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NEURO VISION 2019
MY SINCERE THANKS TO……….
MIGRAINE
DR.B.Suneel kumar
MD,DM
VIJAYASRI clinics
VSKP
outline
• Pathophysiology
• Clinical features and triggers, hits and
misses..
• What can happen if untreated
• Management….
– Last 20 years
– Last 02 years
• Anything else that we can do /advice to
the patient.
 Migraine headache is a complex recurrent headache that
is one of the most common complaints in medicine.
3
Introduction
Neurovascular theory
 Migraine is primarily a neurogenic process with secondary
changes in cerebral perfusion
Cortical spreading depression
 CSD is a well defined wave of neuronal excitation in the cortical
grey matter that spreads from its site of origin at the rate of 2-
6mm/min
 This cellular depolarization causes the primary cortical
phenomenon aura phase, in turn, it activates trigeminal fibers
causing headache.
Patho Physiology
9
Vascular theory
It was believed that ischemia induced by intracranial
vasoconstriction is responsible for the aura of migraine and the
subsequent rebound vasodilation and activation of perivascular
nociceptive nerve resulted in headache.
Based on 2 observations -:
1.Extracranial vessels become distended and pulsatile during an
attack
2.Vasoconstrictors improve the headache and vaso dilators provoke
an attack
Pathophysiology
8
 Approx 70% of patients have a first degree relative with a history
of migraine.
Familial Hemiplegic Migraine
 Migraine with aura that is preceded or followed by hemiplegia
that typically resolves
 FHM type 1 - Linked to mutations in the calcium channel gene –
chromosome 19.May be associated with cerebellar ataxia
 FHM type 2 - mutation in the sodium channel gene ATP1A2 on
chromosome 3
 FHM type 3- mutation in a sodium channel alpha subunit coding
gene
7
Etiology
Migraine in inherited disorders -:
8
lactic
1.MELAS
acidosis)
2.CADASIL
(mitochondrial myopathy, encephalopathy and
(cerebral autosomal dominant arteriopathy with
vasculopathy with
subcortical infarcts and leukoencephalopathy)
3.Genetic vasculopathies like RVCL (retinal
cerebral leukodystrophy) etc.
Etiology
contd…
Childhood periodic syndromes
that are commonly
precursors of migraine
9
History
 U/L, throbbing or pulsatile localized in the frontotemporal and
ocular areas but be felt anywhere around the head or neck.
 Pain builds over 1-2 hrs and become diffuse.
 Many patient prefer to lie in dark room
Other symptoms
 Nausea, vomiting, anorexia and food intolerance occur in about
50 % of patients. Photophobia and phonophobia are commonly
associated with headache.
 Hemiparesis, confusion, apathy and numbness.
15
Clinical
presentation
Prodrome
 Heightened sensitivity to light, sounds and odors.
 Lethargy or uncontrollable yawning.
 Food cravings
 Mental and mood changes
 Excessive thirst and polyuria
 Anorexia
 Constipation or diarrhea
11
Clinical presentation contd…
 It is a complex of neurologic symptoms that may precede or
accompany the headache phase or may occur in isolation.
 Usually develops over 5-20min and lasts less than 60 minutes.
 Can be visual, sensory, motor or combination of these
Negative symptoms -:
 Negative scotoma
 Negative visual phenomenon such as homonymous hemianopia,
central scotoma, tunnel vision, altitudinal visual defects etc.
12
Aura
Positive symptoms
 Scintillating scotoma-highly characteristicof migraine
 Photopsia or flashes of light
 Heat waves
 Micropsia, macropsia
Paresthesia
Occurring in 40%of cases constitute the next most common aura.
 Sensory symptoms rarely occurs in isolation and usually follows visual
aura.
 Motor symptoms may occur in 18% of patients
 Speech and language disturbances have been reported in 17-20% of
patients 13
Aura contd…
Scintillating
Scotoma
14
Central
Scotoma
15
Multiple spotty
scotoma
16
Half visual field
loss
17
 Stress
 Excessive or insufficient sleep
 Medications (OCP, vasodilators)
 Strong odors eg. perfumes, cologne etc.
