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Neuropsychiatric Aspects of Headache
Presented by: Dr. JITHIN T JOSEPH
DNB RESIDNET , MHC TVM
CHAIR: DR.ARUN V ,CONSULTANT IN PSYCHIATRY
INTRODUCTION
• It is said that about 70 percentage of population had experienced
headache once in their life time
• Overall prevalence of migraine is around 12%
• Headache ,especially migraine had caused so much burden to the
patients life.
• There is associated psychiatric and physical co morbidities.
• WHO has launched a global campaign called “Lifting the Burden” to
reduce the burden of headache.
• The new areas of interest in headache researches are newer
treatment agents and evaluation of comorbidities
The aim of this presentation is to?
1. Provide an overview of the diagnostic nomenclature for headache
syndromes.
2. Describe the magnitude, risk factors, and patterns of comorbidity.
3. To describe neuropsychiatric manifestations.
4. Summarize the clinical and laboratory examination necessary for
making a diagnosis.
5. To discuss about current acute and prophylactic treatment
strategies.
CLASSIFICATION
• The International Classification of Headache Disorders - ICHD-2(2004)
• 3 classes
1.Primary headache syndromes
• Migraine
• Tension type headache
• Cluster headache
2. Secondary headache syndrome
• Due to underlying pathology of the brain and adjacent structures
• More severe and more serious
• Needs detailed evaluation
• Temporal arteritis, intracranial mass lesions.
• Idiopathique intra cranial hypertension (pseudotumor cerebri),
• Meningitis , subarachnoid haemorrhage
• Post concussion headaches
3. Cranial neuralgias and other causes of facial pain
Migraine
• Most disabling of the primary headache syndromes
• Characterised by recurrent attacks of
 Recurrent throbbing type of headache that is often
unilateral.
 Gastrointestinal symptoms such as nausea or vomiting
 Hyperesthesia manifested by photophobia or phono
phobia
• Previously migraines were classified as classic and common type.
• Classic is characterised by neurological symptoms and signs but less
common – now called migraine with aura
• Common migraine is more common with 75 % people affected , and
characterised by no neurological symptoms – now called migraine
without aura
ICHD-2 Criteria for Migraine without Aura
A. At least five attacks fulfilling criteria B–D
B. Duration between 4 and 72 hours (untreated or unsuccessfully treated)
C. At least two of the following:
1. Unilateral
2. Pulsating pain
3. Moderate to severe intensity
4. Aggravation by or causing avoidance of routine physical activity (walking or climbing stairs)
D. During headache at least one of the following:
1. Nausea and/or vomiting
2. Photophobia and phonophobia
E. Not attributed to another disorder
ICHD-2 Criteria for Migraine with Aura
A. At least five attacks fulfilling criteria in B–D
B. Aura consisting of at least one of the following but no motor
weakness:
1. Fully reversible visual symptoms
• positive features -flickering lights, spots or lines
• negative features - loss of vision
2. Fully reversible sensory symptoms
• positive features -pins and needles
• negative features - numbness
3. Fully reversible dysphasic speech disturbance
C. At least two of the following:
1. Homonymous visual symptoms and/or unilateral sensory symptoms
2. At least one aura symptom develops gradually over 5 minutes and/or different
aura symptoms occur in succession over 5 or more minutes
3. Each symptom lasts 5 or more minutes and less than or equal to 60 minutes
D. Headache fulfilling criteria B–D for migraine without aura begins during the aura
or follows within 60 minutes
E. Not attributed to another disorder
Aura of migraine
• Aura can be any symptom of brain dysfunction
• Typically precedes or accompanies the headache
• Appear gradually and then evolve over 5–20 minutes, persist for less than
1 hour, and evaporate with the headache’s onset.
• They characteristically consist of a transient visual phenomenon, but
sometimes a simple olfactory hallucination.
• Aura occasionally consists of language impairment similar to aphasia,
sensory misperception, or personality change.
• In children, but not adults, recurrent colic or “cyclic abdominal pain” with
nausea and vomiting may constitute a migraine variant, but not technically
an aura.
• By far the commonest migraine auras are visual hallucinations
• They usually consist of a greying of a region of the visual field
(scotoma) flashing zigzag lines, (scintillating or fortification
scotomata) crescents of brilliant colours , tubular vision, or distortion
of objects(metamorphopsia).
• Migraine auras most often involve the simultaneous appearance of
positive phenomena, such as scintillations, and negative ones, such as
opaque areas.
• Some migraineurs experience premonitory somatic symptoms, such
as fatigue, stiff neck, yawning, hunger, and thirst.
• These patients can frequently predict their impending migraine hours
to days before onset.
SENSORY PHENOMENA
Special Senses
Visual, olfactory, auditory, gustatory
Paraesthesia, Especially Lips and Hand
MOTOR DEFICITS
Hemiparesis, Hemiplegia
NEUROPSYCHOLOGIC CHANGES
Aphasia
Perceptual Impairment, Especially for
Size, Shape,and Time
EMOTIONAL AND BEHAVIORAL
Anxiety, Depression, Irritability,
Hyperactivity
Evolution of migraine
EPIDEMIOLOGY AND COURSE
• About 70 percent of adults endorsing a history of headaches in a
given year.
• Average prevalence of definite migraine is 10.9 percent from
international studies.
• Migraine with aura usually present for the first time in males during
teens.
• In females the peak incidence is around early twenties.
• About half of those with migraine remit, about 35 percent continue
to have intermittent headache, and only 20 percent continue to
develop chronic migraine over time.
• Over 80 percent of those with migraine report some degree of
disability.
• There is enormous personal and social burden
• But only one-half of those individuals who suffer from debilitating
migraine seek professional help.
• Migraine in childhood -associated with gastrointestinal complaints,
:episodic bouts of stomach pain, vomiting, or diarrhoea.
• The duration is shorter than that commonly observed in adults.
• In women, migraine is strongly associated with reproductive system
function
• Increased incidence during puberty and the first trimester of
pregnancy, and is associated with exogenous hormone use.
• After menopause, the frequency of migraine attacks generally
decreases dramatically.
• Family history of migraine is one of the most potent and consistent
risk factors for migraine.
