bagaimana hubungan nyeri kepala dengan epilepsi? epilepsi menyebabkan nyeri kepala? nyeri kepala menyebabkan epilepsi? epilepsi yang manifestasinya nyeri kepala? kapan kita curiga suatu nyeri kepala merupakan bentuk kejang?

1. Seizure-related
Headache
Review & Case Report
Ersifa Fatimah, dr.
FK Universitas Airlangga
RS Dr Soetomo
Surabaya, 2013

2. Introduction
• Abundant clinical and epidemiologic data
demonstrate that headache/migraine and
epilepsy are highly comorbid.
• The disorders share overlapping risk factors,
brain mechanisms, and treatments.
• The clinical presentation of migraine and
epilepsy may overlap, creating a challenge in
differential diagnosis.
Engel & pedley, Epilepsy, A Comprehensive Textbook, 2nd eds, 2008, p 5257 -5273
2

3. Introduction
• Periictal headache (PIH) displays a frequent
ancillary burden to seizures, but identification
of unequivocal predictors is still elusive. PIH is
frequent, severe and undertreated.
Duchaczeck B et al. Interictal and periictal headache in patients with epilepsy.
Eur J Neurol. 2012 Dec 25.
3

4. Introduction
• The relationship between headache and seizures is a
complicated one, since these two conditions are related in
numerous ways.
• In order to improve the care for patients with a clinical
connection between migraine and epilepsy, it is necessary to
try to understand more accurately the exact
pathophysiological point of connection between these two
conditions.
Papetti et al. “Headache and epilepsy”— How are they connected?
Epilepsy&Behavior26(2013)386–393
4

5. Introduction
• Major discrepancies and conflicting data about
comorbidity between headache and epilepsy due
to: [1]
– the confusion and mixture of epidemiological data
between adults and children across studies
– the significant underestimation of headache when it
is comorbid in populations with epilepsy.
• Due to the different methodologies and criteria
used, the studies are quite difficult to compare. [2]
5

6. Migralepsy
Hemicrania epileptica
Epilepgraine
Migrainetriggered
seizure
Post-ictal headache
Hybrid
crisis
6

7. Kasus
Px
LK
SR
PU
FM
SN
Jenis/ Usia
Karakteristik nyeri kepala
(thn)/ Status/
Pekerjaan
P/49/
“Kemeng”, unilateral (kiri)
Menikah/
sekitar mata & hidung,
Ibu rumah
tangga
Gejala
penyerta
Mata kiri
merah, kabur,
mual.
Variabel epilepsi & terapi
EEG
CT/MRI
(Riwayat syncope saat kanak Sharp wave & ISA
& pelo mendadak 5 tahun
temporal kiri
lalu)
Normal
P/29/ Belum
menikah/
Pembantu
rumah tangga
L/33/
Menikah/
“tukang
odongodong”
P/16/ Belum
menikah/
Pelajar
Berdenyut bilateral, 2-3
jam, muncul setelah kejang
Kejang fokal umum sekunder tonik klonik, aura: melihat
sawah
-
Berdenyut, unilateral (kiri),
muncul setelah kejang.
Mual
Automatisme sejak 10 tahun Sharp wave & ISA
lalu, kejang umum tonik
temporal D/S (Interklonik sejak 3 bulan lalu
ictal, 2013)
Toxo dd
Tuberculoma di
cerebellum
Berdenyut, unilateral 
bilateral (mulai kanan), 1
jam, aura (-)
Mual, muntah,
fotofobia
Fokal kiri umum sekunder
tonik sejak usia 3 bulan
Normal (inter-ictal, 4
tahun lalu)
?
P/60/
Menikah/
Penjahit
Berat/ditekan bilateral
Rasa tidak
nyaman di
perut, depresi
Kejang parsial kompleks 7
tahun lalu, kejang umum
tonik-klonik sejak 1 tahun
lalu
Sharp wave di regio
temporal kiri (interictal?, 2012)
Normal
7

