Thunderclap Headache – Pearls and Pitfalls
- Nov 14th, 2016
- Drew A. Long
Authors: Drew A. Long, BS (@drewlong2232, Vanderbilt University School of Medicine) and Brit Long, MD (@long_brit, EM Attending Physician at SAUSHEC) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)
You are working in the ED and see that your next patient is a 38 y/o female complaining of headache. As soon as you enter the room, you notice the patient appears to be in pain, holding her hand to her left temple and wincing. She states she was going on a run about an hour earlier when she experienced a 10/10 intensity headache. When you ask about the onset of the headache, she states “One moment I was running, and suddenly I was bent over in pain.” She also complains of dizziness, nausea, and tingling and numbness of her left hand and foot. The patient has no history of headaches and no pertinent past medical history. She recently gave birth 6 weeks prior via spontaneous vaginal delivery. Her vitals include HR 110, RR 16, BP 173/100, oxygen saturation of 98%, and a normal temperature. As you gather the rest of the history and move to the physical examination, what must you consider in this patient?
What is a thunderclap headache?
A thunderclap headache (TCH) has been defined as a “headache that reaches 7 (out of 10) or more in intensity within less than one minute.”1 TCH is often unexpected and not preceded by any warning signs or symptoms. While the duration and location of the headache are important parts of the history, they do not have a role in defining TCH and are nonspecific for TCH.1 When evaluating a patient with a headache, it is vital the Emergency Physician (EP) determine both the intensity and time it took the headache to reach maximum severity. The EP must keep in mind that a normal neurological exam and absence of any associated symptoms does not exclude a serious cause in a patient with a TCH, and the patient still requires a diagnostic workup for potentially deadly pathologic conditions.1 Additionally, pain relief with treatment does not exclude a serious cause.2-4
The classic teaching in medical school is that a “thunderclap” headache is pathognomonic for subarachnoid hemorrhage (SAH) from a ruptured intracranial aneurysm. However, only 11-25% of TCHs are due to SAH.5,6 What else should the EP think of when a patient presents with a TCH?
Table 1 depicts conditions that may manifest as a TCH.1,7,8
Most cases of SAH occur from a ruptured cerebral aneurysm (about 85% of cases), which occur most commonly at branch points in the Circle of Willis.9 The typical presentation of SAH is a sudden, severe headache that the patient describes as “the worst headache of my life.” A headache will be the primary symptom of SAH in 70% of patients, of which 50% will present with a TCH.6,10-12 The headache usually lasts for several days and very rarely resolves within a few hours.13 Accompanying signs and symptoms include loss of consciousness (one third of patients), seizures (6-9%), delirium (16%), stroke, visual disturbances, N/V, dizziness, neck stiffness, and photophobia.14-16
As TCH is a common presentation of a SAH, any patient that presents with TCH must be evaluated for SAH due to high morbidity and mortality. According to literature, the average fatality rate of SAH is 51%.17 About 10% of patients with aneurysmal SAH die prior to hospital arrival, 25% die within the first 24 hours of SAH onset, and 45% die within 30 days.18
In evaluating for SAH it is helpful to consider a sentinel headache. A sentinel headache is a headache that occurs days or weeks prior to a ruptured cerebral aneurysm. This is thought to arise from a small leak of blood into the subarachnoid space.8 About 10-43% of patients with aneurysmal SAH report a prior similar warning headache.19 Importantly, signs often accompanying SAH, such as a stiff neck, altered mental status, and focal neurological deficits, are usually absent in a sentinel headache.7 However, even if these signs are absent the patient still requires evaluation for a SAH. For more on evaluation of SAH, see http://www.emdocs.net/controversies-in-the-diagnosis-of-subarachnoid-hemorrhage/.
