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Stage 3 Case 1 > Pain associated with head > Flashcards

Pain associated with head Flashcards

1
Q

Idiopathic meaning

A

The cause is unknown. It will have the origin the same the condition. So, if there is an injury underlying the condition that will also be the reason of the pain state.

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2
Q

Trigeminal Neuralgia

A

A type of neuropathic pain around the face. This can rise from the injury of the trigeminal nerve/lingual nerve.

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3
Q

TMD and myofascial pain

A

Pain developed due to changes around muscle function in the face. E.g. TMD is associated with tightness around the muscle jaw. The tightness can also cause nerve pain.

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4
Q

Dental pain

A

Can be acute and chronic. It can also be nerve pain.

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5
Q

Where is the pain is recognised and localised?

A

Cortex

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6
Q

1st order afferents from the face…

A

Projects to pars interpolaris and pars caudalis of medulla /upper cervical cord.

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7
Q

2nd order neurones…

A

Ascend contralaterally to thalamic (via trigemino-thalamic tract)

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8
Q

3rd order neurones…

A

Project to cortex

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9
Q

Trigeminal system (5th cranial nerves)

A

1st order afferents -> 2nd order neurones -> 3rd order neurones

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10
Q

What is the underlying cause of migraine?

A

No injury but It is associated with inflammation and dilation within dura vessels and dura matter.

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11
Q

Migraine pathophysiology

A
  1. That localised inflammation will be associated with the release of the proinflammatory neuropeptides.
  2. This will lead to vasodilation of the dura blood vessels.
  3. Once it reaches the propagation threshold it will, propagate action potential.
  4. This will stimulate the nociceptors in the trigeminal nerve.
  5. Signal travels to the brain stem, then to thalamus, then to cortex.
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12
Q

What is the stimulation in the thalamus associated with?

A

Nausea and vomiting

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13
Q

What happened when the pain signal reached the cortex?

A

It is recognised and initiated (central pain processing)

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14
Q

What is the trigeminal nerve associated with?

A

Peripheral nerve processing

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15
Q

CSD

A

Cortical spreading depression, a slowly propagated wave of slowly propagated depolarisation that leads to depression of neuronal activity.

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16
Q

What is the main factor that tiggers migraine and headache?

A

CSD signal (Cortical spreading depression)

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17
Q

What does CSD signal stimulate? (1st)

A

Astrocyte activation

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18
Q

What does Astrocyte activation lead to? (2nd)

A

Trigeminal system activation and sensitization

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19
Q

What does Trigeminal system activation and sensitization lead to? (3rd)

A

Stimulation of trigeminal ganglion

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20
Q

What does Stimulation of trigeminal ganglion lead to? (4th)

A

Dura matter vasodilation and inflammation

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21
Q

What are the first 5 things in migraine pathophysiology known as?

A

Peripheral sensitization

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22
Q

Peripheral sensitization in migraine/headache pathophysiology (5)

A
  1. CSD signal (Cortical spreading depression)
  2. Astrocyte activation
  3. Trigeminal system activation and sensitization
  4. Stimulation of trigeminal ganglion
  5. Dura matter vasodilation and inflammation
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23
Q

What does peripheral sensitization in migraine/headache lead to? (5th)

A

Stimulation of trigeminal nerve

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24
Q

What does Stimulation of trigeminal nerve lead to? (6th)

A

Processing of the signal from the brain stem, to thalamus, to cortex.

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25
Q

Causes of headache 1 (arteries)

A
  1. Traction or dilatation of intracranial or extracranial arteries.
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26
Q

Causes of headache 2 (veins)

A
  1. Traction of large extracranial veins
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27
Q

Causes of headache 3 (cranial and spinal nerves)

A
  1. Compression, traction or inflammation of cranial and spinal nerves
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28
Q

Causes of headache 4 (cranial and cervical muscles)

A
  1. Spasm and trauma to cranial and cervical muscles.
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29
Q

Causes of headache 5 (Meningeal)

A
  1. Meningeal irritation and raised intracranial pressure
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30
Q

Causes of headache 6 (serotonergic projections)

A
  1. Disturbance of intracerebral serotonergic projections
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31
Q

What are important reports targeted for migraine?

A

Serotonin 5HT receptors

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32
Q

What is serotonin?

