Test 4 Flashcards
Movement is supported by 3 categories of sensory systems
Vision, Vestibular, Somatosensory
neurnons in the visual system create preception of world (images) based on
electromagnetic radiation (light)
eyes have evolved to only detect
visible light (400-700nm)
colour is not inherent in the world, it is the brain’s interpretation of wavelengnths
visual pathway
Retina–> Thalamus–> Primary Visual cortex
Retinofugal projection
“flees the retina”
Retina–> Optic nerve–> optic Chiasm–> Optic Tract–> Leteral Geniculate Nucleus–> primary visual cortex (V1 of Brodman’s 17)
(N before T)
Retinofugal projection- Retina
receives sensory information
Retinofugal projection- optic nerve
before decussation (part of the CNS)
Retinofugal projection- Optic chiasm
decussation (partial)
Retinofugal projection- optic tract
after decussation (CNS)
Retinofugal projection- Lateral Geniculate Nucleus
part of the thalamus
Retinofugal projection- primary visual cortex
V1 or bradmans 17
Brodman’s area 17 in the occipial lobe
-First area of the cortex to receive visual information
-also known as: V1, striate cortex
-Begins mapping and processing visual information
-divides into 2 main pathways
Dorsal Stream
Information passed towards the aprietal lobe
-specialized processing og visual motions
Natigation: perceiving the direction and speed of objects helps us navigate safely
Directing eye movments: sense motion and quickly react to it
Motion perception: interpretation of moving objects
Ventral Stream
Information passed toward the temporal lobe
specialized processing of vison other than motion
-object perception and facial recognition; not only recoginze features but remebering faces (seen even in babies)
AI for facial recignition is getting better at triyng to mimic this
vestibular system
balance equilibrium, posture
Based on the motion of hair cells
vestibular system: lateral line organs
detect movment and vibration in water
-water causes hair cells to deflect
vestibular system: humans
vestibular labyrinth
each part responsible for a specific function
both otolith and semicircular canalas use hair cells to detect changes
~20 000 vestibular axons- cell bodies in scarpa’s ganglion
vestibular labyrinth- otilith organs
acceleration and tilit
vestibular labyrinth- semi-circular canal
head rotation
vestibular system- mechanics review
Aceeleration- change in velocity (measured by ears)
tilt- orientation of head (gravity changes-same structure that detects acceleration)
Rotation- more specifically, angular acceleration (semicircular canals)
The otolith organs (Utricle and Saccule)
measures acceleration and tilit
includes the macula, kinocilim and otocania
otolith organs- macula
epithileum filled pouch with hair cells
otolith organs- kinocilium
tallest and most important cilia. Movement of little cells relative to kinocilium
otolith organs- otoconia
ear stones
calium carbonate crystals
move with fluid (like stones on a waterbed)
otolith organs- how they work
receptor potential: nerve impulses generated in vestibular fiber
Depolarization: when hairs bend towards the kinocilium the hair cell depolarizes, exiciting the nerve fiber, which generates more frequent action potentials (more tilt= more frequent)
hyperpolarization: when hair cells bend away from the kinocilium the hair cells hyperpolarizes inhibtiing the nerve fiber, and decreasing the action potential frequency
macular orientation
array of orientations within organ
saccular maccula-vertically orientented
utricular macula-horizontal orientation
allows measures of all possible linear movment
this movments conteracts the hair cells only being able to more front to back- alloing measurement of movment in 3D
The semiciruclar canals
measure head rotation (angular acceleration)
3 semicircular canaals on each side
Help sense all possible head rotations
each paired on opposite side of head
push-pull activation of vesibular axons (excitatory and inhibitory)
prolonged rotation will keep fluid in motion (dizziness-opposite direction- stop but fluid still deflecting hair cells sepite not moving)
The semiciruclar canals: Crista Ampullaris
capula (bubble) full of cilia found within an ampulla (buldge)
similar idea to macula, but principle of inertia
Endolymph reacts slowly to quick rotatioons which deflect the cupula (and cilia)
semicircular canals (how they work/sense angular acclearation)
at rest, the capula stands upright
-movement of the cupula during rotational acceleration and deceleration
-during rotational acceleration, endolynth moves inside the semicurcular canals in he direction opposite to the rotation (it lages behind the inertia). Endolymph flows bends the cupula and excites the hair cells.
