09 kuliah nyeri kepala dr rd-1

Blok Neurologi:Blok Neurologi:Nyeri KepalaNyeri KepalaRivan Danuaji, dr, M.Kes, Sp.S

OutlineOutline Introduction and approach Pathophysiology Classification:

◦ Primary Headache◦ Secondary Headache

Migraine TTH Cluster Other Headache Conclution

AcuanAcuan

IntroductionIntroduction Headache is the Most Common Symptom that Humans Experience in 99.9% of people with headache there is no sign of tissue damage injuring the brain itself does not cause pain – it causes altered brain function however the membrane and blood vessels of the brain are very pain sensitive

Scale of the problemScale of the problem At least 10% population suffer from headache 1-2% suffer chronic migraine (>15 days/month) 4.4% per year consult GP for headache1

20% of sickness absence from work2

1 Latinovic R et al. JNNP 2006;77:385-387 2 Rasmussen BK. Cephalalgia 2001; 21:774-7

Classification of HeadacheClassification of HeadachePrimary headaches (No underlying cause)

◦Migraine◦Tension-type◦TACs◦Other

Secondary headaches (Underlying cause)◦Medication overuse◦Head/neck injury◦Space-occupying lesion (i.e. brain tumour)◦Vascular cause (i.e. Subarachnoid hemorrhage, intracranial bleed)◦Infectious cause (i.e. meningitis or upper respiratory tract infection)◦+ many others

Headache Classification Committee of the International Headache Society,1988

>65% in patients older than 50

Headache diagnosisHeadache diagnosis Almost entirely on the patients story --> Red Flag Physical Examination always needed Tests, scans etc rarely helpful.

Headache Red Flags - Headache Red Flags - “SNOOP”“SNOOP” Systemic symptoms (fever, weight loss) Secondary risk factors (cancer,

HIV/immunocompromised) Neurologic symptoms or abnormal signs Onset (i.e. new-onset chronic headache) Older patient (i.e. new headaches at age >50 yrs) Previous headache different (i.e. significant

change in headache frequency or clinical features)

Positional component (i.e. increases when upright)

Provocative factors (precipitated by coughing, exercise, sex)

Neurologic Examination of Neurologic Examination of Headache PatientsHeadache Patients Vitals (particularly BP) and Severity of pain (i.e

using VAS) Pupil symmetry, reactivity and fundoscopy Visual fields Eye movements Motor – look for asymmetrical weakness R vs L Reflexes – look for asymmetry (increased

reflexes) R vs L Sensation – extinction to double simultaneous

tactile stimuli Coordination – finger-nose-finger, gain and

tandem gait Examine/touch the head and neck

Olesen J , et al., 2006Pryse –Phyllips WEM, et al., 1997

Adult with Headache

Refer to appropriate on-call hospital team Yes

Headache Management Headache Management PathwayPathwayEmergency

symptoms?

• Thunderclap onset• Accelerated/Malignant hypertension• Acute onset with papilloedema• Acute onset with focal neurological signs• Head trauma with raised ICP headache(see red flags)

• Photophobia + nuchal rigidity + fever +/-rash• Reduced consciousness• Acute red eye: ?acute angle closure glaucoma• New onset headache in:

• 3rd trimester pregnancy/early postpartum• Significant head injury

(esp. elderly/ alcoholics / on anticoagulants)

Adult with Headache

Emergency symptoms? Refer to appropriate on-call hospital team Ye

s

Check ESR, CRP, FBC, LFTPrednisolone 60mg o.d. immediately

Urine and CXR

Consider urgent referral to rheumatology, ophthalmology or

neurology(consideration of temporal artery

biopsy)

Yes

Headache Management PathwayHeadache Management Pathway

Giant cell arteritis?

No

• Symptoms and signs:-• jaw/tongue claudication, amaurosis, scalp

tenderness• temporal artery: prominent, tender, diminished

pulse• other cranial nerve palsies, limb claudication• PMR

• Many headaches respond to high dose steroids, so do not use response as the sole diagnostic factor

• ESR can be normal in 10% (check CRP as well)www.rheumatology.org.uk/includes/documents/cm_docs/2010/m/2_management_of_giant_cell_arteritis.pdf

Adult with Headache


s

Red flags?

