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X
- •Foreword
- •Contents
- •1.1 Introduction
- •1.2 Pathophysiology
- •1.3 Case Presentation
- •1.4 Case Discussion
- •1.5 Clinical Characteristics
- •1.6 Diagnostic Algorithm
- •1.8 Management
- •1.9 Conclusion
- •References
- •2.1 Introduction
- •2.2 Pathophysiology
- •2.3 Case Presentation
- •2.4 Case Discussion
- •2.5 Clinical Characteristics
- •1.7 Differential Diagnosis
- •2.6 Diagnostic Algorithm
- •2.7 Management
- •2.8 Conclusion
- •References
- •3.1 Introduction
- •3.2 Pathophysiology
- •3.3 Case Presentation
- •3.4 Case Discussion
- •3.5 Clinical Characteristics
- •3.6 Diagnostic Algorithm
- •3.7 Management
- •3.8 Conclusion
- •References
- •4.1 Introduction
- •4.2 Pathophysiology
- •4.3 Case Presentation
- •4.4 Case Discussion
- •4.6 Diagnostic Algorithm
- •4.7 Management
- •4.8 Conclusion
- •References
- •5.1 Introduction
- •5.2 Pathophysiology
- •5.3 Case Presentation
- •5.4 Case Discussion
- •5.5 Diagnostic Algorithm
- •5.6 Management
- •5.7 Conclusion
- •References
- •6.1 Introduction
- •6.2 Pathogenesis
- •6.3 Case Presentation
- •6.4 Case Discussion
- •6.5 Diagnostic Algorithm
- •6.6 Management
- •6.7 Conclusion
- •References
- •7.1 Introduction
- •7.2 Pathophysiology
- •7.3 Case Presentation
- •7.5 Differential Diagnosis
- •7.7 The Following Strategies Are Essential
- •7.7.1 Acute Symptom Relief
- •7.7.1.1 Pharmacological Treatment
- •7.7.2.1 Pharmacologic Prophylaxis
- •7.8 Conclusion
- •References
- •8.1 Introduction
- •8.3 Case Study
- •8.4 Case Discussion
- •8.5 Clinical Management
- •8.7 Diagnosis
- •8.8 Treatment
- •8.9 Conclusion
- •References
- •9.1 Introduction
- •9.2 Case Presentation
- •9.4 Diagnosis Algorithm
- •9.5 Secondary SUNCT
- •9.6 Management
- •9.8 Conclusion
- •References
- •10.1 Introduction
- •10.2 Pathophysiology
- •10.3 Case Presentation
- •10.4 Case Discussion
- •10.5 Clinical Characteristics
- •10.6 Diagnostic Algorithm
- •10.7 Management
- •10.8 Conclusion
- •References
- •11.1 Introduction
- •11.2 Pathophysiology
- •11.3 Case Presentation
- •11.4 Case Discussion
- •11.5 Clinical Characteristics
- •11.6 Diagnostic Algorithm
- •11.6.1 Step 1: Detailed Patient History
- •11.8 Management
- •11.9 Conclusions
- •12.2 Pathophysiology
- •12.3 Case Presentation
- •12.4 Case Discussion
- •12.6 Treatment
- •12.7 Conclusion
- •References
- •References
- •12.1 Introduction
- •13.1 Introduction
- •13.2 Pathophysiology
- •13.3 Case Presentation
- •13.4 Case Discussion
- •13.5 Clinical Characteristics
- •13.6 Diagnostic Algorithm
- •13.7 Management
- •13.8 Conclusion
- •References
- •14.1 Introduction
- •14.2 Pathophysiology
- •14.3 Case Presentation
- •14.3.1 Clinical Case 1
- •14.3.2 Clinical Case 2
- •14.4 Case Discussion
- •14.5 Clinical Characteristics
- •14.7 Treatment/Management
- •14.8 Conclusion
- •References
- •15.1 Introduction
- •15.2 Case Presentation
- •15.3 Case Discussion
- •15.4 Diagnostic Algorithm
- •15.5 Pathophysiology
- •15.6 Clinical Presentation
- •15.6.1 External-Compression Headache (ECH)
- •15.6.2 External-Traction Headache (ETH)
- •15.7 Management
- •15.7.1 Nonpharmacological Strategies
- •15.7.2 Pharmacological Strategies
- •15.7.3 Patient Education and Awareness
- •15.8 Conclusion
- •References
- •16.1 Introduction
- •16.2 Pathophysiology
- •16.3 Case Presentation
- •16.4 Case Discussion
- •16.6 Diagnostic Algorithm
- •16.7 Management
- •16.8 Conclusion
- •References
- •17.1 Introduction
