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Systems: Neurology AB > Headache > Flashcards

Headache Flashcards

1
Q

What are most headaches?

A

Primary

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2
Q

Primary headache

A

No underlying medical cause

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3
Q

Secondary headache

A

Has an identifiable structural or biochemical cause

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4
Q

Give examples of primary headaches

A
  • Tension type headache
  • Migraine
  • Cluster headache
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5
Q

Give examples of causes of secondary headaches

A
  • Tumour
  • Meningitis
  • Vascular disorders
  • Systemic infection
  • Head injury
  • Drug-induced
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6
Q

What is the most frequent type of headache?

A

Tension type headache

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7
Q

What is the lifetime prevalence of tension headaches?

A
  • 42% in men

- 49% in women

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8
Q

Describe the headache in tension-type headache

A

Mild, bilateral headache which is often pressing or tightening in quality, has no significant associated features and is not aggravated by routine physical activity

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9
Q

What is the frequency of infrequent episode TTH?

A

<1 day/month

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10
Q

What is the frequency of frequent episodic TTH?

A

1-14 days/month

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11
Q

What is the frequency of chronic TTH?

A

> 15days/month

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12
Q

What is the treatment for TTH?

A

Abortive treatment

  • Aspirin or paracetamol
  • NSAIDs
  • Limit to 10 days per month (~2 days per week) to avoid the development of medication overuse headache

Preventative treatment

  • Rarely required
  • Tricyclic antidepressants (amitriptyline, dothiepin, nortriptyline)
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13
Q

What is the most frequent disabling primary headache?

A

Migraine

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14
Q

What is the epidemiology of migraine?

A
  • 6 million people in the UK
  • Lifetime prevalence: 10% in men and 22% in women
  • Most sufferers aged 20 to 50
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15
Q

What is migraine?

A
  • A chronic disorder with episodic attacks

- Complex changes in the brain

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16
Q

What do people experience during a migraine attack?

A
  • Headache
  • Nausea, photophobia, phonophobia
  • Functional disability
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17
Q

What do people experience in-between migraine attacks?

A
  • Enduring predisposition to future attacks

- Anticipatory anxiety

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18
Q

What do current theories view migraine as?

A

-Current theories view migraine as a neurologic condition in which the brain of
predisposed patients is overresponsive to everyday triggers that normally do not
initiate attacks; alternatively, triggers may be associated with, rather than causing the attack.
-The Brain of a Migraineur Is Hyperresponsive to Normal Stimuli

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19
Q

Give examples of triggers fro migraines

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

Describe the premonitory phase of migraine.

A
  • Mood changes
  • Fatigue
  • Cognitive changes
  • Muscle pain
  • Food craving
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21
Q

Describe the aura phase of migraine.

A
  • Fully reversible
  • Neurological changes
  • Visual somatosensory
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22
Q

Describe the early headache phase of migraine

A
  • Dull headache
  • Nasal congestion
  • Muscle pain
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23
Q

Describe the advanced headaches phase of migraine

A
  • Unilateral
  • Throbbing
  • Nausea
  • Photophobia
  • Phonophobia
  • Osmophobia
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24
Q

Describe the postdrome phase of migraine.

A
  • Fatigue
  • Cognitive changes
  • Muscle pain
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25
Q

How may migraine sufferers are affected by aura?

A

~33%

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26
Q

Aura

A

Transient neurological symptoms resulting from cortical or brainstem dysfunction

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27
Q

What may aura involve?

A

May involve visual, sensory, motor or speech systems

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28
Q

How long does aura last?

A
  • Duration 15-60 minutes

- Slow evolution of symptoms (moves from 1 area to next e.g. vision to sensory to speech)

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29
Q

Why can aura be confused with a TIA?

A
  • Loss of function
  • Sudden onset
  • Symptoms all start at same time and can be localised to a specific vascular area
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30
Q

Chronic migraine

A

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

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31
Q

How does migraine transform?

A
  • History of episodic migraine
  • Increasing frequency 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 or daily headache
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32
Q

When can migraine transformation occur?

A

With or without escalation in mediation use

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33
Q

What can improve headache in patients with medication overuse?

