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53 > 3. Physio > Flashcards

3. Physio Flashcards

1
Q

does touch and pain signal travel separately?

A

yes

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2
Q

contralateral

A

Signals start from left body and ends at right cortex

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3
Q

Spinothalamic pathway is for…

A

pain pathway (start from spinal cord to thalamus)

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4
Q

describe spinothalamic pathway

A

pain efferent (1st order neuron) → enters spinal cord → synapse with 2nd order neuron in dorsal horn of spinal cord → cross over → travels in ventrolateral quadrant → thalamus → synapse to 3rd order neuron → somatosensory cortex

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5
Q

Dorsal column pathway is for…

A

touch pathway (start from dorsal column and synapse in the brain)

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6
Q

describe dorsal column pathway

A

touch afferent (1st order neuron) → moves up dorsal column → at medulla oblongata, synapse with 2nd order neuron → cross over → thalamus → synapse to 3rd order neuron → somatosensory cortex

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7
Q

4 principles underlying sensory processing

A
  1. The relay use action potential (AP) as signal to relay information
  2. The signal travels along topographic lines
  3. The signal travels along labeled line
  4. The signal along the relay encode for properties of the stimuli such as intensity
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8
Q

where is AP generated

A

axon hillock/ trigger zone

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9
Q

topographic lines

A
  • different population of afferents relay information from different region (hand afferent relay info from hand, feet afferent relay info from feet)
  • all relays remain separated, even in the cortex
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10
Q

where does sensory relays end

A

somatosensory cortex

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11
Q

how are neurons in somatosensory arranged

A
  • medial part (middle): receive signal from lower part of body
  • lateral part (towards the sides): receive signal from upper part of body
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12
Q

why does the face takes up a large portion of the somatosensory cortex

A

more sensitive, more neuron pathways

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13
Q

labeled line

A

receptor and primary afferent only respond to one type of stimulus (separation of signal starts from the receptors)

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14
Q

importance of labelled line

A

identification of modality (nature of stimulus), aka separate receptors for different stimuli
- touch receptor activated → Aß fibers → touch sensation
- pain receptor activated → Aδ and C fibers → pain sensation

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15
Q

increasing rate of electrical stimulation through touch will…

A

increase MAGNITUDE of touch sensation (will not cause pain)

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16
Q

The signal along the relay encode for properties of the stimuli such as intensity (meaning)

A

eg intensity: the more intense the stimulus, the more number of AP per unit time (frequency) = more intense sensation

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17
Q

frequency code

A

increase intensity of stimuli = increasing no. of AP per unit time

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18
Q

population coding

A

increase intensity of stimuli = increasing number of receptors activated/ excited

19
Q

quality of sensation is encoded by

A

labelled lines

20
Q

intensity of sensation is determined by

A

frequency and population code

21
Q

3 features of pain

A

individualised/subjective, intensity, unpleasant (emotion)

22
Q

Hyperalgesia

A

increased pain to a given noxious stimuli

23
Q

Allodynia

A

pain to a normally non-painful stimulus (eg pain to touch)

24
Q

Basis of pain pathophysiology - allodynia

A
  1. Change in spinal circuit (lack inhibition of spinothalamic pathway)
  2. Sensitisation (hyperexcitability of spinothalamic tract neuron by Aß fibers) of afferent and 2nd order neuron - due to release of chemicals at damaged site
25
Q

describe change in spinal circuit

A
  • Normally (no tissue damage): when there is a touch sensation, inhibition of spinothalamic neuron (pain) dominates excitation → no pain
  • After tissue damage = loss of inhibitory neuron, Aß fiber (touch) can excite spinothalamic neuron → feel pain when touch (allodynia)
26
Q

describe sensitisation

A

Sensitisation means that after tissue damage:
- potentiates (facilitates/ enhances) the response of pain pathway to a given noxious stimuli
- decreases the threshold for the excitation of pain pathway

