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Revista do Instituto de Medicina Tropical de São Paulo

On-line version ISSN 1678-9946

Rev. Inst. Med. trop. S. Paulo vol.53 no.4 São Paulo July./Aug. 2011 



Acute inflammatory demyelinating polyradiculoneuropathy (Guillain-Barré syndrome) following dengue fever


Polirradiculoneuropatia desmielinizante inflamatória aguda (síndrome de Guillain-Barré) após dengue



Eduardo Gonçalves

Department of Health of Women and Children, Medical School, State University of Montes Claros, Montes Claros, Minas Gerais, Brazil, and Medical School Pitágoras, FIP-MOC, Montes Claros, Minas Gerais, Brazil

Correspondence to




This paper reports a case of dengue in a six-year-old female child who suddenly developed excruciating headaches, fever, myalgia and paresis. Laboratory examinations included blood count, platelet count, biochemical tests (BUN, creatinine, aminotransferases, and total bilirubin and bilirubin fractions) and specific IgM titers (enzyme-immunoassay with recombinant tetravalent dengue). After ten days of hospitalization and having already been in a home environment, a new clinical image emerged, characterized by dysphagia, dysphonia, weakness, peripheral facial palsy and paresthesia. The diagnosis of Guillain-Barré; Syndrome was based on clinical findings, cerebrospinal fluid examination, electrophysiological findings and the exclusion of other pathologies. Our case, as some shown in previous reports, calls attention to the possibility that Guillain-Barré; Syndrome may occur in association with dengue.

Keywords: Acute inflammatory demyelinating polyradiculoneuropathy; Dengue fever; Guillain-Barré Syndrome; Syndrome; Neurological dengue.


Este trabalho relata o caso de uma criança, sexo feminino, seis anos que desenvolveu subitamente cefaléia lancinante, febre, mialgia e paresia. Os exames de investigação clínica, que incluíram hemograma, contagem de plaquetas, dosagens bioquímicas (uréia, creatinina, transferases e billirrubina total e frações) e por títulos específicos de IgM, por enzima-imunoensaio (EIA) com antígeno tetravalente de dengue. Após dez dias de internação e já em ambiente domiciliar, novo quadro clínico surgiu caracterizado por disfagia, disfonia, paresia, paralisia facial periférica e parestesias. O diagnóstico do dengue e da Síndrome de Guillain-Barré foi baseado nos achados clínicos, no exame do líquido cefalorraquidiano, achados eletrofisiológicos e na exclusão de outras patologias. Neste caso, como em alguns relato anteriores, chama a atenção para a possibilidade de que Síndrome de Guillain-Barré pode ocorrer em associação com a dengue.




Dengue is an acute febrile infectious disease caused by arboviruses, which belongs to the Flaviviridae family and are transmitted by two species of mosquitoes, the Aedes aegypti (which is the most common) and the A. albopictus4,7. To date, four serotypes are known: (DEN-1, DEN-2, DEN-3 and DEN-4)7. According to estimates by the World Health Organization, about 80 million people become infected annually and between 2.5 and three billion people are at risk of infection in 100 countries in all continents, except Europe4,7.

Guillain-Barré Syndrome (GBS) is an acute inflammatory demyelinating polyneuroradiculopathy that often develops after infection, mainly viral infection. Cytomegalovirus, Epstein-Barr Virus and HIV are some of the viral agents associated with this neurological syndrome. Some studies call attention to the possible association between dengue and GBS8.

We report a case of a six-year-old female who developed GBS 20 days after the onset of dengue symptoms. This report was approved by the Institutional Ethics Committee and the patient's legal guardian signed a free and clear consent form written in terminology that is easy to understand.



ARN, female, six-year-old child was seen on January 2, 2011 at University Hospital with an excruciating headache, osteomioarticular pain, muscle weakness and fever. She was diagnosed with dengue fever 24 hours later and was hospitalized for ten days. The diagnosis was confirmed after clinical research examinations, which included blood count, platelet count, biochemical tests (BUN, creatinine, aminotransferases, and total bilirubin and bilirubin fractions) and by specific IgM titers (enzyme-immunoassay with recombinant tetravalent dengue) (Table 1).



On January 22, 2011, ten days after discharge, the patient began presenting dysphagia, dysphonia, vomiting and ascending paresthesia (predominantly in the distal third of the limbs). She was referred to the Pediatric Intensive Care Unit (PICU) with what appeared to be tetraparesis, peripheral facial paralysis of the right side, paralysis of eye movements and anarthria. Six days later the patient was diagnosed with GBS, based on cerebrospinal fluid examination (analysis showed lymphocytic pleocytosis with a normal glucose value and negative bacterial and fungal cultures) (Table 2), electrophysiological findings and the exclusion of other pathologies. Electrophysiology in this patient disclosed an abnormal demyelination pattern. She remained hospitalized for 20 days with medication (intravenous immunoglobulin 400 mg/kg/day per five days) and ventilatory support as well as rehabilitation. She returned to daily activities and recovered her gait patterns after two months of rehabilitation.



