Headache Flashcards

(113 cards)

1
Q

How are headaches classified?

A

Into primary and secondary headaches.

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2
Q

What are the main types of primary headaches?

A

• Tension-type
• Migraine
• Trigeminal autonomic cephalalgias (TAC):
- Cluster headache
- Paroxysmal hemicrania
- Short-lasting unilateral neuralgiform headache attacks
- Hemicrania continua

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3
Q

What defines a secondary headache?

A

A headache caused by an underlying abnormality (not a primary headache disorder).

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4
Q

What are some causes of secondary headaches?

A

• Intracranial masses
• Vascular lesions
• Raised intracranial pressure
• Inflammation
• Meningitis

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5
Q

What is an important sign to check for in suspected secondary headaches?

A

Papilledema, which suggests raised intracranial pressure

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6
Q

From where do primary headaches originate?

A

From dysfunction or irritation of pain-sensitive structures in the head (e.g., vascular, muscular, or neural mechanisms) without an underlying structural cause

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7
Q

From where do secondary headaches originate?

A

From underlying structural, infectious, vascular, or inflammatory abnormalities affecting the brain or meninges.

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8
Q

What extracranial disorders can cause secondary headaches?

A

• Carotid/vertebral artery dissection
• Dental disorders
• Glaucoma/decreased visual acuity
• Sinusitis
• Spinal trauma/degenerative disease

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9
Q

What systemic disorders can cause secondary headaches?

A

• Severe hypertension
• Bacteremia/viremia
• Fever
• Giant cell arteritis
• Hypoxia
• Hypercapnia

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10
Q

What intracranial disorders can cause secondary headaches?

A

• Tumours
• Haemorrhage
• Idiopathic intracranial hypertension
• Meningitis
• Encephalitis
• Hydrocephalus
• CSF leak with low pressure
• Reversible cerebral vasoconstriction syndrome (RCVS)
• Post-traumatic

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11
Q

What drugs and toxins can cause secondary headaches?

A

• Analgesic overuse
• Caffeine withdrawal
• Hormones (e.g., estrogen)
• Alcohol
• Proton pump inhibitors
• Nitrates
• Carbon monoxide

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12
Q

What neurological deficits are red flags for secondary headaches?

A

Papilledema, neck stiffness, hemiparesis, cerebellar signs.

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13
Q

Why are immunosuppression or cancer considered red flags in headache?

A

They increase risk for opportunistic infections and intracranial masses.

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14
Q

Why is onset of headache after age 50 a red flag

A

It raises suspicion for secondary causes like giant cell arteritis or intracranial pathology.

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15
Q

Why is a patient’s first or worst headache a red flag?

A

It may indicate subarachnoid haemorrhage or another acute intracranial event.

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16
Q

Why is systemic illness with fever or rash a red flag in headaches?

A

It may indicate meningitis or vasculitis.

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17
Q

Why is pregnancy or postpartum period a red flag in headache?

A

Due to risk of venous sinus thrombosis.

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18
Q

Why is a change in the nature or progressive worsening of a headache a red flag?

A

It may indicate developing intracranial pathology (tumour, raised ICP).

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19
Q

Why is regular eye pain or halos around lights a red flag?

A

Suggests giant cell arteritis or acute glaucoma.

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20
Q

What are the classic features of giant cell arteritis to watch for?

A

Temporal artery tenderness, proximal myalgias, jaw claudication.

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21
Q

Why are headaches provoked by coughing or straining a red flag?

A

They may indicate raised intracranial pressure.

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22
Q

What is a thunderclap headache?

A

A sudden, severe headache described as the “worst headache of life,” reaching peak intensity within 60 seconds

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23
Q

What is the most important cause of thunderclap headache?

A

Subarachnoid haemorrhage (SAH) – seen in 11–25% of cases.

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24
Q

What vascular disorders can cause thunderclap headaches?

A

• Reversible cerebral vasoconstriction syndrome (RCVS)
• Cervical artery dissection
• Cerebral venous thrombosis

