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26 Cerebral Autosomal Dominant Arteriopathy and Subcortical Infarcts…
the current categorization of CADASIL-related headaches within the framework of
vascular disorders may inadequately capture the genetic mechanisms contributing
to these headaches. Sacco etal. advocate for a more nuanced understanding of the
etiology of these headaches, emphasizing the intersection of genetic factors and
headache pathology. This perspective lays the groundwork for a comprehensive
exploration of headache manifestations in CADASIL, which this chapter will further elaborate on [1, 9].
253
26.7 Management
Management of CADASIL-related headaches focuses on symptomatic relief and
preventing stroke. The treatment regimen may include:
• Migraine Prophylaxis: Migraine prophylaxis in CADASIL patients typically
includes medications such as beta-blockers, calcium channel blockers, and anti-
epileptics, which may help reduce migraine frequency. Recent studies, including
detailed case studies, highlight the debilitating nature of migraines in CADASIL,
primarily due to vascular dysfunction linked to NOTCH3 mutations. This
research underscores the refractory nature of traditional migraine treatments in
these patients. It introduces calcitonin gene-related peptide (CGRP) receptor
antagonists as a promising novel therapeutic approach, supported by emerging
literature, for potentially improving headache management in CADASIL
[10, 11].
• Antiplatelet Therapy: Aspirin is commonly used to prevent ischemic events.
• Supportive Care: Physiotherapy, speech therapy, and occupational therapy are
essential in managing progressive neurological decits.
• Genetic Counselling: Given the hereditary nature of CADASIL, counselling for
family members is crucial [10, 12, 13].
26.8 Conclusion
Headaches in CADASIL represent a signicant early symptom of the disease and
may precede other neurological manifestations by many years. Early recognition
and management are key to improving outcomes and preventing further complications. This chapter has provided an overview of the pathophysiology, case presentation, diagnostic approach, and management strategies for headaches associated with
CADASIL, emphasizing the importance of a multidisciplinary approach in caring
for these patients. The insights from recent literature underscore the complexity of
managing CADASIL-related headaches and highlight the need for tailored therapeutic approaches that consider both the neurological and vascular challenges
inherent to this condition.
254
U. Topbaş et al.
References
1. Sacco S, Degan D, Carolei A.Diagnostic criteria for CADASIL in the international classication
of headache disorders (ICHD-II): are they appropriate? J Headache Pain. 2010;11(3):181–6.
https://doi.org/10.1007/s10194- 010- 0203- 6. Epub 2010 Mar 12. PMID: 20224942; PMCID:
PMC3451909
2. Gosalia H, Karsan N, Goadsby P.Genetic mechanisms of migraine: insights from monogenic
migraine mutations. Int J Mol Sci. 2023;24(16):12697. https://doi.org/10.3390/ijms241612697.
3. Su Y, Tay VQ, Singh S, Leary MC, Koss V, Kincaid HM, Yacoub HA, Castaldo J.A retrospective review of sex differences of white matter hyperintensities in brain MRI of patients
with migraine. Headache. 2024;64(6):612–23. https://doi.org/10.1111/head.14714. Epub 2024
May 24. PMID: 38785411.
4. Liem MK, Oberstein SA, van der Grond J, Ferrari MD, Haan J.CADASIL and migraine: a narrative review. Cephalalgia. 2010;30(11):1284–9. https://doi.org/10.1177/0333102410370870.
PMID: 21038489.
5. Guey S, Mawet J, Hervé D, Duering M, Godin O, Jouvent E, Opherk C, Alili N, Dichgans
M, Chabriat H. Prevalence and characteristics of migraine in CADASIL. Cephalalgia.
2016;36(11):1038–47. https://doi.org/10.1177/0333102415620909. Epub 2016 Jul 11. PMID:
26646784.
6. Sacco S, Rasura M, Cao M, Bozzao A, Carolei A.CADASIL presenting as status migraineurs and
persisting aura without infarction. J Headache Pain. 2009;10(1):51–3. https://doi.org/10.1007/
s10194- 008- 0079- x. Epub 2008 Oct 25. PMID: 18953486; PMCID: PMC3451763.
7. Gosalia H, Karsan N, Goadsby PJ.Genetic mechanisms of migraine: insights from monogenic migraine mutations. Int J Mol Sci. 2023;24(16):12697. https://doi.org/10.3390/
ijms241612697. PMID: 37628876; PMCID: PMC10454024.
