SUMMARY:Chikungunya, an alphavirus presenting with fever, rash, and polyarthritis, is derived from the Makonde word that means "that which bends up," in reference to the crippling manifestations of the disease. Most often it is a self-limiting febrile illness. Neurologic complications of Chikungunya infection have been reported. We are reporting the clinical and neuroimaging data in 2 patients with Chikungunya encephalomyeloradiculitis and brain autopsy findings in 1 patient. Chikungunya virus was first isolated in Calcutta, India, in 1963, 1 with several reported outbreaks in India since then. The first isolation of the disease worldwide was in 1952, following an outbreak on the Makonde Plateau. The symptoms include fever, headache, rash, and severe arthralgia. Many of these symptoms are indistinguishable from dengue fever, and simultaneous isolation of both dengue and Chikungunya from sera of patients has been reported.2 Chikungunya virus, an Old World alphavirus, is related antigenically to O'nyongnyong virus and is not known to be neurotropic. However, meningoencephalitis has been reported in outbreaks in India and the Reunion Islands. 3,4 We present the clinical, neuroimaging, and brain autopsy findings of Chikungunya encephalomyeloradiculitis, a relatively unknown and rare complication of the infection. Case Reports Case 1A 65-year-old man had low-grade fever and joint pain, which were treated with analgesics. A few days later he became drowsy. Findings of a complete blood analysis were normal. However, the patient's condition deteriorated clinically. On examination, he was semiconscious with neck rigidity, no limb movements, and an extensor plantar response. CSF analysis revealed elevated proteins, low sugars, and a few cells with lymphocyte predominance. CSF and serum were positive for immunoglobulin M (IgM) antibodies to Chikungunya virus. Intravenous methylprednisolone was administered for 5 days with 5 cycles of plasmapheresis. The patient was shifted to our hospital 45 days after the onset of symptoms. Electromyography (EMG) and nerve-conduction studies revealed acute generalized motor axonal neuropathy with no sensory component. Brain MR imaging revealed bilateral frontoparietal white matter lesions with restricted diffusion (Fig 1A), which enhanced on postcontrast T1-weighted (T1WI) fatsaturated images (Fig 1B). Spinal MR imaging revealed enhancement of the ventral cauda equina nerve roots (Fig 1C). He was administered IV dexamethasone and given supportive treatment; however, he did not improve clinically and was lost to further follow-up. Case 2A 73-year-old man had fever and joint pain, which were treated with analgesics. A few days later, he became drowsy and unresponsive with reduced limb movements. He was admitted 1 week after initial onset of symptoms. Examination revealed absent deep tendon reflexes with an extensor plantar response. CSF studies revealed increased cells (predominantly lymphocytes), elevated proteins, and low sugar. CSF and serum were positive for IgM antibodies to the Chikun...

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A study of 55 patients with heart disease suspected of being viral in origin was carried out at Medical College Hospital, Nagpur, over a period of 2years. Virus studies as well as other routine tests were carried out on all patients.In '9 patients a virus aetiology ofthe heart disease was proved by isolation ofone ofthe subtypes ofCoxsackie B vtrus and/or on the basis offourfold rise in neutralizing antibody titre inpaired sera. Ofthese patients, 5 had acute myocarditis and 5 had acute myopericarditis; 3 had acute pericarditis; 3 had congestive cardiacfailure of obscure aetiology; 2 had pleuropericarditis, and the remaining I developed post-partum heart failure with cardiogenic shock. All had electrocardiographic abnormalities. Thirteen had cardiomegaly; I had a right-sided pleural effusion and 2 had pericardial effusion. Virus could not be isolatedfrom pericardialfluid or pleuralfluid in these 3 patients.Follow-up studies up to Io weeks from discharge revealed that 8 patients were clinically normal but 4 of these 8 had persisting ST-T wave changes, and in 4 the electrocardiogram had returned to normal. Of the remaining II patients, 3 had persistent chronic heartfailure, 3 had vague symptoms ofpraecordialpain but no abnormal signs, and 5 patients were lost to follow-up.