A

In patients with medication overuse, discontinuing the overused medication often (but not always) dramatically improves headache frequency

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34
Q

Medication overuse headache

A

Headache present on ≥15 days / month which has developed or worsened whilst taking regular symptomatic medication

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35
Q

What can medication overuse headache occur in?

A

Primary headache

  • Migraineurs are particularly prone to MOH
  • Migraineurs taking pain medication for another reason can develop chronic headache
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36
Q

What can cause medication overuse headache?

A
  • Use of triptans, ergots, opiods and combination analgesics >10 days / month
  • Use of simple analgesics > 15 days per month
  • Caffeine overuse: coffee, tea, cola, irn brew
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37
Q

What is the treatment for migraine?

A

Abortive treatment

  • Aspirin or NSAIDs
  • Triptans
  • Limit to 10 days per month (~2 days per week) to avoid the development of medication overuse headache

Prophylactic treatment

  • Propranolol, Candesartan
  • Anti-epileptics (Topiramate, Valproate, Gabapentin)
  • Tricyclic antidepressants (amitriptyline, dothiepin, nortriptyline)
  • Venlafaxine
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38
Q

How does pregnancy affect migraines?

A
  • Migraine without aura gets better in pregnancy
  • Migraine with aura usually does not change
  • First migraine can occur during pregnancy, particularly migraine with aura
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39
Q

How should migraine be treated in pregnancy?

A
  • Acute attack: Paracetamol

- Preventative: Propranolol or Amitriptyline

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40
Q

What is contraindicated in active migraine with aura?

A
  • The combined OCP is contraindicated in active migraine with aura
  • Ok if no attacks for > 5 years, but stop if aura recurrs
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41
Q

What are the main sites of pain in cluster headaches?

A

Mainly orbital and temporal

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42
Q

Describe the onset of cluster headaches

A
  • Attacks are strictly unilateral
  • Rapid onset (max within 9 mins in 86%)
  • Duration: 15 mins to 3 hours (majority 45-90 mins)
  • Rapid cessation of pain
43
Q

How do patients appear during cluster headaches attacks?

A
  • Excruciatingly severe (“suicide headache”)

- Patients are restless and agitated during an attack

44
Q

What autonomic symptoms occur with cluster headaches?

A

Prominent ipsilateral autonomic symptoms

45
Q

What migraine symptoms are often present in cluster headaches?

A
  • Premonitory symptoms: tiredness, yawning
  • Associated symptoms: nausea, vomiting, photophobia, phonophobia
  • Typical aura (often under recognised)
46
Q

Describe the episodic (80-90%) nature of cluster headaches

A
  • Attacks “cluster” into bouts typically lasting 1-3 months with periods of remission lasting at least 1 month
  • Attack frequency: 1 every other day to 8 per day
  • May be continuous background pain between attacks
  • Alcohol triggers attacks during a bout, but not in remission
47
Q

What is meant by chronic cluster?

A
  • Bouts last >1 year without remission or

- Remissions last <1 month

48
Q

What is the striking circadian rhythmicity associated with cluster headaches?

A
  • Attacks occur at the same time each day

- Bouts occur at the same time each year

49
Q

What are the main sites of pain in paroxysmal hemicranias?

A

Mainly orbital and temporal

50
Q

Describe the onset of paroxysmal hemicranias?

A
  • Attacks are strictly unilateral
  • Rapid onset
  • Duration: 2-30 mins
  • Rapid cessation of pain
51
Q

How do patients appear during a paroxysmal hemicranias attack?

A
  • Excruciatingly severe

- 50% are restless and agitated during an attack

52
Q

What symptoms may be present in paroxysmal hemicranias?

A
  • Prominent ipsilateral autonomic symptoms

- Migrainous symptoms may be present

53
Q

What is there absolutely no response to in paroxysmal hemicranias?

A

Indometacin

54
Q

What are 10% of paroxysmal hemicranias cases precipitated by?

A

Bending or rotating the head

55
Q

What is the frequency of attacks in paroxysmal hemicranias?

A
  • Frequency: 2-40 attacks per day (no circadian rhythm)

- 80% have chronic PH, 20% have episodic PH

56
Q

What are the main sites of pain in SUNCT?

A

Unilateral orbital, supraorbital or temporal pain

57
Q

What is the characteristic of pain in SUNCT?

A

Stabbing or pulsating pain

58
Q

What can trigger SUNCT?

