Headache Flashcards
(123 cards)
1
Q
What are the 2 broad types of headache?
A
Primary and Secondary
2
Q
What percentage of headaches are primary?
A
Majority (90% GP; 60% A+E)
3
Q
What is a primary headache?
A
A headache with no underlying medical cause
4
Q
What are the 3 types of primary headache?
A
- tension type
- migraine
- cluster
5
Q
What is a secondary headache?
A
A headache with an identifiable structural or biochemical cause
6
Q
Give examples of causes for a secondary headache
A
- tumour
- meningitis
- vascular disorders
- systemic infection
- head injury
- drug-induced
7
Q
What is the most common primary headache?
A
Tension-type
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
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
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)
11
Q
What is some preventative treatment for TTH? (rarely required)
A
Tricyclic antidepressants i.e. amitryptiline, dothiepin, nortriptyline
12
Q
What is the most common DISABLING primary headache?
A
Migraine
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
14
Q
What occurs during a migraine attack?
A
- headache
- nausea; photophobia; phonophobia
- functional disability
15
Q
What can occur between migraine attacks?
A
- enduring predisposition to future attacks
- anticipatory anxiety
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)
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
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
19
Q
What are some triggers for migraine?
A
Dehydration Sleep disturbance Hunger Stress Diet Environmental stimuli Change in oestrogen level in women
20
Q
Describe the brain of a migraineur
A
The brain of a migraineur is hyperresponsive to normal stimuli
21
Q
What are the 5 clinical phases of migraine?
A
Premonitory Aura Early headache Advanced headache Postdrome
22
Q
Features of the premonitory phase of a migraine (predictors of headache attack)?
A
Mood changes, fatigue, cognitive changes, muscle pain, food craving
23
Q
Features of aura phase of migraine?
A
Fully reversible, neurological changes: visual somatosensory
24
Q
What percentage of migraineurs are affected by aura?
A
~33%
25
What is aura defined as?
Transient neurological symptoms resulting from cortical or brainstem dysfunction; may involve visual, sensory, motor or speech systems
26
What is the pattern of symptoms in aura?
Slow evolution; moves from 1 area to next e.g. vision -> sensory -> speech
27
What is the duration of aura?
15-60 minutes
28
What can aura be mistaken for?
TIA (esp in elderly patients who may experience aura without headache (called acephalic migraine))
29
Features of early headache?
Dull headache, nasal congestion, muscle pain
30
Features of advanced headache?
Unilateral, throbbing, nausea, photophobia, phonophobia, osmophobia
31
Features of postdrome headache (symptoms lasting 1-2 days beyond resolution of headache)?
Fatigue, cognitive changes, muscle pain
32
What is chronic migraine defined as?
Headache on >15 days per months, of which >8 days have to be migraine, for more than 3 months
33
What is transformed migraine?
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
34
What is often found to be the cause of chronic migraine?
Medication overuse; but can occur with or without this
| in patients with med overuse, discontinuing overused meds often dramatically improves headache freq
35
What is MOH?
Medication Overuse Headache
| headache present on >15 days/months which has developed or worsened whilst taking reg symptomatic meds
36
Who is more prone to MOH?
Migraineurs (even those taking pain meds for another reasion can develop chronic headache)
37
How can MOH be caused?
- Use of triptans, ergots, opioids & combination analgesics >10 days per month
- Use of simple analgesics >15 days per months
- Caffeine overuse
38
Name abortive treatment for migraine
- Aspirin/NSAIDs
- Triptans
(limit to 10 days per months (~2 per week) to avoid MOH)
39
Name the 4 prophylactic treatments for migraine
- Propanolol (beta blocker), candesartan (ARB)
- Anti-epileptics (topiramate, valproate, gabapentin)
- Tricyclic antidepressants (amitryptiline, dothiepin, nortriptyline)
- Venlafaxine (SNRI)
40
What is the difference in migraine with aura and migraine without aura during pregnancy?
Migraine without aura gets better in pregnancy
| Migraine with aura does not change in pregnancy
41
What contraception is contraindicated in active migraine with aura?
The combined OCP (if women hasnt had attach in >5yrs is okay)
42
What is the appropriate treatment for acute migraine attack during pregnancy?
Paracetamol
43
What is the appropriate preventative treatment for migraine during pregnancy?
