The Sneaky Explanation Behind Increased Painful Lyme Disease Symptoms

While Lyme disease is often associated with painful symptoms, inflammation in the peripheral and central nervous systems can increase the discomfort.

Caused by a bite from a tick with spirochete Borrelia burgdorferi (Bb), Lyme disease has the potential to leave patients in debilitating situations. The illness can lead to arthritis and carditis, and when the nervous system is involved, called Lyme neuroborreliosis (LNB), it can cause muscle weakness, sensory loss, facial nerve palsy, and limb and neurogenic pain in the back, legs, and feet.

Researchers from the Tulane National Primate Research Center and Louisiana State University Health Sciences Center explored how inflammation levels in the central nervous system, spinal nerves, and dorsal root ganglia (DRG) played a role in symptom intensity.

“These results suggest that inflammation has a causal role in the pathogenesis of acute Lyme neuroborreliosis,” one of the authors Mario T. Philipp, PhD, said in a news release.

The team infected 12 rhesus macaques with Bb. They were split into 3 groups of 4 and there were 2 uninfected animals used as the control subjects. The first infected group was treated with the anti-inflammatory steroid dexamethasone, the second with the non-steroidal anti-inflammatory drug (NSAID) meloxicam, and the third were untreated. Half of each group were studied for 8 weeks and the other half for 14 weeks following the initial injection.

All of the infected animals — except for the group treated with dexamethasone – had increased cell counts, mostly made up of white blood cells, along with more of the inflammatory mediators, interleukin.

“Importantly, we found necrotizing myelitis and degeneration in the spinal cord, neurodegeneration in the dorsal root ganglia, and demyelination in the nerve roots only when lymphocytic inflammatory lesions were also observed in both the central nervous system and peripheral nervous system,” Philipp said.

These observations, documented in The American Journal of Pathology, suggested that while the meloxicam only protected the satellite glial apoptosis with a longer term of administration, the dexamethasone treatment provided protection to that as well as the neuronal apoptosis.

“Interestingly, reactions near the injection sites were histologically different from the more diffuse inflammation found along the spinal cord,” the statement noted. “The pathology found in the dorsal root ganglia and sensory nerves may explain the localized pain and motor deficits that Lyme disease patients experience close to the origin of the tick bite.”

The authors concluded that patients can experience more persistent symptoms of pain, fatigue, and cognitive dysfunction, sometimes even with treatment, when cytokine activation continues in the nervous system.