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Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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Dr. Stephanie Wrobel Goldberg from Jefferson University Hospital presents on the relationship between epilepsy and headaches.
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Stephanie Wrobel Goldberg Thomas Jefferson Headache Fellow HEADACHE & EPILEPSY
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Page 1: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

Stephanie Wrobel Goldberg

Thomas Jefferson

Headache Fellow

HEADACHE & EPILEPSY

Page 2: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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

Page 3: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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

Page 4: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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

Page 5: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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

Page 6: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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

Page 7: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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

Page 8: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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.

Page 9: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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

Page 10: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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

Page 11: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014
Page 12: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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

Page 13: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

MA - visual

Page 14: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

ICHD 3 beta• July 2013

• Alignment with the International Classification of Disease edition 11 (ICD-11)

Page 15: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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.

Page 16: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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

Page 17: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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.

Page 18: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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.

Page 19: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

Post-ictal headache • Over 40% of patients with temporal lobe epilepsy or frontal lobe

epilepsy

• 60% of patients with occipital lobe epilepsy.

• Conscious obscuration

Page 20: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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

Page 21: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014
Page 22: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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

Page 23: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

JAMA Neurology June 09, 2008 - Common Pathophysiologic Mechanisms n Migraine and Epilepsy Michael A. Rogawski, MD, PhD

Page 24: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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

Page 25: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

Migraine and Seizure - triggered by neocortical hyperexcitability

MIGRAINE - hyperexcitability thought to transition to cortical spreading depressionSEIZURE - hyperexcitability transitions to hypersynchronous activity

Page 26: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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.

Page 27: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

EEG role in headache

Page 28: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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

Page 29: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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.

Page 30: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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

Page 31: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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)

Page 32: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014
Page 33: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

Levetiracetam (Keppra ) and Zonisamide (Zonegran)

Page 34: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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.

Page 35: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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

Page 36: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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.

Page 37: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

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.

Page 38: Headaches & Epilepsy, Presentation from Epilepsy Education Exchange 2014

THANK YOU

OBRIGADA


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