Quiz 1 Flashcards

(198 cards)

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
what is secondary progressive MS?
a combination of relaping-remitting and primary progressive MS that starts as relapsing-remitting and turns into primary progressive
26
what is progressive relapsing MS?
similar to primary progressive MS where the is a steady decline but this type has relapses of exacerbated symptoms
27
about what % of MS cases are progressive relapsing?
5%
28
how is MS diagnosed?
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!)
29
what is clinically isolated syndrome (CIS)?
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)
30
what syndrome may be the 1st sign of MS?
clinically isolated syndrome
31
what is neuromyelitis optica?
a very rare, severe autoimmune disorder where immune cells primarily attack the optic nerve and SC
32
what are the s/s of neuromyelitis optica?
optic nerve damage (swelling, inflammation, leading to pain and loss of vision) motor and sensory disturbances in the arms/ legs bowel and bladder dysfunction
33
what disease is often misdiagnosed as MS but is much more severe?
neuromyelitis optica
34
what 2 diseases involve demyelination in the PNS?
peripheral neuropathy and Guillain-Barre syndrome
35
what is peripheral neuropathy?
disease that affects large diameter axons 1st (light touch, conscious proprioception) an umbrella term for any pathological changes involving peripheral nerves
36
what are some common causes of peripheral neuropathy?
metabolic abnormalities like diabetes autoimmune disorders viruses trauma toxic chemicals
37
what is Guillain-Barre syndrome (GBS)
an autoimmune disease triggered by bacterial/viral infection in most cases causing acute PNS inflammation and demyelination attacking the Scwann cells
38
what is the most common GBS in North America and Europe?
acute inflammatory demyelinating polyneurpathy (AIDP)
39
what glial cells are attacked in GBS?
Schwann cells
40
can there be regrowth of axons in GBS?
yes, bc it occurs in the PNS!
41
does GBS occur more in males or females?
males
42
what are the s/s of GBS?
decreased sensation limb weakness/skeletal muscle paralysis pain respiratory muscles weakness symptoms are bilateral and move from distal to proximal
43
what CN involvement is there in GBS?
facial palsy and CN 7 and 5
44
what is the disease progression of GBS?
rapid onset with the worst s/s w/in the 2-4 weeks followed by recovery
45
how is GBS diagnosed?
CSF analysis looking for elevated protein w/very few immune cells (WBCs) electromyography and/or nerve conduction study neurological exams
46
what are the 2 synaptic dysfunction diseases?
myasthenia gravis and channelopathy
47
what is myasthenia gravis?
an autoimmune disease causing severe muscles weakness (motor symptoms) from antibodies against ACh receptors so ACh can't bind causing weak/no muscles contractions
48
what receptors are affected in myasthenia gravis?
ACh receptors
49
t/f: there is thymus gland involvement in myasthenia gravis
true bc the thymus makes WBC and T-cells and may contribute to antibody production
50
are males of females usually diagnosed with myasthenia gravis earlier?
females
51
t/f: there is a genetic predisposition to myasthenia gravis
true
52
what are the s/s of myasthenia gravis?
increased weakness and fatigue w/repetative use for skeletal muscles fluctuating weakness that improves after a period of rest progressive symptoms
53
what muscles are commonly affected 1st in myasthenia gravis?
extraocular muscles, causing ptosis (droppy upper eyelid) and diplopia (double vision)
54
how is myasthenia gravis diagnosed?
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
55
what is channelopathy?
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
56
what are 2 examples of a channelopathy?
Lambert-Eaton syndrome and Brugada syndrome
57
what is Lambert-Eaton syndrome?
channelopathy that disrupts voltage gated calcium channels in the axon terminal of the motor neurons causing generalized progressive muscle weakness
58
what is Brugada syndrome?
an inherited channelopathy that affects voltage-gated sodium channels in cardiac muscle causing abnormalities of cardiac rhythm
59
how does spina bifida occur?
the inferior neuropore doesn't close
60
what is the least severe form of spina bifida?
spina bifida oculata
61
what may be the only s/s of spina bifida oculata?
hair at the end of the back
62
what is spina bifida aperta/cystica?
spinal defect clearly visible from the outside 3 forms
63
what are the 3 forms of spina bifida aperta/cystica?
meningocele, myelomeningocele, and myeloschisis
64
what is meningocele spina bifida?
