473 MT 2 Flashcards
1
Q
sensory modalities in the order of decreasing axon size
A
proprioception, superficial touch, deep touch, vibration, pain, temp, itch
2
Q
dermatome
A
sensory area/cutaneous region innervated by a single spinal segment
3
Q
C5 innervates what dermatome C6, C7, C8 T4 T10 L2 L3 L4 L5
A
shoulder hand nipple level belly button thigh knee medial leg lateral leg
4
Q
what sensory info does PMCL carry?
A
vibration, proprioception, tight touch
5
Q
what does antero-lateral pathway carry?
A
pain, temp, crude touch
6
Q
primary sensory neuron in PMCL
A
- cell body in DRG
- bifurcates: axon 1. projects to receptor and 2. enters dorsal horn and splits again–>some to alpha motor neurons in anterior horn, others to posterior column to ascend
7
Q
where do primary sensory neurons for the lower body travel?
A
fasciculus gracilis
medial portion of posterior column
(leg=medial)
8
Q
where do primary neurons for the upper body travel?
A
fasciculus cuneatus
lateral posterior column
(arms=lateral)
9
Q
why would the axons for the legs be more medial?
A
first to enter
avoids crossing of wires
10
Q
where do axons in fasciculus gracilis synapse?
axons in fasciculus cuneatus?
A
nucleus gracilis
nucleus cuneatus
11
Q
2nd order sensory neuron in PMCL
A
nucleus gracilis: cell bodies of afferent for medial part
nucleus cuneatus-cell bodies of afferents for lateral part (more lateral)
-axons cross at caudal medulla, then project to thalamus as medial lemniscus pathway
12
Q
3rd order sensory neuron for PMCL
A
cell body in thalamus, projects to primary sensory cortex
13
Q
antero-lateral pathway consists of
A
spino-thalamic
spino-reticular
spino-mesencephalic
14
Q
what does mesencephalic refer to?
A
midbrain region
15
Q
primary sensory neuron of AL pathway
A
cell body in DRG, synapse w/ 2nd order in dorsal horn of spinal chord
-in 2nd order sensory nuclei
16
Q
2nd order sensory neuron AL pathway
A
crosses midline through anterior comisure over 2-3 segments
ascends in anterolateral white matter
synapse in thalamus
17
Q
3rd order neuron AL pathway
A
thalamus to somatosensory cortex
**only spino-thalamic projects to cortex
18
Q
thalamus functions
A
relay centre for integration of sensory, cerebellar, and basal ganglia inputs and cortical inputs
- there’s a collection of relay nuclei
- ie 1st order of higher level sensory processing
19
Q
somatosensory cortex somatotopic organization
A
mirror image of motor cortex
larger areas for hand, mouth, tongue
20
Q
negative symptoms of somatosensory lesions
A
PMCL pathway
- loss of position and vibration sense
- loss of discriminatory touch (2pt touch)
- astereognosis (can’t recognizing objects)
- sensory ataxia-unsteadiness, poor coordination, worse w/out vision
21
Q
how to test for loss of position sense
A
move joints passively and ask if it was up or down (eyes closed)
22
Q
how to test for vibration sense
A
tuning fork
23
Q
how to test for two-point discrimination
A
ask if being touched in 1 or 2 places
or light touch in one direction and ask which direction
24
Q
tabetic gait
A
from total loss of proprioception in the legs
- high stepping to get limb through swing phase
- foot flaps (no position sense)
- more locked knees b/c it’s clearer where it is
25
what distinct difference does tabetic gate have from foot drop?
in foot drop, toes hit first b/c of weak dorsiflexors
26
what happens from damage to primary sensory neuron (PMCL)?
loss of proprioception + tabetic gate possible
loss of deep tendon reflexes
-PMCL neurons involved in monosynaptic stretch reflex pathways
27
neg. symptoms (spino-thalamic pathway)
loss of pain and temp
| reduced touch sensation
28
how to test for pain and temp
pain: pin prick and see if there's a sharp feeling
temp: hot and cold vials
crude touch is difficult to test if PCML is still intact
29
positive PCML symptoms
tingling, numb sensation
| -parathesia and dysesthesia, meaning abnormal sensations
30
positive antero-lateral symptoms
sharp, burning or searing pain
may by hyperpathia-excessive pain to something normally painful
or allodynia-pain to something normally not painful
31
positive primary sensory neuron symptoms
radicular pain
| numbness and tingling in dermatome
32
trigeminal nerve
- CNV
- 3 branches-1, 2, and 3
- includes motor element (chewing)
- cell bodies in trigeminal ganglion in Merkel's cave
- axons project to pons
33
2nd order sensory neuron (inputs from face)
synapses on ipsi-lateral side at the level of the pons
- crosses midline and continue to thalamus
- 3rd order from thalamus to somatosensory cortex
34
where to pain, temp, and crude touch axons go (facial inputs)?
