About 15% of patients with Lyme disease develop peripheral and central nervous system involvement, often accompanied by debilitating and painful symptoms. New research indicates that inflammation plays a causal role in the array of neurologic changes associated with Lyme disease, according to a study published online on April 16, 2015 in The American Journal of Pathology. The investigators at the Tulane National Primate Research Center and Louisiana State University Health Sciences Center also showed that the anti-inflammatory drug dexamethasone prevents many of these reactions. "These results suggest that inflammation has a causal role in the pathogenesis of acute Lyme neuroborreliosis," explained Mario T. Philipp, Ph.D., Professor of Microbiology and Immunology and Chair of the Division of Bacteriology and Parasitology at Tulane National Primate Research Center (Covington, Louisiana). Lyme disease in humans results from the bite of a tick infected with the spirochete Borrelia burgdorferi (Bb). As Bb disseminates throughout the body, it can cause arthritis, carditis, and neurologic deficits. When the nervous system is involved, it is called Lyme neuroborreliosis (LNB). Clinical symptoms of LNB of the peripheral nervous system may include facial nerve palsy, neurogenic pain radiating along the back into the legs and feet, limb pain, sensory loss, or muscle weakness. Central nervous system involvement can manifest as headache, fatigue, memory loss, learning disability, depression, meningitis, and encephalopathy. To understand further the neuropathologic effects of Bb infection, researchers infected 12 rhesus macaques with live B. burgdorferi; two animals were left uninfected as controls.
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