UHM 2018, Vol. 45, No. 1 – CCAD AND SCUBA: IS THERE A LINK?
Research Article
Cervicocranial artery dissection and scuba diving:
Is there a link or is it serendipity?
Gerald K. Walters, MS, PA-C.
Senior Physician Assistant, Johns Hopkins Bayview Medical Center,
Johns Hopkins School of Medicine, Baltimore, Maryland U.S.
EMAIL: hyperbaric@verizon.net
_____________________________________________________________________________________________________________________________________________________________________
ABSTRACT
Introduction: Numerous reports have documented cervico-
cranial artery dissection (CCAD) associated with scuba diving.
The question remains as to whether there are risk factors
unique to scuba diving related to the occurrence of CCAD.
Objectives: This article aims to perform an examination of
the reported cases to demonstrate any commonality among the
injured divers and association with known risk factors for CCAD.
Methods: A PubMed search was performed utilizing the key
words: carotid artery dissection, dissection, arterial dissection,
cranial artery dissection, scuba, diving, scuba diving.
Articles including reports, reviews, trials, case series, and letters
were considered. Each report was critically dissected for
information specific to the dive itself and the diver and analyzed
for similarities and consistency with known risks.
Results: Twelve (12) reports of CCAD associated with scuba
diving were identified. Activities involved with scuba diving appear
to be consistent with CCAD risk factors. It is unclear if hyper-
baric stress and physiological changes during a dive
present specific risk. Trauma – e.g., environmental protection
and activities associated with diving – was identified as a
common risk factor in all cases. Ten (10) cases involved
arteries at anatomic sites commonly associated with dissections.
Seven divers documented to have dive profiles suspicious of
decompression sickness were identified.
Conclusion: There appears to be a correlation with minor
traumas that occur with diving and CCAD. The inconsistency
of the dive-related specific information reported makes it
impossible for investigation of hyperbaric stress-related risk
factors for CCAD to be analyzed.
___________________________________________________________________________
KEYWORDS: carotid artery dissection; dissection;
arterial dissection; cranial artery dissection; scuba;
diving; scuba diving
Copyright © 2018 Undersea & Hyperbaric Medical Society, Inc.
INTRODUCTION
Cervicocerebral artery dissection (CCAD) is a leading
cause of stroke in younger individuals. Carotid or verte-
bral artery dissection occurs from a tear in the arterial
intima or disruption of the vaso vasorum, with resul-
tant intramural hematoma. The results are narrowing or
occlusion of the affected vessel, with the possibility of
embolization and cerebral infarction. Genetic, environ-
mental and traumatic factors have been identified as
etiologic variables.
Recently, a correlation with cervicocerebral arte-
rial dissection and scuba diving has been postulated. In
1995, Nelson first reported a case of carotid dissection in
a diver [1]. Since then, numerous others have presented
carotid, vertebral and intracranial artery dissection
occurring contemporary with scuba diving. Underwater
diving unquestionably subjects an individual to a unique
environment. Diving subjects individuals to minor
traumas: e.g., jumping from heights to enter the water,
constrictive environmental protection in the form of
wetsuit and drysuits as well as sustained head and neck
positions. Hyperbaric stress, submersion and water
conditions all interact on human physiology while
using scuba. Since a possible link between diving and
arterial dissection is proposed it then becomes reason-
able to explore what, if any, are the unique contributing
factors that are present in this activity.
The intent of this report is to critically review the doc-
umented cases of CCAD associated with scuba diving
to establish some commonality among the patients.
The role of trauma in the development of CCAD is well
established. Are there any traumatic stressors that may
be mitigated while diving to minimize the risk of
CCAD? Does hyperbaric stress in and of itself present
a risk for CCAD?
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METHODS
A PubMed search was performed utilizing the key
words: carotid artery dissection, dissection, arterial dis-
section, cranial artery dissection, scuba, diving, scuba
diving. All articles including reports, reviews, trials,
case series, and letters were considered. Articles were
not limited to only those in peer-reviewed journals.
Each report was critically dissected for information
specific to the dive itself and the diver and analyzed
for similarities and consistency with known risks.
