Systems: Neurology AB > Headache > Flashcards

Headache Flashcards

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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
How may migraine sufferers are affected by aura?
~33%
26
Aura
Transient neurological symptoms resulting from cortical or brainstem dysfunction
27
What may aura involve?
May involve visual, sensory, motor or speech systems
28
How long does aura last?
- Duration 15-60 minutes | - Slow evolution of symptoms (moves from 1 area to next e.g. vision to sensory to speech)
29
Why can aura be confused with a TIA?
- Loss of function - Sudden onset - Symptoms all start at same time and can be localised to a specific vascular area
30
Chronic migraine
Headache on ≥ 15 days per month, of which ≥ 8 days have to be migraine, for more than 3 months
31
How does migraine transform?
- 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
32
When can migraine transformation occur?
With or without escalation in mediation use
33
What can improve headache in patients with medication overuse?
In patients with medication overuse, discontinuing the overused medication often (but not always) dramatically improves headache frequency
34
Medication overuse headache
Headache present on ≥15 days / month which has developed or worsened whilst taking regular symptomatic medication
35
What can medication overuse headache occur in?
Primary headache - Migraineurs are particularly prone to MOH - Migraineurs taking pain medication for another reason can develop chronic headache
36
What can cause medication overuse headache?
- 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
37
What is the treatment for migraine?
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
38
How does pregnancy affect migraines?
- Migraine without aura gets better in pregnancy - Migraine with aura usually does not change - First migraine can occur during pregnancy, particularly migraine with aura
39
How should migraine be treated in pregnancy?
- Acute attack: Paracetamol | - Preventative: Propranolol or Amitriptyline
40
What is contraindicated in active migraine with aura?
- The combined OCP is contraindicated in active migraine with aura - Ok if no attacks for > 5 years, but stop if aura recurrs
41
What are the main sites of pain in cluster headaches?
Mainly orbital and temporal
42
Describe the onset of cluster headaches
- 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
How do patients appear during cluster headaches attacks?
- Excruciatingly severe (“suicide headache”) | - Patients are restless and agitated during an attack
44
What autonomic symptoms occur with cluster headaches?
Prominent ipsilateral autonomic symptoms
45
What migraine symptoms are often present in cluster headaches?
- Premonitory symptoms: tiredness, yawning - Associated symptoms: nausea, vomiting, photophobia, phonophobia - Typical aura (often under recognised)
46
Describe the episodic (80-90%) nature of cluster headaches
- 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
What is meant by chronic cluster?
- Bouts last >1 year without remission or | - Remissions last <1 month
48
What is the striking circadian rhythmicity associated with cluster headaches?
- Attacks occur at the same time each day | - Bouts occur at the same time each year
49
What are the main sites of pain in paroxysmal hemicranias?
Mainly orbital and temporal
50
Describe the onset of paroxysmal hemicranias?
- Attacks are strictly unilateral - Rapid onset - Duration: 2-30 mins - Rapid cessation of pain
51
How do patients appear during a paroxysmal hemicranias attack?
- Excruciatingly severe | - 50% are restless and agitated during an attack
52
What symptoms may be present in paroxysmal hemicranias?
- Prominent ipsilateral autonomic symptoms | - Migrainous symptoms may be present
53
What is there absolutely no response to in paroxysmal hemicranias?
Indometacin
54
What are 10% of paroxysmal hemicranias cases precipitated by?
Bending or rotating the head
55
What is the frequency of attacks in paroxysmal hemicranias?
- Frequency: 2-40 attacks per day (no circadian rhythm) | - 80% have chronic PH, 20% have episodic PH
56
What are the main sites of pain in SUNCT?
Unilateral orbital, supraorbital or temporal pain
57
What is the characteristic of pain in SUNCT?
Stabbing or pulsating pain
58
What can trigger SUNCT?
Cutaneous triggers - Wind , cold - Touch - Chewing
59
What is the duration and frequency of SUNCT attacks?
- 10-240 second duration | - Attack frequency from 3-200/day, no refractory period
60
In SUNCT, what is the pain accompanied by?
Pain is accompanied by conjunctival injection and lacrimation
61
What are the main sites of pain in trigeminal neuralgia?
Unilateral maxillary or mandibular division pain > ophthalmic division
62
What is the characteristic of pain in trigeminal neuralgia?
Stabbing pain
63
What can trigger trigeminal neuralgia?
Cutaneous triggers - Wind , cold - Touch - Chewing
64
What is the frequency and duration of trigeminal neuralgia attacks?