- •17.2 Pathophysiology
- •17.3 Case Presentation
- •17.4 Case Discussion
- •17.5 Clinical Characteristics
- •17.6 Diagnosis
- •17.7 Differential Diagnosis
- •17.8 Treatment
- •17.9 Conclusion
- •References
- •18.1 Introduction
- •18.2 Pathophysiology
- •18.3 Case Presentation
- •18.4 Case Discussion
- •18.5 Clinical Presentation
- •18.6 Diagnosis
- •18.7 Differential Diagnosis
- •18.8 Treatment
- •18.9 Conclusion
- •References
- •19.1 Introduction
- •19.2 Pathophysiology
- •19.3 Case Presentation
- •19.4 Case Discussion
- •19.5 Diagnostic Approach
- •19.6 Management
- •19.7 Conclusion
- •References
- •20.1 Introduction
- •20.3 Case Report
- •20.4 Case Discussion
- •20.6 Clinical Presentation
- •20.7 Diagnostic Algorithm
- •20.8 Conclusion
- •References
- •21.1 Introduction
- •21.2 Case Presentation
- •21.3 Clinical Characteristics
- •21.4 Diagnosis
- •21.5 Treatment
- •References
- •22.1 Introduction
- •22.3 Case Presentation 1
- •22.4 Case Discussion
- •22.5 Case Presentation 2
- •22.6 Case Discussion 2
- •22.7 Clinical Characteristics
- •22.8 Diagnostic Workup
- •22.9 Treatment
- •22.10 Prognosis
- •References
- •23.1 Introduction
- •23.2 Pathophysiology
- •23.3 Case Presentation
- •23.4 Case Discussion
- •23.6 Diagnostic Algorithm
- •23.7 Management
- •23.8 Conclusion
- •References
- •24.1 Introduction
- •24.2 Case Presentation
- •24.3 Case Discussion
- •24.4 Pathophysiology
- •24.6 Clinical Characteristics
- •24.8 Treatment Approaches
- •24.10 Conclusion
- •References
- •25.1 Introduction
- •25.2 Case Presentation
- •25.3 Case Discussion
- •25.4 Conclusion
- •References
- •26.1 Introduction
- •26.2 Pathophysiology
- •26.3 Case Presentation
- •26.4 Case Discussion
- •26.5 Clinical Characteristics
- •26.6 Diagnostic Algorithm
- •26.7 Management
- •26.8 Conclusion
- •References
- •27.1 Introduction
- •27.2 Case Presentations
- •27.3 Clinical Characteristics
- •27.4 Discussion
- •27.5 Conclusion
- •References
- •28.1 Introduction
- •28.2 Case Presentation
- •28.3 Case Discussion
- •28.4 Clinical Characteristics
- •28.5 Diagnosis
- •28.6 Conclusion
- •28.7 Key Messages
- •References
- •29.1 Introduction
- •29.2 Pathophysiology
- •29.3 Case Presentation
- •29.4 Clinical Presentation
- •29.5 Diagnosis
- •29.6 Treatment
- •29.7 Conclusion
- •References
- •30.1 Introduction
- •30.2 Clinical Case
- •30.3 Clinical Presentation
- •30.4 Differential Diagnosis
- •30.5 Diagnosis
- •30.6 Treatment
- •30.7 Conclusion
- •References
- •31.1 Introduction
- •31.2 Pathophysiology
- •31.3 Case Presentation
- •31.4 Case Discussion
- •31.5 Clinical Presentation
- •31.7 Conclusion
- •References
- •32.1 Introduction
- •32.2 Pathophysiology
- •32.3 Case Presentation
- •32.4 Case Discussion
- •32.6 Diagnosis
- •32.7 Additional Diagnostic Evaluations
- •32.8 Apply ICHD-3 Diagnostic Criteria [9]
- •32.10 Management
- •32.11 Conclusion
- •References
- •33.1 Introduction
- •33.2 Pathophysiology
- •33.3 Case Presentation
- •33.4 Clinical Characteristics
- •33.5 Diagnostic Algorithm
- •33.6 Treatment
- •33.7 Conclusion
- •References
- •34.1 Introduction
- •34.2 Pathophysiology
- •34.3 Case Presentation
- •34.4 Case Discussion
- •34.6 Diagnostic Algorithm
- •34.7 Treatment
- •34.8 Conclusion
- •References
- •35.1 Introduction
- •35.3 Case Presentation
- •35.4 Case Discussion
- •35.7 Treatment
- •35.7.1 Oxygen Therapy (100% Oxygen)
- •35.8 Conclusion
- •References
- •36.1 Introduction
- •36.2 Pathophysiology
- •36.3 Case Presentation