-As rotational movement slows, endolymph keeps moving in the direction of the rotation, bending the cupula in the opposite direction from accelerating and inhibting the hair cells
Central vestibular pathways
Pathways of vestibular information and reflexes to control head, body and eye movement
1.Otolith organs + semicircular canals
2.Vestibulocochleat nerve (VIII)- vesibular nerve and choclear nerve (bipolar neurons)
3.Vestibular nuclei (Dorsolateral regions of medulla, integrate with other informatio- visual/motor)
4.sends out information above and below
central vestibular pathways sends information to
cerebellum, thalamus (VPN), extraocular motor neurons
central vestibular pathways- cerebellum
vestibular sensations needed for coordinating movements
central vestibular pathways- thalamus
ventral posterior nucleus
then projects to the post central gyrus
info received by the cortex maintains a represebtation of the body in space
central vestibular pathways- extraocular motor neurons
reflextive eye movement
primary goal: maintain gaze
central vestibular information sends information out to
limbs, neck and truck
central vestibular pathways- Limbs
reflexive limb movements (since doesnt go up to the cortex)
primary goal: keep body upright
central vestibular pathways- neck and trunk
reflexive neck/trunk movements
primary goal: keep head upright
The vestibulo-occular reflex (VOR): function
to fixate line of sight on visual target during head movment
The vestibulo-occular reflex (VOR): mechanism
senses rotation of head, commands compensatory meovment of eyes in opposite direction
chickens vs humans
chickens can heep head very still when body is moving around; very well developed neck motor control
this pathway is better in chickens vs humans since they have a worse vestibulo-occular reflex; therefore they must control their eye movment with their heads.
Vestibular connections mediating horizontal eye movements
eyes turn opposite way to head turn to compensate to maintain gaze
chickens are bad at this- anatomically dosen’t work great.
R and L semicircular canals work in opposites ( 1 inhibits-sends signals for muscles to relax while the other excites-sends excitatory signals so muscles contract)
Vestibualar cahnges with age: peripheral changes
likely occur first
otolith organs: loss of cilis, alterations of otocinia (size and shape)
Semicircular canals: loss of cilia, to a greater extent than the otolith organs, greater impact in VOR (vesibuloccular relfex) and fall risk; if slip, can’t reflex as quickly to maintain gaze.
Vestibualar cahnges with age: central changes
brain is plastic; therefore occurs later (after 60) compared to peripheral changes
vestibular neuclei- slow loss of neurons
cerebellum- slow loss or change in connectivity
what do vestibular changes with aging lead to?
toether, central and perioheral changes lead to reduction in sensory informaiton necessary to control head, eyes, and body and maintain balance
Add this to a multitude of changes to other sensory structures (vison, touch, proprioception) and loss of muscle strength= increased fall risk
** siginficant increase in those admitted to hospital after fall increases significantly after age 60.
Common vestibular pathologies: benign parasomal vertigo (BPPV)
benign: hramless in the long term
Paroxysmal: sudden onset/recurrence of symtoms (<60sec)
Vertigo: sensation of spinning/dizziness (vertigo itself is a symptom not an illness/conditon)
Caused by:
-Ear stones (otoconia) migrating into semicircular canals; disruping the cupula located in ampulla
Treatment:
-often resolves itself (as stones breakdown), specific head maneuvors can reposition debris out
Common vestibular pathologies: Vestibular Neuronitis
caused by: inflammation of the vestibular nerve
symtoms: sudden vertigo that can last for several days. Does NOT affect hearing (since its just the vestibular nerve)
Treatment:
Targets symptoms; anti-nausea medication until inflammation reduces, steroids to reduce inflammtion, physcial therapy/activity can help the body compensate by increasing functional capacity (training balance system to increase baseline).
Common vestibular pathologies: labyrinthitis
caused by: inflammation of the entire inner ear due to infection
symtoms:
sudden vertigo that can last for several days, does impact hearing (sensory also impacted)
treatement: treat infection, anti-nausea medication until inflammation reduces, physical therapy/activity can help body compensate
Common vestibular pathologies: Meniere’s disease
caused by: excessive fluid build up in inner ear, unknon why this occurs (autoimmune in nature)
symtoms:
Sudden episodes of: tinnitus, hearing loss, and or vertigo, each episode can leat minutes to hours, may occur in clusters, then subside for years.
