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6. Neurology (Med) > Headache > Flashcards

Headache Flashcards

1
Q

Are most headaches primary or secondary?

A

Primary

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2
Q

What percentage of headaches are primary and secondary?

A

Primary - 90%

Secondary - 10%

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3
Q

What are primary headaches?

A

Ones with no underlying medical cause

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4
Q

What are secondary headaches?

A

Ones with an identifiable structural or biochemical cause

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5
Q

What are examples of causes of secondary headaches?

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

What are examples of primary headaches?

A
  • Tension type headache
  • Migraine
  • Trigeminal autonomic cephalalgias
    • Cluster headache
    • Paroxysmal hemicrania
    • SUNCT
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7
Q

What is a migraine?

A

A migraine is a chronic disorder with episodic attacks where complex changes occur in the brain:

  • During attacks
    • Headaches
    • Nausea, photophobia, phonophobia
    • Functional disability
  • In-between attacks
    • Enduring predisposition to future attacks
    • Anticipatory anxiety
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8
Q

What is the most frequent primary headache?

A

Tension type headache

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9
Q

What is a 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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10
Q

What are the different kinds of tension type headache?

A
  • Infrequent ETTH
    • <1 day/month
  • Frequent ETTH
    • 1-14 days/month
  • CTTH
    • Equal to or more than 15 days/month
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11
Q

When is a tension type headache an infrequent ETTH?

A

<1day/month

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12
Q

When is a tension type headache a frequent ETTH?

A

1-14 days/month

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13
Q

When is a tension type headache a CTTH?

A

Equal to or more than 15 days/month

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14
Q

What is the treatment for tension type headache?

A
  • Abortive treatment
    • Aspirin or paracetamol
    • NSAIDs
    • Limit to 10 days per month (about 2 days per week) to avoid the development of medication overuse headache
  • Preventative treatment
    • Rarely required
    • Tricyclic antidepressants
      • Amitrptyline, dothiopin, nortriptyline
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15
Q

What is the most common disabling primary headache?

A
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16
Q

What changes occur in the between during a migraine attack?

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

What changes occur in the brain between migraine attacks?

A
  • Enduring predisposition to future attacks
  • Anticipatory anxiety
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18
Q

What are examples of migraine triggers?

A
  • Stress
  • Hunger
  • Sleep disturbances
  • Dehydration
  • Diet
  • Environmental stimuli
  • Changes in oestrogen level in woman
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19
Q

How are migraines manifested clinically?

A

Migraine is manifested clinically as a constellation of symptoms that evolve through the various phases of a migraine attack, the clinical phases of a migraine:

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20
Q

What are the clinical phases of a migraine?

A
  • Premonitory phase
    • 70% of patients experience this
  • Aura phase
    • Involves focal, reversible neurologic symptoms that often precede the headache
    • Believed to be due to electrical disturbances called cortical spreading depression (CSD)
    • Occurs in 15-30% of migraine attacks
    • May involve visual, sensory, motor or speech systems
    • Duration is 15-60 minutes
    • Slow evolution of symptoms
      • Moves from area to the next, for example vision then sensory then speech
    • Can be confused with transient ischaemic attack
      • Loss of function
      • Sudden onset
      • Symptoms all start at the same time and can be localised to a specific vascular area
  • Headache phase
    • Subdivided according to headache pain intensity
      • Early headache
      • Advanced headache
  • Postdrome
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21
Q

What is the aura phase of a migraine believed to be due to?

A
  • Believed to be due to electrical disturbances called cortical spreading depression (CSD)
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22
Q

Why does the aura phase of a migraine have slow evolution of symptoms?

A

Moves from one area of the brain to the next

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23
Q

Why can the aura phase of a migraine be confused with a TIA?

A
  • Loss of function
  • Sudden onset
  • Symptoms all start at the same time and can be localised to a specific vascular area
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24
Q

What can the headache phase of a migraine be divided into?

A
  • Early headache
  • Advanced headache
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25
Q

What is a chronic migraine?

