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PHYSICAL EXAMINATION
Vitals: note fever, HTN
Head and Neck
Trauma, battle’s signs, racoon eyes, hemotympanum, rhinorrhea,
otorrhea, look in mouth (dental abscess), sinus tenderness, discharge
from sinuses, ear infection, temporal/scalp tenderness, auscultation for
AVM, nuchal rigidity, Kernig’s sign, Brudinski’s sign, neck trauma
Neurological Exam
Normal in primary headaches but thorough exam for subtle findings is key
Focal deficit or decreased level of consciouness: must think secondary
Don’t forget fundi examination (papilledema, spontaneous venous
pulsations, subhyloid blood, retinal hemorrhages)
INVESTIGATIONS
Depends on presentation and suspect etiologies
Blood work: CBC, renal fn, liver fn, ESR/CRP (giant cell arteritis), coagulation
(hemorrhage, cerebral venous thrombosis, TIA), drug screen if clinically indicated
CT: initial diagnostic test of choice for any RED FLAGS
LP: after negative CT to look for SAH, infection
MRI, MRA, CTA, Angiography may be used by consultants
PATHOPHYSIOLOGY
Vasoconstriction leads to ischemic brain and produces aura features, ischemia produces
vasoactive mediators which lead to vasodilation. vasodilation leads to headache
Inflammation, seritonin, and dopamine thought to have role in pathophysiology
Dura and dural blood vessels are sensitive. Many vasoactive substances
can stimulate the dural blood vessels and produce vasodilation and
perivascular inflamation which activates the perivascular trigeminal
sensory nerves which leads to headache. These trigeminal sensory
nerves provide a pathway for noxious stimuli from meningeal blood
vessels in the periphery to activate the CNS sensory pathways
(TRIGEMINOVASCULAR system)
Seritonin and Migraines
Goasby 2000. Neurology. Mechanisms of action of serotonin agonists:
insights into migraine pathophysiology.
Serotonin agonists act via 3 mechanisms.......(i) Intracranial
vasoconstriction (ii) Peripheral trigeminal nerve inhibition (iii) Inhibition of
central pain processing
Dopamine and Migraines
Peroutka 1997. Neurology. Dopamine and Migraine
Dopamine administration can mimic symptoms of migraine. Hypothesis of
dopamine hypersensitivity in migraine suffers.
Many dopamine antagonists effective for migraine: metoclopramide,
prochlorperazine, chlorpromazine, domperidone, haloperidol
PRESENTATION
Triggers
Sress, stress letdown, hormonal changes, alcohol, smoke, scents, fumes,
exercise, fatigue, lack of sleep, hunger, head trauma, chocolate, red wine,
MSG, menstrual, altitude changes, chinooks (changing barometric
pressure), caffeine withdrawl
Aggravating/Alleviating
Increase w/: coughing, straining, bending over, mvmt, activity
Decrease w/: rest, immobility, quiet, darkness, scalp pressure, cold press
Migraine Variants
Classical Migraine = preceding aura
Common Migraine = no preceding w/o aura
Status migrainus = > 24hrs
Hemiplegic Migraine: mild –> hemiparesis (dx of exclusion)
Basilar Migraine: dysarthria, vertigo, tinnitus, dec LOC
Ice-Pick Headaches: some classify as migraine variant
Thunder - Clap headache: very sudden onset and severe headache that
reaches maximal intensity within minutes (with negative workup for SAH)
Migraine equivalents: vertigo, tacchycardia, chest pain, abdo pain, pelvic
pain due to autonomic stimulation with or without headache
Ophthalmoplegic Migraine
- usually 3rd nerve palsy (must R/O DM, anerysm)
- cannot distinguish b/w aneurysm
- Tolosa - Hunt syndrome: periarteritis of carotid siphon of
unknown etiology that may simulate opthalmoplegic
migraine; presents with unilateral retrorbital pain that may