Cerebral Venous Thrombosis
A headache occurs in 75-95% of patients with cerebral venous thrombosis (CVT).20,21 While the onset of headache in CVT is usually gradual, about 2-13% of patients experience a TCH as the primary symptom.22 Additionally, patients may experience accompanying neurological symptoms from several vascular territories. Other signs and symptoms include seizures (more commonly focal), papilledema, altered mental status, and focal neurological deficits.7,8 The symptoms can be associated with thrombus location.23,24 Importantly, patients with CVT presenting with TCH as their main symptom are clinically indistinguishable from patients with SAH presenting with TCH.7
While CVT is a relatively rare disorder, 80% of patients with CVT are younger than 50.23,25,26 CVT is more common in women, especially in the peripartum period and in patients with recent surgery.27 CVT is also associated with hypercoagulable states including the use of oral contraceptives, hematologic disorders, factor V Leiden, protein C or S deficiency, and anti-thrombin III deficiency.25,28
For more information about CVT, check out a previous post here: http://www.emdocs.net/cerebral-venous-thrombosis-pearls-and-pitfalls/
Cervical Artery Dissection
A cervical artery dissection can result in an ischemic stroke, transient ischemic attack, or more rarely a SAH.8 Carotid or vertebral artery dissections are an especially important cause of strokes to consider in young and middle aged patients.29-32 A significant risk factor is a history of neck trauma, which can be minor (e.g. manipulation therapy of the neck or sports-related trauma).33 Other risk factors include connective tissue disease, large vessel arteriopathies, hypertension, and a history of migraines.34-36
Headaches are reported in 60-95% of patients with carotid artery dissections and 70% of patients with vertebral artery dissections.36 While headache onset is typically gradual, TCH occurs in about 20% of patients with a cervical artery dissection.38,39 According to the International Headache Society’s diagnostic criteria, headaches from cervical artery dissection must be ipsilateral to the dissected artery.40 The typical first symptom of a cervical artery dissection is unilateral headache (68%), neck pain (39%), or facial pain (10%).41 The headache from a carotid artery dissection is found most commonly in the frontotemporal region.42 Additionally, about 25% of patients will experience a partial Horner’s syndrome (miosis and ptosis).43 A vertebral artery dissection presents with neck pain (66%) and headache (65%), which can be unilateral or bilateral.44 The headache is more commonly posterior in location. Many other symptoms may be present, including facial paresthesia, dizziness, vertigo, nausea/vomiting, visual disturbances (such as diplopia), ataxia, limb weakness or numbness, dysarthria, and hearing loss.42
Acute Hypertensive Crisis/Posterior Reversible Encephalopathy Syndrome
Two case reports describe patients who presented with TCH from either a hypertensive crisis or posterior reversible encephalopathy syndrome (PRES).45,46 In a hypertensive emergency, while the diastolic pressure is often ≥ 120 mmHg, there is no specific threshold, as different patients will manifest signs of end-organ damage at varying blood pressures.47 While about 20% of patients with hypertensive crises have associated headaches, most of these are not a TCH but rather a throbbing headache.48 Additionally, a hypertensive crisis may present with symptoms in addition to headache consistent with end-organ damage. These may include dizziness, dyspnea, vision change, chest pain, psychomotor agitation, change in urine output, fluid overload state, or focal neurological deficits.8
Posterior reversible encephalopathy syndrome (PRES) is a clinical syndrome with radiographic findings that presents with headache, seizures, and visual loss often with extreme hypertension.49 Other symptoms include nausea/vomiting, focal neurological signs, or altered mental status.49,50 Specific radiographic findings are necessary for the diagnosis, most commonly symmetric white matter edema in the posterior cerebral hemispheres.51 The headache associated with PRES generally has an acute onset.7 PRES may occur in conjunction with other disorders including eclampsia, thrombotic thrombocytopenic purpura or hemolytic uremic syndrome, and immunosuppressive therapy.52
It is important to determine whether a patient with TCH is hypertensive due to a stress response to the severe headache or if the TCH is the result of the hypertension. In patients with TCH and extreme hypertension, it is vital to evaluate for signs of end-organ damage suggesting an acute hypertensive crisis and to consider PRES in patients presenting with headache, seizures, and visual loss.
About 25-34% of patients with stroke develop an associated headache.53,54 In 50% of these patients, the headache precedes any other neurological signs or symptoms.54 Typically, the headache is throbbing and ipsilateral to the side of the stroke.54 TCH associated with stroke is rare, but several case reports document patients presenting with TCH due to stroke.5,55,56
Spontaneous Intracranial Hypotension
The most common cause of spontaneous intracranial hypotension is CSF leakage from spinal meningeal defects or dural tears.57 This most commonly occurs after lumbar puncture, but can occur from minor trauma such as falls, lifting, coughing, or sports.1,7 Most commonly intracranial hypotension presents with a positional headache that improves after lying down and worsens when upright.58 However, 15% of patients will present with TCH.59,60 Other symptoms associated with spontaneous intracranial hypotension are nausea/vomiting, dizziness, auditory changes, diplopia, visual blurring, interscapular pain, or upper extremity pain.7,8
Meningitis can very rarely present with TCH. A prospective study of patients presenting with TCH found 2.7% to have an infectious etiology.6 Consider meningitis if the patient is febrile, at increased risk for infection (immunocompromised), or has features of meningitis (e.g. stiff neck).
