TROUBLES IN THE HEAD
| STOP THE SPINNING —Gregory L. Henry, MD, Clinical Professor, Department of Emergency Medicine,
University of Michigan Medical School, Ann Arbor
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 | Dizziness: global term, not medical term; ask patient what he or she means by “dizzy”
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| Vertigo: sensation of motion or spinning; makes no difference whether patient feels like he or she is spinning
or feels that room spinning; physician should not suggest feeling of motion or spinning to patient
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| Presyncope: patient feels he or she is about to faint; completely different differential diagnosis from vertigo,
same differential diagnosis as syncope
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| Multisensory deficit syndrome: particularly in elderly; vision, sensory receptors, auditory canals all integrated
in cerebellum; as day wanes and light decreases, patients’ performance gets worse (sundowning effect); need
bright enough light that visual inputs can overcome deficit in limb input (have them increase light bulb wattage
in their homes)
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| Nonspecific light-headedness: these patients dizzy; have no understandable positive sign; usually suffering
from depression; if symptoms do not correlate with above categories, chances of solving case in emergency
department (ED) near zero (but likelihood patients have problem that will kill them between now and when
they see their own doctor also near zero); mild-to-moderate depression most underdiagnosed condition; experienced
as generalized unwellness and light-headedness
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| History: time of onset key; immediate or delayed? related to motion? present while lying perfectly still? worse
during certain activities? other symptoms?
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| Mild-to-moderate depression: underdiagnosed; “never has a society had more and enjoyed it less,” which
translates into not feeling well and light-headedness
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| Vertigo: movement and rate of onset key (“and it doesn’t matter what moves”; all related to vestibular axis); the
worse the vertigo, the more likely it is benign; the more it is related to slight delay when patient moves, followed
by fatigue, the more likely not so bad; bad prognostic signs include continuous symptoms, no positional
relatedness, or relation to another cranial nerve
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| End-organ vertigo: source outside brain; usually motion dependent
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| Central vertigo: involves brain; immediate sudden onset of whirling vertigo and dysarthria indicates central
disease like stroke; not motion dependent
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| History: most common cause of vertigo related to medication or alcohol; how did it start? how long did it last?
what was its intensity? associated symptoms of nausea and vomiting do not differentiate any other diseases;
intensity of nausea and vomiting worse with relatively benign causes; with hearing change, abnormal
sounds, and voices sounding far away, followed by becoming unsteady, diagnosis almost always end-organ
condition like Meniere’s disease; hearing loss has slightly different differential diagnosis
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| Physical examination: vital signs and orthostatic blood pressure (BP); ask whether patient taking BP medication;
do not normalize BP in acute fashion, do it gradually; “never ask a question you don’t want to know
the answer to”; vital signs should be related to disease process; pulse rate helpful (measure in seated and
standing positions)
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| Neurologic examination: emphasize cranial nerve VIII; check for spontaneous nystagmus; lateral nystagmus
almost always driven by peripheral systems; anything other than lateral nystagmus driven centrally; both
eyes should cross midline; test for hearing loss in ED using speech discrimination, ie, light, might, kite,
right (if patient cannot discriminate between words, likely trouble along nerve itself, eg, acoustic neuroma)
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| Laboratory studies: mostly useless; tests that may be useful cannot be performed in ED (eg, audiometry, electronystagmography,
magnetic resonance imaging [MRI]); nystagmus—brainstem deviation with cortical
correction; cold water in right ear, causes deviation of eyes toward right by brainstem, followed by correction
by cortex; comatose patients cannot have nystagmus; MRI—almost no reason for stat MRI but may
want to inform neurologist and have MRI scheduled
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Diseases Causing Vertigo
| Medications: number one cause of vertigo in United States
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| Cochlear diseases: labyrinthitis—patients generally middle-aged or younger, have rapid onset, hearing loss,
and positional vertigo; vestibular neuronitis—same symptoms as labyrinthitis but no hearing loss; benign paroxysmal
positional vertigo—patient feels awful if moved quickly, but feeling lasts only 30 to 60 sec; meclizine
(Antivert) works, but symptoms recur; patient should be worked up by primary care physician or neurologist;
Meniere’s disease—patients usually middle-aged, have ringing in ears, recruitment problems, sounds in head
that go from very soft to very loud, and peripheral vertigo (most of these patients can be treated medically);
traumatic vestibular syndrome—rare; patients have had significant blows to head and develop vertigo over
next week; if trauma-related, refer to neurosurgery; (patient may develop cerebrospinal fluid [CSF] leak, infection,
meningitis); syphilis—cochlear disease may occur in tertiary syphilis
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| Retrocochlear disease: acoustic schwannoma—patients have intermittent vertigo; can hear words, but sound so
badly distorted they cannot differentiate speech; have pure-tone decay on hearing test (pathognomonic and diagnostic);
meningioma—almost always have mass effect and papilledema by time vertigo manifests; trauma—
rare and must be major
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| Central nervous system (CNS) disease: vascular—eg, basilar artery disease; bigger group than previously
imagined; in study, 25% of elderly who presented with vertigo had central vertigo; demyelinating disease—
