1. D R S A U M Y A M I T T A L
Headache is one of the most common health complaints
in children and adolescents.
Migraine commonly starts in childhood and adolescence.
Early recognition and establishment of acute therapies
and lifestyle adjustments can affect
the disease progression for lifetime of the individual,
prevent long-term discomfort, and
enhance quality of life
It remains under-recognised as a problem by patients,
parents, and practitioners.
The prevalence of migraine has been studied across all
ages starting in early childhood.
There is a slight predominance in boys in the pre-
pubertal years. Overall occurrence increases throughout
adolescence into young adulthood. Then there is a
transition to a predominance in girls.
Age 7-15 years, - 3.9% children
1.7% in 7 year old
5.3% in 15 year old
Similar trend were seen on most studies.
Country to country variations exist.
Overall, this headache disorder remains common.
4. Late Adolescent-Young Adult age group??
Few reports regarding epidemiological for late
adolescents to young adult years.
Split and Neuman- In 2351 individuals aged 15–19
years, up to 28% had migraine.
19% -migraine without aura
9% -migraine with aura.
Stewart et al- Of 10169 individuals aged 12–29 years,
the onset of migraine with or without aura was
significantly earlier in male participants than in
Aura occurred in 25%.
5. How Teachers can be Unfair..
In an study of 4386 adolescents (11, 13,and 15 years)
40% reported having at least one headache a week.
This high frequency of headaches correlated with a
perception of teacher unfairness towards the student
and a poor recognition of the headaches as a
Other studies from Thailand, Germany, Turkey, and
Taiwan reported similar findings.
6. Independent Factors Contributing to Migraine
In children these factors include
a family history of migraine, and
smoking in the household.
There’s an inverse relationship with social economic
7. T h e p a t h o p h y s i o l o g y o f m i g r a i n e i n c h i l d r e n a n d
a d o l e s c e n t s i s p r e s u m e d t o b e t h e s a m e a s i n a d u l t s .
T h e s t u d y o f
M i g r a i n e p a t h o p h y s i o l o g y c a n b e d i v i d e d i n t o t h e
u n d e r l y i n g b a s i s t h e r i s k o f h a v i n g m i g r a i n e a n d f o r t h e
b i o l o g i c a l p r o c e s s e s t h a t o c c u r d u r i n g t h e a t t a c k .
The phenotypic expression migraine depends on a
the genetic inheritance and
the environmental effects.
The best-fitting model showed a genetic influence of
60–70%. Remaining risk derived from a non-shared
While the roles of individual genes in migraine are
beginning to be understood, the genetic risk factors
for migraine remain largely unknown.
9. Individual Gene and Manifestations
A rare subtype of migraine, familial hemiplegic
migraine shows mutations in
a calcium channel gene, CACNA1A,
a sodium/potassium pump gene, ATP1A2, and
a sodium channel gene, SCN1A.
fourth possible gene on chromsome 14q32
This provides insights into the importance of
ion channels (CACNA1A and SCN1A).
astrocytes (ATP1A2) - connection and regulation between
neuron and vessels is implicated in migraine expression.
neurotransmission between neurons contributes to allodynia
10. Genetic Biomarkers
Genetic biomarkers may be potentially used in few
serotonin transporters, a potassium channel (KCNN3),
5’,10’-methylenetetrahydrofolate reductase (MTHFR),
matrix metalloproteinase 3.
Identification of the role of these genes suggests a
complex interaction between neurotransmitters,
channels, and metabolism that needs to be
11. Biological changes
Immunological and inflammatory changes have been
linked to migraine in children.
In a study by Bockowski and colleagues, 36 children with a history of
detectable levels of interleukin 1α (not seen in children with TTH)
concentrations of both soluble tumour necrosis factor receptor
1 and tumour necrosis factor were increased.
Currently no biological markers for migraine.
Potential biomarkers for some groups of patients with
migraine have been identified.
increased levels of calcitonin gene-related peptide and
decreased levels of coenzyme Q10.
12. Hormones and migraine
Hormonal changes might influence paediatric
This partly explains shift in predominance to girls in
The basis for menstrual migraine seems to be a hormonal
13. Neurophysiological changes
Neurophysiological changes in migraine suggests
that migraine is
A vascular disease asthought historically.
