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DPT 520 > Quiz 2 > Flashcards

Quiz 2 Flashcards

1
Q

do we expect to see UMN or LMN signs with PNS injuries?

A

LMN signs

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2
Q

what does the endoneurium surround?

A

individual axons

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3
Q

what does the perineurium surround?

A

fascicles (bundles of neurons)

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4
Q

what does the epineurium cover?

A

bundle of fascicles

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5
Q

what is the point of dynamic protective mechanisms in nerve mobility?

A

provide adequate blood flow for nutrition, oxygen, and removal of waste

movement of the nerve against adjacent structures allows for health of the nerve

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6
Q

t/f: axoplasm flows easily throughout the axon with movement

A

true!

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7
Q

what if dynamic protective mechanisms fail?

A

immobility=numbness

try gentle lengthening and shortening of the nerve

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8
Q

what do nerves look like in resting?

A

folding with wrinkles in endoneurium

stretch gets rid of wrinkles

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9
Q

what are the sensory signs of peripheral nerve injury?

A

decreased/lost sensation

abnormal sensations (dysesthesia, algesia, hyperalgesia)

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10
Q

what are the motor signs of peripheral nerve injury?

A

paralysis/paresis

muscle atrophy (neurogenic)

fasciculation/fibrillation

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11
Q

what are the autonomic signs of peripheral nerve injury?

A

single nerve severance signs are less severe

multiple nerves damaged-difficulty regulating BP, HR, sweating, b/b fxns, impotence

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12
Q

what are the trophic signs of peripheral nerve injury?

A

abnormalities in the lesion of the nerve injury

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13
Q

what are the trophic changes in muscles with peripheral nerve injury?

A

muscle atrophy

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14
Q

what are the trophic changes in skin with peripheral nerve injury?

A

shiny, dry, pigmentation changes

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15
Q

what are the trophic changes in nails with peripheral nerve injury?

A

brittle

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16
Q

what are the trophic changes in subcutaneous tissue in peripheral nerve injury?

A

thicken, ulceration, poor healing of wounds

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17
Q

what are the trophic changes in joints in peripheral nerve injury?

A

neurogenic damage from lack of movement

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18
Q

what are the classifications of peripheral nerve injuries?

A

mononeuropathies, multiple mononeuropathies, and polyneuropathies

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19
Q

what are the 3 mononeuropathies?

A

1) truamatic myelinopathy (neuropraxia)
2) traumatic axonopathy (axonatmesis)
3) traumatic severence (neurotmesis)

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20
Q

what is the usual cause of all 3 mononeuropathies?

A

trauma

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21
Q

what is the pathology of neuropraxia?

A

demyelination

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22
Q

what is the pathology of axonatmesis?

A

axon damage

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23
Q

what is the pathology of neurotmesis?

A

axon and myelin degeneration

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24
Q

what is multiple mononeuropathy?

A

sporadic, non symmetrical pattern of single neuropathy in many places

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25
Q

what is polyneuropathy?

A

symmetric

often complication of diabetes

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26
Q

what is neuropraxia?

A

loss of myelin at the site of injury with no axon damage

temporary impairment of nerve conduction (recovery within hours/weeks)

complete recovery via re-myelination

neuropathic pain

impaired discriminitive touch, proprioception, motor, and DTRs

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27
Q

how long does recovery in neuropraxia take?

A

hours to weeks

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28
Q

what is the least severe mononeuropathy?

A

neuropraxia

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29
Q

what axons are affected first in neuropraxia?

A

large myelinated axons

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30
Q

is there complete recovery with neuropraxia?

A

yes!

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31
Q

what is the prognosis for neuropraxia?

A

good, bc there is complete and rapid recovery via re-myelination

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32
Q

what is axonotmesis?