A

A neurotransmitter

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33
Q

Which two 5-HT receptors are involved in migraine?

A

7 and 2

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34
Q

What happens to serotonin level in the blood during migraine?

A

Low (Low pH)

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35
Q

Why is there a low threshold for migraine?

A

Due to unstable serotonergic neurotransmission

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36
Q

Sinus location

A

Usually behind forehead and/or cheekbones

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37
Q

Cluster location

A

In and around one eye

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38
Q

Tension location

A

Both sides, whole head and neck

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39
Q

Migraine location

A

One side of face (can swap between attacks)

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40
Q

4 types of headaches

A

Sinus
Cluster
Tension
Migraine

41
Q

Two characteristics of a tension headache

A

Pressing/tightening (non-pulsating) quality

Bilateral location

42
Q

Two things are that are not characteristics of a tension headache

A

Nausea and vomiting

Photophobia and phonophobia (or one or the other is present)

43
Q

Tension headache pain type

A

Mild-moderate

Pressure, tightness (Like a band squeezing the head)

44
Q

Duration of tension headaches

A

30 mins – 7 days

45
Q

Migraine pain type

A

Moderate – severe

Pulsating, throbbing

46
Q

Duration of Migraine

A

4 hours – 3 days

47
Q

What is aura?

A

Brief neuronal excitation, events that happen before actual migraine pain develops

48
Q

Stage 1 of migraine name

A

Prodrome

49
Q

Stage 1 of migraine

A

does not feel the pain yet. It is experiences days before the actual pain.

50
Q

Stage 2 of migraine name

A

Aura

51
Q

Stage 2 of migraine

A

lasts or about an hour before the actual pain.

52
Q

Stage 3 of migraine name

A

Headache

53
Q

Stage 3 of migraine

A

can last up to 3 days.

54
Q

Stage 4 of migraine name

A

Postdrome

55
Q

Stage 4 of migraine

A

can last up to a few days after the actual migraine. The tenderness when touching head indicates the presence central sensitizations during the attack and development of allodynia of symptoms around the head.

56
Q

Migraine tiggers food

A

spices, wine , chocolate, citrus, fasting

57
Q

Migraine tiggers food additives

A

monosodium glutamate

58
Q

Migraine tiggers sleep

A

both too much and too little

59
Q

Migraine tiggers stress

A

mainly offset and fatigue

60
Q

Migraine tiggers female hormones

A

fluctuating or falling oestrogen

61
Q

Migraine tiggers medications

A

Birth control pills, vasodilators

62
Q

Migraine tiggers other

A

noise, light and exertion

63
Q

3 biggest tiggers of migraine

A

Stress, hormones and nor eating

64
Q

Two types of aura symptoms

A

Positive neurological and negative neurological symptoms

65
Q

Positive neurological symptoms

A

Reversible brain/neurological symptoms
-Visual flashes, spots, or zig-zag lines
-Traveling tingling sensations
Gradual development over >4 minutes

66
Q

Negative neurological symptoms

A

Reversible brain/neurological symptoms

  • Visual blind spots
  • Numbness
  • Speech or word finding problems
  • Trouble thinking
67
Q

When do Positive neurological and Negative neurological symptoms resolve?

A

Within 1 hour

68
Q

Example of aura (6)

A
  • scotoma (blind spots)
  • Fortification (zig-zag patterns)
  • Scintilla (flashing lights)
  • Unilateral paresthesia/weakness
  • Hallucinations
  • Hemianopsia (blindness in one half of the visual field)
69
Q

What is Allodynia?

A

Sensitivity to hair and scalp. When touching and combing can cause pain.

70
Q

Cluster headache pain type

A

Excruciating

Penetrating, boing, continuous, non-throbbing.

71
Q

Duration of Cluster headache

A

15 mins- 3 hours (same clock time each day)

72
Q

Cluster headache frequency

A

Same time each year/season

73
Q

Cluster headache symptoms

A

Watering eyes, nasal stiffness, runny nose, red eye, swollen eyelids, sweating.