 Hormonal changes such as pregnancy, menstruation
 Head trauma
 Weather changes
 Metabolic or infectious disease
 Physical exertion
 Cold stimulus eg. ice cream
18
Migraine
triggers
 Thorough neurologic examination is essential, results will be
normal in majority
 Possible findings may include
 Cranial/cervical muscle tenderness
 Horner syndrome
 Tachycardia/ bradycardia
 Conjunctival injection
 Hypertension/hypotension
 Hemisensory/ hemiparetic neurological deficits
( complicated migraine)
Physical
Examination
26
 Findings that suggest a headache diagnosis other than
migraine
 Dim scotoma lasting a few seconds to several minutes ie
amaurosis
 Temporal artery tenderness
 Meningisnus
 Mental status changes
 Focal neurologic deficit eg confusion, seizures
20
 Focal neurologic findings suggests a migraine variant
 U/L paralysis or weakness-hemiplegic migraine
 Aphasia, dysarthria, vertigo, tinnitus, syncope, balance
problems-basilar migraine
 Third nerve palsy with sparing of pupillary response-
ophthalmoplegic migraine
21
Physical Examination contd…
 Migraine without aura
Diagnostic criteria:
A. At least 5 attacks fulfilling criteria B-D
B. Headache attacks lasting 4-72 hours (untreated or
unsuccessfully treated)
C. 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)
22
Diagnostic
criteria
 D. During headache at least one of thefollowing:
1. nausea and/or vomiting
2. photophobia and phonophobia
 E. Not attributed to another disorder
Diagnostic criteria contd…
23
Complications of
migraine
2
4
30 year female
Hemiparesis
k/p/o migraine
She had a recent
migraine episode
1week back
Can it be a migrainous infarct?
Migrainous infarct happens
at the height of headache..
…..
Management
26
EDUCATE BEFORE Rx
Specific medications
Triptan (serotonin 1B/1Dreceptor agonists)
 acute management
 Appropriate initial choice in patients with moderate to severe
migraine
 Routes-oral, subcutaneous and nasal
 Drugs – sumatriptan-50-100mg tablet at onset , may repeat after
2hour (max 200mg/d)
 Rizatriptan –most efficacious, early onset of action, 5-10 mg
tablet at onset may repeat after 2hr max 30mg/d)
 Naratriptan, almotriptan,frovatr
42
iptan, zolmitriptan
Specific medications contd…
•  Ergot alkaloids and derivatives-nonselective 5-HT1 agonists)
 Ergotamine PO/PR (and caffeine combination) may be
considered in the treatment of selected patients with
moderate to severe migraine.
 Dose 2mg PO, f/b 1-2mg every 30 min until attack is aborted,
no more than 6mg/day
 Adverse effects-vasospasm, angina, tachycardia, numbness of
extremities, rebound headache, ergotism, gangrene etc
28
May be considered when -:
 Frequency of migraine is >2/months
 Duration of individual attack is longer than 24hrs
 Headache causes major disruption in patients lifestyle
 Abortive therapy fails or is overused
 Symptomatic medications are ineffective
29
Preventive
treatment
ANTIEPILEPTICS
30
 Well tolerated
 Valproic acid is useful as afirst line agent.400-600 mg BD
 Carbamazepine
 Gabapentin
 topiramate
 ANTIHYPERTENSIVES
 Beta-blockers
 Propranolol -40-120mg BD
 Calcium channel blockers
 Diltiazem
 Nimodipine
 Verapamil
31
 ANTIDEPRESSANTS
 Tricyclic antidepressants
 Amitriptyline- 10-75mg at night
 Nortriptyline
Selective serotonin reuptake inhibitors
 Fluoxetine
 Other antidepressants
 Bupropion, mirtazepine, trazodone, venlafaxine
32
SEROTONIN ANTAGONISTS
33
Methysergide-1-4mg OD
 Flunarizine5-15mg OD
 NSAIDS
 Aspirin
 Mefenamic acid
 Ibuprofen
 Naproxen/naproxen sodium
 Other
 Magnesium
 Vitamin B2
Gepants…
Small
Crosses BBB
CNS side effects
Hepatotoxic
NOT APPROVED
MABs
Large
Doesn’t cross BBB
NO CNS side effects
APPROVED
ERENUMAB
Non pharmacological management
Thank You!
