IC3

Question 1

spinothalamic tract

Answer 1

on tissue damage
receptors activated > primary afferent (1st order neuron) > AP movement through 1st order neuron to 2nd order neuron > spinal cord > dorsal horn (grey matter of spinal cord) > medulla > thalamus > AP received at somatosensory cortex

Question 2

movement of AP for pain vs touch

Answer 2

pain:
- first-order afferent > second order in the dorsal horn > cross to the opposite side (left to right) > ventrolateral quadrant > thalamus > somatosensory

touch: first-order afferent > second order in dorsal horn > dorsal column (left side) > medulla > long axon crosses to the right side > thalamus > somatosensory

damage to one side might not affect both sensations

Question 3

contralateral somatosensory cortex

Answer 3

signal starts on the left and ends on the right.

Question 4

principles underlying sensory processing?

Answer 4

1) relay uses AP as signal to relay information

2) signal travels along topographic lines
- each region have their own set of afferent relays
- relays remain separate even in the cortex (occupy different spaces in the somatosensory cortex, ie somatosensory HOMUNCULUS)

3) signal only travels along labelled line IE only responds to one type of stimulus

4) signal along relay encode for properties of the stimuli
- intensity: more intense = higher frequency of AP

Question 5

touch allodynia definition

Answer 5

pain due to a stimulus which does not normally provoke pain (PAIN TO A NORMALLY NON PAINFUL STIMULUS)

due to nerve damage altering the characteristics of the pain pathway.

involves sensitisation

Question 6

define sensitisation

Answer 6

potentiates response of pain pathway to a given noxious stimuli AND decreases threshold for excitation of the pain pathway.

peripheral vs central sensitisation:
peripheral involves first order

central involves second order neurons in the eg spinal cord.

Question 7

receptors activated by innocuous pressure (touch)

Answer 7

merkel cell
meissner corpuscle
pacinian corpuscle
ruffini ending

Question 8

what is hyperalgesia

Answer 8

increased pain to a given noxious stimulus.

(pain sensation)

Question 9

pathophysiology of pain in allodynia

Answer 9

side branch of A beta fibre that enters the spinal cord and (i) makes a synapse on an inhibitory neuron inhibiting the spinothalamic tract AND (ii) direct synapse with the spinothalamic tract directly exciting it.

usually, the inhibition dominates, but scenarios
A) loss of inhibitory neuron
B) hyperexcitability/sensitisation due to the release of various chemicals at the damaged site = second order neuron also becomes hyperexcitable AND DOMINATES OVER INHIBITION

= direct sensitisation of the spinothalamic tract and incite pain.

Question 10

how does sensitisation work in pathophysiology? state chemicals

Answer 10

chemicals released by injury
causes sensitisation of nociceptors
- decreased threshold to stimulus
- increased response to stimulus

chemicals include CGRP, glutamate, substance P…

receptors eg AMPAR, NMDAR of the spinothalamic tract…

Question 11

examples of allodynia

Answer 11

sunburnt
sprained ankle
neuropathy
surgery

Question 12

describe descending pain modulation

Answer 12

morphine, stress, etc
excites neurons in the midbrain periaqueductal gray (PAQ) > signal to nucleus raphe magnus in the medulla > interneuron in spinal cord > inhibits the transfer of signal to spinothalamic neuron (thus blocking the pain).

Question 13

what is enkephalin

Answer 13

inhibitory neuron released at the synapse between the 1st order neuron and the spinothalamic tract neurone = block transfer of signal.

it is an endogenous morphine-like substance

Question 14

mechanism of action of morphine

Answer 14

• act on PAQ neurons
• mimic spinal cord enkaphalin

Question 15

describe segmental modulation in pain modulation

Answer 15

stimulation of large diameter afferents (for touch) excites inhibitory interneuron = decreased transmission of pain signal in the spinal cord.

Question 16

hierarchal features of motor control

Answer 16

cortex = voluntary movement

brainstem = postural reflexes, rhythmic motor patterns

(cortex and brainstem send LONG DESCENDING AXONS to the spinal cord)

spinal cord = site of motor neurons and control of muscle activity

loss of output = flaccid paralysis (muscles lose tone), final common pathway (lower motor neurons)

Question 17

pathway of long neurons in motor behaviour

Answer 17

corticospinal pathway

brainstem pathway

Question 18

damage of cerebellum and effect

Answer 18

involved in coordinating movement

lesions disrupt the coordination of limb and eye movement, impair balance, and decrease muscle tone.

Question 19

effect of basal ganglia and interaction with cortex

Answer 19

basal ganglia involved in initiation of movement and selection of motor program

neurons in basal ganglia = dopamine neurons.

degeneration = parkinsons disease = movement start slow/wrong choice of movement

= disorder of movement (tremor, flicking/chorea, flailing, twisting, bradykinesia) and disorder of posture (rigidity).

Question 20

representation of receptors for somatosensation

Answer 20

higher representation (higher density) of the face than the trunk

relay from the face region is more extensive than from the trunk.

= leads to a more precise sensory experience

Question 21

mechanism of paracetamol in relation to CNS

Answer 21

antagonism of TRPV receptors esp in the spinal cord.

Question 22

intensity encoding depends on two coding?

Answer 22

1) frequency code: intensity of stimulus correlates with the number of AP evoked in labelled line

2) population code: intensity of stimulus correlated with number of reeptors excited