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*Nervous System - Pathology > Headache > Flashcards

Headache Flashcards

1
Q

What are the 2 broad types of headache?

A

Primary and Secondary

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2
Q

What percentage of headaches are primary?

A

Majority (90% GP; 60% A+E)

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3
Q

What is a primary headache?

A

A headache with no underlying medical cause

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4
Q

What are the 3 types of primary headache?

A
  • tension type
  • migraine
  • cluster
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5
Q

What is a secondary headache?

A

A headache with an identifiable structural or biochemical cause

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6
Q

Give examples of causes for a secondary headache

A
  • tumour
  • meningitis
  • vascular disorders
  • systemic infection
  • head injury
  • drug-induced
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7
Q

What is the most common primary headache?

A

Tension-type

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8
Q

Describe a tension-type headache

A

Mild, bilateral headache which is often pressure or tightening in quality; no significant associated features + is not aggravated by routine physical activity

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9
Q

What is the scale for tension type headaches?

A

Infrequent ETTH = <1 day/month
Frequent ETTH = 1-14 days/months
CTTH >15 days/month

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10
Q

What are some abortive treatments for TTH?

A
  • Aspirin or paracetamol
  • NSAIDs
    (limit to 10 days/month (~2 days/week) to avoid development of med overuse headache)
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11
Q

What is some preventative treatment for TTH? (rarely required)

A

Tricyclic antidepressants i.e. amitryptiline, dothiepin, nortriptyline

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12
Q

What is the most common DISABLING primary headache?

A

Migraine

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13
Q

What is migraine?

A

A neurologic chronic disorder with episodic attacks (CDEM) causing complex changes in the brain; characterised by recurrent and reversible attacks of pain and associated symptoms

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14
Q

What occurs during a migraine attack?

A
  • headache
  • nausea; photophobia; phonophobia
  • functional disability
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15
Q

What can occur between migraine attacks?

A
  • enduring predisposition to future attacks

- anticipatory anxiety

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16
Q

What does migraine involve in the CNS?

A

Involves integrated brain mechanisms among a number of CNS structures (cortex, brainstem, trigeminal system, meninges)

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17
Q

What is it generally recognised that migraine arises from?

A

A primary brain dysfunction that leads to activation and sensitization of the trigeminal system

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18
Q

What are the recognised features which can occur during a migraine attack?

A
  • lasts 4-72 hrs
  • unilateral location
  • pulsating quality
  • moderate/severe pain
  • aggravation by or causing avoidance of routine physical activity
  • as well as the other features during headache phase on other card
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19
Q

What are some triggers for migraine?

A 
Dehydration 
Sleep disturbance 
Hunger
Stress
Diet
Environmental stimuli
Change in oestrogen level in women
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20
Q

Describe the brain of a migraineur

A

The brain of a migraineur is hyperresponsive to normal stimuli

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21
Q

What are the 5 clinical phases of migraine?

A 
Premonitory 
Aura
Early headache
Advanced headache
Postdrome
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22
Q

Features of the premonitory phase of a migraine (predictors of headache attack)?

A

Mood changes, fatigue, cognitive changes, muscle pain, food craving

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23
Q

Features of aura phase of migraine?

A

Fully reversible, neurological changes: visual somatosensory

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24
Q

What percentage of migraineurs are affected by aura?

A

~33%

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25
Q

What is aura defined as?

A

Transient neurological symptoms resulting from cortical or brainstem dysfunction; may involve visual, sensory, motor or speech systems

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26
Q

What is the pattern of symptoms in aura?

A

Slow evolution; moves from 1 area to next e.g. vision -> sensory -> speech

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27
Q

What is the duration of aura?

A

15-60 minutes

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28
Q

What can aura be mistaken for?

A

TIA (esp in elderly patients who may experience aura without headache (called acephalic migraine))

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29
Q

Features of early headache?

A

Dull headache, nasal congestion, muscle pain

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30
Q

Features of advanced headache?

A

Unilateral, throbbing, nausea, photophobia, phonophobia, osmophobia

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31
Q

Features of postdrome headache (symptoms lasting 1-2 days beyond resolution of headache)?

A

Fatigue, cognitive changes, muscle pain

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32
Q

What is chronic migraine defined as?

A

Headache on >15 days per months, of which >8 days have to be migraine, for more than 3 months

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33
Q

What is transformed migraine?

