HEADACHE

I Made Oka Adnyana

HEADACHE
Definition:
Headache: Pain above the head
from orbita  occiput.

Facial pain: Pain bellow

orbitomeatal line, above the neck
and the front of the ear.

Headache should be
defferentiated with vertigo.
MECHANISMS OF
HEADACHE

Headache occur doe to stimulation of pain sensitive

craniale structur.
Pain sensitive craniale structur.
Extracraniale structurs :
 Skin, periosteum, muscle( m. frontalis
superfecial, m.occipitalis.
 Extracranial arteries.
 Structur of the eye, ear, nasal cavities
and sinus
Intracraniale structures :
 Intracraniale venous sinuses
 Part of the dura at the base of brain.
 Arteries with in the dura and pia- araachnoid,
and particulary the proximal parts of the anterior
and midle cerebral arteries. And the intracranila
segment of the internal carotid ertery.
Cranial Nerv:
 N. Trigeminal and n. glosopharyngeal
CLASSIFICATION OF
HEADACHE
A. Primary headache.
1. Migraine.
2. Tension type headache.
3. Cluster headache
4. Other primary headache.
- Primary cough headache.
 Primary exertional headache.
Primary headache associated with sexual activity.
Hypnic headache.
Primary thunderclap headache.
Hemicranial continua.
New daily persistent headache (NDPH)
B. Secondary headache (Organic cause headache).
RED FLAG
Red flag in history.
1. Abrupt onset of new type of severe headache.
2. Worst headache the patient ever had.
3. Progressive worsening of headache over period of
days or weeks.
4. Headache precipitated by exertion (exercise,
coughing, sneezing, bending over, or sexual
exciment).
5. Headache accompanied by generalized illness or
fever, nausea,vomiting, or stiff neck.
6. Headache accompanied by neurological symptoms
( aphasia, poor coordination, focal weakness or
numbness,drowsiness, decrease in hiher intelectual
function in personality).
RED flag on examination.
1. Abnormal vital sign ( increase blood
presurre, heart rate, or temperature).
2. Change in higher intellectual functions or
cognition.
3. Alterration in level of conciousness
4. Sign of meningeal irritation.
5. Pailledema.
6. Presence of focal neurlogical signs
(hemipharesis, hemisensory loss, ataxia, or
patholgical reflexes
YELLOW FLAG

Yellow flag in history.

1. Wakes patient from sleep at night

2. New onset side-locked headaches
3. Postural headaches
 HEADACHE

NO RED FLAG YES

PRIMARY
HEADACHE
SECONDARY HEADACHE

PRIMARY HEADACHE
(ATYPICAL SIGN) YES

NO

PRIMARY
HEADACHE
 ASSESMENT OF HEADACHE
1. Headache History

(Mumenthaler dkk, 2006)

(Mumenthaler dkk, 2006)
 ASSESMENT OF HEADACHE ‘Cont

2.

(Mumenthaler dkk, 2006)

 ASSESMENT OF HEADACHE ‘Cont

3.

4
.

(Mumenthaler dkk, 2006)

 Pain Assessment Scale
Verbal Pain Intensity Scale Visual Analog Scale

0–10 Numeric Pain Rating Scale Wong-Baker FACES Pain Rating Scale

Wong dkk, 2001;

McCaffery and Pasero, 1999;
Portenoy and Tanner, 1996
TENSION TYPE HEADACHE.

- The common primary headache.