8. Kasus
Px
LK
SR
PU
FM
SN
Jenis/ Usia
Karakteristik nyeri kepala
(thn)/ Status/
Pekerjaan
P/49/
Kemeng, unilateral (kiri)
Menikah/
sekitar mata & hidung,
Ibu rumah
tangga
Gejala
penyerta
Mata kiri
merah, kabur,
mual.
P/29/ Belum
menikah/
Pembantu
rumah tangga
L/33/
Menikah/
“tukang
odongodong”
P/16/ Belum
menikah/
Pelajar
Berdenyut bilateral, 2-3
jam, muncul setelah kejang
P/60/
Menikah/
Penjahit
Berat/ditekan bilateral
•
•
•
Berdenyut, unilateral 
•
bilateral (mulai kanan), 1
Berdenyut, unilateral (kiri),
muncul setelah kejang.
Variabel epilepsi & terapi
EEG
CT/MRI
(Riwayat syncope saat kanak Sharp wave & ISA
& pelo mendadak 5 tahun
temporal kiri
lalu)
Normal
Kejang fokal umum sekunder tonik klonik, aura: melihat
sawah
-
Perempuan >sejak 10 tahun Sharp wave & ISA
Laki
Automatisme
lalu, kejang
Usia muda >umum tonik temporal D/S (Interklonik sejak 3 bulan lalu
ictal, 2013)
Berdenyut > Nyeri kepala lain
Mual, muntah, Fokal kiri umum sekunder
(inter-ictal, 4
Lobus Temporal > Normallalu)
fotofobia
tonik sejak usia 3 bulan
tahun
Mual
Toxo dd
Tuberculoma di
cerebellum
?
jam, aura (-)
Rasa tidak
nyaman di
perut, depresi
Kejang parsial kompleks 7
tahun lalu, kejang umum
tonik-klonik sejak 1 tahun
lalu
Sharp wave di regio
temporal kiri (interictal?, 2012)
Normal
8

9. Kasus
Px
LK
SR
PU
FM
SN
Jenis/ Usia
Karakteristik nyeri kepala
(thn)/ Status/
Pekerjaan
P/49/
Kemeng, unilateral (kiri)
Menikah/
sekitar mata & hidung,
Ibu rumah
tangga
Gejala
penyerta
Mata kiri
merah, kabur,
mual.
P/29/ Belum
menikah/
Pembantu
rumah tangga
L/33/
Menikah/
“tukang
odongodong”
P/16/ Belum
menikah/
Pelajar
Berdenyut bilateral, 2-3
jam, muncul setelah kejang
P/60/
Menikah/
Penjahit
Berat/ditekan bilateral
•
•
•
Berdenyut, unilateral 
•
bilateral (mulai kanan), 1
Berdenyut, unilateral (kiri),
muncul setelah kejang.
Variabel epilepsi & terapi
EEG
CT/MRI
(Riwayat syncope saat kanak Sharp wave & ISA
& pelo mendadak 5 tahun
temporal kiri (ictal,
lalu)
2013)
Normal
Kejang fokal umum sekunder tonik klonik, aura: melihat
sawah
-
Perempuan >sejak 10 tahun Sharp wave & ISA
Laki
Automatisme
lalu, kejang
Usia muda >umum tonik temporal D/S (Interklonik sejak 3 bulan lalu
ictal, 2013)
Berdenyut > Nyeri kepala lain
Mual, muntah, Fokal kiri umum sekunder
(inter-ictal, 4
Lobus Temporal > Normallalu)
fotofobia
tonik sejak usia 3 bulan
tahun
Mual
Toxo dd
Tuberculoma di
cerebellum
?
jam, aura (-)
Rasa tidak
nyaman di
perut, depresi
Kejang parsial kompleks 7
tahun lalu, kejang umum
tonik-klonik sejak 1 tahun
lalu
Sharp wave di regio
temporal kiri (interictal?, 2012)
Normal
9

10. Association between headache & epileptic seizure
according to their temporal occurrence
Pre-ictal headache
Ictal headache
Post-ictal headache
Inter-ictal headache
Cianchetti C, et al. Epileptic seizures and headache–migraine:
A review on types of association and terminology. Seizure: Eur J Epilepsy (2013)
10

11. Prevalence of headache and migraine in epilepsy
and its relationship with ictal and interictal period
Bianchin MM et al, Migraine and Epilepsy : A Focus on Overlapping Clinical, Pathophysiological, Molecular, and
11
Therapeutic Aspects. Curr Pain Headache Rep (2010)

12. Inter-ictal headache
prevalence
• Migraine in px wth epilepsy: 14-24%
• Epilepsy in px with migraine: 1.1-17%
Andermann et al, 1987, Tellez-Zenteno et al, 2005, Leinger et al, 2003
12

