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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5526_Библиотеки_им_академика_М_И_Перельмана.pdf
10 Short-Lasting Unilateral Neuralgiform Headache Attacks with Cranial Autonomic…
Fig. 10.1 Trigeminal autonomic reex (TAR) and its connectionsThe trigeminal autonomic reex
(TAR) afferent limb is constituted by the nerve endings of the trigeminal nerve that innervate the
intracranial blood vessels. These bers have their cell bodies in the trigeminal ganglion and transmit the signals to the second-order neurons into the trigeminocervical complex (TCC), which is
directly modulated by the hypothalamus. The TCC has a reex connection with the superior salivatory nucleus, from which originate the preganglionic parasympathetic bers that form the efferent
limb of the TAR.Through the greater supercial petrosal nerve, these bers synapse into the sphenopalatine ganglion, where postganglionic parasympathetic bers arise and innervate nasal and
lacrimal glands. Additionally, pain signals reach the cortex by ascending from TCC to the thirdorder neurons in the thalamusCreated in BioRender. https://BioRender.com/f68r610
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10.3 Case Presentation
Our patient is a 38-year-old teacher who presented to the emergency department
due to worsening of her preexisting facial pain and was referred to the headache
team. She had recently moved to the area and had been investigated and treated in
several local services in her previous residence. She has responded poorly to various
treatment options offered previously and was on gabapentin 300mg three times a
day, which had been partially benecial. Over the week preceding her visit, the
frequency and severity of her facial pain had signicantly worsened. She had been
unable to eat or drink and had to take leave from work due to the pain.
Her pain had started at the age of 32years, and she did not recall having any
signicant headache prior to this. Her facial pain was characterized by frequent,
sharp, electrical shock-like pain, mainly affecting the forehead, periorbital and maxillary region on the left side. Attacks last between 30s to 2min, and she described
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multiple attacks in a day, which could be in the range of hundreds when at their most
severe. During an attack, she experienced a series of stabs presenting in a saw tooth
pattern, with the pain not reaching baseline in between stabs. She would be painfree between attacks. Delving further into her headache characteristics, the headache team was able to identify a few CAS which she did not volunteer. These
included grittiness of the left eye, slight congestion of the left nostril, and discomfort and fullness of the left ear during pain. She identied touching the left lower
eyelid and chewing food as triggers; however, the attacks occurred spontaneously
most of the time. If triggered, the pain would continue without a break until she
stopped the trigger itself (e.g., touching the face or eating). Her general examination
and neurological examination were normal. Body weight was 76kg.
A magnetic resonance imaging (MRI) scan of the head, trigeminal nerve, and
internal acoustic meatus with contrast, performed in the past, had shown a loop of
the left superior cerebellar artery near the root entry zone of the left trigeminal
nerve. There was no signal abnormality at the root entry zone itself or distortion,
displacement, abnormal thinning, or enhancement of the trigeminal nerve.
Blood tests, including a pituitary hormone panel, did not show any signicant
abnormalities. When the pain rst started, our patient had consulted a dental practitioner and had treatment for a decayed upper left molar tooth without any improvement in the facial pain. Her local neurology team then saw her. She received a
diagnosis of TN, and was treated with several medications including carbamazepine, oxcarbazepine, pregabalin, amitriptyline, and baclofen with minimal improvement. She had also undergone microvascular decompression of the left trigeminal
nerve, which resulted in pain freedom for 3weeks, followed by a return to her presurgery baseline.
TN and SUNA were considered the most likely explanations for her headache.
Several characteristics supported SUNA over trigeminal neuralgia. These included
the ipsilateral CAS and the lack of a refractory period. Additionally, the pain localization in the distribution of the ophthalmic and maxillary branches of the trigeminal nerve favored the SUNA diagnosis, as TN commonly involves the maxillary and
mandibular branches and involvement of the ophthalmology branch is less common. It is interesting to note that the brain MRI scan showed a blood vessel in close
proximity to the ipsilateral trigeminal nerve. However, there was no distortion or
displacement of the trigeminal nerve. Also, she did not have a sustained, satisfactory
response to microvascular decompression. These factors suggest that TN was less
likely to be the cause of her facial pain.
Due to the signicant impact in her quality-of-life short-term bridging therapies
were considered as a rst step. Greater occipital nerve injection was considered
unsafe due to the previous history of microvascular decompression surgery and a
decision was taken to start lidocaine infusion.
