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ISSN: 2455-5282

GLOBAL JOURNAL OF MEDICAL AND CLINICAL CASE REPORTS

Case Report       Open Access      Peer-Reviewed


FULMINANT REVERSIBLE CEREBRAL VASOCONSTRICTION SYNDROME: THE OTHER THUNDERCLAP
HEADACHE


KEITH A BROWN1*, JAMES BRADY1 AND AMMAR ALIMAM2

AUTHOR AND ARTICLE INFORMATION

1Division of Internal Medicine, Rowan University School of Osteopathic Medicine
at Jefferson Health New Jersey, Stratford, New Jersey, USA
2Division of Pulmonary and Critical Care, Pulmonary and Sleep Associates of
South Jersey, LLC, Cherry Hill, New Jersey, USA
*Corresponding author:Keith A Brown, Division of Internal Medicine, Rowan
University School of Osteopathic Medicine at Jefferson Health New Jersey,
Stratford, New Jersey, USA, E-mail: brownke@rowan.edu; kabrown@atsu.edu
DOI: 10.17352/2455-5282.000113
Received: 16 November, 2020 | Accepted: 02 December, 2020 | Published: 03
December, 2020
Keywords: Reversible cerebral vasoconstriction syndrome; Thunderclap headache;
Ischemic stroke; Migraine

Cite this as

Brown KA, Brady J, Alimam A (2020) Fulminant Reversible Cerebral
Vasoconstriction Syndrome: The Other Thunderclap Headache. Glob J Medical Clin
Case Rep 7(2): 117-120. DOI: 10.17352/2455-5282.000113

ABSTRACT

Reversible Cerebral Vasoconstriction Syndrome (RCVS) is a rare neurologic
clinical syndrome that is often misdiagnosed. The pathophysiology of RCVS is
unknown, but oftentimes presents as a thunderclap headache that is commonly
overlooked once cerebral hemorrhage is ruled out of the differential. Typically
patients follow a benign course and make a full recovery, however, in a small
subset of patients RCVS can result in permanent neurologic damage. We present a
patient with an uncommon clinical course of RCVS and identify pitfalls in the
diagnostic workup.

MAIN ARTICLE TEXT


INTRODUCTION

Reversible Cerebral Vasoconstriction Syndrome (RCVS) is a rare phenomenon that
is underdiagnosed in clinical practice [1]. Oftentimes the presenting symptom of
RCVS is a thunderclap headache leading to evaluation for cerebral hemorrhage.
However, blood work and imaging are usually negative which often leave the
physician without answers or down an arbitrary path to treat atypical migraine
headache [2]. Classically the symptoms of RCVS improve after approximately 2
months, but given the risk of life altering complications which include cerebral
infarction, it is important that RCVS be included high in the differential
diagnosis [2,3]. We present a case of a 56 year old female with thunderclap
headache who was subsequently diagnosed with RCVS after devastating cerebral
infarction.


CASE REPORT

The patient is a 56 year old female with a history of migraines,
gastroesophageal reflux disease, hypertension, and hyperlipidemia that presented
to the hospital with a sudden onset headache that started approximately 1 week
ago. The patient rates the pain a 10/10 at onset and since then the headache has
waxed and waned in intensity. These headaches were described as different from
her typical migraine headache as it presented more suddenly and with greater
intensity. She presented to multiple urgent care facilities to seek treatment
and multiple Computed Tomographies (CT) of the head with CT Angiography (CTA)
were performed throughout the previous week, which were only significant for
bilateral intracranial internal carotid artery aneurysm. Her surgical history
consists of hysterectomy, C3-C4 cervical fusion, and bilateral rotator cuff
repair. Her social history was reviewed and she is a 1 pack per day smoker. Her
home medication regimen included atorvastatin 80mg daily, clopidogrel 75mg
daily, duloxetine 90mg daily, omeprazole 40mg daily, carvedilol 6.25mg daily,
and ranitidine 150mg twice daily, and butalbital-acetaminophen-caffeine
50-325-40mg daily as needed.

On arrival to the hospital, the patient’s vital signs revealed a blood pressure
of 147/78 mmHg.

Her admission laboratory work was unremarkable with the exception of a glucose
of 199 mg/dL. CT of the head and CT angiography of the head and neck were
performed promptly upon arrival, which was approximately 1 week after onset of
headache, revealing atherosclerotic calcification of the bilateral internal
carotid arteries particularly at the level of the cavernous and supraclinoid
segments. Two aneurysms measuring 2mm involving the left and right internal
carotid arteries were observed. However no other acute intracranial pathology or
evidence of large vessel occlusion were demonstrated. The patient was admitted
to the hospital under the Internal Medicine Service with presumed diagnosis of
intractable migraines and 6mg subcutaneous injection of sumatriptan and 10mg
decadron were prescribed upon Neurology evaluation on day 2 of her hospital
stay. The patient became more encephalopathic with fevers and Magnetic Resonance
Imaging (MRI) and Magnetic Resonance Angiography (MRA) were done on day 2 of her
hospital stay, which were unremarkable, and lumbar puncture was completed on day
3 to rule out neurologic infection or autoimmune etiology of her altered
mentation which was also negative.