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
65
what is myelomeningocele spina bifida?
a cyst contains the SC and spinal root with the Sc not where it is should be
66
what is myeloschisis spina bifida?
the most severe form of spina bifida aperta/cystica where the SC isn't formed properly and is exposed
67
what are the s/s of spina bifida?
motor symptoms in the myotomal pattern somatosensory symptoms in the dermatomal pattern autonomic symptoms
68
what is paresis?
partial loss of voluntary motor contraction, weakness, reduced ability to activate any muscles
69
what is paralysis?
complete loss of voluntary motor contraction, complete inability to activate muscles more severe than paresis
70
is meningocele spina bifida more likely to have LE paresis or paralysis?
paresis
71
is myelomeningocele spina bifida more likely to have LE paresis or paralysis?
paresis
72
is myeloschisis spina bifida more likely to have LE paresis or paralysis?
paralysis
73
what are the somatosensory impairments in meningocele spina bifida?
impaired or absent somatosensation
74
what are the somatosensory impairments in myelomeningocele spina bifida?
impaired/absent somatosensation
75
what are the somatosensory impairments in myeloschisis spina bifida?
absent somatosensation
76
what autonomic s/s may occur in spina bifida?
lack of bowel and bladder control in myelomeningocele or myeloschisis (sphincter paralysis is what commonly leads to the lack of b/b control)
77
what may cause spina bifida?
maternal folate deficiency, obesity, diabetes, teratogens, or genetics
78
what is the biggest risk periods for spina bifida
during week 6 of pregnancy
79
what are some clinical characteristics of spina bifida?
surgical treatment b4 birth or shortly after birth may have associations with Arnold-Chiari type 2 and hydrocephalus
80
what is Arnold-Chiari malformation?
a developmental deformity of the hindbrain where the brain tissue extends into the spinal canal
81
what brain structures does Arnold-Chiari malformation affect?
cerebellum, brain stem, and upper SC
82
what is the most sever form of Arnold-Chiari malformation?
type 3
83
what is type 3 Arnold-Chiari malformation?
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
what is type 1 Arnold-Chiari malformation?
reduced volume of the posterior fossa with cerebellar tonsil herniation least severe type with mild symptoms exacerbated by coughing/sneezing
85
what is type 2 Arnold-Chiari malformation?
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
additional s/s of Arnold-Chiari malformation develop due to...
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
what is a syringomyelia?
fluid filled cavity in the SC that can produce pain, weakness, stiffness and may expand causing SC damage
88
what is the most common type of Arnold-Chiari malformation?
type 1
89
which type of Arnold-Chiari malformation is usually found out by accident?
type 1
90
what are common s/s of Arnold-Chiari malformation?
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
what type of Arnold-Chiari malformation is usually asymptomatic?
type 1
92
what is the classic presentation of a syringomyelia?
a cape like distribution of lost pain and temp sensation over the shoulders and lateral upper limbs
93
why would restriction of CSF flow cause visual disturbances?
pressure on the optic chiasm
94
what causes hydrocephalus?
restriction of CSF flow
95
what s/s can hydrocephalus cause?
vomiting and epilepsy
96
what CN involvement may present in Arnold-Chiari malformation?
vertigo and facial and eye muscle weakness (CN 7)
97
how is Arnold-Chiari malformation managed?
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
t/f: there is no gait improvement w/medical management of Arnold-Chiari malformation
true
99
what is a ventriculoperitoneal (VP) shunt?
a catheter is placed in the brain and drains fluid to the lining of the abdomen
100
what is a ventriculoaterial shunt?
a catheter is placed in the ventricle and drains into the atrium
101
what is tethered SC?
the end of the SC (fylum of the conus medullaris) adheres to a lower vertebra causing progressive deficits in the LE
102
why is tethered SC progressive?
as one grows, there will be abnormal stretching of the SC
103
what are the s/s of tethered SC?
sensory deficit/pain in the saddle region and LE b/b dysfunction progressive weakness that can lead to paresis and deterioration of walking
104
what is spinal muscular atrophy?
an autosomal recessive disorder that causes motor neuron degeneration
105
what causes spinal muscular atrophy?
deletion of the survival motor neuron (SMN) 1 gene that makes SMN protein to support survival and maintanance of neurons
106
what happens in spinal muscular atrophy?
progressive weakness and wasting of skeletal muscles
107
what is type 1 spinal muscular atrophy?
the most severe form symptoms present at birth or within the 1st 6 months of life most die b4 their 2nd birthday
108
what type of SMA makes up 60% of cases?
type 1
109
what type of SMA are "non-sitters"?
type 1
110
what is type 2 SMA?
symptoms develop b/w 6-18 months and tends to affect the LE often live into adulthood
111
what type of SMA are "sitters"?
type 2
112
what is type 3 SMA?