She was admitted to the critical care unit and baseline tests including an electrocardiogram (ECG), liver and renal function tests, electrolytes, and a pregnancy test
were arranged, all of which were within expected ranges. She was started on intravenous lidocaine with continuous cardiac monitoring at rate of 1mg/min further
increased by 0.5mg/min daily. She noticed an improvement in the severity and
10 Short-Lasting Unilateral Neuralgiform Headache Attacks with Cranial Autonomic…
frequency of attacks at a dose of 3mg/min. The infusion was continued at this rate
for a total treatment duration of 7 days, at which her symptoms signicantly
improved. She was discharged on her the same dose of gabapentin.
About 4weeks after leaving the hospital she noted a slight worsening of symptoms and lamotrigine was added to her preventive medications, which was titrated
up to 100mg twice a day and the combination resulted in a signicant improvement
of the frequency and severity of attacks.
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10.4 Case Discussion
TACs are often misdiagnosed, leading to an average diagnostic delay of about
5years [18, 19]. This not only delays appropriate treatment but also risks exposing
patients to ineffective or potentially harmful therapies. Our case illustrates these
pitfalls well. Indeed, it showed how delays can result in a signicant negative impact
on quality of life, which could have been minimized if the correct diagnosis had
been made earlier.
A thorough history is paramount in evaluating headache disorders. Rather than
passively listening to the patient, history-taking should be an active data-gathering
process, allowing the clinician to identify key diagnostic clues. An example stemming from this case is the presence of cranial autonomic symptoms and refractory
periods for triggers, which paved the way for a correct diagnosis of SUNA after a
delay of 6years. As Sir William Osler supposedly stated, “Listen to your patient, he
is telling you the diagnosis” [20].
10.5 Clinical Characteristics
SUNA is characterized by unilateral head or facial pain occurring as either single or
multiple stabs and associated with ipsilateral cranial autonomic symptoms. It differs
from SUNCT by the presence of only one or neither between conjunctival injection
and lacrimation (Headache Classication Committee of the International Headache
Society (IHS) The International Classication of Headache Disorders, third edition [3].
The majority of patients with SUNA have a primary chronic form [1, 21–23].
While data regarding periodicity is scarce, a median of four bouts per year lasting
2weeks was noted in those with episodic SUNA [22].
SUNA is typically unilateral, but side variability has been observed in a small
proportion of patients [21, 22, 24, 25]. Pain is most often felt in trigeminal areas;
however, other areas of the head supplied by the C2/C3 nerve roots through the
occipital nerves can also be affected in around a third to a half of the patients [1, 21].
Of the trigeminal areas, pain is most often felt in the distribution of the ophthalmic
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branch of the trigeminal nerve, followed by maxillary branch and less often in the
mandibular distribution [1, 21, 22, 24].
The pain in SUNA is moderate to severe, with a character most often described
as stabbing, jabbing, electric shock-like, or shooting [1, 22, 23, 26]. Three distinct
patterns a attacks have been described (Fig.10.2): single stabs, group of stabs where
the stabs occur back-to-back with the pain returning to the baseline after each stab,
and saw-tooth pattern in which there are multiple stabs in which the pain does not
return to the baseline in between attacks [1, 21, 26, 27]. The duration of an attack
typically ranges between 1 and 600s, and the frequency of attacks ranges between
1 and 100 with an average of around 20 attacks a day [1, 22].
Presence of cranial autonomic symptoms ipsilateral to the pain is essential for
the diagnosis of short-lasting unilateral neuralgiform headache attacks and the presence of only one or neither of conjunctival injection and tearing differentiates SUNA
from SUNCT (Headache Classication Committee of the International Headache
Society (IHS) The International Classication of Headache Disorders, third edition
2018). Lacrimation, nasal symptoms, and ptosis are the most reported cranial autonomic symptom in SUNA [1, 21–23, 25].
Trigger factors are a well-recognized phenomenon in SUNA, and most patients
experience both triggered and spontaneous attacks. While spontaneous attacks can
be completely absent in a small percentage of patients, this is infrequent. Cutaneous
triggers such as light touch and cold wind, and intraoral stimuli such as eating and
brushing are the most frequently reported triggers.
