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Systemic symptoms (fever, weight loss) or
Secondary risk factors (HIV, systemic cancer)
Neurologic symptoms or abnormal signs (confusion, impaired alertness, or
consciousness)
Onset: sudden, abrupt, or split-second
Older: new onset and progressive headache, especially in middle-age >50
(giant cell arteritis)
Previous headache history: first headache or different (change in attack
frequency, severity, or clinical features)
Tension
headaches are the most common presenting headache in the ED and other primary
care settings. They probably exist on a continuum with migraines.27
The IHS divides tension headaches into episodic and chronic, depending on the
length of symptoms. The presence or absence of pericranial muscle tenderness is
key in classifying this form of headache.
Tension headaches are typically episodic, with mild to moderate pain intensity lasting minutes to days. The discomfort is frequently described as "constricting" in nature, bilateral in location, and is normally not worsened with exertion. Typical migraine symptoms of nausea, vomiting, and photophobia are normally absent
IHSS Classification
At least two of the following:
Pressing/tightening nonpulsating quality
Mild or moderate intensity
Bilateral location
Not aggravated by physical activity
Both of the following:
No nausea or vomiting
No photophobia or phonophobia or only one is present
At least one of the following:
Not secondary to another disease
Disease is present but TTH not related.
Migraine is an Episodic Headache lasting 4-72 hrs with:
Any 1 of the associated symptoms:
nausea
vomiting
photophobia and phonophobia
and
Any 2 of the pain qualities:
unilateral pain
throbbing pain
pain worsened by movement
moderate or severe pain
IMPORTANTLY, IHS criteria do not exclude symptoms like sinus pain and pressure, congestion, rhinorrhea, and watery eyes to make a diagnosis of migraine. (Headache Classification Committee of the IHS. Cephalalgia 1998, 8 (suppl 7))
*POUNDing: Pulsatile quality; duration 4-72 hOurs; Unilateral
location; Nausea and vomiting; Disabling intensity.
Cluster-type headache, abnormal findings on neurologic examination, undefined
headache (ie, not cluster-, migraine-, or tension-type), headache with aura,
headache aggravated by exertion or valsalva-like maneuver, headache with
vomiting.
(Rational Clin Exam
JAMA. 2006;296:1274-1283.)
Migraines
may occur with or without an aura. They usually last 4-72 hours, start on one
side (but may later spread bilaterally), and are pulsatile or pounding.
Symptoms may be aggravated by exertion. Almost all patients with migraine
will have nausea, photophobia, or phonophobia.
If the patient with a presumed migraine does not complain of light hurting
their eyes, sound hurting their ears, or nausea, consider an alternative
diagnosis.
Migraines
may be triggered by stress, fatigue, concurrent illness, and even certain
foods.
They can cause hemiplegia, use compazine/benadryl/droperidol
Can use chlorpromazine (thorazine) .1 mg/kg IV (J Emerg Med. 2002; 23(2))
Drop 2.5 mg IV worked as well as compazine 10 mg (Journal of Emergency Medicine Volume 26, Issue 2 , February 2004, Pages 145-150)
RCT of drop vs. placebo (Neurology 2003;60:315)
Some evidence that chest pain with tryptans not ischemic (Intern Med 41(8):622, August 2002)
EFFICACY OF INTRAVENOUS MAGNESIUM SULFATE IN THE TREATMENT OF ACUTE MIGRAINE ATTACKS (1 g over 15 minutes, excellent results in 1 study, others did not work)
(Headache 41:171 February 2001)
MA of Reglan showing efficacy (BMJ 2004;329:1369-1373)
prochlorperazine 10 mg intravenously versus metoclopramide 20 mg intravenously administered during 15 minutes with 25 mg intravenous diphenhydramine. no difference (
[Ann Emerg Med.2008;52:399-406.)
Double Blind prospective study of 30 mg IV Ketorolac vs. 20 mg Nasal Sumatriptan. 7 cm vs. 2 cm VAS change respectively (The American Journal of Emergency Medicine Volume 21, Issue 3 , May 2003, Pages 173-175)
Occipital nerve block 4cc Bupi c 1 cc triamcinolone use 21 G needle at middle 1/3 between occipital prominence and mastoid.