they project through the ganglion into the pons, then descend into long spinal-trigemenal nucleus, which is continuous w/ the spinal chord and extends to the pons
35
loss of sensation on whole side of face?
trigemenal nerve, ipsilateral side
| if cortex was damaged, contralateral side would be affected
36
loss of sensation on right side of face and body?
- pons or above (if IN, sensory loss would be on contralateral side of body)
- likely in the lateral thalamus on the contralateral side
37
loss of sensation on one side of the body?
- likely medial lemniscus pathway, might involve anterolateral
- more ventral would involve pyramids
38
loss of sensation in face on one side and body on the other?
@ the level of the pons
where anterolateral pathways travel together
but body afferents have crossed midline already
39
single dermatome sensation loss?
damage to nerve itself
or dorsal root
**nerve would also involve radicular pain and motor involvement
40
Brown-Sequard syndrome definition + causes
-hemicord lesion
penetrating trauma
compression from a tumour
MS
41
hemicord lesion symptoms
lower MN symptoms on ipsilateral side for muscles innervated by that spinal chord level
upper MN on ipsilateral side for muscles innervated by axons below that level
-loss of proprioception, light touch, and vibration for dermatomes innervated by that level and below on the ipsilateral side
-loss of pain, temp, and crude touch for dermatomes innervated by the segment injured and 1 segment below on the ipsilateral side
-loss of pain, temp, crude touch for dermatomes innervated by 2 segments below and lower on the contralateral side
42
transverse chord lesion causes
trauma, tumor, MS
43
transverse chord lesion symptoms
bilateral lower MN symptoms at that level
bilateral upper MN symptoms below
bilateral PCML loss at that level and below
bilateral anterolateral loss at this level and below
44
central chord syndrome (small lesion)
- starts as a syrinx, then gets inflammed and grows
- small enough not to affect motor pathways
- affects 2nd order neurons crossing in spinal chord in anterolateral pathways
- bilateral loss of sensory info for dermatomes innervated by 1-2 segments below
- anterior horn being unaffected spares levels below
45
posterior chord syndrome causes
- trauma
- tumor
- MS
- vit B12 deficiency (can damage myelin of posterior column axons)
- tabes dorsalis
46
anterior chord syndrome causes
trauma
tumor
MS
infart
-causes anterolateral sensation and motor loss below the neck
-if affecting lateral corticospinal tract, upper MN symptoms in levels below
47
where can herpes zoster lie dormant?
| what is happening when it re-emerges?
```
DRGs
grows down sensory nerve
-pain, rash in dermatome
-allodynia and parasthesias also
-subsides after 2-3 weeks
```
48
what is the name for shingles cases lasting for months?
post-hepatic neuralgia
49
tabes dorsalis
-slow degeneration of dorsal columns, dorsal roots, and ganglia of the spinal chord
-lumbar region
=late symptoms of untreated syphilis (10-30 yrs later)
50
tabes dorsalis symptoms
proprioceptive loss, parasthesias, allodynia
tabetic gate
bad balance w/ out vision
51
mononeuropathy
nerve disorder of one nerve
eg carpal tunnel
-may have sensory symptoms and motor deficits
52
polyneuropathy examples
- diabetes
- overdoes of vit B6
- ganglionopathies
- polyneuritis
53
diabetic neuropathy causes
poor blood supply + inflammation of nerves
- from high levels of glucose
- involves paresthesias and allodynia
54
what does polyneuropathy in the hands and feet immediately rule out?