No


No

Yes Refer

Headache Management Headache Management PathwayPathway


Urine and CXR



biopsy)

Yes

•Raised intracranial pressure:-•Wakes from sleep (but not migraine or cluster)•Precipitated by Valsalva manoeuvres (cough, straining at stool)•Papilloedema•Other symptoms of raised ICP headache include:-

oPresent upon waking and easing once up (MOH can cause this phenomenon)

oWhooshing pulse-synchronous tinnitusoEpisodes of transient visual loss when changing posture (e.g. upon

standing)oVomiting (in context as migraine causes this!)

•New onset seizures•Persistent new or progressive neurological deficit•Increasing in severity and frequency despite appropriate treatment

•Undifferentiated headache of recent origin and present for >8 weeks

•Triggered by exertion•New onset headache (< 6 months) in:-

>50 years old (consider giant cell arteritis); interrogate patient about previous ‘normal headaches’ as it might not be ‘new’Immunosuppressed / HIV / relevant history of cancer

Adult with Headache


s

Migraineor

tension headache?

No

Red flags?

No


No

Yes Refer

Headache Management Headache Management PathwayPathway


Urine and CXR



biopsy)

Yes

Primary or Secondary?

Headache: historyHeadache: history How old were you when the headaches started? How often do they come? Do they come in relationship to anything else? At what time do they come on? How do they start? Where is the pain? How long does it last? How bad is it? Are there other symptoms? Does anything bring it on? What helps? How long does it last?

Overall Approach to Overall Approach to HeadacheHeadache

Wolff HG, et al., 2001

Any secondary Headache disorder can mimic a primary headache disorder

Adult with Headache

•If relevant, stop combined oral contraceptive•Ensure not overusing analgesics or triptans•Modify lifestyle (adequate sleep, hydration, reduce caffeine intake, trigger avoidance)•If prophylaxis necessary, try the following for 3 months at the target dose before judging efficacy:-Migraine prophylaxisa)Propranolol SR 80mg o.d. increase gradually to 240mg o.d. or maximum tolerated below that• If ineffective or contraind: Amitriptyline 10mg o.n. increasing by 10mg/week to ≤75mg• Don’t bother with pizotifen (weight gain, sedation, little benefit)• If above ineffective/not tolerated, try Topiramate 25mg o.d. increasing by 25mg every 2-weeks aiming for a target of 50mg b.d. NOTE: teratogenic and potential interaction with combined oral contraceptive

Tension Type Headache prophylaxisAmitriptyline 10mg o.n. increasing by 10mg a week up to 75mg or maximum tolerated below that


s

Cluster headache

?

No

Continue treatment

for 9-12 months;then consider

stopping

Still troublesome

?

No

Still troublesome

?

No

Nofurther

treatment

Migraineor

tension headache?

No

Red flags?

No


No

No

Stop offending medication

(for 2 months if MOH)

Yes

Yes

Yes Refer

Try acute treatments

Yes

Can you diagnose migraine or

tension headache?

Yes

No

Refer

Yes

Prescribe acute treatment (< 10 times/month)

Yes

Secondary causes?

e.g. sinusitis, TMJ pain

Hb, Ca2+, TFT,ESR, CRP

R/V lifestyle & medication

Treat as necessary

No

Suspect:-•Medication overuse headache (MOH)?•Drug induced?

Yes

Still troublesome

?

Headache Management PathwayHeadache Management Pathway


Urine and CXR



biopsy)

Yes

PATOPHYSIOLOGYPATOPHYSIOLOGY

Basic Pathophysiology of Pain ProcessesBasic Pathophysiology of Pain Processes

Devor, 1996

Stimulus Perception

PNSSpinal cord

Brainstem

BRAIN

Gate-control inhibitionInjury triggered

“central sensitization”

Brainstem collaterals

Peripheral(receptor)

sensitization

NervePathophysiology(ectopic)

Sympathetic-sensory

Coupling,neurogenic

Inflammation?