MgSO4 1 gm over 1 minute, patient will feel hot flush and headache should be significantly better.
Dex 6-8 mg IVP, Some neurologists advocate decadron 24mg and then a rapid taper
Academic Emergency Medicine Volume 11,
Number 5 436, 2004
Brooke Army Medical Center: San Antonio, TX, Wilford Hall Medical Center: San Antonio, TX
ABSTRACT
OBJECTIVE: To evaluate whether the addition of intravenous (IV) dexamethasone to standard ED benign headache therapy would reduce the incidence of severe headache recurrence at 48-72 hours. METHODS:This was a randomized, double-blind, placebo-controlled trial of adult patients presenting with the chief complaint of headache. The study was conducted in the ED of 2 academic, urban level 1 military hospitals. After standard ED headache evaluation and therapy as determined by the treating physician, patients were administered either 10 mg of dexamethasone or placebo (normal saline) IV prior to discharge. Patients were contacted 48 to 72 hours after discharged and asked whether their headache was "better," "worse," or "remained unchanged." Patients with the response of "worse" or "unchanged" were considered to be treatment failures (i.e., recurrence). The patient's headache at follow-up was further categorized as severe (provoking another physician visit or interfering with daily activity) or mild (requiring self-medication or requiring no treatment). RESULTS: 57 patients met the inclusion criteria; 2 patients were lost to follow-up, leaving 55 in the study sample. The treatment groups were similar with regard to baseline characteristics, abortive therapy, IV fluids, and degree of pain relief achieved prior to discharge. At follow-up 9.7% (3/31) of those receiving dexamethasone had headache recurrence; 58.3% (14/24) of those receiving placebo had headache recurrence. This difference was statistically significant (p = 0.001). Additionally, 12.9% (4/31) of the dexamethasone treatment group had severe headaches and 87.1% (27/31) had mild headaches at follow-up. In contrast, 33.3% (8/24) of the placebo group had severe headaches and 66.7% (16/24) had mild headaches. These differences did not reach statistical significance (p = 0.136). CONCLUSIONS: IV dexamethasone decreases the incidence of benign headache recurrences and trended toward a decrease in headache severity at 48-72 hours.
and a shortcut review in (Med J Austr 2002;176:83.)
and (1) Baden EY, et al. Intravenous dexamethasone to prevent the recurrence of benign headache after discharge from the emergency department: a randomized, double-blind, placebo-controlled clinical trial Can J Emerg Med 2006;8(6):393-400.
We find rizatriptan RPD wafer 10 mg to be very effective as a first-line therapy for acute migraine attack diagnosed by physicians in the ED Journal of Emergency Medicine Volume 25, Issue 3 , October 2003, Pages 245-249
25 mg benadryl then 20 mg reglan then 800 mg ibuprofen then 1 liter ns
vasospasm of status migrainosis can be spontaneous carotid artery dissection
Typically seen in malws, ~25 y/o. Associated with heavy drinkers and smokers.
exacerbated by etoh
Characteristic findings include severe, strictly unilateral pain located about the eye. The pain may last from 15-180 minutes and may occur 1-8 times per day. Attacks are usually "clustered" in a short time period, followed by weeks to months of no headaches. Associated symptoms often include conjunctival injection, lacrimation, nasal congestion, rhinorrhea, forehead and facial sweating, miosis, and eyelid edema. As many as 30% of such patients may display ptosis.
Inspect the eye for scleral injection. A unilateral red eye is often seen with either glaucoma or cluster headache. In glaucoma, the cornea is usually cloudy and the pupil mid-position and unreactive. Such patients need measurement of their intraocular pressure.
Rx:
Give high flow oxygen
DHE IV or IM and antiemetics
4% Nasal Lidocaine may also help; use the nostril on the side of the pain
Can discharge on Verapamil 80 mg TID and 1 week steroid taper.
If the patient has facial or frontal pain, tap on the sinuses to elicit tenderness. Similarly, having the patient lean forward will often exacerbate the head pain. However, of all physical findings, studies show that purulent nasal secretion and abnormal sinus transillumination are the best clinical predictors of sinusitis.
Severe headache, decreased vision, opthalmoplegia, hypotension.