- lesion in the brain
| - lesion in the spinal chord
55
overdose of pyridoxine
damages large 1a myelinated fibers, some cases irreversible
| -up to 100x normal does leads to sensory loss
56
ganglionopathies
typically autoimmune
| leads to polyneuropathy
57
polyneuritis
inflammation of many nerves leading to widespread proprioceptive or sensory loss
-eg GL-loss of sensory input below nose (anterolateral largely spared)
58
where is the vestibular system located?
w/in petrous ridge of temporal bone
| continuous w/cochlea
59
what is the bony labarynth
tunnels carved through petrous ridge
| -filled with endolymph fluid
60
which otolith organ is closer to the cochlea?
saccule
61
how many semi-circular canals?
anterior
posterior
inferior
62
which otolith organ is continuous with the semi-circular ducts?
utricle (through ampulla)
63
where do hair cells lie in the semi-circular ducts
crista ampullaris
| axons project to vestibular ganglion
64
cupola
gelatinous material encasing the cilia
| -endolymph pushes against gel-encased hair cell
65
what do hair cells in the ampulla detect?
angular accelreation of the head
| -fluid lags in the ducts and deflects the cupula and cilia
66
where are the utricles located?
| why is that important?
toward midline
for orientation in horizontal movement of the head-when deflected toward utricle (midline), that side depolarizes and other side hyperpolarizes
67
what does rightward movement of the head do to firing rates?
L side inc
| R side decrease
68
anterior and posterior canal firing rates
increase if hair cells are deflected AWAY
| decrease if hair cells deflected toward
69
where are hair cells in the otolith organs?
in macula, with cilia embeded in the otolithic membrane
70
otoconia
Ca carbonate crystals on top the otolithic membrane
| -adds density-->inertia
71
how are hair cells in utricle oriented?
vertically (from floor)
| -ie good for detecting forward/backward/side to side motion
72
how are saccule hair cells oriented?
horizontally from wall
| -ie good for detecting vertical and some backward forward motion
73
otolith firing rates
utricle: increase rate when hair cells are deflected toward striola
saccule: decrease (hair cells face out)
74
which motions have similar vestibular signals?
backward tilt and acceleration b/c hair cells fire normally at constant velocities
75
where are cell bodies of vestibular afferents?
| axons?
vestibular ganglion
| axons travel as CN VIII to ipsilateral vestibular nuclei
76
lateral vestibulospinal tract
control balance and extensor tone in limbs
77
medial vestibulospinal tract (medial and inferior nuclei)
positioning of head and neck
| vestibulo-colic reflexes
78
how are eye muscle reflexes present?
SVN and MVN projections via medial longitudinal fasciculus to 3 cranial nuclei
1. oculo-motor nucleus
2. trochlear nucleus
3. abducens nucleus
79
how does vestibular system influence balance
- reciprocal projections with the cerebellum
- balance, eye control, coordination
- cerebellum maintains some control over eye movements for control
80
how is head orientation and motion consciously perceived?
projections from vestibular nuclei to thalamus to parietal cortex
81
VOR
allows eyes to fix on a target while head is accelerating
| -eyes move in opposite direction of head with the same acceleration (same direction as cupula movement)
82
describe firing w/L movement of head for VOR
L movement causes R endolymph movement
L side increase output to vestibular nuclei
excitation of R side eye muscles pulls eyes to the R
-opposite side muscles inhibited
83
nystagmus
=from continual vestibular stimuli
- eyes snap back to center so VOR can continue when spinning
- named after fast phase (a right VOR response might cause L beating nystagmus)
84
head impulse test
move head passively and quickly while subject wears goggles equiped w/accelerometers
tests canals in all planes
would expect to see equal and opposite eye movements
85
caloric irrigation testing
hot/cold water injection to ear
-cool water causes opposite side nystagmus (endolymph sinks)
-hot water causes same side nystagmus (endolymph rises)
COWS (cold opposite warm same)
86
what test is specific to otolith function?
vestibular evoked myogenic potentials
- sounds of tones or clicks used to stimulate otoliths primarily
- mm activity recorded around neck and head
- sound causes stapes to push into vestibular system that cause stimulation
- largest response is on ipsilateral side
- muscles must be tonically active (ie person is looking up or holding head up)
87
peripheral vestibular lesion
damage to labyrinths or CN VIII
88
central vestibular lesions
damage to vestibular nuclei or pathways projecting to brainstem, thalamus, or cerebellum
89
common symptoms of uni-lateral vestibular lesion
vertigo
nausea
postural instability
90
what causes vertigo?
spontaneous nystagmus
eg if the nerve was damaged, firing rate would be imbalanced
this is interpreted an unexpected head movement
91
cause of nausea as a vestibular lesion symptom
a. sensory mismatch/conflict with visual world
b. vestibular-autonomic connections
- these exist to transmit info about head movement in order to adjust BP but can also cause autonomic response of nausea)
92
postural instibility in vestibular patients
fall or turn (fakuda marching test) toward side of lesion
93
what role does research suggest the vestibular system plays in balance responses?