Interictal trigeminal sensation occurs as shown by an altered
blink reflex, altered visual-evoked responses and altered
The P100 visual response during VEP had a higher latency and
There was a reduction in the N180 latency in response to VEPs, with
a prolongation in N180 in children older than 12 years who had
migraine without aura.
Brainstem auditory-evoked potential did not vary between any of
Transcranial magnetic stimulation to examine cortical excitability in
children showed altered occipital response (but not motor cortex
Phosphene generation was lower for patients with migraine than for
healthy controls for all times tested, whereas the threshold was
increased before an attack in patients.
P300 responses were substantially slower in children with migraine
or TTH than in controls.
15. Conclusion of Neurophysiological changes
These neurophysiological changes indicate that
the altered sensitivity in the migraine brain might be involved
in the initiation and propagation of migraine.
ongoing neurophysiological changes in paediatric patients
with migraine could affect their behavioural presentation.
Cutaneous allodynia occurs due to central
Its studied in adults as a clinical marker that reflects
migraine related neurophysiological changes.
Altered responses to treatment and possible disease
progression occurs in these patients.
In children, allodynia is beginning to be examined
and only small studies have been done so far.
17. A D E T A I L E D H I S T O R Y I S T H E B A S E O F G O O D P A T I E N T C A R E
I N A L L N E U R O L O G I C A L P A T I E N T S . A N D T H I S H O L D S T R U E
F O R H E A D A C H E A S W E L L .
Routine neurological examination should be
neck tenderness and stability,
stability of the temporomandibular joint,
sinus and facial tenderness including peripheral
nerve tenderness, and
general cranial palpation.
Muller’s sign- when patients pressurise their sinus
and then cough to create a brief vacuum, thus
enabling the evaluation of the openness of the
sinuses- assesses sinus related headache.
20. Those cute Drawings give a Clue- Elementary my
In young children, obtaining a complete history can
To assist with this, the use of children’s drawings-
can be both sensitive and specific.
Identification of elements of the children’s drawings
enables differentiation of the three diagnoses.
The drawings also serve as a basis for standardised
drawings for future paediatric patients to examine to
facilitate their diagnosis.
Neurological examination is the most crucial test.
Occipital location warranted further evaluation.
MRI are not usually necessary if
primary headaches are long standing,
do not change
Have a normal neurological examination.
When further evaluation is needed, an MRI examination is the
most sensitive test to identify structural abnormalities and
should be the preferred neuroimaging test. A routine MRI is
usually sufficient, unless there are clinical and physical
findings that would suggest the need to undertake further
imaging studies, such as magnetic resonance angiography
when a vascular disorder is suspected or diffusion-weighted
imaging when there is an acute change or injury.
25. Any headache by ICHD- II classification is first
I. Primary headache
II. Secondary headache
III. Cranial Neuralgia
26. Primary headaches are further classified as
1. Migraine (ICD 10- G43)
2. Tension type headache
3. Cluster headache and other trigeminal neuralgias.
4. Other primary headaches eg cough headache,
exertional headache etc.
27. Migraine is further classified into
1.1 Migraine without aura
1.2 Migraine with aura
1.3 Childhood periodic syndromes that are commonly
precursors to migraine
1.4 Retinal migraines
1.5 Complications of migraines
1.6 Probable migraines
28. Childhood periodic syndromes that are commonly
precursors to migraine are further classified into
1.3.1 Cyclical vomiting (ICD10- G43.82)
1.3.2 Abdominal Migraine (ICD10- G43.820)
1.3.3 Benign Paroxysmal Vertigo of Childhood (ICD10- G43.821)
29. Why the Precursors
In young children, the diagnosis of the childhood
periodic syndromes (thought to be precursors of
migraine) are often first recognised because a child
might not focus on head pain, but instead on some of
the abdominal symptoms (cyclic vomiting and
abdominal migraine) or vertigo (benign paroxysmal
vertigo of childhood). As the child grows older they
are better able to describe the head pain and the
presence of migraine becomes more evident.
30. Purpose of Diagnoses
The desired details
depends on the purpose.
