Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

DPT 520 > Quiz 1 > Flashcards

Quiz 1 Flashcards

1
Q

how does loss of myelination affect the propagation of action potentials in axons?

A

it slows down propagation of action potentials

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the 2 disorders of CNS demylenation?

A

MS and neuromyelitis optica

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what 2 things can happen to axons that lead to pain?

A

ectopic foci or ephaptic transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is ectopic foci?

A

a demyelinated axon region generates an AP in an abnormal place

increase in ion channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is ephaptic transmission?

A

crosstalk b/w areas of demyelination on adjacent axons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

in ephaptic transmission, instead of transmitted APs through synapses, they …

A

jump from one neuron to another through cross talk in areas of demylenation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is multiple sclerosis (MS)?

A

an autoimmune neurodegenerative disease of the CNS that destroys the myelin sheath and attacks oligodendrocytes causing plaques to form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

is MS an CNS or PNS disease?

A

CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what glial cells are attacked in MS?

A

oligodendrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is reactive gliosis?

A

proliferation of glial cells in injured area of CNS leading to scar formation (plaques) in MS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the most common chronic inflammatory condition of the CNS?

A

MS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

who is more likely to be affected by MS, males or females?

A

females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

when is MS usually diagnosed?

A

between the ages of 20-40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what environmental factors may increase risk for MS?

A

inadequate sunlight exposure and low vit D levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are common s/s in MS?

A

visual disturbances (hallmark sign and often the first sign)

positive Lhermitte’s sign (electric shock-like sensation when flexing the neck forward)

sensory disturbance (numbness, tingling, pain)

motor dysfunction (weakness, imbalance, incoordination, reflex changes)

cognitive and memory deficits

heat sensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

why should a PT be cautious of overexertion with a patient who has MS?

A

heat often worsens symptoms or make new ones appear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the 4 types of MS?

A

relapsing-remitting MS

primary progressive MS

secondary progressive MS

progressive relapsing MS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is relapsing-remitting MS?

A

alternating pattern of relapsing and remitting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how long does an MS relapse generally occur?

A

varying b/w 24 hours to months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

how long does an MS remission generally occur?

A

a month or longer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the most common initial course of MS?

A

relapsing-remitting MS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what does relapsing-remitting MS usually progress to?

A

secondary progressive MS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is primary progressive MS?

A

a steady decline in function with no clearly defined relapse periods but rather day-to-day fluctuations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

about what % of MS cases are primary progressive MS?

A

10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is secondary progressive MS?

A

a combination of relaping-remitting and primary progressive MS that starts as relapsing-remitting and turns into primary progressive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is progressive relapsing MS?

A

similar to primary progressive MS where the is a steady decline but this type has relapses of exacerbated symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

about what % of MS cases are progressive relapsing?

A

5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

how is MS diagnosed?

A

with an MRI that shows the plaques in the SC and brain

with a cerebrospinal fluid (CSF) analysis (spinal tap) to detect antibodies associated with MS

neurological exam (PT’s role!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is clinically isolated syndrome (CIS)?

A

a 1st episode of neurologic symptoms that last more than 24 hours and resolve completely with no apparent cause that may be a 1st sign of MS

can be monofocal (a single s/s) or multifocal (many s/s)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what syndrome may be the 1st sign of MS?

A

clinically isolated syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is neuromyelitis optica?

A

a very rare, severe autoimmune disorder where immune cells primarily attack the optic nerve and SC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are the s/s of neuromyelitis optica?

A

optic nerve damage (swelling, inflammation, leading to pain and loss of vision)

motor and sensory disturbances in the arms/ legs

bowel and bladder dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what disease is often misdiagnosed as MS but is much more severe?

A

neuromyelitis optica

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what 2 diseases involve demyelination in the PNS?

A

peripheral neuropathy and Guillain-Barre syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what is peripheral neuropathy?

A

disease that affects large diameter axons 1st (light touch, conscious proprioception)

an umbrella term for any pathological changes involving peripheral nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what are some common causes of peripheral neuropathy?