Descending inhibition

PERCEPTION

MODULATION

CONDUCTION

TRANSDUCTION

PAIN – SERIES OF EVENTSPAIN – SERIES OF EVENTS

PAIN

TRANSMISSION

Pathophysiology Primary Pathophysiology Primary HeadacheHeadache AuraAura

◦Spreading cortical depression, not Spreading cortical depression, not ischemiaischemia

BrainstemBrainstem

◦Migraine “generator” in dorsal raphe, locus Migraine “generator” in dorsal raphe, locus ceruleus and periaqueductal gray matterceruleus and periaqueductal gray matter

◦PET scans show increased blood flowPET scans show increased blood flow

PathophysiologyPathophysiology Threshold surpassed:Threshold surpassed:

◦Brainstem “generator” Brainstem “generator” liberates CGRP (Calcitonin liberates CGRP (Calcitonin Gane-Related Peptide)Gane-Related Peptide)

◦Activation of Activation of trigeminovascular systemtrigeminovascular system

CGRP also elevated with pulsating chronic tension-CGRP also elevated with pulsating chronic tension-type headachestype headaches

PathophysiologyPathophysiology Nitric oxideNitric oxide

◦VasodilatorVasodilator◦Promotes central Promotes central

sensitization of trigeminal sensitization of trigeminal nociceptorsnociceptors

◦Sumatriptan decreases Sumatriptan decreases NO release in addition to NO release in addition to inhibiting CGRP releaseinhibiting CGRP release

PathophysiologyPathophysiology Trigeminal StimulationTrigeminal Stimulation

◦Ca channel activation: substance P Ca channel activation: substance P releaserelease

◦Feedback to DRG: NMDA (Feedback to DRG: NMDA (N-Methyl-D-aspartate) & AMPA ( & AMPA ((α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) release, leading to wind uprelease, leading to wind up

◦Release of prostaglandins, kinins that Release of prostaglandins, kinins that induce perivascular inflammationinduce perivascular inflammation

◦NO and CGRP further capillary leakageNO and CGRP further capillary leakage

PathophysiologyPathophysiology Potentials for future abortive treatment:Potentials for future abortive treatment:

◦Antagonists of: CGRP, NO, GlutamateAntagonists of: CGRP, NO, Glutamate◦Agonists of adenosine A1 receptorsAgonists of adenosine A1 receptors

CLASIFICATIONCLASIFICATION

©International Headache Society 2003/5

INTERNATIONAL CLASSIFICATIONINTERNATIONAL CLASSIFICATIONofofHEADACHE DISORDERSHEADACHE DISORDERS

2nd edition (12nd edition (1stst revision) revision)

(ICHD-IIR1)


ClassificationClassificationPart 1:Primary headache disorders:

no other causative disorderPart 2: Secondary headache disorders

(ie, caused by another disorder):new headache occurring in close

temporal relation to another disorder that is a known cause of headache

coded as attributed to that disorder(in place of previously used term associated

with)

Part 3: Cranial neuralgias, central and primary facial pain and other headaches


ClassificationClassificationPart 1: The primary headaches

1. Migraine2. Tension-type headache3. Cluster headache

and other trigeminal autonomic cephalalgias4. Other primary headaches


Part 2: The secondary Part 2: The secondary headachesheadaches

5. Headache attributed to head and/or neck trauma

6. Headache attributed to cranial or cervical vascular disorder

7. Headache attributed to non-vascular intracranial disorder

8.Headache attributed to a substance or its withdrawal

9. Headache attributed to infection.10. Headache attributed to disorder of homoeostasis 11. Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cranial structures12. Headache attributed to psychiatric disorder


ClassificationClassificationPart 3: Cranial neuralgias, central and primary facial pain and other headaches

13. Cranial neuralgias and central causes of facial pain14. Other headache, cranial neuralgia, central or primary facial pain

MIGRAINEMIGRAINE

MigraineMigraine• Unilateral onset• Throbbing• 4 – 72 hours• Sensory Sensitivity

–Light–Sound–Smells–Movement

migraine behaviour

Common misdiagnosis of Common misdiagnosis of migrainemigraine

Cervicogenic Headache (30% migraine→neck pain)

Chronic Tension Type Headache Eye Strain Dental TMJ dysfunction Sinus headache Hypertensive Headaches

Migraine CriteriaMigraine CriteriaAt least 5 attacks fulfilling the followingHeadache attacks lasting 5 to 72 hours with at least 2 of the following characteristics

◦Unilateral location◦Pulsating quality◦Moderate or severe intensity◦Aggravation by walking stairs or similar

routine physical activity

Migraine Criteria Migraine Criteria (cont.)(cont.) During headache at least 1 of the following

◦Nausea and/or vomiting◦Photophobia and phonophobia

No evidence of organic disorder causing chronic headaches

IHS Migraine Condensed: IHS Migraine Condensed: One Simple QuestionOne Simple Question Have you experienced 5 or more attacks of unprovoked head pain that lasted 4

to 72 hours, were severe enough to inhibit or even prohibit routine activity, and were accompanied by light/sound sensitivity, nausea, or both?