Generally, first 2 digits
diagnoses are usually
applied. In specialist
practice eg at headache
centres, 3rd and 4th digit
levels are appropriate
31. ( I C D 1 0 - G 4 3 . 8 2 )
I t i s a s e l f l i m i t i n g ep i s o d e i n c h i l d h o o d . T h e r e i s a h i s t o r y
o f r e c u r r e n t e p i s o d i c v o m i t t i n g a n d n a u s e a a s s o c i a t e d w i t h
p a l l o r a n d l e t h a r g y w i t h c o m p l e t e r e s o l u t i o n in b e t w e e n
a t t a c k s w i t h n o hi s t o r y a n d s i g n s s u g g e s t i v e o f a
g a s t r o i n t e s t i n a l d i s e a s e .
1. At least 5 attacks with the following (2 and 3)
2. Episodic attacks of intense emesis and nausea
lasting 1 hour to 5 days, stereotypical in individual
3. Emesis during attacks occur at least 4 times per
hour for at least one hour.
4. Sypmtom free in between attacks.
5. Not attributed to another disorder.
33. ( I C D 1 0 - G 4 3 . 8 2 0 )
S e e n m a i nl y i n c h i l d r e n , t h e r e i s i d i o pa t h i c r e c u r r e n t
e p i s o d i c a t t a c k s o f m i d l i n e m o de r a t e t o s e v e r e a b d o m i n a l
p a i n i n t e r f e r i n g w i t h n o r m a l d a i l y a c t i v i t i e s a n d l a s t i n g 1 t o
7 2 h o u r s a s s o c i a t e d w i t h v a s o m o t o r s y m p t o m s ( f l u s h i n g i s
t h e p r e d o m i n a n t s y m p t o m i n f e w ) , n a u s e a a n d e m e s i s . T h e r e
i s n o r m a l c y i n b e t w ee n e p i s o d es . G a s t r o i n t e s t i n a l a n d r e n a l
c a u s e s s h o u l d h a v e b e e n r u l e d o u t o n h i s t o r y , e x a m i n a t i o n o r
i n v e s t i g a t i o n s . T h e p a t i e n t s m a y s h o w p a l l o r a c c o m p a n i e d b y
d a r k s h a d o w s u n d e r t h e e y e s .
1. At least 5 attacks with following (2 to 4)
2. Attacks of abdominal pain last 1 to 72 hours (treated successfully or
3. Abdominal pain with following characters
1. location- midline, periumbilical or poorly localized
2. dull or 'just sore' quality
3. moderate or severe intensitya
4. At least 2 of the following during abdominal pain
5. Not attributed to another disorder.
6. Most children develop migraine headache later in life.
35. ( I C D 1 0 - G 4 3 . 8 2 1 )
VERTIGO OF CHILDHOOD
T h i s h e t e r o g en o u s d i s o r d e r i s c h a r a c t e r i z e d b y r e c u r r e n t
b r i e f a t t a c k s o f v e r t i g o o c c u r i n g w i t h o u t w a r n i n g a n d
r e s o l v i n g s p o n t an e o u s l y i n t h e s e c h i l d r e n w h o a r e o t h e r w i s e
n o r m a l . T h e r e m a y b e a s s o c i a t ed n y s t a g m u s , v o m i t i n g o r
u n i l a t e r a l h e a d a c h e i n s o m e e p i s o d e s .
1. At least 5 attacks with the following criteria (2)
2. Multiple episodes of severe vertigo, without
warning, resolving spontaneously within minutes
3. Normal neurological exam, audiometric and
vestibular function tests.
4. Normal EEG.
37. M i g r a i n e c a n b e s u b d i v i d e d i n t o
•m i g r a i n e w i t h o u t a u r a ,
•m i g r a i n e w i t h a u r a ,
•r e t i n a l m i g r a i n e ,
•m i g r a i n e c o m p l i c a t i o n s ,
•p r o b a b l e m i g r a i n e .
A d d i t i o n al a s p e c t s o f m i g r a i n e i n c h i l d r e n , p a r t i c u l a r l y
d u r i n g t h e i r a d o l e s c e n t y e a r s i n c l u d e
•c h r o n i c m i g r a i n e
•s t a t u s m i g r a i n o s u s .
38. I C D 1 0 - G 4 3 . 0
P r e v i o u s l y c a l l e d c o m m o n m i g r a i n e , h e m i c r a n i a s i m p l e x
MIGRAINE WITHOUT AURA
R e c u r r e n t a t t a c k s o f u n i l a t er a l p u l s a t i l e h e a d a c h e s o f
m o d e r a t e o r s e v e r e i n t e n s i t y l a s t i n g 4 - 7 2 h o u r s a g g r a v a t e d
b y r o u t i n e p h y s i c a l a c t i v i t y a n d a s s o c i a t e d w i t h n a u s e a
a n d / o r p h o t o p h o b i a a n d p h o n o p h o b i a .