• Genetic factors are involved in 1/3rd of the migraine cases.
• The mode of inheritance and the genes involved are still unknown
PATHOPHYSIOLOGY OF MIGRAINE
• Believed to be due to the neuronal hyper excitability.
• Involves mutation in various ion channels.
• The first to be identified was a mutation in the gene, on chromosome
19, for the voltage-gated calcium channel.
• Further studies found out mutation in gene coding for the Na+/K+
pump or in the gene for the neuronal voltage-gated sodium channel.
• Previous hypotheses suggesting that migraine aura was caused by
vasoconstriction, with the headache produced by the subsequent
vasodilation, have now been discarded.
• Migraine is now conceived as being related to events in the cortex
and adjacent meninges on one hand and in the brainstem on the
other.
The final common pathway to the migraine aura is excessive potassium or
glutamate release which facilitates cortical spreading depression
• These events are linked by trigeminal fibres connecting the meninges
to brain stem, and efferent fibres of the parasympathetic system
controlling meningeal blood vessels.
• Cortical spreading depression over the cerebral cortex, is relevant to
the aura of migraine but not to migraine without aura.
• Effects of neuropeptides and other neurotransmitters, particularly 5-
hydroxytryptamine (5HT), on meningeal vasculature and nociceptors.
• Altered function of aminergic brainstem nuclei and their
parasympathetic outflow.
Precipitating factors of migraine
• Hormonal changes - catamenial migraine
• Stress or its cessation.
• Fasting , fatigue, over-sleeping.
• Particular foods and beverages.
• Drug intake, chemical additives.
• Bright light, weather changes.
• Exercise
But these agents/situations vary dramatically within and between
individuals.
Basilar -type migraine or basilar artery
migraine
• Seen in about 10% of cases, episodes are usually interspersed among
classic attacks. Symptoms are often bilateral.
• The attacks begin with a visual aura, sometimes extending to both half-
fields and obscuring vision.
• Then progress to symptoms of brainstem dysfunction such as vertigo,
dysarthria, ataxia, tinnitus.
• Sensory symptoms distally in the limbs and around the lips and tongue.
• This is followed by a gap of around minutes to half hour, following which
headache occurs ,usually occipital
• There may be LOC in between the onset of headache ,and it is believed to
be due to ischemia of RAS
Familial hemiplegic migraine
• Characterised by attacks of transient hemiplegia that are followed by headache
• The hemiparesis is always associated with sensory, language or visual
disturbances and in some cases confusion/drowsiness
• Aura symptoms are of longer duration
• Genetic predisposition
Retinal migraine – very rare
• At least two attacks of fully reversible monocular visual symptoms followed by
migraine headache.(IHS CRITERIA)
• No longer considered as part of migraine
Tension-Type Headache(TTH)
• Most common among primary headache syndromes
• Tension -type headache is characterized by episodes of stable bilateral
pain lasting several days at a time.
• Migraine and TTH can co-exist , or alternate
• Its no longer believed to be due to muscle tension
• Women are more commonly affected than men
• Often affects multiple family members.
• Patients with TTH tolerate their pain and usually go about their
business, unlike people with migraine.
• Fatigue, cervical spondylosis, bright light, loud noise, and, at some
level, emotional factors allegedly produce or precipitate TTH
• But the evidence for the same is less
Differentiated from migraine headache due to its
1. Longer duration.
2. Lack of pulsating quality of the pain.
3. Lack of worsening with physical activity.
4. Absence of gastrointestinal concomitants.
5. Often bilateral
EPIDEMIOLOGY AND COURSE
• The aggregate prevalence of tension-type headache of 32 percent.
• More common in women , but not as prominent as that of migraine.
• More common in young adults
• The incidence comes down with age but not that much as of
migraine.
ICHD-2 Criteria for Tension-Type Headache
• Chronic tension-type headache
• A. Headache occurring on greater than or equal to 15 days per month on average
for more than 3 months (greater than or equal to 180 days per year) and fulfilling
criteria B–D.
Cluster headache
• Cluster headache is a distinct syndrome characterized by frequent
intense attacks (often several per day) over a 1- to 2-month periods.
• Separated by headache-free intervals for as long as 1 or 2 years.
• Initially grouped as part of migraine headache, but researches
distinguished it as a separate entity.
• Cluster refers to a “clustering in time,” with the headache
• Males tend to suffer more from cluster headache than females.
• Characterised by
• Retro -orbital in location.
• Accompanied by autonomic changes
such as lacrimation, rhinorrhoea,
erythema of the eye, and agitation.
• Males are more commonly affected
• Screaming and thrashing that may be
associated with the pain and may
often present as psychotic
• Prior smoking and alcohol use have
been associated with cluster
headache.
• Alcohol use can precipitate it.
• This disorder affects men, typically between the ages of 20 and 40
years.
• Most cluster attacks have a predictable, cyclic pattern. For example,
some patients develop attacks every spring or fall.
• Most strike between 9:00 PM and 9:00 AM and one-half of them
develop during REM sleep.
• Alcohol characteristically precipitates an attack.
• Inhaling 100% high-flow oxygen will abort them. Thus, administering
oxygen can be diagnostic as well as therapeutic.
Headache Attributable to Head or Neck
Trauma
• A headache following head trauma accompanied by a loss of
consciousness, post traumatic amnesia, and abnormal laboratory
tests(ICHD 2)
• Emotional factors are more likely to be a sequela rather than a cause
of posttraumatic headache
• Pathogenesis of posttraumatic headache is unknown. Major
hypothesis are
1. Cerebral oedema.
2. Cortical spreading depression
3. Innate vulnerability to cerebral vasospasm,
4. Transient elevation of intracranial pressure
• No relation between the prevalence of post traumatic headache and
severity of head injury.
• Posttraumatic headache is more common after injuries that do not
result in skull fracture.
• Rare in population -1%
• But common after head injury -28 to 62 %.
• Children and young adults appear to be particularly susceptible
• 50 % had headache at time of discharge.
