Test 2- Sensory CC Flashcards
Kinesthesia
positional awareness info via proprioceptive receptors in muscles.
Proprioceptive receptors in muscles
A-alpha fibers dynamic/stable nuclear bag fibers, golgi tendon organ
Stereognosis
ability to recognize 3D object from texture, size and spatial sensory modalities.
Agnosia
loss of ability to recognize certain sensory modalities. Ex: prosopagnosia- facial recognition lost–damage to fusiform gyrus
What are some trigeminal reflexes?
- Corneal
- Jaw jerk
- Tearing
- Oculocardiac
- **STILL NEED TO ADD SNEEZE REFLEX!**
Corneal
Afferent: Ophthalmic N.
Efferent: CN VII parasympathetic fibers
Corneal
Afferent: Ophthalmic nerve (V1)
Efferent: CN VII to close eyes (orbicularis oculi?)
**Oculocardiac reflex **
Afferent: Opthalmic (V1)
Efferent: Vagus nerve activates PNS (parasympethetics)
**I push on my eyes during tests, now I know why!**
Jaw jerk reflex
Afferent: mesencephalic nucleus has cell bodies of fibers innervating muscle spindles
Efferent: Motor V3 to muscles of mastication to elevate jaw
Complex regional pain syndrome
Chronic pain from increased sensitization to pain within the body due to peripheral nerve damage.
Causes of complex regional pain syndrome?
allodynia, hyperesthesia, increased dendritic spine densitiy, sprouting fibers, glutamate storms, permanent activation of C-fibers
allodynia
lowered stimulus threshold for A-delta fibers. This makes non-painful stimuli painful.
hyperesthesia
lowered stimulus for C-fibers
Most common manifestation of complex regional pain syndrome?
back pain
What happens if there is less input from raphespinal to spinal cord?
pain.
Prostaglandins and pain? treatment?
Prostaglandins usually bind nociceptor receptor= pain.
NSAIDS block COX2 in macrophages and neutrophils = less PG= less pain
Inhibition of capsaicin receptor
Another treatment for pain: inhibition of pain-causing voltage gated sodium channels that respond to inflammation and heat.
Bradykinin Receptor Inhibitor
Pain treatment: Bradykinin is released by leukocytes and binds nociceptor terminal membrane to cause pain. Inhibition= treatment
Gabapentin (aka?)
AKA neurontin- pain drug blocks CALCIUM CHANNELS on nociceptor to prevent neurotransmitter release in the spinal cord.
Symptoms:
- ipsilateral loss of fine touch, vibration and proprioception at and below level of lesion
- contralateral loss of pain and temp below lesion
- IPSilateral paralysis of limbs below/at lesion
_Where is the lesion? What can cause it? _
Lesion an entire half of the spinal cord (ant+post).
Hemisection of spinal cord= Brown Sequard syndrome
Patient has **WIDE STANCE, sensory ataxia, loss of tendon reflex, loss of proprioception in extremity. **
Past medical Hx: Syphillis, but the patient decided he didnt wanna take the meds anymore.
- Where is the lesion? What is this condition called?
- What is a common cause?
- **Posterior column degeneration from demyelention. **Tabes Dorsalis
- Treponema pallidum (I think this must be what causes syphilis). Anyway, an untreated infection causes syphilitic myelopathy
**WIDE STANCE **is because of poor coordination. Probably a hallmark/buzzword.
Why is this dude standing all wide?
Syphilis killed his posterior column = sensory ataxia
Posterior column blood supply
posterior spinal a. (occlusion= loss of post column)
Ischemia to thalamogeniculate a?
- Branch of what artery?
- Area affected
- Symptoms
- Branch of Posterior cerebral.
- VPM and VPL affected.
- Loss of fine touch touch to contralateral body and head.
Function of area 1 of primary somatosensory cortex
- Texture discrimination
- Works with 3B for discrimination of moving stimuli
Area 2-Primary somatosensory cortex function
- Shape and size discrimination
- receptive for palpation of objects (shape and curvature)
It’s dark and you’re holding a penis, but for some reason you can’t figure out it’s size or shape (is it curved?!) But, you can tell it doesn’t have bumps on it, so that’s a relief.
- What is this called?
- **Damage where? **
- Asterognosis= loss of shape discrimination
- damage to area 2 primary sensory cortex
Area 3B primary somatosensory cortex lesion
Texture, size, and shape lost Basically 3B is needed to process stuff from 1 and 2.
HOLY F#*$! THIS LEG ISN’T MINE!
