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Thunderclap headache

Last literature review version 17.3: September 2009  |  This topic last updated: April 8, 2009   (More)

INTRODUCTION AND DEFINITION — Thunderclap headache (TCH) refers to a severe headache of sudden onset. Its explosive and unexpected nature is likened to a "clap of thunder." Although TCH initially referred to pain associated with an unruptured intracranial aneurysm, multiple etiologies have since been described [1] (table 1). These include cerebral venous thrombosis, cervical artery dissection, spontaneous intracranial hypotension, pituitary apoplexy, retroclival hematoma, ischemic stroke, acute hypertensive crisis with reversible posterior leukoencephalopathy syndrome, third ventricular colloid cysts, bacterial and viral meningitis, complicated sinusitis, and reversible cerebral vasoconstriction syndromes.

In addition, the term primary TCH is often used to refer to a benign, idiopathic, and potentially recurrent headache of sudden and severe intensity with a lack of underlying pathology.

This topic will review each of the entities considered in patients with TCH, offer pathophysiologic considerations, and discuss the diagnostic evaluation of TCH.

DIFFERENTIAL DIAGNOSIS — In addition to the pain associated with the onset of subarachnoid hemorrhage from intracranial aneurysm rupture, thunderclap headache may be associated with multiple other causes (table 1).

  • Unruptured intracranial aneurysm (sentinel headache)
  • Cerebral venous thrombosis
  • Cervical artery dissection
  • Spontaneous intracranial hypotension
  • Pituitary apoplexy
  • Retroclival hematoma
  • Ischemic stroke
  • Acute hypertensive crisis
  • Colloid cyst of the third ventricle
  • Infections
  • Reversible cerebral vasoconstriction syndromes
  • Primary thunderclap headache

These are discussed in greater detail in the following sections.

Other conditions that may rarely present with TCH include the following:

  • Acute myocardial infarction [2]
  • Anaplastic oligodendroglioma [3]
  • Aqueductal stenosis [4]
  • Pheochromocytoma [5]
  • Vogt-Koyanagi-Harada syndrome [6]

Unruptured intracranial aneurysm (sentinel headache) — Ten to 43 percent of patients with aneurysmal subarachnoid hemorrhage (SAH) report a history of a sentinel or warning headache [7]. A sentinel headache is an episode of headache similar to that of SAH that occurs days to weeks prior to aneurysm rupture. Sentinel headaches are likely caused by small aneurysmal leaks of blood into the subarachnoid space. Sentinel headaches develop over seconds, reach maximal intensity within minutes, and may endure for hours to days. Features of SAH including stiff neck, altered consciousness, and focal neurologic symptoms and signs are usually absent. (See "Etiology, clinical manifestations, and diagnosis of aneurysmal subarachnoid hemorrhage".)

It is essential to recognize thunderclap headaches (TCHs) as possible warnings of impending aneurysm rupture. In patients in which aneurysms are found, surgical or endovascular intervention, as indicated, may result in avoidance of the catastrophic event. (See "Treatment of aneurysmal subarachnoid hemorrhage" and "Unruptured intracranial aneurysms".)

However, sentinel headaches are often ignored by both patients and clinicians or are misdiagnosed. Approximately 12 to 51 percent of patients with SAH are initially misdiagnosed [8,9]. Misdiagnosis occurs because of failure to recognize the spectrum of possible presentations of SAH, lack of knowledge regarding the limitations of computed tomography (CT), and failure to perform lumbar puncture (LP) and interpret cerebrospinal fluid tests correctly. (See "Etiology, clinical manifestations, and diagnosis of aneurysmal subarachnoid hemorrhage", section on 'Misdiagnosis'.)

Initial evaluation for SAH must include noncontrast CT of the brain. LP is indicated when there is clinical suspicion of SAH and the head CT is normal (algorithm 1).

The diagnosis of SAH as well as the utility of head CT and LP are discussed in greater detail separately. (See "Etiology, clinical manifestations, and diagnosis of aneurysmal subarachnoid hemorrhage", section on 'Diagnosis' and 'Diagnostic evaluation' below.)