- •36.5 Diagnostic Algorithm
- •36.6 Treatment
- •36.7 Conclusion
- •References
- •37.1 Introduction
- •37.2 Pathophysiology
- •37.3 Case Presentation
- •37.4 Headache Characteristics
- •37.5 Case Discussion
- •37.6 Treatment
- •37.7 Conclusion
- •References
- •38.1 Introduction
- •38.2 Pathophysiology
- •38.3 Case Presentation
- •38.4 Clinical Presentation
- •38.5 Diagnostic Algorithm
- •38.6 Treatment
- •38.7 Conclusion
- •References
- •39.1 Introduction
- •39.3 Case Presentation
- •39.4 Case Discussion
- •39.6 ICHD-3 Diagnostic Criteria [28]
- •39.6.1 Diagnostic Criteria
- •39.7 Diagnostic Algorithm
- •39.9 Conclusion
- •References
- •40.1 Introduction
- •40.3 Case Presentation
- •40.4 Case Discussion
- •40.5.1 Diagnostic Algorithm
- •40.6 Treatment
- •40.7 Conclusion
- •References
- •41.1 Introduction
- •41.3 Case Presentation
- •41.4 Clinical Presentation
- •41.5 Differential Diagnosis
- •41.6 Conclusion
- •41.7 Key Messages
- •References
- •42.1 Introduction
- •42.2 Pathophysiology
- •42.3 Case Presentation
- •42.5 Case Discussion
- •42.6 Clinical Presentation
- •42.7 Diagnostic Algorithm [9]
- •42.8 Preeclampsia
- •42.9 Eclampsia
- •42.10 Fetal Assessment
- •42.11 Treatment
- •42.12 Antihypertensive Management [8]
- •42.14 Conclusion
- •References
- •43.1 Introduction
- •43.2 Pathophysiology
- •43.3 Case Presentation
- •43.4 Case Discussion
- •43.5 Clinical Manifestations
- •43.6 Diagnosis
- •43.7 Treatment
- •43.8 Conclusion
- •References
- •44.1 Introduction
- •44.2 Pathophysiology
- •44.3 Case Presentation
- •44.4 Case Discussion
- •44.6 Diagnostic Approach
- •44.7 Management
- •44.8 Conclusion
- •References
- •45.1 Introduction
- •45.2 Pathophysiology
- •45.3 Case Presentation
- •45.6 Treatment
- •45.7 Conclusion
- •References
- •46.1 Introduction
- •46.2 Pathophysiology
- •46.3 Case Presentation
- •46.4 Clinical Characteristics
- •46.5 Differential Diagnosis
- •46.6 Treatment
- •46.7 Conclusion
- •References
- •47.1 Introduction
- •47.2 Pathophysiology
- •47.3 Case Presentation
- •47.4 Case Discussion
- •47.5 Clinical Presentations
- •47.6 Diagnostic Algorithm
- •47.7 Differential Diagnosis
- •47.8 Treatment
- •47.9 Conclusion
- •References
- •48.1 Introduction
- •48.2 Pathophysiology
- •48.3 Case Presentation
- •48.4 Case Discussion
- •48.5 Clinical Characteristics
- •48.7 Treatment
- •48.8 Conclusion
- •References
- •49.1 Introduction
- •49.2 Pathophysiology
- •49.3 Case Presentation
- •49.4 Clinical Presentation
- •49.5 Diagnosis
- •49.6 Treatment
- •49.7 Conclusion
- •References
- •50.1 Introduction
- •50.2 Pathophysiology
- •50.3 Case Presentation
- •50.4 Case Discussion
- •50.5 Clinical Characteristics
- •50.6 Diagnosis
- •50.7 Treatment
- •50.8 Conclusion
- •References
- •51.1 Introduction
- •51.2 Case Presentation
- •51.3 Clinical Characteristics
- •51.4 Diagnosis
- •51.5 Treatment
- •51.6 Conclusion
- •References
- •52.1 Introduction
- •52.2 Pathophysiology
- •52.3 Case Presentation
- •52.4 Case Discussion
- •52.5 Clinical Characteristics
- •52.6 Diagnosis
- •52.6.1 Cervicogenic Headache
- •52.6.2 Migraine
- •52.6.3 Neck Pain
- •52.6.4 Demyelinating Lesions
- •52.6.5 Cervical Myelitis
- •52.6.6 Occipital Allodynia
- •52.6.7 Cervical Muscle Spasms
- •52.7 Treatment
- •52.7.2 Acupuncture
- •52.7.3 Transcutaneous Electrical Nerve Stimulations (TENS)
- •52.8 Minimally Invasive Treatment
- •52.8.1 Nerve Blocks
- •52.8.2 Botulinum Toxin A
- •52.8.3 Radio Frequency
- •52.8.4 Occipital Nerve Stimulation