Treatment:
No cure, managing symptoms. can lead to permantant hearing loss, but rare
mechanorepectors in the skin
most somatosensory repectors are mechanoreceptors- receptive to physcial distortion (causing deformation)
4 primary receptors in skin; vary in terms of: receptive feild (large;deeper vs small;more superficial) and adaptation (rapid vs slow)
4 primary mechanoreceptors in skin
pacinian corpuscles
meissner’s corpuscle
Ruffini endings
Merkel’s disks
Pacinian Corpuscles
largest and deepest machanoreceptor in skin
get compressed and detect pressure and vibration
large receptive feild, rapid adapting
react quickly to inital contact, but not sustained ontact
best at etecting finer textures and high frequency vibrations
Meissner’s Corpuscles
small receptors in upper dermis; common in fingers
detect fine toucj adn pressure
Small receptive feild, Rapid adapting
react quickly to inital contact, but not sustained contact
best at detecting heavier textures and lower frequency vibrations.
rapid adapting mechanoreceptors and vibrations
lower frequency vibration signal (contours/waves are further appart). Meissner’s corpuscles better at low frequency (heavier texutre) eg moving fingers across keys on keyboard
Higher freqeuncy vibration signal (contours/waves are closer together) pacinian corpuscles better at high frequency (finer texture) eg moving hand across the surface of a smooth table.
Ruffini endings
large receptors in the dermis layer
detect stretch and deformation
large receptive feild and slow adapting
react to sustained deformations; best at detecting grip/postion
Merkel’s disks
small receptors in epidermis, common in fingers
detect fnie touch and pressure
small receptive feild, slow adpating
react to sustained deformations, best at static discrimination of shapes/textures
two point discrimination
sensitivity to discriminate small pints caries greatly across the body
more sensitive in important places
accromplished by:
-greater density of mechanirecptors
-smaller feild size (2M’s meissner/Merkel)
-greater brain tissue devoted to tehse areas
barefoot runnig/walking
could barefoot walking/running be better than shod?
to imporve sensory info coming from feet (run/walk=fast adatpators)- barefoot= more signals to improve reaction, power, ect- but nee to cosnider that it also changes a lot of other things
Path to the brain; primary afferent axon
aka first order neuron (first point where sensory info comes in- sensor to spinal cord
enters spinal cord at dorsal root
cell bodies lie in dorsal root ganglion- pseudo unipolar neurons
4 types of primary affecrent axons
AA, AB, AD, C
AB mediates touch
various sizes of primary afferent axons
all A axons are myelinated (larger + myelinated= faster)
C’s are not myelinated (smaller and slower)
2 brances of AB
-directly ascending the spinal cord tot he brain (primary pathway)
-synapses with second-order sensory neuron (for reflexes)
most second order sensort neurons lie in the dorsal horn
Dorsal column-medial lemniscal pathway (DCML)
1.Ascending branch goes up the dorsal column
2.synapse in the dorsal column nuceli in medulla
3.Dorsal column nuclei axons decussate and ascend the medial lemiscus
4.synapse in the VP nucelus of the thalamus
5.Neurons in the Vp nucleus project to the somatosensory cortex
DCML= 3 neuron pathway with 3 synapse points required to reach S1; why are there synapses
these exisit for a reseaon other than simply passing info along
we can assume information is altered at each synapse
adjacent inputs can be inhibited o enhance tactile stimuli
segmentatal organizatinon of spinal cord
Dermatomes diagram- the distribution/mapping of spinal nerves
Herniated disks- clinical example of dermatomes
most common in 30-50s (~2% of adults)- juicy disks + beginign of instability
most common in the lower back (L4/5 and L5/S1-95% cases)
pain- back and leg (glutes, thigh, calf, even foot)
numbness or tingling
weakness
physical exam, imaging and or nerve tests for diagnosis
herniated disk treatment
1.Rest (2-4 weeks), physical therapy, pain medications; 85% resolve in 8-12 weeks
2.surgical- discectomy/microdiscetomy; conservative failed to resolve, progressive/debilittaing pain, numbness and weakness- hernated portion of the disk removed via surgical procedure
Dorsal colum- touch information; lateral inhibtion
-inhibit adjacent inputs to enhace tactile sensitivity
-increases contrast to allow for more precise/finer location of sensation
Dorsal colum- touch information; sensory gating
-corticothalmic feedback influences sensory processing
-cortex helps to filter irrelevant or repetitive information
-feel what you want to feel (emotions, focus and other sensory information impact how we perceive pain)
-complex pathways remain unclear
-may be related to cognitive discorders ie schizophrenia, ADHD
Somatosensory cortex; primary somatosensory cortex (3B)
prinary input for sensory info
How do we know 3b is the primary inpur site?
