Herath et al. Journal of Medical Case Reports (2018) 12:100
https://doi.org/10.1186/s13256-018-1627-x

CASE REPORT

Open Access

Cerebral vasculitis and lateral rectus
palsy – two rare central nervous system
complications of dengue fever: two case
reports and review of the literature
H. M. M. Herath1* , J. S. Hewavithana2, C. M. De Silva2, O. A. R. Kularathna2 and N. P. Weerasinghe3

Abstract
Background: Dengue fever is a common mosquito-borne viral illness with a clinical spectrum ranging from a
simple febrile illness to potentially life-threatening complications such as dengue hemorrhagic fever and dengue
shock syndrome. Dengue infection can affect many organs, including the central nervous system. The neurological
manifestations reported in dengue infections are meningitis, encephalitis, stroke, acute disseminated encephalomyelitis,
and Guillain-Barré syndrome.
Case presentation: We report the cases of two interesting patients with confirmed dengue infection who presented
with complications of possible central nervous system vasculitis and cranial nerve palsy. The first patient was a 53-year-old
previously healthy Singhalese woman who developed acute-onset slurring of speech and ataxia with altered sensorium 1
day after recovery from a critical period of dengue hemorrhagic fever. Subsequent investigations revealed
evidence of encephalopathy with brainstem ischemic infarctions. Her clinical picture was compatible with central
nervous system vasculitis. She was treated successfully with intravenous steroids and had a full functional
recovery. The second patient was a middle-aged Singhalese woman who had otherwise uncomplicated dengue
infection. She developed binocular diplopia on day 4 of fever. An ocular examination revealed a convergent
squint in the left eye with lateral rectus palsy but no other neurological manifestation.
Conclusions: Central nervous system vasculitis due to dengue infection is a very rare phenomenon, and to the
best of our knowledge, only one case of central nervous system vasculitis has been reported to date, in a patient
of pediatric age. Cranial nerve palsy related to dengue infection is also rare, and only a few cases of isolated
abducens nerve palsy have been reported to date. The two cases described in this report illustrate the rare but
important central nervous system manifestations of dengue fever and support the fact that the central nervous
system is one of the important systems that can be affected in patients with dengue infection.
Keywords: Dengue infection, Cerebral vasculitis, Encephalitis, Cranial nerve palsy, Neurological complications

Background
Dengue fever is a common arboviral infection in tropical
and subtropical areas of the world. It is transmitted by
the hematophagous mosquito Aedes aegypti [1]. Around
2.5 billion people in more than 100 countries are at risk
of dengue infection, with about 100 million cases of
* Correspondence: herathtp@gmail.com
1
Department of Medicine, Faculty of Medicine, University of Ruhuna , P.O.
Box 70, Galle, Sri Lanka
Full list of author information is available at the end of the article

symptomatic dengue occurring annually [2]. Being a tropical country with high rainfall, Sri Lanka has experienced
frequent dengue outbreaks for the last several decades. In
2017, over 100,000 cases of dengue infection were reported in Sri Lanka [3]. Dengue infection can be caused
by one of four distinct, antigenically related serotypes:
DEN-1, DEN-2, DEN-3, and DEN-4 [1].
The clinical presentation of dengue infection ranges
from mild clinical febrile illness to potentially lifethreatening dengue hemorrhagic fever (DHF) and dengue

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Herath et al. Journal of Medical Case Reports (2018) 12:100

shock syndrome (DSS) [4]. The main cause of death in
dengue infection is either DHF or DSS, both of which are
due to increased capillary permeability resulting in plasma
leakage [5]. Apart from these complications, dengue
infection is known to cause multiple organ involvement,
including the central nervous system (CNS) [6–10].
Neurological complications in dengue infection can be
explained by three different pathogenic mechanisms: (1)
direct invasion of the CNS, leading to encephalitis, meningitis and myelitis; (2) systemic complications resulting in
encephalopathy and stroke; and (3) para- or postinfectious
immune-mediated effects, such as acute disseminated encephalomyelitis (ADEM), Guillain-Barré syndrome, and
optic neuritis [7, 11].
We report two cases of patients with dengue infection
associated with CNS complications. The first patient
had possible CNS vasculitis related to dengue, and the
second had isolated cranial nerve (abducens nerve)
palsy. These two cases are of importance because, to
the best of our knowledge, CNS vasculitis triggered by
dengue infection has not been described previously in
the literature. Furthermore, only three cases of isolated
cranial nerve palsy related to dengue infection have
been reported previously.

