Review Articles

Unusual Headache Syndromes

Luiz P. Queiroz, MD, PhD
Objective/Background.Some headache syndromes have few cases reported in the literature. Their clinical characteristics,
pathogenesis, and treatment may have not been completely dened. They may not actually be uncommon but rather under-
recognized and/or underreported.
Methods.A literature review of unusual headache syndromes, searching PubMed and ISI Web of Knowledge, was
performed. After deciding which disorders to study, relevant publications in scientic journals, including original articles,
reviews, meeting abstracts, and letters or correspondences to the editors were searched.
Findings.This paper reviewed the clinical characteristics, the pathogenesis, the diagnosis, and the treatment of ve
interesting and unusual headache syndromes: exploding head syndrome, red ear syndrome, neck-tongue syndrome, nummular
headache, and cardiac cephalgia.
Conclusions.Recognizing some unusual headaches, either primary or secondary, may be a challenge for many non-
headache specialist physicians. It is important to study them because the correct diagnosis may result in specic treatments that
may improve the quality of life of these patients, and this can even be life saving.
Key words: unusual headache, exploding head syndrome, red ear syndrome, neck-tongue syndrome, nummular headache,
cardiac cephalgia
(Headache 2013;53:12-22)
The concept of unusual headaches can be applied
to clinical entities whose prevalence rates are lower
than 1% and about which only a few dozen cases have
been reported.
1
Some headache syndromes that were
uncommon when rst described, such as SUNCT,
hemicrania continua, hypnic headache, and reversible
cerebral vasoconstriction syndrome, are nowadays
widely reported in the literature.
There are so many medical conditions that may
present with headache as a main complaint that the
diagnosis of the headache type in these patients may
be overwhelming for the non-specialist.
2
Because of
the low frequency of occurrence, some headache syn-
dromes may pose problems for diagnosis and man-
agement, as their clinical picture, mechanisms, and
treatment are still debated.
3
Although unusual in iso-
lation, uncommon headaches become sizeable when
considered as a group.
2
The differential diagnosis of unusual headache
syndromes in the elderly (typical aura without head-
ache, hypnic headache [HH], cardiac cephalgia [CC],
and exploding head syndrome [EHS])
4
can be differ-
ent from the ones in the pediatric population (neck-
tongue syndrome [NTS] and ophthalmoplegic
migraine)
5
or in the adult population.
In 2006, Evans
6
published a collection of unusual
headaches cases, including exploding head syndrome,
NTS, red ear syndrome (RES), nummular headache
(NH), burning mouth syndrome, hypnic headache,
From the Department of Neurology, Universidade Federal de
Santa Catarina, Florianpolis, Brazil.
Address all correspondence to L.P. Queiroz, Clnica do
Crebro. Rua Presidente Coutinho, 464. 88015-231 Flori-
anpolis, Brazil.
Accepted for publication October 23, 2012. Conict of Interest: No conict.
ISSN 0017-8748
doi: 10.1111/head.12002
Published by Wiley Periodicals, Inc.
Headache
2013 American Headache Society
12
primary cough headache, primary exertional head-
ache, spontaneous intracranial hypotension, and
Alice in Wonderland syndrome. This review paper
will focus on the rst four of these headache syn-
dromes, and include CC, which is also considered an
unusual headache. In fact, they all may not actually be
uncommon but rather under-recognized and/or
underreported in the literature.
METHODS
This review was initiated with a PubMed search
employing the terms unusual headache or unusual
headaches or uncommon headache or uncom-
mon headaches. After deciding which headache
syndromes upon which this review paper would con-
centrate, a second PubMed search was conducted for
each of the 5 disorders. For the term exploding head
syndrome, 21 records were returned, 23 records for
RES or erythromelalgia and ear, 25 records for
NTS, 47 records for numular headache or NH,
and 15 records for CC or cardiac cephalalgia. An
identical search was also performed, utilizing the
same terms, in the ISI Web of Knowledge, in an effort
to extend the comprehensiveness of the review. Some
additional papers were also found by reviewing the
references of published papers. All pertinent publica-
tions in scientic journals published in English-,
Spanish-, or the Portuguese-language, including origi-
nal articles, reviews, meeting abstracts, and letters or
correspondences to the editors, with relevant infor-
mation on the subject matter were included. The
majority of evidence was in the form of case reports.
