Flashcards in 473 MT 2 Deck (122):
sensory modalities in the order of decreasing axon size
proprioception, superficial touch, deep touch, vibration, pain, temp, itch
sensory area/cutaneous region innervated by a single spinal segment
C5 innervates what dermatome
C6, C7, C8
what sensory info does PMCL carry?
vibration, proprioception, tight touch
what does antero-lateral pathway carry?
pain, temp, crude touch
primary sensory neuron in PMCL
-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
where do primary sensory neurons for the lower body travel?
medial portion of posterior column
where do primary neurons for the upper body travel?
lateral posterior column
why would the axons for the legs be more medial?
first to enter
avoids crossing of wires
where do axons in fasciculus gracilis synapse?
axons in fasciculus cuneatus?
2nd order sensory neuron in PMCL
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
3rd order sensory neuron for PMCL
cell body in thalamus, projects to primary sensory cortex
antero-lateral pathway consists of
what does mesencephalic refer to?
primary sensory neuron of AL pathway
cell body in DRG, synapse w/ 2nd order in dorsal horn of spinal chord
-in 2nd order sensory nuclei
2nd order sensory neuron AL pathway
crosses midline through anterior comisure over 2-3 segments
ascends in anterolateral white matter
synapse in thalamus
3rd order neuron AL pathway
thalamus to somatosensory cortex
**only spino-thalamic projects to cortex
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
somatosensory cortex somatotopic organization
mirror image of motor cortex
larger areas for hand, mouth, tongue
negative symptoms of somatosensory lesions
-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
how to test for loss of position sense
move joints passively and ask if it was up or down (eyes closed)
how to test for vibration sense
how to test for two-point discrimination
ask if being touched in 1 or 2 places
or light touch in one direction and ask which direction
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
what distinct difference does tabetic gate have from foot drop?
in foot drop, toes hit first b/c of weak dorsiflexors
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
neg. symptoms (spino-thalamic pathway)
loss of pain and temp
reduced touch sensation
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
positive PCML symptoms
tingling, numb sensation
-parathesia and dysesthesia, meaning abnormal sensations
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
positive primary sensory neuron symptoms
numbness and tingling in dermatome
-3 branches-1, 2, and 3
-includes motor element (chewing)
-cell bodies in trigeminal ganglion in Merkel's cave
-axons project to pons
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
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
loss of sensation on whole side of face?
trigemenal nerve, ipsilateral side
if cortex was damaged, contralateral side would be affected
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
loss of sensation on one side of the body?
-likely medial lemniscus pathway, might involve anterolateral
-more ventral would involve pyramids
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
single dermatome sensation loss?
damage to nerve itself
or dorsal root
**nerve would also involve radicular pain and motor involvement
Brown-Sequard syndrome definition + causes
compression from a tumour
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
transverse chord lesion causes
trauma, tumor, MS
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
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
posterior chord syndrome causes
-vit B12 deficiency (can damage myelin of posterior column axons)
anterior chord syndrome causes
-causes anterolateral sensation and motor loss below the neck
-if affecting lateral corticospinal tract, upper MN symptoms in levels below
where can herpes zoster lie dormant?
what is happening when it re-emerges?
grows down sensory nerve
-pain, rash in dermatome
-allodynia and parasthesias also
-subsides after 2-3 weeks
what is the name for shingles cases lasting for months?
-slow degeneration of dorsal columns, dorsal roots, and ganglia of the spinal chord
=late symptoms of untreated syphilis (10-30 yrs later)
tabes dorsalis symptoms
proprioceptive loss, parasthesias, allodynia
bad balance w/ out vision
nerve disorder of one nerve
eg carpal tunnel
-may have sensory symptoms and motor deficits
-overdoes of vit B6
diabetic neuropathy causes
poor blood supply + inflammation of nerves
-from high levels of glucose
-involves paresthesias and allodynia
what does polyneuropathy in the hands and feet immediately rule out?
-lesion in the brain
-lesion in the spinal chord
overdose of pyridoxine
damages large 1a myelinated fibers, some cases irreversible
-up to 100x normal does leads to sensory loss
leads to polyneuropathy
inflammation of many nerves leading to widespread proprioceptive or sensory loss
-eg GL-loss of sensory input below nose (anterolateral largely spared)
where is the vestibular system located?
w/in petrous ridge of temporal bone
what is the bony labarynth
tunnels carved through petrous ridge
-filled with endolymph fluid
which otolith organ is closer to the cochlea?
how many semi-circular canals?
which otolith organ is continuous with the semi-circular ducts?
utricle (through ampulla)
where do hair cells lie in the semi-circular ducts
axons project to vestibular ganglion
gelatinous material encasing the cilia
-endolymph pushes against gel-encased hair cell
what do hair cells in the ampulla detect?
angular accelreation of the head
-fluid lags in the ducts and deflects the cupula and cilia
where are the utricles located?
why is that important?
for orientation in horizontal movement of the head-when deflected toward utricle (midline), that side depolarizes and other side hyperpolarizes
what does rightward movement of the head do to firing rates?