Preexisting pit tumor bleeds or infarcts, expands and compresses adjoining structures
Precepitates acute
Rx
Steroids-Solumedrol 1 gram
Months after initial insult, accomp. Concentration defects, sleep disorders
increased ICP, HA, papilledema, n/v, change in vision.
Usually has lasted 20 days or greater
usually seen in obese young women,
CT (Should be normal) then do LP, document pressures
Can have permanent visual loss if not discovered.
Also suspect if a normal pattern of migraines is suddenly different
Very difficult to differentiate from dural sinus thrombosis (Emerg Med J 2004; 21:245-247)
All patients given this diagnosis need urgent MRI, either during their initial visit or in next few days
headache, pulsatile intracranial noises, double vision, photophobia, n/v, vision loss with central sparing
can have VI palsy
CSF opening pressure > 25 cm with pt in lateral decub and legs relaxed
20-25 is non-diagnostic
pt's need an MRI
get CTA/CTV if MRI not available
A vasculitide affecting medium and large sized arteries.
almost exclusively affects those >50 y/o with mean onset at 72.
Whites are affected much more frequently than other ethnic groups.
Headache, jaw claudication, polymyalgia rheumatica (PMR), and visual symptoms are the most common symptoms.
Fever, anemia, arterial tenderness, and systemic symptoms are also possible.
The jaw claudication of GCA is worse with hard foods (b/c it is from muscle ischemia) in contrast to tmj disorders, which is often worse with soft foods or with the initiation of chewing. (Med Clin NA 1997;81)
PMR is closely related to GCA and may be a manifestation of same disease process.
Eye symptoms are diplopia or vision loss from occlusion of posterior ciliary artery.
Greatest likelihood ratios were for jaw claudication and diplopia in patients
with sufficient pretest probability to obtain biopsies. Negative likelihood ratios were best with
normal TA on palpation and normal ESR.
(JAMA
287(1):92,
In one study, 18% of patients c GCA had aortic involvement as well. Using PET scans, 50% had involvement. (Am J Med 2000; 108)
Get
ESR
Range of 20-100 mg of
prednisone per day
Abnormal ESR had LR - of 0.2 and LR + of 1.1
jaw claud LR+ 4.2
Diplopia LR+3.4
Beaded or Enlarged Temporal Art LR + 4.6 and 4.3
ASA seems to be non-inferior to coumadin (Neurology 2009;72:1810)
Dissection of the vertebral arteries is often characterized by a sudden, severe occipital headache (often unilateral), associated with neck pain. The pain can occur several days before the onset of neurologic deficits. About half of patients complain of dizziness or vertigo and experience nausea or vomiting. Some have unilateral facial numbness and diplopia.41 Minor trauma (e.g., from sporting activities, chiropractic manipulation, or even head-turning to park a car) frequently occurs within six hours prior to the onset of head and neck pain
Ptosis, Miosis, face pain horrible headache, ha can precede neuro sx by 2 weeks
SPONTANEOUS DISSECTION OF THE CAROTID AND VERTEBRAL ARTERIES
Schievink, W.I., N Engl J Med 344(12):898,
Clinical and Paraclinical Features as Putative Arguments Against or in Favor of Immediate Anticoagulation in Individual CAD Patients at the Time of Diagnosis
|
||||||||||||||||||||||||||||||
(Stroke. 2007;38:2605.)
ASA appears to be as good as anticoag in spont carotid dissection (neuro 2009;72:1810)
Carotid Artery Dissection
Cervical artery dissection is a significant cause of stroke in patients younger
than age 40; approximately 20% of strokes in the young are caused by carotid
artery and vertebral artery dissections in the neck. Although any of the
arteries in the neck may be affected, internal carotid artery dissections are
the most common. They may occur spontaneously or as a result of trauma. However,
the "spontaneous" dissection is often preceded by a trivial trauma - activities
that cause sudden stretch of the pharyngeal portion of the carotid artery.
Ipsilateral facial pain and a partial Horner's syndrome (ptosis with miosis),
are the most frequent clinical manifestations of a spontaneous carotid artery
dissection (1). Pulsatile tinnitus is often reported. Other patients present
with transient or persistent neurologic symptoms. Strokes are often due to the
embolization of thrombus material from the lumen of the dissected artery to the
intracranial arteries, most often the middle cerebral artery. Thus, the
Emergency Physician must consider such dissections in younger patients with
sudden neurologic deficits and no or few risk factors for cerebrovascular
disease
The diagnosis is made via magnetic resonance angiography or CT angiography. If
neither modality is immediately available, carotid duplex scanning may be useful
in diagnosing a carotid artery dissection.