A

Patient:
History of episodic migraine
Increasing freq of headaches over weeks/months/years
Migrainous symptoms become less frequent and less severe
Many patients have episodes of severe migraine on a background of less severe featureless frequent/daily headache

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34
Q

What is often found to be the cause of chronic migraine?

A

Medication overuse; but can occur with or without this

in patients with med overuse, discontinuing overused meds often dramatically improves headache freq

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35
Q

What is MOH?

A

Medication Overuse Headache

headache present on >15 days/months which has developed or worsened whilst taking reg symptomatic meds

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36
Q

Who is more prone to MOH?

A

Migraineurs (even those taking pain meds for another reasion can develop chronic headache)

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37
Q

How can MOH be caused?

A
  • Use of triptans, ergots, opioids & combination analgesics >10 days per month
  • Use of simple analgesics >15 days per months
  • Caffeine overuse
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38
Q

Name abortive treatment for migraine

A
  • Aspirin/NSAIDs
  • Triptans
    (limit to 10 days per months (~2 per week) to avoid MOH)
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39
Q

Name the 4 prophylactic treatments for migraine

A
  • Propanolol (beta blocker), candesartan (ARB)
  • Anti-epileptics (topiramate, valproate, gabapentin)
  • Tricyclic antidepressants (amitryptiline, dothiepin, nortriptyline)
  • Venlafaxine (SNRI)
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40
Q

What is the difference in migraine with aura and migraine without aura during pregnancy?

A

Migraine without aura gets better in pregnancy

Migraine with aura does not change in pregnancy

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41
Q

What contraception is contraindicated in active migraine with aura?

A

The combined OCP (if women hasnt had attach in >5yrs is okay)

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42
Q

What is the appropriate treatment for acute migraine attack during pregnancy?

A

Paracetamol

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43
Q

What is the appropriate preventative treatment for migraine during pregnancy?

A

Propanolol/amitriptyline

AVOID anti-epileptics in pregnancy - teratogenic

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44
Q

What are Trigeminal Autonomic Cephalagias?

A

Group of headache disorders characterised by attacks of moderate to severe/excruciating unilateral pain (mostly V1) in the head or face, with associated ipsilateral cranial autonomic features

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45
Q

What are the associated cranial autonomic symptoms of TACs?

A 
Lacrimation/Conjunctival injection
Nasal congestion (rhinorrhoea)
Eyelid oedema
Forehead/facial sweating
Miosis/ptosis (Horners)
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46
Q

What are the variants among TACs?

A

Attack frequency/duration

Treatment responses

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47
Q

Name 4 TACs

A
  • Cluster headache
  • Paroxysmal hemicrania
  • SUNCT
  • SUNA
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48
Q

What does SUNCT stand for?

A

Short-lasting Unilateral Neuralgiform headache with Conjunctival injecion and Tearing

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49
Q

What does SUNA stand for?

A

Short-lasting Unilateral Neuralgiform headache with Autonomic Symptoms

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50
Q

Where is pain mainly located in cluster headache?

A

Orbital and temporal

51
Q

What are the features of cluster headache?

A
  • Attacks strictly unilateral
  • Rapid onset
  • Duration 15 mins - 3 hrs (majority 45-90 mins)
  • Rapid cessation of pain
52
Q

How does patient present in cluster headache?

A

Excruciatingly severe pain (‘suicide headache’) - patients are restless/agitated
Prominent ipsilateral autonomic symptoms

53
Q

What migrainous symptoms are often present?

A

Premonitary (tiredness, yawning)
Associated (nausea, vomiting, photophobia, phonophobia)
Typical aura (often under recognised)

54
Q

What is a bout in cluster headache?

A

Attacks ‘cluster’ into bouts typically lasting 1-3 months with periods of remission lasting at least 1 month

55
Q

What is the attack frequency during a bout?

A

1 every other day to 8 per day with possible continuous background pain

56
Q

What can occur an attack during a bout?

A

Alcohol

57
Q

What is a striking feature to the pattern of bouts?

A

Striking circadian rhythmicity

  • attacks at same time each day
  • bouts at same time each year
58
Q

What percentage of patients have chronic cluster?

A

10-20% - bouts last year without remission or remissions last <1 month

59
Q

Where is pain located in paroxysmal hemicrania?

A

Mainly orbital and temporal

60
Q

What is the difference between PH and Cluster?