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25
What pituitary condition can cause thunderclap headache?
Pituitary apoplexy.
26
What other causes (besides vascular and pituitary) are associated with thunderclap headaches?
• Infections • Neurovascular disorders • Posterior reversible encephalopathy syndrome (PRES) • Hydrocephalus • Intracranial hypotension
27
What is the first-line investigation for a thunderclap headache?
CT brain (non-contrast)
28
If CT is negative but suspicion remains for SAH, what is the next investigation?
Lumbar puncture (LP) to detect xanthochromia or blood in CSF.
29
What age group is generally considered low risk for headaches not requiring imaging?
Patients younger than 30 years.
30
What type of headache features suggest low risk?
Features typical of primary headaches (e.g., migraine, tension-type).
31
How does headache history help identify low risk?
A chronic history of similar headaches suggests primary headache, not secondary.
32
What neurological findings are seen in low-risk headaches?
None – neurological exam is normal.
33
Why is change in usual headache pattern important?
No concerning change = low risk; progressive change may suggest secondary cause.
34
How do comorbid conditions affect risk stratification in headache?
No high-risk comorbidities (e.g., HIV, cancer) = low risk.
35
What historical or examination features suggest low risk?
No new or concerning findings in history or exam
36
Low risk headaches NOT requiring imaging
- Age <30 years - Features typical of primary headaches - Chronic history of similar headache - No abnormal neurological findings - No concerning change in usual headache pattern - No high-risk comorbid conditions (e.g. HIV) - No new, concerning historical/examination findings
37
How is the diagnosis of a primary headache disorder made?
Based on history (pattern, features, triggers).
38
What is found on neurological exam in primary headache disorders?
No abnormal neurological findings.
39
What is the typical location of tension-type headaches?
Bilateral
40
What is the quality of pain in tension-type headaches?
Pressing or tightening (non-pulsating).
41
What is the intensity of tension-type headache pain?
Mild to moderate
42
Are tension-type headaches aggravated by routine physical activity (e.g., walking, stairs)?
No
43
What gastrointestinal symptoms are associated with tension-type headaches?
No vomiting, and at most mild nausea
44
What sensory symptoms may occur in tension-type headaches?
At most either photophobia or phonophobia, not both
45
How long do tension-type headaches typically last?
Minutes to days.
46
What additional symptom may be present in TTH?
Neck and shoulder muscle tenderness.
47
How is chronic tension-type headache defined?
>14 days per month
48
What should be explained to patients with tension-type headaches?
The pathogenesis and relationship with depression/anxiety.
49
What is the drug treatment for episodic tension-type headache?
Simple analgesics.
50
What is the drug treatment for chronic tension-type headache?
Amitriptyline
51
What is the starting dose of amitriptyline in TTH, and how is it titrated?
Start 10 mg, increase by 10 mg/week, usually up to 30–75 mg.
52
What non-pharmacological strategies help in managing TTH?
• Regular exercise • Stress reduction • Improved sleep • Caffeine reduction • Relaxation training • Cognitive behavioural therapy (CBT)
53
What is the typical location of migraine pain?
Unilateral, usually frontotemporal, but can be facial
54
What is the quality of migraine pain?
Pulsating
55
What is the severity of migraine pain?
Moderate to severe
56
How does physical activity affect migraine?
Aggravated by or causes avoidance of routine physical activity.
57
What gastrointestinal symptoms are common in migraine?
Nausea and/or vomiting.
58
What sensory sensitivities are associated with migraine?
Photophobia and phonophobia
59
What other associated symptoms may occur in migraine?
± Aura, ± cranial autonomic symptoms, ± cutaneous allodynia
60
What proportion of migraine patients experience aura?
About one-third.
61
What are the features of migraine aura?
• Neurological symptoms before headache • Fully reversible • Commonly visual, sensory, speech/language symptoms (motor, brainstem, retinal possible) • Gradual spread over ≥5 minutes • 2 or more symptoms may occur in succession • Usually unilateral • Mix of positive symptoms (e.g. flashing lights) and negative symptoms (e.g. numbness) • Headache typically accompanies or follows within 60 minutes
62
What are red flags in aura suggesting TIA/stroke rather than migraine?
• Onset after age 40 • Exclusively negative symptoms (e.g. hemianopia) • Duration <5 minutes or very prolonged
63
What is first-line treatment for mild to moderate migraine?
Paracetamol or NSAIDs (voltaren, brufen, aspirin, naproxen).
64
What is the next step if first-line treatment fails or in severe attacks?
Triptans (oral, intranasal, wafer, or subcutaneous).
65
How is nausea treated in migraine?
