Headaches Flashcards
What are the 3 primary headache disorders?
Migraine
cluster
tension type
Name some secondary headaches
meningitis SAH GCA Idiopathic intracranial HTN Medication overuse headaches
When to think about a secondary cause of headache? (SNOOP10) critera
Systemic Neurological symptoms and signs Onset sudden Onset >50 Phenotype Pattern change Pregnancy Papillodema Painful eye Pathology Precipitants Posture Post trauma Painkillers
What are the 2 types of migraine
migraine with aura
migraine without aura
Global prevalence of migraine (affects how many people, common age, male or female preponderance)
1 in 7
25-55
females 33%, maes 13% lifetime prevalence
do we know the cause for migraine?
no - mixture between structural, functional, chemical, vascular and inflammatory changes
Features of a typical migraine
- Typically unilateral
- Pulsating / throbbing headache
- Accompanied by nausea, vomiting, photophobia & phonophobia
- Attacks typically last 4-72h
- May have aura which are variable
- Struggle to get comfortable and often prefer to rest in a dark room
Difference between chronic and episodic migraine
chronic = Headaches on more than 15 days of each month 8 of which have migraine features
episodic = less
What percentage of people experience migraine with aura, when does it occur?
1/3rd - hours before the migraine or with the migraine itself
Triggers for migraines
Stress bright lights strong smells certain foods - chocolate, cheese, wine, caffeine dehydration menstruation abnormal sleeping patterns trauma
5 stages of migraine
- Premonitoryor prodromalstage (can begin 3 days before the headache)
- Aura(lasting up to 60 minutes)
- Headachestage (lasts 4-72 hours)
- Resolutionstage (the headache can fade away or be relieved completely by vomiting or sleeping)
- Postdromalorrecovery phase
signs showing red flags for migraine?
- Motor weakness
- Double vision
- Visual disturbances affecting only 1 eye
- Poor balance
- Decreased level of consciousness
For these red flag symptoms, what condition should you worried about and rule out?
- sudden severe onset headache
- worse on standing or lying down
- recent trauma
- triggered by valsalva manoeuvre
- fever, photophobia, neck stiffness
- visual changes
- age over 50
- immunodeficiency
- pregnancy
- sudden severe onset headache - SAH, venous sinus thrombosis, vertebral artery dissection.
- worse on standing or lying down - CSF leak, raised ICP, space occupying lesions.
- recent trauma - sundural haematoma
- triggered by valsalva manoeuvre - posterior fossa lesion or chiari 1 malformation
- fever, photophobia, neck stiffness - meningitis, encephalitis
- visual changes - GCA, glaucoma
- age over 50 - GCA and space occupying lesions
- immunodeficiency - increased risk of malignancy and infection
- pregnancy - pre-eclampsia and venous sinus thrombosis
Acute treatment options for migraine
Analgesia - NSAID or paracetamol (do not use codeine)
Triptans - sumotriptan at onset of headache
Anti-emetics - buccal prochlorperazine for nausea
Prophylaxis for migraine
- avoid triggers
- healthy lifestyle
- propanolol, topiramate
- amitriptyline if first 2 don’t work
- riboflavin
- acupuncture
- botulinum toxin type A
What headache am i typically describing:
severe, unilateral, unbearable headache around the eye
- cluster headache
Symptoms of cluster headaches
Often descibed as the most severe and intolerable pain.
- Typically all unilateral
- Red, swollen and watering eye
- Pupil constriction (miosis)
- Eyelid drooping (ptosis)
- Nasal discharge
- Facial sweating
- People often feel restless and agitated during an attack
typical patient presenting with cluster headache
male, smoker, 30-50 yrs old
triggers for cluster headache
alcohol
strong smells
exercise
acute management of cluster headache
triptans
high flow oxygen
prophylaxis for cluster headache
verapamil - calcium antagonists block entry of calcium ions into smooth muscle. This reduces blood vessel dilation which is responsible for the severe pain.
lithium
prednisolone - breaks cycle
Characteristics of tension type headache
- Bilateral location
- Pressing or tightening quality
- Mild to moderate intensity
- Not aggrevated by routine physical activity such as walking or climbing stairs
- No nausea, no vomiting, no photophobia or phonophobia
Management of episodic tension type headaches
analgesia - paracetamol or nsaid
lifestyle - stress, depression, chronic illness, sleep disorder
what is a medication overuse headache, how often does a person need to be taking medication to classify?
how do we manage it?
This occurs when regular analgesia taken for symptomatic relief of typically primary headache causes or perpetuates the condition.
10/15 or more days a month for 3 months
stops when medication is stopped
what is GCA?
peak incidence?
Commonest vasculitis affecting large and medium sized vessels
peak incidence 70-80yrs, rare below 50
complications of gca
may cause stroke if left untreated 1%
may cause blindness <20%
risk factors for gca
> 50
females
polymyalgia rheumatica in approx 50% of those with GCA
describe the pathogenesis of gca
Inflammation of medium and large sized arteries with preferential involvement of the branches from the carotid including, temporal, opthalmic, occipital.
- initial inflammatory event recruits macrophages into vessel wall
- vessel wall becomes damaged due to cytokine release
- blood vessel wall thickens
- lumen narrows leading to ischaemia and features of GCA
classical features of gca
- New localised headache (abrupt, unilateral & temporal)
- Temporal artery thickening which is visible/palpable and a reduced temporal artery pulse
- Visual symptoms (blurring, amaurosis fugax, diplopia, photopsia, visual loss)
- Scalp tenderness (when brushing hair or resting head on pillow)
- Jaw and tongue claudification caused by chewing or talking (ischaemia of the masseter muscle)
investigations for gca
temporal artery biopsy is the priniciple investigation showing mononuclear cell infiltration or granulomatous inflammation
temporal artery ultrasound can show thickening of wall (halo sign)
management of gca
no delay in corticosteroid treatment - prednisolone
- IV methylprednisolone in those with visual loss followed by oral pred regime
name some features indicting a serious cause of headache
- New severe or unexpected headache
- Progressive or persistent headache or headache which has changed dramatically
- Associated features (fever, papilloedema, personality change, atypical aura, dizziness, visual disturbances, vomiting)
- Contacts with similar symptoms (CO poisoning)
- Precipitating factors (trauma, valsalva manouevre, worse on standing or laying)
- Co-morbidities (immunocompromised or past malignancy)
- Current or recent pregnancy (pre-eclampsia)
presentation of a space occupying lesion?
- new headache with papilloedema, vomiting, posture-related changes, headache waking pt from sleep
- new headache with neurological symptoms or blackouts, change in personality or memory
- unexplained headache becoming progressively worse
- unexplained headache in someone previously diagnosed with cancer or HIV
- new onset of epileptic seizures
For these signs, where would you expect the lesion to be?
- depersonalisation, behaviour changes, emotional changes, hallucinations in smell, taste
- Anosmia
- inability to recognise familiar object if placed in hand, decreased 2-point discrimination
- bitemporal hemianopia
- loss of communication between lobes
- temporal lobe
- frontal lobe
- parietal lobe
- occipital lobe
- corpus callosum
What are some things which can cause TMJ?
trauma - dental procedure, fall on chin, clenching or grinding teeth
psychosocial disorders - stress, anxiety, depression
chronic pain disorders - CFS, fibromyalgia, migraine, IBS
things which affect the joint itself
- osteo or rheumatoid arthritis
- gout, pseudogout, spondyloarthropathy
- infection
- trauma
symptoms of TMJ?
- pain around the tmj (infront of ear) but can spread to head, neck and ear
- restricted jaw movement
- joint noise (popping, cracking)
- ear symptoms (tinnitus, dizziness, headache)
- locking jaw
what is trigeminal neuralgia, where is the pain, what is the most likely cause.
- Characterised by episodes of acute severe facial pain within the distribution of the trigeminal nerve
- pain usually occurs around the jaw and lasts a couple of minutes. Can be triggered by eating, drinking, brushing teeth, talking.
- Most commonly affects the maxillary and mandibular branches of the trigeminal nerve
- 95% due to vascular compression
risk factors for trigeminal neuralgia
- female
- advancing age
- MS
- family hx
treatment for trigeminal neuralgia
carbamazepine
what condition causes a thunderclap headache
SAH
what is the most common cause of SAH?
berry aneurysm rupture
common site of berry aneurysms?
junctions of posterior communicating arteries with internal arteries and anterior communicating with the anterior cerebral artery
risk factors for SAH
previous SAH
smoking, alcohol misuse, increase BP, bleeding disorders, family hx
investigations for SAH (3)
CT 95% sensitive in first 24h and can help localise source
LP must be done if CT normal but SAH expected - look for xanthochromia (wait 12h)
Cerebral angiography to check vessels
SAH management
- resuscitation
- nimodipine - reduced vasospasm
- intervention to stop bleeding
- monitor for complications such as re-bleeding
What headache am I describing?
- Headache worse on waking, coughing, sneezing, straining
- Postural, worse lying down
- Nausea and vomiting
- papilloedema
SOL
In what patients is idiopathic intracranial hypertension most commonly seen?
females
obese
30’s
drugs - tetracycline, steroids, nitrofurantoin, OCP
typical presentation of idiopathic intracranial hypertension
narrowed visual fields blurred vision diplopia 6th cranial nerve palsy enlarged blind spot if papillodema
management of idiopathic intracranial hypertension
weight loss
monitor visual fields (Goldmans)
drugs - acetazolamide, topiramate, loop diuretics
what would a LP & CT head for idiopathic intracranial hypertension show?
high CSF opening pressure but normal constituents
Normal CT head
