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Stephanie Wrobel Goldberg
Thomas Jefferson
Headache Fellow
HEADACHE & EPILEPSY
Headache • 7% of office visits
• As much disability as MS, Parkinson’s disease and epilepsy
• Primary headache much more
common than secondary headache,
but secondary headache more
ominous
Primary vs Secondary• Primary: not accounted by any other underlying diagnosis
1) Migraine
2) Tension-type headache
3) Cluster headache
• Secondary:
1) SVT
2) Pituitary apoplexy
3) Stroke
4) Tumor
5) Infection
Don’t forget “SNOOP” red flagsStands for…
Example… Think of…
2S Systemic
symptoms
Secondary risk
factors
Fever, weight loss, fatigue,
HIV, cancer, immune suppression
Infection, inflammation,
metastatic cancer,
carcinomatous meningitis
NNeurologic
symptoms/signs
Altered consciousness, focal deficits Encephalitis, mass lesion,
stroke
OOnset Thunderclap, abrupt SAH, IPH, RCVS
OOlder New after age 50 Temporal arteritis
PPositional
Prior HA
Papilledema
Change upright vs laying down
Change with neck position
Different in quality
Visual obscurations
Intracranial hypotension,
dysautonomia
cervicogenic headache,
intracranial hypertensionPosterior fossa pathology
How to approach …• History
• Headache onset: age, what were they doing when it started, abrupt vs gradual
• Location of pain: side locked, switches sides, originates from the neck, temporal
• Duration of pain: Migraine 4+hours, Cluster < 3 hours
• Frequency and timing of attacks
Primary Headache Disorders based on duration
Chronic (15+ days/month) Episodic (<15 days/month)
Long (4 hours) • Chronic migraine• Chronic tension-type headache• New daily persistent headache• Hemicrania continua
• Episodic migraine• Episodic tension-type headache
Short (<4 hours) • Chronic cluster headache• Chronic paroxysmal hemicrania• SUNCT
• Episodic cluster headache• Episodic paroxysmal hemicrania
Richard B. Lipton, MD Headache 2011
Epilepsy and Headache• In the general population, the life time prevalence of headache is
about 46 % [1] and that of migraine 10-22 % [2].
• Bi-directional relationship one disorder increases the likelihood that the other is also present.
• 1 to 17% (median of 5.9%) with migraine have epilepsy
• 8 to 15% with epilepsy have migraine
Epilepsy and Migraine• Both chronic disorders characterized by recurrent neurologic attacks
accompanied by gastrointestinal, autonomic, and psychological features.
• Imbalance between excitatory and inhibitory factors results in altered brain function.
• Also linked by common underlying cellular/molecular mechanisms and treatment.
• Heterogeneous disorders influenced by genetic and environmental background clinical features and treatment response profiles.
1,948 adults with epilepsy and 1,411 of their parents and siblings: strong association between migraine and epilepsy, independent of seizure type, etiology, age at onset, or family history of epilepsy. RR 2.4
Epilepsy and Migraine• Mitochondrial myopathy, encephalopathy, lactic acidosis, and
stroke (MELAS), basilar migraine with seizures, migraine with primary generalized absence.
• Benign epilepsy of childhood with occipital paroxysms (BOEP) –partial seizures, may begin with migraine like visual aura and followed by postictal headache.
• Studies in adults less convincing evidence
Epileptic visual hallucinations vs MA visual• Onset within seconds vs slower onset within minutes
• Lasts seconds to minutes vs typically 15-20 minutes up to 1 h
• Colored and circular, may progress into complex forms vs uncolored and linear
• Rising abdominal sensation, fear, deja vu illusion
• The sensory auras of migraine spreads slowly
MA - visual
ICHD 3 beta• July 2013
• Alignment with the International Classification of Disease edition 11 (ICD-11)
ICHD 3 beta – “Migralepsy”• First described by Lennox and Lennox in 1960
1.4.4 Migraine aura-triggered seizure
• Diagnostic criteria:
A. A seizure fulfilling diagnostic criteria for one type of
epileptic attack
B. Occurring in a patient with migraine with aura, and during, or within 1 hour after, an attack of migraine with aura
C. Not better accounted for by another diagnosis.
ICHD 3 beta7.6 Headache attributed to epileptic seizure
Description: Headache caused by an epileptic seizure
1) 7.6.1 Hemicrania epileptica
2) 7.6.2 Post-ictal headache
unavailable ictal EEG make diagnosis difficult
ICHD 3 beta7.6.1 Hemicrania epileptica
Description: Headache occurring during a partial epileptic seizure, ipsilateral to the epileptic discharge, and remitting immediately or soon after the seizure has terminated.
• Diagnostic criteria:
A. Any headache fulfilling criterion C
B. The patient is having a partial epileptic seizure
C. Evidence of causation demonstrated by both of the following:
1. headache has developed simultaneously with onset of the partial seizure
2. both of the following:
a) headache has significantly improved immediately after the partial seizure has terminated
b) headache is ipsilateral to the ictal discharge
D. Not better accounted for by another ICHD-3 diagnosis.
ICHD 3 beta7.6.2 Post-ictal headache
• Diagnostic criteria:
A. Any headache fulfilling criterion C
B. The patient has recently had a partial or generalized epileptic seizure
C. Evidence of causation demonstrated by both of the following:
1) headache has developed within 3 hours after the epileptic seizure has terminated
2) headache has resolved within 72 hours after the epileptic seizure has terminated
D. Not better accounted for by another ICHD-3 diagnosis.
Post-ictal headache • Over 40% of patients with temporal lobe epilepsy or frontal lobe
epilepsy
• 60% of patients with occipital lobe epilepsy.