A

axon and myelin sheath damage with intact endo, peri, and epineurium

Wallerian degeneration at/below level

impaired discriminitive touch, proprioception, motor, DTRs, and autonomic (if severe enough)

decreased nerve conduction velocity and amplitude

complete recovery (1 mm/day of growth)

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33
Q

are the endo, peri, and epineurium intact in axonotmesis?

A

yes!

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34
Q

what size axons are affected in axonotmesis?

A

all sizes

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35
Q

is there complete recovery with axonotmesis?

A

yes!

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36
Q

how long does recovery take in axonotmesis?

A

1 mm/day (1 inch/month)

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37
Q

what is a common cause of neuropraxia and axonotmesis?

A

entrapment or mechanical contriction

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38
Q

what does myelin damage lead to?

A

inflammation in the NS, ectopic foci, and decreased nerve conduction velocity

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39
Q

what is Tinnel’s sign?

A

oversensitivity of the nerve to mechanical stimuli

tapping a superficial nerve may elicit pain

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40
Q

what is neurotmesis?

A

axon, myelin sheath, and CT damaged

wallerian degeneration

incomplete recovery

no nerve conduction

neuroma-hypersensitivity

from severe trauma (gunshot, stabbing)

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41
Q

why is there incomplete recovery in neurotmesis?

A

no covering is guiding the axon growth

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42
Q

what are common UE mononeuropathies?

A

axillary neuropathy

“saturday night” or “honeymooner’s” palsy (radial nerve)

crutch palsy (radial nerve or brachial plexus)

carpal tunnel syndrome (median nerve)

cubital tunnel syndrome (ulnar nerve)

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43
Q

what are common LE mononeuropathies?

A

femoral neuropathy

sciatic neuropathy

peroneal nerve palsy

obturator nerve palsy

morton’s neuroma-wrist drop from radial nerve palsy, atrophy of instrinsic muscles of the hand

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44
Q

what does peroneal nerve palsy cause?

A

foot drop

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45
Q

what does Morton’s neuroma cause?

A

wrist drop and atrophy of intrinsics

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46
Q

what nerve is affected in Morton’s neuroma?

A

radial nerve

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47
Q

what is sciatic neuropathy?

A

compression/irritation of the sciatic nerve causing motor and sensory symptoms

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48
Q

what are some causes of sciatic neuropathy?

A

herniated disc

spinal stenosis/spondylosis

piriformis syndrome

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49
Q

what are the motor symptoms associated with sciatic neuropathy?

A

weakness (specific to the supplied muscles)

severe cramping

reduced DTRs in L4-S1

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50
Q

what are the sensory symptoms associated with sciatic neuropathy?

A

numbness, burning, tingling (specific to the involved dermatome)

sharp shooting pain

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51
Q

what makes sciatic neuropathy worse?

A

prolonged sitting, standing, sneezing, coughing

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52
Q

what are multiple mononeuropathies?

A

involvement of 2/more nerves in dif parts of the body

asymmetric, random presentation of symptoms

occurs with ischemic nerve damages caused by DM or vasculitis (can occur with RA, lupus, and HIV as well)

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53
Q

are multiple mononeuropathies symmetrical or asymmetrical?

A

asymmetrical

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54
Q

what are polyneuropathies?

A

symmetric involvement of sensory, motor, and autonomic fibers that progresses distal to proximal in glove and stocking pattern

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55
Q

what axons are affected first in polyneuropathy?

A

large myelinated

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56
Q

what neuropathy can be metabolic, hereditary, inflammatory, idiopathic, or toxic (alcoholism)?

A

polyneuropathy

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57
Q

what is the most common polyneuropathy?

A

diabetic polyneuropathy

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58
Q

what are some polyneuropathies?

A

diabetic polyneuropathy

GBS

hereditary motor and sensory polyneuropathy (HMSN)-Charcot Marie Tooth disease

chronic inflammatory demyelinating polyneuropathy (CIDP)

idiopathic polyneuropathy

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59
Q

what is the difference b/w GBS and CIDP?