A

metabolic abnormalities like diabetes

autoimmune disorders

viruses

trauma

toxic chemicals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is Guillain-Barre syndrome (GBS)

A

an autoimmune disease triggered by bacterial/viral infection in most cases causing acute PNS inflammation and demyelination attacking the Scwann cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is the most common GBS in North America and Europe?

A

acute inflammatory demyelinating polyneurpathy (AIDP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what glial cells are attacked in GBS?

A

Schwann cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

can there be regrowth of axons in GBS?

A

yes, bc it occurs in the PNS!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

does GBS occur more in males or females?

A

males

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what are the s/s of GBS?

A

decreased sensation

limb weakness/skeletal muscle paralysis

pain

respiratory muscles weakness

symptoms are bilateral and move from distal to proximal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what CN involvement is there in GBS?

A

facial palsy and CN 7 and 5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is the disease progression of GBS?

A

rapid onset with the worst s/s w/in the 2-4 weeks followed by recovery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

how is GBS diagnosed?

A

CSF analysis looking for elevated protein w/very few immune cells (WBCs)

electromyography and/or nerve conduction study

neurological exams

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what are the 2 synaptic dysfunction diseases?

A

myasthenia gravis and channelopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is myasthenia gravis?

A

an autoimmune disease causing severe muscles weakness (motor symptoms) from antibodies against ACh receptors so ACh can’t bind causing weak/no muscles contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what receptors are affected in myasthenia gravis?

A

ACh receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

t/f: there is thymus gland involvement in myasthenia gravis

A

true bc the thymus makes WBC and T-cells and may contribute to antibody production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

are males of females usually diagnosed with myasthenia gravis earlier?

A

females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

t/f: there is a genetic predisposition to myasthenia gravis

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what are the s/s of myasthenia gravis?

A

increased weakness and fatigue w/repetative use for skeletal muscles

fluctuating weakness that improves after a period of rest

progressive symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what muscles are commonly affected 1st in myasthenia gravis?

A

extraocular muscles, causing ptosis (droppy upper eyelid) and diplopia (double vision)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

how is myasthenia gravis diagnosed?

A

tensilon test (administration of a drug (tensilon) that blocks the AChE to activate the muscles) which does nothing for ptosis is not myasthenia gravis

electromyography

blood test for the presence of AChR antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what is channelopathy?

A

an genetic or acquired autoimmune disease causing dysfunction of ion channels that leads to disease in the nervous, cardiovascular, respiratory, endocrine, urinary, and/or immune systems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what are 2 examples of a channelopathy?

A

Lambert-Eaton syndrome and Brugada syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what is Lambert-Eaton syndrome?

A

channelopathy that disrupts voltage gated calcium channels in the axon terminal of the motor neurons causing generalized progressive muscle weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what is Brugada syndrome?

A

an inherited channelopathy that affects voltage-gated sodium channels in cardiac muscle causing abnormalities of cardiac rhythm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

how does spina bifida occur?

A

the inferior neuropore doesn’t close

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what is the least severe form of spina bifida?

A

spina bifida oculata

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what may be the only s/s of spina bifida oculata?

A

hair at the end of the back

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what is spina bifida aperta/cystica?

A

spinal defect clearly visible from the outside

3 forms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what are the 3 forms of spina bifida aperta/cystica?

A

meningocele, myelomeningocele, and myeloschisis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what is meningocele spina bifida?

A

the least severe spina bifida aperta/cystica where the meninges stick out in a balloon shape in the back with the SC enclosed where it should be

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what is myelomeningocele spina bifida?

A

a cyst contains the SC and spinal root with the Sc not where it is should be

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what is myeloschisis spina bifida?

A

the most severe form of spina bifida aperta/cystica where the SC isn’t formed properly and is exposed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what are the s/s of spina bifida?

A

motor symptoms in the myotomal pattern

somatosensory symptoms in the dermatomal pattern

autonomic symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

what is paresis?

A

partial loss of voluntary motor contraction, weakness, reduced ability to activate any muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

what is paralysis?