IHC II auraIHC II aura

• focal neurological symptoms• develop over 5-20 minutes• last for < 60 minutes

AurAuraa

• Fortification spectra = teichopsia

• Photopsia• Scotoma• Shimmering• Paraesthesia• HemiparesisVauban 17th

century

Migrainous AuraMigrainous Aura

What happens during a migraine?What happens during a migraine?

Migraine causeMigraine cause cause unknown but strongly inherited a lower threshold to spontaneously

produce symptoms as if the head and brain had been injured

many effective treatments

TriggersTriggers foods : spices, wine , chocolate, citrus food additives : monosodium

glutamate sleep : both too much and too little stress : mainly offset female hormones : fluctuating or falling

oestrogen

Migraine Treatment: Migraine Treatment: acuteacute

• Aspirin 900mg + metoclopramide (and/or paracetamol)

• NSAID• Triptans: 5-HT 1b/d agonists

– Almotriptan– Eletriptan– Frovatriptan– Naratriptan– Rizatriptan– Sumatriptan

• Antipsychotics: chlorpramazine etc• Steroids?

Generic and fastest acting

Migraine Treatment: Migraine Treatment: ProphylaxisProphylaxis• Propranolol• Amitriptyline• (pizotifen….no evidence…..gain weight and

sleepy)• Topiramate

–Wt loss, paraesthesia common–Memory problems, 1% renal calculi

• Gabapentin

• unusual stuff: Botox, methysergide, lisinopril...• Alternative stuff:

–Feverfew+riboflavin, butterburr, Mg, acupuncture

BMJ 2011;342:d583Pharmacological Prevention of Migraine

TENTION TYPE TENTION TYPE HEADACHEHEADACHE

Tension-Type HeadacheTension-Type Headache Most common headache

syndrome Episodic < 15 days per month Chronic > 15 days per month

TTH - CharacteristicsTTH - Characteristics 30 minutes to 7 days Pressing or tightening Mild to moderate pain Variable location, often bilateral Nausea and vomiting rare

Typical patient : any

Episodic Tension Type Episodic Tension Type HeadacheHeadache..IHS Criteria Tension type headaches < 15 per month. Lasts 30 mins to 7 days No nausea or vomiting No photophobia and phonophobia (1 ok) Headache has at least 2 of the following

criteria:a. pressing/tighteningb. Bilateral Mild-moderate Not aggravated by physical activity.

Chronic Daily HeadacheChronic Daily Headache Affects 4-5% of the population. Definiton: head pain for at least 4

hours for more than 15 days/month. Often develops from an episodic

headache disorder either migraine or episodic tension type headache

Includes chronic tension type headache(CTTH) and chronic daily migraine

Chronic Tension Type Chronic Tension Type Headache.Headache. Develops from episodic tension

type headaches The most common form of CDH. Familial tendency. Medication rebound headache

may be a factor in the transformation of episodic headache to CDH.

Chronic Tension Type Chronic Tension Type HeadacheHeadache Affect women more than men Most common in middle age Stress is often a trigger Average duration is 4-13 hours.

Treatment of CTTH.Treatment of CTTH. Treating each headache increases

the frequency and severity of the headaches.

Reserve medications for worse than usual headache.

Expert opinion: treat 2 headaches a week.

Treatment of TTHTreatment of TTH Simple analgesia:ibuprofen is

more effective than acetaminophen.

Combine analgesics with a sedating anit-histamine eg diphenhydramine.

Limit treatment to 2 days a week to prevent rebound headaches.