RESULTS
Twelve (12) articles were identified as reporting on
CCAD occurring contemporary with scuba diving
(Table 1). Information regarding diver, type of dive,
equipment used, dive profile and past personal and
family history was harvested from the articles. Only
those cases where the diagnosis was confirmed by
imaging were considered. Presentation of symp-
toms, treatment and outcomes varied throughout the
reports. Since the purpose of this paper is to search for
similarities in risk factors and inciting events, details
about symptoms and treatment were not deemed
necessary.
Nelson reported on a 52-year-old male with “mini-
mal” diving experience [1]. On the day of presentation
to the emergency department complaining of headache,
the diver reported he had made three dives:
• to 10 meters of seawater (msw) with a bottom time
of 25 minutes;
• 25 msw for 30 minutes; and
• 30 msw for 25 minutes.
The surface intervals were not elucidated. The headache
worsened after making two subsequent freedives to
5 msw.
On the following day, the diver was noted to have
dysarthria and dysphasia. His past medical history was
positive for hypertension only, and family history was
non-contributory. Expressive aphasia was documented
on examination. Magnetic resonance imaging (MRI)
showed several small left parietal infarcts and a left
internal carotid artery (LICA) occlusion.
Progression of the aphasia and sudden right hemi-
paresis prompted an emergency arteriogram, which
confirmed an occlusion of the (LICA) and a near-total
occlusion of the right internal carotid artery (RICA)
at the skull base. Bilateral carotid artery dissection
was confirmed on MRI.
66
In a letter to the editor from Chojdak-Lukasiewicz,
the case of a 27-year-old male diver was presented
[2]. The dive profile and specifics of the dive were not
reported, only described as having been conducted
in “cold water.” Vertigo and ataxia were present on
initial evaluation. MRI demonstrated a right medulla
oblongata infarct. Right posterior inferior cerebellar
artery (PICA) dissection was demonstrated on a subse-
quent computerized tomography arteriogram (CTA).
Kocigit discussed a 32-year-old diver who presented
for treatment after “diving at sea” three days earlier [3].
Persistent drowsiness was the only chief complaint.
Risk factors for arterial dissection were unremarkable
by physical and laboratory examinations. A left PICA
territory infarct was discovered, and angiography doc-
umented dissection of the posterior medullary segment
of the left PICA.
Minutes after a scuba dive in the Mediterranean Sea,
a 37-year-old female noted left-sided neck pain and
left facial paresthesia accompanied by a feeling of
pressure in the left ear, described by Hafner [4]. The
water temperature was reported as approximately
22° C, and the dive conducted with “adequate
weighting and a well-fitting scuba cylinder.” The
patient endorsed a history of multiple sclerosis (MS),
which was stable. There were no cardiovascular risk
factors other than a 15 pack-year smoking history. A
color Doppler duplex of the cervical arteries revealed
decreased flow velocities in the LICA without evidence
of stenosis or demonstrable lesions. MRI and magnetic
resonance arteriography (MRA) of the brain and
cervical and intracranial arteries was performed. A
2-cm subcranial LICA dissection was noted, along
with changes consistent with MS.
Konno presented a case of an 18-year-old male diver
with a right vertebral artery dissection [5]. The report
was void of information about the dive itself. The pre-
viously healthy patient was evaluated at a local hospital
for right occipital headache and neck pain associated
with vertigo and visual disturbance. Decompression
sickness was suspected; medical treatment resulted in
no improvement of symptoms. The authors did not
elaborate on the specific treatment or if it included
recompression therapy.