A

s/s are very similar but CIDP is more chronic than GBS and can take years to progress and recover

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60
Q

what is diabetic polyneuropathy?

A

a metabolic disorder compromises microvascular blood supply causing oxidative stress, autoimmunity, and chemical disturbances

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61
Q

what is the damage to structures in diabetic polyneuropathy?

A

demyelination and axonal damage=orthostatic hypotension symptoms

greater sensory involvement than motor

glove and stocking pattern of loss

hyporeflexia

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62
Q

why can there be orthostatic hypotension in diabetic polyneuropathy?

A

bc there is a loss of autonomic regulation of blood flow with the demyelination and axon damage

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63
Q

is there a greater motor or sensory involvement in diabetic polyneuropathy?

A

sensory

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64
Q

what is the pattern of loss in diabetic polyneuropathy?

A

glove and stocking

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65
Q

what is Charcot Marie Tooth disease?

A

hereditary motor and sensory neuropathy (HMSN) causing muscle atrophy and paresis distal to the knee and progressing to hands

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66
Q

what is the sensory involvement associated with Charcot Marie Tooth disease?

A

↓ thermal and pain sensation

neuropathic pain

numbness, tingling, burning-not severe

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67
Q

t/f: with charcot marie tooth disease, there is early inflammation, joint dislocation/subluxation, pathological fractures of the foot

A

true

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68
Q

what are the symptoms of Charcot Marie Tooth disease?

A

midfoot swelling (one of the most prominent signs)

shorter 1st metatarsal bone

laterally curved foot

uni or bilateral

hammer toe

high arch/flat foot

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69
Q

what are the neuromuscular junction disorders?

A

myasthenia gravis and botulism

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70
Q

what is myasthenia gravis?

A

decreased amplitude of AP on EMG

repetative use-weaker muscles

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71
Q

what is botulism?

A

acute, progressive weakness

loss of stretch reflexes

usually therapeutically used to decrease spasticity

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72
Q

what are myopathies?

A

degeneration of muscle fibers leading to muscle atrophy and weakness

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73
Q

is there greater weakness proximally or distally with myopathies?

A

proximally

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74
Q

is there sensory or autonomic involvement in myopathies?

A

nope!

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75
Q

what are the 3 myopathies?

A

1) Duchenne’s muscular dystrophy

2) dermatomyositis

3) polymyositis

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76
Q

what are the immune related myopathies?

A

dermatomyosititis and polymyositis

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77
Q

what are the 2 pediatric plexus disorders?

A

Erb’s palsy and Klumpke’s palsy

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78
Q

what roots are involved in Erb’s palsy?

A

C5-6

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79
Q

what is the pathophysiology of Erb’s palsy?

A

fall or traumatic birth

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80
Q

what roots are involved in Klumpke’s palsy?

A

C8-T1

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81
Q

what is the pathophysiology of Klumpke’s palsy?

A

traction of abducted arm

may present with Horner’s disease is severe

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82
Q

is the neurologic level above or below the vertebral level?

A

below

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83
Q

what vertebral bodies are associated with C8 SC segment?

A

C6-7

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84
Q

what vertebral bodies are associated with T1 SC segment?

A

C7-T1

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85
Q

what vertebral bodies are associated with T10-11 SC segment?

A

T9

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86
Q

what vertebral bodies are associated with L2-5 SC segment?

A

T12

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87
Q

what vertebral bodies are associated with S1-5 SC segment?

A

L1

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88
Q

what are the nerve roots of the diaphragm?

A

C3-5

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89
Q

if there is a lesion above C4, is there independent breathing?

A

no

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90
Q

if there is a lesion b/w C4 and C5, is there independent breathing?

A

yes, but heavily rely on accessory muscles

91
Q

what does the pudendal nerve control?

A

b/b sphincters

92
Q

does the pudendal nerve excite or inhibit the sphincters?