A

complete loss of voluntary motor contraction, complete inability to activate muscles

more severe than paresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

is meningocele spina bifida more likely to have LE paresis or paralysis?

A

paresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

is myelomeningocele spina bifida more likely to have LE paresis or paralysis?

A

paresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

is myeloschisis spina bifida more likely to have LE paresis or paralysis?

A

paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

what are the somatosensory impairments in meningocele spina bifida?

A

impaired or absent somatosensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

what are the somatosensory impairments in myelomeningocele spina bifida?

A

impaired/absent somatosensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

what are the somatosensory impairments in myeloschisis spina bifida?

A

absent somatosensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

what autonomic s/s may occur in spina bifida?

A

lack of bowel and bladder control in myelomeningocele or myeloschisis

(sphincter paralysis is what commonly leads to the lack of b/b control)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

what may cause spina bifida?

A

maternal folate deficiency, obesity, diabetes, teratogens, or genetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

what is the biggest risk periods for spina bifida

A

during week 6 of pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what are some clinical characteristics of spina bifida?

A

surgical treatment b4 birth or shortly after birth

may have associations with Arnold-Chiari type 2 and hydrocephalus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

what is Arnold-Chiari malformation?

A

a developmental deformity of the hindbrain where the brain tissue extends into the spinal canal

81
Q

what brain structures does Arnold-Chiari malformation affect?

A

cerebellum, brain stem, and upper SC

82
Q

what is the most sever form of Arnold-Chiari malformation?

A

type 3

83
Q

what is type 3 Arnold-Chiari malformation?

A

the most severe form of Arnold-Chiari malformation where there is an abnormal opening in the back of the skull and the cerebellum and BS structures leak into the opening

higher mortality rate due to severe neurological problems

84
Q

what is type 1 Arnold-Chiari malformation?

A

reduced volume of the posterior fossa with cerebellar tonsil herniation

least severe type with mild symptoms exacerbated by coughing/sneezing

85
Q

what is type 2 Arnold-Chiari malformation?

A

malformation of the BS and cerebellum that is nearly always associated with spina bifida myelomeningocele or myeloschisis

even smaller posterior fossa with an enlarged pons pushing the medulla and 4th ventricle down

enlarged ventricles causing hydrocephalus

86
Q

additional s/s of Arnold-Chiari malformation develop due to…

A

direct compression of neurological structures against the foramen magnum and SC

syringomyelia development

sensory and motor impairments

blocked CSF flow from a blocked foramen magnum

87
Q

what is a syringomyelia?

A

fluid filled cavity in the SC that can produce pain, weakness, stiffness and may expand causing SC damage

88
Q

what is the most common type of Arnold-Chiari malformation?

A

type 1

89
Q

which type of Arnold-Chiari malformation is usually found out by accident?

A

type 1

90
Q

what are common s/s of Arnold-Chiari malformation?

A

occipital headache exacerbated by coughing, sneezing, or straining

neck pain

uncoordinated movement

paresis

impaired fine motor in hands

loss of pain and temp sensation on shoulders and lateral upper limbs

restriction of CSF flow leading to visual disturbances and hydrocephalus

CN involvement

91
Q

what type of Arnold-Chiari malformation is usually asymptomatic?

A

type 1

92
Q

what is the classic presentation of a syringomyelia?

A

a cape like distribution of lost pain and temp sensation over the shoulders and lateral upper limbs

93
Q

why would restriction of CSF flow cause visual disturbances?

A

pressure on the optic chiasm

94
Q

what causes hydrocephalus?

A

restriction of CSF flow

95
Q

what s/s can hydrocephalus cause?

A

vomiting and epilepsy

96
Q

what CN involvement may present in Arnold-Chiari malformation?

A

vertigo and facial and eye muscle weakness (CN 7)

97
Q

how is Arnold-Chiari malformation managed?

A

muscles relaxants, NSAIDs, and use of a cervical collar may be used for pain

re-establishing CSF flow with a VP or VA shunt

98
Q

t/f: there is no gait improvement w/medical management of Arnold-Chiari malformation

A

true

99
Q

what is a ventriculoperitoneal (VP) shunt?