Pituitary apoplexy occurs with hemorrhage or infarction of the pituitary gland.1,7,8 This most commonly occurs in the setting of a pituitary adenoma, but may occur in association with pregnancy, general anesthesia, bromocriptine therapy, or pituitary irradiation.61 Pituitary apoplexy usually presents with a combination of acute headache, ophthalmoplegia, decreased visual acuity, reduction in visual fields, and altered mental status.62 The headache is usually sudden and severe.62
A retroclival hematoma is usually seen as a rare manifestation of severe head and neck injuries in which there is atlantoaxial dislocation.63,64 Patients with retroclival hematomas may present with TCH, which has been described in several patients.65,66
Third Ventricle Colloid Cyst
A colloid cyst of the third ventricle can impede the flow of CSF leading to obstructive hydrocephalus. Third ventricle colloid cysts account for 0.5% of intracranial tumors and are most commonly diagnosed between the third and fifth decades of life.67 The most common symptom is headache, which occurs in 68-100% of patients.68 The headache of a third ventricle colloid cyst usually begins abruptly, lasts for seconds up to one day, and resolves quickly.69 The headache may be relieved with a supine position. Additionally, 50% of patients have associated nausea/vomiting. They can also experience loss of consciousness, altered mental status, seizures, coma, or death.68
Temporal arteritis is a very rare cause of TCH. Temporal arteritis should be suspected in older patients (>50) complaining of a new onset headache, temporal pain, visual symptoms, or jaw claudication. It is also associated with polymyalgia rheumatica, which occurs in 40-50 percent of patients with temporal arteritis.70 For more information on temporal arteritis, check out this previous post: http://www.emdocs.net/can-giant-cell-arteritis-be-ruled-out-in-the-ed/.
Reversible Cerebral Vasoconstriction Syndrome
Reversible Cerebral Vasoconstriction Syndrome (RCVS) includes conditions associated with TCH and diffuse, segmental, reversible vasospasm.71,72 RCVS is thought to account for most cases of TCH that are termed “benign,” or unexplained.1 Risk factors for RCSV include the postpartum period, history of migraine, and use of pharmacologic agents including ergotamine, triptans, SSRIs, pseudoephedrine, cocaine, amphetamines, ecstasy, cannabis, and bromocriptine.73-81 Half of RCVS cases occur during the postpartum period or after exposure to serotoninergic agents, adrenergic agents, or cannabis.81-83
The hallmark of RCVS is multiple thunderclap headaches that recur every day or every few days. These headache recurrences can occur for up to four weeks.72,81 Other symptoms include altered mental status, motor or sensory deficits, seizures, visual changes, ataxia, speech abnormalities, and N/V.7
While RCVS is usually self-limiting, it is not always benign. A minority of patients can experience residual effects including seizures or strokes.72,82,84
Other causes of TCH
Other conditions that have been reported in association with TCH include complicated sinusitis; cluster headache; primary cough, exertional, and sexual headaches; and primary TCH.1,7,8
What is the workup of TCH?
Every patient with TCH must be assumed to have a life-threatening intracranial condition. Management of patients presenting with TCH starts with the ABCs. Once the patient is stabilized, diagnostic evaluation is initiated beginning with specific evaluation for SAH. Schwedt, Matharu, and Dodick proposed an algorithm for TCH evaluation in 2005, beginning with head CT:7
Figure 1. Diagnostic Evaluation of TCH.7 (CVST: cerebral venous sinus thrombosis; SIH: spontaneous intracranial hypotension; PRES: posterior reversible encephalopathy syndrome; RCVS: reversible cerebral vasoconstriction syndrome)
The initial imaging modality is a noncontrast head CT. CT scan has a high sensitivity and specificity for SAH. When conducted within 6 hours of onset of TCH, CT has a specificity of 98% and sensitivity nearing 100%.11 As time from headache onset increases, the sensitivity of CT for SAH declines: 86% on day two, 76% after two days, and 58% after five days.85 However, these numbers are based on head CTs interpreted by neuroradiologists, and the scanners utilized were at least third generation.