Cerebral venous thrombosis — Patients with cerebral venous thrombosis may present with TCH. Headache is the most common presenting symptom in cerebral venous thrombosis, occurring in approximately 90 percent of patients. In addition to headaches, patients with cerebral venous thrombosis usually present with some combination of papilledema, seizures, bilateral focal deficits, and/or altered level of consciousness. However, about 15 percent of patients may present with isolated headache [10]. (See "Etiology, clinical features, and diagnosis of cerebral venous thrombosis", section on 'Clinical aspects'.)

Thunderclap headache is the main symptom of cerebral venous thrombosis in 2 to 13 percent of patients, as suggested by the following reports:

  • A retrospective analysis of 48 patients with cerebral venous thrombosis reported six (13 percent) who presented with TCH [11]

  • A prospective study of 123 consecutive patients with cerebral venous thrombosis found that isolated headache was the only sign in 17 (14 percent), and that TCH was the presenting sign in three (2.4 percent) [10].

Most commonly, however, the headaches of cerebral venous thrombosis have a gradual subacute onset; they may be localized or diffuse, persistent, exacerbated by Valsalva, and positional with worsening on recumbency.

In cases of cerebral venous thrombosis associated with TCH, the initial presentation of cerebral venous thrombosis may be clinically indistinguishable from that of SAH. Magnetic resonance imaging (MRI) with venography should be considered when cerebral venous thrombosis is suspected, as initial testing for a suspected diagnosis of SAH with head CT and LP will not always detect cerebral venous thrombosis. In patients with cerebral venous thrombosis who have normal neurologic exams, the head CT is normal in approximately 25 percent, whereas in patients with cerebral venous thrombosis who have focal neurologic signs, the head CT is normal in less than 10 percent [12,13]. (See "Etiology, clinical features, and diagnosis of cerebral venous thrombosis", section on 'Diagnosis'.)

Cervical artery dissection — Headache is the most frequent presenting symptom of cervical artery dissection, occurring in 60 to 95 percent of patients with carotid artery dissections and in approximately 70 percent of patients with vertebral artery dissections [14].

Although the onset of headache is usually gradual, a sudden and severe onset of pain consistent with a TCH occurs in 20 percent of patients [15]. International Headache Society (IHS) diagnostic criteria for headache secondary to cervical artery dissection stipulate that the headache must be ipsilateral to the dissected artery [16]. Neck pain occurs in one-half of patients with vertebral artery and one-quarter of patients with carotid artery dissections [14].

It is uncommon for patients with cervical artery dissection to present solely with headache and/or neck pain. The majority of patients have additional neurologic symptoms and signs, including amaurosis fugax, Horner's syndrome, pulsatile tinnitus, dysgeusia, diplopia, or other stroke-related manifestations. A history of recent neck manipulation, torsion, or minor trauma has been reported in 12 to 83 percent of patients with cervical artery dissection [17,18].

In the absence of ischemic stroke, CT scanning of the brain and LP are typically unrevealing in patients with dissection. Additional diagnostic tests are necessary if there is clinical suspicion for cervical artery dissection; these could include ultrasound, CT angiography (CTA), magnetic resonance angiography (MRA), conventional angiography, or MRI of the neck with a fat saturation protocol.

Spontaneous intracranial hypotension — Patients with spontaneous intracranial hypotension (SIH) usually present with orthostatic headaches and some combination of nausea/vomiting, dizziness, auditory changes, diplopia, visual blurring, interscapular pain, and/or upper extremity radicular pain. This syndrome is also known as spontaneous low cerebrospinal (CSF) fluid pressure headache.

Cerebrospinal fluid (CSF) leakage from spinal meningeal defects or dural tears may be the most common causes of this syndrome [19]. The headache is caused by displacement of pain-sensitive structures due to the low CSF pressure. (See "Pathophysiology, clinical features, and diagnosis of spontaneous low cerebrospinal fluid pressure headache".)

