Headaches Flashcards

Covers migraine, tension, cluster, temporal arteritis, venous sinus thrombosis

1
Q

What is an occipital nerve block?

A

May be used to treat WHAT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the epidemiology of migraine?

A

More common in women

Most commonly start between 15-24yrs

Occur most frequently in those 35-45yrs

In women, majority resolve after the menopause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are some precipitants of migraine?

A

CHOCOLATE
Chocolate – due to high phenylethylamine content

Hangovers

Oral contraceptive

Caffeine (or withdrawal from) or Cheese(→due to high tryptamine content)

Orgasms

Lie ins/relaxation

Alcohol

Travel or Tumult

Exercise

Other factors: 
Noise/lights 
Obesity 
Patent foramen ovale 
Common around puberty, menstruation, pregnancy, menopause 

Though in 50% of cases triggers are not identified and even if triggers are avoided, doesn’t necessarily mean won’t have a migraine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the pathophysiology of migraine?

A

Not entirely known

Genetic predisposition

Related to dilation/constriction of cerebral blood vessels: 
Neuropeptide CGRP (calcitonin gene related peptide) is thought to be important 

Initial local (occipital cortex) hypovolaemia cause aura → hyperaemia/blood vessel dilatation/oedema → stimulation of nerve endings and causes pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does migraine present?

A

Visual arua – perceived visual disturbances i.e. zig-zag lines, bright flashing lights, distorted objects etc – precede the attack and last 15-60 mins

Sensory aura – pins/needles spreading up limbs

Speech aura – temporary dysarthria

Gradual onset, unilateral, pulsatile, moderate-severe headache aggravated by movement; lasting 4-72hrs; may also be bilateral +/- neck pain

Photophobia

N+V

Heightened sensitivity to all stimuli – become painful i.e. brushing hair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is necessary for a diagnosis of migraine?

A

Headaches lasting 4/72hrs with aura = classical migraine

Headaches lasting 4/72hrs with no aura but with N+V or photophobia + 2x following (common migraine):
Unilateral
Pulsating
Interferes with normal life
Worsened by normal activities i.e. walking, climbing stairs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is necessary for a diagnosis of migraine?

A

Headaches lasting 4/72hrs with aura = classical migraine

Headaches lasting 4/72hrs with no aura but with N+V or photophobia + 2x following (common migraine):
Unilateral
Pulsating
Interferes with normal life
Worsened by normal activities i.e. walking, climbing stairs

Get patients to keep a headache diary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What do you give for acute management of migraines?

A

Triptan e.g. sumatriptan + NSAIDs/paracetamol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What do you give for prophylaxis against migraines?

A

If episodes >2 month:
Propanolol PO daily 60-180mg

Amitriptyline PO at night 25–75 mg

Topiramate (anticonvulsant) PO daily 50-100mg

Acupuncture, CBT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is an analgesic rebound headache?

A

Headaches following stopping long term/excessive use of analgesia

Worse with mixing analgesics i.e. Parecetamol + codeine/opiates

Management:
Withdraw analgesics and limit future use

Aspirin or naproxen may be used to improve symptoms whilst withdrawing from analgesics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the features of a tension headache?

A

Bilateral, non-pulsatile headache ± scalp muscle tenderness

No N+V or sensitivity to head movements

Management:
Stress relief
Scalp massage (mmm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the epidemiology of trigeminal neuralgia?

A

More common in men but more common in Asian women than Asian men

Presents >50yrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the aetiology and pathophysiology of trigeminal neuralgia?

A

Exact mechanisms unknown but believed to be due to loss of myelin sheath around trigeminal nerve

Secondary causes:
Compression of the trigeminal root by arteriovenous malformation or aneurismal intracranial vessels or a tumour (superior cerebellar artery implicated)

Chronic meningeal inflammation

MS

Herpes zoster

Skull base malformation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does trigeminal neuralgia present?

A

Paroxysms of intense, stabbing pain lasing a few seconds (→hours) in the trigeminal nerve distribution

Unilateral, affecting mandibular or maxillary divisions

Triggered by:
Washing affected area, shaving, eating, talking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do you manage trigeminal neuralgia?

A

Carbamazepine

Also: Lamotrigine, Phenytoin, Gabapentin

Surgery

i) If medications are ineffective
ii) Microvascular decompression – moving of any overlying blood vessels over the nerve and placing pads between vessel and nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the epidemiology of giant cell arteritis/temporal arteritis?

A

Common in the elderly

Rare under 50

Strongly associated with polymyalgia rheumetica (PMR)

17
Q

What is the aetiology and pathophysiology of giant cell arteritis?