Although there have been no randomized therapeutic trials in patients with
carotid artery dissection, experience shows that standard anticoagulation in the
form of heparin followed by warfarin is effective in preventing further
artery-to-artery emboli. Some consultants might opt for anti-platelet therapy
alone which may be quite adequate.
References:
(1) Simoens J, et al. Spontaneous carotid artery dissection: a rare cause of
cerebrovascular accident Acta Cardiol 2007;62: 533-6.
(2) Selim M, Caplan LR. Carotid Artery Dissection Curr Treat Options Cardiovasc
Med 2004; 6: 249-253.
(3) Stapf C, Elkind MS, Mohr JP. Carotid artery dissection Annu Rev Med 2000;51:
329-47.
(4) Schievink W. Spontaneous dissection of the Carotid and Vertebral arteries
NEJM 2001;344: 898-906.
(From EMEDHome.com)
Ask about Space Heater Use
Increased CSF pressure or Infxn (most common in 1st 6 months post-op)
Headache after LP is common, and there are several effective treatments. No evidence that symptomatic relief is obtained with post-tap supine bed rest, caffeine (either oral or intravenous; 500 mg of caffeine sodium benzoate in one liter normal saline over one hour) or hydration. (West J Med 176:69, 2002 or Neurology 55:909, October 2000 and Neurology 2004;2:46)
If these measures fail, consider an epidural blood patch which has been shown to be very effective. What has shown to be effective prophylacticly is small needle, appropriate bevel direction, replacing stylet, and operator skill.
dementia, ataxia, incontinence of urine, dilation of ventricles s increased ICP
May have drop attacks.
HA during 2nd half of pregnancy
Spontaneous intracranial hypotension typically presents with subacute onset
of postural headache and there might be features of meningism. Symptoms of
brainstem compression (nausea, vomiting, unsteadiness and coma) and cranial
nerve traction (blurred vision, constriction of visual fields, altered hearing
and sixth nerve palsy) might occur.2 The condition is more common in women and
typically occurs in middle age.2 The aetiology in most cases is thought to be
spontaneous rupture of a dural nerve root sleeve3 and can be precipitated by
trauma (often trivial) or straining. An association with connective tissue
disorders has been described.4
Acute onset of headache has been previously described and the diagnostic
confusion with subarachnoid haemorrhage highlighted.5 The present case was
unusual in that the CSF opening pressure was normal but this is still compatible
with the diagnosis and it has been advocated that the condition is better
explained by CSF hypovolaemia rather than hypotension.6
The neuroimaging features of spontaneous intracranial hypotension include
subdural effusions secondary to dural hyperaemia which might extend into the
spinal canal, dural enhancement with gadolinium, pituitary enlargement, enlarged
cortical and spinal epidural veins, tonsillar herniation and flattening of the
pons against the clivus.7 MR imaging might be normal however. Similar
appearances can be seen following lumbar puncture; however, in the present case
there was no change in the patient's clinical state after the lumbar puncture
and MR imaging was performed within hours. Additionally, abnormalities on the
initial cranial CT scan performed prior to lumbar puncture (presumably the
result of the mass effect exerted by the isodense subdural effusions) also
reverted to normal after treatment.
The optimal management of spontaneous intracranial hypotension is not clear.
Some advocate radioisotope cisternography to identify the site of CSF leakage.8
However, in 50% of cases this cannot be demonstrated and the procedure
necessitates further dural puncture and risk of coning.7 The majority of leaks
occur in the dorsal and lumbar regions and are readily amenable to treatment
with lumbar blood patching.7 We would, therefore, advocate proceeding directly
to lumbar blood patch and only performing cisternography in cases where
treatment fails and neurosurgical intervention is being considered. The
mechanism of action for blood patching is not established, but a tamponade
effect might be important.9 Intravenous caffeine has also been shown to be
beneficial for postdural puncture intracranial hypotension and frequently gives
long lasting relief from headache.10
To the Editor: We report a patient with spontaneous intracranial hypotension (SIH), which is now an increasingly recognised syndrome. Orthostatic headache with typical findings on magnetic resonance imaging (MRI) are the keys to diagnosis. When correctly diagnosed, SIH management is easy and highly effective in most cases.