A

excites them to hold in pee

93
Q

what are the 2 fxns of the SC?

A

1) motor coordination
2) pelvic organ fxn

94
Q

how does the SC control motor coordination?

A

reflexes are integrated into normal functioning

locomotor CPGs

reciprocal inhibition

recurrent (autogenic) inhibition

95
Q

how does recurrent (autogenic) inhibition work?

A

collateral branch of the alpha motor neuron innervates the Renshaw cells

96
Q

are Renshaw cells excitatory or inhibitory?

A

inhibitory

97
Q

what are Renshaw cells innervated by?

A

descending inputs

98
Q

what is the purpose of Renshaw cells?

A

regualte the firing of motor neurons by keeping in check how fast the motor neuron is going

contributes to fine motor fxn

dampens the effects of it own motor neuron, its synergists, and motor neurons to slow them down

99
Q

if there is damage to the descending system what is the effect on Renshaw cells?

A

they are no longer regulated to slow down motor neurons

100
Q

how many anterior arteries supply the SC?

A

just 1

101
Q

how many posterior arteries supply the SC?

A

2

102
Q

how much of the SC is supplied by the anterior artery?

A

2/3 of the SC

103
Q

how much of the SC is supplied by the posterior arteries?

A

1/3 of the SC

104
Q

what is a segmental lesion?

A

a lesion affecting a single level of the SC

focal lesion of the dorsal/ventral root (radiculopathy) or spinal nerve (peripheral neuropathy)

105
Q

are there UMN or LMN signs with a segmental lesion?

A

LMN signs

106
Q

what are the LMN signs associated with a segmental lesion?

A

hypotonia, hyporeflexia, flacidity, fasciculation/fibrillation, paralysis

107
Q

does a segmental lesion affect the levels above and below it?

A

nope!

108
Q

what is a vertical tract lesion?

A

interruption of ascending and descending tracts below the lesion

109
Q

are there UMN or LMN signs with vertical tract lesions?

A

UMN signs

110
Q

what are the UMN signs associated with vertical tract lesions?

A

hypertonicity, spaticity/rigidity, hyperreflexia, Babinski, clasp-knife, CLONUS

111
Q

does a vertical tract lesion affect that segments above/below it?

A

yes, it affects below the lesion

112
Q

if there is both a segmental and vertical tract lesion, are there UMN signs of LMN signs?

A

both

UMN signs below the lesion

LMN signs at the lesion

113
Q

are there significant autonomic s/s with a segmental lesion?

A

no bc there is redundancy in autonomic efferents

114
Q

what is anterior cord syndrome?

A

a lesion of the anterior 2/3 of the SC causing a loss of pain, temp, motor fxn due to disruption in the anterior spinal artery

spinothalamic (sensory) and lateral corticospinal (motor) damage

fxn lost bilaterally

115
Q

is there damage to the DCML or dorsal horn in anterior cord syndrome?

A

no

116
Q

why is proprioception, light touch, and vibration intact in anterior cord syndrome?

A

bc the DCML is not damaged

117
Q

is the ventral horn motor, sensory, or autonomic?

A

motor

118
Q

is the dorsal horn motor, sensory, or autonomic?

A

sensory

119
Q

is the lateral horn motor, sensory, or autonomic?

A

autonomic

120
Q

is anterior cord syndrome bilateral?

A

yes

121
Q

what is central cord syndrome?

A

a centrally located, smaller lesion causes cape-like distribution of loss of pain and temp at the level of the lesion

122
Q

what usually causes central cord syndrome?

A

cervical trauma (hyperextension)

usually upper cervical

123
Q

why is there a loss of pain and temp in central cord syndrome?

A

bc the spinothalamic tract is damaged by of its proximity to the anterior commissure

124
Q

if the lesion in central cord syndrome is larger, what is the order in which lateral corticospinal damage will occur?