A

Chronic migraine is a headache on 15 or more days per month, of which 8 or more days have to be migraine, for a total of more than 3 months:

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26
Q

What is a transformed migraine?

A

Migraine condition that initially began as episodic migraine attacks, which then increase in frequency over a period of month to years

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27
Q

What is the clinical presentation of transformed migraine?

A
  • History of episodic migraine
  • Increasing frequency of headaches over weeks/months/years
  • Migranious symptoms become less frequent and less severe
  • Can occur with or without escalation in medication use
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28
Q

What is a medication overuse headache?

A
  • Headache present on 15 or more days/month which has developed or worsened whilst taking regular symptomatic medication
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29
Q

In what kinds of headaches can medication overuse headaches occur in?

A
  • Can occur in any primary headache
    • Migraineurs are particular prone to MOH
    • Migraineurs taking pain medication for another reason can develop chronic headache
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30
Q

What are medication overuse headaches often caused by?

A
  • Use of triptans, ergots, opiods and combination analgesics more than 10 days/month
  • Use of simple analgesics more than 15 days per month
  • Caffeine overuse
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31
Q

What is the treatment for migraine?

A
  • Abortive treatment
    • Aspirin or NSAIDs
    • Triptans
    • Limit to 10 days per month (about 2 per week) to avoid the development of medication overuse headache
  • Prophylactic treatment
    • Propranolol, candesartan
    • Anti-epileptics
      • Topiramate, valproate, gabapentin
    • Tricyclic antidepressants
      • Amitryptyline, dothiepin, nortriptyline
    • Venlafaxine
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32
Q

What are some specific migraine issues in woman?

A
  • Migraine without aura gets better in pregnancy
  • Migraine with aura usually does not change
  • First migraine can occur during pregnancy
  • The combined OCP is contraindicated in active migraine with aura
  • Avoid if anti-epileptics in woman of child bearing age
  • Treatment is more difficult in pregnancy
    • Acute attack is paracetamol
    • Preventative is propranolol or amitriptyline
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33
Q

What is the acute attack and preventative medication for migraine in pregnant woman?

A

Acute attack - paracetamol

Preventative - propranolol or amitriptyline

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34
Q

What are different kinds of trigeminal autonomic cephalalgias?

A

Cluster headache

Paroxysmal hemicrania

SUNCT

SUNA

Trigeminal neuralgia

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35
Q

What can cluster headaches be seperated into?

A
  • The attack
    • Pain, mainly orbital and temporal
    • Strictly unilateral
    • Rapid onset
    • Duration is 15 mins to 3 hours
    • Rapid cessation of pain
    • Excruciatingly severe (known as suicide headache)
    • Migrainous symptoms often present
      • Tiredness, yawning, nausea, vomiting, photophobia, phonophobia
  • The bout
    • Episodic in 80-90%
      • Attacks cluster into bouts typically lasting 1 to 3 months with periods of remission lasting at least 1 month
      • Attack frequency is 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
    • Striking circadian rhythmicity
      • Attacks occur at the same time every day
      • Bouts occur at the same time each year
    • 10-20% have chronic cluster
      • Bouts last >1 year without remission or remission lasts <1 month
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36
Q

What occurs during the attack of a cluster headache?

A
  • Pain, mainly orbital and temporal
  • Strictly unilateral
  • Rapid onset
  • Duration is 15 mins to 3 hours
  • Rapid cessation of pain
  • Excruciatingly severe (known as suicide headache)
  • Migrainous symptoms often present
    • Tiredness, yawning, nausea, vomiting, photophobia, phonophobia
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37
Q

What are some migrainious symptoms?

A
  • Tiredness, yawning, nausea, vomiting, photophobia, phonophobia
38
Q

Is the attack of a cluster headache unilateral or bilateral?

A

Strictly unilateral

39
Q

Describe the bout of cluster headaches?

A
  • Episodic in 80-90%
    • Attacks cluster into bouts typically lasting 1 to 3 months with periods of remission lasting at least 1 month
    • Attack frequency is 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
  • Striking circadian rhythmicity
    • Attacks occur at the same time every day
    • Bouts occur at the same time each year
  • 10-20% have chronic cluster
    • Bouts last >1 year without remission or remission lasts <1 month
40
Q

Where is the pain located due to paroxysmal hemicrania?

