Lecture 15: Somatosensory Flashcards
Do cells in the DRG have dendrites? Peripheral process becomes…Centrally directed process becomes…
No; spinal nerve; dorsal root
2 submodalities
Touch, pressure, vibration & position and movement; pain and temperature
Accessory structures for touch, pressure, vibration (4)
Meissner (light pressure, sensitive), Pacinian (pick up high frequency vibration, sensitive) and Ruffin’s corpuscles (pressure), Merkel’s disks
Accessory structures for position and movement
Muscle spindle (within skeletal muscle, encodes length) and Golgi tendon organ (encodes tension/stretch at tendon junction)
Pain and temperature use…
Free nerve endings (no myelin); will encode some crude touch
Four principles of encoding
- Each neuron encodes one type of stimulus; 2. Increase in intensity w/ increase in frequency of APs and eventual increase in # axons recruited; 3. Variations in adaption (slowly vs rapidly adapting –> fires AP at onset and offset of stimulus); 4. Receptive fields and perception acuity
About how much overlap in dermatome map vs sensor receptive fields. Same for pain?
50%; no, pain is less overlapped
Order the muscle axons. Which is totally unmyelinated?
Group 1a (primary muscle spindle) –> 1b (Golgi tendon organ) –> II (secondary muscle spindle) –> III and IV (pain and temperature); Group IV
Order the cutaneous axons. Which is totally unmyelinated?
AB (touch, pressure) –> Ad and C (pain, temperature, crude touch); C
What are the two major ascending systems and what do they carry?
- DC-ML (mechanosensation; touch, pressure, vibration = AB; position and movement = Group I, II); 2. Spinothalamic (anterolateral) system (pain and temperature, crude touch = Ad, C; Group III, IV)
F. gracilis where? F. cuneatus where? Significance. What’s above the facilicus? What happens here? What’s the new tract? Where does it travel?
All levels; T6 and above; axons entering above T6 travel on f. cuneatus; the nucleus cuneatus/gracilis; SYNAPSE and then the “great sensory decussation” (arcuate fibers); medial leminscus; thalamus
Do all neurons ascend?
No! Some synapse at the level of the spinal cord (reflexes, cerebellum)
What size of fibers take the lateral route?
Smaller fibers
Lissaurer’s tract and assoicated
Ipsilateral 2-5 segments of bifurcated tract in spinal cord (from Spinothalamic neurons) where synapsing b/t axons and dorsal horn neurons occurs
Where is the first synapse in the Spinothalamic tract? Then what?
In the spinal cord; secondary or tertiary neuron crosses the ventral white commissure to form lateral spinothalamic tract
What are the three distinctions?
- First synapse; 2. Location of decussation
Brown-Sequard Syndrome
Hemi-section of spinal cord. Above lesion: intact; Below lesion: DC-ML on ipsilateral side; Spinothalamic on contralateral side
Syringomyelia can cause…
Bilateral, segmental loss of pain and temperature just at the level of the lesion
Somatotropic organization of spinal cord, medulla, pons, midbrain
Spinal cord (medial –> lateral) organized leg, lower trunk, upper trunk, neck; Mid-medulla (dorsal –> ventral) N, A, T, L; Pons (medial –> lateral) F, N, A, T, L; Midbrain (ventral –> dorsal) L, T, A, N, F
Second order axons from principal sensory nucleus do what?
Decussate and then join medial lemniscus via trigeminal thalamic tract
Primary neurons headed to the spinal nucleus of V do what? Then what?
Travel downward via spinal tract of V; decussate and join SPINOTHALAMIC tract
Mesencephalic nucleus recieves what kind of information? Where are the primary cell bodies? What happens?
Proprioception (Group I, II); within mesencephalic nucleus; Secondary process (still primary cell) sends projections to the motor nucleus of V (jaw jerk reflex)
Trigeminal: medullary lesion
Ipsilateral pain and temperature deficits (mostly)
Trigeminal: pontine lesion
Ipsilateral touch, pressure, proprioception (muscles of mastication); damage to Vm motorneurons (areflexia); deficits in pain and temperature (ipsilateral if V root affected, contralateral if broad lesion affecting spinothalamic)
Trigeminal: above brainstem lesion
All sensory modalities contralateral; motor responses (Vm) not affected because bilaterally innervated
Ventral posterior lateral (VPL)
Receives input coming from dorsal column nuclei (medial lemniscal axons)
Ventral posterior medial (VPM)
Receives input coming from Principal trigeminal nucleus (face)
Somatotropic orgaization of DC-ML system in thalamus
Lateral –> medial: L T A N F (with lips, fingers, toes down)
VPL and VPM cell bodies are ipsi or contralateral?
CONTRALATERAL
T/F: Do we find proportional or disproportional representations of sensation in the VPL/VPM nuclei?
Disproportional
Is place/submodality retained at the level of the thalamus?
Yes for DC-ML but NOT for Spinothalamic (large, promiscuous receptive fields)
Is the cortex ipsi or contralateral? How about proportional representation? How is the body arranged?
Contral; homunculus; (dorsal –> ventral) L T A F
What structure do the axons from the VPM/VPL thalamus project through?
Internal capsule
What are the four separate functional areas of S1? Information.
3a, 3b, 1, 2; proprioception (Group I, II) to 3a and 2; cutaneous (AB) to 3b and 1; pain and temperature to ALL fields of S1
Discuss S1 lesions
3b: all tactile cutaneous information; 1/2: partial deficit in discrimination of texture, size, shape; 3a/2: proprioceptive
Cortex structure relationship to leminscal/spinothalamic projections
Layer IV: lemniscal; Layer I: spinothalamic
What information does S2 get? What is special/different about S2? What does destruction lead to?
Branched axons from thalamic relay neurons headed toward S1; only single representation of information; (anterior –> posterior) E A T L; representation is BILATERAL via fiber tracts from the CC; loss of interhemispheric transfer of info and permanent impairment in object discrimination on basis of size, texture