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
what is type 4 SMA?
rare SMA w/symptoms in late 30s slow progression remain mobile well into adulthood
114
what type of SMA are "walkers"
type 3
115
what is developmental coordination disorder?
dyspraxia lack of motor coordination to perform age-appropriate tasks normal intelligence and no known neuro lesions
116
what are some s/s of developmental coordination disorder?
clumsiness lack of balance frequent falls difficulty planning and executing movement slow and inaccurate movement longer movement planning time
117
are males of females more frequently diagnosed with developmental coordination disorder?
males
118
what are the primitive reflexes?
assymetric tonic neck reflex (ATNR) symmetric tonic neck reflex (STNR) tonic labyrinth reflex
119
what are primitive reflexes?
involuntary motor responses originating in the BS to facilitate survival and gradually disappear as the CNS matures
120
what is the assymetric tonic neck reflex (ATNR)?
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
when does the ATNR reflex last until?
4 months postnatally
122
what is the symmetric tonic neck reflex?
elicited when the neck flexes/extends in sitting or quadruped neck flexion causes arm flexion and leg extension
123
how long does the STNR reflex last?
5-6 months to 8-11 months
124
what is the tonic labyrinth reflex?
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
how long does the tonic labyrinth reflex last?
birth to 4-6 months postnatally
126
what is the Babinski reflex?
scrape the bottom of a baby's foot and the toes fan out
127
how long does the Babinski sign last?
shouldn't persist longer than 24 months
128
what is the palmar grasp reflex?
place a finger in a baby's palm and they squeeze it pyramidal tract integrity test
129
how long should the palmar grasp reflex last?
no more than 6 months
130
what is ataxia?
motor impairment/incoordination not due to muscle weakness
131
what is the dermatome?
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
what is the nerve root innervation of the musculocutaneous nerve?
C5, 6, 7
133
what is the nerve root innervation of the axillary nerve?
C5, 6
134
what is the nerve root innervation of the radial nerve?
C5, 6, 7, 8, T1
135
what is the nerve root innervation of the median nerve?
C5, 6, 7, 8
136
what is the nerve root innervation of the ulnar nerve?
C8, T1
137
what is the dermatomal innervation pattern of C5?
the clavicular area down the inner arm to the wrist and back of the lower neck
138
what is the dermatomal innervation pattern of C6?
top of the shoulder down the arm on the radial side and all of the thumb and back right below C5 innervation
139
what is the dermatomal innervation pattern of C7?
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
what is the dermatomal innervation pattern of C8?
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
what is the dermatomal innervation pattern of T1?
below the clavicle to armpit area down the middle of the inner arm to the wrist and back of scap below C8 innervation
142
median nerve peripheral innervation
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
what are the 2 innervation patterns?
1. dermatomal innervation 2. peripheral innervation
144
what innervation does a radiculopathy follow?
dermatomal innervation
145
what is a radiculopathy?
proximal pathology of a nerve root that follows dermatomal and myotomal patterns
146
what innervation pattern does a neuropathy follow?
peripheral innervation
147
what is a neuropathy?
distal pathology of a nerve branch
148
what is double crush phenomenon?
both a radiculopathy and neuropathy present that can cause a different dermatomal pattern
149
t/f: the intervention is the same for a radiculopathy and a neuropathy?
false!
150
what is peripheral neuropathy?
loss of sensory and/or motor function
151
does sensory or motor loss happen first in peripheral neuropathy?
sensory loss
152
what is the order of sensory loss in peripheral neuropathy?