- 5-10 seconds duration | - Attack frequency similar to SUNCT, has a refractory period
65
What is uncommon in trigeminal neuralgia?
Autonomic features
66
What is the treatment for cluster headaches?
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
What is the treatment for paroxysmal hemicranias?
No abortive treatment Prophylaxis with indometacin -Alternatives – COX-II inhibitors, Topiramate
68
What is the treatment for SUNCT/SUNA?
No abortive treatment Prophylaxis: - Lamotrigine - Topiramate - Gabapentin - Carbamazepine / Oxcarbazepine
69
What is the treatment for trigeminal neuralgia?
No abortive treatment Prophylaxis: - Carbamazepine - Oxcarbazepine Surgical intervention: - Glycerol ganglion injection - Steriotactic radiosurgery - Decompressive surgery
70
What features predict sinister headache?
- Associated head trauma - First or worst - Sudden (thunderclap) onset - New daily persistent headache - Change in headache pattern or type - Returning patient
71
When is serious intracranial pathology very unlikely?
Serious intracranial pathology is very unlikely in longstanding episodic headache
72
What are the red flag signs/symptoms of headaches?
- 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
What would suggest a high pressure headache?
- 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
What would suggest a low pressure headache?
Headache precipitated by sitting / standing up
75
What would suggest giant cell arteritis?
- Jaw claudication or visual disturbance | - Prominent or beaded temporal arteries
76
Define a thunderclap headache
- A high intensity headache reaching maximum intensity in less than 1 minute - Majority peak instantaneously
77
What is the differential diagnosis for thunderclap headache?
- 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
What will the diagnosis be for 1 in 10 patients with thunderclap headache?
Subarachnoid haemorrhage
79
What are 85% of SAH caused by?
Aneurysms
80
What is the prognosis for SAH?
- 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
Who is SAH suspected in?
- 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
How is SAH diagnosed?
- 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
Who should CNS infection be considered in?
CNS infection should be considered in any patient presenting with headache and fever
84
What are the classic features of meningism?
- Nausea +/- vomiting - Photo/phono phobia - Stiff neck
85
What are the classic features of encephalitis?
- Altered mental state/ consciousness - Focal symptoms/signs - Seizures
86
What should you look for in CNS infection?
Non-blanching rash
87
Give examples of causes of raised ICP.
- Glioblastoma multiforme - Cerebral abscess - venous infarct with focal area of haemorrhage - Papilloedema - Hydrocephalus - Meningioma
88
What is a common first presenting feature of a SOL and/or raised ICP?
Headache | -Progressive headache with associated symptoms and signs
89
What are the warning features associated with SOL and/ or raised ICP?
- 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
Why does intracranial hypotension occur?
Dural CSF leak
91
What can cause intracranial hypotension?
- Spontaneous | - Iatrogenic (post LP)
92
Describe the headache associated with intracranial hypotension?
- 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
How should intracranial hypotension be investigated?
MRI brain and spine
94
How should intracranial hypotension be treated?
- Bed rest, fluids, analgesia, caffeine(e.g. 1 can red bull qds) - I.V. caffeine - Epidural blood patch
95
When should giant cell arteritis be considered?
Should be considered in any patient over the age of 50 years presenting with new headache
96
What is giant cell arteritis?
Arteritis of large arteries (on spectrum with polymyalgia rheumatic)
97
Describe the headache associated with giant cell arteritis.
Headache is usually diffuse, persistent and may be severe | The patient may be systemically unwell
98
What may be seen in giant cell arteritis?
Prominent, beaded or enlarged temporal arteries may be present
99
What supports the diagnosis of giant cell arteritis?
- An elevated ESR supports the diagnosis(usually >50, often much higher, rarely normal) - Raised CRP and platelet count are other useful markers
100
What should be done if the likely diagnosis is giant cell arteritis?
If the diagnosis is considered likely high dose prednisolone should be started and a temporal artery biopsy arranged
101
What does SUNCT stand for?
Short-lasting Unilateral Neuralgiform headache with Conjunctival injection and Tearing
102
What does SUNA stand for?
Short-lasting Unilateral Neuralgiform headache with Autonomic Symptoms
103
Give examples of cranial autonomic symtoms
- Conjunctival injection / lacrimation - Nasal congestion / rhinorrhoea - Eyelid oedema - Forehead & facial sweating - Miosis / ptosis (Horner’s syndrome)
104
What specific features other than headache may be present in giant cell arteritis?
Specific features include scalp tenderness, jaw claudication and visual disturbance
Systems: Neurology AB
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