A minority of patients with low CSF pressure headache will present with TCH. In a series of 28 patients with low CSF pressure headache due to CSF leaks from dural tears, TCH was the presenting sign in four (14 percent) [20]. Evaluation for SAH, including CT scans, LPs, and cerebral angiography was nondiagnostic. However, each patient had features of low CSF pressure on brain MRI, including either brain or cerebellar tonsillar descent, and diffuse pachymeningeal gadolinium enhancement.

Pituitary apoplexy — TCH may be the predominant feature of pituitary apoplexy. Pituitary apoplexy usually presents with a combination of acute headache, ophthalmoplegia, decreased visual acuity, and change in mental status. It is caused by hemorrhage or infarction of the pituitary gland in the setting of a pituitary adenoma. The clinical presentation of pituitary apoplexy ranges from relatively mild symptoms to adrenal crisis, coma, or even sudden death.

Pituitary apoplexy can present with TCH in patients who have normal physical examinations, head CT scans, and CSF studies [21,22]. Pituitary tumors that are isodense to normal brain tissue may be easily overlooked on CT studies, even if hemorrhage is present. Brain MRI has a much higher sensitivity than CT for detecting the tumor and associated blood.

Retroclival hematoma — Spontaneous retroclival hematomas may present as TCH [23]. Retroclival hematomas are usually seen as a rare manifestation of severe head and neck injuries in which there is atlantoaxial dislocation. However, spontaneous hemorrhage can occur. Evidence for this comes from a case report of a 49-year-old woman who developed an instantaneous excruciating headache [23]. She had a normal neurologic examination and normal CT scan of the brain, but CSF analysis revealed xanthochromia and MRI of the cervical spine revealed the retroclival hematoma. This case reinforces the recommendation to consider MRI in patients presenting with TCH in which initial tests are nondiagnostic.

Ischemic stroke — TCH may rarely be the presenting feature of ischemic stroke. Approximately 25 to 34 percent of patients with stroke develop an associated headache [24,25]. In about 50 percent of those who develop headache with stroke, the headache occurs prior to other stroke manifestations. In patients with a history of a primary headache disorder, the headache developing in association with stroke may resemble their usual headache. In others, a throbbing headache ipsilateral to the side of the stroke is most common [25]. (See "Headache, migraine, and stroke".)

In the majority of cases, headaches associated with stroke are not consistent with TCH. However, three cases of ischemic stroke associated with TCH have been reported, including one case in which TCH was the primary clinical feature of embolic bilateral cerebellar infarcts [26,27]. CT and LP may be nondiagnostic in patients with TCH and recent stroke, suggesting the necessity of MRI in such cases.

Acute hypertensive crisis — TCH may be a presenting feature of acute hypertensive crisis and reversible posterior leukoencephalopathy syndrome (RPLS). Two such cases have been reported in the literature. In one case report, a patient presented with hypertension, TCH, and white matter abnormalities on MRI involving the parieto-occipital regions consistent with RPLS [28]. In the second case, the patient had recurrent thunderclap headaches and a generalized tonic-clonic seizure [29]. Angiography revealed diffuse, multifocal, segmental vasospasm involving the arteries of the circle of Willis and its branches.

Although headaches occur in approximately 20 percent of patients with hypertensive crisis, they are most often described as throbbing and indistinct [30]. Other manifestations of hypertensive crisis include faintness, dyspnea, chest pain, psychomotor agitation, focal neurologic deficits, and epistaxis.

In the presence of RPLS, patients may have nausea and vomiting, visual changes, altered mental status, seizures, and focal neurologic signs [31,32]. Consideration of acute hypertensive crisis and RPLS as a possible cause of TCH is important for accurate diagnosis. Most commonly, hypertension in the setting of a TCH may arise as a stress response.

Evaluation for underlying SAH with head CT and LP may miss the diagnosis of RPLS. MRI is more sensitive than head CT for revealing the white matter and cortical edema associated with RPLS. These changes typically involve the parietal and occipital lobes and may also involve the basal ganglia, brainstem, and cerebellum [33]. Since the imaging changes are secondary to vasogenic edema and not ischemia or infarction, prompt treatment of the hypertension is essential and should result in correction of the associated clinical syndrome [34].

The pathogenesis, clinical features, diagnosis, neuroimaging and treatment of RPLS is discussed in greater detail separately. (See "Reversible posterior leukoencephalopathy syndrome".)