Two weeks later the patient was noted to have a left
upper quadrant hemianopsia. MRI and cerebral angi-
ography demonstrated infarction in the right cerebellar
hemisphere and medial occipital lobe and occlusion of
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Table 1. Reported cases of CAD and diving

author age/sex diving history missing data PMH/fam Hx risk factors vessel location

Nelson 1 52/male 3 dives/ entry, HTN, non smoker, NS bilateral skull

35”at 10 msw, conditions, FMH-NC ICA base
30” at 25 msw, gear
25” at 30 msw
__________________________________________________________________________________________________________________________________________________________
Chojdak- 27/male NS other than DP, entry, NS NS right IC
Lukasiewicz 2 cold water conditions, gear PICA
__________________________________________________________________________________________________________________________________________________________

Kocigit 3 32/male “diving at sea” DP, entry, NC not left IC
conditions, present PICA
gear
__________________________________________________________________________________________________________________________________________________________
Hafner 4 37/female water-22°C, DP, entry, stable multiple NS left “sub-
adequate weighting conditions sclerosis, ICA cranial”
and well-fitting smoker
cylinder
__________________________________________________________________________________________________________________________________________________________
Konno 5 18/male NS, DCS DP, entry, NS NS right artery second
suspected conditions, vertebral segment
gear artery
__________________________________________________________________________________________________________________________________________________________
Gibbs 6 38/male 36-m dive after entry, NS NS right skull
several hours of conditions, ICA base
diving, rapid direct gear
ascent, did undergo
recompression
__________________________________________________________________________________________________________________________________________________________
Bartch 7 51/male 15” at 5 msw, entry, long smoking NS left skull
15” at 20 msw, conditions, history, ICA base
15” at 5 msw gear otherwise NC
__________________________________________________________________________________________________________________________________________________________
Formento 8 32/male “deep scuba dive,” DP, entry smoker NS left NS
21°C water for conditions, ICA
3 hours, weight of gear
equipment “typical”
__________________________________________________________________________________________________________________________________________________________
Brajkovic 9 52/male NS other than conditions, HTN, BPH, NS LICA skull
cold water gear tension headaches base
__________________________________________________________________________________________________________________________________________________________
Fukuoka 10 51/male 60” at 20 msw entry, NS NS LACA IC
20 years’ diving conditions, except no PFO
experience gear or shunt
__________________________________________________________________________________________________________________________________________________________
Mayer 11 35/female first scuba dive DP, entry, OI? OI bilateral C2 level,
conditions, vertebral, origin of
gear LICA ICA
__________________________________________________________________________________________________________________________________________________________
Shurnik 12 48/female 90” at 8 msw, DP, entry, NS NS LICA distal
carried heavy bag conditions, extracranial
after the dive gear
__________________________________________________________________________________________________________________________________________________________

DP – dive profile; HTN – hypertension; FMH – family medical history; PMH – past medical history; NC – non-contributory,
NS – not stated; ICA – internal carotid artery; PICA – posterior inferior cerebellar artery; IC – intracranial; DCS – decompression sickness;
MCA – middle cerebral artery; HTN – hypertension; BPH – benign prostatic hypertrophy; PFO – patent foramen ovale

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 UHM 2018, Vol. 45, No. 1 – CCAD AND SCUBA: IS THERE A LINK?
the second segment of the right vertebral artery.
In a paper published by Gibbs, a 38-year-old experi-
enced female diver was retrieved from the surface after
losing consciousness while making a rapid direct ascent.
She had made a 36-msw dive after several hours of
diving [6]. The diver suffered nausea, vomiting, neck
pain and headache. She demonstrated a right gaze pref-
erence, expressive aphasia and a left pronator drift.
Recompression utilizing the U.S. Navy Table 6 re-
sulted in resolution of the left-sided weakness. However,
her expressive aphasia persisted. An acute right cortico-
parietal stroke was seen on CT and MRI. MRA revealed
a RICA narrowing at the skull base with a luminal hema-
toma. Right internal carotid artery dissection was sub-
sequently confirmed on CTA. The authors did discuss
a relationship between her recent diving experience but
conceded the dissection was linked to scuba diving
coincidently. Fukuoka described a 51-year-old male with 20 years
Bartch described a 51-year-old male who suffered an
embolic stroke contemporary with scuba diving [7].
The patient made an uneventful dive with the following
profile: 15 minutes at 5 msw; 15 minutes at 20 msw;
and 15 minutes at 5 msw. Three hours after surfacing
he complained of slurred speech and problems with
word-finding, with symptoms lasting 15 minutes.
Two days later he noted difficulty in tongue movement,
dysphagia and left-sided headache. Horner syndrome
was observed four days later.