Metoclopramide 10 mg PO or prochlorperazine (Stemetil).
66
Which medications should be avoided in migraine?
Opiates, barbiturates, and overuse of paracetamol/NSAIDs.
67
What lifestyle measures help in migraine prevention?
Control of chronic migraine risk factors: adequate sleep, limit caffeine.
68
What drugs have RCT evidence for migraine prevention?
• Amitriptyline • Topiramate • Valproate • Propranolol • (Some evidence for gabapentin)
69
What is a common contributing cause of chronic headaches?
Medication overuse headache (MOH)
70
What causes medication overuse headache?
Regular (≥10 days/month), long-term use of simple analgesics for headaches.
71
Which medications are commonly implicated in MOH?
Paracetamol, aspirin, opiates, triptans.
72
What is the key step in managing medication overuse headache?
Withdrawal of simple analgesics (can be done gradually).
73
Besides withdrawal, what is vital in MOH management?
Good explanation to the patient (education about pathogenesis).
74
What is the common underlying mechanism of TACs?
Excessive cranial parasympathetic autonomic reflex activation.
75
What is the typical pain distribution in TACs?
Unilateral pain in the V1 (ophthalmic) distribution of the trigeminal nerve.
76
What type of autonomic features are seen in TACs?
Ipsilateral to the pain.
77
What condition may be associated with TACs?
Trigeminal neuralgia.
78
What ocular features may accompany TACs?
Conjunctival injection, lacrimation, eyelid edema, miosis, ptosis.
79
What nasal features may accompany TACs?
Nasal congestion, rhinorrhea.
80
What skin features may accompany TACs?
Flushing, sweating.
81
What ear feature may accompany TACs?
Ear fullness.
82
What behavioural feature is often seen during TAC attacks?
Restlessness/agitation.
83
What are the “3 A’s” used to diagnose TACs?
• Anteriorly located (unilateral) • Autonomic features (ipsilateral) • Agitation
84
What imaging is recommended to exclude secondary causes in TACs?
MRI brain.
85
What is the acute and chronic treatment for short-lasting unilateral neuralgiform headache attacks (SUNHA)?
• Acute: Steroids • Chronic: Lamotrigine, topiramate, verapamil, gabapentin
86
What is the acute and chronic treatment for paroxysmal hemicrania?
• Acute: Indomethacin • Chronic: Indomethacin, topiramate, amitriptyline
87
What is the acute and chronic treatment for cluster headaches?
• Acute: Oxygen, triptans • Chronic: Verapamil, topiramate, gabapentin
88
What is the acute and chronic treatment for hemicrania continua?
• Acute: Indomethacin • Chronic: Indomethacin, gabapentin, topiramate, amitriptyline
89
What causes trigeminal neuralgia?
A lesion or disease of the trigeminal nerve.
90
How is the pain of trigeminal neuralgia described?
Electric shock-like, shooting, stabbing, or sharp pain.
91
How long do trigeminal neuralgia attacks typically last?
<1 second to 2 minutes (sometimes longer
92
In which nerve distributions does trigeminal neuralgia most often occur?
One or more divisions of the trigeminal nerve, usually V2 (maxillary) or V3 (mandibular).
93
What triggers trigeminal neuralgia pain?
Innocuous stimuli such as chewing, brushing teeth, or talking.
94
What additional pain feature may sometimes occur in trigeminal neuralgia?
Continuous pain in the distribution of the affected division(s).
95
What facial motor symptom may occur in trigeminal neuralgia?
Contraction of facial muscles on the affected side.
96
What autonomic features may be present in trigeminal neuralgia ?
Mild symptoms such as lacrimation or eye redness.
97
Is there a refractory period in trigeminal neuralgia?
Yes, a refractory period between paroxysms
98
When is trigeminal neuralgia pain often worse?
At night.
99
What is the first-line drug for trigeminal neuralgia?
Carbamazepine
100
What investigations are needed in trigeminal neuralgia?
MRI to exclude secondary causes
101
Should patients with trigeminal neuralgia be referred to a specialist?
Yes
102
What type of vessels are affected in giant cell arteritis?
Medium- to large-sized vessels.
103
What age group is usually affected by GCA?
Mostly elderly >70 years, but as young as 50.
104
Which arteries are often involved in GCA?
Cranial arteries such as the superficial temporal artery.
105
What are the classic symptoms of GCA?
Temporal headache and scalp tenderness.
106
What serious complication can GCA cause?
Blindness
107
What associated systemic features are seen in GCA?
Visual symptoms, fever, muscle aches, weight loss, jaw claudication.
108
What investigations support the diagnosis of GCA?
ESR and CRP (usually raised).
109
What is the mainstay of treatment for GCA?
Steroids (long-term, often for months)
110
Who is most commonly affected by idiopathic intracranial hypertension?
Females with rapid weight gain.
111
What important eye finding is present in IIH?
Papilledema
112
What serious complication can occur in IIH?
Blindness
113
What does lumbar puncture show in IIH?
Normal CSF composition but raised opening pressure