• Persistence of headache has been related to
1. Female sex.
2. Age over 45.
3. The presence of dizziness.
4. Lack of skull fracture, intracranial hematoma.
5. Disorders of smell, hearing, or vision
6. Depression , and impaired concentration.
SECONDARY HEADACHES
• Temporal Arteritis / Giant Cell Arteritis
• Intracranial Mass Lesions
• Chronic Meningitis
• Idiopathic Intracranial Hypertension (Pseudotumor Cerebri)
• Post Dural Puncture Headache (PDPH)
• Bacterial Meningitis, Herpes Encephalitis,
• Subarachnoid Haemorrhage
CRANIAL NEURALGIAS
• Most common is trigeminal neuralgia
• Can affect any 3 divisions, most common in V2
• Sufferer has daily agonising sharp pain lasting for few seconds
• Touching the affected area or movements can provoke the pain
• Due to fear of pain patients hesitate to eat, brush their teeth, or
speak.
• More common in females ,after 60 years and not present at night
• Treatment : carbamazepine , gabapentin
Chronic Daily Headache
• Definition - When patients report headaches, each lasting 4 hours or
longer, for at least 15 days each month for at least 3 months.
• Most adult have a primary headache syndrome which progress
• In children it may arise as new onset-New Daily Persistent Headache
(NDPH)
• Patient typically has generalized, waxing and waning, dull, pressing,
and no pulsatile pain.
• Pain is mild to moderate but incapacitating and lost features like aura
and automatic symptoms
• RISK FACTORS
• Medication over use – most powerful risk factor
• The medicines most commonly implicated are aspirin– caffeine compounds triptans, NSAIDs,
benzodiazepines, and opioids.
• Using triptans or opioid for more than 10 days a month – CDH in 2 years
• Non opioid analgesics – 5 years
• Obesity , head trauma.
• Low socioeconomic status.
• Disability , major stressful life events.
• Depression and anxiety.
• Risk factors for adolescents are primarily depression and anxiety.
• Resistant to treatment
• Medication over use has to be taken care of
• Underlying anxiety and depression has to be treated
• TCAs, valproate, and topiramate may help
• modification of lifestyle, behavior therapy, and elimination of
precipitating factors.
Psychiatric aspects
• It is believed that , there is increased psychiatric co morbidities in
patients suffering from migraine.
• The presentation of headache itself can mimic a psychotic episode
• There is increased occurrence of anxiety and depression in migraine
sufferers.
• There are different psychological factors that can precipitate an
attack.
• Psychiatric co morbidity can adversely affect the treatment response
• There are some personality types who may be suffering of migraine
Anxiety and depression
• These are the commonest co morbidities in migraine
• 2-3 fold increase in risk
• Anxiety disorder is more common than depression
• A study by Merikangas et al 1990 found that prevalence of major
depression, bipolar spectrum disorder (i.e. cyclothymia and
hypomania), generalised anxiety and social phobia is more in patients
with migraine.
• Anxiety often manifested in childhood, followed by the development
of migraine some years later, and then by discrete episodes of
depression in early adult life.
• Many cases are found to have mixed anxiety and depression.
• The risk of suicide attempt is also increased in migraine, and it is of
interest that not all this excess risk is explained by the presence of
depression (Breslau 1992).
• Some studies pointed out that there is more chance of developing
migraine in those with anxiety and depression. (Hung et al. 2005;
Oedegaard & Fasmer 2005).
• A study by (Breslau et al. 2000) compared migraine headache with
non migraine headache and those without and could not find any
significant difference in the co morbidities.
• There is a small increase in incidence for those with migraine with
aura.
Personality and stress in migraine
• The evidence that a particular personality type predisposes a person to
suffering migraine is not very strong.
• People with migraine do have higher scores on neuroticism traits,
including harm avoidance, psychasthenia and social introversion as evident
from studies(Fan & Zhou 1999).
• These traits were more common if the patient is seeking treatment.
• There is increased emotional reactivity ,which in turn cause reactivity of
ANS which is responsible for precipitating attacks
• These factors are associated with poor treatment response and chance of
progressing to chronic migraine.
• Studies showed that ,this picture is not only for migraine ,but seen in all
types of headaches. (Di Piero et al. 2001)
Psychological precipitants
• Psychological factors are thought to be the most important precipitating factor as
evident from studies.
• But it is not a must, about one third of people never had a psychological
precipitating factor.
• Periods of stress, or the anticipation of stress, are associated with attacks.
• Sustained emotional tension seems to be more important than acute emotional
disturbance.
• Some patients to develop attacks during the ‘let down period’ after intense
activity and striving.
• Some have attacks quite regularly when a harassing day is over, at weekends or
on the first day of a holiday.
• In a study on patients attending migraine clinic it was found that intrusive
thoughts about work’ and ‘feeling under pressure’ more common .
Psychiatric features associated with attacks
• Feelings of irritability and anxiety may last for several hours before the
attack.
• Sometimes patient may experience unusual health and vigour, amounting
to elation.
• There is history of increased energy and feelings of buoyancy at the
beginning of the attack in some
• In contrast some remain listless and fatigued for several days before attack.
• Anxiety and irritability are common early on, with drowsiness and lethargy
as the headache continues.
• Depression can be severe.
• Klee on detailed evaluation on patients with migraine found that 22%
had some psychiatric presentation.
• Marked impairment of memory in 10%.
• Clouding of consciousness or delirium in 8%.
• Pronounced anxiety in 8%,.
• Complex visual and auditory hallucinations in 6%
• Changes of body image in 6%
• Severe depression in 4%
Work up
• Due to the vast dd’s in headache , a detailed evaluation is mandatory
• A detailed history must be taken with special emphases to following
factors
• Type and location of pain,
• Timing
• Precipitants
• Prodromal events
• Associated symptoms
• Past history – similar episodes, no of episodes
• Past treatment history
• Family history
• Thorough neurological examination - To rule out any secondary
causes of headache
• Look for pathological signs that may indicate a brain disorder
• Psychiatric history
• MSE
Investigation
• Routine blood investigations: to rule out other causes and to get a
baseline before treatment
• Brain imaging is not routinely indicated
• Usually done if
1. Any abnormal neurological findings
2. Poor treatment response
3. Diagnostic clarity
• CT- to rule out haemorrhage
• MRI- in case of tumours, av malformations,hydrocephalus,vasculitis
Management- MIGRAINE
• Mainstay of management is pharmacological
• Include acute management and preventive treatment.
