Transcript Headache - Cleveland Clinic

Headache
Rosen’s Chapters 17 and 105
November 9th, 2006
By George Filiadis
Epidemiology
• 85% of the US population
had significant headaches
at least once
• 3-5% of ED visits have as
chief complaint headache
• 50% accounts for tension
headache while only 8%
of headache has a
potentially serious cause
• Only 1% of headache in
ED have life threatening
cause(usually
subarachnoid hemorrhage)
Rapid Assessment and
Stabilization
• Airway, Breathing, Circulation and Mental Status
assessment in all critical patients with headache.
• If there is change in mental status accompanied by
headache, it must be assumed that cerebral
circulation is compromised
• The main principle of cerebral resuscitation
focuses on 7 causes: lack of substrate (glucose,
oxygen), cerebral edema, mass lesion
intracranially, endogenous or exogenous toxins,
metabolic alterations(fever, seizure), ischemia, or
elevated intracranial pressure.
Pivot Findings in history
• Pattern and onset of
pain
• Activity at onset of
pain
• History of head
trauma
• History of HIV or
immunocompromised
state
• Character of the pain
• Location of head pain
• Intensity of pain
• Exacerbating or
alleviating factors
• Associated symptoms
and risk factors
• Prior history of
headache
Differential Diagnosis
• Subarachnoid
hemorrhage
• Shunt Failure
• Migraine
• Tumor/Masses/ Subdural
hematoma
• Carbon Monoxide
Poisoning, Mountain
Sickness
• Temporal Arteritis
• Glaucoma/Sinusitis
• Tension headaches/
Cervical Sprain
• Cluster
• Bacterial Meningitis/
Encephalitis
• Anoxic Headache/
Anemia
• Hypertensive crisis
Migraine Headaches
• Accounts for 1 million
visits a year in the ED
• Onset is usually in second
decade of life
• More prevalent among
women
• Historically thought to be
due to cerebral
vasoconstriction and
subsequent vasodilatation
• New beliefs indicate that
changes in the
serotonergic activity in
midbrain are precursors to
migraines
• Divided in migraine with
and without aura
• Precipitants are nitrates,
sleep deprivation, alcohol,
hormonal changes, stress,
chocolate, caffeine, oral
contraceptives
Migraine Without Aura
(Common Migraine)
• Most common cause of
migraine (80%)
• A.At least five attacks
with the criteria B,C,D,
and E
• B. Attack lasts 4 to 72
hours with or without
treatment
• C. Has two of the
following: unilateral
location, pulsating quality,
and moderate to severe
intensity, aggravated by
activity
• D. During headache
associated with
nausea/vomiting or
photophobia/phonoph
obia
• E. History, physical
and diagnostic tests
that exclude related
organic disease
Migraine with Aura (Classic
Migraine)
• A. At least two attacks that fulfill criterion B
• B.At least three of the four characteristics:
1)one or more reversible aura symptoms
indicating focal cerebral or brainstem dysfunction
2) at least one aura develops gradually over
more than 4 minutes and no single aura lasts
longer than 60 minutes
3)headache begins during aura or follows with
a symptom-free interval of less than 60 minutes
• C. An appropriate history, physical, and diagnostic
tests that exclude related organic disease.
Clinical Features
• Most common aura is visual
a)scintillating scotomas
b)photopsias
c)teichopsias
d)blurred vision
• Less common auras are somatosensory
a)tingling or numbness
b)motor disturbances
c)cognitive disturbances
Clinical Features
• Ophthalmoplegic migraine
is a rare condition
associated with paresis of
ocular nerves that may last
days to weeks
• Hemiplegic migraine is
characterized by episodic
hemiparesis or hemiplegia
as an aura that is slow or
marching in progression
and lasts 30 to 60 minutes
• Basilar artery migraine
arises with an aura
referable to brainstem and
associated with near
blindness, dysarthria,
tinnitus, vertigo, bilateral
paresthesias, or altered
consciousness
• Status migrainosus
persists longer than 72
hours and requires pain
management
Treatment-Abortive
Mild to Moderate Moderate to Severe
Attacks
Attacks
Acetaminophen
Aspirin
Ibuprofen
Naprosyn
Refractory Attack,
Status Migrainosus
Dihydroergotamine(1mg
Dihydroergotamine
IV or IM), may repeat 1 hr Steroids
Sumatriptan,(6 mg SC/
25-100mg PO)
Rizatriptan, Naratriptan,
Zolmitriptan,
Prochlorpethazine
Metaclopromide
Ketorolac, Meperidine
Treatment-Prophylactic
• More than 2-3 episodes a month, prolonged
attacks, severe and debilitating
*b-blockers like propanolol
*calcium channel blockers
*tricyclic antidepressants
*depakote
*monoamine oxidase inhibitors
New thoughts for treatment of
Migraines-Haldol
• Monzilo PH, Nemoto PH.Acute treatment of
migraine in emergency room: comparative study
between dexamethasone and haloperidol. Arq
Neuropsiquitr. 2004 june:62: 513-8
-29 patients who met HIS criteria for
migraine: 14 pt received Haldol 5mg
and 15 pt received decadron 4 mg .