TTH - TreatmentTTH - Treatment Stress

management◦ Biofeedback◦ Stress reduction◦ Posture correction

Medication rarely needed in ETTH◦ Benzodiazepines◦ amitriptyline

CTTH◦ Abortive

NSAIDs ASA-caffeine-

butalbital Phenacetin

◦ Preventative Antidepressants Muscle relaxants NSAIDs

Prevention of CTTHPrevention of CTTH Tricyclic antidepressants. Stress management Tizanidine SSRIs:prozac Anticonvulsants:gabapentin and

topiramate. Acupuncture

CLUSTER HEADACHECLUSTER HEADACHE


3.1 Cluster headache (IHS)3.1 Cluster headache (IHS)A. At least 5 attacks fulfilling criteria B-DB. Severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15-180 min if untreatedC. Headache is accompanied by ≥1 of the following:

1. ipsilateral conjunctival injection and/or lacrimation2. ipsilateral nasal congestion and/or rhinorrhoea3. ipsilateral eyelid oedema4. ipsilateral forehead and facial sweating5. ipsilateral miosis and/or ptosis6. a sense of restlessness or agitation

D. Attacks have a frequency from 1/2 d to 8/dE. Not attributed to another disorder

Cluster HeadacheCluster Headache Frequency clusters – every time each year or season,

then free

Pain excruciating penetrating, boring continuous, non-

throbbing

Duration 15mins-3 hrs; same clock time each day (2am);

several episodes / day

Location ALWAYS the same side

Symptoms watering eyes nasal stuffiness, runny nosered eye, swollen eyelids osweating

Typical patient : middle aged male smoker

Cluster HeadacheCluster Headache

ClusterCluster Intensely severe

pain Unilateral Periorbital 15 to 180 minutes Nausea and

vomiting uncommon

No aura

Alcohol intolerance

Male predominance

Autonomic hyperactivity◦ Conjunctival

injection◦ Lacrimation◦ Nasal congestion◦ Ptosis

ClusterCluster Episodic

◦ Two episodes per year to one every two or more years 7 days to a year

Chronic◦ Remission phases

less than 14 days◦ Prolonged

remission absent for > one year

Cluster - TreatmentCluster - Treatment Preventative

◦ Calcium channel blockers

◦ Bellergal◦ Lithium◦ Methysergide◦ Steroids◦ Valproate◦ Antihistamines

Abortive◦ Oxygen◦ 5-HT receptor

agonists◦ Intranasal

lidocaine

OTHER HEADACHEOTHER HEADACHE

Secondary headache after injury Should begin within 7 days of head injury

(to meet IHS criteria) Consider diagnosis: subdural, CSF leak,

dissection Headaches may resemble primary

headache disorders (i.e. migraine, tension)

Often assoc with other “post-concussive” symptoms: vertigo, tinnitus, cognitive changes, sleep problems, depression, medication overuse

There is no evidence-based approach and no guidelines

Post-Traumatic HeadachePost-Traumatic Headache

-anterior communicating artery (30-35%),-the bifurcation of the internal carotid and posterior communicating artery (30-35%) --the bifurcation of the middle cerebral artery (20%) -bifurcation of the basilar artery, and the remaining posterior circulation arteries (5%)

http://en.wikipedia.org/wiki/Anterior_communicating_artery

http://en.wikipedia.org/wiki/Internal_carotid

http://en.wikipedia.org/wiki/Posterior_communicating_artery

http://en.wikipedia.org/wiki/Middle_cerebral_artery

SymptomsSymptoms Headache 85-95% Neck stiffness 74-84% n/v , photophobia 48% Mental status 43%

Less common:◦ Focal deficit, seizures, coma, CN palsy, papilledema, ocular

hemorrhage

*sentinel bleed

First primary sexual or exertional First primary sexual or exertional headacheheadache

SAH has to be excluded as 1/3 of SAHs occur during activities such as bending, lifting, defecation or sexual intercourse.

Copyright restrictions may apply.

Wityk, R. J. JAMA 2001;285:2757-2762.

Imaging of Stroke

Copyright restrictions may apply.

Wityk, R. J. JAMA 2001;285:2757-2762.