Classically patients with SUNA would be pain free in between attacks; however,
interictal background pain is not uncommon in clinical practice. In these patients,
Fig. 10.2 Patterns of pain in short-lasting unilateral neuralgiform headache attacks with cranial
autonomic symptoms (SUNA). (Created in BioRender. Sebastianelli, G. (2025) https://BioRender.
com/h08m845)
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the headache phenotype should be carefully evaluated to identify the presence of
other primary headache disorders, such as migraine or hemicrania continua, as well
as secondary headache disorders, particularly medication-overuse headache
[21, 22].
Although neurological examination is generally normal in patients with SUNA,
sensory abnormalities, such as reduced sensation or hyperesthesia, have been noted
occasionally [21].
10.6 Diagnostic Algorithm
Differential diagnoses of SUNA include TN, primary stabbing headache (PSH), and
other TACs, including SUNCT, paroxysmal hemicrania (PH), and cluster headache
(CH). SUNA is a clinical diagnosis, and no tests exist to conrm it. Various clinical
features can help narrow the differentials and guide the correct diagnosis. These
include the types of associated CAS, pain duration, frequency, triggers, refractory
periods, and treatment response.
The distinction between SUNA and SUNCT is mainly due to the obligatory
occurrence of both conjunctival injection and tearing in SUNCT during the pain,
while only one or neither of the symptoms could be present during SUNA attacks.
Additionally, the triggering rate by cutaneous stimuli is reported to be lower in
SUNA than in SUNCT [21].
TN remains the main and the most challenging differential diagnosis. Several
similarities are shared between these diseases, including clinical features, such
as quality, localization, and duration of pain, cutaneous triggers, and response to
similar medications [8]. Indeed, in both TN and SUNA, the pain can involve the
three branches of distribution of the trigeminal nerve [21, 28, 29], with neuralgiform features described as sharp, stabbing, burning, or electrical shock-like,
lasting from a few seconds to a minute. However, SUNA has the presence of
constant pain ipsilateral to the side of the attacks in approximately 50% of
patients [21], which is, by denition, not possible in TN.Indeed, patients with
TN with constant background pain meet the diagnosis of trigeminal neuralgia
with concomitant continuous pain (Headache Classication Committee of the
International Headache Society (IHS) The International Classication of
Headache Disorders, third edition 2018) [3]. Additionally, both SUNA and TN
can be triggered by similar cutaneous/intraoral triggers, including chewing, eating, nose blowing, touching the face, and brushing teeth [21, 30]. However, the
rate of cutaneous stimuli in triggering attacks has a lower frequency in SUNA
than in SUNCT [21] and is lower than in TN [31] and a refractory period, in
which the attacks cannot be triggered or cannot start spontaneously for a few
seconds to minutes immediately after an attack is typical of TN and rare in
SUNA [1, 21, 22, 24, 26, 27, 32].
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Both conditions respond to similar medications, including sodium channel
blockers. However, lamotrigine is considered the rst choice for the preventive
treatment of SUNA, while oxcarbazepine and carbamazepine are considered
second- line treatments for SUNA and rst-line choices in TN [33].
One of the most important distinguishing features between TN and SUNA is the
presence of prominent CAS in the latter. These include conjunctival injection or
tearing, nasal congestion, rhinorrhea, eyelid oedema, facial sweating or ushing,
aural fullness, miosis, and ptosis (Headache Classication Committee of the
International Headache Society (IHS) The International Classication of Headache
Disorders, third edition 2018) [3]. However, it is important to note that CAS symptoms can also be present in TN, including tearing [29, 30], but are mainly described
as mild.
CH and PH are classied as TACs and share the strictly unilateral side of the pain
and cranial autonomic symptoms with SUNA.The duration of pain is crucial in
distinguishing SUNA from CH or PH.By denition, SUNA has the shortest duration, ranging from 1 to 600s, while CH can last from 15 to 180min and PH from 2
to 30min. Then, PH can sometimes mimic SUNA in the shortest attacks. However,
the key element in distinguishing between these two conditions is the response to
indomethacin, which is absolute in PH while being absent in SUNA.Additionally,
in contrast to SUNA, PH attacks are mainly spontaneous and are not caused by
cutaneous facial triggers [34, 35].