- Most complain for out patient.
ETHIOLOGY
1. Oromanibular disfunction
2. Psychology stress
3. Anxiety
4. Depresi
5. Muscle stress
6. Drug abuse
7. Delution phenomena
CLINICAL SYMPTON.
1. Episodic pain, last a few minutes  day.
2. Bilateral location, pressing/tightening must be not throbbing.
3. Mild to moderate intensity.
4. Not aggravated by routine physical activity.
5. No nausea or vomiting.
6. No photophobia and phonophobia, but one of the two can be
present.
TENSION TYPE HEADACHE
A. Infrequent tension type headache:
At least 10 episodes occuring on < 1 day per
month on average (<12 days per year)
1. Infrequyuent episodic TTH. Associated with
pericranial tenderness.
2. Infrequyuent episodic TTH. Associated not
pericranial tenderness.
TENSION TYPE HEADACHE (cont)
B. Frequent tension type headache:
At least 10 episodes occuring on > 1 but < 15
days per month for at least (> 12 and <180
per year)
1. Frequyuent episodic TTH. Associated with
pericranial tenderness.
2. Frequyuent episodic TTH. Associated not
pericranial tenderness.
TENSION TYPE HEADACHE (cont).
C. Chronic tension type headache:
headache occuring on > 15 days per mont on
agerage for > 3 months (> 180 days per years).
Headache lasts hours or may be continous.
1. Chronic TTH. associated with pericranial
tenderness.
2. Chronic TTH. not associated pericranial
tenderness.
TREATMENT PRINCIPLE
1. Life style modification, non-pharmacological
therapy, pharmacological therapy on acute phase
and prophylaxis
2. Education precipitating factor, stress management,
exercise  reducing TTH
3. TTH self-limiting or with OTC analgetics
(accetaminophen, NSAID)
4. Non-pharmachological therapy : relaxation therapy,
cognitive-behavioral therapy, massage
5. Prophylaxys theraphy for frequent headache:
disrupt daily activity (occupation,school,quality of
life) or increasing of OTC analgetics usage (>10-
15 days/month)
TREATMENT.
Acute Prophylaxys

Caffeine combination 65-200 mg Venlafaxine 150 mg

Diclofenac 12.5-100 mg

Naproxen 375-550 mg

Aspirin 500-1000 mg Mirtazapine 15-75 mg

Ketoprofen 25 mg

Ibuprofen 200-800 mg

Paracetamol 1000 mg Amitriptilin 30-75 mg

TREATMENT
1. Pharmacology
 Acute
 Analgesic: aspirin 1000mg/day, acetaminophen
1000mg/day, NSAIDs (Naproxen 660-750mg/day;
ketoprofen 25-50mg/day; tolfenamic 200-
400mg.day; mefenamic acid; fenoprofen; ibuprofen
800mg/day; diclofenac 50-100mg/day. Long term
analgesic caused GI irritation, kidney and liver ds,
and platelet disfunction
 Caffeine (adjuvant analgesic) 65 mg
 Combination: aspirin 325 mg; acetaminophen 65-
200mg; caffein
TREATMENT
1. Pharmacology
 Chronic
 Antidepressant
 Amitriptyline: therapeutic and prevention.
 Reduce firing rate of trigeminal nucleus caudate.
 Long term: increase body weight, cardiac dysfunction,
orthostatic hypertension, and anticholinergic effect
 Antianxiety
 As therapeutic and prevention
 Benzodiazepine and butalbital
 Weaknes: Addictive and hard to control  worsen
headache
TREATMENT
1. Non Pharmacology
 Diet control
 Physical therapy
 Avoid daily used of analgesic sedative, and
ergotamine
 Behaviour treatment
TREATMENT
1. Non Pharmacology
 Physical Therapy
 Posture and position exercise
 Massage, ultrasound, manual therapy, warm or
cold compress
 Acupuncture TENS (transcutaneous electrical
stimulation)
TREATMENT
3. Preventive Pharmacology
 Indication
 Disability because of headache ≥ 4 days/month or no respond
to therapy
 Effective if reduce frequency or severity of headache minimal
50%
 Identification trigger of headache
 Think other comorbid that determine drug of choice therapy
 Drug interaction
 Single based drug and up-titration until tolerate
 Don’t consumed to many drugs  influenced adherence to
taking medicine
 Give patient information about therapy
TREATMENT
3. Preventive Pharmacology
 Drug of choice
Drug Daily dose
First Line
Amitriptyline 10-100 mg
Nortriptyline 10-100 mg

Second line
Mirtazapan 30 mg
Venofaxine 150 mg

Third line
Clomiramine 75-150 mg
Maprotiline 75 mg
Miansering 30-60 mg
CLUSTER HEADACHE
= Migrainus neuralgia, Horton
headache, histamine headache.

Clinical sign.
1. Severa headache, unilateral , orbital, supra orbital or
temporal.
2. Frequency: 1-8 time/day.
3. Follow by:
- conjuctival injection
- lacrimation
- nasal congestion.
- rhinorrhea.
- Forhead and facial sweating.
- Miosis and ptosis,
4. Not attributed to another this order.
CLUSTER HEADACHE