8. Ferrante E, Trimboli M, Erminio C, Martino I, Tiraboschi P.Acute confusional migraine in
CADASIL: a case report and literature review. Clin Neurol Neurosurg. 2022;216:107239.
https://doi.org/10.1016/j.clineuro.2022.107239. Epub 2022 Apr 6. PMID: 35413636.
9. The International Classication of Headache Disorders, 3rd edition. Cephalalgia.
2018;38(1):1–211. Jes Olesen ISSN: 0333-1024.
10. Donnini I, Nannucci S, Valenti R, Pescini F, Bianchi S, Inzitari D, Pantoni L.Acetazolamide
for the prophylaxis of migraine in CADASIL: a preliminary experience. J Headache Pain.
2012;13(4):299–302.
22367627; PMCID: PMC3356473.
11. Goldstein ED, Badi MK, Meschia JF.Treating chronic migraine in CADASIL with calcitonin gene-related peptide receptor antagonism. Neurol Clin Pract. 2019;9(3):277–8. https://doi.
org/10.1212/CPJ.0000000000000651. PMID: 31341718; PMCID: PMC6615658.
12. Gravesteijn G, Dauwerse JG, Overzier M, Brouwer G, Hegeman I, Mulder AA, Baas F, Kruit
MC, Terwindt GM, van Duinen SG, Jost CR, Aartsma-Rus A, Lesnik Oberstein SAJ, Rutten
JW.Naturally occurring NOTCH3 exon skipping attenuates NOTCH3 protein aggregation and
disease severity in CADASIL patients. Hum Mol Genet. 2020;29(11):1853–63. https://doi.
org/10.1093/hmg/ddz285. PMID: 31960911; PMCID: PMC7372551.
13. Yamamoto Y, Liao YC, Lee YC, Ihara M, Choi JC.Update on the epidemiology, pathogenesis,
and biomarkers of cerebral autosomal dominant Arteriopathy with subcortical infarcts and leukoencephalopathy. J Clin Neurol. 2023;19(1):12–27. https://doi.org/10.3988/jcn.2023.19.1.12.
PMID: 36606642; PMCID: PMC9833879.
https://doi.org/10.1007/s10194- 012- 0426- 9. Epub 2012 Feb 25. PMID:
Chapter 27
Headache Attributed toMitochondrial
Encephalopathy, Lactic Acidosis,
andStroke-Like Episodes (MELAS)
NanaNinoTatishvili , TeonaShatirishvili , andSoaTatishvili
27.1 Introduction
Mitochondria are dynamic subcellular organelles with innumerable functions,
including energy generation via oxidative phosphorylation (OXPHOS), calcium
homeostasis, and regulation of apoptotic cell death, placing them at the center of
cellular metabolism and signalling [1].
Mitochondrial diseases are caused by either a mutation in the nuclear DNA
(nDNA) or mitochondrial DNA (mtDNA).
Among the systems most affected by this group of diseases, the nervous system
stands out, primarily due to its high dependence on aerobic metabolism. Due to this,
sleep disorders, headache, and epilepsy are common in mitochondrial disorders
(MDs). These symptoms can be one of the cardinal symptoms that dene some of
the subtypes of these diseases, such as headache in mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) [2].
MDs occur in a large section of the lifespan (from the neonatal period to late adulthood), with an incidence of about 1.6/5000. In the pediatric population, the incidence
ranges from 0.5 to 1.5 per 100,000. In the majority of cases, onset occurs in infancy or
early childhood and is associated with high morbidity and mortality [3, 4].
The most common neurological symptoms present in the majority of children
with mitochondrial disorder (MD) are muscle weakness, peripheral neuropathy,
ophthalmoplegia, movement disorder, epilepsy, and headache, so the neuropediatrician must be one of the key physicians involved in the diagnosis and management
of childhood-onset MDs [5].
N. N. Tatishvili (*) · T. Shatirishvili · S. Tatishvili
David Tvildiani Medical University, Tbilisi, Georgia
Switzerland AG 2026
D. Uludüz et al. (eds.), Rare Causes of Headache Disorders, Headache,
https://doi.org/10.1007/978-3-032-10242-3_27
255© The Author(s), under exclusive license to Springer Nature
256
N. N. Tatishvili et al.
27.2 Case Presentations
We had two patients with MD and headaches. Headache was not the dominant feature of an MD, but only an ancillary feature of the phenotype in both. The headache
was not very severe, but was admitted by both, mostly between acute progressing
episodes, during the stable period.