You probably have a lesion to the PARIETAL ASSOCIATION CORTEX on the contralateral side of the scarey limb. Loss of contralateral body from body map
Phantom limb and chronic pain?
related to platicity. Brain decides it doesnt want to waste space on something that isn’t there. It makes adjacent “areas” larger.
Old man got his leg cut off. What’s his brain about to do?
Nothing. Old people have less plasticity. Ha (walker!)
You also start to lose high frequency sounds when you get old!!! (according to today’s lecture)
Also, thymus gets smaller (immuno). Seems like most things do….
Friedreich Ataxia
Can you see a “Friedreich” playing any sports? nope- i had a Fritz in my high school…lmao thinking about it.
Degeneration of spinocereballar tract= lack of coordination during walking or other movements. Cerebellar inputs not regulating movements.
Symptoms range from numbness, paresthesia, hypesthesi to complete anesthesia (no pain). Where is the lesion?
ALS lesion
Primary hyperalgesia
(In contrast to secondary hyperalgesia)
Pain occurs in the region of damaged skin and is probably from **receptor sensitization. **
Secondary hyperalgesia
(in contrast to primary hyperalgesia)
Increased pain that occurs in the skin immediately around the damaged tissue. Usually involves a central component. (ex: Spinal)
What can cause peripheral sensitization?
Irritating chemicals (capsaicin), inflammatory mediators (bradykinin, prostaglandins), neurotransmitters (serotonin, histamine, norepinephrine) released by damaged tissue.
Central sensitization (this is a doozy)
Tonic input from A-delta and C fibers= increased receptive field of posterior horn neurons= increased response to stimuli, decreased threshold (allodynia= a-delta; hyperesthesia=C fibers), AND activation in response to new inputs.
**A delta is slightly more myelinated than C**
Receptors providing muscle pain sensation from excessive stretch or contraction?
III (a-delta) and IV **(C) **afferents
Muscle injury/ischemia can cause pain by?
releasing algesic compounds that stimulate group IV (C) receptors= pain
Anoxia - what is it? what fibers are at risk?
Low O2 affects large fibers diameter fibers first does NOT= A-delta and C fibers!!
DCML system is affected first!= fine touch, vibration, proprioception.
**mimi this was wrong the first time**
Anesthetics work on ___ fibers by ___.
small. Block sodium channels. So I’m guessing A-delta and group C fibers.
Why might someone STILL have pain after a posterior horn rhizotomy?
Remember- post horn rhizotomy is cutting everything back there (dorsal root). Some C fibers enter the spinal cord via the ANTERIOR horn (tricky bastards) so they’re causing the pain.
Dermatomes to know
- index finger
- Nipps
- bellybutton
- pelvic rim
- big toe
- anus/genitals
- index fiber= C7
- Border of nipple= T4/T5
- Navel= T10
- Pelvic rim= L1
- Big toe= L5
- Genitals/Anus= S4,5.
Postherpetic neuralgia is considered
neuropathic pain
Test for ALS fx
poke them and see if it hurts. compare distal vs. proximal and right vs. left.
Diabetes patients have this type of sensory loss
STOCKING GLOVE sensory loss starts distally (bad circulation…wonder if this could happen to me since my toes-ies are always cold?)
Patchy loss of pain, temp, crude touch on one side of the body. Where is the lesion?
**ALS ischemia= **arterial vasocorona and _sulcal branches of anterior spinal artery _
Lesion would be in contralateral ALS 2 levels below loss of function
- Loss of pain, temperature and crude touch beginning at the UE and moving down.
- Loss of pain, temperature and crude touch beginning at LE and moving upward.
- Intramedullary tumor compressing medial ALS to lateral ALS. Sx: Upper extremity loss followed by lower.
- Extramedullary tumor compressing ALS from lateral to medial. Sx: loss of lower extremity first, then upper.
**MIMI I CHANGED THIS, THEY WERE SWITCHED**
DCML test
- 2 point discrimination (start wide, get smaller until they can’t tell its two points anymore)
- tuning fork to test vibration (vibration= buzzing sensation)
Loss of pain temperature and crude touch in a cape distribution. BILATERAL.
- Where is the lesion
- **What might cause this lesion? **
- Damage to **Anterior white commissure **
- Syringomyelia- Cystic cavitation of central region of spinal cord
- What is **dissociated sensory loss? **
- How does this happen?
- Loss of fine touch and vibration, but pain and temperature still working.
- Lesion has to be in LOWER BRAINSTEM before the two systems come together.