Colloid cyst of the third ventricle — Patients with colloid cysts of the third ventricle may also present with TCH when the cyst, which can act like a ball valve, suddenly impedes the flow of cerebrospinal fluid, causing acute obstructive hydrocephalus. Headache is reported by 68 to 100 percent of patients with third ventricular colloid cysts, making it the most commonly associated symptom.

Typically, the headache has an acute onset and resolution, with a duration of seconds to one day [35]. The pain is often severe and may be relieved by taking the supine position. Headaches may be located in the bilateral frontal, fronto-parietal, or fronto-occipital head regions [36]. Approximately one-half of patients have associated nausea and vomiting. Loss of consciousness, mental status changes, seizures, coma, and death can occur [37].

Third ventricular colloid cysts are diagnosed via CT or MRI of the brain.

Infections — Bacterial and viral meningitis are most commonly associated with headaches of a gradual onset, but may rarely present with TCH. A prospective analysis of 148 patients presenting to their primary care physician with TCH found four (2.7 percent) with infectious etiologies [38]. Lumbar puncture for cerebrospinal fluid examination is required for diagnosis.

Headaches related to acute sinusitis may also rarely be of the thunderclap variety. Although headaches and facial pain are frequent in patients with acute rhinosinusitis, most commonly these are acute to subacute in presentation and not consistent with TCH. However, TCH may occasionally be the presenting manifestation of sinusitis when related intracranial complications have occurred, such as with extension through the sphenoid sinus [39].

Reversible cerebral vasoconstriction syndromes — Conditions associated with TCH and diffuse, segmental, reversible cerebral vasospasm are referred to as reversible cerebral vasoconstriction syndromes (RCVS) [40]. This is a group of disorders with similar clinical and radiologic features that include the following [40-45]:

  • Thunderclap headache with vasospasm
  • Benign angiopathy of the central nervous system (BACNS)
  • Migrainous vasospasm or crash migraine
  • Call-Fleming syndrome (or Call syndrome)
  • Postpartum angiopathy
  • Drug-induced cerebral vasoconstriction

Thus, RCVS may occur in patients who have a history of migraine, in the postpartum period, and in those exposed to different pharmacologic agents, including ergotamine, triptans, selective serotonin reuptake inhibitors, pseudoephedrine, cocaine, amphetamines, ecstasy, cannabis, and bromocriptine [46-55].

Patients with RCVS present with TCH, normal or near-normal cerebrospinal fluid, and reversible cerebral segmental vasospasm involving arteries of the circle of Willis. Thunderclap headache may occur in isolation or in conjunction with other symptoms, such as altered mental status, motor deficits, sensory deficits, seizures, visual changes, ataxia, speech abnormalities, and nausea/vomiting.

Angiographically, RCVS manifest as alternating segments of vasoconstriction and dilation or alternating areas of vasoconstriction and normal vascular caliber in the proximal and distal branches of the circle of Willis. Brain MRI may be normal or have abnormalities consistent with posterior reversible leukoencephalopathy or watershed infarctions in the distal vascular territory of cerebral vessels with severe spasm.

Diagnostic criteria for RCVS have not been validated, but key elements for confirming the diagnosis include all of the following features [40]:

  • Severe acute headaches with or without additional neurologic symptoms or signs
  • No evidence of aneurysmal subarachnoid hemorrhage
  • Multifocal segmental cerebral artery vasoconstriction by contrast angiography or CTA or MRA
  • Normal or near normal CSF analysis (ie, CSF protein <80 mg/dL, CSF leukocytes <10 mm3, and normal CSF glucose)
  • Reversibility of angiographic vasoconstriction within three months of onset

In the majority of cases, RCVS are self-limiting. However, patients may have fluctuating focal neurologic symptoms and signs, including seizures and strokes. (See "Headache, migraine, and stroke", section on 'Reversible cerebral vasoconstriction syndromes'.)

There is limited evidence to suggest that nimodipine may be useful in preventing or ameliorating the risk of a delayed ischemic deficit [56-60]. Significant improvement in vasospasm, even in the absence of specific treatment, is expected within four weeks of symptom onset. Several months may be required for complete normalization of vascular imaging.

