Subdural haematoma and axonal polyneuropathy complicating
dengue fever
Madhukar Mittal, Nirdesh Jain
Department of Medicine, CSM Medical University, Lucknow, India
Correspondence to Dr Madhukar Mittal, mittalspace@gmail.com

Summary
The authors report a case of dengue fever presenting with aseptic meningoencephalitis and developing subdural haematoma and pure motor
quadriparesis due to axonal polyneuropathy. This 27-year-old female patient presented to us during the latter part of the dengue epidemic in
India in 2010. She had mild thrombocytopaenia and subtle signs of capillary leak. Dengue-specific IgM antibody was positive. She presented
initially with recurrent seizures. Initial CT scan of brain was normal with cerebrospinal fluid showing albuminocytologic dissociation. After 6
days, the patient developed quadriparesis with areflexia. MRI showed bilateral subdural haematoma with no evidence of spinal nerve root
compression. The nerve conduction study showed evidence of axonal neuropathy. The patient’s quadriparesis improved such that she was
able to walk with support after 4 weeks with conservative management. This case report highlights a possible association between dengue
and motor axonal neuropathy subtype of Guillain–Barré syndrome.

BACKGROUND
Worldwide, 50–100 million cases of dengue infection occur
each year.1 2 Dengue fever occurs in tropical and subtropical areas of the world. According to the estimates by WHO,
dengue alone costs India almost $30 million every year2
and is part of several western travel advisories on India.
Cyclic epidemics are seen in India and cases of dengue generally start to increase from August onwards, which is the
postmonsoon season and decrease as winter sets in.
Dengue is transmitted by the bite of the Aedes mosquito
infected with any one of the four dengue virus serotypes.
Infection by different serotypes offers no cross protection
and epidemics caused by multiple serotypes can occur.
Infection can be asymptomatic or present with symptoms
ranging from fever, headache, retro-orbital pain, myalgias,
arthralgias and rash to the potentially fatal form of dengue haemorrhagic fever (DHF) or dengue shock syndrome
(DSS). The spectrum of neurological disease in dengue is
not very well elucidated. We present here a case of dengue
fever with neurological involvement as the predominant
manifestation.

CASE PRESENTATION
A 27-year-old woman was admitted in an unconscious
state following multiple episodes of generalised tonicclonic seizures over past 10 h. There was preceding history
of high-grade fever with backache and myalgias for 7 days.
Purpuric rashes or any other bleeding manifestations were
absent. On examination, the patient was febrile and comatose with a Glasgow coma score (GCS) of 10. There were
no signs of meningeal irritation. No cranial nerve involvement was seen. Cardiovascular and respiratory system
examination did not reveal any abnormality.
Laboratory investigations showed a normal total leucocyte count and low platelet count (8200/mm3 and

BMJ Case Reports 2011; doi:10.1136/bcr.12.2010.3672

100 000/mm3, respectively). Both smear and card test for
antigen were negative for malaria. Serology for herpes
simplex virus 1 and 2, Japanese encephalitis, Salmonella
typhi and S paratyphi were all negative. However, denguespecific IgM antibody by commercial micro-well enzyme
immunoassay kit (IVD Research Inc, Carlsbad, California,
USA) was positive. Blood sugar and serum electrolytes
were normal. Serum aminotransferases were raised; however, prothrombin time and partial thromboplastin time
were normal. Ultrasonography showed mild peritoneal
and pleural fluid collection. Fundus examination and CT
scan brain were normal. Total cell count of 10/mm3 (all
lymphocytes) and protein content of 173.7 mg/dl were
present on cerebrospinal fluid (CSF) examination.
Antiepileptic management was instituted in the form
of intravenous infusion of phenytoin sodium followed
by regular maintenance doses. Over a hospital stay of 3
days, the patient’s consciousness improved and her GCS
became 14. The patient was soon able to take oral feeds.
However, she developed weakness of both lower limbs
on day 6 which progressed to involve the upper limbs
over next 24 h. Neurological examination revealed a
power of 2/5 and 1/5 on Medical Research Council scale
in upper and lower limbs, respectively. Weakness was
accompanied with hypotonia, areflexia and non-elicitable
plantar reflexes. Sensory system, cranial nerves and autonomic system function examination were all normal. The
patient developed hypokalemia (table 1) which was corrected by giving oral potassium chloride; however, her
quadriparesis persisted. We repeated her brain imaging
(MRI brain including spine) which showed bilateral subdural haematoma not limited by suture lines over both
cerebral hemispheres with focal petechial haemorrhage in
left parietal region in subcortical white matter (figure 1).
No significant compression over cord and nerve roots in

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Unusual presentation of more common disease/injury