Unfortunately, CT can miss many causes of TCH including SAH (especially if after 12 hours), CVT, CVA dissection, acute hypertensive crisis/PRES, intracranial hypotension, meningitis, pituitary apoplexy, and retroclival hematoma. For CVT, the initial CT may be normal in up to 25-30% of patients.86 In a patient with CVA dissection without an ischemic stroke, head CT is usually normal.1,7 Similarly, CT is typically unrevealing in patients with acute hypertensive crisis, intracranial hypotension, meningitis, pituitary apoplexy, and retroclival hematoma.1,7,8 For patients with an acute hypertensive crisis or PRES, while neuroradiographic changes may be apparent on CT, they are best visualized on MRI.87,88
Some authors recommend always performing a CTA or MRA after negative CT noncontrast.1,7,72,89 If the patient has a SAH, a CTA can detect a ruptured aneurysm. One method is for the TCH patient to receive a CT and CTA, as CTA will additionally further evaluate for SAH or an aneurysm, CVA dissection, stroke, and RCVS.
An LP with opening pressure can aid in diagnosis. LP is the gold standard for the diagnosis of SAH, especially if the patient presents after 12 hours of headache onset.11,89,90 CSF studies including glucose, protein, white cells, and differential are used for diagnosing viral and bacterial meningitis. Additionally, opening pressure can be utilized to detect increased or decreased pressures. CVT may be associated with an elevated opening pressure, while intracranial hypotension is associated with a low opening pressure.1,22 Finally, the CSF should be visually inspected for xanthochromia.
The majority of evidence states that conventional angiography is not necessary in patients with a normal head CT and LP.91 Angiography has a small risk of transient and permanent neurological complications.92 In evaluating patients with TCH and normal head CT and LPs, prospective studies have found no subsequent development of SAH or sudden death in patients with normal head CT and normal LP, supporting the viewpoint that conventional angiography may be more harmful than helpful.93-96
The role of MRI for imaging of the brain and cerebral vasculature has not yet been defined in patients with TCH, especially in the setting of the Emergency Department. Schwedt, Matharu, and Dodick in 2005 recommended that patients presenting with TCH and a normal head CT and LP receive further evaluation with MRI.7 An MRI can help further evaluate for CVT, pituitary apoplexy, PRES, or intracranial hypotension.7 If MRI is normal, Schwedt et al. recommends evaluation with either an MRA or MRV. Ducros and Bousser in 2012 have similar recommendations and state that all patients with TCH and a normal head CT and LP should receive a CTA or MRA.1 If these are normal, they recommend a brain MRI for further evaluation.
Even with a thorough workup, studies estimate that a diagnosis is made in only 27-71% of patients with TCH.5,6,10,95 The most common diagnosed cause of TCH is SAH.5,6,10,95 Other vascular causes are the second most common diagnosed cause, which includes cervical artery dissection, CVT, and RCVS.1,97
In determining workup of patients with TCH, the patient history is essential in determining the necessary diagnostic evaluation. Table 2 provides several suspicious features associated with TCH that may help an Emergency Physician suspect a specific diagnosis. While the physical exam is useful, patients with TCH and a normal exam (specifically a neurological exam) may still have a deadly intracranial condition. The decision to pursue further measures beyond a head CT and/or LP should be made in conjunction with a neurologist, so early consultation is warranted. Neurosurgery may also need to be on board. The ideal mechanism of imaging for each potential condition is shown in Table 2.
Table 2. Features of TCH that aid with diagnostic evaluation1,7,8,42
Upon further questioning, the patient remembers that she was in a minor car accident several days prior. She states she was not injured other than minor neck pain from “whiplash.” However, the pain had been decreasing over the past several days and was barely noticeable prior to today. When asked about neck pain, she admits she is experiencing left sided neck pain, but not nearly as severe as her headache. Now suspicious for a CVA dissection, you order a head CT and CTA. CTA demonstrates a left sided vertebral artery dissection, revealing the cause of this patient’s thunderclap headache.
A thunderclap headache (TCH) is a headache that reaches 7 (out of 10) or more in intensity within less than one minute. Every patient presenting with TCH must be assumed to have a life-threatening intracranial condition. As many conditions can present with TCH (most commonly SAH or RCVS), a thorough history is essential in evaluating for risk factors for other conditions. The Emergency Physician must keep in mind that the absence of associated symptoms and a normal physical and neurological exam does not exclude a serious cause in a patient with a TCH; the patient still requires a diagnostic workup. Due to the high morbidity and mortality of subarachnoid hemorrhage, any patient that presents with TCH must be evaluated for SAH. A noncontrast head CT has a sensitivity for SAH nearing 100% if performed within 6 hours of headache onset. We recommend TCH patients to receive a CTA with the initial head CT, as this will further evaluate for an aneurysm, cervical artery dissection, stroke, or RCVS. Decisions on further imaging and diagnostic evaluation should be made in conjunction with neurology and possibly neurosurgery.
