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Neuroanatomy > 473 MT 2 > Flashcards

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

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2
Q

dermatome

A

sensory area/cutaneous region innervated by a single spinal segment

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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
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4
Q

what sensory info does PMCL carry?

A

vibration, proprioception, tight touch

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5
Q

what does antero-lateral pathway carry?

A

pain, temp, crude touch

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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
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7
Q

where do primary sensory neurons for the lower body travel?

A

fasciculus gracilis
medial portion of posterior column
(leg=medial)

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8
Q

where do primary neurons for the upper body travel?

A

fasciculus cuneatus
lateral posterior column
(arms=lateral)

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9
Q

why would the axons for the legs be more medial?

A

first to enter

avoids crossing of wires

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10
Q

where do axons in fasciculus gracilis synapse?

axons in fasciculus cuneatus?

A

nucleus gracilis

nucleus cuneatus

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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

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12
Q

3rd order sensory neuron for PMCL

A

cell body in thalamus, projects to primary sensory cortex

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13
Q

antero-lateral pathway consists of

A

spino-thalamic
spino-reticular
spino-mesencephalic

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14
Q

what does mesencephalic refer to?

A

midbrain region

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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

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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

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17
Q

3rd order neuron AL pathway

A

thalamus to somatosensory cortex

**only spino-thalamic projects to cortex

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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
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19
Q

somatosensory cortex somatotopic organization

A

mirror image of motor cortex

larger areas for hand, mouth, tongue

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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
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21
Q

how to test for loss of position sense

A

move joints passively and ask if it was up or down (eyes closed)

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22
Q

how to test for vibration sense

A

tuning fork

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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

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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
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25
Q

what distinct difference does tabetic gate have from foot drop?

A

in foot drop, toes hit first b/c of weak dorsiflexors

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26
Q

what happens from damage to primary sensory neuron (PMCL)?

A

loss of proprioception + tabetic gate possible
loss of deep tendon reflexes
-PMCL neurons involved in monosynaptic stretch reflex pathways

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27
Q

neg. symptoms (spino-thalamic pathway)

A

loss of pain and temp

reduced touch sensation

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28
Q

how to test for pain and temp

A

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

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29
Q

positive PCML symptoms

A

tingling, numb sensation

-parathesia and dysesthesia, meaning abnormal sensations

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30
Q

positive antero-lateral symptoms

A

sharp, burning or searing pain
may by hyperpathia-excessive pain to something normally painful
or allodynia-pain to something normally not painful

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31
Q

positive primary sensory neuron symptoms

A

radicular pain

numbness and tingling in dermatome

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32
Q

trigeminal nerve

A
  • CNV
  • 3 branches-1, 2, and 3
  • includes motor element (chewing)
  • cell bodies in trigeminal ganglion in Merkel’s cave
  • axons project to pons
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33
Q

2nd order sensory neuron (inputs from face)

A

synapses on ipsi-lateral side at the level of the pons

  • crosses midline and continue to thalamus
  • 3rd order from thalamus to somatosensory cortex
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34
Q

where to pain, temp, and crude touch axons go (facial inputs)?

A

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

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35
Q

loss of sensation on whole side of face?

A

trigemenal nerve, ipsilateral side

if cortex was damaged, contralateral side would be affected

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36
Q

loss of sensation on right side of face and body?

A
  • pons or above (if IN, sensory loss would be on contralateral side of body)
  • likely in the lateral thalamus on the contralateral side
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37
Q

loss of sensation on one side of the body?

A
  • likely medial lemniscus pathway, might involve anterolateral
  • more ventral would involve pyramids
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38
Q

loss of sensation in face on one side and body on the other?

A

@ the level of the pons
where anterolateral pathways travel together
but body afferents have crossed midline already

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39
Q

single dermatome sensation loss?

A

damage to nerve itself
or dorsal root
**nerve would also involve radicular pain and motor involvement

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40
Q

Brown-Sequard syndrome definition + causes

A

-hemicord lesion

penetrating trauma
compression from a tumour
MS

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41
Q

hemicord lesion symptoms

A

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

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42
Q

transverse chord lesion causes

A

trauma, tumor, MS

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43
Q

transverse chord lesion symptoms

A

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

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44
Q

central chord syndrome (small lesion)

A
  • 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
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45
Q

posterior chord syndrome causes

A
  • trauma
  • tumor
  • MS
  • vit B12 deficiency (can damage myelin of posterior column axons)
  • tabes dorsalis
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46
Q

anterior chord syndrome causes

A

trauma
tumor
MS
infart
-causes anterolateral sensation and motor loss below the neck
-if affecting lateral corticospinal tract, upper MN symptoms in levels below

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47
Q

where can herpes zoster lie dormant?

what is happening when it re-emerges?