13. Inter-ictal headache
Tonini et al, 2012
• Research hypothesis:
comorbidity among patients with either disorder
would be expected to be higher than in the
general population
• Result:
prevalence of comorbidity in patients with
epilepsy and in those with headache roughly
overlaps that of the general population no
association between the two conditions.
13

14. Pre-ictal Headache/Migraine
Variants
• Migraine with aura followed by an
epileptic seizure
• ICHD-2: Migraine-triggered seizure
(Migralepsy)  prevalence is
unknown, associated with basilar-type
migraine & menstrual migraines
• Migraine without
aura followed by an
epileptic seizure
• Headache followed
by an epileptic
seizure
• Pre-ictal headache
• Pre-ictal migraine, migraine-triggered seizure
– Migraine attack, fulfilling migraine criteria, +/- aura,
– Seizure fulfilling diagnostic criteria for 1 type of epileptic attack
– Seizure occurs during/within (conventionally) 1 hour after cessation of the
migraine attack
• Pre-ictal headache
– When criteria for migraine are not met
Bianchin, 2010; Cianchetti et al, 2013
19

15. Pre-ictal Headache/Migraine
• Migrainous aura is the clinical manifestation of
cortical spreading depression(CSD), a potent
excitatory electrical neuronal wave followed
by neuronal inhibition and glial activation
Neuronal activation generated by CSD 
decreases the threshold in the epileptic focus
 increasing the risk of seizures
Bianchin MM et al, Migraine and Epilepsy : A Focus on Overlapping Clinical, Pathophysiological, Molecular,
and Therapeutic Aspects. Curr Pain Headache Rep (2010)
20

16. Pre-ictal Headache/Migraine
Direct surgical observations & neuroimaging
findings:
• Increased blood flow that precedes epileptic
seizures may trigger trigeminovascular
activation & consequent headaches
Bianchin MM et al, Migraine and Epilepsy : A Focus on Overlapping Clinical, Pathophysiological, Molecular,
and Therapeutic Aspects. Curr Pain Headache Rep (2010)
21

17. Ictal headache
Epileptic headache / Ictal epileptic headache
• Headache (whether migraine or not)
• Onset, and cessation if isolated, coinciding with an EEG
pattern of epileptic seizure
(rarely EEG alterations may only be detectable using deep
electrodes)
Cianchetti et al, 2013
Variants
• Not followed by other epileptic • Followed by other epileptic
manifestations
manifestations
• Pure/isolated epileptic
• Epileptic seizure beginning
headache
with headache
• ICHD-2: Hemicrania epileptica
23

18. Ictal headache
Epileptic headache / Ictal epileptic headache
Relatively low prevalence of ictal headaches due
to:
• Cognitive / consciousness impairments
provoked by seizures.
• Seizures propagate to the thalamus 
analgesic status may be rendered (evidence to
support this hypothesis is lacking)
Bianchin MM et al, Migraine and Epilepsy : A Focus on Overlapping Clinical, Pathophysiological, Molecular,
and Therapeutic Aspects. Curr Pain Headache Rep (2010)
24

19. Epileptic headache: Challenge
• Probably underdiagnosed
– Physician & patient tend to emphasize the other
epileptic manifestations
• Requiring a diagnostic differentiation from
other types of headache
– Particularly in pure epileptic headache & no
epileptic abnormalities are present in the
interictal EEG
Cianchetti C, et al. Epileptic seizures and headache–migraine:
A review on types of association and terminology. Seizure: Eur J Epilepsy (2013)
25

20. Migraine vs Epilepsy
• Share many features: chronic, episodic
manifestation, similarities of classification,
ictal progression, symptomology
• Differentiating is usually accomplished on
clinical ground
• EEG not routinely indicated in migraine, may
be useful
Haut S, Differentiating Migraine from Epilepsy. Adv Stud Med. 2005;5(6E):S658-S665
26

21. Migraine vs Epilepsy
Migraine
Epilepsy
Prevalence
Lower during earlier childhood,
decreasing again in older ages
Bimodal pattern, affecting
mostly children and the
Elderly
Sex
Female > Male
//
Consequences
Has not been associated with
reduced lifespan
Stigmatizing disease, being a
life-threatening condition
Bianchin MM et al, Migraine and Epilepsy : A Focus on Overlapping Clinical, Pathophysiological, Molecular,
and Therapeutic Aspects. Curr Pain Headache Rep (2010)
27