A

cervical–>thoracic–>lumbar–>sacrum

125
Q

if the lesion is larger in central cord syndrome, what other tract will be affected?

A

lateral corticospinal

126
Q

what is Brown-Sequard syndrome?

A

hemisection of the SC causing ipsilateral loss of motor fxn, proprioceptionm and discriminitive touch, and contralateral loss of pain and temp

127
Q

is anterior cord syndrome segmental or vertical?

A

vertical

128
Q

is central cord syndrome segmental or vertical?

A

segmental

129
Q

is Brown-Sequad syndrome segmental or vertical?

A

both

130
Q

what is cauda equina syndrome?

A

damage to the lumbar and/or sacral spinal roots causing sensory impairments

131
Q

does cauda equina syndrome cause UMN or LMN signs?

A

LMN signs

132
Q

t/f: cauda equine syndrome causes flaccid paresis

A

true

133
Q

what are the MOIs for traumatic SCI?

A

MVAs, falls, and sports injuries

penetrating wounds

134
Q

with MVAs, falls, and sports injuries, what is the damage due to?

A

crush, hemorrhage, edema, or infarction

135
Q

is there typically a cord severance with MVAs, falls, adn sports injuries?

A

no, so there is some remaining fxn below the lesion

136
Q

is there typically cord severance with penetrating wounds?

A

yes, so there is a complete disconnect b/w above and below the lesion

137
Q

which has more severe presentation of sensory/motor/autonomic symptoms: MVAs, fall and sports injuries; or penetrating wounds?

A

penetrating wounds

138
Q

what is spinal (cerebral) shock?

A

acute UMN lesion interrupts descending motor commands, affecting LMNs to become temporarily inactive

early=LMN
later=UMN

139
Q

how long does it take for LMN signs to leave with spinal (cerebral) shock?

A

days or weeks

140
Q

what are the temporary LMN of spinal (cerebral shock)?

A

paralysis

loss of sensation

somatic reflexes lost

autonomic reflexes lost or impaired

autonomic regulation of blood pressure impaired

control of sweating and piloerection lost

141
Q

what % of pts develop spasticity following spinal shock?

A

80%

142
Q

what is the difference b/w spinal and cerebral shock?

A

spinal chock=SCI

cerebral shock=stroke

143
Q

where is a lesion with presentation of tetraplegia?

A

upper or lower cervical lesion

144
Q

what is the presentation of tetraplegia?

A

loss below head or shoulders depending on lesion location

145
Q

where is the lesion with presentation of paraplegia?

A

thoracic or lumbar lesion

146
Q

does paraplegia have to include the trunk?

A

no, it may just be LEs

147
Q

do higher or lower lesions have greater autonomic impairments?

A

higher

148
Q

what are autonomic dysfunctions associated with SCIs?

A

b/b and sexual dysfxn

paralysis of diaphragm/trunk/abdominals/ intercostals

pressure ulcers

autonomic dysreflexia

VERY frequent UTIs

149
Q

if the lesion is above T6, what is a pt at risk for?

A

autonomic dysreflexia

150
Q

what is autonomic dysreflexia?

A

lesions at or above T6 causing serious abnormalities in autonomic regulation due to loss of descending sympathetic control

151
Q

if the lesion is above C4, is a ventilator required?

A

yes

152
Q

is the lesion is b/w C4-6, is there a need for a ventilator?

A

no

153
Q

if the lesion is b/w T6-S2, is there b/b control?

A

no

154
Q

why may orthostatic hypotension be present in lesions between C4-T6?

A

bc there is inadequate vasoconstriction in the LEs

155
Q

t/f: a pt with a lesion b/w C4-6 is prone to heart stroke bc they can’t sweat below the lesion

A

true

156
Q

t/f: with a lesion b/w C4-5 a pt can pass out just sitting bc of poor BP control

A

true

157
Q

what is autonomic dysreflexia?