1. At least 5 attacks fulfilling criteria 2-4
2. Headache attacks lasting 4-72 hours (untreated or
3. Headache has at least two of the following characteristics:
1. unilateral location
2. pulsating quality
3. moderate or severe pain intensity
4. aggravation by or causing avoidance of routine physical activity (eg,
walking or climbing stairs)
4. During headache at least one of the following:
1. nausea and/or vomiting
2. photophobia and phonophobia
5. Not attributed to another disorder
40. Additional Points
Footnotes for migraine without aura, resulting in an
improvement in the specificity and sensitivity
childhood migraine tends to be shorter in duration (down to 1
h with diary confirmation),
that sleep should be included as part of the duration,
that the location is more likely to be bilateral (typically frontal-
that photophobia and phonophobia could be inferred by the
parents or care providers on the basis of the child’s actions.
if the location is exclusively occipital, further assessment is
41. I C D 1 0 - G 4 3 . 1
P r e v i o u s l y t e r m e d c l a s s i c o r c l a s s i c a l m i g r a i n e ,
o p h t h a l m i c , h e m i p a r a e s t h e t i c , h e m i p l e g i c o r
a p h a s i c m i g r a i n e , m i g r a i n e a c c o m p a g n é e ,
c o m p l i c a t e d m i g r a i n e
MIGRAINE WITH AURA
R e c u r r e n t a t t a c k s o f r e v e r s i b l e f o c al n e u r o l o g ic a l s y m p t o m s
t h a t u s u a l l y d e v e l o p g r a d u a l l y o v e r 5 - 2 0 m i n u t e s a n d l a s t f o r
l e s s t h a n 6 0 m i n u t e s . H e a d a c h e w i t h t h e f e a t u r e s o f m i g r a i n e
w i t h o u t a u r a u s u a l l y f o l l o w s t h e a u r a s y m p t o m s .
1. At least 2 attacks fulfilling criterion 3
2. Not attributed to another disorder
3. Migraine aura fulfilling criteria B and C for one of
the sub forms
1.2.1 Typical aura with migraine headache
1.2.2 Typical aura with non migraine headache
1.2.3 Typical aura without headache
1.2.4 Familial hemiplegic migraine
1.2.5 Sporadic hemiplegic migraine
1,2,6 Basilar type migraine
43. Probable migraine (ICD-10 G43.83)
Individuals who otherwise meet criteria for Migraine
without aura but have had fewer than 5 attacks
should be called Probable migraine without aura
(1.6.3 Probable childhood periodic syndromes that
are commonly precursors of migraine and
1.6.4 Probable retinal migraine are not currently
44. Chronic migraine (ICD 10- G43.3)
When attacks occur on ≥15 days/month for >3
months, the migraine is called Chronic migraine
provided that there is no medication overuse.
Migraine without aura is the disease most prone to accelerate
with frequent use of symptomatic medication, resulting in a
new headache which is Medication-overuse headache coded
45. Status migrainosus (ICD 10- G43.2)
1. The present attack in a patient with 1.1 Migraine without
aura is typical of previous attacks except for its duration
2. Headache has both of the following features:
1. unremitting for >72 hours
2. severe intensity
3. Not attributed to another disorder
Interruption during sleep is disregarded.
Short-lasting relief due to medication is also disregarded.
Status may often be caused by medication overuse and should
be coded accordingly.
Non-debilitating attacks lasting >72 hours but otherwise
meeting these criteria are coded as 1.6.1 Probable migraine
46. Retinal migraine (ICD10- G43.81)
Repeated attacks of monocular visual disturbance,
including scintillations, scotomata or blindness,
associated with migraine headache.