Case presentation
Patient 1

An otherwise healthy 53-year-old Singhalese woman
who was an office worker from Southern Province, Sri
Lanka, presented to a local hospital with an acute febrile illness with no apparent focus of infection. She
had no significant past medical illnesses and did not
smoke or consume alcohol. Three days prior to her
hospital admission, she developed high fever with
chills, myalgia, and moderate headache. She was conscious and rational with no hemodynamic compromise. Her full blood count revealed a hemoglobin level
of 13.6 g/dl, packed cell volume (PCV) of 37.9%, white
blood cell count of 4.2 × 103/mm3, and platelet count
of 105 × 103/mm3. The result of her nonstructural
protein 1 (NS1) antigen test (enzyme-linked immunosorbent assay) was positive. Her liver transaminases were
elevated with aspartate aminotransferase (AST) of 161 U/
L and alanine aminotransferase (ALT) of 113 U/L. In the
next 48 hours, she was observed in the local hospital with
serial full blood count measurements, which showed a
gradual reduction of her platelet count to 41 × 103/mm3
on the fifth day of her illness, at which point her PCV had
risen to 42%. She had evidence of free fluid in the hepatorenal pouch on an ultrasound scan, indicating progression into the critical phase of DHF. She was observed
and managed in the next 48 hours of the critical phase
according to the established national guidelines on dengue management [12]. She went through the critical

Page 2 of 6

phase without any significant complication, such as
bleeding, shock, or multiorgan failure. Following resolution of the critical phase, she was afebrile and clinically improving. Her PCV dropped from 42% to 36.5%,
and her platelets showed a gradual increase to 141 ×
103/mm3. However, on postcritical day 1, she experienced
acute-onset slurring of speech, deviation of the mouth,
difficulty in swallowing, and unsteadiness in gait. At this
juncture, she had no fever, headache, or seizures. An
urgent noncontrast computed tomographic scan did not
demonstrate any particular abnormality in the brain and
brainstem. The patient was transferred to our unit for
further evaluation and management.
On admission to our unit, the patient was hemodynamically stable with a blood pressure of 112/74 mmHg
and pulse rate of 84 beats/minute. She was afebrile but
was slightly drowsy with a Glasgow Coma Scale score of
13/15. She had right-sided lower motor-type facial nerve
(cranial nerve VII) palsy with ipsilateral palatal weakness,
horizontal nystagmus with fast component to the right,
and mild weakness in the left upper and lower limbs with
normal reflexes and sensory and plantar responses. The
rest of the examination, including funduscopy, was unremarkable. Subsequent laboratory investigations, including
septic screening with blood culture and mycoplasma serology, serum electrolytes, and liver and renal function, did
not reveal any significant abnormalities. Apart from
leukopenia (total white cell count of 3400/mm3, 42% neutrophils, 56% lymphocytes), a repeat full blood count
showed no significant abnormalities. The diagnosis of
dengue infection was reconfirmed by the presence of
dengue-specific immunoglobulin G (IgG) and IgM antibodies in serum on day 7 of the patient’s illness (ELISA
method). Analysis of the patient’s cerebrospinal fluid
(CSF) revealed a normal protein level of 53 g/L, a normal
glucose level, and no pleocytosis. An electroencephalogram (EEG) showed features of encephalitis (Fig. 1).
Magnetic resonance imaging (MRI) of the brain revealed
multiple infarctions involving the pons and medulla regions (Fig. 2).
The patient was treated with intravenous dexamethasone to reduce cerebral inflammation. Supportive measures, including physiotherapy and speech therapy, were
initiated. She had gradual but progressive improvement
over the next few weeks and had a full functional recovery
around 1 month after the illness. CNS vasculitis due to
dengue infection was the presumptive diagnosis, based on
the clinical presentation of acute onset of focal neurological signs with evidence of brainstem infarction and
encephalopathy.
Patient 2