A 38-year-old woman presented to our hospital after having daily headaches for 3 weeks. The acute onset of severe headache occurred initially when she bent down and tried to lift her 16-month-old child. The headache began as a sharp pain over the right side of her occiput and rapidly spread to her frontal area. The headache was particularly bad in the morning and while standing, and was relieved by assuming a recumbent posture. Apart from nausea, she had no other associated symptoms. General and systemic examination findings were normal.
MRI of the brain showed diffuse dural enhancement and smooth thickening of the dura (Box, A) and a total spinal magnetic resonance image showed fluid in the posterior soft tissues at C1/C2 level (Box, B). These findings confirmed the leak of cerebrospinal fluid that accounted for the intracranial hypotension and orthostatic headache. Initial treatment with bed rest, increased fluid intake and non-steroidal anti-inflammatory drugs relieved her symptoms marginally. After a failed lumbar epidural blood patch, 10 mL of autologous blood was injected at the site of the cervical level leak. The patient’s symptoms resolved, and she was asymptomatic and had had no recurrence at follow-up at 4 months.
Also known as Schaltenbrand syndrome, SIH is very rare, with a prevalence of about 1 in 50 000 population, and a female preponderance of 3:1.1 Patients with connective tissue diseases2 or Chiari malformation may be more susceptible to SIH. Orthostatic headache is the cardinal feature of this syndrome. Headache is usually holocranial, although it might be localised to the frontal or occipital regions. Patients may have other symptoms such as diplopia and photophobia. MRI with gadolinium is critical in diagnosing this syndrome. The condition of most patients improves with conservative therapy (bed rest, increased fluid intake and caffeine). Epidural autologous blood patch is effective in relieving low intracranial pressure headaches.3 Surgical repair of the leak is rarely used and should be used only if medical therapy fails.4
Almost always from leaks either from connective tissue disorder, trauma or from traumatic spinal tap
sagging of diencephalon and brain stem can lead to stupor or coma which may only resolve with the patient in trend.
can alos result in subdural hematomas as blood must make up for the neg pressure
patients actually do worse if the sdh is evacuated
may occur at multiple levels, so if first patch doesn't work, scan for additional leaks
Brain Tumors
The edema surrounding brain tumors is believed to be primarily vasogenic, due to
breakdown of the blood brain barrier, with a lesser component of cytotoxic
(intracellular) edema. Electron microscopy studies of peritumoral tissue have
revealed swelling of astrocytes, axons, and myelin sheaths, tissue necrosis, and
enlargement of the extracellular space in the white matter. Other studies have
also documented improvement of histologic abnormalities that correlate with the
use of DXM and parallel clinical improvement (77).
Clinically, a dramatic response to GC can be observed in patients with brain
neoplasms, edema, and mass effect. Ingraham et al. (78) first used GC in an
attempt to ameliorate postoperative adrenal insufficiency in patients undergoing
craniotomy for craniopharyngioma resection. They noted the favorable effect that
GC had on postoperative cerebral edema, and this observation had a lasting
effect on neurosurgical practice (78). Hormonal manipulation of brain tumors and
antineoplastic effects of GC were then investigated a few years later. Although
many of these patients had dramatic improvement, the investigators concluded
that it was attributable to an anti-edema effect rather than to any
antineoplastic activity (79). Galicich et al. (80) evaluated the use of GC in a
large number of patients with brain tumors and established the beneficial role
of DXM in this setting. French (81) reported an even greater response in
patients with metastatic brain tumors. Subsequently, computerized tomographic
confirmation of the edema-reducing effect of GC became available, and
modification of tumor enhancement patterns was reported (82). Diffusion
tensor–magnetic resonance imaging of peritumoral edematous brain in patients
treated with DXM suggested a localized reduction in the magnitude of
extracellular water mobility and therefore water content (83). Given the
perception of an unequivocal treatment effect, a randomized controlled trial of
GC vs. placebo has never been undertaken and likely never will be.