• Acute treatment
• patients are advised to make a headache diary to note migraine days, meals,
menses, school examinations, stressful episodes, and other potential
precipitants.
• For some patients, relaxation techniques or other forms of CBT may be
helpful.
• Evidence for hypnosis , acupuncture, transcutaneous electrical stimulation, or
spinal manipulation is poor
• Main aim is to treat the pain ,associated nausea and vomiting and to maintain
hydration.
TRIPTANS :
• 5HT1B/1D receptor agonists with
vasoconstrictive effects on blood vessels.
• Can be given as oral, intra nasal spray or
injection
• Choice of triptan depends on efficacy, side
effects, duration of headache, and coexistent
vomiting and cost.
• Efficacy data at 2 hours favour eletriptan and
rizatriptan
• Zumatriptan is available in India
• Common A/E: injection site reaction,
paraesthesia, dizziness, warm sensation.
• Avoided in individuals with uncontrolled
hypertension, cardiovascular, or
cerebrovascular disease
Ergot derivatives
• ergotamine and dihydroergotamine
• MOA: CEREBRAL VASO CONSTRICTION
• Previously used very commonly to treat
moderate to severe attacks
• Should be used along with anti emetics to
reduce nausea and vomiting.
• Excessive use may lead to persistent,excessive
vasoconstriction (ergotism) in the coronary
arteries, digits, and elsewhere.
• Might precipitate a miscarriage or cause
foetal malformations, so NEVER TO BE USED
IN PREGNANCY.
Anti emetics:
• To treat the nausea and vomiting associated
• Vomiting can result in reduced drug
absorption
• Drugs like narcotics and ergort alkaloids can
cause nausea and vomiting
• Metoclopramide , ondansetron etc can be
given parenterally
• Chance of dystonia with metoclopramide
• Adequate hydration must be maintained
• Those who have severe symptoms may need
admission and iv fluids.
Preventive treatment
• Prevention medicine - antidepressants, antihypertensive, and
antiepileptic's.
Migraine occurring more than four times a month
Migraine causing 3–4 days of disability per month
Acute medicines losing their effectiveness
Patients taking excessive medicine
Treating migraine with psychiatric co
morbidities
• While treating special consideration has to be given
• Aim is not just to reduce headache
• Equal or more importance should be given in managing co morbid
anxiety or depression
• Drugs that can cause depressive symptoms should be avoided- beta
blockers
• Role of psycho therapy
• Drug Treatment for Children and Adolescents.
• The only effective agents that have been effective in migraine prophylaxis for
children in multiple controlled trials are topiramate and flunarizine.
• cyproheptadine is commonly used as a preventative medication – no
evidence
Nonpharmacological Treatments
• Use of behavioural treatments including biofeedback, relaxation training, and
cognitive behavioural therapy.
• Herbal treatments such as feverfew
• Dietary supplements such as magnesium and vitamin D
Tension-Type Headache
• Acute management
 Pharmacological – given when headache occurs less than twice a week
 Ibuprofen (800 mg) is the first DOC, followed by naproxen (825mg)
 Naproxen has less chance of GI disturbance
 Simple analgesics like paracetamol, NSAIDS, aspirin can be used
 Adding caffeine (130 mg or 200 mg) significantly increases the efficacy of simple
analgesics.
• Preventive treatment- indications
• Headaches occur more frequently than two or three times per week
• Acute therapy is ineffective
• Analgesic consumption becomes excessive.
• Drugs used
• Amitriptyline or topiramate can be used
• Amitriptyline should be started in low doses (10-15mg) and then tapered
up
• 50 to 75 mg per day is needed to control symptoms
• Should be discontinued after 6 months of use, have to taper and stop
• MOA: not clearly understood
• Possible – increase in levels of serotonin and endorphin , decreasing NMDA
activity involved in pain pathway – so no role for SSRI
• Non pharmacological treatment
• Behavioural treatments: relaxation and biofeedback alone or in
combination
• Cognitive behavioural treatments – stress management
• Can be used with behavioural treatments
• The effects are produced slowly but long lasting
• Combination of this with prophylactic pharmacological treatment
have the best result
• Physiotherapy, spinal manipulation, massage, TENS, the application of
heat or cold failed to show any long lasting effect
• spinal manipulation can result in vertebral artery dissection
Cluster Headache
• First-line abortive therapy is subcutaneous sumatriptan –gives immediate
relief
• 100% O2 via a non-rebreathable mask at 12 to 15 L/min for up to 20
minutes can also be used as an effective treatment method
• Prophylactic medicine is almost always indicated- because of the extreme
severity of attacks
• Drugs shown some effect are lithium, corticosteroids, methysergide, CCB’s,
β-blockers, valproic acid. Often need combination
• Topiramate can be used as adjuvant
• Histamine desensitization and surgical intervention are options upon
exhaustion of traditional agents.
Posttraumatic Headache
• No clear guidelines
• Treatment should be tailored to the symptoms of the individual
patient
• Patient may have migraine/TTH type of headache ,so treatment is
modified accordingly.
• Muscular or ligament pathology – physical treatment
Legal implication may be the reason for poor
treatment response
Features Migraine Tension headache Cluster headache
Pain features
• Unilateral
• Pulsating
• Moderate to severe
• Worsened by activity
• Last for few hours to 1day
• Bilateral
• Pressing type
• Mild to moderate
• No relation to activity
• Last for many days
• Unilateral
• Stabbing ,retro orbital
• Severe
• Night time occurrence
• Multiple episodes per day
Associated symptoms
• Nausea/vomiting
• Sensory symptoms
• Aura symptoms
• Psychiatric presentation
• No much symptoms • Lacrimation
• Red eye
• Rhinorrhoea
• No aura
• Horner's syndrome
Precipitating factors • Stress
• Hormonal change
• Exercise and activity
• Food and medicines
• Weather changes
• Fatigue
• Cervical spondylosis
• Bright light ,loud noise
• Stress
• Alcohol
• Smoking
Treatment • Acute , preventive
• Behavioural therapy
• Acute
• Prophylactic therapy-rare
• Acute
• Prophylactic
Thank you ….