- •52.9 Surgical Treatments
- •52.10 Conclusions
- •References
- •53.1 Introduction
- •53.2 Pathophysiology
- •53.3 Characteristics of Pain
- •53.4 Case Presentation
- •53.5 Case Discussion
- •53.6 Clinical Characteristics
- •53.8 Treatment
- •53.9 Conclusion
- •References
- •54.1 Introduction
- •54.2 Pathophysiology
- •54.3 Case Presentation
- •54.4 Case Discussion
- •54.5 Clinical Characteristics
- •54.6 Diagnostic Algorithm
- •54.7 Management
- •54.8 Conclusion
- •References
- •55.1 Introduction
- •55.2 Pathophysiology
- •55.3 Case Presentation

384
C. I. Deligianni and T. Mavridis
40.6 Treatment
The treatment of headache in pheochromocytoma is focused on controlling the
underlying cause—excess catecholamine secretion—and managing the associated
hypertension. Several therapeutic strategies are employed:
1. Antihypertensive therapy: α-blockers, such as phenoxybenzamine, are used to
control hypertension and prevent the vasoconstrictive effects of excessive catecholamines. These medications also help alleviate headaches by reducing blood
pressure uctuations.
2. Heart rate: β-blockers (e.g., propranolol) can be added to control tachycardia and
reduce the adrenergic stimulation that contributes to the headache. Nevertheless,
β-blockers should never be started before α-blockers, as unopposed alphaadrenergic stimulation may worsen the hypertensive crisis.
3. Surgical resection: The denitive treatment for pheochromocytoma is surgical
resection of the tumor, which leads to normalization of catecholamine levels
and, therefore, most patients experience resolution of symptoms, including
headaches.
4. Management of hypertensive crises: Intravenous medications such as nitroprus-
side or labetalol may be used to control acute blood pressure elevations, which
can also lead to headache relief if present.
40.7 Conclusion
Headache is a common but often overlooked symptom in patients with pheochromocytoma, and it is essential to consider this diagnosis in patients presenting with
unexplained headache, primarily when associated with other systemic symptoms
such as hypertension, palpitations, and sweating. Clinical suspicion leads to early
diagnosis and treatment, which are crucial for preventing complications and improving outcomes. Physicians must be vigilant when evaluating prolonged headaches in
the emergency setting. Medical management, including alpha and beta blockade,
followed by surgical resection of the tumor, remains the cornerstone of treatment.
Prompt recognition and appropriate intervention can provide signicant relief from
the debilitating symptoms associated with this rare but signicant condition.
References
1. Anyfanti P, Mastrogiannis Κ, Lazaridis Α, Tasios Κ, Vasilakou D, Kyriazidou Α, Aroutsidis
F, Pavlidou O, Papoutsopoulou Ε, Tiritidou A, Kotsis V, Triantafyllou Α, Zaris Ι, Douma S,
Gkaliagkousi Ε. Clinical presentation and diagnostic evaluation of pheochromocytoma: case
series and literature review. Clin Exp Hypertens. 2023;45(1):2132012. https://doi.org/10.108
0/10641963.2022.2132012.

40 Headache Attributed toPheochromocytoma
2. Farrugia FA, Martikos G, Tzanetis P, Charalampopoulos A, Misiakos E, Zavras N, Sotiropoulos
D. Pheochromocytoma, diagnosis and treatment: review of the literature. Endocr Regul.
2017;51(3):168–81.
3. Gupta PK, Marwaha B. Pheochromocytoma. [Updated 2024 Nov 7]. In: StatPearls [Internet].
Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.
nih.gov/books/NBK589700/.