FINDINGS
Exploding Head Syndrome.Exploding head
syndrome (EHS) was rst described by Armstrong-
Jones, in 1920, as a snapping of the brain.
7
He
described a complaint by some patients of a sudden
crash or noise as if something had snapped or given
way on my brain. He associated this disorder with
the suffering of early melancholia, neurasthenia, and
psychastenia. Presently, some authors do not think
that this syndrome is related to neurosis,
8
although
others state that it may be related to emotional tense-
ness, as many patients report a stressful life situation
in periods when attacks are intense and frequent.
9
This syndrome is considered a benign sleepwake
transition disorder of unknown etiology. Attacks
occur predominantly in relaxed wakefulness or at the
transition from wakefulness to sleep;
10
but less often
patients waken during the night with it and then fall
sleep.
11
The attacks typically present with sudden loud
banging noises, like a bomb explosion or a gun
shot. There is no real headache, but patients are so
alarmed that at rst they may inaccurately describe it
as a pain; upon closer questioning, there is no descrip-
tion of pain but rather a noise in the center or back of
the head.
8
The attacks can be mild, but they are
usually so unpleasant and sometimes terrifying
to patients that they may raise concern in doctors
that an acute subarachnoid hemorrhage may have
occurred.
10
Patients become concerned and may
develop tachycardia, sweating and have difculty
breathing.
8,11
In 1020% of patients, attacks are
accompanied by a sensation of ashing lights.
10
Some
cases of EHS are followed by a sleep paralysis.
12,13
EHS may exacerbate migraine attacks, in patients
with chronic migraine.
10
The pattern of episodes is variable. Some may
have 24 attacks followed by a prolonged, or total,
remission while others have frequent attacks, up to 7
in one night, for several nights each week.
11
The
prevalence of EHS is unknown.
The differential diagnosis includes thunderclap
headaches, hypnic headache, migraine, cluster head-
ache, and paroxysmal hemicranias, as well as noctur-
nal nightmares and sleep myoclonus (sleep starts).
13,14
Sacks and Svanborgn
9
have recorded attacks
during polysomnography in 5 patients, all when they
were awake and relaxed. In 2 patients, they found an
alerting effect; the others had no electroencephalog-
raphy (EEG) changes. In 3 cases, the patients stated
afterwards that they had attacks when sleeping, but
there were no signs of sudden increasing of alertness
in EEG to support their reports. In another case,
15
a
video-EEG showed that attacks correlated with the
transition from nonrapid eye movement (REM)
stage 1 sleep to wake. Some of the events were asso-
ciated with a hypnic jerk. A video- polysomnography
of 11 attacks showed the phenomenon occurring
during non-REM sleep stages 1 and 2, and that the
attacks were preceded by mild snoring.
16
Headache 13
The basis of this syndrome may be a delay in the
reduction of activity in selected areas of the brain-
stem reticular formation as the patient passes from
wakefulness to sleep.
12
At the onset of sleep, the neu-
ronal activity in the brainstem reticular formation
subsides. This, in turn, switches off the motor, sensory,
visual, and auditory parts of the cerebral hemi-
spheres; if there is a delay in selected areas of the
reticular formation in switching off, then a paroxysm
of neuronal activity is manifested by the alarming
experiences, such as a loud noise, a ash of light, or a
myoclonus.
17
Jacome
18
has reported a case of a patient
with EHS and idiopathic stabbing headache relieved
by nifedipine, a calcium channel blocker, 90 mg a day,
speculating that EHS is perhaps a paroxysmal
symptom arising from transient calcium channel dys-
function, similar to the one observed in patients with
episodic ataxia and familial hemiplegic migraine that
results from a mutation in the CACNA1A gene.
To date, there have been no clinical trials of
therapies for EHS. In the majority of cases, rm reas-
surance that the condition is benign is appropriate;
patients are not treated with medication.
8,14
In
patients who complain of sleeping difculties due to
frequent attacks, clomipramine, 50 mg at night, has
been used with success.
9
Topiramate, 200 mg per
day;
15
nifedipine, 90 mg per day;
18
unarizine, 10 mg
per day;
19
and imipramine 10 mg plus alprazolam
0.25 mg, at night
13
have been reported as effective.
Red Ear Syndrome.The RES was rst described
by Lance, in 1994.