A 
DRGs
grows down sensory nerve
-pain, rash in dermatome
-allodynia and parasthesias also
-subsides after 2-3 weeks
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48
Q

what is the name for shingles cases lasting for months?

A

post-hepatic neuralgia

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49
Q

tabes dorsalis

A

-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
Q

tabes dorsalis symptoms

A

proprioceptive loss, parasthesias, allodynia
tabetic gate
bad balance w/ out vision

51
Q

mononeuropathy

A

nerve disorder of one nerve
eg carpal tunnel
-may have sensory symptoms and motor deficits

52
Q

polyneuropathy examples

A
  • diabetes
  • overdoes of vit B6
  • ganglionopathies
  • polyneuritis
53
Q

diabetic neuropathy causes

A

poor blood supply + inflammation of nerves

  • from high levels of glucose
  • involves paresthesias and allodynia
54
Q

what does polyneuropathy in the hands and feet immediately rule out?

A
  • lesion in the brain

- lesion in the spinal chord

55
Q

overdose of pyridoxine

A

damages large 1a myelinated fibers, some cases irreversible

-up to 100x normal does leads to sensory loss

56
Q

ganglionopathies

A

typically autoimmune

leads to polyneuropathy

57
Q

polyneuritis

A

inflammation of many nerves leading to widespread proprioceptive or sensory loss
-eg GL-loss of sensory input below nose (anterolateral largely spared)

58
Q

where is the vestibular system located?

A

w/in petrous ridge of temporal bone

continuous w/cochlea

59
Q

what is the bony labarynth

A

tunnels carved through petrous ridge

-filled with endolymph fluid

60
Q

which otolith organ is closer to the cochlea?

A

saccule

61
Q

how many semi-circular canals?

A

anterior
posterior
inferior

62
Q

which otolith organ is continuous with the semi-circular ducts?

A

utricle (through ampulla)

63
Q

where do hair cells lie in the semi-circular ducts

A

crista ampullaris

axons project to vestibular ganglion

64
Q

cupola

A

gelatinous material encasing the cilia

-endolymph pushes against gel-encased hair cell

65
Q

what do hair cells in the ampulla detect?

A

angular accelreation of the head

-fluid lags in the ducts and deflects the cupula and cilia

66
Q

where are the utricles located?

why is that important?

A

toward midline
for orientation in horizontal movement of the head-when deflected toward utricle (midline), that side depolarizes and other side hyperpolarizes

67
Q

what does rightward movement of the head do to firing rates?

A

L side inc

R side decrease

68
Q

anterior and posterior canal firing rates

A

increase if hair cells are deflected AWAY

decrease if hair cells deflected toward

69
Q

where are hair cells in the otolith organs?

A

in macula, with cilia embeded in the otolithic membrane

70
Q

otoconia

A

Ca carbonate crystals on top the otolithic membrane

-adds density–>inertia

71
Q

how are hair cells in utricle oriented?

A

vertically (from floor)

-ie good for detecting forward/backward/side to side motion

72
Q

how are saccule hair cells oriented?

A

horizontally from wall

-ie good for detecting vertical and some backward forward motion

73
Q

otolith firing rates

A

utricle: increase rate when hair cells are deflected toward striola
saccule: decrease (hair cells face out)

74
Q

which motions have similar vestibular signals?

A

backward tilt and acceleration b/c hair cells fire normally at constant velocities

75
Q

where are cell bodies of vestibular afferents?

axons?

A

vestibular ganglion

axons travel as CN VIII to ipsilateral vestibular nuclei

76
Q

lateral vestibulospinal tract

A

control balance and extensor tone in limbs

77
Q

medial vestibulospinal tract (medial and inferior nuclei)

A

positioning of head and neck

vestibulo-colic reflexes

78
Q

how are eye muscle reflexes present?

A

SVN and MVN projections via medial longitudinal fasciculus to 3 cranial nuclei

  1. oculo-motor nucleus
  2. trochlear nucleus
  3. abducens nucleus
79
Q

how does vestibular system influence balance

A
  • reciprocal projections with the cerebellum
  • balance, eye control, coordination
  • cerebellum maintains some control over eye movements for control
80
Q

how is head orientation and motion consciously perceived?

A

projections from vestibular nuclei to thalamus to parietal cortex

81
Q

VOR

A

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
Q

describe firing w/L movement of head for VOR

A

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
Q

nystagmus

A

=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
Q

head impulse test

A

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
Q

caloric irrigation testing

A

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
Q

what test is specific to otolith function?