Six days into the patient’s hospitalization a stroke alert was activated as the
patient had acute neurologic changes with increased lethargy and was unable to
move her left arm. A teleneurology evaluation was done and a CT of the head was
performed revealing large subacute appearing infarcts of the right and left
posterior frontal, parietal, and occipital lobes, as well as the right
cerebellum (Figure 1). CTA revealed mild to moderate stenosis in the cavernous
and infraclinoid internal carotid arteries bilaterally with diminutive anterior
cerebral arteries and possible occlusion of a distal segment or branch of the
left anterior cerebral artery. Moderate stenosis was seen in the distal right
vertebral artery, however the posterior cerebral arteries were not well
visualized on this imaging study (Figure 2). The patient developed seizures
which were refractory to lorazepam and she was intubated and started on versed
continuous infusion. Continuous electroencephalogram revealed focal seizures
originating the right occipital lobe. She was started on levetiracetam and
lacosamide. On day 6, MRI was able to be done at that time revealing infarcts as
previously described on CT with petechial hemorrhagic conversion. An
echocardiogram was performed and significant for grade I left ventricular
diastolic dysfunction consistent with impaired relaxation. In the setting of
multiple cerebral infarctions and the ongoing pandemic of coronavirus-2019
(COVID-19), she was tested for the virus and was found to be negative. The
patient was transferred to our facility for Neurosurgery evaluation as the
admitting facility did not provide neurosurgical services.


Figure 1: (A) Coronal View CT angiogram of head without evidence of large vessel
occlusion. (B) Coronal view CT angiogram of head with severe focal stenosis of
supaclinoid right internal carotid artery and moderate stenosis of right
M1-middle cerebral artery segment. Multifocal stenoses of right A2-anterior
cerebral artery segments. (C) Axial view CT angiogram of head without evidence
of large vessel occlusion. (D) Coronal view CT angiogram of head with severe
focal stenosis of supraclinoid right internal carotid artery and moderate
stenosis of right M1-middle cerebral artery segment. Multifocal stenoses of
right A2- anterior cerebral artery segments.

Figure 2: (A) MRI FLAIR and T2 signal hyperintensity at inferior right
cerebellar hemisphere. (B) MRI FLAIR and T2 signal hyperintensity involving
posterior occipital lobes. (C) MRI FLAIR and T2 signal hyper intensity involving
bilateral parietal lobes and posterior right frontal lobe.

Upon arrival to our facility the patient was intubated and sedated on versed and
propofol and admitted to the Critical Care Service with Neurology and
Neurosurgery consultation. Sedation was weaned and she was able to be extubated.
The patient was provisionally diagnosed with RCVS at this time and 4 grams (g)
of Intravenous (IV) magnesium and oral amlodipine 10mg were prescribed and her
previous levetiracetam and lacosamide were continued. A repeat CTA of the head
and neck were done on day 7 revealing known findings of bilateral occipital lobe
infarcts, however arteries were patent with no findings of significant stenosis
or occlusion. After starting the patient on this regimen she became
progressively more awake, alert, and oriented after several days of treatment.
However she was found to be blind bilaterally, with ⅗ strength in the right
upper and lower extremities with left sided hemiplegia. Over the course of her
hospital stay she received amlodipine 10mg daily and 2g of magnesium daily for 7
days. The patient continued to work with physical therapy to optimize her
physical mobility and strength. At the conclusion of her 21 day hospitalization,
her vision did improve significantly and she only required reading glasses for
correction of her vision. Unfortunately, she remained with residual left sided
hemineglect. She was discharged to an acute rehabilitation facility and will
continue to follow up with her Neurology specialist for ongoing evaluation and
management.


DISCUSSION

In 2007, multiple unexplained vasculopathies and vasoconstriction syndromes to
include CallFleming syndrome, postpartum angiopathy, and acute benign cerebral
angiopathy were unified as one clinical syndrome called RCVS [4,5]. Since this
time few cases have been reported in the literature of patients with RCVS with
poor outcomes and death as it is generally observed to have a self-limiting
course [5]. RCVS appears to predominantly affect young females between the ages
of 20 to 50 years of age, but according to a single cohort study, men who
present with RCVS are significantly younger and symptoms are often associated
with sexual activity [6]. The hallmark of the disease is thunderclap headache as
well as reports of photophobia and phonophobia leading the physician to a
diagnosis of migraine after cerebral hemorrhage has been ruled out [1,7]. The
exact mechanism for this clinical syndrome is unknown, but susceptibility to
developing RCVS may be influenced by genetics or a potential trigger [8]. Common
triggers have been reported to include alcohol, sexual intercourse, triptans,
postpartum states, and Valsalva maneuver; however, many patients are diagnosed
without a known trigger [2]. Specific attention should be paid to the use of
triptans as patients are often prescribed this for migraine, which this clinical
syndrome is often mistaken for. Previous case reports have linked triptans to
induce or at the very least exacerbate RCVS [8]. Our patient was also prescribed
triptans which may have contributed to her rapid neurologic decline after
hospitalization.