4. Ghanizada H, Al-Karagholi MA, Arngrim N, Mørch-Rasmussen M, Walker CS, Hay DL,
Ashina M. Effect of adrenomedullin on migraine-like attacks in patients with migraine: a
randomized crossover study. Neurology. 2021;96(20):e2488–99. https://doi.org/10.1212/
WNL.0000000000011930. Epub 2021 Apr 7. PMID: 33827963.
5. D'Andrea G, D'Arrigo A, Dalle Carbonare M, Leon A. Pathogenesis of migraine:
role of neuromodulators. Headache. 2012;52(7):1155–63. https://doi.org/10.1111/
j.1526- 4610.2012.02168.x. Epub 2012 Jun 1. PMID: 22671857.
6. Leonard JB, Munir KM, Kim HK.Metoclopramide induced pheochromocytoma crisis. Am J
Emerg Med. 2018;36(6):1124.e1–2.
7. Neumann HPH, Young WF Jr, Eng C.Pheochromocytoma and Paraganglioma. N Engl J Med.
2019;381(6):552–65.
8. The International Classication of Headache Disorders, 3rd edition. Cephalalgia.
2018;38(1):1–211. Jes Olesen ISSN: 0333-1024.
9. Do TP, Remmers A, Schytz HW, Schankin C, Nelson SE, Obermann M, Hansen JM, Sinclair
AJ, Gantenbein AR, Schoonman GG. Red and orange ags for secondary headaches in
clinical practice: SNNOOP10 list. Neurology. 2019;92(3):134–44. https://doi.org/10.1212/
WNL.0000000000006697.
10. Bravo EL, Gifford RW Jr. Pheochromocytoma. Endocrinol Metab Clin N Am.
1993;22(2):329–41.
11. Manger WM, Gifford RW. Pheochromocytoma. J Clin Hypertens (Greenwich).
2002;4(1):62–72.
12. Bravo EL.Pheochromocytoma: new concepts and future trends. Kidney Int. 1991;40(3):544–56.
13. Nehs MA, Ruan DT.Minimally invasive adrenal surgery: an update. Curr Opin Endocrinol
Diabetes Obes. 2011;18(3):193–7.
14. Ando Y, Ono Y, Sano A, Fujita N, Ono S, Tanaka Y.Clinical characteristics and outcomes
of pheochromocytoma crisis: a literature review of 200 cases. J Endocrinol Investig.
2022;45(12):2313–28.
PMID: 35857218.
15. Schwedt TJ. Thunderclap Headache. Continuum (Minneap Minn). 2015;21(4
Headache):1058–71. https://doi.org/10.1212/CON.0000000000000201. PMID: 26252591.
16. Patel D, Phay JE, Yen TWF, Dickson PV, Wang TS, Garcia R, Yang AD, Solórzano CC, Kim
LT.Update on pheochromocytoma and paraganglioma from the SSO endocrine/head and neck
disease-site work group. Part 1 of 2: advances in pathogenesis and diagnosis of pheochromocytoma and paraganglioma. Ann Surg Oncol. 2020;27(5):1329–37. https://doi.org/10.1245/
s10434- 020- 08220- 3. Epub 2020 Feb 28. PMID: 32112212; PMCID: PMC8655649.
17. Taïeb D, Timmers HJ, Hindié E, Guillet BA, Neumann HP, Walz MK, Opocher G, de Herder
WW, Boedeker CC, de Krijger RR, Chiti A, Al-Nahhas A, Pacak K, Rubello D, European
Association of Nuclear Medicine. EANM 2012 guidelines for radionuclide imaging of phaeochromocytoma and paraganglioma. Eur J Nucl Med Mol Imaging. 2012;39(12):1977–95.
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PMC4714772.
https://doi.org/10.1515/enr- 2017- 0018.
https://doi.org/10.1007/s40618- 022- 01868- 6. Epub 2022 Jul 20.
385

Chapter 41
Headache Attributed toHypertensive
Encephalopathy
MarioFernandoPrietoPeres
41.1 Introduction
Headaches are one of the most common symptoms seen in emergency departments.
However, when associated with an acute rise in blood pressure and neurological
changes, it can signal a life-threatening condition called hypertensive encephalopathy. This syndrome is characterised by a breakdown in cerebral autoregulation leading to vasogenic oedema and, if not recognised promptly, can lead to seizures, coma
or death [1, 2].