ARTICLE 51A(H) IN THE CONSTITUTION OF INDIA 1949
It is the fundamental duty of a citizen to develop the
scientific temper, humanism and the spirit of inquiry and
reform

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Neuropsychiatric aspects of headache

  • 1. Neuropsychiatric Aspects of Headache Presented by: Dr. JITHIN T JOSEPH DNB RESIDNET , MHC TVM CHAIR: DR.ARUN V ,CONSULTANT IN PSYCHIATRY
  • 2. INTRODUCTION • It is said that about 70 percentage of population had experienced headache once in their life time • Overall prevalence of migraine is around 12% • Headache ,especially migraine had caused so much burden to the patients life. • There is associated psychiatric and physical co morbidities. • WHO has launched a global campaign called “Lifting the Burden” to reduce the burden of headache. • The new areas of interest in headache researches are newer treatment agents and evaluation of comorbidities
  • 3. The aim of this presentation is to? 1. Provide an overview of the diagnostic nomenclature for headache syndromes. 2. Describe the magnitude, risk factors, and patterns of comorbidity. 3. To describe neuropsychiatric manifestations. 4. Summarize the clinical and laboratory examination necessary for making a diagnosis. 5. To discuss about current acute and prophylactic treatment strategies.
  • 4. CLASSIFICATION • The International Classification of Headache Disorders - ICHD-2(2004) • 3 classes 1.Primary headache syndromes • Migraine • Tension type headache • Cluster headache 2. Secondary headache syndrome • Due to underlying pathology of the brain and adjacent structures • More severe and more serious • Needs detailed evaluation
  • 5. • Temporal arteritis, intracranial mass lesions. • Idiopathique intra cranial hypertension (pseudotumor cerebri), • Meningitis , subarachnoid haemorrhage • Post concussion headaches 3. Cranial neuralgias and other causes of facial pain
  • 6.
  • 7. Migraine • Most disabling of the primary headache syndromes • Characterised by recurrent attacks of  Recurrent throbbing type of headache that is often unilateral.  Gastrointestinal symptoms such as nausea or vomiting  Hyperesthesia manifested by photophobia or phono phobia
  • 8. • Previously migraines were classified as classic and common type. • Classic is characterised by neurological symptoms and signs but less common – now called migraine with aura • Common migraine is more common with 75 % people affected , and characterised by no neurological symptoms – now called migraine without aura
  • 9. ICHD-2 Criteria for Migraine without Aura A. At least five attacks fulfilling criteria B–D B. Duration between 4 and 72 hours (untreated or unsuccessfully treated) C. At least two of the following: 1. Unilateral 2. Pulsating pain 3. Moderate to severe intensity 4. Aggravation by or causing avoidance of routine physical activity (walking or climbing stairs) D. During headache at least one of the following: 1. Nausea and/or vomiting 2. Photophobia and phonophobia E. Not attributed to another disorder
  • 10. ICHD-2 Criteria for Migraine with Aura A. At least five attacks fulfilling criteria in B–D B. Aura consisting of at least one of the following but no motor weakness: 1. Fully reversible visual symptoms • positive features -flickering lights, spots or lines • negative features - loss of vision 2. Fully reversible sensory symptoms • positive features -pins and needles • negative features - numbness 3. Fully reversible dysphasic speech disturbance
  • 11. C. At least two of the following: 1. Homonymous visual symptoms and/or unilateral sensory symptoms 2. At least one aura symptom develops gradually over 5 minutes and/or different aura symptoms occur in succession over 5 or more minutes 3. Each symptom lasts 5 or more minutes and less than or equal to 60 minutes D. Headache fulfilling criteria B–D for migraine without aura begins during the aura or follows within 60 minutes E. Not attributed to another disorder
  • 12. Aura of migraine • Aura can be any symptom of brain dysfunction • Typically precedes or accompanies the headache • Appear gradually and then evolve over 5–20 minutes, persist for less than 1 hour, and evaporate with the headache’s onset. • They characteristically consist of a transient visual phenomenon, but sometimes a simple olfactory hallucination. • Aura occasionally consists of language impairment similar to aphasia, sensory misperception, or personality change. • In children, but not adults, recurrent colic or “cyclic abdominal pain” with nausea and vomiting may constitute a migraine variant, but not technically an aura.
  • 13. • By far the commonest migraine auras are visual hallucinations • They usually consist of a greying of a region of the visual field (scotoma) flashing zigzag lines, (scintillating or fortification scotomata) crescents of brilliant colours , tubular vision, or distortion of objects(metamorphopsia). • Migraine auras most often involve the simultaneous appearance of positive phenomena, such as scintillations, and negative ones, such as opaque areas. • Some migraineurs experience premonitory somatic symptoms, such as fatigue, stiff neck, yawning, hunger, and thirst. • These patients can frequently predict their impending migraine hours to days before onset.
  • 14.
  • 15. SENSORY PHENOMENA Special Senses Visual, olfactory, auditory, gustatory Paraesthesia, Especially Lips and Hand MOTOR DEFICITS Hemiparesis, Hemiplegia NEUROPSYCHOLOGIC CHANGES Aphasia Perceptual Impairment, Especially for Size, Shape,and Time EMOTIONAL AND BEHAVIORAL Anxiety, Depression, Irritability, Hyperactivity
  • 17.
  • 18. EPIDEMIOLOGY AND COURSE • About 70 percent of adults endorsing a history of headaches in a given year. • Average prevalence of definite migraine is 10.9 percent from international studies. • Migraine with aura usually present for the first time in males during teens. • In females the peak incidence is around early twenties. • About half of those with migraine remit, about 35 percent continue to have intermittent headache, and only 20 percent continue to develop chronic migraine over time.
