction of Brown sequard syndrome?

A

Ipsilateral motor loss below level of lesion

116
Q

Sensory dysfunction of Brown sequard syndrome?

A

Ipsilateral loss of proprioception/touch/vibration below level of lesion
&
Contralateral loss of pain/temp below level

117
Q

Prognosis of Brown sequard syndrome?

A

Better than other SC syndromes

118
Q

Region of SC damaged w/ anterior cord lesion?

A

Incomplete lesion: anterior 2/3 of cord

119
Q

Motor dysfunction of anterior cord lesion?

A

Bilateral loss below level

120
Q

Sensory dysfunction of anterior cord lesion?

A

Bilateral loss of pain/temp below level
***No loss of proprioception, or discrimination between touch/vibration

121
Q

Prognosis of anterior cord lesion?

A

Poor for ambulation and B/B function

122
Q

Region of the SC damaged w/ posterior cord lesion?

A

Incomplete lesion: posterior columns damaged

123
Q

Motor dysfunction of posterior cord lesion?

124
Q

Sensory dysfunction of posterior cord lesion?

A

No loss of pain/temp
Bilateral loss of proprioception/discrimination between vibration/touch below level

125
Q

What sign is positive with posterior cord lesion?

A

Romberg’s

126
Q

Region of SC damaged w/ central cord lesion?

A

Incomplete lesion: area around central canal of cord is damaged
*impair spinothalamic tracts as they cross midline

127
Q

Motor dysfunction of central cord lesion?

128
Q

Sensory dysfunction of central cord lesion?

A

Cervical level: loss of pain/temp in classic cape distribution of UE
*no loss of proprioception or discriminating between touch/vibration

129
Q

Region of SC damaged w/ transverse cord lesion?

A

Complete lesion: all columns & grey matter damaged

130
Q

Motor dysfunction with transverse cord lesion?

A

Bilateral loss below lesion

131
Q

Sensory dysfunction with transverse cord lesion?

A

Bilateral loss of proprioception, discrimination between vibration/touch, & pain/temp below lesion

Patho II Final (4 decks)

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