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
what is the most common cause of chronic peripheral neuropathy?
diabetic neuropathy
154
what is carpal tunnel syndrome?
median nerve neuropathy
155
what are the 3 types of ataxia?
sensory, vestibular, and cerebellar
156
what is sensory ataxia?
a proprioceptive pathway lesion affecting the DCML
157
what are the s/s of sensory ataxia?
wide BOS, slow gait, over/undershooting, positive Romberg test
158
what is a positive Romberg test?
when the patient keeps the eyes open and stand with the feet together, they can balance, but with the eyes closed they cannot
159
why would someone with sensory ataxia not be able to balance with their eyes closed?
because their is no visual compensation for lost proprioceptive information
160
what time of day would sensory ataxia coordination be worse?
at night bc the darkness diminished the visual compensation for proprioceptive loss
161
why can vision only compensate for CONSCIOUS proprioception?
vision is a conscious pathway and so it can only compensate for other conscious pathways, not unconscious ones
162
where is the first order neuron in the DCML?
periphery to SC
163
where is the 2nd order neuron in the DCML?
caudal medulla decussation to synapse in the VPL (thalamus)
164
where is the 3rd order neuron in the DCML?
VPL to S1 (primary somatosensory cortex)
165
what are the DCML somatosensory modalities?
conscious proprioception and light touch
166
where does the DCML decussated?
caudal medulla
167
where does the DCML terminate?
cerebral cortex
168
where in the thalamus does the DCML go?
VPL
169
what are the somatosensory modalities of the trigeminal pathway for light touch?
conscious proprioception and light touch
170
where does the trigeminal pathway for light touch decussate?
pons
171
where does the trigeminal pathway for light touch terminate?
cerebral cortex
172
where in the thalamus does the trigeminal pathway for light touch go?
VPM
173
what makes of the medial system?
DCML and trigeminal pathway for light touch
174
what makes up the antero-lateral system?
spinothalamic pathway and trigeminal pathway for pain
175
what are the somatosensory modalities for the spinothalamic pathway?
fast nociception temp crude touch
176
where does the spinothalamic pathway decussate?
in the SC at the level of the 1st order neuron entry
177
where does the spinothalamic pathway terminate?
cerebral cortex
178
where in the thalamus does the spinothalamic pathway go?
VPL
179
what are the somatosensory modalities for the trigeminal pathway for pain?
nociception temp crude touch
180
where does the trigeminal pathway for pain decussate?
caudal medulla
181
where does the trigeminal pathway for pain terminate?
cerebral cortex
182
where in the thalamus does the trigeminal pathway for pain go?
VPM
183
what are the somatosensory modalities of the nonconscious spinocerebellar pathway?
nonconscious proprioception
184
where does the spinocerebellar pathway decussate?
mostly no decussation, some double decussation
185
where does the spinocerebellar pathway terminate?
cerebellum
186
what are the somatosensory modalities of the divergent pathway (medial nociceptive system w/in anterolateral system) ?
slow nociception
187
where does the divergent pathway decussate?
same as spinothalamic, at the SC at the level of 1st order neuron entry
188
where does the divergent pathway terminate?
reticular formation periaqueductal gray insula amygdala dorsolateral prefrontal cortex (DLPFC) cerebral cortex
189
with a cortical lesion, what sensory loss is there?
contralateral loss of all sensory modalities (proprioception, light touch, and nociception), decreased stereognosis and impaired graphesthesia
190
with a thalamus lesion (VPM/VPL), what sensory loss is there?
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
what is the most common brain stem stroke?
lateral medullary lesion
192
what is the 2nd most common brain stem stroke?
lateral pontine lesion
193
with a lateral pontine lesion, what is the sensory loss of the body?
contralateral loss of pain and temperature sensation in the body (spinothalamic tract)
194
with a lateral pontine lesion, what is the sensory loss of the face?
ipsilateral loss of pain and temp sensation in the face and ipsilateral loss of discriminitive touch and proprioception in the face
195
with a lateral medullary lesion, what is the sensory loss of the body?
contralateral loss of pain and temp sensation in the body
196
with a lateral medullary lesion, what is the sensory loss of the face?
ipsilateral loss of pain and temp sensation, but unaffected touch and proprioception of the face
197
what is vestibular ataxia?
pathology in vestibular system causing dizziness, vertigo, difficulty hearing, tinnitus, motor incoordination feels like the world is spinning (may cause vomiting)
198
what is cerebellar ataxia?
pathology in cerebellum negative Romberg test (can't do with eye opened or closed) lateral hemispheres: finger ataxia paravermis: limb ataxia vermis: trunk ataxia