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Headache & epilepsy
STEPHANIE WROBEL GOLDBERG
THOMAS JEFFERSON
HEADACHE FELLOW
Headache
7% of office visits
As much disability as MS, Parkinson’s disease and epilepsy
Primary headache much more
common ...
Primary vs Secondary
Primary: not accounted by any other underlying diagnosis
1) Migraine
2) Tension-type headache
3) Clus...
Don’t forget “SNOOP” red flags
Stands for… Example… Think of…
S
Systemic
symptoms
Secondary risk
factors
Fever, weight los...
How to approach …
History
Headache onset: age, what were they doing when it started, abrupt vs
gradual
Location of pain: s...
Primary Headache Disorders
based on duration
Chronic (15+ days/month) Episodic (<15 days/month)
Long (4 hours) • Chronic m...
Epilepsy and Headache
In the general population, the life time prevalence of headache is about
46 % [1] and that of migrai...
Epilepsy and Migraine
Both chronic disorders characterized by recurrent neurologic attacks accompanied by
gastrointestinal...
1,948 adults with epilepsy and 1,411 of their parents and siblings: strong association
between migraine and epilepsy, inde...
Epilepsy and Migraine
Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke
(MELAS), basilar migraine with s...
Epileptic visual hallucinations vs
MA visual
Onset within seconds vs slower onset within minutes
Lasts seconds to minutes ...
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 ...
ICHD 3 beta
7.6 Headache attributed to epileptic seizure
Description: Headache caused by an epileptic seizure
1) 7.6.1 He...
ICHD 3 beta
7.6.1 Hemicrania epileptica
Description: Headache occurring during a partial epileptic seizure, ipsilateral t...
ICHD 3 beta
7.6.2 Post-ictal headache
Diagnostic criteria:
A. Any headache fulfilling criterion C
B. The patient has rece...
Post-ictal headache
Over 40% of patients with temporal lobe epilepsy or frontal lobe
epilepsy
60% of patients with occipit...
What hurts?
The brain parenchyma is insensate.
Dura mater, dural vessels, extra and intracranial vessels, venous sinus,
cr...
Cortical Spreading Depression
1940 - Discovered by Aristides Leao at the department of physiology at
Harvard med school
Wa...
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 gl...
Migraine and Seizure - triggered by neocortical hyperexcitability
MIGRAINE - hyperexcitability thought to transition to co...
EEGs recorded during a migraine with aura are usually normal.
Most reported EEG abnormalities in migraine are nonspecific,...
EEG role in headache
Genetics
Imbalance between inhibitory and excitatory cortical function seem to
have a major role in both migraine and epil...
FHM type 1
CACNA1A
Encodes subunit ( α1A) of neuronal P/Q calcium channels  gain of function
First familial hemiplegic mi...
FHM type 2
ATP1A2 (early 2003)
Encodes a subunit (α2) of Na+-K+ -ATPase transporter (primarily astrocytes
and pia/arachnoi...
FHM type 3
SCN1A
Encodes subunit of neuronal VG Na channel  gain of function
Correlation with generalized epilepsy with f...
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...
Take home points
Although migraine and epilepsy are associated, the mechanisms of the
association are uncertain.
Unlikely ...
References
[1] Stovner L, Hagen K, Jensen R, et al. The global burden of headache: a documentation of
headache prevalence ...
References
[7] Winawer MR, Connors R. Evidence for a shared genetic susceptibility to migraine and
epilepsy. Epilepsia. 20...
Thank you
Obrigada
Epilepsy and Headaches
Epilepsy and Headaches
Epilepsy and Headaches
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Epilepsy and Headaches

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A presentation by Stephanie Wrobel Goldberg, MD, Headache Fellow a

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Epilepsy and Headaches

  1. 1. Headache & epilepsy STEPHANIE WROBEL GOLDBERG THOMAS JEFFERSON HEADACHE FELLOW
  2. 2. 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
  3. 3. 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
  4. 4. Don’t forget “SNOOP” red flags Stands for… Example… Think of… S Systemic symptoms Secondary risk factors Fever, weight loss, fatigue, HIV, cancer, immune suppression Infection, inflammation, metastatic cancer, carcinomatous meningitis N Neurologic symptoms/signs Altered consciousness, focal deficits Encephalitis, mass lesion, stroke O Onset Thunderclap, abrupt SAH, IPH, RCVS O Older New after age 50 Temporal arteritis P Positional Prior HA Papilledema Change upright vs laying down Change with neck position Different in quality Visual obscurations Intracranial hypotension, dysautonomia cervicogenic headache, intracranial hypertension Posterior fossa pathology
  5. 5. 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
  6. 6. 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
  7. 7. 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
  8. 8. 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.
  9. 9. 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
  10. 10. 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
  11. 11. 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
  12. 12. MA - visual
  13. 13. ICHD 3 beta July 2013 Alignment with the International Classification of Disease edition 11 (ICD-11)
  14. 14. 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.
  15. 15. ICHD 3 beta 7.6 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
  16. 16. ICHD 3 beta 7.6.1 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.
  17. 17. ICHD 3 beta 7.6.2 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.
  18. 18. Post-ictal headache Over 40% of patients with temporal lobe epilepsy or frontal lobe epilepsy 60% of patients with occipital lobe epilepsy. Conscious obscuration
  19. 19. 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
  20. 20. 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
  21. 21. JAMA Neurology June 09, 2008 - Common Pathophysiologic Mechanisms n Migraine and Epilepsy Michael A. Rogawski, MD, PhD
  22. 22. 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
  23. 23. Migraine and Seizure - triggered by neocortical hyperexcitability MIGRAINE - hyperexcitability thought to transition to cortical spreading depression SEIZURE - hyperexcitability transitions to hypersynchronous activity
  24. 24. 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.
  25. 25. EEG role in headache
  26. 26. 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
  27. 27. 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.
  28. 28. 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
  29. 29. 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 Dravet syndrome)
  30. 30. Levetiracetam (Keppra ) and Zonisamide (Zonegran)
  31. 31. 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.
  32. 32. 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
  33. 33. 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.
  34. 34. 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 Neurol Neurosci 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.
  35. 35. Thank you Obrigada

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