Case 27.1 Male, 5years old, early development was normal.
At the age 5, he lost consciousness and presented with right-sided hemiparesis.
At that point, a cranial magnetic resonance imaging (MRI) showed normal ndings.
A second episode occurred at 7years of age: during a respiratory infection complicated with pneumonia, he transiently lost consciousness and vision. It was evaluated
as an epileptic seizure, he was treated with carbamazepine, and his electroencephalography (EEG) was normal. An MRI showed non-specic changes of the bilateral
occipital white matter. After this, he had periods of headache without any other
signs; he could not describe the type of headache, it was of moderate severity, and
sometimes nonsteroidal anti-inammatory drugs (NSAIDs) were needed. His third
episode occurred at the age of 10years. Again, after an unspecic illness, focal
convulsive status epilepticus (epilepsia partialis continua) occurred with deviation
of head and eyes to the right and twitching of the right side of the face, accompanied
by left-sided focal spike and slow-wave activity. All blood tests, including liver
enzymes, were normal. The MRI was unchanged.
The patient was treated with i/v antiseizure medication (ASM) in the pediatric
intensive care unit (PICU). Status epilepticus was not controlled. Then thiopentone
anaesthesia was used. He was alert and responsive for 3days. However, acute severe
deterioration occurred, and the boy died within 10h due to recurrent status epilepticus, acidosis, anuria, and respiratory failure.
Genetic analysis revealed that our patient and sibling had MD Alpers- and mitochondrial neurogastointestinal encephalomyopathy (MNGIE)-like disease with disturbed cerebrospinal uid (CSF) folate transport and an unusual mode of genetic
transmission of POLG mutations. In the blood DNA of our patient and his sibling,
two heterozygous variants were detected, while multiplex ligation-dependent probe
amplication (MLPA) analysis was normal. One of these NM_002693.2: c.680G>A
p.(Arg227Gln) is a missense variant that has recently been described in three infants
with mitochondrial depletion syndrome (MDS) and Alpers-Huttenlocher syndrome
(AHS) [6–8] This variant was also present in blood DNA of the deceased brother
but not in the parents and the healthy brother. A buccal swab, saliva, and hair bulbs
of the father were also negative for this mutation. Paternal blood DNA was additionally tested by deep targeted next- generation sequencing (coverage >2500) for this
POLG variant and was negative [6].
Case 27.2 A 9-year-old male patient developed bilateral sensorineural hearing loss
followed by a generalized tonic–clonic seizure. From this period, he had monthly
headaches without other signs, usually of moderate severity, and rare NSAIDs were
27 Headache Attributed to Mitochondrial Encephalopathy, Lactic Acidosis…
257
ab c
Fig. 27.1 Brain MRI: Stroke-like episode (SLE) (A-C) demonstrating hyperintensities in the left
occipital and parietal lobes, extending into white matter—a suspected area of cortical and subcortical ischemia not respecting the borders of large and medium-sized arterial territories.
(T.Shatirishvili etal. [6])
used. From age 15, he exhibited progressive fatigue, muscle weakness, and strokelike episodes.
MRI revealed stroke-like lesions in the brain (Fig.27.1). Over 2years, he experienced multiple hospital admissions for severe symptoms including right-sided
hemiparesis, hemianopia, seizures, and encephalopathy, periodically with nonmigraineous headaches. Despite treatment, his condition deteriorated, leading to
multi-organ failure and death at the age 16years. Molecular genetic analysis identied a heteroplasmic m.3764C>G variant in MT-ND1.
The case was evaluated as MELAS with a new mutation [9].
27.3 Clinical Characteristics
Headache is a common feature of MD and can manifest as a migraine-like headache, cluster headache, non-classied headache, or tension headache. Headache
may be the dominant feature of a MD or only an ancillary feature of the phenotype [10].
Due to the absence of a structured diagnostic headache tool, specic questionnaires, interviews, and objective clinical examination, the prevalence of headache/
migraine in MDs patients uctuates noticeably in the scientic literature [2].
