Thunderclap Headache (2024)

Continuing Education Activity

Patients presenting with a thunderclap headache (TCH) may describe their pain as “the worst headache ever” or “worst headache of my life.” What differentiates TCHs from other headache types is how rapidly they reach their peak intensity, not the headache intensity itself. TCH is often associated with a potentially fatal etiology, such as subarachnoid hemorrhage (SAH), and is considered a medical emergency, requiring a rapid, focused evaluation. According to the ICHD-3, “Evidence that thunderclap headache exists as a primary disorder is poor: the search for an underlying cause should be both expedited and exhaustive.” This activity reviews the clinical presentation and recommended workup of patients who present with TCH and highlights the role of the interprofessional team in prompt and timely recognition and management to improve outcomes.

Objectives:

• Describe the recommended steps of a rapid, focused history and physical in patients with a thunderclap headache.

• Differentiate thunderclap headache from other headache types.

• Identify the signs and symptoms associated with secondary thunderclap headache causes.

• Implement evidence-based diagnostic criteria for thunderclap headache with a focus on the initial testing phase.

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Introduction

Day and Raskin are creditedwith coining the term thunderclap headache (TCH). The term was used in a case report published in 1986 of a 42-year-old woman who presented with an intense, sudden-onset headache she described as "like a hammer hitting my head."They concluded, "Hemorrhage into the wall of an aneurysm is a possible cause of thunderclap headache attacks before rupture."[1][2][3]

Primary TCH is an "other primary headache disorder" in the third edition of the International Classification of Headache Disorders (ICHD-3).TCH is defined as a high-intensity headache of abrupt onset, mimicking that of a ruptured cerebral aneurysm, in the absence of any intracranial pathology. However, according to the ICHD-3, "Evidence that thunderclap headache exists as a primary disorder is poor: the search for an underlying cause should be both expedited and exhaustive."[4]

What differentiates thunderclap headaches from other headache types is how rapidly they reach their peak intensity, not the headache intensity itself.[5]TCH is often associated with a potentially fatal etiology, such as subarachnoid hemorrhage (SAH), and is considered a medical emergency.

Etiology

In a systematic review of causes of a sudden and severe headache (thunderclap headache), the authors, Devenney, Neale, and Forbes, conclude, “There are over 100 different published causes of sudden and severe headache, other than aneurysmal subarachnoid hemorrhage.”[6]

The2 most common causes of secondary TCH are subarachnoid hemorrhage and reversible cerebral vasoconstriction syndrome (RCVS).[5]

Other causes include the following:

• Intracerebral hemorrhage, subdural hematoma, cervical artery dissection

• Ischemic stroke, cerebral venous sinus thrombosis (CVT)

• Spontaneous intracranial hypotension (SIH), acute hypertensive crisis

• Intracranial infection, complicated sinusitis

• Intracranial tumor, third ventricle colloid cyst, pituitary apoplexy

• Posterior reversible encephalopathy syndrome (PRES)

Epidemiology

A systematic literature review reported poor population-based data to accurately identify the true incidence and prevalence of thunderclap headaches.[6] The authors determined that the only estimate of a population-based incidence is from the study of a subset of a Swedish population. The incidence is reportedly43 per 100,000 inhabitants older than 18 years annually.[7]

A population-based study in Italy showed a 0.3% lifetime prevalence of TCH in men and women aged 55to 94.[8]

TCH in the pediatric population is considered very rare, but dataare limited. In a recent retrospective study of children and adolescents aged 6to 18 years presenting to a pediatric emergency department, TCH was diagnosed in 19 out of 2290 (0.8%) of the included patients.[9]

In patients presenting with a TCH, subarachnoid hemorrhage is found in 11 to 25% and other intracranial hemorrhages in 5 and 10%.[5][10]

TCH is the presenting symptom in 20% of patients with cervical artery dissection, 2 to 16% with cerebral venous thrombosis, 15% with intracranial hypotension, and 2% with bacterial or viral meningitis.[10]

Reversible cerebral vasoconstriction syndrome (RCVS) is a group of disorders characterized by severe headaches and cerebral vasoconstriction.The most common symptom of RCVS is a sudden, intense,thunderclap headache. RCVS represents a multitude of pathologies, so the true incidence of thunderclap is unknown.