A. Episodic cluter headache

attacks occurirng I periods lasting 7 days to 1 year
seperated by pain-free periods lasting 1 month or
longer.
B. Chronic cluter headache
attacks occurring for more than 1 year without
remission or with remission lasting less than 1
month.
Hypothesis of Cluster headache
TREATMENT.
1. Oksigen 100%, 7 lt/minutes (10-15 minutes).
Combination 1-2 mg ergotamin and oksigen
100%.
2. Sumatriptan
- subcutan 6 mg (5-15mg).
3. Zolmatriptan 5 mg.
4. Dehydroergotamin (o,5-1,5mg).
5. Ergotamin 1-2 mg sup.
6. Analgetic and narcotic.
PROPHYLACTIC

1. Ergotamine 1-2 mg, verapamil 360-480mg)

2. Metisergid 1-2 mg( 3-4 time/day).
3. Kortiokosteroid (prednison 60-100 mg, metilprednisolon
40-60mg/day, dexametason 8mg/day)
4. Lithium carbonate.
5. Sodium valproate.
6. Pizotipen
7. Nerve block.
PREVENTION

1. Live and rest regularly

2. Avoid alcohol
3. Avoid precipitated factor  glare and bright light,
noise
4. Sleep regulation  Avoid sleeping at evening
5. Avoid stress, smooking, and excessive working.
MIGRAINE
PATHOPHYSIOLOGY 0
Figure 4.5 Line drawing (panel
1. Cortical spreading depression (Leo) a) of the spreading oligemia
observed with studies of cerebral
blood flow (CBF) during aura
after Lauritzen. Adapted with
permission from Lauritzen M.
Cortical spreading depression as
a putative migraine mechanism.
Trends Neurosci 1987;10:8–13,
with permission from
Elsevier Science. Panel b
illustrates the variable time
course and relationship of the
changes in cerebral blood flow
and the symptomatology of
migraine. Adapted with
permission from Olesen J, Friberg
L, Skyhoj-Olesen T, et al. Timing
and topography of cerebral blood
flow, aura and headache during
migraine attacks. Ann Neurol
PATHOPHYSIOLOGY (CONTINUES)
2.
2. System
Systemtrigeminovascular
trigeminovascular
MIGRAINE.

A. Migraine with out aura = common

migraine.
A. Recurrent headache (5 X).
B. Headache last with in 4 – 72 hours.
C. Headache has at least two of the following
characteristic:
1. Unilateral.
2. Throbbing or pulsating headache.
3. Moderate or severe pain intensity.
4. Aggravated by routine physical activity such as
bending, climbing stairs.
D. During headache at least one of the following:
A.Nause and or vomiting.
B.Photophobia and phonophobia.
E.Not atributed to another disorder
B. Migraine with aura = classic
migraine, opthalmic, hemiphlegic,
aphasia, complicated migraine.
1. Recurent headache.
2. Aura sympton precede headache ( 5-20
minute) and last less than 60 minute.
3. Headache is throbing or pulsating.
MANAGEMENT.

A. General principles.
Avoid precipitated factor.
1. Food (chocoate, ice cream, mono sodium
glutamate).
2. Stress
3. Changing climate.
4. Sleep regulation.
B. Abortive treatment.
Attenttion:
1. Rapid and constant effect of the drug.
2. Minimal/ with out side effect.
3. Long term effect to prevent recurrent
headache.
4. Drug efectiveness that help patients return back
to normal activity.
5. Unexpensive and avaible
Drug for abortive treatment.
1. Ergotamin derivat.
- Ergotamin tartrat
- Dehydroergotamin.
2. Triptan
- sumtriptan
3. Analgetic
- Acetaminophen.
- Paracetamol.
- NSAIDs.
Successful therapy

 Free pain 2 hours after treatment

 Pain resolution from pain scale 2 or 3 to scale
1 or 0 after 2 hours
 Drug efficacy consistent after 2 -3 attack
 No recurrent pain and no drug use after 24
hours aftrer treatment success
 PROPHYLACTIC
Goal of therapy:

1. Reducing frequency, severity, and duration of

migraine attack
2. Increasing patient response to acute therapy
3. Improve daily activity and reducing disability
4. Prevent usage of excessive analgetics  MOH
5. Reducing cost
 PROPHYLACTIC
Indication:

1. Recurrent migraine, disturb daily avtivities.

2. More than 2 times attack/week.
3. Failure abortive treatment or exceed abortive
treatment.
4. Side efect with abortive treatment.
5. Patient choice.
6. Uncommon migraine ( hemiphlegic migraine,
basilar migraine, migraine with prolonged
aura, aura infarc migraine).
DRUG FOR PROPHYLACTIC
1. Beta blocker ( propanolol, metoprolol, timolol
Efective for; hypertension, angina.
2. Antidepresant; amitriptilin, flouxetin.
3. Calcium chanel blocker: flunarizin,
nimodipin, nipedipin, verapamil.
4. Anti convulsant: sodium valproate,
gabapentine, topiramate.
5. Serotonon antagonis: metisergid, pizotifen.
6. Botox ( botolinum toxin). .
SUCCESSFUL
PROPHYLAXIS