  • 19. • Over 80 percent of those with migraine report some degree of disability. • There is enormous personal and social burden • But only one-half of those individuals who suffer from debilitating migraine seek professional help. • Migraine in childhood -associated with gastrointestinal complaints, :episodic bouts of stomach pain, vomiting, or diarrhoea. • The duration is shorter than that commonly observed in adults. • In women, migraine is strongly associated with reproductive system function
  • 20. • Increased incidence during puberty and the first trimester of pregnancy, and is associated with exogenous hormone use. • After menopause, the frequency of migraine attacks generally decreases dramatically. • Family history of migraine is one of the most potent and consistent risk factors for migraine. • Genetic factors are involved in 1/3rd of the migraine cases. • The mode of inheritance and the genes involved are still unknown
  • 21. PATHOPHYSIOLOGY OF MIGRAINE • Believed to be due to the neuronal hyper excitability. • Involves mutation in various ion channels. • The first to be identified was a mutation in the gene, on chromosome 19, for the voltage-gated calcium channel. • Further studies found out mutation in gene coding for the Na+/K+ pump or in the gene for the neuronal voltage-gated sodium channel.
  • 22. • Previous hypotheses suggesting that migraine aura was caused by vasoconstriction, with the headache produced by the subsequent vasodilation, have now been discarded. • Migraine is now conceived as being related to events in the cortex and adjacent meninges on one hand and in the brainstem on the other. The final common pathway to the migraine aura is excessive potassium or glutamate release which facilitates cortical spreading depression
  • 23. • These events are linked by trigeminal fibres connecting the meninges to brain stem, and efferent fibres of the parasympathetic system controlling meningeal blood vessels. • Cortical spreading depression over the cerebral cortex, is relevant to the aura of migraine but not to migraine without aura. • Effects of neuropeptides and other neurotransmitters, particularly 5- hydroxytryptamine (5HT), on meningeal vasculature and nociceptors. • Altered function of aminergic brainstem nuclei and their parasympathetic outflow.
  • 24. Precipitating factors of migraine • Hormonal changes - catamenial migraine • Stress or its cessation. • Fasting , fatigue, over-sleeping. • Particular foods and beverages. • Drug intake, chemical additives. • Bright light, weather changes. • Exercise But these agents/situations vary dramatically within and between individuals.
  • 25. Basilar -type migraine or basilar artery migraine • Seen in about 10% of cases, episodes are usually interspersed among classic attacks. Symptoms are often bilateral. • The attacks begin with a visual aura, sometimes extending to both half- fields and obscuring vision. • Then progress to symptoms of brainstem dysfunction such as vertigo, dysarthria, ataxia, tinnitus. • Sensory symptoms distally in the limbs and around the lips and tongue. • This is followed by a gap of around minutes to half hour, following which headache occurs ,usually occipital • There may be LOC in between the onset of headache ,and it is believed to be due to ischemia of RAS
  • 26. Familial hemiplegic migraine • Characterised by attacks of transient hemiplegia that are followed by headache • The hemiparesis is always associated with sensory, language or visual disturbances and in some cases confusion/drowsiness • Aura symptoms are of longer duration • Genetic predisposition Retinal migraine – very rare • At least two attacks of fully reversible monocular visual symptoms followed by migraine headache.(IHS CRITERIA) • No longer considered as part of migraine
  • 27. Tension-Type Headache(TTH) • Most common among primary headache syndromes • Tension -type headache is characterized by episodes of stable bilateral pain lasting several days at a time. • Migraine and TTH can co-exist , or alternate • Its no longer believed to be due to muscle tension
  • 28. • Women are more commonly affected than men • Often affects multiple family members. • Patients with TTH tolerate their pain and usually go about their business, unlike people with migraine. • Fatigue, cervical spondylosis, bright light, loud noise, and, at some level, emotional factors allegedly produce or precipitate TTH • But the evidence for the same is less
  • 29. Differentiated from migraine headache due to its 1. Longer duration. 2. Lack of pulsating quality of the pain. 3. Lack of worsening with physical activity. 4. Absence of gastrointestinal concomitants. 5. Often bilateral
  • 30. EPIDEMIOLOGY AND COURSE • The aggregate prevalence of tension-type headache of 32 percent. • More common in women , but not as prominent as that of migraine. • More common in young adults • The incidence comes down with age but not that much as of migraine.
  • 31. ICHD-2 Criteria for Tension-Type Headache
  • 32. • Chronic tension-type headache • A. Headache occurring on greater than or equal to 15 days per month on average for more than 3 months (greater than or equal to 180 days per year) and fulfilling criteria B–D.
  • 33.
  • 34. Cluster headache • Cluster headache is a distinct syndrome characterized by frequent intense attacks (often several per day) over a 1- to 2-month periods. • Separated by headache-free intervals for as long as 1 or 2 years. • Initially grouped as part of migraine headache, but researches distinguished it as a separate entity. • Cluster refers to a “clustering in time,” with the headache • Males tend to suffer more from cluster headache than females.
  • 35. • Characterised by • Retro -orbital in location. • Accompanied by autonomic changes such as lacrimation, rhinorrhoea, erythema of the eye, and agitation. • Males are more commonly affected • Screaming and thrashing that may be associated with the pain and may often present as psychotic • Prior smoking and alcohol use have been associated with cluster headache. • Alcohol use can precipitate it.
  • 36. • This disorder affects men, typically between the ages of 20 and 40 years. • Most cluster attacks have a predictable, cyclic pattern. For example, some patients develop attacks every spring or fall. • Most strike between 9:00 PM and 9:00 AM and one-half of them develop during REM sleep. • Alcohol characteristically precipitates an attack. • Inhaling 100% high-flow oxygen will abort them. Thus, administering oxygen can be diagnostic as well as therapeutic.
  • 37.
  • 38. Headache Attributable to Head or Neck Trauma • A headache following head trauma accompanied by a loss of consciousness, post traumatic amnesia, and abnormal laboratory tests(ICHD 2) • Emotional factors are more likely to be a sequela rather than a cause of posttraumatic headache • Pathogenesis of posttraumatic headache is unknown. Major hypothesis are 1. Cerebral oedema. 2. Cortical spreading depression 3. Innate vulnerability to cerebral vasospasm, 4. Transient elevation of intracranial pressure
  • 39. • No relation between the prevalence of post traumatic headache and severity of head injury. • Posttraumatic headache is more common after injuries that do not result in skull fracture. • Rare in population -1% • But common after head injury -28 to 62 %. • Children and young adults appear to be particularly susceptible • 50 % had headache at time of discharge.