Pathophysiology

Once the etiology of secondary TCH in a patient is known, the pathophysiology of the specific condition applies. However, generally speaking, the pathophysiology of primary and secondary TCH is unclear. Evidence suggests the sympathetic nervous system plays a central role in the abnormal cerebrovascular tone causing vasoconstriction and vasospasm, leading to head pain.[11]

History and Physical

TCH is often associated with a potentially fatal etiology, such as subarachnoid hemorrhage (SAH), and is considered a medical emergency. Therefore, a rapid, focused history and physical examination are essential for evaluating a patient presenting with TCH. Patients may describe their pain as “the worst headache ever” or “worst headache of my life.”

A focused history and neurologic examination will help differentiate TCH from other headache types, narrow the secondary TCH differential diagnoses, and guide the initial testing phase. What differentiates thunderclap headaches from other types of headaches is how rapidly they reach their peak intensity, not the headache intensity itself.[5]Primary and secondary TCH diagnostic criteria are (1) severe head pain with abrupt onset, (2) pain reaching maximum intensity in less than one minute, (3) pain lasting at least5 minutes, and (4) headache not better accounted for by another ICHD-3 diagnosis.[4]

Remember that the2 most common causes of TCH are SAH and RCVS, which can be difficult to distinguish by history and physical alone when the patient presents with an isolated TCH. Asking the patient about common RCVS precipitants may be helpful. RSVS precipitants include vasoactive substances such as cannabis, cocaine, amphetamines, triptans, noradrenergic and selective serotonergic antidepressants, and nasal decongestants; eclampsia and postpartum; binge alcohol consumption; surgical manipulation causing direct vessel injury; and strenuous physical exertion, sexual activity, and Valsalva maneuvers.[10][12][13]

Multiple (2-10) excruciating, short-lived thunderclap headaches over a few days to weeks arehighly suggestive of RCVS.[5][12]

SAH usually occurs during routine activity, including rest or sleep, but can occur during physical activity.Accompanyingsymptoms may include neck pain or stiffness, photophobia, vomiting, altered mental status, and loss of consciousness. Some patients report a sentinel headache, occurring days or weeks before presentation.[14]Potential focal exam findings include the following unilateral vision loss, visuospatial neglect, and ophthalmoplegia; retinal, subhyaloid, and vitreous hemorrhage; third and sixth nerve palsy; and hemiparesis, aphasia, and abulia.[15]

The neurological examination can be categorized using the Hunt Hess scale or the World Federation of Neurological Surgeons scale.[14]

The following are signs and symptoms associated with other secondary TCH causes:

• Intracerebral hemorrhage - seizure, focal neurological deficits, altered level of consciousness

• Cervical artery dissection - neck pain, Horner syndrome, altered level of consciousness

• Cerebral venous thrombosis (CVT) - seizure, focal neurological deficits, the patient avoids lying flat

• Spontaneous intracranial hypotension (SIH) - patient avoids sitting up or standing up

• Meningitis - fever and neck stiffness

• Complicated sinusitis - fever, sinus pressure, the patient avoids lying flat

• Third ventricle colloid cyst - confusion, seizure, loss of consciousness

• Pituitary apoplexy - confusion, vision loss, diplopia, ophthalmoplegia, nausea, vomiting

• Posterior reversible encephalopathy syndrome (PRES) - seizure, focal neurological deficits, hypertension

Evaluation

The absence of associated symptoms and a normal physical examination do not exclude a serious etiology of secondary TCH.[10][16]The clinician must be cognizant of the numerous conditions that can presentas secondary TCH because many are associated with significant morbidity and mortality.

Although diagnostic algorithms vary slightly, emergent noncontrast head computed tomography (CT) is the recommended first step after the history and physical, primarily to assess for SAH.[1][5][10][16][17][16]In addition to evaluating for SAH, noncontrast head CT may demonstrate findings associated with other intracranial causes of secondary TCH. Authors of a recent clinical review propose a diagnostic algorithm that includes adding head and neck CT angiography (CTA) to the initial imaging studies if there is a concern for cervical artery dissection or RCVS.[16]

Noncontrast head CT should be performed as soon as possible. Within the first 6to 12 hours after headache onset,noncontrast head CThas a sensitivity of up to 100% for detecting SAH but decreases to 85-95% onday 2, 75% on day 3, and 50 to 60% after5 days.[1][5]Because patients presenting with a TCH may have a mass lesion, brain imaging is required before performing a lumbar puncture (LP).