With a long half-life and minimal mineralocorticoid effect, DXM has become the
GC of choice for this patient population. Most subjects respond to starting
doses of 4–8 mg/day, although higher doses have been used (up to 100 mg/day).
About 75% of patients with brain metastases show marked improvement within 24–72
hrs, and generalized symptoms such as headache and altered mental status tend to
improve more than focal ones. Although approximately 25% of patients require
long-term GC use, most patients are successfully weaned off GC after several
weeks. In patients with metastatic brain tumors, DXM, when used as the only form
of treatment, slightly increases the median survival and results in remission of
symptoms for about 4 wks (84).
Subarachnoid hemorrhage
Meningitis and encephalitis
Cervico-cranial artery dissections
Temporal arteritis
Acute narrow angle closure glaucoma
Hypertensive emergencies
Carbon monoxide poisoning
Pseudotumor cerebri
Cerebral venous and sinus (dural
or cavernous) thrombosis
Acute strokes: hemorrhagic or ischemic
Mass lesions
Tumor
Abscess
Intracranial hematomas (parenchymal, subdural, epidural)
Parameningeal infections
· response to therapy is irrelevant
· LP without CT if no papilledema, normal fundi, no neurodeficit, and normal mental status
· Image: Neuro findings, HIV (Scan all c HA or Δ in MS), >50 y/o c new type of HA
· Do not need angio with neg. CT/LP (with normal opening pressure), just give close neuro f/u
Is the combination of CT and lumbar puncture enough for all patients with thunderclap headache? Here, we believe that the art of medicine should not be lost. There are a number of situations in which the clinician may suspect rarer alternative diagnoses based on a careful history and examination. From our perspective, extracranial or intracranial arterial dissection is the most important of these alternatives, because specific management would be indicated. Other diagnoses include cerebral venous thrombosis and vasculitis. In these settings, we would generally use MRI/MR angiography/MR venography, but CT angiography techniques may be a reasonable alternative.
For most of these conditions the diagnosis rests on the performance of additional investigations. Cervicocranial vascular imaging studies such as magnetic resonance angiography, CT angiography, or catheter angiography are essential for diagnosing cervical or cerebral arterial dissections, vasospasm, arterial occlusions (when early CT demonstrates no evidence of ischemia), vasculitis, and aneurysms. MR venography, CT venography, and venous phase angiography may confirm dural sinus thrombosis or cortical vein thrombosis. Finally, routine MRI can readily identify hemorrhagic or ischemic pituitary apoplexy as well as posterior circulation vasogenic edema from hypertensive crises, and fat-suppression techniques have become the gold-standard for visualizing intramural hemorrhage related to dissection. (Mayer)
thunderclap and normal CT
Dural sinus thrombosis
Expansion or thrombosis of an unruptured intracranial aneurysm
Pituitary apoplexy
Dissection of the cerebral or cervical arteries
Hypertensive crisis
Posterior reversible leukoenceophalopathy syndrome
Sympathomimetic-induced vasospasm
Cerebral vasculitis
Vasoconstrictive angiopathies (postpartum, exertional, coital)
Spontaneous intracranial hypotension
Viral or bacterial meningoencephalitis
Sphenoid sinusitis
CSF spectrophotometry remains 100% sensitive for detecting SAH when analyzed between 12 hours and 2 weeks from the time of ictus.8 (Mayer)
Preventive measures
• Try
to reduce stress
•
Drink at least one gallon of water per day
Activity
•
Exercise regularly
•
Rest in a dark, quiet room while you have a headache
• Do
not drive, swim, or operate heavy machinery during the headache
•
Keep a record of what triggers the headache
Diet
• Do
not skip meals
•
Avoid alcohol and tobacco
•
Avoid triggers of the headache (for example, red wine, foods that may contain
nitrites, and certain cheeses)
•
Keep a record of food eaten prior to the onset of the headache
Medications
•
Take all medications as prescribed
Return to the emergency
department if you have:
• A
headache that persists, becomes worse, or if you have any change in vision
•
Numbness or weakness of your arms or legs
•
Neck stiffness, sensitivity to light, or any fever greater than 100.3ºF
•
Drowsiness, lethargy, abdominal pain, or continued nausea and vomiting
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15
in intracranial dissection,32 eg, vertebral artery
dissection.