patient with nonlateral nystagmus and internuclear ophthalmoplegia (caused by lesion in median longitudinal
fasciculus) has multiple sclerosis until proven otherwise, and MRI indicated; drugs—anticonvulsants, alcohols,
hypnotics
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| If uncertain, do nothing: meclizine—does not fix everything; only treats irritation coming from end-organ
vertigo; makes every other form of dizziness worse; also makes syncope and near-syncope worse; helpful in
patients with end-organ vertigo related to semicircular canals
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| Retrocochlear or CNS disease: nothing works well, except fixing problem; start aspirin if transient ischemic attack
(TIA) suspected; patient needs further testing but not necessarily immediately; check heart rate and
rhythm (looking for atrial fibrillation); check patient’s medications; no advantage to placing patient on coumadin;
check for neck lesion; do not admit elderly patient suspected of having posterior fossa TIA; symptoms
will probably recur
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| Cochlear problems: use antihistamines, meclizine, phenothiazines, or belladonna alkaloids, eg, atropine
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| THUNDERCLAP HEADACHE — David W. Dodick, MD, Professor of Neurology, Mayo Clinic College of
Medicine, Scottsdale, Arizona
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| Key points: how headache began—10% of patients who present with thunderclap headache and normal examination
have serious underlying cause; most patients do not tell physician how headache began because they
are overwhelmed by pain, vomiting, and prostration; physician must elicit that information by asking, “how
did this headache begin?” or “what were you doing when the headache began?” or “how quickly did the pain
peak, going from no headache to 10 on pain scale?”; if patient says headache peaked within seconds, condition
may be serious; blood vessels—most serious conditions involve blood vessels (pain-sensitive; besides
dura, blood vessels only pain-sensitive structures inside head) all patients with negative computed tomography
(CT) and negative CSF examination must have MRI of brain and cerebral vasculature
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| Primary thunderclap headache: sudden-onset headache reaching maximum intensity within 1 min; may recur
within first week after onset; patients have normal CSF and brain imaging (do very well); benign causes
outweigh malignant causes by 9 to 1; no clinical or headache features that reliably distinguish between primary
and secondary thunderclap headache (cannot tell by history if patient has something bad or benign); all
patients require diagnostic imaging
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| Subarachnoid hemorrhage: 30,000 cases/yr in United States; results in serious disability or death in 40% to
60%; only 33% have good quality of life 1.5 yr later; if missed, 1 of 8 rebleed within 24 hr, 40% rebleed
within 1 mo; outcome highly dependent on early diagnosis and aggressive intervention; patients who have
normal neurologic examination benefit most from early intervention, but often go undiagnosed; headache
most common presentation of subarachnoid hemorrhage (90%); 1% to 4% of all headache patients coming
into ED have subarachnoid hemorrhage; of patients presenting with “worst headache of life,” only 1 in 10
have subarachnoid hemorrhage (ask about mode of onset); 25% of “worst headache” presentations with abnormal
examination have subarachnoid hemorrhage; sentinel headaches occur in 10% to 40%
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| Diagnostic pitfalls: 10% do not present with headache; headache mild or progresses gradually in ≈18%; headache
may be overshadowed by other presentations (eg, coma or obtundation); failure to perform, interpret,
or understand limitations of CT, eg, of patients who wait 3 days before presenting to ED, 1 in 4 have negative
CT; failure to perform or correctly interpret lumbar puncture (LP); in patients with thunderclap headache
and negative CT, LP must be performed
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| LP: traumatic LPs occur in ≈20% of patients; visual inspection for xanthochromia falsely negative in up to 50%
of specimens; “3-tube test” notoriously unreliable; perform LP if index of suspicion high, no matter when patient
presents; if LP negative and was done within 1 to 2 hr, proceed to imaging if index of suspicion high
(takes up to 6 hr for oxyhemoglobin from lysed erythrocytes to reach lumbar thecal sac); CSF must be centrifuged
immediately upon collection to prevent false-negative results from in vitro lysis of erythrocytes
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| Imaging: CT positive almost 100% of time if done within 24 hr of headache onset; MRI FLAIR (Fluid Attenuated
Inversion Recovery) equally sensitive as CT and more sensitive than CT up to 1 mo after ictus; magnetic
resonance angiography (MRA) and CT angiography detect reasonably sized aneurysm (≥5 mm) 90%
to 100% of time
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| Venous sinus thrombosis: may not be detected on routine MRI; thunderclap headache occurs in ≈10%; CT
normal in 25%; CSF normal in ≈70%; up to 40% may have elevated CSF opening pressure; if suspected, perform
MRI and MR venography (reliable tests for this condition)
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| Arterial dissection: presents with thunderclap headache 13% of time; pain often unilateral or in jaw, face,
around eyes or temple; almost always on same side as dissection; may have Horner’s syndrome (may be subtle
and easily missed); may also present with unilateral headache and delayed focal ischemia (may be 1-3 wk
later); CT and CSF almost always normal, unless patient has had silent stroke; MRI/MRA diagnostic procedure
of choice
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| Summary: of patients presenting with thunderclap headache, 10% have serious cause; ask about mode of onset,
especially for patient in ED and those seeking help for particular headache; know differential diagnosis
and look at arteries and veins; all patients should be aggressively evaluated with CT and LP and if negative,
image brain as soon as possible
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Educational Objectives
| The goal of this program is to educate the listener about dizziness and thunderclap headache. After hearing and
assimilating this program, the clinician will be better able to:
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| 1. Define the various types of vertigo.