20
This syndrome is commonly uni-
lateral and implies discomfort or burning pain as well
as change in color (erythema) that may involve the
adjacent skin of the cheek. The pain may radiate to
the cheek, forehead, a strip behind or below the man-
dible, the area behind the ear, occiput, and the upper
posterior aspect of the neck on the same side.
21,22
Attacks may be either spontaneous or may be pre-
cipitated by exercise, stress, exposure to heat or cold,
touching the ear, drinking, coughing, chewing, sneez-
ing, or neck movement.
23,24
The involvement, in fact,
may be unilateral or bilateral;
23,25,26
symptoms are
often present beyond the ear, and color change is only
one of the many symptoms reported by patients.
27
The
duration of the pain is variable, lasting from 10
minutes to many hours.
22
The frequency is also vari-
able, from less than one per month to four per day.
22
The cutaneous erythema should be observable to the
patient and the examiner, during the attack.
28
Various
case reports have shown that the disorder need not
necessarily result in signicant ear pain but rather
only redness of the ear.
29
More than 80 cases have
been reported, so far. About 60% of the cases are in
women and 40% are in men.
30
No association with primary headache disorders,
including migraine, hemicrania continua, chronic par-
oxysmal hemicrania, and SUNCT has been reported
in adults. Raieli et al
23,31,32
have shown that this syn-
drome is very frequent (24%) in children and adoles-
cents with migraine with and without aura. In this
population, RES was signicantly more prevalent in
males, with throbbing pain and vomiting.
31
If patients
also experience migraine, RES may be in association
with migraine attacks or not.
22
Because of varied etiology, this entity may have
primary and secondary forms. RES may exist as an
idiopathic, primary trigeminal or cervical autonomic
cephalgia, it may coexist with migraine and other
trigeminal autonomic cephalgias,
33
and there may be
secondary forms, in association upper cervical disor-
ders with irritation of the third cervical root, temporo-
mandibular joint dysfunction, glossopharyngeal, and
trigeminal neuralgia, or thalamic syndrome.
21,29,30
Probably, the idiopathic forms are more frequent in
children while the secondary ones are more common
in the elderly.
24,34
In a child with systemic lupus
erythematosus, a thalamic lesion, caused by a vascu-
litis of the middle cerebral artery, was the most
probable cause of RES.
35
Activation of the trigemi-
novascular system may represent a common patho-
physiologic mechanism of all etiologies,
23
with an
antidromic discharge of impulses along the third cer-
vical root, and release of vasodilator peptides in the
ear, such as substance P, calcitonin gene-related
peptide, and nitric oxide, which are responsible for
pain and vasodilatation.
21,27,30,36
Differential diagnoses of RES includes erysi-
pelas, herpes zoster, diffuse otitis externa (Pseudomo-
nas aeroginosa), streptococcal infections, borrelial
lymphocytoma, Hansens disease, erythromelalgia,
relapsing polychondritis, chondrodermatitis, nodu-
laris helices, cartilaginous pseudocyst, eczematous
14 January 2013
diseases, granulomatous diseases, and photoderma-
toses.
30,37
Erythromelalgia is the main differential
diagnosis. Most patients with erythromelalgia experi-
ence the symptoms in the feet (90%) and/or in the
hands (25%), but only rarely involves just the ears.
38,39
It is usually bilateral, but may be unilateral, especially
in secondary cases. Since RES and erythromelalgia
have several diagnostic criteria in common
(erythema, elevated temperature, burning pain, and
pain aggravated by warmth and relieved by coldness),
they probably have a similar pathogenesis. Today,
some authors believe that erythromelalgia is a com-
ponent of RES, and it is possible that RES is the
auricular variant of erythromelalgia.
37
A variety of treatments have been used for RES.
Because of the multiplicity of potential causes, there
is no a treatment of choice, and many patients are
resistant to all treatments.
28,29
A temporary or perma-
nent relief can be achieved by a local anesthetic block
or even section of the third cervical root.
21,24
A case of
brosis surrounding the C
3
root and the vertebral
artery responded dramatically to microvascular cer-
vical decompression.
33
Some cases have responded to
amitriptyline,
21,39,40
gabapentin,
22,41
indomethacin,
22,40
unarizine,
23
nimodipine,
23
and ibuprofen.
29,41
Neck-Tongue Syndrome.The term NTS was
coined by Lance and Anthony, in 1980.