A 57-year-old previously healthy Singhalese woman who
was a schoolteacher was admitted to our unit with a

Herath et al. Journal of Medical Case Reports (2018) 12:100

Fig. 1 Electroencephalogram showing generalized spike and
wave discharges and periodicity compatible with encephalopathy

history of fever, headache, malaise, nausea, and anorexia
of 3 days’ duration. She did not smoke or use alcohol or
recreational drugs. On examination, she had a
temperature of 39.5 °C and was hemodynamically
stable with a pulse rate of 66 beats/minute and blood
pressure of 112/66 mmHg with no significant postural
drop. The rest of her examination was unremarkable.
Her full blood count revealed a total leukocyte count
of 4100/mm3 with 42% lymphocytes, hemoglobin of
13.4 g/dl, PCV of 40%, platelet count of 94,000/mm3,
and elevated liver transaminases (ALT of 77 U/L and AST
of 86 U/L). Dengue infection was confirmed by detection
of the NS1 antigen.

Fig. 2 Magnetic resonance imaging scan of the brainstem showing
multiple infarctions involving the pons and medulla regions (arrow)

Page 3 of 6

The patient was started on treatment for uncomplicated dengue fever. However, on the second day of her
hospital admission, she started complaining of bilateral
diplopia, which worsened upon left gaze. She did not
complain of headache, and her consciousness level was
not reduced at this stage. An ocular examination revealed a convergent squint in the left eye with evidence
of isolated lateral rectus weakness. The results of the rest
of the CNS examination, including the vision and fundus
of both eyes, were normal. The patient was investigated
with an MRI scan of the brain, which ruled out a spaceoccupying lesion or any other significant pathology.
During the patient’s hospital stay, her platelet count
dropped gradually to 44,000/mm3 on the fifth day of
fever, before it started to rise. Apart from isolated lateral
rectus weakness, she did not develop any other complications, such as plasma leakage, shock, hemorrhage, or
liver failure.
She was managed with intravenous and oral fluids according to the national guideline for the management of
dengue fever [12]. She recovered from dengue fever and
was discharged from the hospital on day 7 of her illness.
She had evidence of improvement of her lateral rectus
palsy at the time of discharge, and it completely resolved
within 4 weeks without any specific treatment.

Discussion
The two patients with dengue infection whom we describe in this report, one with possible CNS vasculitis
and the other with isolated cranial nerve (abducens
nerve) palsy, had extremely rare CNS manifestations of
dengue infection. Particularly, CNS vasculitis triggered
by dengue infection has not been described in the literature previously, to the best of our knowledge. Furthermore, only three cases of isolated cranial nerve palsy
related to dengue infection have been reported previously.
Dengue infections pose a significant health challenge
in affected countries in the tropics [2]. CNS manifestations are increasingly recognized and can cause diagnostic and management dilemmas [13]. A wide variety of
CNS manifestations of dengue have been described,
ranging from meningitis [14–16] to immune-mediated
disease such as Guillain-Barré syndrome [17, 18] and
optic neuritis [19]. CNS involvement of dengue infection
was first described by Sanguansermsri et al. in 1976 in a
patient who presented with encephalopathy [20]. Since
then, many different types of CNS involvement have
been described. Even though the pathogenesis of CNS involvement of dengue infection is still poorly understood,
direct viral invasion, autoimmune reaction, and metabolic
and hemorrhagic disturbances are widely considered as
possible mechanisms. Murthy categorized CNS manifestations in dengue infection into three groups [21]: (1) CNS
involvement due to direct neurotropic effects such as