A

a catheter is placed in the brain and drains fluid to the lining of the abdomen

100
Q

what is a ventriculoaterial shunt?

A

a catheter is placed in the ventricle and drains into the atrium

101
Q

what is tethered SC?

A

the end of the SC (fylum of the conus medullaris) adheres to a lower vertebra causing progressive deficits in the LE

102
Q

why is tethered SC progressive?

A

as one grows, there will be abnormal stretching of the SC

103
Q

what are the s/s of tethered SC?

A

sensory deficit/pain in the saddle region and LE

b/b dysfunction

progressive weakness that can lead to paresis and deterioration of walking

104
Q

what is spinal muscular atrophy?

A

an autosomal recessive disorder that causes motor neuron degeneration

105
Q

what causes spinal muscular atrophy?

A

deletion of the survival motor neuron (SMN) 1 gene that makes SMN protein to support survival and maintanance of neurons

106
Q

what happens in spinal muscular atrophy?

A

progressive weakness and wasting of skeletal muscles

107
Q

what is type 1 spinal muscular atrophy?

A

the most severe form

symptoms present at birth or within the 1st 6 months of life

most die b4 their 2nd birthday

108
Q

what type of SMA makes up 60% of cases?

A

type 1

109
Q

what type of SMA are “non-sitters”?

A

type 1

110
Q

what is type 2 SMA?

A

symptoms develop b/w 6-18 months and tends to affect the LE

often live into adulthood

111
Q

what type of SMA are “sitters”?

A

type 2

112
Q

what is type 3 SMA?

A

symptoms occur after 18 months or some show no signs until early adulthood

mild proximal muscles weakness, frequent, respiratory infections

doesn’t really affect life expectancy

113
Q

what is type 4 SMA?

A

rare SMA w/symptoms in late 30s

slow progression

remain mobile well into adulthood

114
Q

what type of SMA are “walkers”

A

type 3

115
Q

what is developmental coordination disorder?

A

dyspraxia

lack of motor coordination to perform age-appropriate tasks

normal intelligence and no known neuro lesions

116
Q

what are some s/s of developmental coordination disorder?

A

clumsiness

lack of balance

frequent falls

difficulty planning and executing movement

slow and inaccurate movement

longer movement planning time

117
Q

are males of females more frequently diagnosed with developmental coordination disorder?

A

males

118
Q

what are the primitive reflexes?

A

assymetric tonic neck reflex (ATNR)

symmetric tonic neck reflex (STNR)

tonic labyrinth reflex

119
Q

what are primitive reflexes?

A

involuntary motor responses originating in the BS to facilitate survival and gradually disappear as the CNS matures

120
Q

what is the assymetric tonic neck reflex (ATNR)?

A

elicited by turning the head to one side

the arm and leg on the side that the head is turned toward extend and the limbs on the other side flex

121
Q

when does the ATNR reflex last until?

A

4 months postnatally

122
Q

what is the symmetric tonic neck reflex?

A

elicited when the neck flexes/extends in sitting or quadruped

neck flexion causes arm flexion and leg extension

123
Q

how long does the STNR reflex last?

A

5-6 months to 8-11 months

124
Q

what is the tonic labyrinth reflex?

A

elicited when the neck flexes/extends in supine

forward tilting of the head causes shoulder protraction and hip-knee flexion

backward tilting of the head causes shoulder retraction and leg extension and adduction

125
Q

how long does the tonic labyrinth reflex last?

A

birth to 4-6 months postnatally

126
Q

what is the Babinski reflex?

A

scrape the bottom of a baby’s foot and the toes fan out

127
Q

how long does the Babinski sign last?

A

shouldn’t persist longer than 24 months

128
Q

what is the palmar grasp reflex?

A

place a finger in a baby’s palm and they squeeze it

pyramidal tract integrity test

129
Q

how long should the palmar grasp reflex last?

A

no more than 6 months

130
Q

what is ataxia?

A

motor impairment/incoordination not due to muscle weakness

131
Q

what is the dermatome?