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| 2. Describe the differential diagnosis of the “dizzy” patient.
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| 3. Discuss the diseases that cause vertigo and their treatment.
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| 4. List some key points in the evaluation of a patient with the complaint of thunderclap headache.
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| 5. Review the differential diagnosis and evaluation of thunderclap headache.
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Discussed on This Program
Atropine sulfate (many trade names)
Clopidogrel bisulfate [Plavix]
Dipyridamole and aspirin [Aggrenox]
Meclizine [Antivert, others]
Phenytoin sodium [Dilantin]
Warfarin sodium [Coumadin]
For NYACEP’s next Emergency Medicine Scientific Assembly visit: www.nyacep.org
Programs of Related Interest
Falk JL, Cassidy D: Stroke. Audio-Digest Emergency Medicine 20:05(Mar 7), 2003; Rauch SD et al: The
dizzy patient: concepts in care. Audio-Digest Otolaryngology 37:02(Jan 21), 2004; Slattery DE, Ginther B:
Vascular emergencies. Audio-Digest Emergency Medicine 22:08(Apr 21), 2005; Smith WS, Johnston SC:
Problems in the head. Audio-Digest Emergency Medicine 21:04(Feb 21), 2004.
To Order, Contact Subscriber Service (1-800-423-2308)
Suggested Reading
American College of Emergency Physicians: Clinical policy: critical issues in the evaluation and management
of patients presenting to the emergency department with acute headache. Ann Emerg Med 39:108, 2002;
Davenport R: Acute headache in the emergency department. J Neurol Neurosurg Psychiatry 72 Suppl 2:ii33,
2002; Edlow JA: Diagnosis of subarachnoid hemorrhage in the emergency department. Emerg Med Clin North
Am 21:73, 2003; Foot C et al: How valuable is a lumbar puncture in the management of patients with suspected
subarachnoid haemorrhage? Emerg Med (Fremantle) 13:326, 2001; Grotta JC: Cerebral Venous Thrombosis - a
new diagnosis in travel medicine. J Travel Med 3:137, 1996; Kappes JN et al: Headache and visual changes at
triage: do not allow the patient’s assumptions to cloud your critical thinking. J Emerg Nurs 29:584, 2003; Lalive
PH et al: Is measurement of D-dimer useful in the diagnosis of cerebral venous thrombosis? Neurology
61:1057, 2003; Perry JJ et al: Attitudes and judgment of emergency physicians in the management of patients
with acute headache. Acad Emerg Med 12:33, 2005; Peters KS: Secondary headache and head pain emergencies.
Prim Care 31:381, 2004; Schievink WI et al: Spontaneous intracranial hypotension mimicking aneurysmal
subarachnoid hemorrhage. Neurosurgery 48:513, 2001; Schwartz DT: Evidence-based emergency
medicine. Feedback: computed tomography and lumbar puncture for the diagnosis of subarachnoid hemorrhage:
the importance of accurate interpretation. Ann Emerg Med 39:190, 2002.
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant
financial relationship with the manufacturer or provider of any commercial product or service discussed.
For this issue, the faculty reported nothing to disclose.
Dr. Henry was recorded July 7, 2004, in Bolton Landing, New York, at the 2004 Scientific Assembly, sponsored
by the New York chapter of the American College of Emergency Physicians; Dr. Dodick, April 19, 2005, in
Scottsdale, Arizona, at Emergency Medicine 2005: Moving Forward, sponsored by the Mayo Clinic College of
Medicine at Scottsdale. The Audio-Digest Foundation thanks the speakers and the sponsors for their cooperation
in the production of this program.
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