PSH is characterized by localized stabs of pain in the head that last up to a few
seconds (Headache Classication Committee of the International Headache Society
(IHS) The International Classication of Headache Disorders, third edition 2018)
[3]. Unlike SUNA, there are no cranial autonomic symptoms in PSH.In most cases,
the pain is not triggerable and is located in extra trigeminal regions, primarily in the
auricular, posterior parietal, occipital, and nuchal areas [36].
Finally, it is important to exclude secondary causes in patients with clinical features of SUNA, as different secondary causes that can mimic short-lasting unilateral
neuralgiform headache attacks are reported in the literature [37]. These include vascular loops compressing the entry zone of the trigeminal root [37, 38] and pathologies involving the cerebellopontine angle [39], brainstem [40–42], or cavernous
sinus. Additional investigations, such as neuroimaging, are required in all patients
with a clinical presentation of SUNA.
Step 1: Clinical Suspicion.
• Identify key symptoms:
– Moderate or severe strictly unilateral head pain, with trigeminal
distribution.
– Pain lasts for 1–600s and occurs as single stabs, series of stabs, or in a
saw-tooth pattern.
– Presence of cranial autonomic symptoms ipsilateral to the pain.
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Step 2: Narrow the Differentials and Differentiate from Other TACs:
• Identify clinical differences:
– Response to indomethacin.
– Pain features: location, radiation, and duration.
– Triggers.
– Refractory period.
– Entity of cranial autonomic symptoms.
– Other accompanying symptoms.
Step 3: Apply ICHD-3 Diagnostic Criteria for Short-Lasting Unilateral Neuralgiform
Headache Attacks (2018).
A. At least 20 attacks fullling criteria B–D.
B. Moderate or severe unilateral head pain, with orbital, supraorbital, temporal,
and/or other trigeminal distribution, lasting for 1–600s and occurring as
single stabs, series of stabs, or in a saw-tooth pattern.
C. At least one of the following ve cranial autonomic symptoms or signs, ipsi-
lateral to the pain:
(a) Conjunctival injection and/or lacrimation.
(b) Nasal congestion and/or rhinorrhea.
(c) Eyelid oedema.
(d) Forehead and facial sweating.
(e) Forehead and facial ushing.
(f) Sensation of fullness in the ear.
(g) Miosis and/or ptosis.
D. Occurring with a frequency of at least one a day.
E. Not better accounted for by another ICHD-3 diagnosis.
Step 4: Distinguish SUNA from SUNCT.
• Apply ICHD-3 diagnostic criteria for SUNA (2018):
A. Attacks fullling criteria for 3.3 short-lasting unilateral neuralgiform
headache attacks and criterion B below.
B. Only one or neither of conjunctival injection and lacrimation (tearing).
Step 5: Distinguish episodic from chronic SUNA.
• Investigate for pain-free periods lasting at least 3months (2018):
– Episodic: At least two bouts lasting from 7days to 1year (when untreated)
and separated by pain-free remission periods of ≥3months.
– Chronic: Attacks occurring without a remission period or with remissions
lasting <3months, for at least 1year.
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Step 6: Exclude secondary causes and neurovascular compression:
• Perform brain MRI:
– Dedicated views of the pituitary glands and the trigeminal nerves.
10.7 Management
Due to the short-lasting nature of the attacks, acute treatment options are unlikely to
be of any benet in SUNA.For patients with infrequent and non-debilitating attacks
preventive medications can be considered, while those with frequent and debilitating attacks may benet from short-term bridging treatments as a rst step to improve
the quality of life. Invasive surgical procedures have been used for patients refractory to conventional treatment options; however, these need further research to
determine their effectiveness in the management of SUNA.
Intravenous lidocaine is considered as the rst-line bridging treatment option for
both SUNCT and SUNA.Intravenous lidocaine can lead to a signicant improvement of symptoms in 80–90% of patients with SUNA and the benet can last about
3weeks on average [25, 27, 33]. Lidocaine is usually administered as an intravenous infusion at a rate of 1–4mg/min up to 7days and requires continuous cardiac
monitoring during the infusion [43].
Greater occipital nerve blockade is another short-term treatment option which is
used for most primary headache disorders. Although not as effective as lidocaine, a
benecial effect lasting about 40days on average can be seen in around 40% of
patients with SUNA.