- Ducros A, Bousser MG. Thunderclap Headache. BMJ 2013 Jan 8;346:e8557.
- Pope JV, Edlow JA. Favorable Response to Analgesics does not predict a benign etiology of headache. Headache 2008;48:944-950.
- Rosenberg JH, Silberstein SD. The Headache of SAH responds to Sumatriptan. Headache 2005;45:597-598.
- Seymour JJ, Moscati RM, Jehle DV. Response of headaches to nonnarcotic analgesics resulting in missed intracranial hemorrhage. Am J Emerg Med 1995;13:43-45.
- Landtblom AM, Fridriksson S, Boivie J, et al. Sudden onset headache: a prospective study of features, incidence and causes. Cephalalgia 2002;22:354-60.
- Linn FJ, Wijdicks EF, van der Graff Y, Weerdesteyn-van Vliet FA, Bartelds AI, van Gijn J. Prospective study of sentinel headache in aneurysmal subarachnoid hemorrhage. Lancet 1994:344:590-93.
- Schwedt TJ, Matharu MS, Dodick DW. Thunderclap headache. Lancet Neurol 2006 Jul;5(7):621-31.
- Schwedt TJ, Dodick DW. Thunderclap Headache. UpToDate 2014 Dec 10.
- van Gijn J, Rinkel GJ. Subarachnoid hemorrhage: diagnosis, causes and management. Brain 2001;124:249-78.
- Linn FJ, Rinkel GJ, Algra A, van Gijn J. Headache characteristics in subarachnoid hemorrhage and benign thunderclap headache. J Neurol Neurosurg Psychiatry 1998;65:791-3.
- Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. N Engl J Med 2000;344:29-36.
- van Gijn J, Kerr RS, Rinkel GJ. Subarachnoid hemorrhage. Lancet 2007;369:306-18.
- Sandercock PAG, Hankey GJ, van Gijn J, et al. Stroke: a practical guide to management. 2nd Oxford: Blackwell Science Ltd;2000.
- Hasan D, Schonck RS, Avezaat CJ, Tanghe HL, van Gijn J, van der Lugt PJ. Epileptic seizures after subarachnoid hemorrhage. Ann Neurol 1993;33:286-91.
- Pinto AN, Canhao P, Ferro JM. Seizures at the onset of subarachnoid hemorrhage. J Neurol 1996;243:161-164.
- Caeiro L, Menger C, Ferro JM, Albuquerque R, Figueira ML. Delirium in acute subarachnoid hemorrhage. Cerebrovasc Dis 2005;19:31-38.
- Hop JW, Rinkel GJ, Algra A, van Gijn J. Case-fatality rates and functional outcome after subarachnoid hemorrhage: a systematic review. Stroke 1997;28(3):660.
- Broderick JP, Brott TG, Duldner JE, Tomsick T, Leach A. Initial and recurrent bleeding are the major causes of death following subarachnoid hemorrhage. Stroke 1994;25(7):1342.
- Polmear A. Sentinel headaches in aneurysmal subarachnoid hemorrhage: what is the true incidence? A systemic review. Cephalalgia 2003;23:935.
- Terazzi E, Mittino D, Ruda R, et al. Cerebral venous thrombosis: a retrospective multicenter study of 48 patients. Neurol Sci 2005;25:311-315.
- de Bruijn SFTM, de Hann RJ, Stam J, et al. Clinical features and prognostic factors of cerebral venous sinus thrombosis in a prospective series of 59 patients. J Neurol Neurosurg Psychiatry 2001;70:105-8.
- de Bruijn SF, Stam J, Kappelle LJ. Thunderclap headache as first symptom of cerebral venous sinus thrombosis. CVST Study Group. Lancet 1996;348(9042):
- Bousser MG, Ferro JM. Cerebral venous thrombosis: an update. Lancet Neurol 2007;6:162-70.
- Stam J. Thrombosis of the cerebral veins and sinuses. N Engl J Med 2005;352:1791-8.
- Piazza G. Cerebral venous thrombosis. Circulation 2012;125:1704-1709.
