Chikungunya encephalitis: report of a fatal case in Northeastern Brazil.

Chikungunya, a viral infection that presents with fever, rash and polyarthritis, is usually an acute febrile illness. Uncommon neurological manifestations include meningoencephalitis, encephalitis, myelitis, Guillain-Barre syndrome, myelopathy and neuropathy. During an outbreak of the disease in La Reunion Island, abnormalities were observed in the magnetic resonance imaging (MRI) of patients with encephalitis and acute disseminated encephalomyelitis, showing bilateral, frontoparietal, white matter lesions with restricted diffusion, similar to our case. We report a 57-year-old male patient with comorbidities, admitted with high fever, arthralgia, asthenia, vomiting, psychomotor agitation, behavioral changes and seizures. Cerebrospinal fluid (CSF) values revealed pleocytosis (98 cells/mm3 with 68% lymphocytes and 12% monocytes) and high levels of protein (161 mg%). Brain MRI showed hyperintense lesions in the temporal and frontal lobes and bilaterally in the posterior thalamus. CSF serology was positive for IgM antibodies to Chikungunya virus. Encephalitis due to an acute viral infection by Chikungunya was diagnosed. The patient's clinical condition worsened and he died on the twenty-fourth day of admission to our hospital.

Primary hyperparathyroidism is associated with subclinical peripheral neural alterations.

OBJECTIVE: Some case reports have suggested primary hyperparathyroidism (PHPT) and peripheral polyneuropathy (PPN) are associated; however, there are no reports of studies examining this possible relationship. The aim of this study was to evaluate peripheral nerve conduction in subjects with PHPT. METHODS: The study involved 17 patients with PHPT. Mean patient age was 60.5 ± 12.9 years, serum calcium concentration was 11.5 ± 1.0 mg/dL, and the serum parathyroid hormone (PTH) level was 315 ± 569 pg/dL. The control group comprised 17 individuals without PHPT. The mean age of controls was 60.8 ± 12.5 years and the serum calcium concentration was 9.8 ± 0.3 mg/dL. Motor and sensory nerve conduction was assessed by electroneurography (ENG). RESULTS: The following ENG parameters differed significantly between the PHPT and control groups: right (R) sural sensory nerve action potential conduction velocity (52.7 ± 6.3 m/s versus 58.0 ± 8.0 m/s; P = .041); R median compound muscle action potential (CMAP) amplitude (7.4 ± 1.6 mV versus 8.9 ± 1.7 mV; P = .002); R median CMAP latency (4.3 ± 1.2 ms versus 3.6 ± 0.6 ms; P = .032); R tibial CMAP latency (4.2 ± 1.1 ms versus 3.3 ± 0.4 ms; P = .001). The neurological examination was normal in all patients. CONCLUSION: Our data demonstrate an association between PHPT and peripheral neurological alterations, consistent with subclinical sensory-motor PPN.