lecture_headache

8/7/2019 lecture_headache

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ea ac e

Jennifer McCombe

-September 15, 2006


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Overview

Basics of headache S ecific headache

Epidemiology Anatomy

disorders Thunderclap headache

Diagnostic work-up

thrombosis

Cervical artery dissection gra ne

Trigeminal neuralgia

Post LP headache

Idiopathic intracranialhypertension

Chronic dail headache


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Epidemiology

Headache is the resentin s m tom in 1-2.5% of

emergency visits Patients present to the emergency with 2 types of

1. First or worst syndrome

2. Last straw syndrome

medical specialties

Most headaches dont re resent a serious medical

condition However, has one of the longest lists of differential


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Anatomy

Pain sensitive structures include:

Skin and its blood supply Muscles of the head and neck

Portions of the meninges including the dura mater at the

base of the skull ura ar er es

Intracerebral arteries

Cervical nerves

Select cranial nerves

Pain sensitive structures are affected by tension,, , ,


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Evaluation

based on the International Headache Societyclassification s stem u dated in 2003

Headache divided into two main types: Primary

and secondary

The most important diagnostic tool is a

detailed history

Diagnostic tests only help to establish or

exclude causes of secondar headache


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Evaluation

Histor : Past headache histor

Onset Duration

(including meds tried) Past medical history

Course

Character

e ca ons

Family history Severity

Location

Associated s m toms

alcohol and drugs,sleep, eating and

Precipitants or triggers

Prodromes

exerc se a s, owheadache affectsfunction)


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Evaluation

diary documenting headaches, possibletri ers and treatment tried is often ver

helpful in clarifying details of the history


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Evaluation

KEY POINTS: Vitals

Fundoscopy

Palpation of areas of head and neck Auscultation of eyes, neck

Nuchal rigidity and meningeal signs


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Further evaluation of headache


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Further evaluation of headache


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When to consider neuroimaging Temporal profile and headache features:

1. e rs or wors ea ac e un erc ap ea ac e

2. Subacute headache with increasing frequency or severity3. Progressive or new daily persistent headache

4. Chronic daily headache

5. Side-locked

6. Headache not responding to treatment

Demo ra hics:1. New headache in patient with cancer or HIV

2. New headache age > 50

3. Headache and seizures

Associated symptoms and signs:1. Fever, stiff neck, nausea and vomiting

2. Focal neurological symptoms or signs

3. Papilledema, cognitive impairment or personality change


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Overview

Basics of headache S ecific headache

Epidemiology Anatomy disorders Thunderclap headache

Diagnostic work-up

thrombosis

Cervical artery dissection gra ne

Trigeminal neuralgia

Post LP headache

Idiopathic intracranialhypertension

Chronic dail headache


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Thunderclap headache

onset

associated with subarachnoid hemorrhage

If the work-up for SAH is negative, however,

etiology


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Causes of thunderclap headache


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Subarachnoid hemorrhage

thunderclap headache and should be thefocus of the initial investi ations

11-25% of patients presenting with thunderclap

headache have SAH

Etiology of SAH:

Ruptured aneurysm 85%

Non aneurysmal perimesencephalic bleed 10%

Other causes 5%


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minutes

days

-

isolated headache

-have a history of a sentinel headache days to


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Sensitivity with new scanners nears 100% withinthe first 12 hours

This is provided that the images are interpreted by an

experienced neuroradiologist (or Dr. Mike Saka) ens v y a s o y wee

Therefore, in cases where clinical suspicion

s g , nee an o ru e ou LP needs to be analyzed for xanthochromia


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Cerebral venous sinus thrombosis

onset exacerbated by increases inintracranial ressure that occur with

coughing, sneezing, and valsalva

-

Up to 10% of patients can present with a


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Cerebral venous sinus thrombosis

CT head:

