Headache and Facial Pain Flashcards

1
Q

Headache classification

A

-Primary headache syndromes
=Migraine
=Tension-type
=Trigeminal autonomic cephalgias (TACs, cluster headaches)
=Benign Cough/Exertional Headache
=Benign Orgasmic Cephalgia
=Ice-pick headache
-Secondary (due to other problem)

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2
Q

Presentation of Tension-type headache

A

-Typical Pattern:
=Generally bilateral
=Often Tightness/pressure; band-like headache (non-pulsating)
=Often worse end of day
=None of the systemic or neurological symptoms associated with migraine (can co-exist)
=Lower intensity than migraine (mild to moderate)
=Can be related to stress but not aggravated by routine physical activity

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3
Q

Presentation of TACs (cluster headache)

A

-Unilateral headaches with accompanying autonomic features
=Severe pain (typically around the orbit, intense sharp, stabbing pain occurring 1-2 times a day with episodes lasting 15mins-2hours)
=Red/watering eye
=Drooping/ swelling eyelid
=Constriction of pupil
Blocked/runny nose= all usually ipsilateral to pain
=Agitation and restlessness during attack

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4
Q

Time factors

A

-Migraine
=Several hours; variable frequency

-Tension-type
=Several hours; variable frequency

-Trigeminal Neuralgia
=Seconds-minutes, triggered

-Cluster headache
=15-60+ mins, several times a day, typically ‘cluster’

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5
Q

Epidemiology of Migraine

A

A very common disorder, average population prevalence: ~12%
-F:M 2-3:1
-Often occurring in families
-Heritability element ~65%
-A major cause of disability

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6
Q

Age group for migraine

A

-Affects all age groups
=20-45 age group

-Onset often around puberty
=children are affected, and late-set migraines occur

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7
Q

Primary headache syndrome symptoms

A

-Headache
-Systemic symptoms
-Neurological disturbances

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8
Q

Describe a migraine headache

A

-Typically throbbing or pounding
-Classically unilateral (can be bilateral)
-Severity variable (mild to very bad)
-Typically made worse by movement (stay still/ lie down)

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9
Q

Systemic symptoms of migraine

A

-Nausea and vomiting
-Photo/phono/osmo- phobia
-Sweating/ polyuria
-Poor concentration/ mood change
-Abdominal pain (usually in children)
-Malaise/ tiredness

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10
Q

Neurological disturbances of migraine

A

-Visual
=Blurring, scotomata, fortification spectra, coloured blobs

-Somatosensory
=Classically spreading tingling/ numbness arm/ face

-Vertigo

-Dysphasia
=Usually expressive

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11
Q

Types of migraine

A

-Common migraine (without aura)- 80%
-Classical migraine (with aura)- 20%

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12
Q

Pattern of migraine

A

-Intermittent attacks
-Variable frequency
-Variable duration (few hours-2+ days)
-Chronic migraine is recognized
=Very frequent/Persistent over long periods

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13
Q

Triggers for migraine attacks

A

-Stress/ relief from stress
-Bright loud/ loud noises/ strong smells
-Sleep disturbances/ sleep pattern changes
-Atmospheric pressure/ weather changes
-Coffee/ alcohol/ dietary items
-Hormonal factors (menstrual cycle, pregnancy, OCP, menopause)

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14
Q

Diagnosis of migraine

A

International Headache Society Criteria

A: At least 5 attacks fulfilling criteria B-D
B: Headache attacks lasting 4-72hrs
C: At least 2: unilateral, pulsating, moderate to severe intensity, aggravation by routine physical activity
During: nausea and/or vomiting/ photophobia and phonophobia
E: Not attributed to another disorder

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15
Q

Treatment of acute migraine attacks

A

-Lie in bed in darkened room
-Simple analgesia (NSAID/ paracetamol)
-Triptans (oral)
-Anti-emetic (metoclopramide)
-Consider triggers

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16
Q

Prophylactic treatment of migraine

A

Generally indicated only if frequent/ severe attacks
-Topiramate
-Sodium Valproate
-Beta blockers (propranolol)
-Others

17
Q

What is trigeminal neuralgia?

A

-A facial pain condition
-Typically begins after age of 50
-Females>Men
-Incidence 1:8000 people/year

18
Q

Typical clinical picture of Trigeminal Neuralgia

A

-Brief (seconds-minutes) episodes
-Shooting/ lancinating pain unilateral

-Triggered
=Washing/ shaving/ cleaning teeth/ talking/ eating/ cold wind/ touching face

19
Q

Causes of trigeminal neuralgia

A

-May be no apparent cause
-Arterial compression/ compression of trigeminal roots by tumour
-Other disease (MS)

20
Q

Treatment of trigeminal neuralgia

A

-Medical:
=Carbamazepine
=Other drugs

-Surgical:
=Microvascular Decompression

-Other:
=Trigeminal Destructive Techniques

21
Q

Causes of physical activation of pain receptors

A

-In blood vessels
-Meninges

=Displacement/ stretching by mass lesions/ RICP/ Irritation by inflammation/ blood products

22
Q

Causes of secondary headaches

A

-Vascular
=Subarachnoid haemorrhage
=Intracerebral haemorrhage
=Intracranial venous thrombosis
=Giant Cell Arteritis

-Infection
=Meningitis
=Encephalitis

-RICP
=Intracranial tumour
=Idiopathic intracranial hypertension

23
Q

Headache timeline and urgent considerations

A

-New, acute headache
=Intracranial infection and haemorrhage

-Recent, subacute headache
=Raised ICP
=GCA (giant cell arteritis)