Anatomy of Carotid Artery Dissection

2cm distal to carotid origin-ends at skull base

Subintimal dissection -stenosis

Mickey mouse ears: expansion by hyperintense hematoma of the outer lumen of the artery

Carotid DissectionCarotid Dissection Fronto-orbital headache before ischemia: 55-100%

Painful Horner’s, Painful tinnitus Carotid bruit, dysguesia, ipsilateral neck pain,

cerebral or retinal ischemia

Triggers: cough, sneeze, trauma Risks: syphilis, Marfans, Ehlers-Danlos, FMD Prognosis: good (60% resolve spont.;85% do well)

37 year old after a motorcycle accident Sara Mazzucco, MD; and Nicolo` Rizzuto, MD

Neurology 2006

cavernomacavernoma

MRI demonstrating a left-sided cavernoma (a and b) with an associated developmental venous anomaly (c) in the dorsal midbrain region adjacent to the periaqueductal grey matter. Cephalalgia, Vol. 22, No. 2, 107-111 (2002)

MSMS

MS patients with a plaque located within the midbrain, in proximity to the PAG, showed a four-fold increase in migraine-like headaches (odds ratio 3.91, 95% confidence interval 2.01 to 7.32; P < .0001) when compared to MS patients without a plaque in this location

Headache 2005 Jun;45(6):670-7

occipital arteriovenous malformationoccipital arteriovenous malformation

Kurita, H. et al. Arch Neurol 2000;57:1219

34-year-old man started to experience monthly headaches: visual prodrome consisting of scintillating bright lights in the left visual field that slowly expanded over several minutes. Shortly after the visual symptom subsided, right-sided throbbing headaches developed along with nausea and vomiting, which usually lasted 2 to 4 hours. Normal neuro exam. He was treated by radiosurgery with obliteration of the AVM and resolution of the headaches

Erle C.H. Lim, Raymond C.S. Seet: Sudden-Onset Headache And Seizures In A Young Man. The Internet Journal of Neurology. 2005. Volume 4 Number 2

Trigeminal NeuralgiaTrigeminal Neuralgia

VERY short (<1 sec) severe pain

Knife-like Local triggering : eating

etc

Typical patient : middle aged / elderly woman

Sinus InnervationSinus Innervation Ophthalmic and maxillary

branches of 5th cranial nerve Greater superficial petrosal

branch of 7th cranial nerve Ostiomeatal complex > turbinates

> septum > sinus mucosa

Frontal SinusFrontal Sinus Ophthalmic

branch of 5th cranial nerve

Pain referred to forehead and anterior cranial fossa

Anterior EthmoidAnterior Ethmoid Ophthalmic

division Anterior ethmoid

nerve off nasociliary

Anterior septum, turbinates, ostiomeatal complex

Posterior Ethmoid and Posterior Ethmoid and SphenoidSphenoid Maxillary division

◦ Posterior ethmoid nerve

◦ Posterior septum, parts of superior and middle turbinates

Ophthalmic division

Greater superficial petrosal nerve

Maxillary SinusMaxillary Sinus Maxillary

division of 5th cranial nerve◦Posterior

superior alveolar◦Infraorbital◦Anterior superior

alveolar

Referred OtalgiaReferred Otalgia Oral cavity

◦Mandibular division of 5th cranial nerve

◦Auriculotemporal nerve Pharynx

◦Jacobson’s branch of 9th cranial nerve Hypopharynx and supraglottic

larynx◦Arnold’s branch of 10th cranial nerve

HistoryHistory First occurrence Timing Quality Treatments Associated symptoms Precipitating factors

Past Medical HistoryPast Medical History Head injuries, infections,

surgeries Psychiatric diagnoses Medications

◦OTC analgesics ◦OCP ◦Herbal medications◦Antihypertensives & vasodilators

Alcohol, tobacco, drugs

Physical ExaminationPhysical Examination Complete head & neck exam

◦Cranial nerves◦TMJ & muscles of mastication◦Scalp vessels◦Trigger points

Neurological exam

Diagnostic TestsDiagnostic Tests EEG CT and/or MRI EMG TMJ radiography Cervical spine films Labs Psychometric testing

Conclusion of Secondary causesConclusion of Secondary causesDisruption of outflow-venous thrombosis, dural fistula-radical neck dissection-right heart failure-COPD-(obesity)

