What are the epidemiology of Neuro Lyme?
The rate of Lyme disease reported to the CDC was 7.85 per 100,000 in 2005, with approximately 10% to 15% of these developing nervous system involvement.
Peak incidence is in the summer months with an endemic area in the continental United States focused in the Northeast.
What is the pathogenesis of Neuro Lyme?
The spirochete Borrelia burgdorferi is injected into the skin by the Ioxodes ricinus tick and spreads hematogenously to affect other organs.
The characteristic target-shaped erythema migrans rash appears at the site of inoculation as well as elsewhere on the body in the first few days to weeks following infection.
Meningeal irritation and other neurologic symptoms develop after several weeks to months.
What are the typical clinical features?
The most common clinical manifestations of neuro-Lyme are referred to as Garin–Bujadoux–Bannwarth syndrome , which consists of the triad of lymphocytic meningitis, cranial neuritis, and polyradiculitis.
Meningitis typically follows a longer, more subacute course than viral etiologies.
Cranial neuropathy typically affected CN VII, often bilaterally, with occasional involvement of CN III, IV, VI, and VIII. Polyradiculitis is difficult to distinguish clinically from mechanical compression and is characterized by dermatomal pain, weakness, and decreased reflexes.
How is Lyme disease diagnosed?
Two tiered serologic testing is required to diagnose Lyme disease in the serum. Patients are screened with enzyme-linked immunosorbent assay (ELISA) for anti- B. burgdorferi antibodies.
If positive, they are then tested for specific antigens by Western blot for both IgM and IgG antibodies.
CNS involvement is confirmed when a patient has a typical neurologic neuro-Lyme syndrome and when CSF analysis reveals that the relative concentration of specific antibody in the CSF exceeds that in the serum.
What is the differential diagnosis of neuro Lyme?
Neuro-Lyme disease can affect both the central and peripheral nervous system, and diagnostic considerations should be based according to presentation.
Chronic meningitis may mimic tuberculous, syphilitic, lupus, or sarcoidosis meningitis.
Cranial neuropathies typically involve the seventh nerve and may present similarly to idiopathic facial nerve palsy, Guillain–Barré syndrome, HIV, and basilar meningitides such as sarcoidosis, TB, or fungal infections.
Radiculoneuritis develops subacutely to chronically and may mimic mechanical compression of the nerve root as well as a host of other toxic, metabolic, infectious, autoimmune, paraneoplastic, and neoplastic radiculoneuropathies.
What are the expected CSF findings in neuro Lyme?
CSF findings are those of an aseptic meningitis with lymphocytic pleocytosis, typically <200 cells/μL, protein typically <150 mg/dL, and normal glucose.
How is neuro Lyme treated ?
Treatment typically consists of oral doxycycline for 2 to 4 weeks with intravenous ceftriaxone, cefotaxime, or penicillin G used in severe or refractory cases.
What are the complications of neuro Lyme?
Rarely, patients will develop inflammation of the brain parenchyma leading to acute encephalitis with MRI changes and hypermetabolism on positron emission tomography.
Patients may develop “Lyme encephalopathy” with fatigue, cognitive slowing, and memory trouble. This entity is more likely due to systemic inflammation and is not associated with irreversible brain damage.