IF FREQUENCY OF MIGRAINE ATTACKS

REDUCE AT LEAST 50% PER MONTH
WITHIN 3 MONTHS
Trigeminal Neuralgia

Unilateral pain in the face, characterized by a

short sharp pain electric shock-like, is limited
to one or more parts of the trigeminal Nerve
(N.V) and triggered by non noxious stimulus.
Epidemiology

 The incidence of occurrence ranged 70 from

100,000 population
 Most commonly found in people over the age
of 50 years or older.
 Incidence will increase in accordance with
increasing age.
 Rarely found at a young age.
 Man : woman = 2 : 3
Etiology

 Mechanicals pressure of blood vessels

 Pressure by the lesion or tumor
 Multiple sclerosis
 Physical damage of the trigeminal nerve due
to surgery or infection
 Idiopathic
Pathophysiology

 Glutamate secretion  activated AMPA receptor

in post synapse causing depolarization and action
potential.
 NMDA receptor will activated after magnesium ion
channel receptors that clog that receptor 
calcium ions influx  increase intracellular calcium
 This mechanism explains the occurrence of central
sensitization.
 Trigeminal neuralgia is classified into idiopathic
and symptomatic.
Pathophysiology

Medscape, 2014
Symptom

 Neuropathic pain proximal severe pain,

sharp, such as stabbing, shot, electrocuted,
hit by lightning, or burning, the brief few
seconds to a few minutes but less than two
minutes, sudden and repetitive.
 Between attacks there is usually a pain-free
interval, or only a mild dull taste.
 There is Trigger Area
Pain distribution:
 N.V1 : 4%
 N.V2 : 35%
 N.V3 : 30%
 N.V1+V2: 10%
 N.V2+V3: 20%
Diagnosis

 Classic Neuralgia Trigeminal :

a. Paroxysmal pain attacks a few seconds to two minutes
involving one or more branches N.Trigeminus and
meet criteria b and c.
b. Pain at least meet one the following criteria :
 Strong, sharp, superficial or stabbing
 Precipitated from trigger areas or by trigger factors
c. Stereotyped attacks on each individual
d. No neurological defisist
e. Not associated with other disorders
 Symptomatic Neuralgia trigeminal
a. Paroxysmal pain attacks for a few seconds to two minutes
with or without persistent pain among paroxysmal
attacks, involving one or more branch / division of the
trigeminal nerve.
b. Pain at least meet one the following criteria :
 Strong, sharp, superficial or stabbing
 Precipitated from triger areas or by trigger factors
c. Stereotyped attacks on each individual
d. Lesions caused by other than vascular
compression, real structural abnormalities also seen
in advanced inspection and / posterior fossa
exploration. Machfoed, 2010
Diagnostic Examination

 In TN Primary, found no interference in the

lab and radiology. In emng showed a normal
response.
 In TN Secondary (due to structuring lesions)
can do a CT scan, MRI or MRA
Treatment

 Pharmacology
 Surgery
Therapy
 Pharmacology:
1. Anticonvulsant :
  Carbamazepine 100-600 mg/day
 Oxcarbazepine 300-2400 mg/day
 Phenytoin 200-400 mg/day
 Gabapentin 1200-3600 mg/day
 Pregabalin 150-300 mg/day
 Lamotrigine 100-400 mg/day
 Topiramat 150-300 mg/day

2. Muscle Relaxant :
 Baclofen 60-80 mg/day
Therapy

 Non-Pharmacologic:
 Information and education to patient
 Surgery : intractable pain, side effect of oral
therapy

Note: Symptomatic therapy is similar in other

neuralgia
THANK YOU
TREATMENT.
4. Muscle relaxant: tizaniden, eperison hcl, baclophen and
diazepam.
5. Injection botox.
6. Non farmacology treatment.
- Cognitive behavior theraphy
- Relaxation.
- Physiotheraphy.
TREATMENT.
1. Simple analgetic
- Aspirin, acetaminophen
2. NSAIDs (ibuprophen, sod. naproxen, sod, diclofenac).
3. Combination analgetic, sedative, minor transquilizer.