This case highlights 2 interesting points. Firstly, the rare complication of parkinsonism following dengue virus infection. Secondly, the extensive post-infectious neurological manifestations in a previously well young man with no history of chronic illness. We aim to address these issues in the next few paragraphs in turn.
The family Flaviviridae has been known to cause muscle weakness. Poliomyelitis-like weakness has been associated with Japanese encephalitis virus infection and West Nile virus infection [4, 5]. To our knowledge, our patient is only the second reported case of dengue-fever associated brachial plexopathy .
Acute cerebellar ataxia is quite common following a viral infection; Varicella Zoster virus, Mumps virus and Epstein-Barr virus being the common culprits . Cerebellar ataxia following dengue fever is less commonly reported .
Virus as the etiological agent for parkinsonism is not a novel concept. Von Economo first described seven patients presenting with parkinsonism, somnolence and diplopia; almost all had at least one cranial nerve involvement . Although now a topic of much debate, initially the trigger was thought to be the influenza virus.
We feel that our patient developed features of parkinsonism as a post-infectious immune-mediated consequence of dengue fever. NS1 antigen has been shown to have a 93.4% sensitivity rate and 100% specificity rate in diagnosing acute dengue fever . The diagnosis was further confirmed by the subsequent positive IgM and IgG for dengue antibodies in the serum. An acute parkinsonian syndrome has been described following Japanese Encephalitis virus and West Nile virus infection, but to our knowledge, our patient represents the first case of acute parkinsonian syndrome afflicting a patient following a dengue infection [11, 12].
The absence of the dengue virus in the cerebrospinal fluid of our patient highlights an important point, and suggests that the mechanism by which the virus is causing the symptoms is not via a direct neurotropic effect . There have been previous reports of viral encephalitis with no evidence of the virus apart from the presence of oligoclonal bands in the cerebrospinal fluid, suggesting an immune-mediated mechanism [14, 15]. We did not test for oligoclonal bands but there was evidence of pleocytosis in the cerebrospinal fluid of our patient.
The absence of any abnormal findings on brain MRI scan further reinforces this hypothesis. Cranial neuropathy arising from post-infectious immune mediated dengue fever with normal brain MRI findings have been previously reported .
Although the phenomenology of viral parkinsonism may share similar characteristics with idiopathic Parkinson’s disease, it is unlikely that the pathophysiology is due to abnormal Lewy body and neurofibrillary tangle deposition in brain tissue . The usual anti-parkinson’s medication such as levodopa and dopamine agonist may not be as effective. Indeed, as our case demonstrates, there is a role for immunosuppression with methylprednisolone in selected patients.
Our patient developed quite extensive neurological symptoms involving the extra-pyramidal system, cranial and peripheral nerves. The patient was an otherwise fit young man with no history of chronic illness, apart from having chicken pox 3 months earlier. Although remote, the possibility of varicella zoster virus playing a role in the subsequent neurological complication of dengue fever should not be dismissed out of hand.
One-way to explain this unusual phenomenon is the ‘double-hit’ hypothesis. It is known that influenza virus has the capability to prime the innate CNS immune system . If varicella zoster virus has the same capability in up-regulating the CNS immune system, a ‘second-hit’ in the form of dengue fever may explain why our patient was afflicted with such diverse neurological manifestation, namely, parkinsonism, multiple cranial neuropathies, cerebellar ataxia and plexopathy.