A

areas of skin innervated by a single nerve root or a part of the somite that gives rise to the skin innervated by the neurons from the neural crest

132
Q

what is the nerve root innervation of the musculocutaneous nerve?

A

C5, 6, 7

133
Q

what is the nerve root innervation of the axillary nerve?

A

C5, 6

134
Q

what is the nerve root innervation of the radial nerve?

A

C5, 6, 7, 8, T1

135
Q

what is the nerve root innervation of the median nerve?

A

C5, 6, 7, 8

136
Q

what is the nerve root innervation of the ulnar nerve?

A

C8, T1

137
Q

what is the dermatomal innervation pattern of C5?

A

the clavicular area down the inner arm to the wrist and back of the lower neck

138
Q

what is the dermatomal innervation pattern of C6?

A

top of the shoulder down the arm on the radial side and all of the thumb and back right below C5 innervation

139
Q

what is the dermatomal innervation pattern of C7?

A

back right below C6, back of shoulder down the back of the arm and index and middle finger on palmar and dorsal side of hand

140
Q

what is the dermatomal innervation pattern of C8?

A

low back of the shoulder/scap down the back of the arm on the ulnar side and the palmar and dorsal side of the ring and pinky fingers

141
Q

what is the dermatomal innervation pattern of T1?

A

below the clavicle to armpit area down the middle of the inner arm to the wrist and back of scap below C8 innervation

142
Q

median nerve peripheral innervation

A

tips of middle and index fingers and half of ring finger on dorsal side, and thumb, index, and middle fingers and half in ring finger on palmar side

143
Q

what are the 2 innervation patterns?

A
  1. dermatomal innervation
  2. peripheral innervation
144
Q

what innervation does a radiculopathy follow?

A

dermatomal innervation

145
Q

what is a radiculopathy?

A

proximal pathology of a nerve root that follows dermatomal and myotomal patterns

146
Q

what innervation pattern does a neuropathy follow?

A

peripheral innervation

147
Q

what is a neuropathy?

A

distal pathology of a nerve branch

148
Q

what is double crush phenomenon?

A

both a radiculopathy and neuropathy present that can cause a different dermatomal pattern

149
Q

t/f: the intervention is the same for a radiculopathy and a neuropathy?

A

false!

150
Q

what is peripheral neuropathy?

A

loss of sensory and/or motor function

151
Q

does sensory or motor loss happen first in peripheral neuropathy?

A

sensory loss

152
Q

what is the order of sensory loss in peripheral neuropathy?

A

heavily myelinated large diameter axon neurons damaged 1st (1a/b and A beta-proprioception and light touch)

  1. proprioception
  2. light touch
  3. cold sensation
  4. fast nociception
  5. heat
  6. slow nociception
153
Q

what is the most common cause of chronic peripheral neuropathy?

A

diabetic neuropathy

154
Q

what is carpal tunnel syndrome?

A

median nerve neuropathy

155
Q

what are the 3 types of ataxia?

A

sensory, vestibular, and cerebellar

156
Q

what is sensory ataxia?

A

a proprioceptive pathway lesion affecting the DCML

157
Q

what are the s/s of sensory ataxia?

A

wide BOS, slow gait, over/undershooting, positive Romberg test

158
Q

what is a positive Romberg test?

A

when the patient keeps the eyes open and stand with the feet together, they can balance, but with the eyes closed they cannot

159
Q

why would someone with sensory ataxia not be able to balance with their eyes closed?

A

because their is no visual compensation for lost proprioceptive information

160
Q

what time of day would sensory ataxia coordination be worse?

A

at night bc the darkness diminished the visual compensation for proprioceptive loss

161
Q

why can vision only compensate for CONSCIOUS proprioception?

A

vision is a conscious pathway and so it can only compensate for other conscious pathways, not unconscious ones

162
Q

where is the first order neuron in the DCML?

A

periphery to SC

163
Q

where is the 2nd order neuron in the DCML?

A

caudal medulla decussation to synapse in the VPL (thalamus)

164
Q

where is the 3rd order neuron in the DCML?