Conclusion. Pt who received haldol reached
50% reduction in pain in 30 min, while
patients who received decadron reached the
same level of anesthesia at 2 hrs.
New thoughts for treatment of
Migraines-Haldol
• Honkaniemi, Jari, Liimatainen Suvi,
Rainesalo(2006) Haloperidol in the Acute
Treatment of Migraine: A Randomized, DoubleBlind, Placebo-Controlled Study. Headache: The
Journal of Head and Face pain. 46 (5), 781-787
-40 patients were enrolled in a double-blind,
placebo-controlled study. 80% of patients who
were fiest treated with haldol showed significant
relief while 79% of the patients treated with
placebo first and subsequently with haldol felt
significant pain relief.
Cluster Headache
• More common in men
• Associated with several episodes over 24
hrs that can last minutes up to 2 hrs
• Clinical features include
-unilateral sharp stabbing pain in eye
-involves the distribution of CN V
-30% of patients have partial Horner’s
-eye is often injected, tearing
Cluster Headache-Treatment
•
•
•
•
High flow oxygen of 7-10 l/min
Sumatriptan, DHE
Prednisone tapering dose
Sphenopalatine nerve anesthesia with
intranasal cocaine or lidocaine-controversial
Tension Headache
•
•
•
•
Most common type of headache
Higher prevalence in middle aged women
Usual frequency is 5 episodes per month
Clinical features include
-tight, band-like discomfort around the head
-intensity of pain is not severe and thus not
debilitating
-headache does not worsen with physical
activity
-coexisting anxiety and depression are
common
Tension headache-Treatment
• Aspirin, acetaminophen, NSAIDs
• Exercise program
• Nonpharmacologic regimen like massage,
mediation, and biofeedback
• Psychotherapy
Brain Tumor
• In elderly, brain tumor is usually metastatic from
lung or breast carcinoma.
• Primary brain tumor are more common in adults
younger than 50 years
• HA is caused either by direct pressure on the brain
or elevated ICP
• Typical presentation is headache that worsens over
over weeks to months
• HA is usually present on awakening initially, then
it becomes continuous.
Brain Tumor
• HA is often worse
with sneezing,
bending, coughing.
• Diagnostic tools
include CT with IV
contrast or MRI(best
test)
Subarachnoid Hemorrhage
(SAH)
• Extravasation of blood in subarachnoid space
activates meningeal nocireceptors causing
occipital pain and meningismus.
• SAH accounts for 10% of all strokes and is most
common cause of death from a stroke.
• Causes are saccular aneurysms (80%), blood
dyscrasias, arteriovenous malformations, mycotic
aneurysms, cavernous angiomas.
• Risk factors include increased age,hypertension,
smoking, excessive alcohol consumption and
sympathomimetic drugs.