Examination revealed leftward tongue and uvula
deviation. The patient endorsed a long history of ciga-
rette use but had an otherwise unremarkable past or
family history. MRI/MRA confirmed several small
embolic infarcts in the left middle cerebral artery
(MCA) territory and occlusion of the LICA below
the skull base. Carotid dissection was confirmed by
the presence of an intramural hematoma on MRA.
Minutes following a “deep scuba dive,” a 32-year-old
male diver experienced left neck pain and a full feeling
in his left ear, as reported by Formento [8]. This ex-
perienced diver had conducted an uneventful dive
in 21°C water for three hours. The other details of the
dive were not reported except to state that the weight
of his equipment was typical for recreational diving.
Six days later he was found to have Horner syndrome,
with ptosis and myosis. He did endorse cigarette use.
Past medical history, detailed neurologic examination,
laboratory testing and CT of the neck and head were
68
non-contributory. A LICA dissection was subsequently
documented on MRI/MRA. There was no mention of
cerebral infarction or other focal neurologic symptom
elucidated in the report.
Following a scuba dive in cold water, a 52-year-old
male complained of persistent neck pain with pain ra-
diating behind the left eye. As reported by Brajkovic, the
continuing headache – associated now with left-sided
facial edema, left ptosis, myosis and neck pain – led the
patient to seek evaluation [9]. Incomplete Horner
syndrome was discovered as well as dysesthesia of the
left scalp and leftward deviation of the tongue.
The patient’s past medical history was remarkable
for hypertension, benign prostatic hypertrophy and
tension headaches. Magnetic resonance imaging re-
vealed dissection of the LICA near the skull base and
an incidental left MCA aneurysm.
of dive experience who suffered sudden right hemipa-
resis during a one-hour scuba dive to 20 msw [10]. On
presentation to the hospital he displayed a right hemi-
paresis. A head CT did not demonstrate hemorrhage
or infarcts. MRI/MRA revealed hyperdense areas in
the left superior frontal and cingulate gyri and stenosis
of the left anterior cerebral artery (LACA). Additional
MRA imaging subsequently demonstrated a double
lumen finding consistent with dissection of the LACA.
Patent foramen ovale or other right-to-left cardiac shunt
was ruled out.
A genetic collagen disorder was reported by Mayer
in this 35-year-old female who suffered multiple cere-
bral artery dissections following her first scuba dive [11].
Eight days after her uneventful scuba dive, she was
evaluated for vertigo, nausea and headache. Her symp-
toms intensified over several days, and she was ob-
served to have nystagmus, right facial weakness and
severe ataxia. She subsequently required intubation for
severe dysphagia and respiratory compromise. Sub-
sequently, she displayed bilateral brainstem deficits,
right Horner syndrome, left facial weakness, bilateral
palate and tongue weakness, nystagmus and ataxia.
General physical examination revealed bluish sclerae.
The past medical and family histories were non-contrib-
utory. MRI and angiography demonstrated left superior
cerebellum and right posterolateral medulla infarction.
Bilateral vertebral artery dissections were seen at the C-2
level along with dissection of the origin of the LICA.
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 UHM 2018, Vol. 45, No. 1 – CCAD AND SCUBA: IS THERE A LINK?
The presence of the blue sclerae prompted a work-up for
a suspected genetic abnormality which demonstrated
findings consistent with osteogenesis imperfecta.
Skurnik reviewed a 48-year-old male who experienced
severe pain on the left neck and face two days following
a dive to 8 msw for 1.5 hours [12]. He also complained
of dysgeusia (all food tasted bitter) and anisocoria.
He could recall 10 minutes of some dizziness and stiff
neck immediately upon surfacing. He noted carrying
a heavy dive bag on his left shoulder after the dive.
Horner syndrome was confirmed on his initial exam-
ination. A CT scan was normal, and the MRA demon-
strated dissection of the distal part of the extracranial
LICA.
DISCUSSION
Spontaneous vs. traumatic CCAD
Cervicocerebral artery dissection may be categorized
as either spontaneous or traumatic. Spontaneous dissec-
tion implies a lack of trauma as a contributing factor.