L side inc
R side decrease
anterior and posterior canal firing rates
increase if hair cells are deflected AWAY
decrease if hair cells deflected toward
where are hair cells in the otolith organs?
in macula, with cilia embeded in the otolithic membrane
Ca carbonate crystals on top the otolithic membrane
how are hair cells in utricle oriented?
vertically (from floor)
-ie good for detecting forward/backward/side to side motion
how are saccule hair cells oriented?
horizontally from wall
-ie good for detecting vertical and some backward forward motion
otolith firing rates
utricle: increase rate when hair cells are deflected toward striola
saccule: decrease (hair cells face out)
which motions have similar vestibular signals?
backward tilt and acceleration b/c hair cells fire normally at constant velocities
where are cell bodies of vestibular afferents?
axons travel as CN VIII to ipsilateral vestibular nuclei
lateral vestibulospinal tract
control balance and extensor tone in limbs
medial vestibulospinal tract (medial and inferior nuclei)
positioning of head and neck
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
how does vestibular system influence balance
-reciprocal projections with the cerebellum
-balance, eye control, coordination
-cerebellum maintains some control over eye movements for control
how is head orientation and motion consciously perceived?
projections from vestibular nuclei to thalamus to parietal cortex
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)
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
=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)
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
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)
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)
peripheral vestibular lesion
damage to labyrinths or CN VIII
central vestibular lesions
damage to vestibular nuclei or pathways projecting to brainstem, thalamus, or cerebellum
common symptoms of uni-lateral vestibular lesion
what causes vertigo?
eg if the nerve was damaged, firing rate would be imbalanced
this is interpreted an unexpected head movement
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)
postural instibility in vestibular patients
fall or turn (fakuda marching test) toward side of lesion
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)
6 possible causes of uni-lateral vestibular lesions
vestibular neuritis (CN VIII)
benign paroxysmal peripheral nystagmus
cerebellar pontine angle tumor
can impinge on CN VIII coming from pons level and possibly some vestibular nuclei
vestibular neuritis cause
viral infection of vestibular nerve
40% recover after a month, some have partial deficits
damaging one side to allow for compensation is sometimes a better route
-labyrinthectomy (plug canals or damage hair cells)
-vestibular nerve section
-increased endolymph volume and pressure
-small ruptures of membranous labyrinth
-unknown/maybe viral or autoimmune or genetic
treatment: lifestyle change, surgery
round/oval window rupture, which separates middle ear
-traumatic injury or severe pressure damage (eg scuba diving)
-treated w/rest or surgery
signs of perilymph fistula
abnormal nystagmus with additional pressure changes (in fistula test)
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
how is BPPN identified?
dix hallpike-turn head in certain directions
what causes BPPN?
or massive head acceleration (eg a fall)
bilateral vestibular loss symptoms
postural instability (especially w/out vision)
blurry vision (when moving and trying to fixate)
missing postural responses
possible causes of bilateral vestibular loss
ototoxic medicaiton (ie gentomicin)
meniere's disease can be bilateral
what does abnormal VOR and normal optokinetic reflex suggest?
damage at the canal (intact visual system)
what would happen to the VOR and optokinetic reflexes if medial vestibular nuclei were damaged?
what type of vestibular lesion is this?
-optokinetic bypasses receptors but goes to medial vestibular nucleus and then follows VOR path to adjusts eyes to reduce retinal slip
unimodal association cortex
higher level processing of 1 function
multimodal association cortex
integration of several sensory modalities for higher level processing
motor association cortex
involved in formulating motor programs
-supplimental motor area superior and medial
-pre-motor cortex lateral
motor association area projections
-primary motor cortex
-spinal chord (corticospinal tract fibers)
what does stimulation of the pre-motor cortex cause?
multiple contractions at multiple joints of the same limb
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)
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
normal percept stripped of all meaning
stereoagnosis-inability to recognize/name objects
agraphesthesia-inability to recognize symbols, numbers, etc. from light touch
somatosensory association cortex lesion
basic elements of where and what but that information can't be integrated and given meaning to
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
parietal association cortex
integrates visual, somatosensory, vestibular, and auditory inputs
-primarily parietal but also frontal (ie multimodal)
-outputs include motor association areas
which hemisphere deals with skilled motor formulation?
also called praxis
-particularly when interacting w/tools or the environment
dominant hemisphere functions
-musical sequencing and analytical skills
non-dominant hemisphere functions
sense or direction-spatial orientation
visual-spatial analysis and spatial attention
prosody (emotion in tone of voice)