-Longer-standing, chronic headache
=Primary Headache Syndrome

24
Q

History of headache and facial pain

A

-General context: age, sex
-When, what, where
=How long? Had it before?
=Mode of onset: sudden (intracranial haemorrhage), subacute, gradual
=Intermittent (frequency and duration- migraine) vs constant (variable/ increasing/ decreasing)

25
Q

Other history taking aspects

A

-Severity
=How to measure- how it interferes with life
=How useful

-Other symptoms
=Nausea/ vomiting/ photo-phonophobia/ neurological/ fever/ malaise

-Exacerbating/ relieving factors
=Relationship to activity
=Drugs
=Jaw claudication/ scalp tenderness
=Triggered by touch, cold

26
Q

Examination for headache and facial pain

A

-Intermittent/ chronic headache
=Often unhelpful

-Acute/ subacute
=Temperature
=Conscious level
=Neurological deficits
=Rash
=Signs of meningeal irritation
=Signs of RICP
=Cranial artery tenderness

27
Q

Investigations of possible serious underlying cause

A

-Blood tests
-Cranial imaging
-CSF examination
-Temporal artery biopsy (GCA)

28
Q

Diagnosis of cluster headaches

A

At least five attacks of severe or very severe unilateral orbital, supraorbital, and/or temporal pain lasting 15–180 minutes (untreated), and the headache is associated with a sense of restlessness or agitation and/or at least one of the autonomic symptoms.
=Clusters lasting several weeks (4-12) typically once a year
=More common in men (3:1) and smokers
=Alcohol may trigger attack/ relation to nocturnal sleep
=Neuroimaging for underlying brain lesions- MRI with gadolinium contrast

29
Q

Management of cluster headaches

A

-Acute= 100% oxygen, subcutaneous triptan
-Prophylaxis= verapamil, tapering dose of prednisolone, discuss triggers

30
Q

Diagnosis of tension-type headaches

A

Definition: Recurrent episodes of headache lasting from 30 minutes to 7 days which are not associated with nausea or vomiting.

-Infrequent episodic — less than 1 day of headache per month (usually self-limiting).

-Frequent episodic — at least 10 episodes of headache occurring on fewer than 15 days per month on average, for more than 3 months.

-Chronic tension-type headache defined as tension headache occurring on 15 or more days per month.

31
Q

Management of tension-type headaches

A

-Acute treatment: aspirin, paracetamol or an NSAID are first line
-Prophylaxis: up to 10 sessions of acupuncture over 5-8 weeks/ low-dose amitriptyline

32
Q

Definition of medication overuse headache

A

-Headache occurring on 15 or more days per month in a person with a pre-existing primary headache disorder, which develops as a consequence of regular overuse of one or more drugs that can be taken for acute and/or symptomatic treatment of headache, for more than 3 months.
-Ergotamines, triptans, opioids, or combination analgesics are taken on 10 days or more per month.
-Simple analgesics are taken on 15 days or more per month.

33
Q

Management of medication overuse headache

A

-Simple analgesics and triptans should be withdrawn abruptly (may initially worsen headaches) 1 month
-Opioid analgesics should be gradually withdrawn
-Withdrawal symptoms such as vomiting, hypotension, tachycardia, restlessness, sleep disturbances and anxiety may occur when medication is stopped

34
Q

Presentation of subarachnoid haemorrhage

A

-Sudden-onset thunderclap headache, severe, occipital, peaking in intensity 1-5 minutes
-Maybe history of less-severe ‘sentinel’ headache in weeks prior
-Nausea and vomiting
-Meningism
-Coma
-Seizures

35
Q

Diagnosis of subarachnoid haemorrhage

A

-Non-contrast CT head= hyperdense/ bright on CT
-If CT done more than 6 hours after symptom onset and is normal= LP
-CT angiography to identify cause

36
Q

Management of subarachnoid haemorrhage

A

-Pain relief
-Enteral nimodipine for ruptured aneurysm
-Endovascular coiling
-Neurosurgical clipping

37
Q

Presentation of temporal arteritis

A

-Typically, patient > 60 years old
-Usually rapid onset (e.g. < 1 month)
-Headache (mostly temporal)
-Jaw claudication
-Anterior ischemic optic neuropathy (occlusion of the posterior ciliary artery- a branch of the ophthalmic artery- so ischaemia of optic nerve head)
-Amaurosis fugax (temporary visual loss)
-Permanent visual loss
-Diplopia (involvement of any part of the oculomotor system- cranial nerves)
-Tender, palpable temporal artery (thickening and nodularity)
-Around 50% have features of PMR: aching, morning stiffness in proximal limb muscles (not weakness)
-Lethargy
-Depression
-Low-grade fever
-Anorexia
-Night sweats

38
Q

Investigation of temporal arteritis

A

-Vision testing- Fundoscopy typically shows a swollen pale disc and blurred margins.
-Raised inflammatory marker (ESR>50, CRP elevated),
-Temporal artery biopsy (skip lesions may be present) or ultrasound
-Creatine kinase and EMG normal.

39
Q

Management of temporal arteritis

A

-Urgent high-dose glucocorticoids before the temporal artery biopsy
-If there is no visual loss then high-dose prednisolone is used
-If there is evolving visual loss IV methylprednisolone is usually given prior to starting high-dose prednisolone
-Urgent ophthalmology review
-Bone protection with bisphosphonates is required as long, tapering course of steroids is required
-Low-dose aspirin