-recives input from VP nucleus
-highly response to somatosensory input
-Damage impairs sensation
-electrical stimulus creates sensations
Somatosensory cortex; Somatosensory 3a
dense thalamus input, but more body postion (vs just raw info)
Somatosensory cortex; somatosensory 1 & 2
receives information from 3b
geenrally realted to texture, size and shape
beging integrating info
Wilder penfeild
canadina neurosurgeon, lots of work wth mapping the somatosensory cortex (+ brain in general)–> related sensory info to specific regions
did lots of work with people with seizure disorders
posterior parietal cortex
allows for processing of basic sensory information and integration with other senses
* areas 5 and 7
Posterior parietal cortex 5
sensory (tactile) integration for the planning and organization of movment
Posterior parietal cortex 7
sensory integration for object recognition and spatial relationships (not visual)
Pain an nociception
nociceptiors: receptors of painful stimuli (dangerous or damaging stimuli)
-strong mehcanical stimulation, temperature extremes, oxygen deprivation, chemicals. een substances released by damaged cells (ie lactic acid, histamine)
nociception is not the same as pain
nociception= sensory process that provides signal that may trigger pain
pain= sore, aching, throbbing sensation we feel; can be infleunced by past experiences or other thigns going on
nociception can exist without pain
and pan can exist without nocicpetion
nocicpetors
free nerve endings which bring the sensation of pain to CNS
types of nociceptors:
-Mehcanical nociceptors- respond to damge such as cutting, crushing or pinching
-termal nociceptors: respond to temperature extrems
-chemical nociceptors: repsond to histamine and otehr chemicals
polymodal nociceptors: respond equally to all kinds of damaging stimuli (many)
Fast pain
nociceptor: mechanical and thermal
fiber: myelinated Ad fibers
pain: sharp, prickling sensation
Localiating: easily localized
Timing: Fast, occurs first
slow pain
nociceptor: polymodal
fiber: unmyelinated C fibers
pain: Dull, acheing, buring sensation
Localiating: poorly localized
Timing: Slow, occurs second and for longer time
Spinothalmic tract
to carry nociceptive info to brain
cell bodies in dorsal root ganglion
axon enter dorsal horn of spinal cord
1.Enter zone of lissauer (ascend or descend slightly in spinal cord)
2.synapse in the substantia gelatinosa (at top of dorsal horn)
3.second order neruons in the spinal cord immediately decussate
4.acsend to the brain n the ventrolateral lateral surfac of the spinal cord (up towards brain)
5.synapse with VP nucelus (and other areas) in the thalamus
6.Information then projected the somatosensory cortex
*but pain is complex and impacted by other things
General organization of major pathways
DCML: upper body tracts are more lateral, lower body tracts are more medial
Spinothalmic: Upper body tracts more deep, lower body tracts are more superficial
Pain regulation- Adfferent regulation; Gate control theory
pain can be reduced by activity of mechanorecptors
-neruons in the spinothalmic tract may be inhibited by Ab or Aa sensory nerves (touch) in the dorsal horn of the spinal cord
ie hit something and rub it, KT taping, TENS machines, foam rolling
Pain regulation- Descending regulation
brain can do powerful things when it comes to controlling pain.
Strong emotion, stress, ect can supress pain
Pain regulation- Descending regulation; periaqueductal gray matter (PAG)
- Receives input from many areas in the cortex (often emotional)
- Neurons descend to medulla (Raphe nuceli)
3.Neurons descend to spinal cord to depress activity (pain)
Hyperalgesia (primary and secondary)
Reduction in the pain threashold, increased sensitivity, or spontaneous pain
Primary hyperalgesia: super-sensitivity within the damaged area
Secondary hyperalgesia: super-sensitivity in the surrounding area
Primary changes occur peripherally:
inflammatin: bodies attempt to eliminate injury and stimulate healing
A variety of neurotransmitters, perptides, lipids ect. are released which can attatch to receptors in/around injury to lower their threashold for activation
hyperalgesia vs allodynia
allodynia is a similar concept, but pain response from stimuli that would normally not cuase pain
Central sensitization
Amplification of neural signaling (eg, nociceptive information) within the CNS that elicits pain hypersensitivity or even normal stimuli (allodynia)
-changes in the synapses and potentially the organization of interconnecting neurons may increase excitability/reducing inhibition of pain pathways
-contribuutions are difficult to identify and treatments difficult to target
Initially debated, but now an accpeted factor realted to: osteoarthritis and various MSK disorders, Fibromyalgia, other chronic pain conditions
Referred pain
cross talk between sensory neurons
convergence of visceral and somatic afferent neruons
shared dorsal root ganglion- if shared can get referred pain.
Temperature
thermorecetors:
-Varying sensitivites to hot anf cold temperatures
-cold (Ad and C fibers); exciting in response to cold and hot (C fibers); excite in response to hot– bot fast adapting
-Adapt to long durations of stimuli
Follow the same pathway as pain
Proprioception- concious proprioceptive information
-Dorsal coloumn medial lemniscus pathways to cortex
Proprioception- unconcious proprioceptive information
unconcious proprioceptive information (reflecive)
-Spinocerebella tracts- To cerebellum
-Spinal interneurons- Spinal reflexes