A

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
Q

peripheral vestibular lesion

A

damage to labyrinths or CN VIII

88
Q

central vestibular lesions

A

damage to vestibular nuclei or pathways projecting to brainstem, thalamus, or cerebellum

89
Q

common symptoms of uni-lateral vestibular lesion

A

vertigo
nausea
postural instability

90
Q

what causes vertigo?

A

spontaneous nystagmus
eg if the nerve was damaged, firing rate would be imbalanced
this is interpreted an unexpected head movement

91
Q

cause of nausea as a vestibular lesion symptom

A

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
Q

postural instibility in vestibular patients

A

fall or turn (fakuda marching test) toward side of lesion

93
Q

what role does research suggest the vestibular system plays in balance responses?

A

regulating amount and coordination

NOT for initiating the response (slower responses than reflexes)

94
Q

6 possible causes of uni-lateral vestibular lesions

A 
tumor 
vestibular neuritis (CN VIII)
surgery
Meniere's disease
perilymph fistula
benign paroxysmal peripheral nystagmus
95
Q

cerebellar pontine angle tumor

A

can impinge on CN VIII coming from pons level and possibly some vestibular nuclei

96
Q

vestibular neuritis cause

A

viral infection of vestibular nerve

40% recover after a month, some have partial deficits

97
Q

surgery

A

damaging one side to allow for compensation is sometimes a better route

  • labyrinthectomy (plug canals or damage hair cells)
  • vestibular nerve section
98
Q

Meniere’s disease

A 
mechanism
-increased endolymph volume and pressure
-small ruptures of membranous labyrinth
cause
-unknown/maybe viral or autoimmune or genetic
treatment: lifestyle change, surgery
99
Q

perilymph fistula

A

round/oval window rupture, which separates middle ear

  • traumatic injury or severe pressure damage (eg scuba diving)
  • treated w/rest or surgery
100
Q

signs of perilymph fistula

A

abnormal nystagmus with additional pressure changes (in fistula test)

101
Q

benign paroxysmal peripheral nystagmus

A

due to otoconia getting dislodged and traveling in canals

  • symptoms w/sudden head changes
  • they usually dissolve w/in a few weeks
102
Q

how is BPPN identified?

A

dix hallpike-turn head in certain directions

103
Q

what causes BPPN?

A

age

or massive head acceleration (eg a fall)

104
Q

bilateral vestibular loss symptoms

A 
postural instability (especially w/out vision)
blurry vision (when moving and trying to fixate)
missing postural responses
105
Q

possible causes of bilateral vestibular loss

A

ototoxic medicaiton (ie gentomicin)
meningitis itself
meniere’s disease can be bilateral

106
Q

what does abnormal VOR and normal optokinetic reflex suggest?

A

damage at the canal (intact visual system)

107
Q

what would happen to the VOR and optokinetic reflexes if medial vestibular nuclei were damaged?
what type of vestibular lesion is this?

A

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
Q

unimodal association cortex

A

higher level processing of 1 function

109
Q

multimodal association cortex

A

integration of several sensory modalities for higher level processing

110
Q

motor association cortex

A

involved in formulating motor programs

  • supplimental motor area superior and medial
  • pre-motor cortex lateral
111
Q

motor association area projections

A
  • primary motor cortex
  • brainstem
  • spinal chord (corticospinal tract fibers)
112
Q

what does stimulation of the pre-motor cortex cause?

A

multiple contractions at multiple joints of the same limb

113
Q

what is the pre-motor cortex involved in?

A

preparation of voluntary movements and activating multiple muscles in the limb
-set related movements and directionally specific (affects contralateral limbs)

114
Q

supplementary motor area

A
  • 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
Q

agnosia

A

normal percept stripped of all meaning
stereoagnosis-inability to recognize/name objects
agraphesthesia-inability to recognize symbols, numbers, etc. from light touch

116
Q

somatosensory association cortex lesion

A

agnosia

basic elements of where and what but that information can’t be integrated and given meaning to

117
Q

visual agnosia

A

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
Q

parietal association cortex

A

integrates visual, somatosensory, vestibular, and auditory inputs

  • primarily parietal but also frontal (ie multimodal)
  • outputs include motor association areas
119
Q

which hemisphere deals with skilled motor formulation?

A

dominant
also called praxis
ie Left
-particularly when interacting w/tools or the environment

120
Q

dominant hemisphere functions

A
  • language
  • analytic skills
  • musical sequencing and analytical skills
121
Q

non-dominant hemisphere functions

A

musical ability
sense or direction-spatial orientation
visual-spatial analysis and spatial attention
prosody (emotion in tone of voice)

122
Q

apraxia

A

damage to either motor association areas or L parietal association cortex
–inability to perform complex sequences of tasks

Neuroanatomy (3 decks)

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