Herath et al. Journal of Medical Case Reports (2018) 12:100

meningitis, encephalitis, and myelitis; (2) CNS involvement due to metabolic complications such as encephalopathy, hypokalemic paralysis, and stroke; and (3) postviral
immune-mediated CNS complications such as encephalomyelitis, optic neuritis, and Guillain-Barré syndrome [21].
Based on patient 1’s presentation and investigations,
CNS vasculitis was considered as the most likely diagnosis. Most patients with isolated CNS vasculitis typically
have headache and features of encephalopathy, with
evidence of multiple cerebral infarctions [22]. Patient 1
developed ischemic stroke, as evidenced by acute onset
of focal neurological symptoms (dysarthria and ataxia)
and signs of brainstem lesions (such as palatal palsy and
lower motor facial nerve palsy) with evidence of brainstem infarctions involving the pons and medulla regions
on an MRI scan. In addition, patient 1 had clear evidence
of encephalopathy, as indicated by altered sensorium and
typical EEG abnormalities observed in encephalopathy.
Alternative causes for patient 1’s encephalopathy were
considered unlikely, given that there was no evidence of
hemodynamic compromise, metabolic derangement such
as hypoglycemia, electrolyte imbalance, or liver failure.
This was further confirmed by the presence of a normal
CSF study. Dengue encephalitis was considered as one of
the possibilities. However, the combination of stroke with
multiple infarctions, encephalopathy with altered sensorium, headache, and absence of CNS pleocytosis made
CNS vasculitis more likely. Furthermore, the main features of dengue encephalitis, such as seizures and CNS
pleocytosis, were absent in patient 1 [23]. Even though
CNS pleocytosis may be absent in some patients with
dengue encephalitis, it is a well-recognized feature of the
disease [13, 15, 23]. For example, the diagnostic criteria
for dengue encephalitis proposed by Carod-Artal et al.
included CSF pleocytosis [11].
There are many challenges in making a definitive diagnosis of isolated cerebral vasculitis [22]. The lack of uniform consensus regarding diagnostic criteria, as well as
diagnostic limitations of specific investigations such as
angiography and imaging, present important challenges.
Angiography was not considered in patient 1 because
she responded to the treatment well and she was unwilling to undergo further testing due to her prolonged
hospital stay. CNS vasculitis due to dengue infection is
a very rare phenomenon, and to the best of our

Page 4 of 6

knowledge, only one case of CNS vasculitis has been reported to date, in a patient of pediatric age [24]. As far
as we are aware, there are no previous cases of CNS
vasculitis reported in adults with dengue.
Regarding treatment, the mainstay of treatment for
dengue infection and its associated CNS complications
is supportive therapy based on locally available guidelines [7, 12, 23, 25]; however, steroids may have a place
in treating some of the immune-mediated CNS complications. There is some evidence that CNS complications
such as ADEM [26, 27] and myelitis [25, 28] have a favorable response to steroid therapy. Patient 1 also had a
good response to an intravenous steroid (dexamethasone), which may suggest that an underlying immunemediated pathological process was the most likely reason
for the CNS manifestation.
Patient 2 had isolated sixth cranial nerve palsy that developed on the fourth day of her illness. Cranial nerve
palsy associated with dengue infection is also relatively
rare, with only a few cases reported previously [8, 29].
Optic neuropathy [19], oculomotor nerve palsy [30], and
facial nerve palsy [9, 31] associated with dengue infection
have been described previously. Abducens nerve palsy has
also been described, but only in a few cases [8, 9, 29]. All
reported cases of abducens nerve palsy were in male patients, and none of them had features of DHF (plasma
leakage) or DSS. Most patients developed abducens nerve
palsy roughly 1 week after the onset of fever. However, patient 2 and the patient reported by Mazliha et al. [9] developed abducens nerve palsy within the first 5 days of the
onset of fever (Table 1). Even though some authors have
suggested that the underlying pathophysiology behind
cranial palsy could be due to an immune-mediated
mechanism, direct viral invasion of cranial nerves is
more likely, considering the fact that some patients developed abducens nerve palsy at an early stage of their
illness (days 2–4). The fact that all patients recovered
fairly rapidly without any specific therapies such as
steroids favors direct viral invasion over immunemediated mechanisms [7, 9].
Specific therapies, such as steroids or immunoglobulins, are not generally required in the management of
dengue-related abducens nerve palsy [8, 9, 29]. Patient 2
was managed with supportive therapy with fluid and
paracetamol during the acute stage. She had a complete

Table 1 Characteristics of previously reported patients with abducens nerve palsy
Study

Patient age (years)

Sex

Day of onset of
mononeuropathy in
relation to fever

Type of mononeuropathy

Associated with
DHF or DSS

Associated with other
CNS manifestation

Mishra, et al. [29]

52

Male

Day 8

Lateral rectus palsy

No

No

Shivanthan MC et al.