40

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MIGRAINE neurovision 2019.pptx

  • 1. NEURO VISION 2019 MY SINCERE THANKS TO………. MIGRAINE DR.B.Suneel kumar MD,DM VIJAYASRI clinics VSKP
  • 2. outline • Pathophysiology • Clinical features and triggers, hits and misses.. • What can happen if untreated • Management…. – Last 20 years – Last 02 years • Anything else that we can do /advice to the patient.
  • 3.  Migraine headache is a complex recurrent headache that is one of the most common complaints in medicine. 3 Introduction
  • 4. Neurovascular theory  Migraine is primarily a neurogenic process with secondary changes in cerebral perfusion Cortical spreading depression  CSD is a well defined wave of neuronal excitation in the cortical grey matter that spreads from its site of origin at the rate of 2- 6mm/min  This cellular depolarization causes the primary cortical phenomenon aura phase, in turn, it activates trigeminal fibers causing headache. Patho Physiology 9
  • 5. Vascular theory It was believed that ischemia induced by intracranial vasoconstriction is responsible for the aura of migraine and the subsequent rebound vasodilation and activation of perivascular nociceptive nerve resulted in headache. Based on 2 observations -: 1.Extracranial vessels become distended and pulsatile during an attack 2.Vasoconstrictors improve the headache and vaso dilators provoke an attack Pathophysiology 8
  • 6.
  • 7.  Approx 70% of patients have a first degree relative with a history of migraine. Familial Hemiplegic Migraine  Migraine with aura that is preceded or followed by hemiplegia that typically resolves  FHM type 1 - Linked to mutations in the calcium channel gene – chromosome 19.May be associated with cerebellar ataxia  FHM type 2 - mutation in the sodium channel gene ATP1A2 on chromosome 3  FHM type 3- mutation in a sodium channel alpha subunit coding gene 7 Etiology
  • 8. Migraine in inherited disorders -: 8 lactic 1.MELAS acidosis) 2.CADASIL (mitochondrial myopathy, encephalopathy and (cerebral autosomal dominant arteriopathy with vasculopathy with subcortical infarcts and leukoencephalopathy) 3.Genetic vasculopathies like RVCL (retinal cerebral leukodystrophy) etc. Etiology contd…
  • 9. Childhood periodic syndromes that are commonly precursors of migraine 9
  • 10. History  U/L, throbbing or pulsatile localized in the frontotemporal and ocular areas but be felt anywhere around the head or neck.  Pain builds over 1-2 hrs and become diffuse.  Many patient prefer to lie in dark room Other symptoms  Nausea, vomiting, anorexia and food intolerance occur in about 50 % of patients. Photophobia and phonophobia are commonly associated with headache.  Hemiparesis, confusion, apathy and numbness. 15 Clinical presentation
  • 11. Prodrome  Heightened sensitivity to light, sounds and odors.  Lethargy or uncontrollable yawning.  Food cravings  Mental and mood changes  Excessive thirst and polyuria  Anorexia  Constipation or diarrhea 11 Clinical presentation contd…
  • 12.  It is a complex of neurologic symptoms that may precede or accompany the headache phase or may occur in isolation.  Usually develops over 5-20min and lasts less than 60 minutes.  Can be visual, sensory, motor or combination of these Negative symptoms -:  Negative scotoma  Negative visual phenomenon such as homonymous hemianopia, central scotoma, tunnel vision, altitudinal visual defects etc. 12 Aura
  • 13. Positive symptoms  Scintillating scotoma-highly characteristicof migraine  Photopsia or flashes of light  Heat waves  Micropsia, macropsia Paresthesia Occurring in 40%of cases constitute the next most common aura.  Sensory symptoms rarely occurs in isolation and usually follows visual aura.  Motor symptoms may occur in 18% of patients  Speech and language disturbances have been reported in 17-20% of patients 13 Aura contd…