A

Cutaneous triggers

  • Wind , cold
  • Touch
  • Chewing
59
Q

What is the duration and frequency of SUNCT attacks?

A
  • 10-240 second duration

- Attack frequency from 3-200/day, no refractory period

60
Q

In SUNCT, what is the pain accompanied by?

A

Pain is accompanied by conjunctival injection and lacrimation

61
Q

What are the main sites of pain in trigeminal neuralgia?

A

Unilateral maxillary or mandibular division pain > ophthalmic division

62
Q

What is the characteristic of pain in trigeminal neuralgia?

A

Stabbing pain

63
Q

What can trigger trigeminal neuralgia?

A

Cutaneous triggers

  • Wind , cold
  • Touch
  • Chewing
64
Q

What is the frequency and duration of trigeminal neuralgia attacks?

A
  • 5-10 seconds duration

- Attack frequency similar to SUNCT, has a refractory period

65
Q

What is uncommon in trigeminal neuralgia?

A

Autonomic features

66
Q

What is the treatment for cluster headaches?

A

Abortive (Headache)

  • Subcutaneous sumatriptan 6mg or nasal zolmatriptan 5mg
  • 100% oxygen 7-12 l/min via a tight fitting non-rebreathing max is effective and safe

Abortive (Headache bout)

  • Occipital depomedrone injection (same side as the headache)
  • Or tapering course of oral prednisone

Preventative

  • Verapamil (high doses may be required)
  • Lithium
  • Methysergide (risk of retroperitoneal fibrosis)
  • Topiramate
67
Q

What is the treatment for paroxysmal hemicranias?

A

No abortive treatment

Prophylaxis with indometacin
-Alternatives – COX-II inhibitors, Topiramate

68
Q

What is the treatment for SUNCT/SUNA?

A

No abortive treatment

Prophylaxis:

  • Lamotrigine
  • Topiramate
  • Gabapentin
  • Carbamazepine / Oxcarbazepine
69
Q

What is the treatment for trigeminal neuralgia?

A

No abortive treatment

Prophylaxis:

  • Carbamazepine
  • Oxcarbazepine

Surgical intervention:

  • Glycerol ganglion injection
  • Steriotactic radiosurgery
  • Decompressive surgery
70
Q

What features predict sinister headache?

A
  • Associated head trauma
  • First or worst
  • Sudden (thunderclap) onset
  • New daily persistent headache
  • Change in headache pattern or type
  • Returning patient
71
Q

When is serious intracranial pathology very unlikely?

A

Serious intracranial pathology is very unlikely in longstanding episodic headache

72
Q

What are the red flag signs/symptoms of headaches?

A
  • New onset headache
  • New or change in headache (aged over 50, immunosupression or cancer)
  • Change in headache frequency, characteristics or associated symptoms
  • Focal neurological symptoms
  • Non-focal neurological symptoms
  • Abnormal neurological examination
  • Neck stiffness/fever
  • High pressure
  • Low pressure
  • Giant cell artertitis
73
Q

What would suggest a high pressure headache?

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
74
Q

What would suggest a low pressure headache?

A

Headache precipitated by sitting / standing up

75
Q

What would suggest giant cell arteritis?

A
  • Jaw claudication or visual disturbance

- Prominent or beaded temporal arteries

76
Q

Define a thunderclap headache

A
  • A high intensity headache reaching maximum intensity in less than 1 minute
  • Majority peak instantaneously
77
Q

What is the differential diagnosis for thunderclap headache?

A
  • Primary (migraine, primary thunderclap headache, primary exertional headache, primary headache associated with sexual activity)
  • Subarachnoid haemorrhage
  • Intracerebral haemorrhage
  • TIA / stroke
  • Carotid / vertebral dissection
  • Cerebral venous sinus thrombosis
  • Meningitis / encephalitis
  • Pituitary apoplexy
  • Spontaneous intracranial hypotension
78
Q

What will the diagnosis be for 1 in 10 patients with thunderclap headache?

A

Subarachnoid haemorrhage

79
Q

What are 85% of SAH caused by?

A

Aneurysms

80
Q

What is the prognosis for SAH?