- Thorell SE, Parry-Jones AR, Punter M, Hurford R, Thachil J. Cerebral venous thrombosis – A primer for the haematologist. Blood Reviews 2015;29:45-50.
- Alvis-Miranda HR, Milena Castellar-Leones S, Alcala-Cerra G, Rafael Moscote-Salazar L: Cerebral sinus venous thrombosis. J Neurosci Rural Pract 4:427,2013.
- Canhao P, Ferro JM, Lindgren AG, Bousser MG, Stam J, Barinagarrementeria F, et al. Causes and predictors of death in cerebral venous thrombosis. Stroke 2005;36:1720-5.
- Leys D, Bandu L, Henon H, Lucas C, Mounier-Vehier F, Rondepierre P, Godefroy O. Clinical outcome in 287 consecutive young adults (15 to 45 years) with ischemic stroke. Neurology 2002;59(1):26.
- Rasura M, Spalloni A, Ferrari M, De Castro S, Patella R, Lisi F, Beccia M. A case series of young stroke in Rome. Eur J Neurol 2006;13(2):146.
- Cerrato P, Grasso M, Imperiale D, Priano L, Baima C, Giraudo M et al. Stroke in young patients: etiopathogenesis and risk factors in different age classes. Cerebrovasc Dis 2004;18(2):154.
- Nedeltchev K, der Maur TA, Georgiadis D, Arnold M, Caso V, Mattle HP et al. Ischaemic stroke in young adults: predictors of outcome and recurrence. J Neurol Neurosurg Psychiatry 2005;76(2):191.
- Debate S. Pathophysiology and risk factors of carotid artery dissection: what have we learnt from large hospital-based cohorts? Curr Opin Neurol 2014;27:20
- Grond-Ginsbach C, Debette S. The association of connective tissue disorders with cervical artery dissections. Curr Mol Med 2009;9(2):210
- Southerland AM, Meschia JF, Worrall BB. Shared associations of nonatherosclerotic, large-vessel, cerebrovascular arteriopathies: considering intracranial aneurysms, cervical artery dissection, moyamoya disease and fibromuscular dysplasia. Curr Opin Neurol 2013;26:13.
- Arnold M, Pannier B, Chabriat H et al. Vascular risk factors and morphometric data in cervical artery dissection: a case-control study. J Neurol Neurosurg Psychiatry 2009;80:232.
- Silbert PL, Mokri B, Schievink WI. Headache and neck pain in spontaneous internal carotid and vertebral artery dissections. Neurology 1995;45:1517-22.
- Mitsias P, Ramadan NM. HA in ischemic cerebrovascular disease. Part I: Clinical features. Cephalalgia 1992;12(5):269.
- Maruyama H, Nagoya H, Kato Y, Deguchi I, Fukuoka T, Ohe Y, et al. Spontaneous cervicocephalic arterial dissection with headache and neck pain as the only symptom. J Headache Pain 2012 Apr;13(3):247-53.
- Headache Classification Committee of the International Headache Society. The international classification of headache disorders. Cephalalgia 2004;24:1-151.
- Schievink WI. Spontaneous dissection of the carotid and vertebral arteries. N Engl J Med 2001;344:898.
- Tintinalli JE, Stapczynski JS, Ma OJ, Yearly GD, Meckler GD, Cline DM. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 8th New York: McGraw-Hill, 2016.
- Lee VH, Brown RD Jr, Mandrekar JN, Mokri B. Incidence and outcome of cervical artery dissection: a population-based study. Neurology 2006;67:1809.
- Debette S, Grond-Ginsbach C, Bodenant M et al. Differential features of carotid and vertebral artery dissections: the CADISP study. Neurology 2011;77:1174.
- Tang-Wai DF, Phan TG, Wijdicks EFM. Hypertensive encephalopathy presenting with thunderclap headache. Headache 2001;41:198-2000.
- Dodick DW, Eross EJ, Drazkowski JF, et al. Thunderclap headache associated with reversible vasospasm and posterior leukoencephalopathy syndrome. Cephalalgia 2003;23:994-97.
- Lenfant C, Chobanian AV, Jones DW, Roccella EJ. Seventh report of the Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7): resetting the hypertension sails. Hypertension 2003;41(6):1178-9.
- Zampaglione B, Pascale C, Marchisio M, et al. Hypertensive urgencies and emergencies: Prevalence and clinical presentation. Hypertension 1996;27:144-147.