regulating amount and coordination
| NOT for initiating the response (slower responses than reflexes)
94
6 possible causes of uni-lateral vestibular lesions
```
tumor
vestibular neuritis (CN VIII)
surgery
Meniere's disease
perilymph fistula
benign paroxysmal peripheral nystagmus
```
95
cerebellar pontine angle tumor
can impinge on CN VIII coming from pons level and possibly some vestibular nuclei
96
vestibular neuritis cause
viral infection of vestibular nerve
| 40% recover after a month, some have partial deficits
97
surgery
damaging one side to allow for compensation is sometimes a better route
- labyrinthectomy (plug canals or damage hair cells)
- vestibular nerve section
98
Meniere's disease
```
mechanism
-increased endolymph volume and pressure
-small ruptures of membranous labyrinth
cause
-unknown/maybe viral or autoimmune or genetic
treatment: lifestyle change, surgery
```
99
perilymph fistula
round/oval window rupture, which separates middle ear
- traumatic injury or severe pressure damage (eg scuba diving)
- treated w/rest or surgery
100
signs of perilymph fistula
abnormal nystagmus with additional pressure changes (in fistula test)
101
benign paroxysmal peripheral nystagmus
due to otoconia getting dislodged and traveling in canals
- symptoms w/sudden head changes
- they usually dissolve w/in a few weeks
102
how is BPPN identified?
dix hallpike-turn head in certain directions
103
what causes BPPN?
age
| or massive head acceleration (eg a fall)
104
bilateral vestibular loss symptoms
```
postural instability (especially w/out vision)
blurry vision (when moving and trying to fixate)
missing postural responses
```
105
possible causes of bilateral vestibular loss
ototoxic medicaiton (ie gentomicin)
meningitis itself
meniere's disease can be bilateral
106
what does abnormal VOR and normal optokinetic reflex suggest?
damage at the canal (intact visual system)
107
what would happen to the VOR and optokinetic reflexes if medial vestibular nuclei were damaged?
what type of vestibular lesion is this?
both affected
- optokinetic bypasses receptors but goes to medial vestibular nucleus and then follows VOR path to adjusts eyes to reduce retinal slip
* *central lesion
108
unimodal association cortex
higher level processing of 1 function
109
multimodal association cortex
integration of several sensory modalities for higher level processing
110
motor association cortex
involved in formulating motor programs
- supplimental motor area superior and medial
- pre-motor cortex lateral
111
motor association area projections
- primary motor cortex
- brainstem
- spinal chord (corticospinal tract fibers)
112
what does stimulation of the pre-motor cortex cause?
multiple contractions at multiple joints of the same limb
113
what is the pre-motor cortex involved in?
preparation of voluntary movements and activating multiple muscles in the limb
-set related movements and directionally specific (affects contralateral limbs)
114
supplementary motor area
- complex sequences of movements
- bilateral coordination of limbs
- affects contralateral limbs
- influences proximal muscles directly
- influences distal muscles via primary motor cortex
- inter-hemispheric connections exist b/t the two sides
115
agnosia
normal percept stripped of all meaning
stereoagnosis-inability to recognize/name objects
agraphesthesia-inability to recognize symbols, numbers, etc. from light touch
116
somatosensory association cortex lesion
agnosia
| basic elements of where and what but that information can't be integrated and given meaning to
117
visual agnosia
features can be identified but can't be integrated to give meaning and name too
- facial recognition intact (frontal cortex)
- motor function intact: sometimes the motion of a tool happens in their hands and then they can identify it
- also could name objects if they picked them up with eyes closed
118
parietal association cortex
integrates visual, somatosensory, vestibular, and auditory inputs
- primarily parietal but also frontal (ie multimodal)
- outputs include motor association areas
119
which hemisphere deals with skilled motor formulation?
dominant
also called praxis
ie Left
-particularly when interacting w/tools or the environment
120
dominant hemisphere functions
- language
- analytic skills
- musical sequencing and analytical skills
121
non-dominant hemisphere functions
musical ability
sense or direction-spatial orientation
visual-spatial analysis and spatial attention
prosody (emotion in tone of voice)
122
apraxia
damage to either motor association areas or L parietal association cortex
--inability to perform complex sequences of tasks
