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-secondOlder: 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
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:
- photophobia and phonophobia
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
Intravenous Dexamethasone to Prevent the Recurrence of Benign Headache Following Discharge from the Emergency Department: A Randomized, Placebo-controlled Clinical Trial
Eric Y. Baden and Curtis L. Hunter
Brooke Army Medical Center: San Antonio, TX, Wilford Hall Medical Center: San Antonio, TX
OBJECTIVE: To evaluate whether the addition of intravenous (IV)dexamethasone to standard ED benign headache therapy would reducethe incidence of severe headache recurrence at 48-72 hours.METHODS:This was a randomized, double-blind, placebo-controlledtrial of adult patients presenting with the chief complaintof headache. The study was conducted in the ED of 2 academic,urban level 1 military hospitals. After standard ED headacheevaluation and therapy as determined by the treating physician,patients were administered either 10 mg of dexamethasone orplacebo (normal saline) IV prior to discharge. Patients werecontacted 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 lostto follow-up, leaving 55 in the study sample. The treatmentgroups were similar with regard to baseline characteristics,abortive therapy, IV fluids, and degree of pain relief achievedprior to discharge. At follow-up 9.7% (3/31) of those receivingdexamethasone had headache recurrence; 58.3% (14/24) of thosereceiving placebo had headache recurrence. This difference wasstatistically significant (p = 0.001). Additionally, 12.9% (4/31)of the dexamethasone treatment group had severe headaches and87.1% (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 reachstatistical significance (p = 0.136). CONCLUSIONS: IV dexamethasonedecreases the incidence of benign headache recurrences and trendedtoward 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
Compazine is still better than reglan (Emerg Med J 2013;30:595-596 doi:10.1136/emermed-2013-202853.1)
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.
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.
Subarachnoid Hemorrhage (SAH)
Severe headache, decreased vision, opthalmoplegia, hypotension.
Preexisting pit tumor bleeds or infarcts, expands and compresses adjoining structures
Precepitates acute addisonian crisis from no ACTH secretion.
Steroids-Solumedrol 1 gram
Months after initial insult, accomp. Concentration defects, sleep disorders
Cerebral Venous Thrombosis
Idiopathic Intracranial Hypertension (Pseudotumor Cerebri)
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
Giant Cell (Temporal) Arteritis
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.
beading, swelling, and tenderness of the temp arteries
ha may actually be occipital
PMR-shoulder girdle pain
vision loss is from flicking off clots from swollen, inflamed arteries
can be intermittent
may have fovea sparing depending on blood supply
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, January 2, 2002)
In one study, 18% of patients c GCA had aortic involvement as well. Using PET scans, 50% had involvement. (Am J Med 2000; 108)
and CRP. ESR should be corrected to increase accuracy. (Men 17.3+0.18 x Age) (Women 22.1 + 0.18 x Age). CRP does not need to be corrected. 2-9% of GCA cases will have an ESR in the normal range (Am J Med 1986; 80)
Range of 20-100 mg of prednisone per day
. In ED, send home on Prednisone 60 mg OD with close f/u.