Normal exam: CT normal 25% of the time Abnormal exam: CT normal 10% of the time

LP can have subtle abnormalities (RBC, protein,

mild lymphocytic pleocytosis, opening pressure) ere ore, one nee s a g n ex o susp c on

especially in women who are pregnant or post-

artum in atients with a histor of DVT

Requires an MRI with MRV to establish or exclude

the diagnosis


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Cervical artery dissection

Most commonl associated with a headache of

subacute onset 20% of patients present with a thunderclap

Headache reported by 60-95% of patients with

carotid arter dissection and 70% of atients withvertebral artery dissection

Headache generally ipsilateral to the dissection and

, , , ,temporal regions; with neck pain in 25-50% ofpatients


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Cervical artery dissection

neurological symptoms is 4 days with carotiddissection and 14.5 hours with vertebral

artery dissection

with a history of TIA or stroke and a history of

trauma or chiro ractic mani ulation


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Migraine

predisposition to headaches, GI dysfunction,and neurolo ical d sfunction

Inherited in an autosomal dominant fashion

encountered; triggers include hormonal

, , , ,

alcohol, smells, sleep disturbance etc


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Migraine

,

throbbing, worse with activity and associatedwith nausea vomitin hoto hobia and

sonnophobia

that the HIS criteria are too strict


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Migraine

Princi les of Treatment:

Goal is to stop headache and progression of the pain Are treatment options which are migraine specific and

ose w c are non-spec c

Is best to treat early in the course of the headache to

prevent central sensitization and treatment refractory pain

Use different agents for different intensities of pain and limit

abortive therapies to 2 times per week to avoid medication

If requiring more frequent abortive therapies need to

recommend prophylaxis


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Migraine

Treatment of the acute headache NSAIDs

Hydration/ iv fluids Triptans

the coronary arteries therefore contraindicated in those with a historyof CAD

DHE os common s e e ec s nausea ere ore pre rea w an

antiemetic

Neuroleptics (metoclopromide, promethazine, prochlorperazine,chlorpromazine)

Can cause hypotension when given iv therefore give with saline Corticosteroids

Used in status migrainosis


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Trigeminal Neuralgia

The most common cranial neuralgia

More common in women with an average age ofonset at 50 years

Characterized by brief lancinating pain limited to the

distribution of one or more divisions of the trigeminal,

Pain intensity is excruciating, described as sudden,sharp, superficial, stabbing or burning

Paroxysmal and usually lasts a few seconds May occur in volleys with pain free periods lasting

seconds to hours


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Painful e isodes associated with tri er

zones around the mouth and nostril Can be tri ered b wind on the face,

brushing teeth, shaving, chewing or even

talking Majority of cases are idiopathic

Suspicion of a secondary cause should arise

w en a c ron c con nuous pa n s punc ua eby paroxysms of pain or when the is signs of


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Diagnosis in younger patients should prompt

MS, posterior fossa tumours, or aneurysmal

10% of patients harbour an intracranial lesion

patients


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Treatment:

Spontaneousremissions are

common

After 8 weeks of

,slow drug taper is

recommended


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Approximately 30% of patients will fail medicalthera and ma re uire sur ical or ablative

procedures

Microvascular decompression is considered to bethe definitive process for idiopathic trigeminal

neuralgia


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Post LP headache

Defined as a bilateral headache that

develops within 7 days after LP anddisappears within 14 days after LP

Headache worsens within 15 minutes of

assuming the upright position and disappearsor mproves w n m nu es o resum ngthe recumbent position

areas, and may also involve the neck andu er shoulders


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Post LP headache

,

vomiting, visual disturbances, and hearingalteration

Visual symptoms most commonly due to 6th

10% of patients with LP have some alteration

,

range


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Post LP headache

The fre uenc of headache is inversel related to

age The greatest influence on the incidence is technique

and choice of needle

Ensuring the direction of the bevel is parallel to the

headache

Smaller needles also have a lower incidence of headache

Many recommend bedrest following dural puncturehowever, studies do not support this


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Post LP headache

Treatment:

Conservative measures: Bedrest

Analgesia

Hydration

Caffeine Sumatriptan

Autologous epidural blood patch

g success ra e, ow comp ca on ra e Performing the blood patch too early increases the risk

of failure; optimal time is 24 hours post LP


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Idiopathic Intracranial Hypertension

Condition of increased intracranial ressure without

clinical, laboratory, or radiological evidence ofintracranial pathology

Typical patient is an obese, but otherwise healthy

woman of childbearing age with symptoms of

Seen in all ages with an incidence of 21:100000

- , .