22. Migraine vs Epilepsy
Ictal Progression
Migraine
Preaura
prodrome/
Premonitory
phase
Aura
Epilepsy
Irritability, joy, or sadness
Talkactiveness or social withdrawal
Appetite change or anorexia
Water retention
Sleep diturbances
Heaviness, depression,
irritability
GI upset
(next table)
Ictus
Prolonged (4-72 hours) unilateral
Brief , self limited (1-2
throbbing headache with associated minute), exception:
features
status epilepticus
Automatism absent
Post-ictal
Impaired concentration, malaise, or
euphoria
Common post-ictal
state, marked after GTCS
Haut S, Differentiating Migraine from Epilepsy. Adv Stud Med. 2005;5(6E):S658-S665
28

23. Migraine vs Epilepsy
Aura
Migraine
Epilepsy
Definition
Complex of symtoms occuring
prior to, at onset, or during
migraine
Simple partial seizure, no
alteration on consciousness
Mechanism
Cortical spreading depression
Synchronous neuronal discharge,
limited distribution
Functional
imaging
Wave of decreased CBF
Increased cerebral blood flow &
metabolism
Duration
15-60 minutes, develops slowly
Brief (less than 1 minute)
Occur in
isolation
Yes. Acephalgic migraine, aura
without headache
Yes. Simple partial seizure
Common
symptoms
Visual: most common
Sensory: paresthesias
Motor: unilateral weakness
Limbic: abdominal sensation, fear,
deja vu
Sensory: paresthesias
Motor: twitching
Haut S, Differentiating Migraine from Epilepsy. Adv Stud Med. 2005;5(6E):S658-S665
29

24. Keywords
• Status migrainosus unresponsive to analgesic
therapy  iv administration of lorazepam
induced the prompt resolution of the
symptoms.
Belcastro et al. Ictal epileptic headache mimicking status migrainosus: EEG and DWI-MRI
findings. Headache. 2011 Jan;51(1):160-2.
• Brief episodes (of a few minutes) of severe
frontal headache..
Chiancetti et al. Pure epileptic headache and related manifestations: a video-EEG report and
discussion of terminology. Epileptic Disord. 2013 Mar;15(1):84-92.
31

25. EEG in the evaluation of Headache
A new list from the American Academy of Neurology
(AAN) calls into question 5 clinical practices judged
to be of little or no benefit for patients.
• Don't perform electroencephalography (EEG) for
headaches.
– Recurrent headache is the most common pain
problem, affecting up to 20% of the general population.
– EEG has no advantage over clinical evaluation in
diagnosing headache, does not improve outcomes, and
increases costs.
Jeffrey S. AAN Points to 5 Questionable Practices in Neurology. Medscape,
Feb 22, 2013. http://www.medscape.com/viewarticle/779756
32

26. EEG in the evaluation of Headache
• A total of 50 patients yielded 50 routine EEGs
(headache NOS, n = 32; migraine n = 18).
• Overall, there were 37 (74%) normal EEGs and 13
(26%) abnormal.
• Routine EEGs are mostly normal in young patients
(18-40 years of age) who are referred to our
laboratory with a diagnosis of headache NOS or
migraine.
Senthi NK et al. Diagnostic utility of routine EEG study in identifying seizure as the
etiology of the index event in patients referred with a diagnosis of migraine and not
otherwise specified headache disorders. Clin EEG Neurosci. 2012 Oct;43(4):323-5.
33

27. EEG in the evaluation of Headache
• Contributed greatly to increasing understanding
of the pathogenesis of primary headache, but
little / no value in the clinical setting.
• Interictal EEG is not routinely indicated in the
diagnostic evaluation of patients with headache.
• Interictal EEG is, however, indicated if the clinical
history suggests a possible diagnosis of epilepsy
(differential diagnosis).
• Ictal EEG could be useful in certain patients
suffering from hemiplegic or basilar migraine.
Sandrini G et al, Neurophysiological tests and neuroimaging procedures in nonacute headache (2nd edition). Eur J Neurol. 2011 Mar;18(3):373-81.
34

