Neurophysiology of nociception Flashcards Preview

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Flashcards in Neurophysiology of nociception Deck (58)
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1
Q

Define pain

A

Unpleasant sensory and emotional experience associated with actual or potential tissues damage

2
Q

Define nociception

A

Mechanism that provide notice of potential noxious substance/stimuli or injury

The mechanism that provides the notice of pain

3
Q

Define ganglion

A

An encapsulated neural structure containing a collection of neuronal cell bodies

4
Q

Define afferent nerve

A

Sensory nerve conveying signals from receptor to CNS

5
Q

Define efferent nerve

A

Motor nerve conveying signals from CNS to effector

6
Q

What nerve provides the majority of sensory innervation to the face?

A

Trigeminal nerve (CN 5)

7
Q

What is the only feature of the face in which the trigeminal nerve does not provide sensory innervation?
What is this supplied by?

A

Angle of the mandible

Upper cervical nerves

8
Q

What are the 3 branches of the trigeminal nerve?

A

Opthalmic, maxillary, mandibular

9
Q

How is the mandibular division of the trigeminal nerve divided?

A

Anterior and posterior

10
Q

What is the function of the thalamus?

A

Processes and relays sensory information to varying parts of the brain

11
Q

What part of the brain is responsible for memory, language skills, consciousness and governing of voluntary control?

A

Cerebral cortex

12
Q

What is the function fo the cerebral cortex?

A

Responsible for memory, language, consciousness and governing of voluntary control

13
Q

What are algogenic substances?

A

Substances released after tissue damage associated with pain, the brain interpreters these as pain

14
Q

Name 2 algognenic substances that can be inhibited by analgesics

A

Substance P

Prostaglandin

15
Q

What detects algogenic substances?

A

Nociceptors

16
Q

What are nociceptors?

A

Receptors on a neurone that detect the actual/potential noxious stimuli

17
Q

What kind of stimuli can nociceptors respond to?

A

Chemical, thermal or mechanical

18
Q

Name the 2 main types of nociceptive axons (fibres)

A

A delta

C fibres

19
Q

What are the difference between A delta and C fibres

a) speed
b) myelination
c) stimuli they respond to
d) type of pain
e) location in the tooth
f) diagnosis of tooth depending on pain they feel

A
a) a delta = fast (act first)
C = slower
b) A delta = myelinated, C = unmyelinated
c) a delta = mechanical 
C = mechanical, thermal and chemical
d) A delta = short sharp
C = dull ache
e) A delta = periphery of pulp
C = centre of pulp
f) A delta = reversibel pulpitis
C = irreversibel pulpitis
20
Q

Algogenic substances are released and stimulate nociceptors on A delta or C fibres, where are these nociceptors found (in terms of facial pain)?

A

Trigeminal ganglion

21
Q

Algogenic substances are released and stimulate …… on ……. or …….. fibres.

A

Nociceptors
A delta
C

22
Q

From the trigeminal ganglion, where are pain signals transmitted?

A

Brianstem

23
Q

Via what pathway are pain signals transmitted from trigeminal ganglion to brainstem?

A

Sensory root

24
Q

What part of the brainstem do the pain signals from the trigeminal ganglion enter?

A

Pons

25
Q

Why is dental pain relatively well localised?

A

The pain signal is carried along one signal axon from the tooth to the brainstem = very little cross over

26
Q

From the brainstem, where do the primary afferents of the trigeminal nerve go?

A

Sensory nuclei of the trigeminal nucleus caudalis (TNC)

27
Q

What is to note about the structure of the TNC (trigeminal nucleus caudalis)?

A

Multiple different nucleic within the TNC that are responsible for different types of pain

28
Q

What structure within the TNC receives the majority of nociception from the primary afferents of the trigeminal nerve?

A

Spinal nucleus

29
Q

What kind of neurones will synapse with the primary afferents of the trigeminal nerve in the TNC?

A

Second order neurones

30
Q

Second order neurones that have synapsed with primary afferents in the spinal nuclei (TNC) can feedback to the spinal nuclei as they ascend, what is the advantage of this?

A

This can be used to modulate pain

31
Q

How can second order neurones help to modulate pain?

A

They can feedback to the spinal nuclei as they ascend

32
Q

Where do second order neurones synapse?

A

Thalamus

33
Q

What do second order neurones synapse with?

Where do these go?

A

Third order neurones

Higher centres of brain which allow individual to interpret pain

34
Q

What is the pathway termed as from tissue damage to interpreting pain?

A

Ascending (sensory) pathway

35
Q

What is the pathway that is sent out by the brain once it has interpreted the signals?

A

Descending (motor) pathway

36
Q

List 2 mechanisms of modulating nociception we can control outside the body?

A

Altering stimuli

Pharmacological intervention

37
Q

Name 2 mechanisms of nociception modulation that occur in the body

A

Descending impulses

Sensitisation

38
Q

How can descending impulses from the brain modulate nociception? (2)

A

Endogenous chemical messengers can effect transmission of impulses from primary afferents

Gate theory - touch pressure activates A beta fibres which are faster than A delta - generates descending impulse and closes the gate at TNC

39
Q

Describe the gate theory?

A

A beta fibres are activated from touch - hoses are faster than A delta or C fibres, clsoingthe gate to the TNC so the TNC finds it harder to relay the nociceptive fibres

40
Q

What is sensitisation?

A

Increase in pain response

41
Q

In what 2 was can sensitisation occur?

A

Hyperalgesia - increase in painful signal

Allodynia - a previously neutral stimuli is now interpreted as painful

42
Q

How can sensitisation be classified?

A

Peripheral and central

43
Q

How is sensitisation helpful?

A

It has a protective role. It ensures you do not damage the area more

44
Q

How can sensitisation be harmful?

A

Chronic pain

45
Q

What is peripheral sensitisation?

A

Peripheral nociceptors have increased responsiveness or respond at lower thresholds (hyperalgesia)

46
Q

What causes peripheral sensitisation?

A

Constant chronic tissue damage releasing continual allogenic substances causing: the recruitment of sleeping nociceptors, making nociceptors prone to spontaneous activity, lower threshold

47
Q

What is central sensitisation?

A

When second order neurones receive prolonged stimulus of nociceptive input.

Increase strength fo pain sensation (hyperalgesia)or allodynia

48
Q

What causes both hyperalgesia and allodynia?

A

Central sensitisation

49
Q

What causes only hyperalgesia?

A

Peripheral sensitsation

50
Q

What causes central sensitisation?

A

Nerve trauma
Hormonal, genetic and environmental factors
peripheral sensitisation
Psychological factors

51
Q

What is convergence? What does it cause

A

Brain struggles to tell which area an impulse came from- causes referred pain

52
Q

What is divergence?

A

Radiation of pain

53
Q

What causes divergence?

A

Primary afferents synapse several other second order neurones - signals come from a large area

54
Q

How can central sensitisation be exploited?

A

Can be caused by psychological factors, so can be treated with this

55
Q

What is persistent idiopathic dentoalveolar pain?

A

Persistent pain derived from a tooth that has been removed or a root has been removed

56
Q

What are the warning signs of persistent pain?

A
Difficulty localising pain
No obvious pathology
Burning/electric shock pain
LA does not reduce pain
Pain fro longer than healing process
Does not respond to further treatment 
Unusual triggers and abnormal response
Doesn't disturb sleep
57
Q

What are the 3 features of biopsychosocial model of pain?

A

Biological, psychological, sociological

58
Q

How does the BSP model link to management of persistent pain?

A

Multidisciplinary management

persistent pain has same effect as depression - psychological

Aim to improve pt management of pain with cognitive techniques