42
In doing so,
they acknowledged a previous report of 2 similar
cases by Cyriax, an orthopedic surgeon, in 1962. In
NTS patients, a sudden rotation of the neck induces a
sharp pain on the side of the upper neck or occiput,
followed immediately by transient ipsilateral numb-
ness of the tongue on the same side. The pain lasts a
few seconds to 1 minute and the paresthesia
seconds to 5 minutes.
42
Other symptoms may occur,
less frequently, such as dysarthria, dysphagia, tongue
paralysis, or movements of the tongue.
43-47
NTS may
present as transient symptoms, which may persist,
resolve, and relapse, or may become permanent, with
continuous decits.
45
Although symptoms remain
always on the same side, the rotation may be to either
side. Rarely, the whole constellation of symptoms can
change to the opposite side, including any unilateral
precipitating maneuver.
48
The estimated prevalence of NTS in the Vaga
study was 0.22%.
48
There are approximately 50 cases
described in the literature. A few cases of NTS
have a familial (probably autosomal dominant)
aggregation.
49,50
The proposed mechanism for the site of the pain
is related to an irritation of the second and/or third
cervical roots, with tongue involvement due to affer-
ent impulses traveling from the lingual nerve via the
hypoglossal nerve to the C
1
-C
2
roots.
42
The anatomical
basis for the NTS was demonstrated by Bogduk,
51
dissecting 5 cadavers. The mechanical disability of the
upper cervical spine that induces compression of the
C
2
root (C
2
dorsal root ganglion and the C
2
ventral
ramus
51
) on sudden rotation of the neck certainly
involves some degree of unilateral subluxation of the
facets of the atlantoaxial joint.
42
An abnormality of
the posterior atlantoaxial ligaments, including the
accessory atlantoaxial ligament (Arnolds ligament),
can be the cause of NTS.
52
There are probably 2 types of NTS: (1) compli-
cated NTS, as a result of an underlying disease
(inammatory or degenerative), and (2) uncompli-
cated NTS (idiopathic, hereditary, or trauma-
related).
52
Any pathology of the occipito-atlantoaxial
joints has been noted in about a quarter of the
reported cases. Adult patients have more anatomical
abnormalities than pediatric patients (65% 21%).
50
Secondary NTS includes congenital anomalies of
cervical spine, Chiari-1 malformation, ankylosing
spondylitis, degenerative spondylosis, rheumatoid
arthritis, tuberculous atlantoaxial osteoarthritis, cervi-
cal acute transverse myelopathy, and also following
head and neck trauma.
49,53-55
The efcacy of any therapeutic approach to NTS
is uncertain. Conservative treatment includes avoid-
ance of neck trauma and the use of nonsteroidal anti-
inammatory drugs (NSAIDs) and drugs to alleviate
neuropathic pain.
56
Treatment commonly used
includes cervical collars, manipulation, analgesics,
NSAIDs, muscle relaxants, carbamazepine, gabapen-
tin, amitriptyline, steroids, injections of local anes-
thetic, nerve resection, and cervical fusion.
45,46,53,56
Nummular Headache.NH was rst described by
Pareja et al in 2002.
57
Two years later, in 2004, it was
included in the appendix of the International Classi-
cation of Headache Disorders, 2nd edition (ICHD-
II).
58
There are currently more than 200 cases reported
Headache 15
in the literature. In a hospital-based tertiary center, the
estimated incidence of NH was 6.4/100,000/year.
59
The pain affects exclusively a circumscribed
cranial area, round (70%) or elliptical (30%), typically
with 16 cm of diameter, most at the parietal region,
and with no changes in size or shape with time. Pain is
usually mildtomoderate (but may be severe), continu-
ous, persisting for days to years, with lancinating exac-
erbations lasting for several seconds or gradually
increasing for 10 minutes to 2 hours.
57
Exacerbations
commonly have a throbbing, electric, or stabbing
quality. They may be precipitated by touching the
symptomatic area, by combing the hair, by head move-
ments, or Valsalva maneuvers.
59,60
Periods of remis-
sion, for weeks or months, are frequently reported.
Most patients also describe a combination of hypoes-
thesia, hyperesthesia, dysesthesia, tenderness, and/or
touch-evoked paresthesias.
57,59,61
The pain is usually
unifocal, but bifocal and even multifocal cases have
been reported.
60,62-66
Patients, when explaining their
symptoms, usually nger point to a specic area of the
head. Some patients have shown trophic changes
withinthe painful area, including thinness of the skin,
67
and one patient had hair heterochromia at the pain
site.