precede or follow IIIrd nerve palsy
CHLORPROMAZINE (Thorazine)
0.1 mg/kg iv q15 min X 3 prn
50 mg im q15 min X 3 prn
Pretreat with 500ml NS to prevent orthostatic hypotension (alpha effect)
80 - 90% effective
18% get orthostasis
Higher s/e :. not 1st line
Lane 1989: CPZ = demerol + gravol
ERGOTAMINES
Serotonin agonism leads to vasoconstriction
Contraindications: CAD, PVD, HTN (vasoconstriction), pregnant (oxytocic effects), use of
sumitriptin within 24hrs
Various preparations: ergotamine, + caffeine, tablet, suppository, intranasal, inhalor
Ergotamine
1 - 2 mg po, sl q1hr X 3
Success 75%
DiHydroErgotamine (DHE)
0.5 - 1.0 mg iv/sc/im/in, repeat 0.75 mg prn in 30 min
Hanna 1991: 71% complete relief
Carleton 1998: DHE = demerol
SUMITRIPTAN (Imitrex)
6 mg sc, repeat at 1hr minimum prn
50 - 100 mg po
Intranasal preparations available
Seritonin agonist that causes vasoconstriction, reduction of inflammatory mediators;
does not cross BBB thus no CNS effects
Other seritonin agonists: rizatriptan, naratriptan, zolmitriptan
Contraindications: CAD, PVD, HTN, pregnant, ergotamine w/i 24hrs
Gawel 2001: Effectiveness 77% at 1hr, 83% at 2hr, 60% at 24hr
Cady 1998: Effectiveness 69% at 1hr, 79% at 2hr
High rate of rebound headaches (40% at 24hr) and cost make this a 2nd line drug
Effectiveness at 1hr better for sc > po > in
OTHER
Lidocaine
4% topical solution in nostril of side of h/a
55% response in 5 min but 42% relapse rate in 1 hr
JAMA 1995, 1996
NSAIDs
Good evidence from RCTs for effectiveness > placebo
Should add to ED regimen for additive effect
Naprosyn: 250 - 500 mg po q2-6hr
Ibuprofen: 400 - 600 mg po q2-6hr
Toradol: 60 mg im (maximum 120 mg w/i 24hrs)
- Shustha 1996: ketorolac = CPZ
- Duarte 1992: ketorolac = meperidine
- Larkin 1992: ketorolac < demerol
Steroids
Some recommend for recurrent, prolonged headaches > 72hrs
Dexamethasone (10 - 20mg iv), prednisone, methylprednisone
Poor evidence
Opiods
Last resort, potential for abuse, LOWER efficacy documented by many
studies (50%), HIGHER relapse rates (40%), 3rd line
Prevention
Beta - blockers, TCAs, phenytoin, CCBs, ergotamines
DISPOSITION
Admission for pain control or status migrainus rarely required: DHE + maxeran Q8hr +/-
steroids
Consider referral to headache clinic
Chronic headaches requiring prophylaxis
Disabling headaches
TENSION/MUSCLE CONTRACTION
Most common type
Usu bilateral, often described as a tight band, squeezing
Not aggravated by physical activity, no prodrome/aura
May be associated w/ nausea or photophobia
Usu waxes and wanes
May last for several days
Tx: tylenol or NSAIDs
CLUSTER
Much less common
“Ice-Pick Headache”
More common in men (9:1), onset in late 20s
Severe, stabbing, periorbital pain
Associated w/ ipsilateral tearing, nasal congestion, rhinorrhea, conjucntival injection,
ptosis, eyelid swelling, flushing of forehead, can see horner’s
Precipitants: alcohol, heavy smoking, NTG
Onset frequently at night, usu lasts 30min - 3hrs
Each attack is similar, often occurring at the same time of day (“alarm - clock headache”)
Pt prefers to pace and keep acitive during attack
Cluster refers to the seasonal occurrence of episodes
Acute tx: 02 > 7 L/min (90% effective), intranasal DHE, sumitriptan
Prophylaxis: CCBs, valproate, lithium carbonate
EFFORT/COITAL HEADACHE
Presentation worrisome for SAH
More common in men
Dx of exclusion
Effort headache: any valsalva
SECONDARY HEADACHES
MENINGITIS
Headache + fever/meningismus/rash
Headache esp common in bacterial and viral and often is presenting feature
Must R/O meningitis if fever, meningismus, or rash is present