A

Mainly orbital and temporal

41
Q

Is paroxysmal hemicrania unilateral or bilateral?

A

Strictly unilateral

42
Q

What is the onset of paroxysmal hemicrania?

A

Rapid onset

43
Q

What is the onset of the attack of a cluster headache?

A

Sudden onset

44
Q

What is the duration of an attack of cluster headache?

A

15 minutes to 3 hours

45
Q

What is the duraiton of paroxysmal hemicrania?

A

2 to 30 minutes

46
Q

Describe the cessation of pain due to an attack of cluster headache?

A

Rapid cessation

47
Q

Describe the cessation of pain due to paroxysmal hemicrania?

A

Rapid cessation of pain

48
Q

What is the clinical presentation of paroxysmal hemicrania?

A
  • Pain is mainly orbital and temporal
  • Strictly unilateral
  • Rapid onset
  • Duration is 2 to 30 minutes
  • Rapid cessation of pain
  • Excruciatingly severe
  • Prominent ipsilateral autonomic symptoms
  • Migrainous symptoms may be present
  • Background continuous pain can be present
  • 80% have chronic, 20% have episodic
  • Frequency is 2-40 attacks per day (no circadian rhythm)
  • Absolute response to indometacin
49
Q

What is the treatment for paroxysmal hemicrania?

A
  • Absolute response to indometacin
50
Q

What is SUNCT?

A
  • Short-lasting unilateral neuralgiform headache with conjunctival injection and tearing
51
Q

Describe the pain due to SUNCT?

A
  • Unilateral orbital, supraorbital or temporal pain
  • Stabbing or pulsating pain
52
Q

What is the duration of SUNCT?

A

10-240 seconds

53
Q

What triggers SUNCT?

A
  • Cutaneous triggers
    • Wind, cold, touch, chewing
54
Q

What is the frequency of SUNCT?

A
  • Frequency 3-200/day, no refractory period
55
Q

What is the frequency of paroxysmal hemicrania?

A
  • Frequency is 2-40 attacks per day (no circadian rhythm)
56
Q

What is the frequency of cluster headache?

A
  • Attack frequency is 1 every other day to 8 per day
57
Q

What kind of pain does trigeminal autonomic cephalalgias present as?

A

Presents as unilateral head pain predominantly V1, which is very severe/excruciating

58
Q

What are some cranial autonomic symptoms due to trigeminal autonomic cephalalgias?

A
  • Conjunctival injection/lacrimation
  • Nasal congestion/rhinorrhoea
  • Eyelid oedema
  • Forehead and facial sweating
  • Miosis/ptosis (Horner’s syndrome)
59
Q

What is the treatment for cluster headache?

A
60
Q

What is the treatment for paroxysmal hemicrania?

A
61
Q

What is the treatment for SUNCT?

A
62
Q

What is the treatment for SUNA?

A
63
Q

What is the treatment for trigeminal neuralgia?

A
64
Q

What is the attack frequency (daily) of cluster headache, paroxysmal hemicrania and SUNCT?

A
65
Q

What is the duration of attack of cluster headache, paroxysmal hemicrania and SUNCT?

A
66
Q

Describe the pain quality of cluster headache, paroxysmal hemicrania and SUNCT?

A
67
Q

Describe the pain intensity of cluster headache, paroxysmal hemicrania and SUNCT?

A
68
Q

What are some features that predict a sinister secondary headache?

A
  • Serious intracranial pathology is very unlikely in longstanding episodic headache
  • Presentation more likely to have sinister cause
    • Associated head trauma
    • First or worst
    • Sudden (thunderclap) onset
    • New daily persistent headache
    • Change in headache pattern or type
    • Returning patient
69
Q

What are some red flags for a sinister secondary headache?