Controversy exists as to whether there are cases with a
true absence of an instigating trauma or an injury that
may be trivial and overlooked. A group of 24 non-diving
patients who sustained a stroke related to a confirmed
carotid or vertebral artery dissection was compared
with matched subjects who had stroke without dissec-
tion [13]. In the dissection group, 17 (71%) reported a
history of trauma prior to presentation. Three categories
of trauma were described: intense physical efforts, jerky
or abrupt neck movement, and sustained extreme neck
positions. Suspected head movements included sporting
activities that involved hyperextension or lateral devia-
tion of the neck. Intense physical effort, including the
lifting of heavy objects, has been identified as an incit-
ing event. Hyperextension of the neck has been cited as
sufficient trauma in the development of CCAD [13-15].
Risk factors associated with CCAD
Diving vs. non-diving events
Additionally, events common to scuba diving have
been implicated in CCAD. These include: prolonged
neck hyperextension; falls from less than 3 meters;
lifting heavy objects; Valsalva maneuver; and external
vasocompression [13-16]. Data from the Cervical Artery
Dissection and Ischemic Stroke consortium reported
on a cohort of 1,618 patients with ischemic stroke not
associated with diving [17]. The study compared
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genetic and environmental risk factors in 960 patients
with CCAD and stroke and 658 ischemic stroke patients
without CCAD. One intriguing comparison was the
relationship between time of year, autumn-winter vs.
spring-summer, and the occurrence of CCAD. A signifi-
cant majority of patients suffered CCAD in the autumn-
winter months, (P=0.007). Additionally, more infec-
tions were noted in the autumn-winter group. This
connection could suggest that the presence of a
current or recent infection might be related to
CCAD.
Recent infections
Grau presented three cases of CCAD associated with
recent infection [18]. These patients suffered both
carotid and vertebral artery dissection, with concurrent
febrile respiratory infections. In fact, one patient experi-
enced a second dissection five years following a previous
one, both associated with infection. All patients in this
small series denied any recent trauma or congenital or
hereditary conditions known to be associated with
CCAD.
Triggering mechanisms that may contribute to CCAD
associated with a recent infection may include me-
chanical stress caused by vomiting or coughing,
injury to the arterial wall from antibiotic use, or
increased inflammatory parameters [19].
Altered vascular function
The hyperbaric environment elicits many physiologic
changes on the human body, including altered vascular
function and vasospasm [20]. A link between cerebral
vasospasm and cervical artery dissection has been
previously established by Mawet, et al. [21]. Their
observations “strongly suggest that the association of
reversible cerebral vasoconstriction (RCVS) and cer-
vical artery dissection is unlikely by chance.” RCVS
is associated with numerous conditions, including
migraine and thunderclap headaches [22]. Certain
medication commonly used by divers – e.g., pseudo-
ephedrine – may cause vasoconstriction.
Cerebrovascular dysfunction occurring during scuba
diving has been documented [23]. Sixteen (16) divers
were monitored for MCA and PCA blood flow follow-
ing no-decompression dives in a water temperature
of 15°C and using air. Following the dives, increased
velocities were observed in the anterior and posterior
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cerebral arteries as recorded by transcranial Doppler.
The proposed reasons for these findings were changes
in arterial blood gases, cerebrovascular endovascular
dysfunction and cerebral vasospasm.
Other evidence of the correlation between vascular
changes with decompression stress has been shown to
be a result of microparticle shedding [24]. Lambrechts
studied nine experienced divers who made a decom-
pression dive in 15°C water [25]. After the experimental
dive, impairment of both cutaneous microcirculation
as well as dysfunction in large conduit arteries was
observed. Intracardiac bubbles were also detected in all
divers without any suspected cases of decompression
illness (DCI). There was no correlation between degree
of vascular function and bubble formation. It was
therefore unclear how hyperbaric stress induced these
changes. The results demonstrated that both macro- and
microvascular dysfunction resulted from the study
dives. Although it is evident hyperbaric stress alters
vascular function, it has yet to be proven these
changes contribute to CCAD in divers.