Migraine may also be part of the clinical presentation of a stroke-like episode
(SLE). Regarding headache, it is still unclear whether headache is a primary disorder associated with MDs or a secondary migraine-like headache caused by mitochondrial disease. In the study population, 71% (43/61) indicated headache, and
29% (18/61) reported not suffering any headache [11].
258
N. N. Tatishvili et al.
The pathophysiology of migraine-like headache is poorly understood. Still, there
are indications that it is a vascular pathology, resulting in initial hyperperfusion,
which results from activation of the calcitonin-related protein or enhanced inux of
calcium into mitochondria, resulting in increased oxidative stress [10].
A SLE, which can have an acute or subacute neurological manifestation, typically affects young individuals and is caused by focal brain dysfunction of an epileptic nature.
MD-associated migraine tends to be chronic and more disabling than in the general population. Non-classied headache has been reported in patients carrying
POLG1 mutations [10]. A higher frequency of headache, other than migraine, has
also been observed in patients with MELAS syndrome, suggesting the presence of
a characteristic headache subtype in these patients. In this way, mitochondrial dysfunction could be one of the pathophysiological mechanisms of headache migrainous or non-migrainous and constitute a factor of chronication and severity in this
entity [2].
27.4 Discussion
Mitochondria play a central role in a variety of cellular functions, including energy
generation, production of reactive oxygen species (ROS), control of Ca2+ homeostasis, and regulation of apoptosis [7].
Mitochondrial diseases are caused by either mutation in the nuclear DNA(nDNA)
or mitochondrial DNA(mtDNA). The mtDNA encodes only for approximately 1%
of all estimated 1500 (nuclear and mtDN encoded) proteins needed for normal
structure and function of mitochondria [7, 8]. Pathogenic variants in mtDNA include
single-nucleotide variants as well as single large-scale deletions/rearrangements.
The integrity of mtDNA can also be affected by multiple deletions arising in the
context of primary defects in one of over 30 nuclear genes that control mtDNA
maintenance. This can also result in reduced mtDNA content (mtDNA depletion).
According to O.Heath, R.G.Feichtinger etal. (2025), pathogenic variants in the
nuclear gene POLG account for the most prevalent mtDNA maintenance defect in
childhood [12].
Mitochondrial diseases presenting in childhood are characterized by clinical,
biochemical, and genetic complexity. Some children are affected by well-described
syndromes, and many have nonclassical multisystemic disease presentations involving any organ in the body. Each child has a unique combination of clinical features
and disease trajectory, leading to enormous challenges in the diagnosis and management of these heterogeneous disorders [2].
Fifty-ve percent of all participants reported a headache. Forty-eight percent of
women and 31% of all men in the population reported headache as one of the ve
most essential complaints due to their mitochondrial disease [10].
Despite many publications about the high frequency of headache in MD, it is still
unclear whether headache is a primary disorder associated with or coincidental to
27 Headache Attributed to Mitochondrial Encephalopathy, Lactic Acidosis…
259
MDs, mainly manifested as migraine, or a secondary migraine-like headache caused
by mitochondrial disease.
The current edition of the International Classication of Headache Disorders
(ICHD-3 beta) only includes headache in MELAS among headache attributed to
genetic vasculopathy, without other references to headache in the context of
MDs [13].
About 80% of the MD cases are associated with the pathogenic m.3243A>G
mutation in the MT-TL1 gene, the rst genetic defect linked to MELAS syndrome.
However, other rare mtDNA mutations and recessive POLG1 mutations are wellrecognized causes of SLEs [5].
POLG1 patients have an explosive onset and a rapid progression, with a higher
risk of death due to status epilepticus [14], as was the case in our case 27.1. The
patient developed suprarefractory status epilepticus, which led to the patient’s death.
Patients with the 3243A>G mutation usually show a protracted disease course with
an insidious onset and mainly die from complications not related to central nervous
system (CNS). Moreover, around half of POLG1 patients have no other symptoms
outside of CNS features before the rst SLE.The patient in case 27.1 also had
purely CNS signs.
A. H. San Martin, C. D. Gonzalez et al. (2023) performed a cross-sectional
cohort study. Of the 203 patients interviewed, 92 (45.3%) reported suffering regularly from headache of any type (at least one headache day per month), the prevalence being more frequent in women than in men (53.2 vs. 32.9%, respectively).