Intravenous dihydroergotamine, sumatriptan, high-ow oxygen, corticosteroids.
and intramuscular indomethacin injections have not shown consistent efcacy to be
considered as short-term bridging treatments for SUNA [25, 44].
Lamotrigine is the most effective preventive treatment. A single-center, prospective, open-label study reported at least some degree of headache improvement in
72% of patients with SUNA, and at least 50% improvement in the number of attacks,
attack severity, or duration in 58% of patients [33, 45].
Alternative medical treatment options that can be considered if lamotrigine is not
tolerated or ineffective include oxcarbazepine, carbamazepine, gabapentin, pregabalin, and topiramate. Limited data suggest that duloxetine, lacosamide, and mexiletine can also be considered as treatment options. Topiramate has the highest rate
of discontinuation (32%), followed by pregabalin, carbamazepine and oxcarbazepine [23, 25, 27, 33, 45].
Non-invasive vagal nerve stimulation (nVNS) has shown some efcacy in primary headache disorders including migraine, cluster headache, and indomethacin
responsive headache disorders; however, data on the efcacy of nVNS in SUNA
from a single case series with two patients have not been encouraging and needs
further research [46, 47].
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Several studies have demonstrated an increased prevalence of neurovascular contact on the ipsilateral trigeminal nerve in patients with short-lasting unilateral neuralgiform headache attacks [7, 27]. Based on this observation, microvascular
decompression of the trigeminal nerve has been considered as a treatment option for
patients with refractory SUNA.A series of 47 patients with short-lasting unilateral
neuralgiform headache attacks which included 16 patients with SUNA reported a
positive response to microvascular decompression in 62.5% of the SUNA cohort
(mean follow-up of 57months) [48]. Cerebrospinal uid leak, neuropathic pain on
the wound site, and facial numbness were the most frequent complications [48].
Occipital nerve stimulation has been used for the treatment of primary headache
disorders and limited data suggests that this can be effective in about two-thirds of
the patients with short-lasting unilateral neuralgiform headache attacks [49]. Leadrelated problems and infections were the common causes of surgical revision in
patients who had occipital nerve stimulation for headache disorders [50].
In a small case series, pulsed radiofrequency targeting the sphenopalatine ganglion was reported to be benecial in seven out of nine patients for a median of
6months [51]. Several studies have also reported benecial effects of deep brain
stimulation in patients with short-lasting unilateral neuralgiform headache attacks,
targeting the hypothalamus or the ventral tegmental area [15, 16, 49]. Further studies are needed to conrm the efcacy of these treatment modalities in the treatment
of SUNA.
Destructive procedures targeting the trigeminal nerve and the sphenopalatine
ganglion including glycerol rhizotomy, radiofrequency thermocoagulation, and
gamma knife radiosurgery have been used to treat short-lasting unilateral neuralgiform headache attacks [52–54]. However, symptoms recurrence after these procedures is not uncommon and caution is needed when considering these treatment
options due to complications associated with these procedures such as anesthesia
dolorosa and trigeminal sensory impairment [52, 53, 55].
10.8 Conclusion
SUNA is a rare and challenging primary headache disorder that is often misdiagnosed. Investigating subtle symptoms, such as the lack of refractory period, the
presence of CAS, and the localization of pain, is crucial to distinguishing SUNA
from other diseases with similar presentations. Additionally, it is mandatory to
exclude secondary causes in all patients presenting with clinical features suggestive
of SUNA.
This chapter has provided an overview of the pathophysiology, case presentation,
diagnostic approach, and management strategies for SUNA, emphasizing the importance of detailed history-taking to identify key diagnostic clues. By improving the
identication of this rare disease, clinicians can select the most appropriate treatment and reduce the burden of disability associated with it.
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References
1. Larsen JG, Henningsen MJ, Karlsson WK, Christensen RH, Al-Khazali HM, Amin FM,
Ashina H.Epidemiology and clinical features of short-lasting unilateral neuralgiform headache
attacks: a systematic review and meta-analysis. Cephalalgia. 2024;44(8):03331024241271976.
https://doi.org/10.1177/03331024241271976.
2. Hagen K.One-year prevalence of cluster headache, hemicrania continua, paroxysmal hemicrania and SUNCT in Norway: a population-based nationwide registry study. J Headache Pain.
2024;25(1):30.