Arterial abnormalities and hereditary disorders
Primary arterial abnormalities or anatomical varia-
tions have been documented in patients with CCAD
[13]. Anomalous arterial anatomy was documented in
several patients with CCAD as well as arterial fibro-
muscular dysplasia. Genetic factors associated with
connective tissue anomalies identified in patients with
CCAD include Ehlers-Danlos syndrome, Marfan’s syn-
drome and osteogenesis imperfecta (OI) [23]. OI was
diagnosed in a patient sustaining multivessel dissections
following a scuba dive [11]. In an interesting review of
84 patients with CCAD, none were identified with either
clinical or molecular finding meeting diagnostic criteria
for hereditary connective tissue disorder (HCTD) [27].
However, 96% displayed at least one historical, physical
and/or symptomatic feature of 68 findings known to be
associated with HCTD. This led the authors to conclude
that “systemic aberrations of connective tissue might be
implicated in the pathogenesis of the disease (CCAD).”
Only one of the reported cases clearly displayed a
hereditary disorder known to be a risk factor for
CCAD: osteogenesis imperfecta [11]. The other reports
failed to provide any specific information regarding
hereditary or other genetic factors, except Kocigit,
who reported the absence of these factors [3]. Given
70
the lack of frequency of HCTD or other genetic risk
factors in the series of scuba-related dissections, it ap-
pears that this would not be a significant causal factor.
Internal carotid arteries
In the 12 cases presented, involvement of multiple ves-
sels in the same patient was reported twice [1,11].
A total of 15 arteries were affected in the reported cases.
The ICA was affected in nine arteries, with seven on
the left side and two on the right. Intracranial arteries
– two PICAs and an ACA – represented three of 15
vessels with dissection. The vertebral artery was identi-
fied in three of the affected arteries. In the seven divers
with ICA dissections, the location was described as at
the skull base in four, “sub-cranial” in one, distal part
of extracranial in one, and at the carotid origin in one.
One author did not report the location. The skull base
is where the cervical carotid passes through the carotid
foramen and courses through the petrous bone (Fig-
ures 1 and 2). This anatomical location leaves the artery
susceptible to trauma and is the most common location
for ICA dissections to occur [28,29].
Diving-related vertebral dissection:
hyperextension, direct trauma, equipment
Regarding the vertebral dissections, the V2 portion,
defined as that part of the vertebral artery contained
within the foramina of the cervical vertebral transverse
processes, is reported to be particularly vulnerable
to stretching and tearing [28]. This observation is
consistent with the location of the described diving-
related vertebral dissection. Caplan noted as well that
stretching movements are probably responsible for
contributing to intracranial dissections [28].
The location of arterial involvement and its relation-
ship to stretching or movement suggests the physical
activities of scuba diving may be a common risk factor.
First, entry to the water while diving occurs in several
ways. Divers may simply walk into the water from the
shore or make a shallow jump from a platform. One
common form of entry is the “giant stride.” The giant
stride is typically utilized when entry is gained from
an elevated platform or boat deck. Divers positions
themselves at the edge of the platform and take a
large step entering the water feet-first. Hypothetically,
performing this entry may cause hyperextension or
direct trauma to the neck. Once in the water divers will
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FIGURE 1
➠

Figure 1: Angiogram demonstrating carotid artery entering the petrous

bone. Solid line – base of the skull Arrow – point where the cervical
portion of the carotid artery enter the fixed bony structure.

Figure 2: ICA dissection originating at the skull base. ➠ FIGURE 2

attempt to maintain neutral buoyancy. Their attitude
in the water column ideally will be horizontal. In this
position the diver is more streamlined and requires
less energy. The neck will be hyperextended and
frequently rotated to allow the diver to observe the sur-
rounding environment. Thomas has listed sustained
extreme positions of the neck and abrupt head move-
ment as potential sources of trauma in CCAD [13].
Another common feature in several reported scuba-
related dissections is the environmental protection
required. To prevent hypothermia and remain comfort-
able in the water, divers may employ either a wetsuit or
drysuit. Both garments employ tight seals or neoprene
around the neck. Sufficient external compression, which
is possible with various dive suits, has been implicated
in CCAD [14,30]. Diving in cold water, which neces-
sitates use of environmental protection, was reported
in three cases.