At the neurological examination held on May 10, 2011, residual sequelae were found. The physical examination showed tetraparesis and sensory disorders (tactile hypoesthesia, temperature and pain in the distal third of the limbs, and hypopallesthestia). The patient recovered completely from the neurologic impairment caused by the involvement of the nuclei of the cranial nerves, except for the pitch and intensity of her voice (dysphonia). The gait patterns were unchanged; however, the speed as well as the timing of the ascent and descent of stairs was affected. With exception to the patellar reflex (bilateral hyporeflexia), the remaining deep reflexes also appear unaffected. Because the patient reports instability and insecurity while walking, she was directed to continue with rehabilitation.



Dengue is the most common human arboviral infection and has been recognized as a clinical entity since 17806. During the nineteenth century, dengue was considered a sporadic disease, causing epidemics at long intervals. However, dramatic changes in this pattern occurred and currently dengue is considered the most common viral disease transmitted by mosquitoes across the globe, being endemic in 112 countries. In tropical countries, annual outbreaks have occurred since 19863.

In most cases, the disease has a self-limited course, with nonspecific symptoms such as fever, feeling ill and weakness. The most striking characteristics include intense muscle pain and retro-ocular headache, which may or may not be associated with a cutaneous rash8.

Many neurological symptoms are associated with dengue and have been recognized for over a century. The classic signs of acute infection are headache, dizziness, lightheadedness, insomnia, agitation, irritability and depression. A minority of symptoms manifests as encephalopathy. The post-infectious sequelae are mainly amnesia, dementia, manic psychosis, Reye's syndrome and meningoencephalitis3. However, most cases do not describe demyelination as a specific complication. Laboratory tests show elevated liver enzymes, leukopenia and thrombocytopenia, but these changes are not specific to dengue1.

Despite frequent and severe dengue epidemics, there have been few reported cases involving neurological complications associated with the infection of this virus. This fact can be explained because, unlike other arboviruses2, this virus rarely affects the central nervous system. The pathophysiology of these neurological complications can be explained by the occurrence of cerebral edema, cerebral hemorrhage, hyponatremia, liver failure associated with portasystemic encephalopathy, cerebral anoxia, microcapillary hemorrhage and/or the release of toxic products, which can occur separately or together9. Among the neurological manifestations that appear post-dengue, which may occur after the dengue fever and the following hemorrhagic dengue, post-infectious encephalitis, meningoencephalomyelitis, transverse myelitis, epilepsy, tremors, Bell's palsy, mononeuropathies and GBS stand out5.

GBS occurs at an incidence of between 0.6 and 1.9 per 100,000 inhabitants and is characterized by ascending flaccid paralysis, deep areflexia and sensory changes. The examination of the cerebrospinal fluid reveals an albumin-cytologic dissociation.

Some previous reports, as with our case, call attention to the possibility that GBS may occur in association with dengue3, although the mechanisms that relate to this infection are not known. However, there is evidence that this is an immune-mediated neurological disease9. The same pro-inflammatory substances that participate in the immune response to the dengue virus (tumor necrosis factor-α, complement, interleukins) also have an important role in the pathogenesis of GBS, which can establish the relationship between the two conditions5. In all previous reports, the onset of GBS occurred after the recovery of the initial infection. This fact was also observed in the patient in question.

The first report of post-dengue infection GBS in children is referred in the study of SULEKHA et al.10. The authors describe three children, all under the age of eight, who suddenly experienced ascending motor paralysis, sensory disturbances and albumin-cytological dissociation in the CSF after being infected by dengue some days before.

In 2004 CUNHA-MATTA et al.1 reported the case of a 14-year-old patient with what appeared to be ascending flaccid, areflexic tetraparesis, with electrophysiological findings consistent with GBS, beginning ten days after the classical form of dengue appeared. There was a complete functional recuperation, leaving only a deep areflexia. This recovery also occurred in our patient who, after recovery, was able to walk without support for independent daily living activities, although there were some residual sequelae.



Our case calls for special attention because the dengue infection remains a serious public health problem in many countries and yet little is known about the actual incidence of neurological complications caused by the infection of the dengue virus. Therefore, it is important to consider dengue as a possible cause of GBS.



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Correspondence to:
Eduardo Goncalves
M.D, Department of Health of Women and Children, Medical School
State University of Montes Claros - UNIMONTES
Rua Gabriel Passos 116, Apto 201
39400-112 Montes Claros, Minas Gerais, Brasil
Tel.: +55-38-8822-2575
Fax.: +55-38-3214-7775

Received: 23 May 2011
Accepted: 5 July 2011



Conflict of Interest: None

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