Primary thunderclap headache — TCH may occur as a benign and potentially recurrent headache disorder in the absence of underlying organic intracranial pathology. However, it cannot be overstated that primary TCH must be a diagnosis made only after exclusion of all possible underlying causes.

International Headache Society diagnostic criteria for primary TCH stipulate that head pain must be severe, sudden in onset, reach maximum intensity in less than one minute, endure from one hour to 10 days, not recur regularly over subsequent weeks or months (although headache may recur within the first week after onset), and not be accounted for by another disorder [16]. In addition, normal cerebrospinal fluid and brain imaging are required. Primary TCH may occur spontaneously, while a patient is at rest, or may be precipitated by exertion or Valsalva. Exercise, weight lifting, or sexual activity is a precipitating event in up to one-third of cases.

Reversible cerebral vasoconstriction may be part of the spectrum of primary thunderclap headache. Supporting evidence comes from a series of 56 consecutive patients with recurrent thunderclap headache of unknown etiology referred to a headache clinic in Taiwan [60]. Magnetic resonance angiography (MRA) performed at a mean interval of 11 days after the first headache attack showed segmental vasoconstriction involving Circle of Willis vessels in 22 patients (39 percent). This finding must be interpreted cautiously, since the utility of MRA for determination of segmental vasoconstriction is not established. (See 'Reversible cerebral vasoconstriction syndromes' above.)

PATHOPHYSIOLOGY — The underlying pathophysiology of primary thunderclap headache (TCH) and reversible cerebral vasoconstriction syndromes (RCVS) is unclear. Excessive sympathetic activity or an abnormal vascular response to circulating catecholamines may be involved. This would explain the occurrence of TCH during physical activity, in patients with pheochromocytoma, acute hypertensive crises, and in patients who take sympathomimetic drugs or tyramine containing foods concurrently with MAO inhibitors. In further support of this hypothesis, reversible cerebral vasospasm has been documented in pheochromocytoma, eclampsia, and sympathomimetic drug intoxication [61-64].

Although vasospasm can be initiated by mechanical, biochemical, and neurogenic stimuli, the abrupt onset of headache and vasospasm implies a neurogenic mechanism. Sympathetic afferents that innervate the intracranial vasculature contain neuropeptide Y and noradrenaline, both vasoconstrictors [65,66]. Vascular caliber may be a reflection of sympathetic tone and sympathetic receptor sensitivity, and primary TCH may be a result of spontaneous and abnormal central sympathetic response. This theory is supported by models of vasospasm in SAH as well as the clinical finding of multifocal vasospasm in patients with pheochromocytoma and sympathomimetic drug intoxication [61,63,64,67,68].

DIAGNOSTIC EVALUATION — Given the potentially serious nature of possible underlying intracranial etiologies, thunderclap headache (TCH) must be considered and treated as a medical emergency.

Initial testing (algorithm 1) focuses on evaluation for subarachnoid hemorrhage (SAH). Brain CT without contrast, the first test in this evaluation, is highly sensitive and specific for the diagnosis of SAH within the first 12 to 24 hours. During the first 12 hours following onset of headache, third-generation CT scanners have a sensitivity nearing 100 percent and a specificity of 98 percent [8]. However, these numbers are based upon studies that used expert neuroradiologists to interpret the scans.

In general practice, clinicians may easily overlook subtle imaging abnormalities suggestive of SAH. In addition, the sensitivity of head CT in SAH declines rapidly over time, decreasing to 86 percent on day two, 76 percent after two days, and 58 percent after five days [69]. Therefore, lumbar puncture (LP) is required in the evaluation of patients presenting with TCH who have CT scans interpreted as normal or inadequate. LP should include measurement of opening pressure (which may be elevated in patients with SAH or cerebral venous thrombosis), routine cerebrospinal fluid (CSF) analyses including cell counts, and visual inspection for xanthochromia.