  • 40. • Persistence of headache has been related to 1. Female sex. 2. Age over 45. 3. The presence of dizziness. 4. Lack of skull fracture, intracranial hematoma. 5. Disorders of smell, hearing, or vision 6. Depression , and impaired concentration.
  • 41. SECONDARY HEADACHES • Temporal Arteritis / Giant Cell Arteritis • Intracranial Mass Lesions • Chronic Meningitis • Idiopathic Intracranial Hypertension (Pseudotumor Cerebri) • Post Dural Puncture Headache (PDPH) • Bacterial Meningitis, Herpes Encephalitis, • Subarachnoid Haemorrhage
  • 42. CRANIAL NEURALGIAS • Most common is trigeminal neuralgia • Can affect any 3 divisions, most common in V2 • Sufferer has daily agonising sharp pain lasting for few seconds • Touching the affected area or movements can provoke the pain • Due to fear of pain patients hesitate to eat, brush their teeth, or speak. • More common in females ,after 60 years and not present at night • Treatment : carbamazepine , gabapentin
  • 43. Chronic Daily Headache • Definition - When patients report headaches, each lasting 4 hours or longer, for at least 15 days each month for at least 3 months. • Most adult have a primary headache syndrome which progress • In children it may arise as new onset-New Daily Persistent Headache (NDPH) • Patient typically has generalized, waxing and waning, dull, pressing, and no pulsatile pain. • Pain is mild to moderate but incapacitating and lost features like aura and automatic symptoms
  • 44. • RISK FACTORS • Medication over use – most powerful risk factor • The medicines most commonly implicated are aspirin– caffeine compounds triptans, NSAIDs, benzodiazepines, and opioids. • Using triptans or opioid for more than 10 days a month – CDH in 2 years • Non opioid analgesics – 5 years • Obesity , head trauma. • Low socioeconomic status. • Disability , major stressful life events. • Depression and anxiety. • Risk factors for adolescents are primarily depression and anxiety.
  • 45. • Resistant to treatment • Medication over use has to be taken care of • Underlying anxiety and depression has to be treated • TCAs, valproate, and topiramate may help • modification of lifestyle, behavior therapy, and elimination of precipitating factors.
  • 46. Psychiatric aspects • It is believed that , there is increased psychiatric co morbidities in patients suffering from migraine. • The presentation of headache itself can mimic a psychotic episode • There is increased occurrence of anxiety and depression in migraine sufferers. • There are different psychological factors that can precipitate an attack. • Psychiatric co morbidity can adversely affect the treatment response • There are some personality types who may be suffering of migraine
  • 47. Anxiety and depression • These are the commonest co morbidities in migraine • 2-3 fold increase in risk • Anxiety disorder is more common than depression • A study by Merikangas et al 1990 found that prevalence of major depression, bipolar spectrum disorder (i.e. cyclothymia and hypomania), generalised anxiety and social phobia is more in patients with migraine. • Anxiety often manifested in childhood, followed by the development of migraine some years later, and then by discrete episodes of depression in early adult life.
  • 48. • Many cases are found to have mixed anxiety and depression. • The risk of suicide attempt is also increased in migraine, and it is of interest that not all this excess risk is explained by the presence of depression (Breslau 1992). • Some studies pointed out that there is more chance of developing migraine in those with anxiety and depression. (Hung et al. 2005; Oedegaard & Fasmer 2005). • A study by (Breslau et al. 2000) compared migraine headache with non migraine headache and those without and could not find any significant difference in the co morbidities. • There is a small increase in incidence for those with migraine with aura.
  • 49. Personality and stress in migraine • The evidence that a particular personality type predisposes a person to suffering migraine is not very strong. • People with migraine do have higher scores on neuroticism traits, including harm avoidance, psychasthenia and social introversion as evident from studies(Fan & Zhou 1999). • These traits were more common if the patient is seeking treatment. • There is increased emotional reactivity ,which in turn cause reactivity of ANS which is responsible for precipitating attacks • These factors are associated with poor treatment response and chance of progressing to chronic migraine. • Studies showed that ,this picture is not only for migraine ,but seen in all types of headaches. (Di Piero et al. 2001)
  • 50. Psychological precipitants • Psychological factors are thought to be the most important precipitating factor as evident from studies. • But it is not a must, about one third of people never had a psychological precipitating factor. • Periods of stress, or the anticipation of stress, are associated with attacks. • Sustained emotional tension seems to be more important than acute emotional disturbance. • Some patients to develop attacks during the ‘let down period’ after intense activity and striving. • Some have attacks quite regularly when a harassing day is over, at weekends or on the first day of a holiday. • In a study on patients attending migraine clinic it was found that intrusive thoughts about work’ and ‘feeling under pressure’ more common .
  • 51. Psychiatric features associated with attacks • Feelings of irritability and anxiety may last for several hours before the attack. • Sometimes patient may experience unusual health and vigour, amounting to elation. • There is history of increased energy and feelings of buoyancy at the beginning of the attack in some • In contrast some remain listless and fatigued for several days before attack. • Anxiety and irritability are common early on, with drowsiness and lethargy as the headache continues. • Depression can be severe.
  • 52. • Klee on detailed evaluation on patients with migraine found that 22% had some psychiatric presentation. • Marked impairment of memory in 10%. • Clouding of consciousness or delirium in 8%. • Pronounced anxiety in 8%,. • Complex visual and auditory hallucinations in 6% • Changes of body image in 6% • Severe depression in 4%
  • 53. Work up • Due to the vast dd’s in headache , a detailed evaluation is mandatory • A detailed history must be taken with special emphases to following factors • Type and location of pain, • Timing • Precipitants • Prodromal events • Associated symptoms
  • 54.
  • 55. • Past history – similar episodes, no of episodes • Past treatment history • Family history • Thorough neurological examination - To rule out any secondary causes of headache • Look for pathological signs that may indicate a brain disorder • Psychiatric history • MSE
  • 56.