Figure 2 Normal MRI cervical spine.
cervical region was seen (figure 2). Neurosurgical opinion
was taken and conservative management was advised.
Nerve conduction study (NCS) included normal latencies,
sensory nerve action potential and velocity in sensory
NCS when checked in bilateral median, ulnar and sural
nerve. Normal latencies, low compound muscle action
potential and normal velocities were seen in the motor
NCS (table 2); features suggestive of acute motor axonal
polyneuropathy (AMAN).
Conservative management and general supportive care
of the patient was continued. We could not offer plasma
exchange to the patient, as the facility was not available in

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our hospital and cost was a constraint for giving intravenous immunoglobulin. Corticosteroid therapy is of uncertain benefit for patients of Guillain–Barré syndrome (GBS)
and was not given. No ventilatory support was required
during the course of her illness. The patient showed a
slow but gradual improvement in power (3/5 in upper
limbs and 2/5 in lower limbs) over several days and was
discharged on day 17. Weekly review of the patient on
follow-up showed further improvement, with a power of
4/5 in upper limbs and 3/5 in lower limbs after 2 weeks
and gradually the patient was able to walk with support
over another 2 weeks.

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Figure 1 (A) Normal CT scan brain, (B) bilateral extra-axial concavo convex lesion, displaying hypointense on T1W image (arrow), (C)
coronal section T2W FLAIR image showing focal haemorrhage in left parietal region subcortical white matter (arrow).

Table 1 Laboratory parameters
Parameters (Reference ranges)

Date: November 2010
11

Haematocrit (35–44% for female)
Total WBC count (4000–11 500 cells/mm3)
Platelet count (1.5–4.5 lacs/mm3)
Random blood sugar (mg/dl)
S. Sodium (135–148 meq/l)
S. Potassium (3.5–5 meq/l)
S. Urea (15–43 mg %)
S. Creatinine (0.6–1.2 mg %)
PT (12–16 s)
INR (0.8–1.2)
aPTT (25–36 s)
S. Bilirubin (0.5–1.2 mg/dl)
SGPT (9–45 IU/l)
CSF
Cells (<5/mm3)
Protein (15–60 mg/dl)
Sugar (50–80 mg/dl)
ADA (<10U/l)

12

24.3
11 400
1.0
121
142
3.4
162
1.94
14
1.0
30

14

16

17

26.2
7790
0.59

1.56

60
137
4.8
64
1.4

153
2.9

1.5
651

21

22

23

24

7500
2.98
156
162
2.6

136
165
2.7

157
4.3

152
138
5.1

0.5
202

10
173.2
162
9.13

ADA, adenosine deaminase; aPTT, activated partial thromboplastin time; CSF, cerebrospinal fluid, INR, International Normalised Ratio; PT, prothrombin time; SGPT, serum
glutamic pyruvic transaminase; WBC, white blood cell.

Table 2

Nerve conduction and EMG study with reference ranges
Nerves

Sensory NCV

Latencies (ms)

Left median
Right median
Left ulnar
Right ulnar
Right sural
Left median
Right median
Left ulnar
Right ulnar
Left common peroneal
Left tibial

Motor NCV

Peak amplitude (µV)

Patient

Reference

Patient

Reference

Patient

Reference

3.1
3.2
3.1
3.4
3.1
4.15
3.65
2.9
3.5
3.5
4.75

<3.5

15.6
17.2
17.9
20.9
19.2
3.6
3.9
2.9
2.6
3.5
2.4

15

>50

≥4

52.5
55.1
51
62.3
64.2
46.3
48.2
42.8
41.3
38.3
40.1

EMG

<4.4
<3.3
<6.5
<5.8

17

≥6
≥2
≥4

≥44
≥45
≥40
≥40

Summary table
Spontaneous

L. Quadriceps
L. Tib. Ant.
R.
Brachioradialis
Impression

Velocities (m/s)

MUAP

Recruitment

IA

Fib

PSW

Fasc

HF

Amp

Dur

PPP

Pattern

N
N
N

None
None
None

None
None
None

None
None
None

None
None
None

N
N
N

1+
N
N

1+
1+
N

Reduced
Reduced
Reduced

Neuropathic pattern

Amp, amplitude; Dur, duration; EMG, Electromyography; Fib, fibrillation; HF, high frequency potentials for myotonia and paramyotonia; IA, insertional activity; MUAP, motor
unit action potential; NCV, nerve conduction velocity; PPP, poly phasic potential; PSW, positive sharp waves.

TREATMENT
Conservative management and general supportive care
of the patient was continued. We could not offer plasma
exchange to the patient as the facility was not available in
our hospital and cost was a constraint for giving intravenous immunoglobulin. Corticosteroid therapy is of uncertain benefit for patients of GBS and was not given.