Subarachnoid Hemorrhage(SAH)
• There is familial association of cerebral aneurysms
with several diseases
-autosomal dominant polycystic kidney
disease
-coarctation of the aorta
-Marfan’s syndrome
-Ehlers-Danlos Syndrome type IV
• 1 to 4% of all ED patients with headache have
SAH with 50% associated morbidity and mortality
Clinical Features of SAH
• Sudden “thunderclap”
headache
• Can be associated with
exertional activities
• Nausea/vomitng-75%
• Neck stiffness-25%
• Seizures-10%
• Meningismus-50%
• Subhyloid or retinal
hemorrhages
• Oculomotor nerve
pulsy with dilated
pupil
• Restlessness and
altered level of
consciousness
Prognosis
Grade Condition
• It depends on neurological
status at the time of
presentation
• Hunt and Hess scale
• Grades I and II have good
prognosis
• Grades IV and V have
grave prognosis
0
Unruptured Aneurysm
I
No symptoms or minimal
headache
Moderate/Severe HA,
nuchal rigidity, no neuro
deficit other than CN pulsy
Drowsiness, confusion, or
mild focal deficit
II
III
IV
Stupor, severe
hemiparesis
V
Deep coma, decerebrate
Diagnostic Studies
• Emergent CT scan of
head
• CT is greater than
90% sensitive for
acute bleeding-less
than 24 hr
• Sensitivity decreases
to 50% by the end of
the first week
Diagnostic Studies
• When CT is negative a lumbar
puncture should be performed
• The CSF should be spun and
the supernatant fluid should be
observed for xanthochromia
(develops after 12 hrs)
•
CSF xanthochromia with
negative CT is diagnostic
• Xanthochromia by
spectophotometry is more
sensitive
Diagnostic Studies
• Patients with persistent bloody CSF without
xanthochromia should go vascular imaging
• Up to 90% of patients with SAH have
cardiac arrhythmias or EKG findings
suggestive of ischemia
• Typical EKG changes include ST-T wave
changes, U waves, and QT prolongation
Treatment
• Airway, breathing, circulation and
neurosurgical consultation.
• Patients with Grade III SAH usually require
endotracheal intubation
• Nimodipine 60 mg PO or NG to lessen the
chance of ischemic stroke due to vasospasm
• Anticonvulsants for patients with evident
seizure
Giant Cell Arteritis
• Systemic inflammatory
process of small and
medium size arteries.
• Mean age of onset is 71
years, rare before 50
• Headache is intermittent,
worse at night or on
exposure to cold
• Associated symptoms
include jaw claudication,
fever, anorexia, pain and
stiffness in joints aka
polymyalgia rheumatica
• On exam there is
tenderness of temporal
artery.
• It’s a medical emergency
because long term
sequelae is permanent
visual loss.
• Diagnostic tests include
ESR, CRP, LFTs, platelet
count
• Definite diagnosis is by
temporal artery biopsy
• Treatment is prednisone
60-120mg daily.
Carotid and Vertebral Artery
Dissection
• Most common cause of stroke in persons younger
than 45 years.
• Associated with sudden neck movement or trauma
following neck torsion, chiropractic manipulation,
coughing, minor falls, MVA.
• The pathologic lesion is an intramural hemorrhage
in the media of the arterial wall that can be subtle
in the early phase leading to thrombus formation
over time with emboli or significant enough to
occlude the vessel.
• Patients can present with stroke symptoms days to
years after dissection.
Carotid artery Dissection
• Classic triad includes
unilateral headache,
ipsilateral partial Horner’s
syndrome, and
contralateral hemispheric
findings like aphasia,
neglect, visual disturbance
or hemiparesis.
• Older age, occlusive
disease, stroke on initial
presentation has worse
prognosis
• Diagnosis is via CT angio,
MRI/MRA
Vertebral Artery Dissection
• Unilateral posterior
headache, and
neurological findings like
vertigo, ataxia, diplopia,
hemiparesis, and unilateral
facial weakness, tinnitus
• Diagnosis is same as in
carotid dissection
• Treatment includes early
anticoagulation followed
by antiplatelet therapy
Idiopathic Intracranial
Hypertension
• Also known as
Pseudotumor Cerebri.
• Commonly seen in young
obese women o
• Predisposing factors
include anabolic steroids,
oral contraceptives,
tetracyclines, Vitamin A
• Caused by increased brain
water content and
decreased CSF ouflow.
• Most common symptom is
generalized headache.
• Eye movement, bending
forward or Valsava may
worsen headache
• On exam patients have
papilledema and visual
defects, including an
enlarged blind spot
followed by loss of
peripheral lesion.
Idiopathic Intracranial
Hypertension(IIP)
• Treatment
-stop offending med
-lower CSF
production with
acetazolomide and
furosemide.
-steroids
-repeat LPs
-ventricular shunt if
with impending
visual loss.
