What happens to the brain during acute Lyme neuroborreliosis?
A group of researchers from Tulane National Primate Research Center in Louisiana have found that inflammation plays a “causal role” in the pathogenesis of acute Lyme neuroborreliosis.
Individuals diagnosed with Lyme neuroborreliosis typically suffer from headaches, fatigue, memory loss, learning disabilities, and depression. Clinical findings have included meningitis, cranial neuritis, radiculoneuritis, encephalopathy, encephalitis, encephalomyelitis, radiculitis, radiculoneuritis, mononeuropathies, plexopathies, and demyelinating neuropathies.
Dr. Mario T. Philipp and colleagues at the Tulane National Primate Research Center launched an investigation to examine the role of inflammation on the central nervous system of subjects infected with Borrelia burgdorferi (Bb). Rhesus monkeys were injected with live Bb spirochete. Several monkeys received a potent steroid prior to being injected with the spirochete, while another group was pretreated with a non-steroidal (NSAID) medicine.
The NSAID and control group experienced extensive neurologic damage. The cerebrospinal fluid revealed significantly elevated levels of IL-6, IL-8, chemokine ligand 2, and CXCL13 and pleocytosis in the monkeys, according to a study published in The American Journal of Pathology. Additional pathological changes included:
- Leptomeningitis (meningitis)
- Vasculitis (inflammation of blood vessels in the brain)
- Focal inflammation in the central nervous system
- Necrotizing focal myelitis in the cervical spinal cord
- Radiculitis (pain that radiates along the nerve due to inflammation on the nerve root at its connection to the spinal column)
- Neuritis (inflammation of the nerves)
- Demyelination in the spinal roots (erosion of the myelin sheath that normally protects nerve fibers)
- Inflammation with neurodegeneration in the dorsal root ganglia (Inflammation and progressive loss of structure or function of neurons in the dorsal root ganglia, or spinal ganglion. The dorsal root ganglion contains the cell bodies of sensory neurons that bring information from the periphery to the spinal cord.)
- Neuronal and satellite glial cell apoptosis
- Persistent abnormal F-wave chrono dispersions localized to the nerve roots, suggesting damage to axons or demyelination, that were similar to several inflammatory demyelinating peripheral neuropathic disorders, including Guillain-Barré. (Guillain-Barre syndrome is a rare disorder in which your body’s immune system attacks your nerves.)
However, there were no inflammation in the central nervous system of the monkeys that were pretreated with the potent steroid, dexamethasone.
While the monkey study provides insight into the benefits steroids can play when inflammation is present, it’s also important for clinicians to keep in mind the risks steroids can pose to patients with Lyme disease, as steroids can weaken an already overtaxed immune system.
Clinicians should not prescribe steroids to patients suspected of having Lyme disease, based on this primate study. Unfortunately, pretreatment with the non-steroidal medicine was not effective. Researchers and clinicians must continue to search out ways to control the immune response to Lyme disease without exposing patients to steroids.