- Hinchey J, Chaves C, Appignani B, Breen J, Pao L, Wang A, et al. A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996;334(8):494
- Healton E, Burst J, Feinfield D, Thompson G. Hypertensive encephalopathy and the neurologic manifestations of malignant hypertension. Neurology 1982;32:127-32.
- Lamy C, Oppenheim C, Meder JF, Mas JL. Neuroimaging in posterior reversible encephalopathy syndrome. J Neuroimaging 2004;14(2):89.
- Stott, Hurrell MA, Anderson TJ. Reversible posterior leukoencephalopathy syndrome: a misnomer reviewed. Intern Med J 2005;35:83-90.
- Ferro JM, Melo TP, Oliveira V, Salgado AV, Crespo M, Canhao P, Pinto AN. A multivariate study of headache associated with ischemic stroke. Headache 1995;35(6):315.
- Vestergaard K, Andersen G, Nielsen MI, Jensen TS. Headache in stroke. Stroke 1993;24(11):1621.
- Schwedt TJ, Dodick DW. Thunderclap stroke: embolic cerebellar infarcts presenting as thunderclap headache. Headache 2006;46(3):520.
- Edvardsson BA, Persson S. Cerebral infarct presenting with thunderclap headache. J Headache Pain 2009 Jun;10(3):207-9.
- Rando TA, Fishman RA. Spontaneous intracranial hypotension: report of two cases and review of the literature. Neurology 1992;42(3 Pt 1):481.
- Mokri B. Headaches caused by decreased intracranial pressure: diagnosis and management. Curr Opin Neurol 2003;16:319-26.
- Schievink WI, Wijdicks EF, Meyer FB, et al. Spontaneous intracranial hypotension mimicking aneurysmal subarachnoid hemorrhage. Neurosurgery 2001;48:513-7.
- Ferrante E, Savino A. Thunderclap headache caused by spontaneous intracranial hypotension. Neurol Sci 2005;26:S155-57.
- Mohr G, Hardy J. Hemorrhage, necrosis, and apoplexy in pituitary adenomas. Surg Neurol 1982;18:181-189.
- Randeva HS, Schoebel J, Byrne J, et al. Classical pituitary apoplexy: clinical features, management and outcome. Clin Endocrinol (Oxf) 1999;51:181-88.
- Kuroso A, Amano K, Kubo O, et al. Clivus epidural hematoma. J Neurosurg 1990;72:660-62.
- Orrison WW, Rogde S, Kinard RE, et al. Clivus epidural hematoma: a case report. Neurosurgery 1986;18:194-6.
- Tomaras C, Horowitz BL, Harper RL. Spontaneous clivus hematoma: case report and literature review. Neurosurgery 1995;37:123-24.
- Schievink WI, Thompson RC, Loh CT, Maya MM. Spontaneous retroclival hematoma presenting as thunderclap headache. J Neurosurg 2001;95:522-24.
- Spears RC. Colloid cyst headache. Curr Pain Headache Rep 2004;8:297-300.
- Young WB, Silberstein SD. Paroxysmal headache caused by colloid cyst of the third ventricle: case report and review of the literature. Headache 1997;37:15-20.
- Kelly R. Colloid cysts of the third ventricle; analysis of twenty-nine cases. Brain 1951;74:23-65.
- Gonzalez-Gay MA, Barros S, Lopez-Diaz MJ, Garcia-Porrua C, Sanchez-Andrade A, Llorca J. Giant cell arteritis: disease patterns of clinical presentation in a series of 240 patients. Medicine (Baltimore) 2005;84(5):269.
- Calabrese LH, Dodick DW, Schwedt TJ, Singhal AB. Narrative review: reversible cerebral vasoconstriction syndromes. Ann Intern med 2007;146(1):34.
- Ducros A. Reversible cerebral vasoconstriction syndrome. Lancet Neurol 2012 Oct;11(10):906-17.
- Schluter A, Kissig B. MR angiography in migrainous vasospasm. Neurology 2002;59(11):1772.
- Farine D, Andreyko J, Lysikiewicz A, Simha S, Addison A. Isolated angiitis of brain in pregnancy and puerperium. Obstet Gynecol 1984;63(4):586.
- Janssens E, Hommel M, Mounier-Vehier F, Leclerc X, Guerin du Masgenet B, Leys D. Postpartum cerebral angiopathy possibly due to bromocriptine therapy. Stroke 1995;26(1):128.