A

Attacks are shorter and more frequent

61
Q

What are the features of PH?

A
  • Attacks strictly unilateral
  • Rapid onset
  • Duration: 2-30 mins
  • Rapid cessation of pain
62
Q

What does patient present with in PH?

A

Excruciating pain, but only 50% are restless and agitated
Prominent ipsilateral autonomic symptoms
Migrainous symptoms and continuous background pain may be present

63
Q

In 10% of patients how can attacks be precipitated?

A

Bending/rotating head

64
Q

What percentage of patients have chronic PH?

A

80% (20% have episodic) (reverse of cluster)

65
Q

What is the frequency of PH attacks?

A

2-40 attacks per day (NO circadian rhythm - diff to cluster)

66
Q

What does PH show absolute response to?

A

INDOMETHACIN (NSAID)

67
Q

Where is pain located in SUNCT?

A

Unilateral orbital, supraorbital or temporal pain

68
Q

What is the character of pain found in SUNCT?

A

Stabbing/pulsating pain

69
Q

What is the duration of a SUNCT attack?

A

10-240 secs

70
Q

What are the cutaneous triggers for SUNCT?

A
  • Wind/cold
  • Touch
  • Chewing
71
Q

What is the frequency for SUNCT attacks?

A

3-200/day, no refractory period

72
Q

What are the autonomic symptoms found in SUNCT?

A

Conjunctival injection and lacrimation

73
Q

What is trigeminal neuralgia?

A

A chronic pain condition that affects the trigeminal nerve

74
Q

Where is pain felt in trigeminal neuralgia?

A

Unilateral maxillary or mandibular division pain > opthalmic division

75
Q

What is the character of the pain felt in trigeminal neuralgia?

A

Stabbing

76
Q

What is the duration of a TN attack?

A

5-10 secs

77
Q

What are the cutaneous triggers for TN?

A

(same as SUNCT)

  • Wind, cold
  • Touch
  • Chewing
78
Q

What is the attack frequency for TN?

A

Similar to SUNCT, except has a refractory period

79
Q

Are autonomic features common in TN?

A

No

80
Q

What is the abortive treatment for cluster headache (not bout)?

A
  • Subcutaneous sumatriptan 6mg or nasal zoimatriptan 5mg

- 100% oxygen 7-12 l/min via tight mask

81
Q

What is the abortive treatment for a cluster headache bout?

A
  • Occipital depomedrone injection (on same side as headache)

- Or tapering course of oral predisnolone

82
Q

What are 4 options for preventative meds for cluster? (V, L, M, T)

A
  • Verapamil (high dose may be required)
  • Lithium
  • Methysergide (risk of retroperitoneal fibrosis)
  • Topiramate
83
Q

What is the abortive treatment for PH?

A

There is none

84
Q

What is the prophylactic treatment for PH?

A

Indomethacin

alternatives - COX-II inhibitors, topiramate

85
Q

What is the abortive treatment for SUNCT/SUNA?

A

There is none

86
Q

What is the prophylactic treatment for SUNCT/SUNA? (L, T, G, C)

A
  • Lamotrigine
  • Topiramate
  • Gabapentin
  • Carbamazepine/Oxcarbazepine
87
Q

What is the abortive treatment for TN?

A

There is none

88
Q

What is the prophylactic treatment for TN? (C, O)

A
  • Carbamezapine

- Oxcarbazepine

89
Q

What is the surgical treatment for TN?

A
  • Glycerol ganglion injection
  • Steriotactic radiosurgery
  • Decompressive surgery
90
Q

In what cases is serious intracranial pathology very unlikely in?

A

Longstanding episodic headache

91
Q

What presentations are more likely to have a sinister cause? (6)

A
  • Associated head trauma
  • First or worst
  • Sudden (thunderclap) onset
  • New daily persistent headache
  • Change in headache pattern or type
  • Returning patient
92
Q

What are red flags for sinister underlying causes?

A 
New onset 
New or change >50, on immunosuppresion, have cancer 
Changes in headache frequency, characteristics or associated symptoms 
Focal/ non-focal neurological symptoms 
Abnormal examination 
Neck stiffness/fever, photophobia
High pressure/Low pressure
GCA symptoms
93
Q

What are signs of high pressure?