Diagnosis of SAH relies on noncontrast head CT, followed by LP if the CT findings are negative and the clinical suspicion is high. In a recent study, the diagnosis of SAH was 95% sensitive and 100% specific when the Ottawa SAH rule was used when interpreting a CT scanperformed within6 hours of headache onset.[18]CTA may be considered when evaluating SAH; however, if inconclusive, digital subtraction catheter angiography (DSA) with 3-dimensional reconstruction is the gold standard study for detecting aneurysms.[19][20]

When LP is indicated, it should be performed as soon as possible after the noncontrast head CT. However, the sensitivity of the cerebrospinal fluid (CSF) analysis for detecting SAH is higher if the LP isperformed at least6 hours after symptom onset.[21]LP should include measuring the opening pressure because a high pressure may point to CVT and a low pressure to SIH.[10][16]CSF analysis should include white and red blood cell counts, protein and glucose concentrations, and visual inspection for xanthochromia.[1][5][10][16][17]When available, spectrophotometry is recommended because visual inspection for xanthochromia is associated with a high rate of false negatives. Spectrophotometry also helps to decrease false-positive interpretations.[1]Spectrophotometry has a high sensitivity for detecting SAH when the CSF is obtained between 12 hours and2 weeks following the SAH.[5][17]Other CSF studies following LP, such as testing for central nervous system infections, may also be indicated.

Suppose the noncontrast head CT and CSF analyses are nondiagnostic. In that case, further imaging studies may include contrast-enhanced brain magnetic resonance (MR) imaging, head and neck CTA, and head and neck MR angiography.[5][10]Digital subtraction angiography (DSA) may be used for definitive imaging when RCVS is strongly suspected, or the patient’s clinical condition worsens, and noninvasive methods have been unremarkable.[13]

Treatment / Management

There are only a few case reports on primary TCH treatment, and evidence supporting that TCH exists as a primary disorder is poor. Therefore, the treatment and management are focused almost exclusively on secondary TCH.[1][4]Once the diagnosis has been established, secondary TCH management should be tailored to the underlying cause.

Differential Diagnosis

According totheICHD-3, “Vasoconstrictions may not be observed in the early stage of RCVS. For this reason, probable primary thunderclap headache is not a diagnosis that should be made even temporarily.”[4]

The differential diagnosis includes other primary headache disorders and secondary TCH causes. Primary cough headache, primary exercise headache, and primary headache associated with sexual activity can all present as TCH.[4]The2 most common causes of secondary TCH are SAH and RCVS.[5]Other causes include the following intracerebral hemorrhage, subdural hematoma, cervical artery dissection, ischemic stroke, CVT, SIH, acute hypertensive crisis, intracranial infection, complicated sinusitis, intracranial tumor, third ventricle colloid cyst, pituitary apoplexy, and PRES.[4][5][10][17][22][23]

Prognosis

The differential diagnosis of secondary TCH is extensive; therefore, this section is limited to the2 most common causes, SAH and RCVS, and comments on the pediatric population.

Approximately 10 to 18% of patients with SAH die before arriving at a hospital. Mortality at one year is 35 to 65%, and 25 to 33% of survivors will suffer reduced activities of daily living, decreased quality of life, and neurological disability.[14][24][25][26]

Importantly, "reversible" in the acronym RCVS refers to reversible vasoconstriction, not necessarily signs and symptoms associated with the syndrome. For example, over half of the patients report headaches years after diagnosis.[27]Most patients with RCVS have a self-limited course lasting days to weeks, with vasoconstriction usually resolving within3 months. Overall, the long-term clinical outcomesassociated with RCVS are excellent in over 90% of patients.[28][29]

In a recent United States population study, patient factors independently associated with a poor outcome or death in patients with RCVS were advanced age, female sex, intracerebral hemorrhage, ischemic stroke, seizure disorder, reversible brain edema, atrial fibrillation, and chronic kidney disease.[30]Glucocorticoid exposure may also contribute to worsening RCVS outcomes.[28]