68
There are a few cases reported with the painful
area larger than 6 cm of diameter up to 10 cm.
69,70
Some studies have shown evidence of increased sensi-
tivity a lower pain threshold with pressure algometry
restricted to the symptomatic area, with no pericra-
nial tenderness in the remainder of the scalp, and with
no signs of a generalized pain state.
71-73
The characteristics of clinical observations
suggest a non-psychogenic origin. Fernndez-de-las-
Peas and colleagues
74
have shown that NH is not
associated with either depression or anxiety. A few
patients have reported mild head trauma previous to
the onset of NH.
57,66,70
Many patients have also a past
or present diagnosis of migraine, but the pain from a
migraine headache can be easily distinguished from
the NH pain.
57,70,75-78
Similar to menstrually related
migraine, there is a case report of menstrually related
NH.
75
Focal headaches may result from a variety of
underlying causes, including metastatic disease or
myeloma of the skull, focal intracranial tumors
involving the dura mater, Pagets disease, and local
infection or inammatory diseases.
79
A diagnostic
evaluation should include a complete clinical and
neurological examination, laboratory tests, and neu-
roimaging studies.
61
NH seems to be mainly a primary
disorder, but secondary forms have been described: a
fusiform extracranial aneurysm of the scalp,
80
a
cranial wall lesion,
61
post-transsphenoidal surgery for
pituitary adenoma,
61
meningioma in the left posterior
fossa,
81
arachnoid cysts,
82
and Varicella-zoster virus
infection.
83
Chen et al
84
have noticed an extraordinar-
ily high (65%) association of NH with autoimmune
disorders, including Sjogren/sicca syndrome,
rheumatoid arthritis, and antiphospholipid antibody
syndrome.
The pathogenesis of NH is still not completely
known. The supercial location and consistent char-
acteristics of the pain, local sensory symptoms, the
focal increased sensitivity with algometry, and the
trophic changes conned to the affected area, provide
evidence for an epicranial source of the pain, stem-
ming from the bone, scalp, or pericranial nerves.
59,85
Some authors, however, suggest that there may be
also NH of central origin because of some migrainous
features in some cases and the absence of pain relief
with local nerve blocks.
78,86
Patients are usually more concerned with the
possibility of having a serious disease than with the
pain or with the sensory disturbances.
57
To date, no
specic therapy was identied to be effective for most
patients. As there are a rather high percentage of
patients with spontaneous remission of the pain, we
should be careful when analyzing isolated good
results of any treatment.
66
Local subcutaneous anes-
thetic injections are considered as not effective, but
occasionally it may work.
65
NH may respond to
onabolulinumtoxinA, but the response is not univer-
sal.
77,87,88
Gabapentin seems to be the most used pre-
ventive treatment for NH, although the results are
inconsistent.
60,63,66,89-91
Other treatments potentially
helpful are naproxen,
76
indomethacin,
86
cyclobenza-
prine,
75
nortriptyline,
79
carbamazepine,
69
lamot-
rigine,
60
neurotropin,
92
and transcutaneous
electrical nerve stimulation.
93
Cardiac Cephalgia.The term CC was coined by
Lipton et al in 1997,
94
as a form of exertional head-
ache. In the ICHD-II, it was included in group 10,
16 January 2013
headaches attributed to disorders of homeostasis.
58
The association of headache and ischemic heart
disease, however, has been described at least since
1978.
95
Bini et al in 2009,
96
reviewing the literature,
compiled 30 cases of CC. After that, 6 cases have been
reported.
97-101
Of the 36 cases, 21 (58.3%) were men
and 15 (41.7%) women.
CCusually occurs after 50 years of age, in subjects
at risk for cardiovascular diseases. They may have or
not a previous history of headache. The clinical char-
acteristic of the pain is not homogeneous. It may
involve any part of the head; it may be unilateral or
bilateral; it is generallysevereor excruciating, constric-
tive, and oppressive; but it may be similar to a migraine
headache, with accompanying symptoms such as pho-
tophobia, phonophobia, osmophobia, and nausea.
96
Nausea is probably not prevalent enough (23%) to be
considered an important accompanying symptom.
102
Some cases have presented as a thunderclap head-
ache.
97,100,103,104
Although most patients with CC were
older than 50 years, 22% of them (8/36) were younger
than that the youngest being 35 years old.