Some experts recommend the use of CSF spectrophotometry, if available, to measure xanthochromia, especially when a traumatic tap makes CSF interpretation difficult or when the specimen has been improperly processed. The sensitivity of spectrophotometry approaches 100 percent when LP is performed 12 hours to two weeks after SAH onset [70].

Despite its high sensitivity, spectrophotometry has only low to moderate specificity for the diagnosis of SAH and is not universally recommended. As a practical matter, spectrophotometry is rarely available in North American hospitals. (See "Etiology, clinical manifestations, and diagnosis of aneurysmal subarachnoid hemorrhage", section on 'Spectrophotometry'.)

The necessity of performing conventional angiography to evaluate for unruptured intracranial aneurysms in patients with TCH who have normal neurologic exams, normal head CT, and normal LP is still debatable. However, the bulk of evidence suggests that conventional angiography is not necessary in this setting. In a retrospective study of 71 patients with TCH and normal CT and LP, none had SAH during an average follow-up of 3.3 years [71]. Prospective analyses have had similar results. Among a total of 225 patients with primary TCH in four prospective studies, no patient had SAH or sudden death during at least one year of follow-up [72-75]. In addition, conventional angiography carries a small but real risk of transient and permanent neurologic complications (1 and 0.5 percent respectively). This risk may be higher in patients with TCH, especially if they have associated vasospasm [76,77].

Magnetic resonance angiography (MRA) or CT angiography (CTA) may be considered in patients who have nondiagnostic CSF studies when spectrophotometry is not available, or when the index of suspicion for intracranial aneurysm is very high. The sensitivity of MRA ranges from 69 to 100 percent and is dependent upon the size of the aneurysm [78]. For aneurysms 6 mm or larger, MRA sensitivity is greater than 95 percent. Although CTA has been studied less extensively, it has an overall detection rate of 85 to 98 percent [79,80]. CTA requires patient exposure to radiation and carries a small risk of allergic reaction to contrast material and deterioration of renal function.

The exact role of brain MRI in the evaluation of TCH has not yet been defined, but MRI appears to be more sensitive than head CT for many of the possible underlying causes of TCH, such as cerebral venous thrombosis, cervical artery dissection, spontaneous intracranial hypotension, and reversible posterior leukoencephalopathy syndrome.

Therefore, for patients with TCH who have non-diagnostic head CT and LP, we suggest obtaining brain MRI. In cases of suspected arterial dissection, imaging of the cranial and cervical arteries may also be indicated. Imaging of the intracranial venous system may be necessary when cerebral sinus venous or cortical vein thrombosis is suspected.

SUMMARY AND CONCLUSIONS — Thunderclap headache (TCH) refers to a severe headache of sudden onset. (See 'Introduction and definition' above.)

  • Thunderclap headache requires urgent evaluation as such headaches may be harbingers of subarachnoid hemorrhage. However, a wide range of different etiologies must be considered when evaluating a patient with TCH (table 1). These include unruptured intracranial aneurysm, cerebral venous thrombosis, cervical artery dissection, spontaneous intracranial hypotension, pituitary apoplexy, retroclival hematoma, acute hypertensive crisis, third ventricular colloid cysts, viral and bacterial meningitis, acute complicated sinusitis, reversible cerebral vasoconstriction syndromes, and primary thunderclap headache. (See 'Differential diagnosis' above.)

  • Primary TCH is a diagnosis that should be made only after exclusion of all other possible underlying causes. A comprehensive evaluation for underlying pathology must be performed prior to diagnosis of primary TCH. (See 'Primary thunderclap headache' above.)

  • The underlying pathophysiology of TCH with or without vasospasm is unclear. Excessive sympathetic activity or an abnormal vascular response to circulating catecholamines may be involved. (See 'Pathophysiology' above.)

  • Initial testing for TCH generally includes head CT. Lumbar puncture with measurement of opening pressure and cerebrospinal fluid analysis is indicated when there is clinical suspicion of subarachnoid hemorrhage and the head CT is normal (algorithm 1). For patients with TCH who have nondiagnostic head CT and LP, we suggest obtaining brain MRI. Additional studies that may be indicated on a case-by-case basis include angiography and venography. (See 'Diagnostic evaluation' above.)

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