A
  • headache worse lying down
  • headache wakening the patient up
  • headache precipitated by physical exertion
  • headache precipitated by valsalva manoeuvre
  • risk factors for cerebral venous sinus thrombosis
94
Q

What is the sign for low pressure?

A

headache precipitated by sitting/standing up

95
Q

What are the signs of GCA (giant cell arteritis)?

A

Jaw claudication or visual disturbance

Prominent or beaded temporal arteries

96
Q

What is a thunderclap headache?

A

A high intensity headache reaching max intensity in less than one minute (majority peak instantly)

97
Q

What is the main concern with thunderclap headaches?

A

Subarachnoid haemhorrage

98
Q

What are some other differentials for thunderclap headaches?

A 
Primary (can be primary or secondary - no reliable differentiation) - migraine, primary thunderclap, exertional etc
ICH
TIA/stroke
Carotid/vertebral dissection
Meningitis/encephalitis
Cerebral venous sinus thrombosis
Pituitary apoplexy
Spontaneous intracranial hypotension
99
Q

What percentage of patients with thunderclap headache will have SAH?

A

10%

100
Q

What is the most common cause for SAH?

A

Aneurysm (85%) - berry aneurysms

101
Q

What is the mortality rate for SAH?

A

50%

102
Q

What is most important to do early to save lives in SAH?

A

Coiling/clipping of the aneurysm

103
Q

Describe presentation of SAH

A
  • All patients present with sudden severe headache that peaks within a few mins and lasts for at least 1hr
  • Examination is often normal
  • Never consider patient ‘too well’ for SAH
104
Q

How is SAH investigated?

A
  • SAME DAY hosp assessment
  • CT brain (3% neg at 12hrs, 7% neg at 24hrs)
  • LP
105
Q

When should LP be done?

A

> 12 hrs after onset

106
Q

What investigation should be carried out beyond 2 weeks of onset?

A

CT +/- LP is unreliable beyond 2 weeks and angiography is required beyond this time

107
Q

What should be considered in any patient presenting with headache and fever?

A

CNS infection e.g. meningism and encephalitis

108
Q

What are the symptoms of meningitis?

A

Nausea +/- vomiting, photo/phono phobia, stiff neck

109
Q

What are the symptoms of encephalitis?

A

Altered mental state/consciousness, focal symptoms/signs, seizures

110
Q

What should be looked for when looking for CNS infection?

A

A rash

111
Q

What is a common 1st presenting feature of a space occupying lesion and/or raised intracranial pressure?

A

Headache (progressive headache with associated symptoms)

112
Q

What are other warning features of a space occupying lesion and/or raised intracranial pressure?

A
  • Headache: worse in morning/wakes patient, worse lying flat/valsava triggered
  • Focal symptoms/signs
  • Non-focal e.g. cognitive/personality change, drowsy
  • Seizures
  • Visual obscurations/pusatile tinnitus
113
Q

What is pulsatile tinnitus?

A

Ear noise heard in time with heartbeat

114
Q

What is intracranial hypotension due to?

A

Dural CSF leak

115
Q

What are the 2 types of causes of IC hypotension?

A

Spontaneous or iatrogenic (post lumbar puncture)

116
Q

What is the main sign of IC hypotension?

A

Headache develops or worsens soon after assuming an upright posture + lessens or resolves shortly after lying down; often loses postural component when becomes chronic

117
Q

What investigation should be down in IC hypotension?

A

MRI brain + spine

118
Q

What is the treatment for IC hypotension?

A
  • Bed rest, fluids, analgesia, caffeine (e.g. 1 can red bull qds)
  • I.V. caffeine
  • Epidural blood patch
119
Q

What is giant cell arteritis?

A

Arteritis of large arteries

120
Q

Should be considered in any patient over…

A

age of 50 years presenting with new headache

121
Q

What does a patient present with in GCA?

A
  • Headache usually diffuse, persistent + may be severe
  • Patient may be systemically unwell
  • Scalp tenderness, jaw claudication + visual disturbance
  • Prominent/beaded/enlarged temporal arteries
122
Q

What investigations should be done in GCA?

A

Elevated ESR supports diagnosis (usually >50, often higher, rarely normal)
Raised CRP and platelet count are other useful markers

123
Q

What treatment should be given in GCA?

A

If diagnosis is likely - high dose prednisolone should be started and temporal artery biopsy arranged

*Nervous System - Pathology (13 decks)

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