A

SCI at or above T6

vasomotor response to noxious stimuli below the level of injury

HTN with bradycardia, excessive sweating above the lesion, flushed face, pounding headache

158
Q

how is autonomic dysreflexia treated?

A

remove the noxious stimulus if possible and get pt into sitting (DO NOT LAY THEM DOWN)

159
Q

how is the bladder voluntarily controlled?

A

the frontal cortex disinhibits the pontine micturation center which facilitates the sacral micturation center and causes contraction of the bladder wall and relaxation of the sphincters and pelvic floor muscles for voiding

160
Q

where is the sacral micturation center?

A

b/w S2-4

161
Q

if the lesion is above S2, is the bladder UMN type or LMN type?

A

UMN type bladder

162
Q

what is an UMN type bladder?

A

hyperreflexive bladder

reflexive voiding with little urine in the bladder

causes bladder to shrink

163
Q

if the lesion is at/below S2-4, is the bladder UMN type or LMN type?

A

LMN type bladder

164
Q

what is a LMN type bladder?

A

areflexive bladder

the bladder won’t void even when full, so voiding schedule is important

165
Q

what is the purpose of the NS?

A

speed of communication b/w the body and brain

166
Q

what are 3 causes of nerve impairments?

A

1) trauma
2) autoimmune disease
3) compression

167
Q

what are pt symptoms of nerve impairment and how do we differentiate them b/w other conditions with similar s/s?

A

pain, weakness, paresthesias

differentiate by using diagnositic medical tests

168
Q

what are the ancillary lab tests?

A

EMG/NCS

MRI

x-ray

bone scan

CAT scan

169
Q

why are the EMG/NCS combined?

A

bc they have weaknesses on their own

170
Q

t/f: EMG and NCS study must be completed sequentially or on the same day for Medicare coverage

A

true

171
Q

what does NCS test?

A

sensory and motor neurons

how long and how strong they conduct

172
Q

is there wallerian degneration with axon damage or myelin damage?

A

axon damage

173
Q

site of lesion with axon damage

A

distal

174
Q

is nerve damage usually a slowing or loss of AP

A

both

175
Q

what is the goal of EMG testing?

A

read electricity inside muscle tissue that may suggest nerve damage

176
Q

are abnormalities above or below the lesion in EMG testing?

A

below

177
Q

t/f: you can evaluate the age of a nerve injury with EMG testing

A

true (but after 2 years, there are limited findings)

178
Q

what does a snap sound and/or positive sharp wave on an EMG indicate?

A

acute motor axon nerve damage

179
Q

t/f: grading EMGs is objective

A

false, it can be subjective

180
Q

how are EMGs graded?

A

+1–>+4; large/small; inc/dec; long/short

181
Q

does NCS or EMG measure sensory and motor nerves?

A

NCS

182
Q

does NCS or EMG measure motor axons?

A

EMG

183
Q

what are common UE peripheral entrapment neuropathies (in order)

A

carpal tunnel
cubital tunnel
radial tunnel
axillary nerve
suprascapular nerve

184
Q

t/f: the PT is free to choose the test based on clinical suspicion, pt age, sex, and comorbidities

A

true

185
Q

when myelin is impaired, the AP is slowed or gone?

A

slowed

186
Q

when the axon is damaged, the AP is slowed or gone?

A

gone

187
Q

what does a slowed/prolonged segment on an EMG indidcate?

A

that is the problem area

188
Q

what are the hyperkinetic disorders?

A

dystonia, Tourette’s, and dyskinesia

189
Q

what is dystonia?

A

abnormal postures or twisting caused by involuntary, sustained muscle contractions

genetic, non-progressive

increases w/stress, decreases w/sleep

190
Q

what is focal dystonia?

A

dystonia affecting just one area

191
Q

what is the most common dystonia?

A

focal dystonia

192
Q

what is cervical dystonia?