  • 18.  Stress  Excessive or insufficient sleep  Medications (OCP, vasodilators)  Strong odors eg. perfumes, cologne etc.  Hormonal changes such as pregnancy, menstruation  Head trauma  Weather changes  Metabolic or infectious disease  Physical exertion  Cold stimulus eg. ice cream 18 Migraine triggers
  • 19.  Thorough neurologic examination is essential, results will be normal in majority  Possible findings may include  Cranial/cervical muscle tenderness  Horner syndrome  Tachycardia/ bradycardia  Conjunctival injection  Hypertension/hypotension  Hemisensory/ hemiparetic neurological deficits ( complicated migraine) Physical Examination 26
  • 20.  Findings that suggest a headache diagnosis other than migraine  Dim scotoma lasting a few seconds to several minutes ie amaurosis  Temporal artery tenderness  Meningisnus  Mental status changes  Focal neurologic deficit eg confusion, seizures 20
  • 21.  Focal neurologic findings suggests a migraine variant  U/L paralysis or weakness-hemiplegic migraine  Aphasia, dysarthria, vertigo, tinnitus, syncope, balance problems-basilar migraine  Third nerve palsy with sparing of pupillary response- ophthalmoplegic migraine 21 Physical Examination contd…
  • 22.  Migraine without aura Diagnostic criteria: A. At least 5 attacks fulfilling criteria B-D B. Headache attacks lasting 4-72 hours (untreated or unsuccessfully treated) C. 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) 22 Diagnostic criteria
  • 23.  D. During headache at least one of thefollowing: 1. nausea and/or vomiting 2. photophobia and phonophobia  E. Not attributed to another disorder Diagnostic criteria contd… 23
  • 25. 30 year female Hemiparesis k/p/o migraine She had a recent migraine episode 1week back Can it be a migrainous infarct? Migrainous infarct happens at the height of headache.. …..
  • 27. Specific medications Triptan (serotonin 1B/1Dreceptor agonists)  acute management  Appropriate initial choice in patients with moderate to severe migraine  Routes-oral, subcutaneous and nasal  Drugs – sumatriptan-50-100mg tablet at onset , may repeat after 2hour (max 200mg/d)  Rizatriptan –most efficacious, early onset of action, 5-10 mg tablet at onset may repeat after 2hr max 30mg/d)  Naratriptan, almotriptan,frovatr 42 iptan, zolmitriptan
  • 28. Specific medications contd… •  Ergot alkaloids and derivatives-nonselective 5-HT1 agonists)  Ergotamine PO/PR (and caffeine combination) may be considered in the treatment of selected patients with moderate to severe migraine.  Dose 2mg PO, f/b 1-2mg every 30 min until attack is aborted, no more than 6mg/day  Adverse effects-vasospasm, angina, tachycardia, numbness of extremities, rebound headache, ergotism, gangrene etc 28
  • 29. May be considered when -:  Frequency of migraine is >2/months  Duration of individual attack is longer than 24hrs  Headache causes major disruption in patients lifestyle  Abortive therapy fails or is overused  Symptomatic medications are ineffective 29 Preventive treatment
  • 30. ANTIEPILEPTICS 30  Well tolerated  Valproic acid is useful as afirst line agent.400-600 mg BD  Carbamazepine  Gabapentin  topiramate
  • 31.  ANTIHYPERTENSIVES  Beta-blockers  Propranolol -40-120mg BD  Calcium channel blockers  Diltiazem  Nimodipine  Verapamil 31
  • 32.  ANTIDEPRESSANTS  Tricyclic antidepressants  Amitriptyline- 10-75mg at night  Nortriptyline Selective serotonin reuptake inhibitors  Fluoxetine  Other antidepressants  Bupropion, mirtazepine, trazodone, venlafaxine 32
  • 33. SEROTONIN ANTAGONISTS 33 Methysergide-1-4mg OD  Flunarizine5-15mg OD  NSAIDS  Aspirin  Mefenamic acid  Ibuprofen  Naproxen/naproxen sodium  Other  Magnesium  Vitamin B2
  • 34.
  • 35. Gepants… Small Crosses BBB CNS side effects Hepatotoxic NOT APPROVED MABs Large Doesn’t cross BBB NO CNS side effects APPROVED ERENUMAB
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  • 39.