Propanolol/amitriptyline
| AVOID anti-epileptics in pregnancy - teratogenic
44
What are Trigeminal Autonomic Cephalagias?
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
45
What are the associated cranial autonomic symptoms of TACs?
```
Lacrimation/Conjunctival injection
Nasal congestion (rhinorrhoea)
Eyelid oedema
Forehead/facial sweating
Miosis/ptosis (Horners)
```
46
What are the variants among TACs?
Attack frequency/duration
| Treatment responses
47
Name 4 TACs
- Cluster headache
- Paroxysmal hemicrania
- SUNCT
- SUNA
48
What does SUNCT stand for?
Short-lasting Unilateral Neuralgiform headache with Conjunctival injecion and Tearing
49
What does SUNA stand for?
Short-lasting Unilateral Neuralgiform headache with Autonomic Symptoms
50
Where is pain mainly located in cluster headache?
Orbital and temporal
51
What are the features of cluster headache?
- Attacks strictly unilateral
- Rapid onset
- Duration 15 mins - 3 hrs (majority 45-90 mins)
- Rapid cessation of pain
52
How does patient present in cluster headache?
Excruciatingly severe pain ('suicide headache') - patients are restless/agitated
Prominent ipsilateral autonomic symptoms
53
What migrainous symptoms are often present?
Premonitary (tiredness, yawning)
Associated (nausea, vomiting, photophobia, phonophobia)
Typical aura (often under recognised)
54
What is a bout in cluster headache?
Attacks 'cluster' into bouts typically lasting 1-3 months with periods of remission lasting at least 1 month
55
What is the attack frequency during a bout?
1 every other day to 8 per day with possible continuous background pain
56
What can occur an attack during a bout?
Alcohol
57
What is a striking feature to the pattern of bouts?
Striking circadian rhythmicity
- attacks at same time each day
- bouts at same time each year
58
What percentage of patients have chronic cluster?
10-20% - bouts last year without remission or remissions last <1 month
59
Where is pain located in paroxysmal hemicrania?
Mainly orbital and temporal
60
What is the difference between PH and Cluster?
Attacks are shorter and more frequent
61
What are the features of PH?
- Attacks strictly unilateral
- Rapid onset
- Duration: 2-30 mins
- Rapid cessation of pain
62
What does patient present with in PH?
Excruciating pain, but only 50% are restless and agitated
Prominent ipsilateral autonomic symptoms
Migrainous symptoms and continuous background pain may be present
63
In 10% of patients how can attacks be precipitated?
Bending/rotating head
64
What percentage of patients have chronic PH?
80% (20% have episodic) (reverse of cluster)
65
What is the frequency of PH attacks?
2-40 attacks per day (NO circadian rhythm - diff to cluster)
66
What does PH show absolute response to?
INDOMETHACIN (NSAID)
67
Where is pain located in SUNCT?
Unilateral orbital, supraorbital or temporal pain
68
What is the character of pain found in SUNCT?
Stabbing/pulsating pain
69
What is the duration of a SUNCT attack?
10-240 secs
70
What are the cutaneous triggers for SUNCT?
- Wind/cold
- Touch
- Chewing
71
What is the frequency for SUNCT attacks?
3-200/day, no refractory period
72
What are the autonomic symptoms found in SUNCT?
Conjunctival injection and lacrimation
73
What is trigeminal neuralgia?
A chronic pain condition that affects the trigeminal nerve
74
Where is pain felt in trigeminal neuralgia?
Unilateral maxillary or mandibular division pain > opthalmic division
75
What is the character of the pain felt in trigeminal neuralgia?
Stabbing
76
What is the duration of a TN attack?
5-10 secs
77
What are the cutaneous triggers for TN?
(same as SUNCT)
- Wind, cold
- Touch
- Chewing
78
What is the attack frequency for TN?
Similar to SUNCT, except has a refractory period
79
Are autonomic features common in TN?
No
80
What is the abortive treatment for cluster headache (not bout)?
- Subcutaneous sumatriptan 6mg or nasal zoimatriptan 5mg
| - 100% oxygen 7-12 l/min via tight mask
81
What is the abortive treatment for a cluster headache bout?