As mentioned previously, TCH in the pediatric population is very rare. In a 3-year retrospective study of children and adolescents aged 6to 18 years, all patients diagnosed with TCH had a benign course.[9]

Complications

The complications associated with secondary TCH depend on the attributable cause. Secondary brain injury can occur in SAH due to intracerebral hemorrhage, intraventricular hemorrhage, intracranial pressure, hydrocephalus, subdural hematoma, or delayed cerebral ischemia. Medical complications are common and significantly impact outcomes. Reported complications include pyrexia, sepsis, aspiration pneumonia, cardiac dysfunction, anemia, hyponatremia, hyperglycemia, and deep venous thrombosis.[14][31]

Although one- to two-thirds of patients with RCVS develop ischemic or hemorrhagic brain lesions (or both), most achieve functional recovery and independence. Overall, the long-term recurrence rate of RCVS is low, and the relapse is typically benign.[27][28]However, anxiety or depression may be associated with decreased quality of life.[27]

Deterrence and Patient Education

Due to the lengthy differential diagnosis for secondary TCH and the heterogeneity of causes for each potential diagnosis, deterrence and patient education fall in the domain of each diagnosis. Several of the common causes are neurovascular. Selected patients should be educated on modifiable risk factors associated with vascular diseases, including physical inactivity, dyslipidemia, diet and nutrition, hypertension, obesity, diabetes mellitus, and cigarette smoking.

Several groups of people have been identified that may benefit from aneurysmal SAH screening. Individuals with2 or more affected first-degree relatives with aneurysmal SAH and those with autosomal dominant polycystic kidney disease are candidates for intracranial aneurysm screening. Patient counseling before ordering imaging is essential to allow patients to make an informed decision on whether or not screening is appropriate for them.[32]

Enhancing Healthcare Team Outcomes

Managing patients presenting with TCH requires an interprofessional team of clinicians, including physicians, physician assistants, nurses, nurse practitioners, pharmacists, and ancillary staff. Thespecialists involved will vary depending on the underlying cause, but medical teams commonly include emergency medicine clinicians, neurologists, radiologists, pharmacists, critical care specialists, and neurosurgeons. Thecare of patients with TCH may not end in the emergency department. Effective communication during the handoff between emergency and inpatient teams is essential. Planning and coordinationamong teams of professionals involved in patient care arecritical for favorable healthcare outcomes and require open communication channelsamong all team members.[33][Level 1]

While clinicians, particularly specialists, will direct the overall management course, other interprofessional team members must make significant contributions because treatment regimens vary widely based on the underlying cause.Nurses play a valuable role in coordinating activitiesamong the various clinicians on the case, ensuring the patient is informed about the latest developments. They will also assist in evaluating the patient and providing patient counsel. If medicationtherapy isa central aspect of case management, pharmacists must provide patient medication counseling, coordinate with prescribing clinicians, perform medication reconciliation, report any concerns to the rest of the team, and serve as the subject matter expert for pharmacotherapy. All professionals in patient care must maintain accurate and updated notes, documenting each interaction with the patient and intervention. Current patient data are necessary and must be accessible to assist the interprofessional team in their decision-making processes. This interprofessional paradigm will result in the best patient outcomes with the fewest adverse events. [Level 5]

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References

1.

Ferrante E, Tassorelli C, Rossi P, Lisotto C, Nappi G. Focus on the management of thunderclap headache: from nosography to treatment. J Headache Pain. 2011 Apr;12(2):251-8. [PMC free article: PMC3072477] [PubMed: 21331755]

2.

Ravishankar K. Looking at "thunderclap headache" differently? Circa 2016. Ann Indian Acad Neurol. 2016 Jul-Sep;19(3):295-301. [PMC free article: PMC4980948] [PubMed: 27570377]

3.

Day JW, Raskin NH. Thunderclap headache: symptom of unruptured cerebral aneurysm. Lancet. 1986 Nov 29;2(8518):1247-8. [PubMed: 2878133]

4.

Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition. Cephalalgia. 2018 Jan;38(1):1-211. [PubMed: 29368949]

5.

Schwedt TJ. Thunderclap Headache. Continuum (Minneap Minn). 2015 Aug;21(4 Headache):1058-71. [PubMed: 26252591]

6.