Is a diagnosis of exclusion


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Etiolo and atho enesis are unknown

Symptoms include headache, pulsatile tinnitus,transitory visual obscurations, nausea, blurred vision

and diplopia

Headache is episodic in onset and usually developsover wee s o a y pa n o mo era e n ens y,

worse in the morning and during physical activity,

with valsalva maneuvres and with ostural chan es

Quality and location of the headache are non-

specific


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E isodes of visual obscurations can be monocularor binocular and usually last less than a minute

Episodes are provoked by postural changes and the

No way to predict those at risk of developing

ermanent visual deficits Transient sixth nerve palsy is the most common

cause of episodes of diplopia

er, ess common symp oms exper ence nc u etransient sensory symptoms, decreasedconcentration and memory difficulties


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On examination, one usually sees bilateralpapilledema (blurring of the disc border, absent

venous pulsations, distended retinal veins, and laterprotrusion of the optic disc, peripapillary

emorr ages an exu a es

The risk of permanent deficit increases with the

duration of edema Transient visual field deficits occur in 96% of

patients; enlargement of the blind spot being themost fre uent

Defect is usually asymptomatic and resolves whenthe edema resolves


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Measurement of CSF ressure necessar for

diagnosis For accurate measurement, needs to be assessed in the

a era ecu us pos on w egs ex en e an as

relaxed as possible

Pressure readings between 200 and 250 mm are a non-diagnostic grey zone

93% of patients have an elevated, steady state,

pressure monitoring to catch transient pathological

elevations in ressure


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CSF analysis within normal limits by definition

be carried out before the diagnosis of

given


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Treatment

Symptomatic: focused on lowering ICP and preventingpermanent visual deficits and headache

nc u es:

1. Weight loss

2. Acetazolamide (carbonic anhydrase inhibitor)3. Furosemide

4. Topiramate

.

6. Surgical options: shunting and optic nerve sheet fenestration

7. Controversial: repeated lumbar punctures


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Pro nosis: Spontaneous recovery is common

Cessation of symptoms in 70-85% of patients within 2-3

Up to 25% have a more protracted course

Recurrence not unusual (10-40%)

ery s g permanen v sua e e c s common normaformal testing in only 43% of patients) but largelyasymptomatic

o pa en s exper ence severe permanen v sua edeficits

Up to 5% develop blindness in one or both eyes


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h d l h d h


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Chronic daily headache

Refers to the resence of headache for more than

15 days per month for longer than 3 months

Is a category that contains many disorders

representing primary and secondary headaches

70-80% of patients presenting to headache clinics

ave a y or near- a y ea ac es

Transformed migraine and medication-overuse

Ch i d il h d h


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Risk factors include obesit a histor of fre uentheadache (more than 1 per week), caffeine

consumption, and overuse (more than 10 days per,

analgesics, ergots, and triptans

Greater than 50% of patients have sleepdisturbances and mood disorders

Most patients with transformed migraine are women,,

transformation in which the headaches becamemore frequent until the current pattern developed

Ch i d il h d h


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Reasons to ima e:

1. Development of progressively frequent and severe

headache within a period of 3 months

2. euro og c symp oms

3. Focal or lateralizing neurologic signs

4. Pa illedema5. Headaches aggravated or relieved by assuming an

upright or supine posture

6. ea ac es provo e y a sa va

7. Systemic symptoms or fever

8. Histor of new headache after the a e of fift

Ch i d il h d h


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In medication overuse headaches there are var inintervals from the time of frequent intake of

medications to the development of chronic daily

Triptans: 1.7 years

Ergots: 2.7 years

Simple analgesics: 4.8 years

Accurate diagnosis and treatment requires thewithdrawal of these medications if an e isodic

pattern of headache recurs within 2 months ofwithdrawal, medication-overuse headache is

Ch i d il h d h


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Treatment strate ies:

Lifestyle modification: Limiting caffeine consumption

Regular exercise

Regular mealtimes

Re ular slee schedule Preventative medications:

Tricyclic antidepressants, low dose

a apen n

Topiramate, low dose

Botulinum toxin type A

Ch i d il h d h


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medications, there are a few strategies tolimit withdrawal s m toms

Use NSAIDS and DHE to treat breakthrough

headaches as these are considered at lower riskof medication overuse headache

Prednisone 100 mg daily for 5 days may reduce

e num er o ours o severe w rawa

headache (Pageler et al., 2004)

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