A

VPL to S1 (primary somatosensory cortex)

165
Q

what are the DCML somatosensory modalities?

A

conscious proprioception and light touch

166
Q

where does the DCML decussated?

A

caudal medulla

167
Q

where does the DCML terminate?

A

cerebral cortex

168
Q

where in the thalamus does the DCML go?

A

VPL

169
Q

what are the somatosensory modalities of the trigeminal pathway for light touch?

A

conscious proprioception and light touch

170
Q

where does the trigeminal pathway for light touch decussate?

A

pons

171
Q

where does the trigeminal pathway for light touch terminate?

A

cerebral cortex

172
Q

where in the thalamus does the trigeminal pathway for light touch go?

A

VPM

173
Q

what makes of the medial system?

A

DCML and trigeminal pathway for light touch

174
Q

what makes up the antero-lateral system?

A

spinothalamic pathway and trigeminal pathway for pain

175
Q

what are the somatosensory modalities for the spinothalamic pathway?

A

fast nociception
temp
crude touch

176
Q

where does the spinothalamic pathway decussate?

A

in the SC at the level of the 1st order neuron entry

177
Q

where does the spinothalamic pathway terminate?

A

cerebral cortex

178
Q

where in the thalamus does the spinothalamic pathway go?

A

VPL

179
Q

what are the somatosensory modalities for the trigeminal pathway for pain?

A

nociception
temp
crude touch

180
Q

where does the trigeminal pathway for pain decussate?

A

caudal medulla

181
Q

where does the trigeminal pathway for pain terminate?

A

cerebral cortex

182
Q

where in the thalamus does the trigeminal pathway for pain go?

A

VPM

183
Q

what are the somatosensory modalities of the nonconscious spinocerebellar pathway?

A

nonconscious proprioception

184
Q

where does the spinocerebellar pathway decussate?

A

mostly no decussation, some double decussation

185
Q

where does the spinocerebellar pathway terminate?

A

cerebellum

186
Q

what are the somatosensory modalities of the divergent pathway (medial nociceptive system w/in anterolateral system) ?

A

slow nociception

187
Q

where does the divergent pathway decussate?

A

same as spinothalamic, at the SC at the level of 1st order neuron entry

188
Q

where does the divergent pathway terminate?

A

reticular formation
periaqueductal gray
insula
amygdala
dorsolateral prefrontal cortex (DLPFC)
cerebral cortex

189
Q

with a cortical lesion, what sensory loss is there?

A

contralateral loss of all sensory modalities (proprioception, light touch, and nociception), decreased stereognosis and impaired graphesthesia

190
Q

with a thalamus lesion (VPM/VPL), what sensory loss is there?

A

contralateral sensory loss of the face and body with normal nonconscious proprioception and slow nociception bc the nonconscious and divergent pathways are not affected

191
Q

what is the most common brain stem stroke?

A

lateral medullary lesion

192
Q

what is the 2nd most common brain stem stroke?

A

lateral pontine lesion

193
Q

with a lateral pontine lesion, what is the sensory loss of the body?

A

contralateral loss of pain and temperature sensation in the body (spinothalamic tract)

194
Q

with a lateral pontine lesion, what is the sensory loss of the face?

A

ipsilateral loss of pain and temp sensation in the face and ipsilateral loss of discriminitive touch and proprioception in the face

195
Q

with a lateral medullary lesion, what is the sensory loss of the body?

A

contralateral loss of pain and temp sensation in the body

196
Q

with a lateral medullary lesion, what is the sensory loss of the face?

A

ipsilateral loss of pain and temp sensation, but unaffected touch and proprioception of the face

197
Q

what is vestibular ataxia?

A

pathology in vestibular system causing dizziness, vertigo, difficulty hearing, tinnitus, motor incoordination

feels like the world is spinning (may cause vomiting)

198
Q

what is cerebellar ataxia?

A

pathology in cerebellum

negative Romberg test (can’t do with eye opened or closed)

lateral hemispheres: finger ataxia

paravermis: limb ataxia

vermis: trunk ataxia

DPT 520 (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions