Headaches

Question 1

Headaches

Answer 1

One year prevalence of headache is 50%

Question 2

Headaches criteria

Answer 2

Primary headache symptoms:
Migraines,tension type headache,trigeminal autonomic cephalalgias,cluster headache

Secondary headaches
Headache is spercipitated by another condition-local or systemic.. serious causes of secondary headache are uncommon

Question 3

Long lasting vs short lasting

Answer 3

Long lasting:
Duration >4 hours
Migraine
Tension type headache

Short lasting headache
Duration < 4 hours,trigeminal autonomic cephalalgia which leads to cluster headaches

Question 4

Clinical approach

Answer 4

History and examination

Question 5

Red flags suggesting secondary headache

Answer 5

Systemic-history of malignancy,immunosuppresion,HIV,fevers,chills at night,weight loss,jaw claudication
Neurological-change in behavior,personality,diplopia,visual obscurations,pulsatile tinnitus,motor weakness,ataxia
Onset sudden-reaches intensity in less than one minute
Onset age <5 or >65
Pattern change-progressive headache,precipitated by valsalva manouvre,postural aggravation
Papilledema-n/a
Pregnancy-new onset headache during pregnancy,change in headache
Phenotype of rare headache-trigeminal autonomic cephalagia,exrcuse,cough or sec induced

Question 6

Migraine

Answer 6

Unilateral location
Pulsating quality
Moderate or severe pain intensity
Aggravation by physical routine
Lasts hours or days
Nausea and vomiting
Photophobia/phonophobia
With or without aura

Question 7

Migraine visual aura

Answer 7

Complex array of symptoms reflecting focal corticol or brainstem dysfunction
Gradual evolution 5-20 minutes
Usually before headache

Question 8

Migraine phases

Answer 8

Premonitory-yawning,polyuria,mood change,irritable,light sensitive,neck pain,concentration difficulty

Headache-head and body pain,nausea ,photophobia

Recovery-recovery-mood,disturbed,food intolerance,feeling hungover,can take 48 hours

Question 9

Migraine management

Answer 9

Lifestyle-avoid triggers,diet,sleep,exercise mindfulness

Pharmacological therapy-
Acute-paracetamol,NSAIDS,prokinetiks,triptans (5HT agonists)

Long term
>5days/month
Low and slow with doses until at optimum

Avoid opiate based and mixed analgesics

Question 10

Migraine preventatives

Answer 10

TCA
SNRIS
Bblockers
Seratonin antagonists
Anticonvulsant
Calcium channel blockers
Angiotensin converting enzyme inhibitor
Non prescription eg mg,riboflavin,
Parenteral eg acupuncture,botulinum toxin,greater occipital nerve block

CGRP antibodies

Question 11

Tension type headaches episodic

Answer 11

Feels like tight muscles around head and neck
Lasts 30 mins
Bilateral,mild or moderate,not aggravated by movement
No nausea,no vomiting,no photophobia/phonophobia

Question 12

Treatment for tension type headache

Answer 12

Reassurance
Simple analgesics eg aspirin and paracetamol

Question 13

Cluster headache

Answer 13

Severe unilateral pain
Lasts 15 to 180 mins if left untreated
At least one of the following ipsilaterally:
Conjunctival redness/lacrimation
Nasal congestion/rhinorrhoea
Eyelid Oedema
Forehead and facial sweating,miosis/ptosis
Restlessness or agitation
Not associated with brain lesion or MRI

Question 14

Cluster headache treatment

Answer 14

Acute
Triptan (nasal or subcutaneous)
High flow oxygen . Oxyge inhibits neuronal activation in the trigeminocervical complex

Prevention
Verapamil (calcium channel inhibitor get an ECG first)
Greater occipital nerve block

Question 15

Pathophysiology

Answer 15

Abnormal cortical hyperexcitability (calcium,glu,mg decreases)——>cortical spreading depression (auras develop)—->activation of trigemino vascular system ——>central sensitization and vasodilation neurogenic inflammation which causes pain

Question 16

Trigeminal vs sphenopalatine ganglion

Answer 16

Trigeminal function is sensory relay for pain temperature and touch and plays a role insipidus pain generation and trigeminovascular activation. Its key neurotransmitters are CGRP and NO

The sphenopalatine ganglion has a function in parasympathetic control of autonomic functions eg tearing and nasal congestion. Involved in cluster headache and migraines . Neurotransmitters involved are acetylcholine

Question 17

Pathophysiology in more detail

Answer 17

Trigger activates trigeminal nerve which releases CGRP substance p and neurokinin A causing vasodilation and increased vascular permeability
The SPG in activated indirectly by its connection to the trigeminal nerve causing autonomic symptoms such as tearing . The trigeminocervical complex integrates input from trigeminal nerve

More CGRP released etc

Inflammation and vasodilation → 2. Trigeminal activation → 3. CGRP release → 4. More vasodilation and pain.