1. David Kernick Exeter Headache Clinic

2. Two default diagnoses
< 50 years Migraine

3. >50 years Temporal arteritis Systemically unwell
Tender artery with allodynia
CRP better than ESR
Problem with skip lesions

4. History and examination (Primary care perspective)
Headache is in the history
Examination
In theory:
For diagnosis
To reassure the patient
To keep out of the law courts

5. History and examination (Primary care perspective)
Examination in reality:
To keep out of the law courts
To reassure the patient
For diagnosis
BP, Fundoscopy
Giles Elrington 3 minute neurol examination

6. 6 month non specific headache
Buzzing in ears

7. What other ocular test?

8. Pain extra-cranial.
Innervation of head

9. Pain Intracranial - Innervation of dura

10. Dura stretched, compressed or inflamed
CSF – 20 mls/hr, 150 mls capacity

11. Pain - cervicogenic

12. 45 year old male 3 months continuous background headache generalised
Not postural
Featureless
No medication
Family history

14. IHS Headache classification Primary Secondary
Traumatic
Vascular
Non-vascular (SOL)
Substance induced
Infection
Disturbed homoestasis
Facial structures
Migraine
Tension type
Autonomic cephalalgias (cluster)

15. Headache impact Adults Children Community Primary Care Secondary care
20% have impact
50% visit GP
Primary Care
4.4% consultations
3% referred
Secondary care
30% of consultations
>50% investigated
Adults
Community
20% have impact
10% visit GP
Primary Care
0.6% consultations
25% referred
Secondary care ?
Children
Kernick 2009, Latinovic 2006

16. University new entrants Kernick 2002
1124 consecutive students
Headache that impacted on life 21%
13% > 15 days of the month
45% seen a GP
<5% prescribed medications for headache

17. What do patients have when they present to A and E with headache
What do patients have when they present to A and E with headache? Valade 2000
Migraine % 80%
TTH 25%
Cluster %
Trauma %
Trig Neuralgia 1.6%
Sinusitis %
Vascular disorders 1.2%
Low Pressure 1.2%
Meningitis %
Tumour %
Other Misc < 5%

18. 29 year old male Thunderclap headache CT, LP normal
Headache easing after 3 months
Has coital headache X 2 in past year
GP increased sertraline 4 months ago
Heavy cannabis user

19. Reversible vasoconstriction syndrome

20. Thunderclap Headache

21. Cerebral venous sinus thrombosis – any phenotype

23. Cluster treatment Injectable Sumatriptan Short term steroids
Oxygen 100%

24. Central sensitivity (movement, light, sound, touch)
Cluster
Migraine
Peri-orbital
Unilateral.
Any part of head
Uni or bi-lateral
Attack 15 minutes- 2 hours.
4-72 hours
Biochronicity -
Autonomic features
Central sensitivity (movement, light, sound, touch)
Active ++
Inactive
Aura 30%

26. Annual Migraine incidence

27. Some problems Migraine – a complex biopsychosocial disease
No clinical markers
Mechanisms poorly understood
Doesn’t come alone – epilepsy, anxiety, depression, asthma, IBS, fibromyalgia
Stigmatised

28. Implications for gastric stasis and neck pain

29. Migraine generator – gastric and cervical implications
Central and peripheral sensitisation
Activation trigeminal nerve
Peripheral inflammation
Cortical depolarisation and vasoconstriction
Classifying headache 2