28. EEG in the evaluation of Migraine
• Striking EEG patterns have been described in specific subtypes of
migraine.
• The brain regions most often involved in the published EEG samples
in basilar-type migraine include the posterior temporal, parietal,
and occipital regions. The posterior electrographic localization may
not pertain to other forms of migraine.
• Paroxysmal lateralizing epileptiform discharges (PLEDs) or PLED-like
activity has been associated with hemiplegic migraine, prolonged
migraine aura, or incipient migrainous infarction. Those patients
with PLED-like activity did not have any of the usual entities
associated with PLEDs, such as stroke, brain abscess, glioblastoma,
or viral encephalitis, and their PLEDs usually resolved within 24
hours. Certain migralepsy patients had clinical seizures when PLEDs
were present on their EEGs.
Schachter SC (ed). Differential diagnosis of migraine and epilepsy.
http://professionals.epilepsy.com/page/migraine_eeg.html
35

29. Post-ictal Headache
• Features of tension-type headache OR
migraine headache (in px with migraine)
• Develops within 3 hours after seizure
• Diseappears within 72 hours after the seizure
• Partial or generalized epileptic seizure
ICHD-2, International Headache Society, 2004
Ekstein D, Schachter SC. Postictal headache. Epilepsy & Behavior 19 (2010) 151–155
43

30. Post-ictal headache
Risk Factor
Age
Significantly higher in younger patient [1]
Sex
Significantly higher in female [2]
Male : Female = 1:1.8 (pediatric) [3]
Relationship to interictal
headache
Occurrence of IIH appears to increase the risk
of PIH [4], especially with migraine [5]
PIH shorter duration than IIH [6]
Relationship to family history
of headache
No association [7]
Ekstein & Schachter, 2010
Controversy.
Other studies: not statistically significant association
44

31. Post-ictal headache
Association with epilepsy-related variables
Duration
Younger age of onset epilepsy
(HELP study, 2010: 22.1 vs 28.8)
Longer duration of disease
(HELP study, 2010: 9.9 years vs 7.3 years)
Severity
PIH correlated with AED polytherapy [1]
Characteristic of seizure
PIH more frequent after GTCS & more severe after
prolonged/repetitive seizure [2]
Occurred in 96 & 28 % GTCS, 88-62& secondary GTCS, 43%
partial seizure, 70-22% CPS
GTCS ~ nonmigraineous/ steady
CPS ~ throbbing
Classification/location of
epilepsy
No clear association
PIH is more frequent in OLE (59-62%) > FLE (40-42%) > TLE
(23-41%) [3]
Ekstein & Schachter, 2010
45

32. Post-ictal headache
Pathophysiology
• Headaches may occur as following brainstem
activation, with consequent trigeminal
activation and vasodilation
(as for pre-ictal headaches)
Bianchin MM et al, Migraine and Epilepsy : A Focus on Overlapping Clinical, Pathophysiological, Molecular,
and Therapeutic Aspects. Curr Pain Headache Rep (2010)
46

33. Patofisiologi Kejang
Gangguan permeabilitas membran neuron
Ketidakseimbangan inhibisi dan eksitasi
Disfungsi sel glia
Kejang  “Energy failure” Edema serebri  Nyeri kepala

34. Pathophysiology of Primary Headache
Migraine [Suharjanti, 2009 & 2013; Sjahrir, 2008]
•
•
•
•
•
Hyperexcitability neuronal
Cortical spreading depression
Trigeminal activation: peripheral & central
PAG: progressive changes
Genetic
Tension-type Headache [Suharjanti, 2009; Machfoed, 2008; Basir, 2012]
•
•
•
•
Muscle contraction
Vascular theory
Humoral theory
Posture
Cluster Headache [Suharjanti, 2009; Blanda, 2012]
•
•
•
•
•
Periodicity ~hypothalamus, central disinhibition of nociceptive & autonomic pathways
Trigeminal-facial neuronal circuitry alteration due to central sensitization
Substance P neurons in V1&2
Vascular dilatation (neurogenic)
Histamine?
52

35. • The mechanisms underlying the association of
migraine and epilepsy are yet to be elucidated
• Several subtypes of migraine disorders & of
epilepsy  mechanisms are likely to be
diverse
• Pathophysiological common aspects do exist
53

36. Migraine & Epilepsy
are characterized by
lower neuronal threshold
in the cortex
• Occipital cortex is particularly vulnerable to CSD
• Postictal headaches often having migraine-like
characteristics occur more in occipital epilepsy
• AEDs (eg, valproic acid, topiramate, gabapentin)
work for migraine prophylaxis
Bianchin et al, 2010
54