Within the group of 92 patients with headaches, migraine prevalence was 35%,
which is higher compared to the general population. Sixteen (69.6%) of these
patients met the criteria of migraine, while the remaining seven had non-migrainetype headaches. Patients with migraine had a median of 10 headache days per
month, while patients with non-migraine headaches, like our case 27.2 patient, had
a median of 3 headache days per month. Both our patients had non-migrainous
headaches, frequency was not high, and severity was moderate [2].
Patients with the pathogenic variant m.8344 A>G in the MTTK gene were those
with the highest prevalence of headache. A total of 39 patients with the m.3243
A>G mutation in the MTTL1 gene (58.2%) presented headache, with 69% of cases
fullling migraine criteria [2]. This prevalence was reported to be independent of
sex, phenotype, or genotype, which, together with dysfunction of mitochondrial
metabolism in migraine observed in several studies, supports the hypothesis that
mitochondrial dysfunction could play an important role in the pathophysiology of
migraine. Moreover, there is emerging evidence that monoclonal antibodies acting
on calcitonin gene-related peptide (CGRP) (CGRP-mAbs), widely used in the treatment of patients with migraine, are also safe and effective in the treatment of refractory headaches associated with mitochondrial diseases. This data also supports the
theory about common pathophysiological pathways between MDs and migraine.
Based on the phenotype of the patients with MD, a statistically signicant relationship was found between the MELAS syndrome and the presence of headache,
in contrast with other phenotypes, with a p-value of less than 0.01 [2].
260
N. N. Tatishvili et al.
The exciting fact is that in MD patients with epilepsy, myoclonus, and SLEs are
more frequent in patients with headache/migraine compared to patients without it.
In both of our cases, there was a combination of epilepsy (in one, myoclonus) and
headache. The nding of a higher prevalence of epilepsy in the population of mitochondrial migraineurs (33.33%; 11/33) compared with non-migraineurs (11.66%;
7/60) presumably means that the association between migraine and epilepsy is not
fortuitous in these patients, but could underlie common pathophysiological mechanisms [15].
It is essential to mention that the pharmacological management of MDs patients
with headache/migraine could be particularly challenging, probably due to poor
tolerance to drugs commonly used for headaches.
We can admit that mitochondrial dysfunction could be one of the pathophysiological mechanisms of headache/migraine, mainly through the production of ROS,
apoptosis, Ca2þ homeostasis, and global increased neuronal excitability, and it can
also constitute one of the mechanisms of chronication and severity of migraine.
27.5 Conclusion
Headache/migraine has a higher prevalence in MDs compared with general
population- based data, independently of genotype or phenotype. Headache is not
merely a phenotypic aspect of specic MDs. Still, it is rather the expression of vulnerability of the central nervous system, probably directly related to defects of the
respiratory chain.
A headache can be a cardinal sign of clinical presentation, as well as an ancillary
feature. It can be migrainous as well as non-migrainous or unclassied, as in our
cases. New data is needed for a better understanding of pathophysiologic mechanisms and the relationship between MD and headache in mitochondrial disorders,
especially in MELAS and SLE.
References
1. Rahman S.Mitochondrial disease in children. J Intern Med. 2020;287:609–33. https://doi.
org/10.1111/joim.13054.
2. San Martin AH, Gonzalez CD, Conejo MM, Hernandez Salas ME, Gallego JH.Headache and
sleep quality in mitochondrial diseases. Cephalalgia Rep. 2023;6:1–7.
3. Tolomeo D, Orsucci D, Nesti C, Baldacci J, Battini R, Bruno C, Bruno G, Cassandrini D,
Doccini S, Donati MA, Ferrari A, Fiori S, Fiorillo C, Guerrini R, Mari F, Montomoli M,
Pochiero F, Procopio E, Ruggiero L, Sampaolo S, Sicca F, Ticci C, Rubegni A, Santorelli
FM. The diagnostic approach to mitochondrial disorders in children in the era of nextgeneration sequencing: a 4-year cohort study. J Clin Med. 2021;10(15):3222. https://doi.
org/10.3390/jcm10153222.
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4. Tan J, Wagner M, Stenton SL, Strom TM, Wortmann SB, Prokisch H, Meitinger T, Oexle K,
Klopstock T.Lifetime risk of autosomal recessive mitochondrial disorders calculated from
genetic databases. EBioMedicine. 2020;54:102730.