30. Migraine: A Featureful Headache
Cady, p 206, C1 Par 2 L 1-12
Cady, p 206, C2 Par 2 L 1-4
Premonitory
Mood changes
Fatigue
Cognitive changes
Muscle pain
Food craving
Fully reversible
Neurological changes: Visual somatosensory
Aura
Dull headache
Nasal congestion
Muscle pain
Early Headache
Unilateral
Throbbing
Nausea
Photophobia
Phonophobia
Osmophobia
Advanced Headache
Fatigue
Cognitive changes
Muscle pain
Postdrome
Cady, p 206, C2 Par 3 L 4-6
Cady, p 207, C1 Par 1 L 1-11
Linde, p 71, C2 Par 1 L 4-9
Linde, p 74, C1 Par 3 L 1-15
Key point: Migraine is manifested clinically as a constellation of symptoms that evolve through the
various phases of a migraine attack; clinical experience indicates that symptoms typically associated
with each phase of an attack often recur during other phases of the attack, resulting in a continuum of
symptoms, rather than a succession of distinct phases.
CLINICAL PHASES OF MIGRAINE1
A migraine attack can take days to develop and resolve; headache is only 1 of several symptoms associated with migraine.1
Although the symptoms of migraine often overlap, the classic view is to separate an attack into phases.1
The Premonitory Phase1
Seventy percent of patients suffering from migraine with or without aura experience premonitory symptoms.1
Premonitory symptoms are often seen as predictors of the headache attack. 1
Mood alterations, muscle pain, food cravings, cognitive changes, fluid retention, and yawning are common premonitory symptoms.1
Eighty-three percent of subjects with premonitory symptoms could predict over 50% of their attacks.1
The Aura Phase 1
An aura involves focal, reversible neurologic symptoms that often precede the headache.1
Aura symptoms are believed to arise from an electrical disturbance called cortical spreading depression (CSD); it occurs in approximately was 15-32% of migraine attacks.1,2,3
Auras are not always followed by headache pain; such auras are called acephalgic migraine or migraine aura without headache.1
The Headache Phase1
The headache phase is subdivided according to headache pain intensity into an early phase and an advanced phase.1
Early headache: mild pain without the associated symptoms of migraine1
Advanced headache: moderate to severe pain with the associated symptoms of nausea, photophobia, phonophobia, or disability; used to confirm a migraine diagnosis1
Postdrome1
Phase of migraine-associated symptoms beyond the resolution of the headache; often entails significant disability that can last for 1 or 2 days.1
R1, p 206, C1,
Par 1, L 1-14
Preheadache
Mild
Moderate
Severe
Post headache
Time
R1, p 206, C1,
Par 2, L 1-12
and C2, Par 1,
L 1-9
Headache
R1, p 206, C2,
Par 2, L 1-13
R2, p5, para3, L1-2
R3, p222-3, last para-cont, L11-12
R1, p 206, C2,
Par 3, L 1-7
and p 207, C1,
Par 1 and Par 2
R1, p 207, C1,
Par 3, L 1-4 30
References:
Cady R, Schreiber C, Farmer K, Sheftell F. Primary headaches: a convergence hypothesis. Headache. 2002;42(3):204–216
Launer LJ, Terwindt GM, Ferrari MD. The prevalence and characteristics of migraine in a population-based cohort: the GEM study.
Neurology. 1999; 53(3): 537—542.
3. Rasmussen BK, Olesen J. Migraine with aura and migraine without aura: an epidemiological study. Cephalalgia.1992;12(4): .

31. Migraine Acute treatment
Paracetamol, Aspirin, Prokinetic (Domperidone/metochlorpropramide).
Triptan
Not opiates

32. 30 year old
Migraine with aura
GP given Sumatriptan 50mg
Not effective

33. Problems Gastric stasis Change formulation (nasal, (wafer), inj)
Takes too late or in aura phase
Change the Triptan (failure not a class effect)
Medication overuse headache

34. Medication overuse Headache
3% of population
Analgesics > 15 days of month
Triptans > 10 days of month

35. Medication overuse headache
Withdrawal of all analgesia
Increased frequency of headache,
associated with increased frequency of analgesia use.
Return of episodic
headache
Daily headache with spikes of more severe pain
Headache intensity
Migraine attacks
Frequent ‘daily’ headaches 35

36. Migraine with aura taking Sumatriptan 100mg Which cause you concern?
On Loestrin 20
Age 69
Past history TIA
Started SSRI

38. Loestin 20
Absolute risk of stroke Bejot 2016

39. Stroke relative risks Schurks 09
MA ( ) > MwA 1.2 ( )
Female>male: 2.08 ( ) > 1.37 ( )
Under 45>over 45: 3.65 ( )

40. Incidence MI/100,000 Cheng-Han 14

41. Myocardial infact Sacco 2009
Meta analysis 15 studies
All migraine RR 1.33 ( )
MA (n-1) ( )

43. Possible mechanisms Endothelial dysfunction Platelet dysfunction
Mitochondrial dysfunction
Patent foramen ovale

44. The white matter story

45. The white matter story Krutz 2004, Swartz 2004, Xie 2018
Nature of lesions unclear (? Microvascular)
Increase with age
Associated with posterior circulation infarcts (? More vunerable)
Female>male
Migraine>non-migraine
Aura>without aura
Related to migraine frequency