27
Q

process of sensitisation

A
  1. Damage to the skin release chemicals (histamine, bradykinin, 5HT, prostaglandin, K+
  2. Chemicals cause nociceptor to be hyperexcited
  3. Hyperexcitability of the nociceptor cause changes.
  4. Sensitised nociceptor (1st order neuron) makes 2nd order neuron more sensitisable
28
Q

how does the released chemicals cause hyperexcitability of the nociceptor

A
  • increase no of TRPV1 receptors (nociceptor)
  • decrease threshold to excite TRPV1 receptors
  • Effect: make nociceptor more excitable (when noxious stimuli applied, more AP is generated) = sensitisation/ sensitised nociceptor
29
Q

how does the sensitised nociceptor makes 2nd order neuron more sensitisable

A

Excitatory NT (glutamate) released from sensitised nociceptor bind to NMDAR/AMPAR receptors (glutamate receptors) causing:

  1. excites 2nd order neuron
  2. sensitisation of 2nd order neuron (structural changes in 2nd order neuron) by:
  • increasing AMPAR on spinothalamic tract neuron
  • decreasing threshold to excite spinothalamic tract neuron through AMPAR receptors
30
Q

effect of sensitisation

A

in tissue damage, the whole system will be sensitised and the effect is multiplied several folds

31
Q

Pain modulation (modifying sensory relays)

A
  • Suppressed: pain may be decreased by regulating the signal along pain pathway (soldiers in battlefield do not feel much pain)
  • Enhanced: pain increased in anxiety
32
Q

how is pain modulated in the descending pathway

A
  1. Stress/ morphine/ expectation/ context →excite neurons in the periaqueductal gray (PAG, found in midbrain)
  2. Excited neurons in PAG → excites neurons in medulla (nucleus raphe magnus)
  3. Excited neurons in medulla → excites inhibitory neurons in spinal cord (interneuron)
33
Q

how does the inhibitory neuron inhibit pain

A

Inhibitory neurons inhibit the transfer of signal from 1st order neuron (nociceptor) to spinothalamic tract neuron by releasing enkephalin (inhibitory NT) into synaptic cleft

34
Q

enkephalin

A

an endogenous morphine-like substance → pain relief by inhibiting the transfer of signal from 1st order neuron (nociceptor) to spinothalamic tract neuron

35
Q

morphine

A

mimic effect of enkephalin in spinal cord to inhibit pain signal in spinal cord
- acts on the PAG neurons to activate descending pathway (PAG → NRM → spinal cord)

36
Q

Segmental modulation (Gate theory)

A

stimulation of large diameter afferents (Aß fibers for touch) excite inhibitory interneurons → decrease transmission of pain signal in spinal cord

37
Q

cortex is important for what motor behaviour

A

important for voluntary movement

38
Q

brain stem is important for what motor behaviour

A

important for rhythmic motor patterns

39
Q

why spinal cord is important for motor behaviour

A

contains efferent fibers to control motor behaviour. Loss/ damage of efferent causes flaccid paralysis

40
Q

how do cortex/brainstem influence movement?

A
  • via efferent neurons that send long axons from site of origin to spinal cord (descending control of efferent)
  • cortex → brainstem → efferent (found in ventral horn)
41
Q

importance of cerebellum

A

indirectly coordinate movement by adjusting output of efferent from cortex/brainstem

42
Q

damaged to cerebellum

A

Lesion in cerebellum disrupt coordination of limb and eye movement, impair balance, decrease muscle tone

43
Q

function of basal ganglia (a cluster of neurons) - a combination of structures in the brain

A

initiation of movement, selection of motor program

44
Q

damaged to basal ganglia

A
  • disorder of movement: tremor at rest, rapid flicking movement, violent flailing movement, slow writhing/twisting, bradykinesia (slow movement & speed with progressive halts)
  • disorder of posture: rigidity

eg Parkinson’s disease - marked by tremor, rigidity, bradykinesia

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