Within the spectrum of hypertensive crises, hypertensive encephalopathy stands
out because of its complex clinical-radiological overlap with other neurological
emergencies. It can present with acute or subacute onset of headache, visual disturbances, altered mental status and even focal neurological decits—features that
often mimic stroke, pre-eclampsia/eclampsia or cerebral venous thrombosis [3, 4].
The most recognised radiological correlate is posterior reversible encephalopathy
syndrome (PRES), which is associated with reversible vasogenic oedema, predominantly in the parieto-occipital lobes [5–7]. However, PRES represents only one
aspect of the spectrum of hypertensive encephalopathy and should not be considered synonymous with it [8, 9].
Clinical diagnosis is further challenged by the broad differential diagnosis, particularly in special populations such as pregnant women, where the distinction
between hypertensive encephalopathy, eclampsia and migraine with aura may be
blurred [10, 11]. In addition, unusual imaging patterns—including brainstem,
M. F. P. Peres (*)
Elect International Headache Society, Institute of Psychiatry, University of Sao Paulo,
Sao Paulo, Brazil
Hospital Israelita Albert Einstein, Sao Paulo, Brazil
Switzerland AG 2026
D. Uludüz et al. (eds.), Rare Causes of Headache Disorders, Headache,
https://doi.org/10.1007/978-3-032-10242-3_41
387© The Author(s), under exclusive license to Springer Nature

388
M. F. P. Peres
cerebellar, spinal cord and frontal lobe involvement—may be seen in hypertensive
encephalopathy, which may delay diagnosis [12–14].
Emerging evidence also suggests that reversible cerebral vasoconstriction syndrome (RCVS) may coexist with or mimic hypertensive encephalopathy, especially
when it presents with thunderclap headache and dynamic vascular changes on magnetic resonance (MR) angiography [15–17].
This chapter focuses on headaches attributed to hypertensive encephalopathy,
illustrated through a representative clinical case involving a third-trimester pregnant
woman with hypertensive crisis and radiological features of PRES.Beyond the classical narrative, we will explore atypical imaging patterns, potential overlaps with
RCVS and diagnostic dilemmas in differential diagnosis, particularly in pregnancyrelated hypertensive states. We will also provide practical clinical guidance on neuroimaging, ophthalmological signs and management strategies to prevent irreversible
neurological damage.
41.2 Pathophysiology (Fig.41.1)
Hypertensive encephalopathy is a neurologic emergency that lies on the spectrum of
hypertensive crises. Its pathophysiology is primarily attributed to the failure of cerebral autoregulation under acute, severe blood pressure elevations. This leads to a
Fig. 41.1 Pathophysiological mechanism of headache in hypertensive encephalopathy. (This g-
ure was created on the Biorender)

41 Headache Attributed toHypertensive Encephalopathy
389
hyperperfusion state, endothelial dysfunction and leakage of plasma and proteins
into the interstitial space, resulting in vasogenic oedema, most prominent in posterior brain regions due to their relatively sparse sympathetic innervation [5, 7]. While
posterior reversible encephalopathy syndrome (PRES) is the most widely recognised neuroimaging pattern of this process, not all hypertensive encephalopathy
cases meet the PRES criteria. Conversely, not all cases of PRES are of hypertensive
origin [6, 8].
41.3 Case Presentation
Zeynep, a 42-year-old woman in her 32nd week of pregnancy with her third child,
presented to the emergency department with a sudden and intensely distressing
headache that had started approximately 2 hours prior. She described the onset as
abrupt and explosive, ‘as if something burst inside my head’, with immediate full
intensity. The pain was primarily located at the occipital region, radiating upward
and forward toward the vertex and bilateral temples. She noted that it throbbed and
pulsed with each heartbeat, but with periods where it felt like a tightening band
pressing against her skull.
She rated the headache intensity as 9 out of 10, unresponsive to rest or the
paracetamol she had taken at home. Unlike previous mild, tension-type headaches
during her earlier pregnancies, this episode was profoundly different in both quality
and severity. Associated symptoms included nausea, phonophobia and dizziness,
particularly when changing positions. She also reported neck stiffness and a feeling
of restlessness, frequently shifting in bed and unable to nd relief. She denied fever,
trauma or preceding aura symptoms. While visual blurring and ashing lights were
present, she was more troubled by a heavy, internal head pressure and a sense of
‘mental fog’ that made it difcult to concentrate or respond promptly to questions.
She had no prior history of hypertension or migraines but had missed several
prenatal follow-ups. Her two previous pregnancies were uncomplicated.