37. Migraine & Epilepsy
common genetic & molecular aspect
Gene/Locus
Migraine Epilepsy
CACNA1A (19p13)
pore-forming α1A-subunit of
voltage-dependent P/Q-type
calcium channels
FHM1
Different forms
of epilepsy
ATP1A2 (1q23)
poreforming α2 subunit of the
electrogenic Na+, K+-ATPase
FHM2
(occipitotempor
al epilepsy)
SCN1A
voltage-gated
Sodium (Na) channel α1-subunit
FHM3
Different forms
of epilepsy
SLC1A3
Excitatory aminoacid transporter1
POLG
mitochondrial DNA polymerase &
helicase
C10orF2
mitochondrial DNA polymerase &
helicase
Bianchin et al, 2010
55

38. Mutations
- Channelopathies  ionic homeostasis
- GABAergic/Glutamatergic systems
- Mitochondrial functions
Spectrum of nervous system diseases
with frequent migraine/epilepsy
comorbidity
Bianchin MM et al, Migraine and Epilepsy : A Focus on Overlapping Clinical, Pathophysiological,
Molecular, and Therapeutic Aspects. Curr Pain Headache Rep (2010)
56

39. Therapeutic Aspects
• Migraine & epilepsy are associated  clinicians
should be aware that individuals with one
disorder are more likely to have the other.
• Comorbidity should be considered when
developing treatment plan:
– TCA & neuroleptic drugs for migraine may lower
seizure thresholds
– Antimigraine anticonvulsants should be considered as
a simultaneous treatment for both disorders
Bianchin et al, 2010
57

40. Case
58

41. ?
Jenis nyeri kepala yang mana?
Kaitan nyeri kepala dengan kejang?
Penyebab nyeri kepala?
Terapi?
59

42. Tn. PU/ L/33/ Menikah/ “tukang odong-odong”
• Kejang seluruh tubuh saat sedang tidur, sejak seminggu
sebelum berobat ke Poli, kedua lengan & tungkai kaku
menghentak-hentak selama 5 menit. Lidah tergigit +. Sebelum
kejang tidak ada gejala khusus. Setelah kejang pasien segera
sadar dan mengalami nyeri kepala berdenyut sebelah kiri, VAS
5-6, disertai mual, menghilang sendiri dalam beberapa jam
atau setelah minum obat dari toko. Kejang berulang 2-3x
seminggu, muncul sewaktu-waktu, dengan pola yang sama.
Pasien juga mengeluhkan nyeri kepala berdenyut & tegang di
bagian depan kepala kadang kumat saat kecapekan sejak 6
bulan ini. (Karakteristik nyeri kepala sama dengan yang setelah
kejang).
61

43. • Kejang sejak 10 tahun yang lalu (usia 23 thn),
gerakan seperti meniup & menepuk-nepuk tangan,
jalan mondar-mandir tanpa ingat arah, pasien tdk
ingat saat kejang.
• Tx: Valproat 2x250mg, Paracetamol prn
•
•
•
•
Pemeriksaan fisik: refleks palmomental +/+
EEG: Sharp wave & ISA temporal D/S
Lab: IgG Toxo (+), HIV (-)
MRI+K: infeksi di serebelum
62

44. Migren?
Unilateral
Sedang
Segera setelah
kejang
Mual-muntah
Infeksi otak
Post iktal
1-beberapa jam
Berdenyut
Interiktal
Primer
Migren
Nyeri
kepala
Infeksi
Post-ictal headache?
Migren
Focal secondarily
generalized
Berkembang dalam
3 jam
Hilang dalam 72 jam
63

45. Faktor Risiko
SR
PU
Wanita
+
-
Interictal headache
-
+
Onset epilepsi usia muda
26 thn
23 tahun
Durasi epilepsi
3 tahun
>10 tahun
Politerapi
-
-
GTCS
secondarily
+
Muda
64

46. Case Challenge
65

47. Mrs. Lk/ F/49/ Married/ Housewife
• Headache, in left periorbital, dull, VAS 8-9, accompanied by
nausea, tearing & conjunctival injection of the left eye, begin
4 months ago, occur almost everyday and persist whole day
History of syncope in childhood and sudden slurred speech 5
years ago
66

48. • Physical examination: normal
• Blood work up: normal
• Brain imaging: normal
• EEG: Sharp wave & ISA in left temporal lobe
• Improved with valproate 250 mg bid
ictal cluster headache
???
67

49. End.