Hormonal-hypoparathyroidism-hyper/hypothyroidism-Cushing's ?Addison's-PCO

Toxins/meds-vitamin A-Nalidixic acid,tetracycline,nitrofurantoin,indocid,steroids/withdrawal,others

Medical conditionsCRF, SLE, Anemia/polycythemia

Infectious-meningitis,encephalitis,Lyme,HIV

Trauma

MANAGEMENTMANAGEMENT

TreatmentTreatmentExplanation, set realistic objectives

Lifestyle change

Treatment of the attack

Treatment to reduce attack frequency

Treatment of the attackTreatment of the attack1. General pain relievers2. Migraine-specific treatments

- triptans and ergots

3. Cluster specific treatment- oxygen- triptans

General pain relievers : General pain relievers : migraine, tensionmigraine, tension

aspirin

paracetamol

ibuprofen

codeine

tramadol

Fast? ✔✔ ✔ ✔Safe? ✔✔OK

for long term?

✖ ✔✔ ✖ ✖✖✖

Not suitable : dextropropoxyphene “Doloxene; Di-Gesic” morphine, pethidine

Additives : metoclopramide (nausea) caffeine

Effective Abortive AgentsEffective Abortive Agents TriptansTriptans DihydroergotamineDihydroergotamine NSAIDsNSAIDs Anti-emeticsAnti-emetics Lidocaine?Lidocaine? Opioids?Opioids?

TriptansTriptans 5-HT5-HT1B 1B action: vasoconstriction by action: vasoconstriction by

acting against NOacting against NO 5-HT5-HT1D1D action: inhibit CGRP release action: inhibit CGRP release

Should be very effective, yet only Should be very effective, yet only 70-80% effective, with 50% 70-80% effective, with 50% headache recurrence.headache recurrence.◦Cardiac risk, side effects further limit Cardiac risk, side effects further limit

useuse

TriptansTriptans PO versions require 60-90 PO versions require 60-90

minutes to effectminutes to effect 50% success rate PO vs. 75-80% 50% success rate PO vs. 75-80%

s/cs/c Newer triptans offer no real Newer triptans offer no real

advantage over originaladvantage over original Subset of patients do respond Subset of patients do respond

well to this abortive agent in well to this abortive agent in home settinghome setting

DihydroergotamineDihydroergotamine Same 5-HT action, but slower bindingSame 5-HT action, but slower binding

◦Impact of IM may require 2 hoursImpact of IM may require 2 hours◦Nasal version requires up to 4 hoursNasal version requires up to 4 hours

If given IV may initially increase CGRP If given IV may initially increase CGRP release, producing dramatic headache release, producing dramatic headache increaseincrease

Does not increase N&VDoes not increase N&V Most initial research success probably Most initial research success probably

due to adjunctive anti-emeticsdue to adjunctive anti-emetics

NSAIDsNSAIDs Excellent for mild to moderate Excellent for mild to moderate

migrainesmigraines No effect on neurotransmittersNo effect on neurotransmitters Direct inhibition of most Direct inhibition of most

perivascular inflammationperivascular inflammation Ketorolac at best 50-60% success Ketorolac at best 50-60% success

as abortive for severe migrainesas abortive for severe migraines

Dopamine AntagonistsDopamine Antagonists PhenothiazinesPhenothiazines ButyrophenonesButyrophenones MetoclopramideMetoclopramide

Dopamine AntagonistsDopamine Antagonists High adverse event rateHigh adverse event rate

◦Need to treat prophylactically: Need to treat prophylactically: benztropine, lorazepam, benztropine, lorazepam, diphenhydraminediphenhydramine

Low headache recurrence rateLow headache recurrence rate Only droperidol as effective IM as Only droperidol as effective IM as

IVIV Dysphoria cannot be treated, found Dysphoria cannot be treated, found

to be horrible by some patientsto be horrible by some patients

LidocaineLidocaine Intranasal lidocaine found Intranasal lidocaine found

effective in two studies, but of effective in two studies, but of very short duration, 70% very short duration, 70% headache recurrenceheadache recurrence

Mechanism of action uncertain as Mechanism of action uncertain as blocks Na+ channels not Ca++ blocks Na+ channels not Ca++ onesones

