Somatosensory System and Thalamus Flashcards
Touch pressure vibration receptors
Meissner’s corpuscle, pacinian corpuscle, ruffini corpuscles, merkel’s disks
Pain and temp reception
Free nerve ending
1a Fibers
1b
AB
2
Muscle spindle fibers
GTO fibers
Touch, proprioception
Spindle
Large diameter, heavy myelin, fast conducting.
Group III
AD
Group IV
C
Thin myelinated
Thin unmyelinated
Pain and temperature sense
DC-ML system senses
Proprioception, touch, vibration
Spinothalamic (anterolateral) tract
Pain and temp
Where does DC-ML ascend?
Ipsilaterally in the fasciculus gracilis, fasciculus cuneatus (above T6) to their respective nuclei. (1st synapse) Then decussate at medial lemniscus in medulla.
Where does the spinothalamic tract ascend
Enters 1-2 levels higher via Lissauer’s tract, (enters and synpases) then crosses immediately via ventral white commissure, then rises in the lateral spinothalamic tract to the thalamus.
Brown sequard syndrome
Hemisection of spinal cord leads to ipsilateral weakness/loss of touch and position, and contralateral reduction of pain/temp.
Mechanosensation from face
AB fibers from face (whose cell bodies live in trigeminal ganglion in pons) synapse in the principal sensory nucleus (pons), and ascend contralaterally in the medial lemniscus.
Pain/temp from face
AD and C fibers from face (whose cell bodies live in trigeminal ganglion in pons) descend to spinal nucleus of V, then synapse, cross and ascend in spinothalamic tract.
How is the DCML organized in the thalamus?
Legs lateral, trunk arm neck in VPL. Face medial in the VPM. Proportional representation, strong and faithful synapses.
How is spinothalamic system organized in the thalamus?
Very little somatotopic organization, little proportional representation, large receptive fields, no convergence of info.
Somatotopy in SI
Leg medial, Face lateral
Do AD and C fibers run with AB fibers to places in S1?
Yes. Just not as organized in the thalamus.
Areas 3a, 3b, 1 and 2 in S1
Sagitally anterior to posterior. 3A and 2 are proprioception. 3b and 1 are cutaneous. Pain and temp everywhere in S1. .
Where do DCMLs synapse in the cortex?
Layer 4 on stellate cells
Where to spinothalamic neurons synapse in the cortex?
Nowhere, run directly to pial layer.
S2
Second somatosensory cortex, organized face rostral, legs caudal. Receives bilateral input via fibers running through corpus callosum.
TRN
Thalamic reticular nucleus (Ventral Thalamus). Sheet of 100% gabaergic inhibitory neurons. Surrounds dorsal thalamus, sends axons only to dorsal thalamus relay neurons.
Draw the circuits from sensory inputs to Dorsal Thalamus and interaction with TRN and cortex
Do it!
What is the purpose of the TRN/Dorsal thalamus circuit?
Regulates states of consciousness
Awake EEG
Low voltage, high frequency
Spindle Waves
Stage 2 sleep, mid frequency
Delta Waves
Stage IV sleep, low frequency, synchronized oscillations. High amplitude
Oscillatory (burst) mode of relay cells
Cell hyperpolarized due to input from TRN. Hyperpolarization activated current activated, spike with Ca 2 influx, so depolarization happens. This then activates TRN neurons. Cycle repeats
Tonic mode of relay cells
During consciousness. Thalamic relay cell relatively depolarized because inputs from reticular activating system depolarize the membrane of relay cells.
Reticular activating system
Parabrachial nucleus, raphe, locus ceruleus, hypothalamus (produces histamine).
Thalamic syndrome
Damage to posterior thalamus (which includes VPL and VPM) causes hemianesthesia with excruciating central pain.
Tremor states
Rhythmic bursts in motor thalamus
Amnesia
Lesions of anterior/medial thalamus
Descending modulatory systems of pain
S1 -> PAG ->Raphe/LC/PBN -> Enkephalin inhibitory interneurons in dorsal horn -> Ad or C fibers which project back up to thalamus
What does activation of opiate receptors do?
Decreases duration of sensory neuron AP coming from periphery, so less released onto dorsal horn projection neurons.
Decreases EPSP, hyperpolarizes projection neuron.
Nociceptive pain
Physiological pain produced by noxious stimuli. Everything is correct
Gate theory
Light tough decreases pain because activates inhibitory interneuron that stops dorsal horn projection neuron from firing.
Inflammatory pain
Pain hypersensitivity due to peripheral inflammation. Pain with no stimulus. All stimuli more painful.
Allodynia
Normally non-painful stimulus is painful
Hyperalgesia
Normally painful stimulus is more painful.
Dysfunctional Pain
Neither protects nor supports healing/repair (fibromyalgia).
Neuropathic pain
Maladaptive plasticity cause by disease causes nociceptive processing. HUGE pain.
Central sensitization
Pain felt with enhanced synaptic signalling