Devenney E, Neale H, Forbes RB. A systematic review of causes of sudden and severe headache (Thunderclap Headache): should lists be evidence based? J Headache Pain. 2014 Aug 14;15(1):49. [PMC free article: PMC4231167] [PubMed: 25123846]

7.

Landtblom AM, Fridriksson S, Boivie J, Hillman J, Johansson G, Johansson I. Sudden onset headache: a prospective study of features, incidence and causes. Cephalalgia. 2002 Jun;22(5):354-60. [PubMed: 12110111]

8.

Schwaiger J, Kiechl S, Seppi K, Sawires M, Stockner H, Erlacher T, Mairhofer ML, Niederkofler H, Rungger G, Gasperi A, Poewe W, Willeit J. Prevalence of primary headaches and cranial neuralgias in men and women aged 55-94 years (Bruneck Study). Cephalalgia. 2009 Feb;29(2):179-87. [PubMed: 18823362]

9.

Levinsky Y, Waisman Y, Eidlitz-Markus T. Severe abrupt (thunderclap) non-traumatic headache at the pediatric emergency department - a retrospective study. Cephalalgia. 2021 Oct;41(11-12):1172-1180. [PubMed: 33982624]

10.

Ducros A, Bousser MG. Thunderclap headache. BMJ. 2013 Jan 08;346:e8557. [PubMed: 23303883]

11.

Agostoni E, Rigamonti A, Aliprandi A. Thunderclap headache and benign angiopathy of the central nervous system: a common pathogenetic basis. Neurol Sci. 2011 May;32 Suppl 1:S55-9. [PubMed: 21533714]

12.

Ducros A, Wolff V. The Typical Thunderclap Headache of Reversible Cerebral Vasoconstriction Syndrome and its Various Triggers. Headache. 2016 Apr;56(4):657-73. [PubMed: 27015869]

13.

Burton TM, Bushnell CD. Reversible Cerebral Vasoconstriction Syndrome. Stroke. 2019 Aug;50(8):2253-2258. [PubMed: 31272323]

14.

Claassen J, Park S. Spontaneous subarachnoid haemorrhage. Lancet. 2022 Sep 10;400(10355):846-862. [PMC free article: PMC9987649] [PubMed: 35985353]

15.

Suarez JI. Diagnosis and Management of Subarachnoid Hemorrhage. Continuum (Minneap Minn). 2015 Oct;21(5 Neurocritical Care):1263-87. [PubMed: 26426230]

16.

Long D, Koyfman A, Long B. The Thunderclap Headache: Approach and Management in the Emergency Department. J Emerg Med. 2019 Jun;56(6):633-641. [PubMed: 30879843]

17.

Ju YE, Schwedt TJ. Abrupt-onset severe headaches. Semin Neurol. 2010 Apr;30(2):192-200. [PMC free article: PMC3558726] [PubMed: 20352589]

18.

Perry JJ, Sivilotti MLA, Émond M, Hohl CM, Khan M, Lesiuk H, Abdulaziz K, Wells GA, Stiell IG. Prospective Implementation of the Ottawa Subarachnoid Hemorrhage Rule and 6-Hour Computed Tomography Rule. Stroke. 2020 Feb;51(2):424-430. [PubMed: 31805846]

19.

Cho WS, Kim JE, Park SQ, Ko JK, Kim DW, Park JC, Yeon JY, Chung SY, Chung J, Joo SP, Hwang G, Kim DY, Chang WH, Choi KS, Lee SH, Sheen SH, Kang HS, Kim BM, Bae HJ, Oh CW, Park HS., Quality Control Committees from the Korean Society of Cerebrovascular Surgeons. Society of Korean Endovascular Neurosurgeons. Korean Society of Interventional Neuroradiology. Korean Stroke Society and Korean Academy of Rehabilitation Medicine. Korean Clinical Practice Guidelines for Aneurysmal Subarachnoid Hemorrhage. J Korean Neurosurg Soc. 2018 Mar;61(2):127-166. [PMC free article: PMC5853198] [PubMed: 29526058]

20.