- Occipital depomedrone injection (on same side as headache)
| - Or tapering course of oral predisnolone
82
What are 4 options for preventative meds for cluster? (V, L, M, T)
- Verapamil (high dose may be required)
- Lithium
- Methysergide (risk of retroperitoneal fibrosis)
- Topiramate
83
What is the abortive treatment for PH?
There is none
84
What is the prophylactic treatment for PH?
Indomethacin
| alternatives - COX-II inhibitors, topiramate
85
What is the abortive treatment for SUNCT/SUNA?
There is none
86
What is the prophylactic treatment for SUNCT/SUNA? (L, T, G, C)
- Lamotrigine
- Topiramate
- Gabapentin
- Carbamazepine/Oxcarbazepine
87
What is the abortive treatment for TN?
There is none
88
What is the prophylactic treatment for TN? (C, O)
- Carbamezapine
| - Oxcarbazepine
89
What is the surgical treatment for TN?
- Glycerol ganglion injection
- Steriotactic radiosurgery
- Decompressive surgery
90
In what cases is serious intracranial pathology very unlikely in?
Longstanding episodic headache
91
What presentations are more likely to have a sinister cause? (6)
- Associated head trauma
- First or worst
- Sudden (thunderclap) onset
- New daily persistent headache
- Change in headache pattern or type
- Returning patient
92
What are red flags for sinister underlying causes?
```
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
What are signs of high pressure?
- 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
What is the sign for low pressure?
headache precipitated by sitting/standing up
95
What are the signs of GCA (giant cell arteritis)?
Jaw claudication or visual disturbance
| Prominent or beaded temporal arteries
96
What is a thunderclap headache?
A high intensity headache reaching max intensity in less than one minute (majority peak instantly)
97
What is the main concern with thunderclap headaches?
Subarachnoid haemhorrage
98
What are some other differentials for thunderclap headaches?
```
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
What percentage of patients with thunderclap headache will have SAH?
10%
100
What is the most common cause for SAH?
Aneurysm (85%) - berry aneurysms
101
What is the mortality rate for SAH?
50%
102
What is most important to do early to save lives in SAH?
Coiling/clipping of the aneurysm
103
Describe presentation of SAH
- 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
How is SAH investigated?
- SAME DAY hosp assessment
- CT brain (3% neg at 12hrs, 7% neg at 24hrs)
- LP
105
When should LP be done?
>12 hrs after onset
106
What investigation should be carried out beyond 2 weeks of onset?
CT +/- LP is unreliable beyond 2 weeks and angiography is required beyond this time
107
What should be considered in any patient presenting with headache and fever?
CNS infection e.g. meningism and encephalitis
108
What are the symptoms of meningitis?
Nausea +/- vomiting, photo/phono phobia, stiff neck
109
What are the symptoms of encephalitis?
Altered mental state/consciousness, focal symptoms/signs, seizures
110
What should be looked for when looking for CNS infection?
A rash
111
What is a common 1st presenting feature of a space occupying lesion and/or raised intracranial pressure?
Headache (progressive headache with associated symptoms)
112
What are other warning features of a space occupying lesion and/or raised intracranial pressure?
- 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
What is pulsatile tinnitus?
Ear noise heard in time with heartbeat
114
What is intracranial hypotension due to?
Dural CSF leak
115
What are the 2 types of causes of IC hypotension?
Spontaneous or iatrogenic (post lumbar puncture)
116
What is the main sign of IC hypotension?
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
What investigation should be down in IC hypotension?
MRI brain + spine
118
What is the treatment for IC hypotension?
- Bed rest, fluids, analgesia, caffeine (e.g. 1 can red bull qds)
- I.V. caffeine
- Epidural blood patch
119
What is giant cell arteritis?
Arteritis of large arteries
120
Should be considered in any patient over...
age of 50 years presenting with new headache
121
What does a patient present with in GCA?
- Headache usually diffuse, persistent + may be severe
- Patient may be systemically unwell
- Scalp tenderness, jaw claudication + visual disturbance
- Prominent/beaded/enlarged temporal arteries
122
What investigations should be done in GCA?
Elevated ESR supports diagnosis (usually >50, often higher, rarely normal)
Raised CRP and platelet count are other useful markers
123
What treatment should be given in GCA?
If diagnosis is likely - high dose prednisolone should be started and temporal artery biopsy arranged