  • 57. Investigation • Routine blood investigations: to rule out other causes and to get a baseline before treatment • Brain imaging is not routinely indicated • Usually done if 1. Any abnormal neurological findings 2. Poor treatment response 3. Diagnostic clarity • CT- to rule out haemorrhage • MRI- in case of tumours, av malformations,hydrocephalus,vasculitis
  • 58. Management- MIGRAINE • Mainstay of management is pharmacological • Include acute management and preventive treatment. • Acute treatment • patients are advised to make a headache diary to note migraine days, meals, menses, school examinations, stressful episodes, and other potential precipitants. • For some patients, relaxation techniques or other forms of CBT may be helpful. • Evidence for hypnosis , acupuncture, transcutaneous electrical stimulation, or spinal manipulation is poor • Main aim is to treat the pain ,associated nausea and vomiting and to maintain hydration.
  • 59. TRIPTANS : • 5HT1B/1D receptor agonists with vasoconstrictive effects on blood vessels. • Can be given as oral, intra nasal spray or injection • Choice of triptan depends on efficacy, side effects, duration of headache, and coexistent vomiting and cost. • Efficacy data at 2 hours favour eletriptan and rizatriptan • Zumatriptan is available in India • Common A/E: injection site reaction, paraesthesia, dizziness, warm sensation. • Avoided in individuals with uncontrolled hypertension, cardiovascular, or cerebrovascular disease Ergot derivatives • ergotamine and dihydroergotamine • MOA: CEREBRAL VASO CONSTRICTION • Previously used very commonly to treat moderate to severe attacks • Should be used along with anti emetics to reduce nausea and vomiting. • Excessive use may lead to persistent,excessive vasoconstriction (ergotism) in the coronary arteries, digits, and elsewhere. • Might precipitate a miscarriage or cause foetal malformations, so NEVER TO BE USED IN PREGNANCY.
  • 60. Anti emetics: • To treat the nausea and vomiting associated • Vomiting can result in reduced drug absorption • Drugs like narcotics and ergort alkaloids can cause nausea and vomiting • Metoclopramide , ondansetron etc can be given parenterally • Chance of dystonia with metoclopramide • Adequate hydration must be maintained • Those who have severe symptoms may need admission and iv fluids.
  • 61. Preventive treatment • Prevention medicine - antidepressants, antihypertensive, and antiepileptic's. Migraine occurring more than four times a month Migraine causing 3–4 days of disability per month Acute medicines losing their effectiveness Patients taking excessive medicine
  • 62.
  • 63. Treating migraine with psychiatric co morbidities • While treating special consideration has to be given • Aim is not just to reduce headache • Equal or more importance should be given in managing co morbid anxiety or depression • Drugs that can cause depressive symptoms should be avoided- beta blockers • Role of psycho therapy
  • 64. • Drug Treatment for Children and Adolescents. • The only effective agents that have been effective in migraine prophylaxis for children in multiple controlled trials are topiramate and flunarizine. • cyproheptadine is commonly used as a preventative medication – no evidence Nonpharmacological Treatments • Use of behavioural treatments including biofeedback, relaxation training, and cognitive behavioural therapy. • Herbal treatments such as feverfew • Dietary supplements such as magnesium and vitamin D
  • 65. Tension-Type Headache • Acute management  Pharmacological – given when headache occurs less than twice a week  Ibuprofen (800 mg) is the first DOC, followed by naproxen (825mg)  Naproxen has less chance of GI disturbance  Simple analgesics like paracetamol, NSAIDS, aspirin can be used  Adding caffeine (130 mg or 200 mg) significantly increases the efficacy of simple analgesics.
  • 66. • Preventive treatment- indications • Headaches occur more frequently than two or three times per week • Acute therapy is ineffective • Analgesic consumption becomes excessive. • Drugs used • Amitriptyline or topiramate can be used • Amitriptyline should be started in low doses (10-15mg) and then tapered up • 50 to 75 mg per day is needed to control symptoms • Should be discontinued after 6 months of use, have to taper and stop • MOA: not clearly understood • Possible – increase in levels of serotonin and endorphin , decreasing NMDA activity involved in pain pathway – so no role for SSRI
  • 67. • Non pharmacological treatment • Behavioural treatments: relaxation and biofeedback alone or in combination • Cognitive behavioural treatments – stress management • Can be used with behavioural treatments • The effects are produced slowly but long lasting • Combination of this with prophylactic pharmacological treatment have the best result • Physiotherapy, spinal manipulation, massage, TENS, the application of heat or cold failed to show any long lasting effect • spinal manipulation can result in vertebral artery dissection
  • 68. Cluster Headache • First-line abortive therapy is subcutaneous sumatriptan –gives immediate relief • 100% O2 via a non-rebreathable mask at 12 to 15 L/min for up to 20 minutes can also be used as an effective treatment method • Prophylactic medicine is almost always indicated- because of the extreme severity of attacks • Drugs shown some effect are lithium, corticosteroids, methysergide, CCB’s, β-blockers, valproic acid. Often need combination • Topiramate can be used as adjuvant • Histamine desensitization and surgical intervention are options upon exhaustion of traditional agents.
  • 69. Posttraumatic Headache • No clear guidelines • Treatment should be tailored to the symptoms of the individual patient • Patient may have migraine/TTH type of headache ,so treatment is modified accordingly. • Muscular or ligament pathology – physical treatment Legal implication may be the reason for poor treatment response
  • 70. Features Migraine Tension headache Cluster headache Pain features • Unilateral • Pulsating • Moderate to severe • Worsened by activity • Last for few hours to 1day • Bilateral • Pressing type • Mild to moderate • No relation to activity • Last for many days • Unilateral • Stabbing ,retro orbital • Severe • Night time occurrence • Multiple episodes per day Associated symptoms • Nausea/vomiting • Sensory symptoms • Aura symptoms • Psychiatric presentation • No much symptoms • Lacrimation • Red eye • Rhinorrhoea • No aura • Horner's syndrome Precipitating factors • Stress • Hormonal change • Exercise and activity • Food and medicines • Weather changes • Fatigue • Cervical spondylosis • Bright light ,loud noise • Stress • Alcohol • Smoking Treatment • Acute , preventive • Behavioural therapy • Acute • Prophylactic therapy-rare • Acute • Prophylactic
  • 71. Thank you …. ARTICLE 51A(H) IN THE CONSTITUTION OF INDIA 1949 It is the fundamental duty of a citizen to develop the scientific temper, humanism and the spirit of inquiry and reform