Somatosensory System and Thalamus Flashcards

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1
Q

Touch pressure vibration receptors

A

Meissner’s corpuscle, pacinian corpuscle, ruffini corpuscles, merkel’s disks

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2
Q

Pain and temp reception

A

Free nerve ending

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3
Q

1a Fibers
1b

AB

2

A

Muscle spindle fibers
GTO fibers

Touch, proprioception

Spindle

Large diameter, heavy myelin, fast conducting.

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4
Q

Group III
AD

Group IV
C

A

Thin myelinated

Thin unmyelinated

Pain and temperature sense

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5
Q

DC-ML system senses

A

Proprioception, touch, vibration

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6
Q

Spinothalamic (anterolateral) tract

A

Pain and temp

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7
Q

Where does DC-ML ascend?

A

Ipsilaterally in the fasciculus gracilis, fasciculus cuneatus (above T6) to their respective nuclei. (1st synapse) Then decussate at medial lemniscus in medulla.

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8
Q

Where does the spinothalamic tract ascend

A

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.

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9
Q

Brown sequard syndrome

A

Hemisection of spinal cord leads to ipsilateral weakness/loss of touch and position, and contralateral reduction of pain/temp.

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10
Q

Mechanosensation from face

A

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.

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11
Q

Pain/temp from face

A

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.

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12
Q

How is the DCML organized in the thalamus?

A

Legs lateral, trunk arm neck in VPL. Face medial in the VPM. Proportional representation, strong and faithful synapses.

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13
Q

How is spinothalamic system organized in the thalamus?

A

Very little somatotopic organization, little proportional representation, large receptive fields, no convergence of info.

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14
Q

Somatotopy in SI

A

Leg medial, Face lateral

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15
Q

Do AD and C fibers run with AB fibers to places in S1?

A

Yes. Just not as organized in the thalamus.

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16
Q

Areas 3a, 3b, 1 and 2 in S1

A

Sagitally anterior to posterior. 3A and 2 are proprioception. 3b and 1 are cutaneous. Pain and temp everywhere in S1. .

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17
Q

Where do DCMLs synapse in the cortex?

A

Layer 4 on stellate cells

18
Q

Where to spinothalamic neurons synapse in the cortex?

A

Nowhere, run directly to pial layer.

19
Q

S2

A

Second somatosensory cortex, organized face rostral, legs caudal. Receives bilateral input via fibers running through corpus callosum.

20
Q

TRN

A

Thalamic reticular nucleus (Ventral Thalamus). Sheet of 100% gabaergic inhibitory neurons. Surrounds dorsal thalamus, sends axons only to dorsal thalamus relay neurons.

21
Q

Draw the circuits from sensory inputs to Dorsal Thalamus and interaction with TRN and cortex

A

Do it!

22
Q

What is the purpose of the TRN/Dorsal thalamus circuit?

A

Regulates states of consciousness

23
Q

Awake EEG

A

Low voltage, high frequency

24
Q

Spindle Waves

A

Stage 2 sleep, mid frequency

25
Q

Delta Waves

A

Stage IV sleep, low frequency, synchronized oscillations. High amplitude

26
Q

Oscillatory (burst) mode of relay cells

A

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

27
Q

Tonic mode of relay cells

A

During consciousness. Thalamic relay cell relatively depolarized because inputs from reticular activating system depolarize the membrane of relay cells.

28
Q

Reticular activating system

A

Parabrachial nucleus, raphe, locus ceruleus, hypothalamus (produces histamine).

29
Q

Thalamic syndrome

A

Damage to posterior thalamus (which includes VPL and VPM) causes hemianesthesia with excruciating central pain.

30
Q

Tremor states

A

Rhythmic bursts in motor thalamus

31
Q

Amnesia

A

Lesions of anterior/medial thalamus

32
Q

Descending modulatory systems of pain

A

S1 -> PAG ->Raphe/LC/PBN -> Enkephalin inhibitory interneurons in dorsal horn -> Ad or C fibers which project back up to thalamus

33
Q

What does activation of opiate receptors do?

A

Decreases duration of sensory neuron AP coming from periphery, so less released onto dorsal horn projection neurons.
Decreases EPSP, hyperpolarizes projection neuron.

34
Q

Nociceptive pain

A

Physiological pain produced by noxious stimuli. Everything is correct

35
Q

Gate theory

A

Light tough decreases pain because activates inhibitory interneuron that stops dorsal horn projection neuron from firing.

36
Q

Inflammatory pain

A

Pain hypersensitivity due to peripheral inflammation. Pain with no stimulus. All stimuli more painful.

37
Q

Allodynia

A

Normally non-painful stimulus is painful

38
Q

Hyperalgesia

A

Normally painful stimulus is more painful.

39
Q

Dysfunctional Pain

A

Neither protects nor supports healing/repair (fibromyalgia).

40
Q

Neuropathic pain

A

Maladaptive plasticity cause by disease causes nociceptive processing. HUGE pain.

41
Q

Central sensitization

A

Pain felt with enhanced synaptic signalling