A
  • 50% mortality, 20% of survivors remain dependant
  • Risk of re-bleed 4-6% in first 24-48 hours, 40% in first month
  • Early coiling (or clipping) of the aneurysm saves lives
81
Q

Who is SAH suspected in?

A
  • All patients presenting with a sudden severe headache that peaks within a few minutes and lasts for at least 1 hour
  • Examination is often normal!
  • Never consider a patient ‘too well’ for SAH
82
Q

How is SAH diagnosed?

A
  • SAME DAY hospital assessment
  • Does the patient have SAH or another secondary cause
  • CT brain (3% negative at 12 hrs, 7% negative at 24 hrs)
  • LP (must be done >12hrs after headache onset)
  • CT +/- LP is unreliable beyond 2 weeks and angiography is required beyond this time
83
Q

Who should CNS infection be considered in?

A

CNS infection should be considered in any patient presenting with headache and fever

84
Q

What are the classic features of meningism?

A
  • Nausea +/- vomiting
  • Photo/phono phobia
  • Stiff neck
85
Q

What are the classic features of encephalitis?

A
  • Altered mental state/ consciousness
  • Focal symptoms/signs
  • Seizures
86
Q

What should you look for in CNS infection?

A

Non-blanching rash

87
Q

Give examples of causes of raised ICP.

A
  • Glioblastoma multiforme
  • Cerebral abscess
  • venous infarct with focal area of haemorrhage
  • Papilloedema
  • Hydrocephalus
  • Meningioma
88
Q

What is a common first presenting feature of a SOL and/or raised ICP?

A

Headache

-Progressive headache with associated symptoms and signs

89
Q

What are the warning features associated with SOL and/ or raised ICP?

A
  • Headache worse in morning or wakes patient from sleep
  • Headache worse lying flat or brought on by valsalva (cough, stooping, straining)
  • Focal symptoms or signs
  • Non-focal symptoms e.g. cognitive or personality change, drowsiness
  • Seizures
  • Visual obscurations and pulsatile tinnitus
90
Q

Why does intracranial hypotension occur?

A

Dural CSF leak

91
Q

What can cause intracranial hypotension?

A
  • Spontaneous

- Iatrogenic (post LP)

92
Q

Describe the headache associated with intracranial hypotension?

A
  • Clear postural component to the headache
  • Headache develops or worsens soon after assuming an upright posture and lessens or resolves shortly after lying down
  • Once the headache becomes chronic it often loses its postural component
93
Q

How should intracranial hypotension be investigated?

A

MRI brain and spine

94
Q

How should intracranial hypotension be treated?

A
  • Bed rest, fluids, analgesia, caffeine(e.g. 1 can red bull qds)
  • I.V. caffeine
  • Epidural blood patch
95
Q

When should giant cell arteritis be considered?

A

Should be considered in any patient over the age of 50 years presenting with new headache

96
Q

What is giant cell arteritis?

A

Arteritis of large arteries (on spectrum with polymyalgia rheumatic)

97
Q

Describe the headache associated with giant cell arteritis.

A

Headache is usually diffuse, persistent and may be severe

The patient may be systemically unwell

98
Q

What may be seen in giant cell arteritis?

A

Prominent, beaded or enlarged temporal arteries may be present

99
Q

What supports the diagnosis of giant cell arteritis?

A
  • An elevated ESR supports the diagnosis(usually >50, often much higher, rarely normal)
  • Raised CRP and platelet count are other useful markers
100
Q

What should be done if the likely diagnosis is giant cell arteritis?

A

If the diagnosis is considered likely high dose prednisolone should be started and a temporal artery biopsy arranged

101
Q

What does SUNCT stand for?

A

Short-lasting Unilateral Neuralgiform headache with Conjunctival injection and Tearing

102
Q

What does SUNA stand for?

A

Short-lasting Unilateral Neuralgiform headache with Autonomic Symptoms

103
Q

Give examples of cranial autonomic symtoms

A
  • Conjunctival injection / lacrimation
  • Nasal congestion / rhinorrhoea
  • Eyelid oedema
  • Forehead & facial sweating
  • Miosis / ptosis (Horner’s syndrome)
104
Q

What specific features other than headache may be present in giant cell arteritis?

A

Specific features include scalp tenderness, jaw claudication and visual disturbance

Systems: Neurology AB (51 decks)

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