Scuba diving is an equipment-dependent sport, and
the scuba cylinder is obviously an essential component.
The cylinder, manufactured from aluminum or steel,
is worn on the diver’s back and secured there by straps
or a buoyancy compensation device. An empty cylinder
of that size can weigh approximately 15 kg. Larger-
capacity cylinders obviously weigh more, and some
divers utilize more than one at a time. In addition
to other equipment required, the total weight bur-
den could be a risk factor for CCAD. External com-
pression of the neck may occur as well from various
straps securing the tank. Interestingly, there were no
reports of CCAD associated with the use of rebreather
units. Typically, these units are heavier than open-circuit
equipment and are utilized often on technical dives.
DCI and CCAD
The role of decompression illness (DCI) in the etiology
of CCAD is unknown. Analysis of known dive profiles
and presenting symptoms in the reported cases could
bring a suspicion of DCI in these divers. In fact, two of
the 12 divers discussed were treated with recompression
therapy [5,6]. In the case presented by Gibbs, the diver
made a rapid ascent from depth and lost consciousness
immediately, which would be consistent with an arterial
gas embolism [6]. Additionally, this diver was reported
to have made a 36-msw dive after several hours of
diving, which would have increased to risk for DCS.

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Nelson reported the diver as making three dives. Per
the U.S. Navy dive tables, none of the dives exceeded
the no-decompression limits but would have violated
their directive of no more than two dives within a
12-hour period [31]. Since these were repetitive dives,
however, the surface intervals would dictate the overall
nitrogen load and the risk of DCS.
Alonso Formento and Fukuoka similarly presented
dive profiles that could be suspicious for DCS [8,10].
One dive was described as a “deep scuba dive” in cold
water for three hours. The other was a one-hour dive
at 20 msw, which is the no-decompression limit for
depth. One subject’s presentation was inconsistent with
CCAD and cerebral infarction. That diver’s only
symptom was persistent drowsiness, which has been
described with DCS [32].
Whether CCAD is yet another manifestation of DCI
remains a question. An interesting hypothesis could
involve the role of microbubbles in disruption of the
vaso vasorum. Commercially available microbubble so-
lutions have been used to image the vaso vasorum of
the coronary arteries to identify unstable plaques [33].
Filling of the vaso vasorum with microbubbles is ac-
complished by intra-arterial injection of the contrast
solution. Intravascular ultrasound can then provide
diagnostic images of the vaso vasorum. It could there-
fore be feasible that nitrogen bubbles arising from
decompression might enter the vaso vasorum.
While bubbles in the vaso vasorum have never been
documented in DCS, their presence can conceivably
lead to intramural hemorrhage and CCAD.
72
CONCLUSION
The typical locations of reported scuba-related CCAD
suggest the physical activities of scuba, trivial trauma,
and equipment represent a common feature. Trauma
associated with the prolonged extension and rotation
of the neck as well as the eternal compression from
environmental protection garments could be a sufficient
trigger for CCAD. The giant-stride entry may induce
significant traction on the carotid and vertebral arteries
sufficient to cause a dissection. Vasoconstriction that
occurs from hyperbaric stress has yet to be correlated
with CCAD, as it has in the non-diving population.
A standardized approach in the reporting of these
cases should include a description of the presence or
absence of known risk factors for CCAD. Similarly,
factors such as composition of the dive gas, water
temperature, decompression versus no-decompression
dive, specific details of the dive itself and dive pro-
file, body habitus, and past personal and family history
should be consistently reported. Vague descriptions
of dives, such as in Alonso Formento’s report, leave
details unavailable for analysis [8]. A report of a “deep”
dive for three hours, which would be an atypical recre-
ational dive, lacks details required for thorough review.
Future standardized and detailed reports of CCAD
and scuba diving, would aid the dive medicine com-
munity in the analysis of these cases. Subsequently, a
risk factor unique to scuba diving may be identified
and a possible mitigation of risk offered.
n
The author declares that no conflicts of interest exist
with this submission.
Walters GK
 UHM 2018, Vol. 45, No. 1 – CCAD AND SCUBA: IS THERE A LINK?
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