CT b/f LP if possible
BRAIN TUMOR
60% will have headaches, especially if rapid grwoing
Neurological examination usu abnormal
Usu gradual progression over weeks to months
Red Flags for possible brain tumor
Focal neurologic symptoms or findings
Wakes in am with headaches
Headaches recently with no prior hx
Headache that is chronic, persistent over days –> months with no prior hx
Weight loss
VASCULAR ETIOLOGY
Unruptured AVM or aneurysm
Ischemic stroke or TIA: headache in 20% or less
Cervicocephalic Arterial Dissection
Headache, facial pain, neck pain
May or may not be associated w/ trauma
Carotid: ipsilateral, steady, nonthrobbing headache and ipsilateral
horner’s; throat pain, focal cerebral ischemia
Vertebrobasilar: occipital headache or neck pain, may be assoc/ w/
whiplash
Cerebral Venous Thrombosis
Blood drains from brain veins into venous sinuses (superior saggital sinus,
inferior saggital sinus, transverse sinus, straight sinus, cavernous sinus —
> confluence of sinuses and drainage into jugular system)
Thrombosis: underlying hypercoagulable states, meningitis, abcess, etc
Presents with headaches and neurological symptoms (may be
asymptomatic)
Dx: CT with enhancement (delta sign for SSS thrombosis)
Cavernous Sinus Thrombosis
- venous sinus lateral to sella turcica that drains blood from
face, pterygoid, eyes
- infectious spread from eyes, nose, face, palate, tonsils,
middle ear, mastoid, sinuses, teeth ------> thrombosis
- headache, proptosis, fever, eye swelling, edema
- CN palsies: CN III, IV, V1, V2, VI and ICA
- Dx: evidence on CT
- Mx: heparin, abx
GIANT CELL ARTERITIS
Over 50 yo and average is 70: 4 females to 1 male
Headache + visual loss, jaw claudication, tenderness of scalp over temporal arteries
Pain is piercing or buring quality, usually unilateral
Note: pain can be located more in jaw than temporal skull region
Fundoscopy: can see edema or papillitis but usually are normal
Association with PolyMyalgia Rheumatica (50%)
ESR elevated, mild anemia, mild leukocytosis
Risks: blindness, CB infarct, basilar artery infarct
Tx: prednisone 60 - 100 mg po od
Treat with steroids even b/f lab results if you suspect this dx
Bx usu diagnostic
TRIGEMINAL NEURALGIA
Tic Douloreux = sudden wincing of facial muscles in response to severe facial pain
Facial pain that occurs suddenly, lasts seconds to minutes, lancating/electrical quality,
progression to constant ache, UNILATERAL 95%
V2 and V3 more common distribution than V1
May have “trigger spot” on face, may be precipitated by talking, chewing, facial
movement, or tapping on the trigger zone to reproduce symptoms
2 females: 1 male, most > 50yo
Theories: HSV irritation of CNV, dental disease, anatomic nerve lesion, vascular
compression by adjacent vessels, MS, cerebellopontine angle mass
Diagnosis: history with NORMAL physical examination (CNV: normal sensation to face,
muscles of mastication normal, normal corneal reflex)
Ddx: glossopharyngeal neuralgia, post - herpetic neuralgia, TMJ pain, dental dz,
sinusitis, trauma, cluster h/a, GCA
CT/MRI: normal, should be done to r/o posterior fossa tumor
Management
Tegretol: 100 - 200 mg/day and titrate up (some start at 200 mg po tid)
Alternative: dilantin
Failure of medical Rx: injections, peripheral neurectomy, radiation, or
surgical decompression
GLAUCOMA
Acute onset of orbital pain
Visual changes: decreased acuity, haziness, or visual loss
Conjunctival injection
Pupil mid position, corneal edematous or slightly hazy
Dx: tonometry
Tx
Acetazolamide
Miotics
Mannitol
Betablockers
Corticosteroids
Antiemetics
VP SHUNT COMPLICATIONS
Obstruction or infection