5. Conti F, Di Martino S, Drago F, Bucolo C, Micale V, Montano V, Siciliano G, Mancuso M,
Lopriore P.Red ags in primary mitochondrial diseases: what should we recognize? Int J Mol
Sci. 2023;24:16746.
6. Shatirishvili T, Katsitadze Z, Yi Shiau Ng, Achuthaprasad A, Alston CL, Blakey E, Turnbull
DM, Bregvadze K, Tkemaladze T, Tatishvili NN. Novel m.3764C>G variant in MT-ND1
linked to severe MELAS syndrome: a case report. Brain Dev Case Rep. 2025;3:100059.
7. Tiehuis LH, Koene S, Saris CGJ, Janssen MCH.Mitochondrial migraine; a prevalence, impact
and treatment efcacy cohort study. Mitochondrion. 2020;53:128–32.
8. El-Hattab AW, Craigen WJ, Scaglia F. Mitochondrial DNA maintenance defects. Biochim
Biophys Acta (BBA)– Mol Basis Dis. 2017;1863(6):1539–55.
9. Korinthenberg R, Kirschner J, Eckenweiler M, Steinfeld R, Tatishvili NN, Horvath R, Kleinle
S, Abicht A.Alpers- and MNGIE-like disease with disturbed CSF folate transport and an
unusual mode of genetic transmission of POLG mutations: a case report. J Int Child Neurol
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10. Finsterer J, Torres de Carvalho EH.Cerebral manifestations of mitochondrial disorders. Can J
Neurol Sci. 2017;44:654–63. https://doi.org/10.1017/cjn.2017.211.
11. Burow P, Meyer A, Naegel S, Watzke S, Zierz S, Kraya T.Headache and migraine in mitochondrial disease and its impact on life—results from a cross-sectional, questionnaire-based
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12. Heath O, Feichtinger Ren’e G, Achleitner MT, Hofbauer P, Doris M, Merkevicius K, Spenger
J, Steinbrücker K, Steindl C, Tiefenthaler E, Mayr JA, Wortmann SB. Mitochondrial disorder diagnosis and management– what the pediatric neurologist wants to know. Eur J Paediatr
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E, Ostergaard E, de Coo IFM, Pias-Peleteiro L, Isohanni P, Uusimaa J, Darin N, Rahman S,
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261
Chapter 28
Headache Attributed toMoyamoya
Angiopathy
EsraKochanKizilkilic andDeryaUluduz
28.1 Introduction
Moyamoya disease (MMD) is a chronic, progressive cerebrovascular disorder characterized by bilateral stenosis or occlusion of the terminal portion of the internal
carotid arteries (ICA) and the development of compensatory basal collateral vessels. These vessels appear as a “puff of smoke” on cerebral angiography—hence the
name “Moyamoya,” which means “hazy” or “smoky” in Japanese [1, 2].
While MMD is traditionally recognized for its ischemic and hemorrhagic stroke
presentations, headache is an increasingly acknowledged, yet underdiagnosed,
manifestation of the disease, particularly in adults [3]. Clinical series and case
reports suggest that headache can be the initial and sometimes the only presenting
symptom of Moyamoya disease, preceding more serious cerebrovascular events by
months or even years [4, 5].
Headaches in MMD can mimic primary headache disorders, particularly
migraine without aura, and are often misclassied due to overlapping clinical features such as throbbing pain, photophobia, nausea, and unilateral localization [6, 7].
In some cases, patients may be labelled as having refractory migraine or chronic
tension-type headache, delaying the correct diagnosis and appropriate management
[8, 9]. In a recent case series from Indonesia, Moyamoya-related headache was
among the most challenging initial presentations to identify, often requiring
advanced neurovascular imaging for diagnosis [10]. Headaches associated with
MMD can occur both in the ischemic phase, due to cerebral hypoperfusion, and in
the hemorrhagic phase, due to the rupture of fragile collateral vessels [6]. Moreover,
E. KochanKizilkilic · D. Uluduz (*)
Department of Neurology, University of Health Sciences,
Prof. Dr. Cemil Tascioglu City Hospital, Istanbul, Turkey
Medical Faculty, Neurology Department, Istanbul University Cerrahpasa, Samatya, Türkiye
Switzerland AG 2026
D. Uludüz et al. (eds.), Rare Causes of Headache Disorders, Headache,
https://doi.org/10.1007/978-3-032-10242-3_28
263© The Author(s), under exclusive license to Springer Nature