- Henry PY, Larre P, Aupy M, Lafforgue JL, Orgogozo JM. Reversible cerebral arteriopathy associated with the administration of ergot derivatives. Cephalalgia 1984;4(3):171.
- Meschia JF, Malkoff MD, Biller J. Reversible segmental cerebral arterial vasospasm and cerebral infarction: possible association with excessive use of sumatriptan and Midrin. Arch Neurol 1998;55(5):712.
- Singhal AB, Caviness VS, Begleiter AF, Mark EJ, Rordorf G, Koroshetz WJ. Cerebral vasoconstriction and stroke after use of serotonergic drugs. Neurology 2002;58(1):130.
- Levine SR, Washington JM, Jefferson MF, Kieran SN, Moen M, Feit H, Welch KM. “Crack” cocaine-associated stroke. Neurology 1987;37(12):1849.
- Reneman L, Habraken JB, Majoie CB, Booij J, den Heeten GJ. MDMA (“ecstasy”) and its association with cerebrovascular accidents: preliminary findings. AJNR Am J Neuroradiol 2000;21(6):1001.
- Ducros A, Boukobza M, Porcher R, Sarov M, Valade D, Bousser MG. The clinical and radiological spectrum of reversible cerebral vasoconstriction syndrome. A prospective series of 67 patients. Brain 2007;130(Pt 12):3091.
- Singhal AB, Hajj-Ali RA, Topcuoglu MA, Fok J, Bena J, Tang D, et al. Reversible cerebral vasoconstriction syndrome: analysis of 139 cases. Arch Neurol 2011;68:1005-12.
- Fugate JE, Ameriso SF, Ortiz G, Schottlaender LV, Wijdicks EF, Flemming KD, et al. Variable presentations of postpartum angiopathy. Stroke 2012;43:670-6.
- Ducros A, Fiedler U, Porcher R, Boukobza M, Stapf C, Bousser MG. Hemorrhagic manifestations of reversible cerebral vasoconstriction syndrome. Frequency, features, and risk factors. Stroke 2010;41:2505-11.
- van Gijn J, van Dongen KJ. The time course of aneurysmal haemorrhage on computed tomograms. Neuroradiology 1982;23(3):153.
- Rao KC, Knipp HC, Wagner EJ. Computed tomographic findings in cerebral sinus and venous thrombosis. Radiology 1981;140(2):391.
- Oppenheim C, Logak M, Dormont D, Lehericy S, Manai R, Samson Y, Marsault C, Rancurel G. Diagnosis of acute ischemic stroke with fluid-attenuated inversion recovery and diffusion-weighted sequences. Neuroradiology 2000;42(8):602.
- Schwartz RB, Jones KM, Kalina P, Bajakian RL, Mantello MT, Garada B, Holman BL. Hypertensive encephalopathy: findings on CT, MR imaging, and SPECT imaging in 14 cases. AJR Am J Roentgenol 1992;159(2):379.
- Moussouttas M, Mayer SA. Thunderclap headache with normal CT and lumbar puncture: further investigations are unnecessary: Stroke 2008;39:1394-5.
- Savitz SI, Edlow J. Thunderclap headache with normal CT and lumbar puncture: further investigations are unnecessary: Stroke 2008;39:1392-3.
- Savitz SI, Levitan EB, Wears R, Edlow JA. Pooled analysis of patients with thunderclap headache evaluated by CT and LP: is angiography necessary in patients with negative evaluations? J Neurol Sci 2009 Jan;276(1-2):123-5.
- Warnock NG, Gandhi MR, Bergvall U, Powell T. Complications of intraarterial digital subtraction angiography in patients investigated for cerebral vascular disease. Br J Radiol 1993;66(790):855.
- Markus HS. A prospective follow up of thunderclap headache mimicking subarachnoid hemorrhage. J Neurol Neurosurg Psychiatry 1991;54(12):1117.
- Linn FJ, Rinkel GJ, Algra A, van Gijn J. Follow-up of idiopathic thunderclap headache in general practice. J Neurol 1999;246(10):946.
- Harling DW, Peatfield RC, Van Hile PT, Abbott RJ. Thunderclap headache: is it a migraine? Cephalalgia 1989;9(2):87.
- Landtblom AM, Boivie J, Fridriksson S, et al. Thunderclap headache: final results form a prospective study of consecutive cases. Acta Neurol Scand 1996;167(Suppl 94):23.
- Schwedt TJ. Clinical spectrum of thunderclap headache. Expert Rev Neurother 2007 Sep;7(9):1135-44.