Appropriate investigations exclude other causes of
transient monocular blindness (amaurosis fugax)
1. At least 2 attacks fulfilling criteria 2-3
2. Fully reversible monocular positive and/or negative
visual phenomena (eg, scintillations, scotomata or
blindness) confirmed by examination during an attack
or (after proper instruction) by the patient's drawing of
a monocular field defect during an attack
3. Headache fulfilling criteria 2-4 for 1.1 Migraine
without aura begins during the visual symptoms or
follows them within 60 minutes
4. Normal ophthalmological examination between attacks
5. Not attributed to another disorder
49. In Paediatric Population
The treatment of paediatric migraine can be divided
biobehavioural interventions to minimise the effects of the
50. Acute treatment
The goal of acute treatment of paediatric migraine should be
a consistent response with minimum side-effects and
rapid return to normal function.
Drugs approved for acute treatment of adolescent migraine
only almotriptan by US FDA
Nasal sumatriptan and zolmitriptan approved EMEA.
Effective acute drugs fell into two broad groups:
non-steroidal anti-inflammatory drugs (NSAIDs) and
Subsequently, additional studies have indicated that NSAIDs
(particularly ibuprofen) are effective when used early in the
attacks at an adequate dose (7.5–10 mg/kg per dose) and that
triptans are effective when NSAIDs do not completely relieve
symptoms, particularly during the more severe attacks.
51. When acute treatment doesnt relieve headache
Patients visit the emergency department or infusion
The paediatric ER treat these children with dopamine
antagonists (adult ER use opiates).
When these emergency department treatments are not
successful, inpatient treatment might be necessary-
adults use dihydroergotamine.
52. Preventive Therapy
When the headaches are frequent (more than once a week) or disabling
(PedMIDAS score >30 [grade III or IV]), preventive treatment should be
The goal of preventive treatment is to reduce the headache frequency (to
<1–2 per month), with a decreased disability (PedMIDAS <10) for a
sustained period of time (4–6 months).
No drugs are approved in the USA for the prevention of paediatric
migraine. The American Academy of Neurology practice guidelines for
headache identified flunarazine as having sufficient evidence for efficacy
but this drug is not available in the USA, whereas flunarizine has been
approved for use in Europe.
Drugs that have been used for prevention of paediatric migraine include
antidepressants (eg, amitriptyline),
antihypertensives (eg, propranolol),
antiserotonergics (eg, cyproheptadine), and
anti epileptic medications (eg, valproic acid and topiramate).
Nutraceuticals might be effective in treating
Coenzyme Q deficiency has been found in many
young migrainers. Supplementation was associated
with an improvement in headache frequency.
Other options include
54. Behavioral Therapy
Biobehavioural therapy, or the incorporation of
adherence, education, lifestyle adjustment, and
coping skills, is essential to the management of
These changes can include
reduced intake of caffeine-containing beverages,
a healthy, balanced diet without skipping meals,
regular exercise, and
sufficient sleep on a regular basis
55. Educating the patient and their family about the
proper use of their acute and preventive therapies,
with a discussion about the importance of treatment
and inclusion of the child in the decision-making
process, can greatly improve the adherence to
57. Needs More Work
These suggestions increased the number of children who met the
criteria, but there remained a subgroup of patients with migraine
who did not meet the criteria.
Further work is necessary to develop improved markers for the
identification of paediatric migraine.
Even with these limitations, the evaluation and diagnosis of
paediatric headaches should involve the use of these criteria as a
Standardised questionnaires with a semi-structured interview can
be used to obtain a more thorough evaluation.
Such an approach has been shown to be very sensitive and specific
in making the appropriate diagnosis of headache.
This evaluation must incorporate the children’s responses and
should not just be completed by the parents. Parents might not
always be completely aware of the child’s symptoms or the effect of
In a study from a tertiary headache centre, the menstrual pattern was evident even before girls began menarche, and became consistent once menarche had started. In a population-based study, the onset of menarche was associated with an increased risk of recurrent headaches, although the frequency of headaches was not affected.
The P100 visual response during visual-evoked potential testing had a higher latency and amplitude in patients with migraine.
There was a reduction in the N180 latency in response to visual-evoked potentials, with a prolongation in N180 in children older than 12 years who had migraine without aura.
Brainstem auditory-evoked potential did not vary between any of the groups.
Transcranial magnetic stimulation to examine cortical excitability in children showed altered occipital response (but not motor cortex response).
Phosphene generation was lower for patients with migraine than for healthy controls for all times tested, whereas the threshold was increased before an attack in patients.
P300 responses were substantially slower in children with migraine or TTH than in controls.