On examination, she was hypertensive with a blood pressure of 210/120mmHg
and mildly confused. Neurologically, she had brisk deep tendon reexes and bilateral ankle clonus. An ophthalmological bedside exam revealed mild bilateral papilledema. Visual acuity was decreased but correctable, and she had difculty with
visual eld testing. The fundoscopic examination showed blurred disc margins and
venous engorgement, with mild ame-shaped haemorrhages suggestive of grade II
hypertensive retinopathy.
A comprehensive neuroimaging workup was performed. MRI Brain (T2-FLAIRdiffusion) The MRI ndings in this case are highly consistent with posterior reversible encephalopathy syndrome (PRES) secondary to hypertensive encephalopathy.
On T2-weighted and uid-attenuated inversion recovery (FLAIR) sequences, there
are bilateral, symmetrical hyperintense signal changes predominantly involving the
parieto-occipital lobes, affecting both the cortical and subcortical white matter.
These regions demonstrate no mass effect or enhancement, and the pattern is typical

390
M. F. P. Peres
for vasogenic oedema. Additionally, subtle hyperintensities in the cerebellar hemispheres—particularly on the right—further support a posterior circulation vulnerability. Diffusion-weighted imaging (DWI) shows mild hyperintensities without
corresponding low signal on apparent diffusion coefcient (ADC) maps; instead,
the ADC values are elevated, indicating facilitated diffusion and conrming the
presence of vasogenic rather than cytotoxic oedema. The absence of true diffusion
restriction effectively rules out acute infarction. These ndings reect the pathophysiology of PRES, in which severe hypertension overwhelms the cerebral autoregulatory mechanisms, especially in posterior circulation territories with relatively
less sympathetic innervation, leading to transient blood–brain barrier disruption and
uid extravasation into the interstitium. Collectively, the imaging demonstrates the
classic radiologic pattern of PRES, supporting a diagnosis of reversible vasogenic
oedema due to hypertensive encephalopathy. Given the clinical and radiological
ndings, Zeynep was diagnosed with hypertensive encephalopathy in the context of
severe preeclampsia, with radiological features of PRES.
Treatment was initiated with intravenous labetalol to stabilise her blood pressure
and magnesium sulphate for seizure prophylaxis. Obstetrics was consulted immediately. After maternal stabilisation, she was transferred to the high-risk maternal care
unit. Delivery planning was initiated in close collaboration with the perinatology team.
Over the next 72hours, the intensity of her headache gradually lessened, and her
visual symptoms began to resolve. Serial ophthalmological assessments showed
improving disc clarity and resolution of venous dilation. A follow-up MRI 1 month
later revealed partial regression of the T2-FLAIR abnormalities.
41.4 Clinical Presentation
Headache is often the earliest and most prominent symptom in hypertensive encephalopathy. It may precede more overt signs, such as altered mental status, visual
disturbances or seizures, as a crucial diagnostic clue [1, 10]. The headache is typically bilateral, throbbing and in the occipital region, though variations exist. The
presence of a new-onset severe headache, particularly in a patient with markedly
elevated blood pressure and neurological complaints, should prompt urgent investigation for hypertensive encephalopathy [16].
The headache phenomenology in hypertensive encephalopathy may mimic or
overlap with other secondary headache causes, especially in pregnant or peripartum
individuals. This emphasises the need for structured symptom evaluation and a high
index of suspicion in emergency and primary care settings.

41 Headache Attributed toHypertensive Encephalopathy
391
41.5 Differential Diagnosis
• Preeclampsia/Eclampsia: Both share overlapping features with hypertensive
encephalopathy, including elevated blood pressure, headache and visual distur-
bances. However, systemic ndings such as proteinuria, elevated liver enzymes
and thrombocytopenia help differentiate them [3].
• Reversible Cerebral Vasoconstriction Syndrome (RCVS): It is characterised by
thunderclap headaches and reversible narrowing of cerebral arteries. MRA is
critical in identifying dynamic segmental vasoconstriction [15].
• Cerebral Venous Sinus Thrombosis (CVST): It can present with subacute head-
ache and visual symptoms, sometimes with preserved consciousness. MRV is
essential for differentiation.
• Hypertensive Intracerebral Haemorrhage: It often presents with sudden, focal
decits and altered consciousness. Non-contrast computed tomography (CT) is
the rst-line investigation in suspected cases.
• Pituitary Apoplexy and Posterior Fossa Mass Lesions: Although less common,
these should be considered in cases of headaches with visual loss, particularly in
pregnant women.