OpioidsOpioids At best 50% effective, high At best 50% effective, high

recurrence raterecurrence rate Often required in combination for Often required in combination for

complex casescomplex cases Biggest effect: allows patient to Biggest effect: allows patient to

enter REM sleep, which shuts enter REM sleep, which shuts down dorsal raphe activitydown dorsal raphe activity

Analgesia-induced rebound Analgesia-induced rebound headachesheadaches Obtain good headache medication Obtain good headache medication

historyhistory May occur with simple analgesics or May occur with simple analgesics or

with opioidswith opioids If cessation of medication may take 3 If cessation of medication may take 3

months to return to baseline headache months to return to baseline headache frequencyfrequency

DHE IV q8h x 2-3 days resolves DHE IV q8h x 2-3 days resolves problemproblem

Preventing Future Preventing Future HeadachesHeadaches Headache diary: identifying Headache diary: identifying

triggerstriggers ProphylaxisProphylaxis

◦DietDiet◦ExerciseExercise◦SleepSleep◦Stress modificationStress modification

Preventing Future Preventing Future HeadachesHeadaches Medications:Medications:

◦Valproate: 45% patients more than Valproate: 45% patients more than placebo with 50% decrease in placebo with 50% decrease in headache rateheadache rate

◦Beta Blockers: 40%Beta Blockers: 40%◦Flunarazine: 42%Flunarazine: 42%◦Pizotifen: 20%Pizotifen: 20%◦Riboflavin: 37%Riboflavin: 37%

Preventative drugsPreventative drugs “mixed bag” of drugs used for other conditions

found to be effective in headache usually by chance usually for high blood pressure, depression,

epilepsy all work in somebody ; none works in everybody generally reduce frequency but do not change

attacks key to success : trial and error : persist need to start at low dose and increase until effective

or not tolerated about 50 % of patients will get 50% or more

reduction in attacks

Main migraine preventersMain migraine preventersEffectiveness

Tolerability / safety

Good Fair Poor

Good propranolol verapamilBotox

Fair amitriptylinetopiramatevalproate

pizotifenibuprofen

Poor methysergide

Tension preventersTension preventersEffectiveness


Good Fair Poor

Good

Fair amitriptyline ibuprofen

Poor

Cluster preventers - balance of Cluster preventers - balance of effectiveness and safety / tolerabilityeffectiveness and safety / tolerability

Effectiveness


Good Fair Poor

Good verapamil

Fair topiramate

Poor methysergidesteroids

lithium

Non drugNon drugHerbalManual therapies

◦physiotherapy – caution◦acupuncture – probable

Electrical occipital nerve stimulation : possiblyClosure of hole in heart - no

Anger

Fear

Anxiety

Depression

PERCEPTION OF PAIN

Noxious Stimuli

PS Y

CH

OL O

GI C

AL

NOCICEPTIVE

A

B

MELIALA 2004

PERILAKU NYERI(PAIN BEHAVIOUR)

PENDERITAAN(SUFFERING)

NYERI(PAIN)

BIOPSIKOSOSIAL(BIOPSYCHOSOCIAL)

NOSISEPSI(NOCICEPTION)

PENGERTIAN MODEL NYERI

BYERS AND BONICA, 2001MODIFIKASI PENULIS

•Terapi kognitif•Restorasi fungsional

•Opioid•Tramadol

•Oxcarbazepine•Gabapentin

•Eperisone HCL•Paracetamol

•OAINS

•Antidepresan•Psikotropika•Relaksasi•Spiritual

•Diklofenak•Etodolac•Dexketoprofen•Celecoxib•Modalitas fisik

ConclusionConclusion Headache & facial pain are

common complaints History most important in making

accurate diagnosis Recognize psychological aspects

of pain Recognize “Red Flag” Do a proper management based

on pathophysiology

The task of a doctor:The task of a doctor:

TO CURE IS SOMETIMES TO TREAT IS OFTEN TO COMFORT IS ALWAYS

A. Pare (1598)

AKU TELAH MEMBERIKAN OBAT YANG AKU KENAL TERHADAP PENYAKIT

YANG AKU PAHAMI KEPADA PASIEN YANG

SEBAGIAN BESAR TIDAK TAHU APA-APA

THANK YOU THANK YOU

09 kuliah nyeri kepala dr rd-1

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