46. Preventative Medications in Migraine
Cupboard 1
Propranolol
Amitriptyline
Topiramate

47. CGRP monoclonals Eptinezumab Alder IV Erenumab1 AIMOVIG Novartis SC
Galcanezumab2
EMAGALITY
Lily
Fremenezumab3
AJOVY
Teva
EU Approval
1 =July 18
2= Nov 18
3 = Likely April 19

48. Chronic Migraine CGRP v Current Therapies

49. Needles – occipital nerve injection

50. BOTOX® for Chronic Migraine
Needles - Botox
BOTOX® for Chronic Migraine
UK licence for Chronic Migraine, NICE approved
≥15 days headache of which ≥8 days are migraine
Rejected by SMC (2011 and 2013)
Starting to be used in patients where most other treatments have failed
Mean change in frequency of headache days from baseline (days/28-day period) 52 48 44 40 36 32 28 24 16 12 8 4
Study week 20 56 -2 -4 -6 -8
-10
-12
-14
BOTOX® (n=688)
Placebo (n=696)
p=0.019
p=0.047
p=0.007
p=0.01
p=0.008
p<0.001
Double-blind phase:
BOTOX® vs. placebo
Open-label phase:
All patients on BOTOX®
p=0.011

52. Transcutaneous vagal nerve stimulation

53. Supra-orbital nerve stimulator

54. Exercise headache 35 yr female Migraine 1-2 each year
Noticed headache on running
Diagnosis?

55. Exercise headache Migraine 10% Sub arachnoid SOL AC malformation
Primary exercise headache

56. Pressure too low

57. 35 yr male
Car shunt one week ago
3 days non specific headache
Diagnosis?

59. Brain injury Direct neuronal damage
Secondary damage due to vascular insult
Inflammatory response and resolution

60. Post Traumatic Headache
(Post Traumatic syndrome)

61. Predominant clinical feature
Classification
Current terms
Time to onset
Length of symptoms
Insult
Predominant clinical feature
Pathophysiology
Traumatic brain injury with immediate effects
Acute traumatic brain injury
Concussion
Immediate
Days
Single episode of trauma
Alterations in consciousness
Direct axonal damage
Traumatic brain injury with early effects
Sub-acute traumatic brain injury
Hours to days
Weeks to months
Headache
(IHS < 7 days)
Inappropriate inflammatory cascade
Traumatic brain injury with late effects
Chronic traumatic encephalopathy
Years
Multiple small traumas. E.g. boxing, heading of the football
Cognitive dysfunction
Pragmatic classification of traumatic brain injury with associated features

64. Brain tumour primary or secondary

65. Tumour diagnosis setting65

66. Presentations
New onset seizure has the highest positive predictive value of 1-2%
Headache most common 23-56% of patients present with headache as their initial symptom

67. Red Flags Headache with: Abnormal neurological symptoms or signs
New seizure
Headache with exercise
History of cancer elsewhere

68. Orange Flags Aggregated by Valsalva manoeuvre
Headache with significant change in character
Awakes from sleep
New headache over 50 years
Memory loss
Personality change
If a primary headache diagnosis has not emerged in an isolated headache after 8 weeks

69. Primary Brain Tumour Population investigated Risk of tumour
All consultations with GP for headache
0.09%
All consultations with GP where a diagnosis of migraine is made
0.045%
All consultations with GP with special interest in headache with headache in intermediate care setting
0.6%
All consultations with secondary care neurology with headache
Casualty
0.8%
0.17%
Primary Brain Tumour
Population incidence 10/100,000 per year

70. Two default diagnoses
< 50 years Migraine

71. >50 years Temporal arteritis Systemically unwell
Tender artery with allodynia
CRP better than ESR
Problem with skip lesions

72. Primary Brain Tumour Population investigated Risk of tumour
All consultations with GP for headache
0.09%
All consultations with GP where a diagnosis of migraine is made
0.045%
All consultations with GP with special interest in headache with headache in intermediate care setting
0.6%
All consultations with secondary care neurology with headache
Casualty
0.8%
0.17%
Primary Brain Tumour
Population incidence 10/100,000 per year