• Primary Headaches Exacerbated by Blood Pressure Elevation: Migraine, tension-
type and cluster headaches can all trigger transient increases in blood pressure,
but in these cases, the hypertension is usually secondary, not causal.
However, the diagnostic process is complicated by the broad differential diagnosis of headaches in hypertensive and pregnant patients. In pregnant individuals like
the case presented, differentials include preeclampsia/eclampsia, cerebral venous
sinus thrombosis (CVST), reversible cerebral vasoconstriction syndrome (RCVS),
pituitary apoplexy and even migraine with aura. Each may present with similar
neurological signs and symptoms, including headache, visual changes and altered
consciousness [3, 11].
Differentiating hypertensive encephalopathy from eclampsia is particularly critical in obstetric patients. Both conditions may involve elevated blood pressure, seizures and cerebral oedema, yet eclampsia often includes additional systemic features
such as proteinuria, hepatic dysfunction and thrombocytopenia. Neuroimaging in
both conditions may show PRES patterns, further complicating the diagnosis.
Nonetheless, the presence of isolated neurological symptoms with a radiologic
PRES pattern, in the absence of systemic signs, leans toward primary hypertensive
encephalopathy [4].
Similarly, RCVS is a signicant diagnostic consideration. Thunderclap headache
is the hallmark of RCVS, and MRA often reveals segmental vasoconstriction in
cerebral arteries, a nding that may also be observed in hypertensive encephalopathy [15]. Both syndromes may coexist or mimic each other, especially in postpartum or peripartum patients. The key distinction lies in the dynamic reversibility of
vascular narrowing in RCVS and the dominant oedema patterns in PRES-like
hypertensive encephalopathy [5, 6].

392
Imaging plays a pivotal role in diagnosis. MRI is superior to CT in detecting the
hallmark vasogenic oedema of hypertensive encephalopathy. Typical ndings
include bilateral, symmetrical hyperintensities in the parieto-occipital white matter
on T2- and FLAIR-weighted sequences. However, less typical presentations involve
the frontal lobes, cerebellum, brainstem and spinal cord. Imaging abnormalities
may persist long after symptom resolution, especially in chronic or undertreated
conditions [14].
Ophthalmological examination is another essential, often underutilised, diagnostic tool. Papilledema and hypertensive retinopathy provide real-time evidence of
elevated intracranial pressure and systemic vascular injury. In the case of hypertensive encephalopathy, ndings such as blurred disc margins, venous engorgement,
ame haemorrhages or cotton wool spots reinforce the urgency of neurological
evaluation [2, 4].
M. F. P. Peres
41.6 Conclusion
In summary, headache is not merely a symptom in hypertensive encephalopathy—it
is a diagnostic cornerstone. Its characteristics, evolution and associated ndings
guide the clinician toward or away from competing diagnoses. It is key to timely
diagnosis and management to understand its role, alongside careful systemic evaluation, neuroimaging and fundoscopic examination. Failure to act on these early
clues can lead to irreversible cerebral injury, seizures or death [13, 17].
41.7 Key Messages
• Headache can be the earliest and most critical clue in diagnosing hypertensive
encephalopathy. New-onset severe headache in the presence of acute hyperten-
sion should prompt urgent neurological evaluation.
• Hypertensive encephalopathy is pathophysiologically distinct from but radio-
logically overlapping with posterior reversible encephalopathy syndrome
(PRES). Not all PRES is hypertensive in origin, and not all cases of hypertensive
encephalopathy manifest as classical PRES.
• In pregnant patients, hypertensive encephalopathy should be differentiated from
preeclampsia/eclampsia, cerebral venous sinus thrombosis, RCVS and migraine
with aura. Systemic ndings and dynamic neuroimaging features aid in differen-
tial diagnosis.
• MRI with advanced sequences (T2-FLAIR, DWI, MRA, MRV) is essential for
identifying vasogenic oedema, ruling out infarction or haemorrhage and evaluat-
ing vascular changes suggestive of RCVS or CVST.

41 Headache Attributed toHypertensive Encephalopathy
393
• Ophthalmological examination, including fundoscopy, is a valuable bedside tool.
Papilledema and hypertensive retinopathy ndings can guide urgency and indi-
cate elevated intracranial pressure.
• Prompt treatment, including blood pressure control and seizure prophylaxis, can
lead to complete recovery and radiological reversal in most cases, especially
when diagnosed early.
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