A

Inflammation of walls of arteries

Inflamed superficial temporal or occipital arteries cause pain → touching skin over vessels will cause pain

Vessel may become hardened (due to the chronic inflammation) → loss of pulse

18
Q

How does giant cell arteritis present?

A

Generalised headache

Scalp tenderness

Claudication of the jaw

Painless temporary or permanent visual loss (if more than one of the temporal or occipital arteries are affected)

Generalised malaise, fever, fatigue

19
Q

How does polymyalgia rheumetica present?

A

Pain, stiffness and inflammation of the muscles of the shoulders, neck and hips - mostly in the morning, lasting longer than 45 mins

Fatigue

Loss of appetite and weight

Depression

Similarly rare in the under 50’s (most are in 70’s)

20
Q

How do you investigate giant cell arteritis?

A

Bloods:
Raised ESR/CRP
LFT - Low albumin, Raised ALP, Raised gamma-glutamyltransferase

Temporal arterial biopsy = diagnostic
Do not hesitate to start steroids though as risk of slight loss is high and biopsy should still remain +ve for a few weeks after starting treatment
Hypertrophy and inflammation of the intima
Degredation and presence of giant cells, lymphocytes and plasma cells in the elastic lamina

21
Q

How do you manage giant cell arteritis?

A

Corticosteroids: Predinsolone – ASAP - probably a long course (1-2+yrs)

To reduce the risk of sight loss

75mg aspirin PO OD - to reduce clot risks

PPI - gastroprotection as long course steds + NSAID

22
Q

What is the epidemiology of venous sinus thrombosis?

A

Rare but most common in the 3rd decade and in women

23
Q

What are some risk factors/aetiology for developing a VST?

A

Thrombophilia

Nephrotic syndrome, dehydration

IBD, lupus
Pregnancy and recent birth

Polycythaemia rubra vera, sickle cell

Oestrogen contraceptives

Meningitis, sepsis

Trauma/head/neck surgery

24
Q

What is the pathophysiology of VST?

A

Blood clot in the dural venous sinuses – congestion – venous infarction due to insufficient blood supply – cerebral oedema – further hypoxic injury

25
Q

How does a VST present?

A

Subacute (worsening over up to 7 days) or sudden onset headache – may be the only symptom

Papillodema – blurring of vision

Focal neurology –limb weakness slurred speech – though not necessarily confined to one side

Seizure – usually unilateral localised but sometimes tonic clonic

In the elderly – change in mental status or decreased GCS

Can embolise causing a PE – rare but poor prognosis

26
Q

How do you investigate VST?

A

MRI/CT head

Bloods – any infection or underlying cause

27
Q

How do you manage a VST?

A

Anticoagulants – heparin/LMWH/warfarin

Rarely thrombolysis

Complicated by raised ICP - dexamethasone to reduce swelling

28
Q

What is the epidemiology of cluster headaches?

A

Much more common in men

More common in smokers

Much rarer than migraine

Often disappears after age 55

29
Q

What is the aetiology and pathophysiology of cluster headaches?

A

Unknown
Potentially
Superficial temporal artery smooth muscle hyperreactivity to 5HT

Also hypothalamic grey matter abnormalities

30
Q

How do cluster headaches present?

A

Rapid onset excruciating pain around one eye only, almost always affects the same side, lasts 15-160 mins

Eye becomes watery + bloodshot, lid swelling

Rhinorrhoea

Occurs 1-2 times a day for 4-12wks then periods of relapse (up to 2 years) but can also be chronic

31
Q

How do you manage cluster headaches?

A

Acute attack:
100% oxygen for 15min+ via non-rebreathable mask (unless COPD)

Sumatriptan (SC) or zolmitriptan (nasal) (DMT analogues)

Preventative:
Suboccipital steroid injections

Verapamil + lithium + melatonin

(magic mushrooms + LSD)

32
Q

What are the features of acute glaucoma?

A

Epidemiology:
i) Elderly, long sited people

Presentation: 
Constant aching pain, develops rapidly over one eye, radiates to forehead 	Marked loss in vision 
N+V	
Red, congested eye
Dilated non responsive pupil 	

Treatment:

i) Seek help asap
ii) Acetazolamide

33
Q

Why is it important to ask about whether household members have similar symptoms?

A

If present, need to consider the possibility of CO poisoning

34
Q

Why is it important to know blood pressure?

A

Malignant hypertension - cranial HTN

35
Q

Why is it important to know whether they are pregnant/or are in the puerperium?

A

Might be pre-eclampsia/eclampsia

36
Q

Why is it important to ask about DH?

A

Side effects e.g. nitrates

Also illegal use e.g. cocaine; also in withdrawal