A

spasmotic torticollis

tight neck muscles like the SCM

head off midline

193
Q

who is focal hand dystonia most common in?

A

ppl who play an instrument

194
Q

what is Tourrette’s disorder?

A

hyperkinetic disorder causing vocal and motor tics that increase with stress, and decrease with sleep

abrupt involuntary and repetitive

tics last longer than a year

195
Q

what is dyskinesia?

A

abnormal involuntary movement

can be medication induced

196
Q

what is a basal ganglia stroke?

A

supplied by deep branch of the middle cerebral artery (MCA)

contralateral s/s (mostly affecting lateral corticospinal)

197
Q

what is post-hemiplegic athetosis?

A

lesions in the internal capsule and GP

198
Q

what is post-hemiplegic hemiballismus?

A

lesions in the STN (rare)

involuntary, jerky movements, not rhythmic

severe form of chorea

199
Q

what is flaccid paralysis?

A

extensive lesions in the lenticular nucleus (not what we would normally expect in the basal ganglia which is usually rigidity)

200
Q

what is the msot common pediatric condition seen by PTs?

A

cerebral palsy

201
Q

can all people with CP walk?

A

some can, some can’t

202
Q

what is CP?

A

permanent, non-progressive brain damage perinatally (80% of cases b4 labor)

movement and postural disorder

especially traumatic to white matter

cognitive, somatosensory, visual, auditory, and/or speech deficits

203
Q

is growing into the deficit common in CP?

A

yes, very common

204
Q

is CP progressive?

A

only if seizures are involved

205
Q

when are fetuses most susecptible to CP?

A

in the 3rd trimester when a lot of sulci and gyri are being made

206
Q

what are the 5 types of CP?

A

1) spastic
2) dyskinetic
3) ataxic
4) hypotonic
5) mixed

207
Q

what is spastic CP?

A

mainly shows increased muscle tone

motor cortex lesion

208
Q

what is dyskinetic CP?

A

basal ganglia lesion

when trying to do one motion, there’s a lot of involuntary accessory motions

non-rhythmic, abrupt, involuntary movement

atypical, abnormal muscle tone

choreoathetoid - fluctuating muscle tone

209
Q

what is choreatic movement?

A

jerky, non-rhythmic movement, lot of twisting

210
Q

what is athetotic movement?

A

slow and complex movements with twisting

211
Q

what is ataxic CP?

A

cerebellar lesion

uncoordinated movement

dysmetria

212
Q

what is hypotonic CP?

A

no specific lesion location, more extensive lesion

more extensive cognitive dysfunction

more difficult to treat

213
Q

what is mixed CP?

A

dyskinetic and ataxic, hypotnoic and ataxic

214
Q

what are the types of CP reflecting the body parts invovled?

A

quadriplegic, diplegic, hemiplegic

215
Q

what is quadriplegic CP?

A

includes lack of control of head, arms, legs, and trunk

no walking

216
Q

what is diplegic CP?

A

leg motor control is more severly affected than UE control

may walk

217
Q

what is hemiplegic CP?

A

half the body (L/R) involved

can walk most times

218
Q

what type of CP is being described?: spasticity of UE and LE, worse in the LE

A

spastic diplegic

219
Q

what is spastic diplegic gait?

A

toe walking, flexed knees, speed up scissoring gait, shortening adductors

if no Botox or release=don’t walk very long due to energy use

220
Q

is spastic hemiplegic or spastic diplegic gait smoother?

A

spastic hemiplegic

221
Q

what is the most common visual problem in CP?

A

strabismus (asymmetric crossed eyes/lazy eye)

222
Q

what does uncorrected strabismus result in?

A

the brain learns to block input from the one eye -no depth perception if young

223
Q

is CP frequently associated with intellectual disability and language deficits?

A

yes

224
Q

what is the result of synaptic pruning not happening correctly in CP?

A

greater motor dysfunction

DPT 520 (13 decks)

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