Only SX: Loss of pain/temp/crude touch on contralateral side.
- Where is the lesion
- What artery supplies this area?
DISSOCIATED PAIN LOSS
- MEDULLA ALS! The two sensory systems move closer together in the pons.
- Depends on the exact level of the medulla. **Lower medulla= verterbal a. Upper= PICA. **
SX: Loss of CONTRALATERAL vibration, proprioception and fine touch ONLY.
- Where is the lesion
- What artery supplies this?
- What if it was ipsilateral?
- **Medulla ML **system (above decussation)
- Mostly anterior spinal artery. In upper medulla= **vertebral a. **
- Ipsilateral= dorsal columns in spinal cord
What fibers contribute to “dull aching pain”
Ex?
C fibers. Ex: Pulp inflammation (in your tooth area, I guess)
Dull people get C’s in high school
What fibers contribute to “sharp” pain? Ex?
**A-delta fibers. **Dental hypersensitivity
Sharp people got A’s in HS.
Headaches from CN V?
I guess the meninges are a theory for initiation of headaches. They’re supplied by CNV.
Occlusion of an artery caused loss of ALL sensations from the contralateral side of the body. The blockage was removed. What’s the order that sensations come back? (not location, but function).
PAIN!!! ==>crude touch ==> thermal ==> DCML
DCML might never come back.
Where should the clot go to:
- Paralyze and remove sensation from LE and trunk?
- UE and face?
- Trunk and LE = ACA
- UE and face= MCA
What part of the brain causes PAIN?
Primary somatosensory cortex=**neospinothalamic **
What causes SUFFERING?
**PALEOSPINOTHALAMIC= **hypothalamus and limbic system (via reticular formation and periaqueductal gray)
What do Valium users report?
No suffering, but pain is still there.
Deep brain stimulation
Treatment for chronic or deafferentiated pain. Stimulus is applied to somatosensory thalamus, centromedian-parafascicular complex or PAG to activate neurons in the pain matrix to modulate painful sensation. stimulation-induced analgesia.
Sounds like they’re desensitizing it with repeated stimulation.
Stimulation of the somatosensory thalamus may also activate pain modulation circuits that involve _________.
**Thalamocortical thermal pathways. **
Why might you have pain from visual, auditory or olfactory stimuli following CNS lesions?
**Central Pain syndrome **
A lesion of the ALS in the thalamus or below can result in a plasticity in the cortex that causes pain from other stimuli. The book says the method isn’t super well known. **Deafferentiation phenomenon= **removeal of primary afferent influence on central neurons results in formation of new and innapropriate connections.
Treatment for central pain syndrome
- Analgesiscs don’t work. They’ve tried some antidepressants and anti-epileptic drugs that maybe kind of work.
- Temporary relief from these methods. Nothing longterm
- Transcutanous electrical nerve stimulation (TENS) or stimulation of posterior columns
- Chronic stimulation of PAG, PVG with deep brain stimulation
- They also tried removing lots of shit like ALS, trigeminal tract, thalamus, cortical ablation….
Referred pain
We know what this is. Visceral pain activates somatic pain. Look at a pic to make sure you remember where it all is.
Cerebellar ataxia can have lots of different symptoms.
**What is it called when you cant time movements? **
DysRHYTHMIA
You reach out for your water bottle and accidentally hit the furry friend standing BEHIND IT.
OR
You try to pick up the remote and miss.
dysMETRIA
Inability to judge distances. Hypermetria (ex 1) or Hypometria (Ex 2)= overshoot and undershoot movements.
You walk all wide stanced like you just peed yourself. Do you remember what this is characteristic of?
**TRUNCAL ataxia. **
(it was called sensory ataxia earlier, donno if they’re the same? but damage to posterior column)
Nystagmus
Eye can’t keep up with moving objects. Cause dby **lack of vestibular input to cerebellum **(I’d expect it would go both ways? blockage of cerebellar ouput too?)
Mimi, you were on a run and you ran into a tree. What happened?
Vestibulo-ocular reflex impairment
compensatory eye movement to keep eyes focused on stuff while you’re moving.
**SX: What structure is affected with each sx? Where is the lesion? and what are other names for this condition? **
- Ipsilateral loss of sensation to face,
- contralateral loss of pain/temp to body
- Nausea, vomitting
- Hoarseness, dysphagia, uvular deviation
- Ataxia
Lateral MEDULLARY syndrome. PICA syndrome
- Spinal trigeminal tract
- ALS
- Vestibular nuclei
- Nucleus accumbens
- Restiform body