Clinical presentation is misleading as thunderclap headache is the most common
clinical presentation of RCVS although it is not specific for the syndrome
[1,4]. In fact, when physicians encounter thunderclap headache the differential
is often limited to subarachnoid hemorrhage, migrainous headache disorder,
Primary Angiitis of the Central Nervous System (PACNS), and cervical arterial
dissection. More specific characteristics of thunderclap headache that are
associated with RCVS include a waxing and waning course often that repeats over
1 to 3 weeks [4]. This distinction is particularly important to consider during
initial examination in a patient with RCVS as presentation of subarachnoid
hemorrhage presents with more abrupt onset. Seizures can be present at onset as
well, but their recurrence is rare [9]. Rapid progression of the disease is very
unusual in RCVS [5], but our patient did develop rapid neurological decline
after she was hospitalized. This type of fulminant course is encountered in
5-10% of patients with RCVS resulting in permanent disability and death [10].

Diagnostic criteria for RCVS include acute and severe onset headache, with or
without additional neurologic signs or symptoms that are uniphasic without new
symptoms after 1 month of onset. On cerebrovascular imaging there is evidence of
multifocal segmental cerebral artery vasoconstriction without evidence of
aneurysmal SAH [4,9]. A clinical and radiologic distinction must be made between
RCVS and PRES. MRI with diffuse weighted imaging and cerebral angiographic
imaging remains the radiologic test of choice for both clinical entities and in
RCVS lesions are typically asymmetric while in PRES lesions are more symmetric.
MRI should be performed when CT are non diagnostic and do not adequately explain
the patients symptoms. In RCVS there are also ischemic lesions noted bilaterally
while ischemic lesions are uncommon in PRES. In RCVS vasoconstriction on
vascular imaging is a distinctive finding 6. Our patient demonstrated findings
of asymmetric lesions with associated ischemia with vasoconstriction on vascular
imaging which is more typical with RCVS. Given results of imaging, a lumbar
puncture was performed to exclude pleocytosis in the setting of headache.
Infectious workup to include CSF analysis was unremarkable, which was done to
exclude infectious as well as paraneoplastic and autoimmune etiology. Most
importantly there is reversibility of angiographic abnormalities within 12 weeks
after onset of disease, separating it from the etiology and findings in acute
ischemia secondary to vascular occlusion from thrombosis or progressive
atherosclerosis [4,9]. Infarction on baseline imaging, use of intra-arterial
vasodilator therapy, and glucocorticoid therapy may be associated with poor
outcomes [10].

There are no clear treatment modalities for the treatment of RCVS and specific
treatment is based on observational studies and clinical experience. Like any
clinical entity with potential triggers, these offending agents must be
discontinued [9], such as sumatriptan in our patient. Other pharmacologic agents
thought to be potential precipitating factors are triptans, ergotamines,
pseudoephedrine, amphetamines, cannabis, cocaine, and bromocriptine [1].
Treatment of the vasospasm should be considered for cerebral vasoconstriction
with calcium channel blockers and continued for 4-12 weeks. Our patient was
treated with amlodipine and magnesium upon diagnosis which has been used as well
in the treatment of acute RCVS with success. The decision to use amlodipine
opposed to nimodipine, nicardipine, or verapamil was arbitrary and based off of
the attending physician preference. There are no evidence based guidelines
regarding calcium channel blockers although nimodipine and verapamil are most
common reported in previous cases. Intra-arterial administration of
epoprostenol, milrinone, and nimodipine as well balloon angioplasty have all
been reported in more severe cases with variable success. However, this
intervention should be utilized based on access to intervention and operator
experience as this procedure is higher risk [1,9]. Although magnesium and
calcium channel blockers have been used in previous reported cases of RCVS, no
standard treatment regimen has been established [1]. However, long term
management with neurologic specialists is imperative as symptom recurrence and
complications until death may rarely occur [10].


CONCLUSION

RCVS presents a diagnostic challenge in physicians as it is not a commonly
encountered clinical syndrome. However, given the life altering complications
such as cerebral hemorrhage and infarction, it is imperative to be aware of this
clinical entity. Patients who present with thunderclap headache without
significant findings on neuroimaging are often diagnosed with migraines even if
the clinical history does not fit properly. Unfortunately, this leads to
prescription of vasoconstrictive drugs which can often worsen RCVS. Through this
case it is our goal to bring awareness to RCVS and bring the condition into
physicians’ differential diagnosis as the other thunderclap headache.

ACKNOWLEDGEMENTS

Institutional financial and material support were not provided for the creation
of this manuscript.

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COPYRIGHT

© 2020 Brown KA, et al. This is an open-access article distributed under the
terms of the Creative Commons Attribution License, which permits unrestricted
use, distribution, and reproduction in any medium, provided the original author
and source are credited.

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