95,98-100,104-107
CC is frequently related to exertion, even when mild,
such as walking. It is not obligatorily precipitated by
exercise. Cardiac symptoms, such as chest, mandible,
left arm, or epigastric pain are present in one half of
the patients.
96
The frequency of headache is variable,
from bouts of a few weeks to several years.
There are 4 theories as to the pathogenesis of
CC:
96,97,105
1. Anginal pain is mediated by sympathetic bers in
5060% of cases, by vagal bers in 1020%, and by
both in 3040%. The convergence of autonomic
sensory bers and trigeminal somatic bers into
the descending trigeminal nucleus is responsible
for referred pain into the lower dental arch and in
the head; the convergence of autonomic and
somatic bers in the upper cervical spinal cord
could cause referred pain in the occipital region.
2. The sudden reduction of cardiac output, caused
by cardiac ischemia, increases pressure in the left
ventricle and in the right atrium. Consequently,
there is a reduction of venous blood ow from
the brain, an elevation of intracranial pressure,
and distention of intracranial structures, causing
pain.
3. As a result of myocardial ischemia, there is a
release of neurochemical mediators (serotonin,
bradykinin, histamine, substance P, and atrial natri-
uretic factor), with potent vasodilating action in
the brain, causing headache.
4. CC could be secondary to a concomitant occur-
rence of vasospasm in both coronary and cerebral
vessels.
To make the diagnosis of CC, it is necessary to
have a medical history demonstrating the onset of
the headache in close temporal relationship with
acute myocardial ischemia. An electrocardiogram
(ECG) must be performed at rest and under stress.
The baseline ECG may be normal or show patho-
logical alterations (in 57%); these alterations may
only appear under stress ECG. Elevated cardiac
markers (CPK-MB, myoglobin, and troponin) may
occur. In doubtful cases, coronary angiography can
conrm the diagnosis, by detecting coronary artery
stenosis.
96
It is uncommon for myocardial ischemia
to produce headache as its only presenting symp-
tom.
108
If CC manifests without cardiac symptoms,
physicians should think about this diagnosis when
patients are over 50 years of age, have signicant
risk factors for cardiovascular diseases (male sex,
smoking, diabetes, hypertension, hypercholester-
olemia, and obesity), and the onset of headache is
during/after exertion.
96,102,109
Distinguishing CC from migraine is of great
importance. Migraine-like characteristics of CC can
lead to use of vasoconstrictor agents (triptans, ergota-
mine, and dihydroergotamine), which are contraindi-
cated for these patients because of their ability to
constrict coronary arteries. CC usually responds to
therapy with nitrates, which are used to treat cardio-
vascular diseases.
94,96,99,109-111
Nitrates, by vasodilating
cerebral arteries, may precipitate a headache
in normal subjects and a migraine attack in
migraineurs.
112
The response to nitrates by abating
the headache corroborates the diagnosis of CC.
110
Patients submitted to angioplasty or bypass surgery
nd that both their cardiac condition and also the
headache resolve. CC may occur again, if there is
restenosis of the coronary artery.
96,98,113
Potential risk
of mortality exists.
106,110
Headache 17
CONCLUSIONS
The ICHD-II comprises almost 200 headache
types and subtypes.
58
Diagnosing and treating the
most common headache disorders are not so difcult.
Recognizing some unusual and uncommon head-
aches, either primary or secondary, may be a chal-
lenge for many non-headache specialist physicians.
Some of these syndromes are scarcely reported in the
literature. However, it is important to learn about
them because correct diagnosis may result in specic
treatments that improve the quality of life of these
patients and can even be life saving, such as in the
case of CC.
This paper reviewed the clinical characteristics,
pathogenesis, diagnosis, and the treatment of ve
unusual, uncommon, and interesting headache syn-
dromes: EHS, RES, NTS, NH, and CC.
Acknowledgment: The author wishes to thank Dr.
Alan M. Rapoport (University of California Los Angeles,
USA) for reviewing the manuscript.
STATEMENT OF AUTHORSHIP
Category 1
(a) Conception and Design
Luiz P. Queiroz
(b) Acquisition of Data
Luiz P. Queiroz
(c) Analysis and Interpretation of Data
Luiz P. Queiroz
Category 2
(a) Drafting the Manuscript
Luiz P. Queiroz
(b) Revising It for Intellectual Content
Luiz P. Queiroz
Category 3
(a) Final Approval of the Completed Manuscript
Luiz P. Queiroz
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