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
Cervical Artery Dissection
ASA seems to be non-inferior to coumadin (Neurology 2009;72:1810)
Vertebral Artery Dissection
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
Carotid Artery Dissection
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, March 22, 2001
Clinical and Paraclinical Features as Putative Arguments Against or in Favor of Immediate Anticoagulation in Individual CAD Patients at the Time of Diagnosis Against Immediate Anticoagulation
Severe strokes, ie, NIHSS score 15 In analogy to findings of increased rate of symptomatic hemorrhagic transformation in severe strokes in TOAST.51 Applying general ASA guidelines for anticoagulation.52 No brain imaging available CAD can present with bleedings.53,54 Applying general ASA guidelines for anticoagulation.52 Accompanying intracranial dissection Bleeding risk seems in intracranial dissection,32 eg, vertebral artery dissection. Local compression syndromes without stroke/TIA Subadventitial dissection may have less risk for ischemic events.36 Concomitant diseases with increased bleeding risk (extra/intracranial) Translating atrial fibrillation studies to CAD.90 Insufficient intracranial collaterals Delayed ICA occlusion under heparin.45,46 Watershed infarct in a patient without collaterals.44However, low intracranial flow may favor anticoagulants to prevent intracranial thrombus formation. In Favor of Immediate Anticoagulation
HITS despite (dual) antiplatelets HITS more frequent in patients with recurrent ischemia.20,23 Few studies. HITS surrogate marker of “microclots”? Occlusion/ pseudo-occlusion Embolization may occur during recanalization.42 Multiple TIAs/strokes affecting multiple regions (same circulation) Clinical course may suggest repetitive emboli Free-floating thrombus Rare finding38,39
In the absence of evidence-based treatment guidelines, this synopsis is based on pathophysiological considerations, observations and conclusions by analogy and reflects the view of the authors. Neither clinical/paraclinical features nor the comments/references claim to be exhaustive. TIA indicates transient ischemic attack; ASA, American Stroke Association; NIHSS, National Institutes of Health Stroke Scale.
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.
Ask about Space Heater Use
Narrow Angle Glaucoma
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.
Aminophylline for treatment of postdural puncture headache: A randomized clinical trial. Neurology. 2018 Mar 23. pii: 10.1212/WNL.0000000000005351. doi: 10.1212/WNL.0000000000005351. [Epub ahead of print]
Anesthesia & Analgesia December 2018, Volume 127 (6), p 1434–1439. Addition of Neostigmine and Atropine to Conventional Management of Postdural Puncture Headache : A Randomized Controlled Trial
Hoovers sign, cup one heel, ask pt to raise other leg, if dont push down on your hand, they are faking. Psychogenic Coma-try nasal tickle, open eyes, they should close slowly in a coma.
Normal Pressure Hydrocephalus
dementia, ataxia, incontinence of urine, dilation of ventricles s increased ICP
May have drop attacks.
HA during 2nd half of pregnancy
Spontaneous Intracranial Hypotension
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
Mohamed Asif Chinnaratha, Ronald A Criddle and Paul J GraziottiMJA 2007; 187 (1): 59
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 patients 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 tensormagnetic 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 48 mg/day, although higher doses have been used (up to 100 mg/day). About 75% of patients with brain metastases show marked improvement within 2472 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).
Can’t miss diagnoses in HA
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
- Idiopathic Thunderclap
- Without reversible vasospasm
- With Reversible Vasospasm (Call-Fleming syndrome)
- Cerebral Venous Sinus Thrombosis
- Carotid Artery Dissection
- Pituitary Apoplexy
- Spont. Intracranial Hypotension
- Malignant Hypertension
- Spont. Retroclival Hematoma
- Unruptured Inracranial Aneurysm
What does CT + LP Miss
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 restson the performance of additional investigations. Cervicocranialvascular 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, andvenous phase angiography may confirm dural sinus thrombosisor cortical vein thrombosis. Finally, routine MRI can readilyidentify hemorrhagic or ischemic pituitary apoplexy as wellas posterior circulation vasogenic edema from hypertensive crises,and fat-suppression techniques have become the gold-standardfor visualizing intramural hemorrhage related to dissection. (Mayer)
thunderclap and normal CT
Dural sinus thrombosis
Expansion or thrombosis of an unruptured intracranial aneurysm
Dissection of the cerebral or cervical arteries
Posterior reversible leukoenceophalopathy syndrome
Vasoconstrictive angiopathies (postpartum, exertional, coital)
Spontaneous intracranial hypotension
Viral or bacterial meningoencephalitis
CSF spectrophotometryremains 100% sensitive for detecting SAH when analyzed between12 hours and 2 weeks from the time of ictus.8 (Mayer)
Try to reduce stress
Drink at least one gallon of water per day
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
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
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