Connolly ES, Rabinstein AA, Carhuapoma JR, Derdeyn CP, Dion J, Higashida RT, Hoh BL, Kirkness CJ, Naidech AM, Ogilvy CS, Patel AB, Thompson BG, Vespa P., American Heart Association Stroke Council. Council on Cardiovascular Radiology and Intervention. Council on Cardiovascular Nursing. Council on Cardiovascular Surgery and Anesthesia. Council on Clinical Cardiology. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. Stroke. 2012 Jun;43(6):1711-37. [PubMed: 22556195]

21.

van Gijn J, Rinkel GJ. Subarachnoid haemorrhage: diagnosis, causes and management. Brain. 2001 Feb;124(Pt 2):249-78. [PubMed: 11157554]

22.

Guryildirim M, Kontzialis M, Ozen M, Kocak M. Acute Headache in the Emergency Setting. Radiographics. 2019 Oct;39(6):1739-1759. [PubMed: 31589569]

23.

Bahra A. Other primary headaches-thunderclap-, cough-, exertional-, and sexual headache. J Neurol. 2020 May;267(5):1554-1566. [PMC free article: PMC7184054] [PubMed: 32130497]

24.

Martin CO, Rymer MM. Hemorrhagic stroke: aneurysmal subarachnoid hemorrhage. Mo Med. 2011 Mar-Apr;108(2):124-7. [PMC free article: PMC6189155] [PubMed: 21568235]

25.

Steiner T, Juvela S, Unterberg A, Jung C, Forsting M, Rinkel G., European Stroke Organization. European Stroke Organization guidelines for the management of intracranial aneurysms and subarachnoid haemorrhage. Cerebrovasc Dis. 2013;35(2):93-112. [PubMed: 23406828]

26.

Lindbohm JV, Kaprio J, Jousilahti P, Salomaa V, Korja M. Risk Factors of Sudden Death From Subarachnoid Hemorrhage. Stroke. 2017 Sep;48(9):2399-2404. [PubMed: 28739833]

27.

John S, Singhal AB, Calabrese L, Uchino K, Hammad T, Tepper S, Stillman M, Mills B, Thankachan T, Hajj-Ali RA. Long-term outcomes after reversible cerebral vasoconstriction syndrome. Cephalalgia. 2016 Apr;36(4):387-94. [PubMed: 26088331]

28.

Singhal AB, Topcuoglu MA. Glucocorticoid-associated worsening in reversible cerebral vasoconstriction syndrome. Neurology. 2017 Jan 17;88(3):228-236. [PMC free article: PMC5272793] [PubMed: 27940651]

29.

Boitet R, de Gaalon S, Duflos C, Marin G, Mawet J, Burcin C, Roos C, Fiedler U, Bousser MG, Ducros A. Long-Term Outcomes After Reversible Cerebral Vasoconstriction Syndrome. Stroke. 2020 Feb;51(2):670-673. [PubMed: 31842705]

30.

Patel SD, Topiwala K, Otite Oliver F, Saber H, Panza G, Mui G, Liebeskind DS, Saver JL, Alberts M, Ducros A. Outcomes Among Patients With Reversible Cerebral Vasoconstriction Syndrome: A Nationwide United States Analysis. Stroke. 2021 Dec;52(12):3970-3977. [PubMed: 34470494]

31.

Hammer A, Ranaie G, Erbguth F, Hohenhaus M, Wenzl M, Killer-Oberpfalzer M, Steiner HH, Janssen H. Impact of Complications and Comorbidities on the Intensive Care Length of Stay after Aneurysmal Subarachnoid Haemorrhage. Sci Rep. 2020 Apr 10;10(1):6228. [PMC free article: PMC7148333] [PubMed: 32277142]

32.

Rinkel GJ, Ruigrok YM. Preventive screening for intracranial aneurysms. Int J Stroke. 2022 Jan;17(1):30-36. [PMC free article: PMC8739572] [PubMed: 34042530]

33.

Allen D, Gillen E, Rixson L. The Effectiveness of Integrated Care Pathways for Adults and Children in Health Care Settings: A Systematic Review. JBI Libr Syst Rev. 2009;7(3):80-129. [PubMed: 27820426]

Disclosure: Sandeep Sekhon declares no relevant financial relationships with ineligible companies.

Disclosure: Roopa Sharma declares no relevant financial relationships with ineligible companies.

Disclosure: Marco Cascella declares no relevant financial relationships with ineligible companies.