Diagnostic Criteria for IIP
Increased intracranial
pressure(>200mmHg) measured by
lumbar puncture
Signs and symptoms of increased
ICP, without localizing signs
No mass lesions or hydrocephalus
on imaging
Normal or low CSF protein
No clinical or neuroimaging
suspicion of venous sinus thrombosis
Posttraumatic Headache(PTHA)
• Estimated that 30-50% of
2 million closed head
injuries per year develop
headache.
• Associated with dizziness,
fatigue, insomnia,
irritability, memory loss,
and difficulty with
concentration.
• Acute PTHA develops
hours to days after injury
and may last up to 8
weeks.
• Chronic PTHA may last
from several months to
years.
• Patients have normal
neurological examination
and imaging
• Treatment for acute PTHA
is symptomatic while for
chronic PTHA, adjunct
therapies include betablockers and
antidepressants.
Acute Glaucoma
• Sudden onset of eye
pain radiating to head,
ear, teeth, and sinuses.
• Visual symptoms
include blurriness,
halos around lights,
and scotomas.
• Nausea and Vomiting
• Due to congenital
narrowing of the
anterior chamber angle
that leads to elevated
intraocular pressure
(IOP)
• Medications that
elevate IOP include
mydriatics,
sympathomimetics
Acute Glaucoma
• Physical exam shows a red
eye with a fixed
middilated pupil and
shallow anterior chamber
(separates it from cluster
HA)
• IOP in the range of 60 to
90 mmHg ( not found in
iritis)
• Treatment includes topical
miotics, b-blockers,
carbonic anhydrase
inhibitors, optho consult
Postdural Puncture Headache
• Most common
complication following
lumbar puncture (up to
40%)
• Most common in 18 to 30
year old patients
• It can last up to 5 days
• Bilateral throbbing HA
that worsens with upright
position
• Thought to be due to
persistent leak of CSF
that exceeds its
production
• Treatment includes
rest, fluids, and blood
patch, caffeine or
theophylline for
persistent HA
Intracranial Infection
Meningitis
Severe HA, nuchal
rigidity,
• HA is common
meningismus
complaint in meningitis,
Encephalitis HA, confusion,
brain abscess,
fever, change of
encephalitis or AIDS
mental status,
• Diagnostic tools include
seizures
CT of head and LP
Brain
HA, vomiting, focal
Abscess
neurological signs,
depressed level of
consciousness
AIDS
Toxoplasmosis,
CMV, Cryptococcus
Hypertensive Headache
• Elevated blood pressure is
not as important in HA as
the rate by which the
blood pressure increases
• Nonetheless, HA with
severe HTN is well
documented especially in
hypertensive
encephalopathy
• Treatment is directed at
lowering blood pressure
slowly
• HA may last for days until
brain edema has resolved
Medication-Induced Headache
• Medication use, abuse or
withdrawal s the cause.
• Common in patients with
chronic headache
disorders like migraine or
tension-type.
• Most common meds
include ASA, NSAIDs,
Tylenol, barbiturateanalgesic combinations,
caffeine, and ergotamine
• Patients build
tolerance to the meds
and subsequently
require higher doses
for symptomatic relief.
• Treatment includes
withdrawal of the
overused medications
Carbon Monoxide Poisoning
• Usually gradual, subtle, dull, nonfocal throbbing
pain associated with nausea, chest pain.
• Symptoms may wax and wane as patients may
enter and leave the area of carbon monoxide
• Exposure to engine exhaust, old or defective
heating systems, most common in winter months.
• Non focal neurological exams.
• Diagnosis is made by elevated
carboxyhemoglobin
• Treatment is oxygen
High Altitude Headache
• Main symptom of Acute Mountain Sickness
• Can occur at altitudes higher than 5000 feet
in unacclimatized individuals.
• HA is throbbing, located in temporal or
occipital area and worsens at night or early
in the morning.
• Treatment includes supplemental oxygen
and descent to a lower altitude.
Key Concepts
• HA is a challenging yet common complaint in ED
• Diseases that we cannot afford to miss are SAH,
CO poisoning, temporal arteritis, bacterial
meningitis/encephalitis
• Be liberal with use of CT
• Remember CT doesn’t rule out SAH-need LP.
• If CT and LP are negative think of temporal
arteritis if older than 50 years, and CO poisoning.
• Don’t forget the eyes!