CT to look for hydrocephalus
Aspiration of CSF to look for infection
Consult neurosurgery if problem suspected
SUBARACHNOID HEMORRHAGE
AND INTRACRANIAL ANEURYSMS
EPIDEMIOLOGY
Incidence: 20 per 100,000/yr (5th - 7th decade); Prevalence: 1% of population
Morgenstern 1998: prospective study of 38,730 consecutive ED patients, headache was
cc in 450, worst h/a of life in 170 (37%), SAH was ultimate dx of 4% of
“severe”headaches and 17% of “worst ever” headaches
SAH is a relatively common entity with serious consequences
Headache is 1 - 2% of ED visits, SAH is 1% of all headaches, SAH is 10% of “worst
ever”h/a
MC age is between 20 - 60yr old; Peak rupture rate is in 50s; Pediatrics RARE but does
occur
SAH is 5 - 10% of strokes
Increased risk with Ehlers-Danlos, Marfan’s, coarctation, Polycystic kidney disease
HTN is NOT a major factor in formation but is a major factor in rupture
Prognosis BEFORE rupture: rupture 1% per year, surgery risk low :. most electively
clipped
Rupture
Peaks of BP very important THUS association with lifting, bending,
valsalva, coitus, orgasm, coughing, urination, parturition
Smoking, EtOH, cocaine, phencyclidine, other stimulants, poorly
controlled HTN, chronic ASA also increases risk of rupture
Note: 1/3 occur in sleep or not related to activity
ALERT(I/II) 74 8 4 1 13
DROUSY (III) 53 11 6 2 28
STUPOR (IV) 30 14 8 4 44
MISDIAGNOSIS OF SAH
Misdiagnosis is common and important b/c of high rates of death and disability
Especially common in patient with NORMAL level of consciousness and physical exam
Retrospective reviews of initial misdiagnosis: Niel - Dwyer 1997 (51%), Mayer 1996
(25%), Kassel 1985 (23%), Adams 1980 (32%) —> Overall initial misdiagnosis in 32%
Reasons for misdiagnosis of SAH
Failure to appreciate spectrum of SAH
- failure to evaluate “warning headaches” w/ CT and LP
- failure to recognize that h/a can improve spontaneously
- failure to recognize mild or atypical presentations
- focus on secondary injury resulting from syncope
- focus on ECG abnormality (misdx as MI)
- focus on BP (misdx as HTN headache)
Failure to appreciate the limitations of CT
- decreasing sensitivity with time
- accuracy depend on reader (neurorad > rad > emerg > res)
- sensitivity depends on volume of bleed
- sensitivity depends on technical factors (3rd / 4th generation
scanner, thin slices at base of brain)
- false -ve with Hct < 30
Failure to perform and interpret LP correctly
- LP not done if CT -ve
- xanthochromia insensitive < 12hr and > 2weeks
- visual inspection for xanthochromia unreliable
- failure to distinguish b/w traumatic tap and true SAH
ETIOLOGY OF ANEURYSMS
Congenital
Familial intracranial aneurysms (dominant)
Genetic predisposing condition (Marfan’s, Ehler’s - Danlos, etc)
Acquired
Traumatic: skull#, penetration, post op, hemodynamic damage
Infectious: syphillus, mycotic
Inflammatory: vasculitis
Degenerative: atherosclerotic
LOCATION/SIZE
95% are associated with the Circle of Willis
Locations usually distal to carina of bifurcation of vessels and point in the direction of
flow usually on the convexity of the curve
Rupture rates increase after 3mm, symptoms increase after 7mm
Multiple aneurysms in 15%
PERIMESENCEPHALIC SAH
5 - 10% of SAH
Not caused by aneurym: represents 50% of non-aneurysmal SAH
Typical presentation for SAH except slightly slower onset (minutes vs seconds) and
tends to have lower Hunt - Hess score (higher LOC and less neuro findings)
Extravasated blood mainly or only in interpeduncular cistern or quadrigeminal cistern
Thought to be a VENOUS or CAPILLARY source
CT or LP +ve but angiogram is negative