A
  • New onset headache
  • New or change in headache
    • Age over 50
    • Immunosuppression or cancer
  • Change in headache frequency, characteristic or associated symptoms
  • Focal neurological symptoms
  • Non-focal neurological symptoms
  • Abnormal neurological examination
  • Neck stiffness/fever
  • High pressure
    • Headache worse lying down
    • Headache wakening the patient up
    • Precipitated by physical exertion
    • Precipitated by Valsalva manoeuvre
    • Risk factors for cerebral sinus thrombosis
  • Low pressure
    • Headache precipitated by sitting/standing up
  • GCA
    • Jaw claudication or visual disturbance
    • Prominent or breaded temporal arteries
70
Q

What are some indicators that a headache is caused by high pressure?

A
  • Headache worse lying down
  • Headache wakening the patient up
  • Precipitated by physical exertion
  • Precipitated by Valsalva manoeuvre
  • Risk factors for cerebral sinus thrombosis
71
Q

What are some different causes of secondary headaches?

A
  • Thunderclap headache
  • Meningitis and encephalitis
  • Raised intracranial pressure
  • Intracranial hypotension
  • Giant cell arteritis
72
Q

What is a thunderclap headache?

A

A high intensity headache reaching maximum intensity in less than 1 minute

73
Q

Is a thunderclap headache primary or secondary?

A

May be primary or secondary, no reliable differentiating features

74
Q

What is the differential diagnosis for thunderclap headache?

A
75
Q

What dangerous thing is thunderclap associated with?

A

1 in 10 patients with thunderclap headache will have a subarachnoid haemorrhage (SAH):

  • 85% aneurysmal
  • 50% mortality
76
Q

What investigations are done for thunderclap headache?

A
  • Same day hospital assessment
  • CT brain
  • LP must be done >12 hours after headache onset
  • CT with or without LP is unreliable beyond 2 weeks and angiography is required beyond this time
77
Q

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

A

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

  • Meningism
    • Nausea with or without vomiting
    • Photo/phonophobia
    • Stiff neck
  • Encephalitis
    • Altered mental state/consciousness
    • Focal symptoms
    • Signs, seizures
78
Q

Compare the presentations of meningism and encephalitis?

A
  • Meningism
    • Nausea with or without vomiting
    • Photo/phonophobia
    • Stiff neck
  • Encephalitis
    • Altered mental state/consciousness
    • Focal symptoms
    • Signs, seizures
79
Q

What are warning features that the cause of the headache is raised intracranial pressure?

A
  • Headache is worse in morning or wakes patient from sleep
  • Headache worse lying flat or brought on by Valsalva (cough, stooping, straining0
  • Focal symptoms or signs
  • Non-focal symptoms such as cognitive or personality change, drowsiness
  • Seizures
  • Visual obscuration’s and pulsatile tinnitus
80
Q

What is intracranial hypotension often due to?

A

Dural CSF leak

81
Q

What is the presentaiton of intracranial hypotenison?

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 lose its postural component

82
Q

What investigation is done for intracranial hypotension?

A
  • MRI brain and spine
83
Q

What is the treatment for intracranial hypotension?

A
  • Bed rest, fluids, analgesia, caffeine
  • IV caffeine
  • Epidural blood patch
84
Q

What is giant cell arteritis?

A

Arteritis of large arteries

85
Q

When should giant cell arteritis be considered as the cause for a headache?

A

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

86
Q

Describe the headache due to giant cell arteritis?

A

Headache is usually diffuse, persistent and may be severe

87
Q

What is the presentation of a headache due to giant cell arteritis?

A

Headache is usually diffuse, persistent and may be severe

Patient is systemically unwell

Specific features include scalp tenderness, jaw claudication and visual disturbance

Prominent, beaded or enlarge temporal arteries may be present

88
Q

What does ESR stand for?

A

Erythrocyte sedimentation rate

89
Q

What blood finding supports giant cell arteritis being the cause of a headache?

A

An elevated ESR supports the diagnosis:

  • Usually >50, often much higher, rarely normal
  • Raised CRP and platelet count are other useful markers
90
Q

What is the treatment for giant cell arteritis?

A

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

6. Neurology (Med) (47 decks)

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