3. Headache Classication Committee of the International Headache Society (IHS). The international classication of headache disorders, 3rd edition. Cephalalgia. 2018;38(1):1–211. https://
doi.org/10.1177/0333102417738202.
4. May A, Goadsby PJ.The trigeminovascular system in humans: pathophysiologic implications
for primary headache syndromes. J Cereb Blood Flow Metab. 1999;19(2):115–27. https://doi.
org/10.1097/00004647- 199902000- 00001.
5. Eller M, Goadsby P.Trigeminal autonomic cephalalgias. Oral Dis. 2016;22(1):1–8. https://doi.
org/10.1111/odi.12263.
6. Coppola G, Abagnale C, Sebastianelli G, Goadsby PJ. Pathophysiology of cluster
headache: from the trigeminovascular system to the cerebral networks. Cephalalgia.
2024;44(2):3331024231209317. https://doi.org/10.1177/03331024231209317.
7. Lambru G, Rantell K, O’Connor E, Levy A, Davagnanam I, Zrinzo L, Matharu M.Trigeminal
neurovascular contact in SUNCT and SUNA: a cross-sectional magnetic resonance study.
Brain. 2020;143(12):3619–28. https://doi.org/10.1093/brain/awaa331.
8. Lambru G, Matharu MS. SUNCT, SUNA and trigeminal neuralgia: different disorders or
variants of the same disorder? Curr Opin Neurol. 2014;27(3):325. https://doi.org/10.1097/
WCO.0000000000000090.
9. Leone M, Bussone G.Pathophysiology of trigeminal autonomic cephalalgias. Lancet Neurol.
2009;8(8):755–64.
10. May A, Bahra A, Büchel C, Turner R, Goadsby PJ.Functional magnetic resonance imaging in
spontaneous attacks of SUNCT.Ann Neurol. 1999;46(5):791–4. https://doi.org/10.1002/1531-
8249(199911)46:5<791::AID- ANA18>3.0.CO;2- 8.
11. Sprenger T, Valet M, Platzer S, Pfaffenrath V, Steude U, Tölle TR.SUNCT: bilateral hypothalamic activation during headache attacks and resolving of symptoms after trigeminal decompression. Pain. 2005;113(3):422–6. https://doi.org/10.1016/j.pain.2004.09.021.
12. Malick A, Burstein R.Cells of origin of the trigeminohypothalamic tract in the rat. J Comp
Neurol. 1998;400(1):125–44.
::AID- CNE9>3.0.CO;2- B.
13. Malick A, Strassman RM, Burstein R.Trigeminohypothalamic and reticulohypothalamic tract
neurons. J Neurophysiol. 2000;84(4):2078–112. https://doi.org/10.1152/jn.2000.84.4.2078.
14. Bartsch T, Levy MJ, Knight YE, Goadsby PJ.Differential modulation of nociceptive dural
input to orexin receptors in the posterior hypothalamic area. Pain. 2004;109(3):367–78. https://
doi.org/10.1016/j.pain.2004.02.005.
15. Leone M, Franzini A, D’Andrea G, Broggi G, Casucci G, Bussone G.Deep brain stimulation to relieve drug-resistant SUNCT.Ann Neurol. 2005;57(6):924–7. https://doi.org/10.1002/
ana.20507.
16. Lyons MK, Dodick DW, Evidente VG.Responsiveness of SUNCT to hypothalamic deep brain
stimulation. J Neurosurg. 2009;110(2):279–81. https://doi.org/10.3171/2008.4.17493.
17. Bartsch T, et al. Deep brain stimulation in intractable SUNCT. Cephalalgia.
2011;31(13):1405–8. https://doi.org/10.1177/0333102411409070.
18. Viana M, etal. Diagnostic and therapeutic errors in TACs and hemicrania continua: a systematic review. J Headache Pain. 2013;14(1):14.
19. Wei DY, Moreno-Ajona D, Renton T, Goadsby PJ.TACs presenting in an orofacial pain clinic.
J Headache Pain. 2019;20(1):69.
https://doi.org/10.1186/s10194- 024- 01738- x.
https://doi.org/10.1016/S1474- 4422(09)70133- 4.
https://doi.org/10.1002/(SICI)1096- 9861(19981012)400:1<125
https://doi.org/10.1186/1129- 2377- 14- 14.
https://doi.org/10.1186/s10194- 019- 1019- 7.