74
Q

Cluster headache risk factor

A

Male, middle aged, smoker

75
Q

Characteristics of trigeminal neuralgia

A

Sudden, intense, sharp, superficial, stabbing or during. (electric-shock like pain)

76
Q

Causes of trigeminal neuralgia

A
  • Pressure from blood vessel on the root of the trigeminal nerve
  • Demyelination of the nerve. In
  • Pressure from tumour on trigeminal nerve
  • Pressure damaged to the nerve caused by dental or surgical procedures, injury to face or infections.
  • Sometimes unknow
77
Q

3 branches of the trigeminal nerve

A

Ophthalmic
Maxillary
Mandibular

78
Q

Ophthalmic nerve (CN V1)

A

lies in the lateral wall of the cavernous sinus
enters the orbit via the superior orbital fissure
(forehead and nose)

79
Q

Maxillary nerve (CN V2)

A

lies in the lateral wall of the cavernous sinus
exits the cranial vault via the foramen rotundum
(Above lips, Cheekbones and temples)

80
Q

Mandibular nerve (CN V3)

A

exits the cranial vault via the foramen ovale

(Jaw and around ear)

81
Q

Pain in symptomatic side vs non symptomatic (trigeminal neuralgia)

A

The pain responses in the non-symptomatic side are significantly higher. Showing the importance of the secondary hyperalgesia and central sensitization.
Symptomatic side directly associated with injury.

82
Q

Two types of therapy for antimigraine

A

Prophylactic and acute

83
Q

Medications that inhibit an effect on cortical spreading depression (CSD) (prophylactic)

A 
Topiramate
 Valproate
 Gabapentin
 Lamotrigine
 Topiramate
 Propranolol
 Methysergide
84
Q

Medications that inhibit an effect on cortical spreading depression (CSD) (acute)

A

Ocelgepant
Telkagepant
MK-3207
BI 44370 TA

85
Q

Triptans acting site

A

Serotonin 5HT1B/1Dreceptor agonists, with additional activity at 5HT1Freceptor.

86
Q

How triptans work

A

They prevent the vasodilation and therefore the triggering of the migraine.

87
Q

Triptans effects

A
  • Intracranial vasoconstriction,
  • Inhibition of neurotransmission in the trigeminocervical complex,
  • Inhibition of release of pro-inflammatory and vasoactive mediators,
  • Blood-brain barrier?
  • Relieve from pain and the nausea associated with migraine.
88
Q

MOA of triptans

A

Drug targets 5HT 1B in the dura. This causes vasoconstriction.
Also has anti-inflammatory effect, causing the inhibition of the activation of the trigeminal system.
The biding to 5HT 1B and 1D causes a decease in the pain transmission.

89
Q

What do triptans not target?

A

The central pain transmission is not targeted by the treatment.

90
Q

No Allodynia (central sensitization ), only peripheral sensitization and triptans

A

When they are treated with triptan they are pain free.

91
Q

Allodynia (central sensitization ) and triptans

A

Not targeted by triptan. Pain is only managed a moderate amount.

92
Q

Ergotamine’s are a bad option…

A

Relatively poor absorption after oral administration.

Side effects due to alpha 1 adrenal receptors and dopamine D2 receptors.

93
Q

Prophylactic drug: Beta-adrenoreceptor antagonists

A

Antimigraine action related to the reflex vasoconstriction

94
Q

Prophylactic drug: Antiepileptic drugs

A

Not well understood!

Multiple mechanisms including GABA-mediated suppression of neurotransmission in the brainstem.

95
Q

Prophylactic drug: Amitryptyline

A

Not well understood!

Multiple receptor-neurotransmitter interactions that modulate nociception.

96
Q

Prophylactic drug: Pizotifen

A

5H2 receptor antagonist

97
Q

Prophylactic drug: Methysergide

A

5H2 receptor antagonist, 5HT 1B and 1D agonist.

98
Q

What two types of drug are used for other orofacial pains other than migraine?

A

Antiepileptic and Amitryptyline

99
Q

Prophylactic drug: Botulinum toxin

A

Did not respond to at least three prior
Inhibits the release of neurotransmitters from presynaptic nerve endings (suppression of ACh release at the neuromuscular junction) like substance P or CGRP! Therefore, inhibition of peripheral sensitisation may lead to indirect inhibition of central sensitisation and this is a possible mechanism for the efficacy of botulinum toxin in chronic pain.

Stage 3 Case 1 (12 decks)

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