• Conscious obscuration
What hurts? • The brain parenchyma is insensate.
• Dura mater, dural vessels, extra and intracranial vessels, venous sinus, cranial nerves, upper cervical roots, muscles and nasopharynx.
• Trigeminal nerve, mostly its first division (ophthalmic nerve V1)
• Trigeminocervical complex
Cortical Spreading Depression• 1940 - Discovered by Aristides Leao at the department of physiology
at Harvard med school
• Wave of cortical excitation followed by a wave of inhibition.
• Wave marches over the cortical mantle at a rate of 3 mm/min
• Elevated extracellular potassium and glutamate
JAMA Neurology June 09, 2008 - Common Pathophysiologic Mechanisms n Migraine and Epilepsy Michael A. Rogawski, MD, PhD
Role of Glutamate• Important neurotransmitter that plays the principal role in neural
activation.
• Elevated extracellular glutamate plays critical role in epileptiform activity
• Also triggers CSD
• Target treatment: Magnesium, Topamax
Migraine and Seizure - triggered by neocortical hyperexcitability
MIGRAINE - hyperexcitability thought to transition to cortical spreading depressionSEIZURE - hyperexcitability transitions to hypersynchronous activity
EEGs recorded during a migraine with aura are usually normal.Most reported EEG abnormalities in migraine are nonspecific, such as focal or diffuse slowing and abnormalities during procedures such as hyperventilation.
EEG role in headache
Genetics• Imbalance between inhibitory and excitatory cortical function seem
to have a major role in both migraine and epilepsy
• Genetically channelopathies leading to alter cortical excitability.
• FHM
• Comorbid non-syndromic migraine and epilepsy complex interplay of multiple genes and environmental factors
FHM type 1• CACNA1A
• Encodes subunit ( α1A) of neuronal P/Q calcium channels gain of function
• First familial hemiplegic migraine gene to be described (1996)
• Increased intracellular calcium
• Synaptic release of glutamate, no change in GABA release lower CSD threshold
• Linked to cases of generalized epilepsy and absence-like seizures.
FHM type 2• ATP1A2 (early 2003)
• Encodes a subunit (α2) of Na+-K+ -ATPase transporter (primarily astrocytes and pia/arachnoid cells) loss of function
• In neonates predominantly expressed in neurons infantile convulsions
• Inhibition of this transporter can induce seizures by lowering membrane threshold.
• Most frequent association with epilepsy (20% of families) - partial seizures, benign familial infantile convulsions, febrile seizures
FHM type 3• SCN1A
• Encodes subunit of neuronal VG Na channel gain of function
• Correlation with generalized epilepsy with febrile seizures plus (GEFS+) and severe myoclonic epilepsy of infancy (SMEI or Dravetsyndrome)
Levetiracetam (Keppra ) and Zonisamide (Zonegran)
Take home points• Patients with epilepsy tend to under report presence of pre and
peri-ictal headaches.
• The presence of one disorder increases the likelihood the other is also present.
• Headaches adds to the already significant burden of epilepsy and so it is fundamental for physicians to be aware, diagnose and address this comorbid condition.
• In patients with migraine, a history of epilepsy should be investigated tricyclic antidepressants or neuroleptics may lower seizure thresholds.
Take home points• Although migraine and epilepsy are associated, the mechanisms of
the association are uncertain.
• Unlikely unidirectional
• Altered brain state (increased excitability) might increase the risk of both disorders.
• Shared pathophysiology/molecular genetic factors
References[1] Stovner L, Hagen K, Jensen R, et al. The global burden of headache: a documentation of headache prevalence and disability worldwide. Cephalalgia. 2007;27(3):193–210.
[2] Smitherman TA, Burch R, Sheikh H, Loder E. The prevalence, impact, and treatment of migraine and severe headaches in the United States: a review of statistics from national surveillance studies. Headache. 2013
[3] MacDonald BK, Cockerell OC, Sander JW, Shorvon SD. The incidence and lifetime prevalence of neurological disorders in a prospective community-based study in the UK. Brain. 2000;123:665–76.
[4] Forsgren L, Beghi E, Oun A, Sillanpää M. The epidemiology of epilepsy in Europe - a systematic review. Eur J Neurol. 2005;12(4):245–53.
[5] Sander JW. The epidemiology of epilepsy revisited. Curr Opin
Neurol. 2003;16(2):165–70.
[6] Kelley SA, Hartman AL, Kossoff EH. Comorbidity of migraine in
children presenting with epilepsy to a tertiary care center. Neurology. 2012;79(5):468–73.
References[7] Winawer MR, Connors R. Evidence for a shared genetic susceptibility to migraine and epilepsy. Epilepsia. 2013.
[8] Crepeau AZ. Migralepsy: a borderland of wavy lines. Curr NeurolNeurosci Rep. 2014 Feb;14(2):427
[9] Schon F, Blau JN. J Neurol Neurosurg Psychiatry. Post-epileptic headache and migraine. 1987 Sep;50(9):1148-52.
[10] Sethi NK, Ulloa CM, Solomon GE, Lopez L. 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.
[11] Marks DA, Ehrenberg BL. Migraine-related seizures in adults with epilepsy, with EEG correlation. Neurology. 1993 Dec;43(12):2476-83.
[12] Bigal ME, Lipton RB, Cohen J, Silberstein SD. Epilepsy and migraine. Epilepsy Behav. 2003 Oct;4 Suppl 2:S13-24.
[13] Ottman R, Lipton RB Comorbidity of migraine and epilepsy. Neurology 1994 Nov;44(11):2105-10.
THANK YOU
OBRIGADA