OUTCOME AND FOLLOW-UP
No ventilatory support was required during the course
of her illness. The patient showed a slow but gradual

BMJ Case Reports 2011; doi:10.1136/bcr.12.2010.3672

improvement in power (3/5 in upper limbs and 2/5 in
lower limbs) over several days and was discharged on day
17. Weekly review of the patient on follow-up showed further improvement, with a power of 4/5 in upper limbs and
3/5 in lower limbs after 2 weeks and gradually the patient
was able to walk with support over another 2 weeks.

DISCUSSION
Neurological manifestations were first reported in 1976
as atypical manifestations in dengue infection.3 The frequency of central nervous system involvement in dengue
fever remains largely unknown. So far, the incidence of

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INVESTIGATIONS

4 of 5

3 was the predominant serotype in a report from India in
2005.14
In this report, we describe a patient of dengue fever with
mild thrombocytopaenia and involvement of both central
as well as peripheral nervous system as the predominant
presentation for the disease. Axonal polyneuropathy could
possibly be associated with dengue as in this case. A high
index of suspicion needs to be maintained in patients with
short duration of febrile illness with atypical neurological
manifestations especially in areas of endemicity for the
disease.

Learning points
Aseptic meningoencephalitis as a presentation for
dengue fever.
▶ Subtle manifestations of capillary leak (small peritoneal
and pleural fluid collection with or without subdural
haematoma) as a pointer towards dengue.
▶ Quadriparesis in dengue due to motor axonal
neuropathy type of GBS.
▶

Competing interests None.
Patient consent Obtained.

REFERENCES
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October 1999. Geneva: WHO, 2000.
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with dengue viral infection clinical and neuroimaging features. Clin Neurol
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presentation as atypical acute subdural hematoma. Pediatr Neurosurg
2008;44:490–2.
11. Kalita J, Misra UK, Mahadevan A, et al. Acute pure motor quadriparesis: is it
dengue myositis? Electromyogr Clin Neurophysiol 2005;45:357–61.
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Neurol India 2010;58:592–4.
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neurological manifestations in patients with dengue fever
has been reported to vary from 3% to 25% in different
studies.4
A wide array of neurological manifestations such as
headache, seizures, altered sensorium and behavioural
disturbances as part of encephalitis or aseptic meningitis,
in patients with dengue infection have been described.
The CSF picture in our patient had elevated protein with
normal sugar levels. She presented with seizures which
responded to first-line antiepileptic treatment.
Isolated cases of mononeuropathy,5 polyneuropathy
including GBS,6 7 myelitis,8 intracranial thrombosis and
haemorrhage9 10 have been reported. Electrophysiologically,
demyelinating, axonal and mixed forms of GBS are known
with demyelinating pattern as the most common form.
Besides GBS, other causes reported for quadriparesis in
dengue fever patients are myositis11 and hypokalemia.12
Bleeding into segmental nerves can lead to manifestations;
however, our patient had symmetrical quadriparesis and
MRI spine focussing on cervical segment was normal.
Our patient presented with fever, seizures and loss of
consciousness followed by axonal polyneuropathy (possibly AMAN type of GBS as suggested by NCS) and
quadriparesis. Since the patient was residing in a dengue
endemic area and her clinical presentation and lab investigations (mild thrombocytopaenia and evidence of capillary
leakage in the form of small peritoneal and pleural fluid
collection and subdural haematoma) suggested a clinical
picture of dengue fever, the patient’s blood was tested for
IgM antibodies against dengue virus. A positive serology
confirmed infection by dengue virus. We could not perform quantitative testing for the dengue antibody titres.
Screening MRI for whole spine with particularly focus on
cervical segment was normal. Collective features such as
acute onset, areflexic, ascending and symmetric pattern of
paralysis without bladder, bowel and sensory involvement
suggested GBS. AMAN subgroup was distinguished by
electrodiagnostic study results that are consistent with a
pure motor axonopathy. However, antibodies to gangliosides (like anti-GM1 antibodies) were not done.
The most severe well known forms of dengue infection
are DHF and DSS. Prior infection with heterogeneous serotypes and production of non-protective antiviral antibodies that bind to Fc receptor of macrophages and monocytes
may have an antibody dependent enhancement phenomenon.13 It results in increased cytokine production and
activation of complement system, leading to increased
vascular permeability, capillary fragility and thrombocytopenia and ultimately contributes to mortality. However,
neurological manifestations of dengue entail greater morbidity. Whether neurological disease in dengue now being
increasingly recognised is because of increased awareness
for the disease or is part of new virological strains is a matter of speculation and further research. Dengue serotype

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