Excellent prognosis
PRESENTATION
Subarachnoid hemorrhage has a wide spectrum of presentation from mild h/a –> coma
History
SUDDEN onset of SEVERE headache (“worst H/A of my life”)
Associated w/ nausea, vomiting, menigismus, mild fever, photophobia,
decreased LOC -----> syncope
Onset with activity is common (2/3): sex, straining, lifting, bending,
valsalva
Physical
Labile BP (hypertension common), decreased LOC, subhyloid
hemorrhage, retinal hemorrhages, cranial nerve palsies, neurologic
findings (may be focal, hemparesis)
Findings may localize hemorrhage: IIIrd nerve palsy (PCA or Pcom), VI
nerve palsy (posterior fossa), bilateral leg weakness (Acom), nystagmus
or ataxia (post fossa), hemiparesis/aphasia/neglect (MCA)
Ocular hemorrhage
- subhyaloid (preretinal): bright red blood near optic disc that
obscures underlying retinal vessels
- intraretinal hemorrhage
- vitreous humor hemorrhage (Terson’s syndrome)
Warning signs
Unusual headache; sudden onset, severe but less often related to activity,
more relief with NSAIDS, more generalized
Consider on ddx of “Thunderclap headache” (sudden onset of severe
headache with -ve work up for subarachnoid hemorrhage)
Warning signs and symptoms occur in 20 - 60% which can be the result of
stretching, pressure, or leakage; ave interval b/w warning and bleed is 3
weeks
Note: sensitivity of CT is decreased with small bleeds (50%)
Sahs A. (Cooperative study)
headache 48% - motor/sensory change 6%
dizziness 10% - seizures 4%
orbital pain 7% - ptosis 3%
diplopia 4% - dysphagia 2%
Sarner M. (1967)
Meningism 64%
Coma 52%
N/V 45%
H/A (gen) 32%
H/A (occipital) 21%
Reflex changes 19%
<10%: motor change, sensory change, papilledema, anisocoria, 3rd nerve
ALERT I/II
DROUSY III
STUPOROUS IV
COMATOSE V
95 - 85 - 75 RULE
Timing Sensitivity
12hrs - 2wks 100%
2 - 3wks 91% (71 - 79)
3 - 4 wks 71% (42 - 92)
Summary on LP
Best to delay LP to 10 - 12hrs after onset of headache: 12 hours is not a
“gold standard”, realize that sensitivity increases with time
Spectophotometry dx of xanthochromia seems to be superior to visual dx
although literature is unclear
Study of LP on CT-ve patients has not been done.
Getting sample analyzed within 1hr is important
Only alternative to keeping patient until 10-12hrs is too find a reliable way
to distinguish between traumatic tap and SAH before xanthochromia
develops
ED MANAGEMENT
ABCD
Airway: intubate for hypoventilation, hypoxia, hypercarbia, loss of airway
reflexes, pulmonary edema, signs of increased intracranial pressure
RSI: lidocaine/fentanyl/thiopentothal/succ
D: elevate head of bed, hyperventilate to PaCO2 of 30 and mannitol 1
gm/kg if signs of increased ICP, phenytoin prophylaxis (20 mg/kg @ 50
mg/min), consult neurosurgery for craniotomy and clipping or angiographic
coiling
Complications
Rebleeding: high morbidity and mortality
Hypertension: increases risk of rebleeding, keep BP < 160 systolic with 10
- 20 mg labetolol prn (alternatives are captopril 12.5 mg po, nitroprusside
0.5 ug/kg/min, esmolol, hydralazine 10 - 20 mg)
Seizures (rare but disasterous): prophylaxis with dilantin controversial
Hydrocephalus due to scarring, may require shunts
Vasospasm: blood in SAS irritates the blood vessels in the SAS causing
vasospasm which can cause infarction, must delay Sx until vasospasm
under control, Rx: CCBs (nimodipine 60mg po q4h), fluids, increase BP
Cardiac: ST changes (may be missdx as AMI), ischemia, prolonged QT,
virtually any brady or tacchyarrythmia; do ECG
DEFINITIVE MANAGEMENT
Angiography +/- coiling
CT angiography and MR angiography yet to be defined