Headache and Facial Pain Flashcards

1
Q

Headache classification

A

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

-Secondary (due to other problem)
-Acute
=Meningitis
=Encephalitis
=SAH
=Head injury
=Sinusitis
=Glaucoma (acute angle-closure)
=Tropical illness (Malaria)

-Chronic
=Chronically raised IC
=Paget’s disease
=Psychological

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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, may be related to stress
=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

-Men (3:1), smokers, alcohol trigger, nocturnal sleep
-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

-Clusters typically last 4-12 weeks

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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 , recurrent
-Classically unilateral (can be bilateral)
-Severity variable (mild to very bad)
-Typically made worse by movement (stay still/ lie down): Aggravated by, or causes avoidance of, routine activities of daily living. Patients often describe ‘going to bed’.
In women may be associated with menstruation

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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

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17
Q

What is trigeminal neuralgia?

A

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

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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. Patients using opioids and triptans are at most risk
-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

Acute: Symptoms usually develop within 48 hours of injury, characterised by rapid neurological deterioration
Subacute: Symptoms manifest within days to weeks post-injury, with a more gradual progression.
Chronic: Common in the elderly, developing over weeks to months. Patients may not recall a specific head injury.

36
Q

Management of subarachnoid haemorrhage

A

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

37
Q

Presentation of subdural haemorrhage

A

Neurological Symptoms:
Altered Mental Status: Ranging from mild confusion to deep coma. Fluctuations in the level of consciousness are common.
Focal Neurological Deficits: Weakness on one side of the body, aphasia, or visual field defects, depending on the haematoma’s location.
Headache: Often localised to one side, worsening over time.
Seizures: May occur, particularly in acute or expanding hematomas.
Recent head trauma, Patients frequently exhibit a lucid interval followed by a gradual decline in consciousness. This pattern is particularly common in chronic SDH. Other hallmark features include headache, confusion, and lethargy.

Physical Examination Findings:
Papilloedema: Indicates raised intracranial pressure.
Pupil Changes: Unilateral dilated pupil, especially on the side of the haematoma, indicating compression of the third cranial nerve.
Gait Abnormalities: Including ataxia or weakness in one leg.
Hemiparesis or Hemiplegia: Reflecting the mass effect and midline shift.

Behavioural and Cognitive Changes:
Memory Loss: Especially in chronic SDH.
Personality Changes: Irritability, apathy, or depression.
Cognitive Impairment: Difficulty with attention, problem-solving, and other executive functions.

Other Associated Features:
Nausea and Vomiting: Secondary to increased intracranial pressure.
Drowsiness: Progressing to stupor and coma in severe cases.
Signs of Increased Intracranial Pressure: Such as bradycardia, hypertension, and respiratory irregularities (Cushing’s triad).

38
Q

Investigation of subdural haemorrhage

A

-CT: crescentic collection not limited by suture lines
=They will appear hyperdense (bright) in comparison to the brain (acute) vs chronic hypodense. Large acute subdural haematomas will push on the brain (‘mass effect’) and cause midline shift or herniation.

=Rupture of the small bridging veins within the subdural space rupture and cause slow bleeding. Elderly and alcoholic patients are particularly at risk of subdural haematomas since they have brain atrophy and therefore fragile or taut bridging veins.
=Confsuion, reduced consciousness, neurological deficit

39
Q

Management of subdural haemorrhage

A

-Small or incidental acute subdurals can be observed conservatively. Surgical options include monitoring of intracranial pressure and decompressive craniectomy.

If the chronic subdural is an incidental finding or if it is small in size with no associated neurological deficit then it can be managed conservatively with the hope that it will dissolve with time. If the patient is confused, has an associated neurological deficit or has severe imaging findings then surgical decompression with burr holes is required.

40
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. Blurred margins and swollen pale disc on fundoscopy)
-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

41
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.

42
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

43
Q

Headache red flags

A

-Compromised immunity, caused, for example, by HIV or immunosuppressive drugs
-Age under 20 years and a history of malignancy
-A history of malignancy known to metastasis to the brain
-Vomiting without other obvious cause
-Worsening headache with fever
-Sudden-onset headache reaching maximum intensity within 5 minutes - ‘thunderclap’
-New-onset neurological deficit
-New-onset cognitive dysfunction
-Change in personality
-Impaired level of consciousness
-Recent (typically within the past 3 months) head trauma
-Headache triggered by cough, valsalva (trying to breathe out with nose and mouth blocked), sneeze or exercise
-Orthostatic headache (headache that changes with posture)
-Symptoms suggestive of giant cell arteritis or acute narrow-angle glaucoma
-A substantial change in the characteristics of their headache