29

Male

Day 7

Lateral rectus palsy

No

No

Mazliha, et al. [9]

40

Male

Day 2

Lateral rectus

No

No

Abbreviations: CNS Central nervous system, DHF Dengue hemorrhagic fever, DSS Dengue shock syndrome

Herath et al. Journal of Medical Case Reports (2018) 12:100

recovery from the nerve palsy within the first 4 weeks of
the illness. Similar to patient 2, other patients with
dengue-associated cranial nerve palsies, including abducens nerve palsy, Bell’s palsy, and oculomotor nerve
palsy, have been reported to improve without any specific therapy [8, 9]. The prognosis for dengue-related
cranial nerve palsies is good, and complete recovery was
observed in all previously reported cases [8, 9, 25].

Conclusions
Even though most cases of dengue infection have a selflimiting course, some patients develop devastating and
life-threatening complications such as DHF and DSS. In
addition to these two complications, dengue infection
can affect many other organ systems, including the CNS.
Even though a wide variety of CNS manifestations of
dengue infection have been reported, CNS vasculitis associated with dengue infection has not been described
previously among adults. To the best of our knowledge,
we report the first case of CNS vasculitis in an adult patient with dengue infection. Furthermore, abducens
nerve palsy in the setting of fever in a tropical country
such as Sri Lanka could very well be due to dengue infection, and dengue infection should be considered as a
cause of abducens nerve palsy.
Abbreviations
ADEM: Acute disseminated encephalomyelitis; ALT: Alanine aminotransferase;
AST: Aspartate aminotransferase; CNS: Central nervous system; CSF: Cerebrospinal
fluid; DHF: Dengue hemorrhagic fever; DSS: Dengue shock syndrome;
EEG: Electroencephalogram; ELISA: Enzyme-linked immunosorbent assay;
Ig: Immunoglobulin; MRI: Magnetic resonance imaging; NS1: Nonstructural
protein 1; PCV: Packed cell volume
Acknowledgements
The authors acknowledge the two patients profiled in this case report for
permitting us to publish this case report. The authors also acknowledge
Dr. Krishantha Jayasekara, consultant physician at Balapitiya Base Hospital,
and all the staff of the university medical unit of Karapitiya Teaching Hospital
for their assistance in investigating and managing the two patients
presented in this case report.
Funding
No funding was received for this report.
Availability of data and materials
Data sharing is not applicable to this article, because no datasets were
generated or analyzed. The two reported patients’ hospital records are not
shared, because they contain personally identifiable information.
Authors’ contributions
HMMH was involved in patient diagnosis and management and in writing
the manuscript. JSH, CMDS, and OARK were involved in investigations and
writing the manuscript. NPW was involved in writing the manuscript. All
authors read and approved the final manuscript.
Ethics approval and consent to participate
Not applicable.
Consent for publication
Written informed consent was obtained from the patients for publication of
this case report and any accompanying images. Copies of the written
consent are available for review by the Editor-in-Chief of this journal.

Page 5 of 6

Competing interests
The authors declare that they have no competing interests.

Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in
published maps and institutional affiliations.
Author details
1
Department of Medicine, Faculty of Medicine, University of Ruhuna , P.O.
Box 70, Galle, Sri Lanka. 2University Unit, Karapitiya Teaching Hospital, Galle,
Sri Lanka. 3Department of Microbiology, Faculty of Medicine, University of
Ruhuna, Galle, Sri Lanka.
Received: 11 October 2017 Accepted: 19 February 2018

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